2

INTRODUCTION

This booklet is designed to provide you with a better understanding of all the
core surgical topics that you’ll encounter throughout the “Surgery 351” course. The aim
of this booklet was to create a single study source that is concise, yet covers the breadth
of the course’s topics, which will help you make the most of this course, and prepare you
for the corresponding examinations. The content of this booklet is based on the “Surgery
351” course outline. It is a compilation of lecture notes provided by the faculty members
to students throughout the year, handouts and notes provided by former students, and
further explanations obtained from books.

Features include:
 All chapters are color-coded according to theme, with a structured layout for all
topics.
 Includes all topics covered in “Surgery 351” course for the year 2012/2013.
 Free space on the right margin of each page that allows you to add
comments/notes of your own.
 Different symbols have been used throughout this booklet:
a. Frequently tested high-yield facts noted by 
b. Extra notes for further explanation noted by 
c. OSCE hints noted by 
d. Clinical case 
 MCQs section after each topic serves as a self-assessment tool for you to test your
knowledge
 Margin boxes highlight important notes and provide further explanations
 Illustrations, tables, and clinical images to enhance understanding
 Available in softcopy and hardcopy

We hope that you find this booklet useful, and we wish you good luck in all of your future
medical endeavors. We also value your feedback and would like to hear from you if you
have any general suggestions or any corrections for any errors that may have crept in.

2
 3

CONTRIBUTORS

Ismail Raslan

Badra'a Muharib Roa Alsajjan

Mohammed Alrasheed Mohammed Bohlega
Aliya Alawaji Leena Alshaman
Sara Alsukait Hadeel Alsajjan
Layan Akkielah Aos Aboabat

Design & format editing: Cover art by:

Roa Alsajjan Sarah Mahasin
Hadeel Alsajjan

3
4

ACKNOWLEDGEMENT
Thanks to all of those who contributed to 429 surgery team & 430 surgery
team:

Reham Alhenaki Nouf Saati

Sarah Bin Hussain Rafif Mattar
Nourhan El Shamma' Abdullah Alaogayil
Eman Alrashidi Fatima Alkhashram
Shoog Alaqeel Bedoor Alqadrah
Nouf Alzendi Suhail Asiri
Abdulmajeed Al-Sadhan Dona Barakah
Rana Al-Khelaif Suhaib Almasry
Amira Al-Jaber Mashael Al-Towairqi
Albatool Al-Ammari Afnan Al-Tamimi
Manahel Al-Ansari Noura Al-Syefi
Morooj Allabban Maha Al-Balharith
Sultan Al-Salem Sara Mahasin
Hamda Bawazeer Mohammed Al Watban

Maysoon Alhaizan Alaa AlSaad

Jawaher AlAskar Ruah AlYamany

Special thanks to 428 and 427 surgery teams

4
 5

CONTENTS

Introduction 2
Contributors 3
Acknowledgement 4
Contents 5
Section I: Introduction to Surgery
Burns and Wound Healing…………………………………………………………….. 7
Shock…………………………………………………………………………………………… 18
IV Fluids………………………………………………………………………………………. 31
Blood Products…………………………………………………………………………….. 47
Nutrition………………………………………………………………………………………. 56
Complications of Surgery………………………………………………………………. 61
Surgical Infections………………………………………………………………………… 67
Sterilization…………………………………………………………………………………... 75
Principles of Surgical Oncology……………………………………………………… 85
Section II: Cardiothoracic Surgery
Cardiac Surgical Disease………………………………………………………………... 93
Thoracic Disease…………………………………………………………………………… 101
Section III: Urology
Pediatric Urology………………………………………………………………………….. 113
Adult Urological Disorders…………………………………………………………….. 123
Emergencies in Urology………………………………………………………………… 134
Genitourinary Oncology………………………………………………………………… 149
Section IV: Pediatric Surgery
Acute Abdomen in Children…………………………………………………………… 161
Inguinoscrotal Conditions……………………………………………………………… 165
Section V: General Surgery/Gastroenterology
Acute Abdomen……………………………………………………………………………. 174
Esophageal Diseases……………………………………………………………………... 181
Gastric & Duodenal Diseases…………………………………………………………. 203
Inflammatory Bowel Disease………………………………………………………… 210
Anorectal Conditions…………………………………………………………………….. 217
Colorectal Cancer…………………………………………………………………………. 229
Cholelithiasis………………………………………………………………………………... 238
Portal HTN…………………………………………………………………………………… 249
Pancreatic Disease………………………………………………………………………... 255
Section VI: General Surgery
Superficial Lumps…………………………………………………………………………. 263
Hernias…………………………………………………………………………………………. 271

5
6

Section VII: General Surgery/Trauma Surgery

Introduction…………………………………………………………………………………. 287
ATLS…………………………………………………………………………………………….. 297
Abdominal Trauma……………………………………………………………………….. 307
Section VIII: Neurosurgery
Raised ICP…………………………………………………………………………………….. 318
Congenital Neurosurgical Diseases………………………………………………… 330
Section IX: Endocrine Surgery
Common Neck Swellings……………………………………………………………….. 345
Breast Diseases……………………………………………………………………………... 352
Adrenal Diseases…………………………………………………………………………… 371
Section X: Vascular Surgery
Venous Disease……………………………………………………………………………... 382
Atherosclerosis……………………………………………………………………………... 392
Vascular Investigations…………………………………………………………………. 399
Section XI: Plastic Surgery
Peripheral Nerve Injuries………………………………………………………………. 412
Hand Injuries………………………………………………………………………………… 423
Skin Tumors…………………………………………………………………………………. 438

6
 Introduction 1

BURNS AND WOUND HEALING

1 INTRODUCTION Skin appendages
examples:
1.1 SKIN FUNCTION  Sebaceous
Glands
 Body Covering  Sweat Glands
 Permit movement of underlying muscles & joint  Hair Follicles
 Sensors for touch, pain, and temperature  Nails
 Vitamin D production
 Temperature regulation
o Sweating, blood flow
 Sun protection
o Detoxification/activation of drugs and chemicals
 Immuno-surveillance
o Langerhans cells, t-lymphocytes
1.2 SKIN LAYERS

 Epidermis
o Outer layer contains the stratum corneum
o The rate limiting step in dermal or percutaneous absorption is
diffusion through the epidermis
 Dermis (Appendages)
o Much thicker than epidermis
o True skin & is the main natural protection against trauma
o Contains
- Sweat glands
- Sebaceous glands
- Blood vessels
- Hair
- Nails
 Subcutaneous Layer (Fat)
o Contains the fatty tissues which cushion & insulate

7
2 Burns and wound healing

2 BURNS  We can classify

burns according to the
2.1 CAUSES OF DEATH cause:
Thermal, chemical,
 Smoke inhalation, sepsis, pneumonia, shock electrical and friction
o More common in elderly injuries
o (Age + BSA= %mortality)
o most with>70% die
2.2 RISK FACTORS FOR DEATH:
 > 40% BSA (Body Surface Area),
 > 60 years
 Inhalation injury

2.3 PATHOPHYSIOLOGY OF BURNS Zones of Injury

 Dynamic injuries Our aim after a burn
o Cellular damage at >45° C injury at the zone of
o Dependent on temperature and duration stasis has occurred is to
direct it towards the zone
 Three zones of injury of hyperemia and away
o Central necrosis from the possibility of
o Zone of stasis (at risk of necrosis) necrosis.
o Zone of hyperemia
 Thermal injury triggers intense inflammatory response SIRS
o Initial release of histamine, bradykinin
o Release of prostanoids, free radicals, proteases
 Leading to:
o Hypermetabolism. Sepsis is one of the
o Bacterial translocation. major causes of death in
burn patients
o MOF. (Multi-organ failure)

 Central Zone Of We can classify burns

Necrosis according to the cause:
Irreversible Thermal, chemical,
 Intermediate Zone Of electrical, friction injuries
Stasis
Reversible (The
damage is not enough
to be irreversible)
 Outer Zone Of
Hyperemia
Inflammatory response,
vasodilatation

8
 Burns 3

Examples:

st
Sun burn 1
degree burn
 Spilled hot water
nd
mostly cause 2
degree
 Flame burn
rd
mostly cause 3
degree

Superficial Deep Second Third Degree

Second Degree
Burns Degree Burns Burns
• Epidermis and the • Epidermis and most of • All Skin Layers
upper dermis the Dermis • Severe scarring
• Usually no scarring • Lead to scarring • Painless
• Severe Pain • Less Pain (Due to nerve • Whitish of Black in color
• Blanches with pressure damage) • Thrombosed vessels/No
• Pinkish in color • Doesn't blanch with blood flow
• Small Blisters pressure • Skin feels like leather
• Treatment --> • Whitish or Cherry Red • Eschar formation
Flamazine • Larger Blisters --> (Needs Escharotomy)
Sometimes with • Treatment --> Surgery
Hemorrhage and Skin grafing
• Treatment --> Surgical

 Compartment Syndrome:
 Is the compression of nerves, blood
vessels, and muscle inside a closed
space (compartment) within the
body.
 This leads to tissue death from lack
of oxygenation due to the blood
vessels being compressed by the
raised pressure within the
compartment.
 You must always look for
circumferential burns around the
chest, abdomen, limbs, etc… and
perform an Escharotomy to release
the pressure

9
4 Burns and wound healing

2.4 DETERMINING EXTENT OF INJURY Blisters are always

seen in second degree
 Burn extent determines therapy and prognosis burns
 Burn size estimate is often inaccurate
 Extent of injury described using percentage of total body surface area that is
burned (TBSA)
 For patients > 9 “rule of nines” may be used
 For small burns, the patient’s palm covers 1%
 With young children proportions differ
2.5 EVALUATION OF BURNS

 Look for circumferential burns to chest, neck and limbs that may
compromise ventilation or circulation
 Loss of distal pulses late
 Assess for warmth, sensation, motor, rigidity
 Doppler exam is helpful
 Identify potential abuse  (Mostly suspected if the patient is a child or an elderly,
check if the story matches the burns type and sit)
 Well circumscribed, feet, ankles, buttocks

Once the burn injury is more than 30% of the body surface area the
inflammatory response will be systemic
 (SIRS: Systemic Inflammatory Response Syndrome)
 There will be systemic vasodilatation,
 Fluid will shift from the intravascular space to the extra vascular space  How do we
 Which leads to hypo-perfusion to vital organs such as the kidneys; causing calculate the surface
renal failure. area?
 Hypo-perfusion to the intestines may happen causing Intestinal ischemia
 Bacteria will shift into the blood stream (Bacterial Translocation)  Leading to By using the rule of nine
for normal sized adults
sepsis (un-managed will lead to death).
(The body is divided into
9 areas) as the
Following:
Adults
  All lower limbs 18%
(9%front 9% back)
 All upper limbs 9%
 trunk: anterior 18%
posterior 18%
 Head and neck 9%
Kids
 Head & neck: 18%
 Each Lower Limb:
4%
 Or by using the
Lund-Browder chart
How can we calculate
scattered burns?
 The palm of the
patient is 1%, use it
for measurement.

10
 Inhalation Injury 5

3 INHALATION INJURY What to do in the

ER:
3.1 SMOKE INHALATION 1. ABC (A= Air way, B=
breathing, C=
 Carbon Monoxide Poisoning Circulation)
o CO has stronger affinity for HGB than O2 2. Take detailed history
3. IV access
 Signs of CO poisoning: 4. Blood test
o Confusion, dizziness, HA, NV, flushed skin 5. Allergy (mainly to
o Treatment 100% FiO2 sulfa because
 Upper Airway Obstruction Flamazine contains
it)
o Common in head and neck burns and smoke inhalation
6. Quick general exam
o Edema continues at least 24 hours 7. Estimate the
o Protect airway with intubation percentage and
o Edema usually decreases by post burn day 3 depth of the burn.
 Pulmonary Injury from Chemical Inhalation
o Develops ARDS within 24 hours post injury
o Pneumonia may occur as late as post burn day 10
 Inflammation and systemic reactions
 Poisoning: When fire affects furniture (flame burn in closed space)
Toxins get released into the air  inhaling these toxins affects the
lungs directly causing" inflammation pneumonitis" and later
pneumonia. There could also be systemic poisoning due to inhaled
fumes like Cyanide

11
6 Burns and wound healing

4 FLUID RESUSCITATION

 Hypovolemia was major cause of death

 Massive transudation of fluids from vessels due to increased permeability
 Edema intensifies over 8-48 hours
 Goal: preservation of organ perfusion and urine output

How much IV fluids should we give a burn patient? (If needed)

 PARKLAND formula (crystalloid)  most common
 4cc X (% of burn) X weight of patient = total amount of fluid needed in 24 hrs
 Half of the amount calculated is given in first 8 hrs, the other half is to be given in
the next 16 hrs (start counting from the time of burn NOT when you see the
patient in the ER).

5 ELECTRICAL BURNS

 4th degree if the current passes through the body

 Caused by passage of electric current
 Damage increased in small bony areas
o Fingers, feet, lower legs, forearm
 Systemic effects
o Low voltage (<1000 V) (May cause arrhythmias)
o High voltage (>1000 V): Massive tissue damage, respiratory and
cardiac arrest
 ECG, CPK, UA, monitor
 Local care often necessitates grafting and amputation
 Electrical burns are the only type of burns that have an entry and exit point.
 They may be minimal on the surface; we should check the muscles and bones for
any injuries.
 Damage mostly affects the small bones (feet, hands, and forearms)
 Damage is due to resistance which generates heat, that’s why it’s common in small
bones (Because bones have the highest resistance in the body)

12
 Chemical Burns 7

6 CHEMICAL BURNS
Types of Chemical
 4th degree if it reaches the fat and muscle Burns:
1- Acids: cause
 Delayed and progressive injury coagulation and regular
 Deceptively superficial at first burn necrosis and will
 Acid more limited (coagulation necrosis) stop at that level
(limited).
 Alkalis more destructive (liquefaction) 2- Alkaline: “worse"
 HFl: significant necrosis, arrhythmias (Worst chemical burn because it causes liquefaction that
has both mechanisms of acid and alkaline. It burns like an acid because it is may continue for hours
an acid and when the fluoride (alkaline) is released it reaches the bone and after the injury (deep)
causes decalcification leading to hypocalcaemia and arrhythmias)
 Hypo Calcemia
 Removal of causative agent
 Brush off metals and powders
 Copious irrigation with water
7 WOUND HEALING (THREE PHASES)

 Wound: a disruption of normal anatomic relations as a result of injury

intentional or unintentional. Regardless of causation or tissue type, wound
healing presents with identical biochemical and physiologic processes,
though wound healing may vary in timing and intensity.

7.1 INFLAMMATORY PHASE Neutrophils are

the first cells to arrive
 Substrate or reactive phase, immediate at the site of injury
o Typically days 1-10
 Response to limit and prevent further injury, inflammation, hemostasis,
sealing surface, removing necrotic tissue and debris, migration of cells
into wound by chemotaxis, cytokines, and growth factors
 Initial intense local vasoconstriction of arterioles and capillaries followed
by vasodilation and vascular permeability
 Tissue injury & blood vessel damage

13
8 Burns and wound healing

 Exposure of subendothelial collagen to platelets and vWF activates the

coagulation pathway
 Plugging: Platelet and fibrin
 Provisional matrix:
o Platelets, fibrin, and fibronectin
 Platelet aggregation:
o Thromboxane (vasoconstrict), thrombin, platelet factor 4
7.1.1 PLATELETS
 Alpha granules contain:
o Platelet factor 4: aggregation
o Beta-thrombomodulin: binds thrombin
o PDGF: chemoattractant
o TGF-beta: key component tissue repair
 Dense granules contain vasoactive substances: adenosine, serotonin, and
calcium
 Other factors released: TXA, Platelet activate factor, Transform. growth
factor alpha, Fibroblast growth factor, Beta lysin (antimicrobial), PGE2 and
PGI2 (vasodilate) and PGF2 (vasoconstrict).
7.1.2 POLYMORPHONUCLEAR CELLS
 Chemotoxins attract after extravasation
 Migrate through the ECM by transient interaction with integrins
 PMNs scavenge, present antigens, provide cytotoxicity-free radicals
(H2O2)
 Migration PMNs stops with wound contamination control usually a few
days
 Persistent contaminant: continuous influx PMN’s and tissue destruction,
necrosis, abscess, & systemic infection
 PMNs are not essential to wound healing
7.1.3 MACROPHAGES
 Macrophages are
 Necessary the most important cells
 Monocytes migrate & activate: Macrophages in the inflammatory
 Appear when PMN’s disappear 24-48 hr phase of wound healing
 Do the same activities as PMN’s
 Plus orchestrate release of enzymes (collagenase, elastase), PGE’s,
cytokines (IL-1, TNF alpha, IFN ), growth factors (TGF & PDGF), and
fibronectin (scaffold/anchor for fibroblasts)
 Activate fibroblasts, endothelial and epithelial cells to form Granulation
Tissue
7.2 PROLIFERATIVE PHASE The Proliferative
phase depends on
 Regenerative or Reparative Fibroblasts.
o day 5 to 3 weeks
 Angiogenesis: endothelial cells activate & degrade basement membrane,
migrate, and divide to form more tubules
 Granulation Tissue: capillary ingrowth, collagen, Macrophages,
Fibroblasts, Hyaluronic acid (GAG)

14
 Abnormalities 9

7.2.1 FIBROBLASTS
 Differentiate from resting mesenchymal cells in connective tissue 3-5 days
migrate from wound edge
 Fibroplasia: Fibroblasts proliferate replace fibronectin-fibrin with collagen
contribute ECM  The most common
collagen type in normal
7.2.2 COLLAGEN woundless skin is
type1 followed by type 2
 Type III predominant collagen synthesis days 1 to 2
 Type I days 3 to 4 The most common type
in wounded (scarred)
 Type III replaced by Type I in 3 weeks skin is type 3

7.2.3 WOUND STRENGTH

 Week 6 = 60% original, 80% final strength
 Week 8 to 1 year ≈ 80% original (Max)
 Net Collagen = 6 weeks amount stays the same but cont. crosslink increase  Granulation tissue
strength = maturation contains:
I 80% of skin Capillary ingrowths,
Most Common: skin, bone, tendon. Primary type in wound healing. Collagen, Macrophages,
Fibroblasts, Hyaluronic
II Cartilage acid (GAG)
III 20% of skin
Increased Ratio in healing wound, also blood vessels and skin
IV Basement Membrane
V Widespread, particularly in the cornea

7.3 MATURATIONAL PHASE

 Remodeling of wound 3 week-1+year

 Type I replaces Type III Collagen: net amount doesn’t change after 6
weeks, organization & cross-linking
 Decreased vascularity, less fibroblasts & hyaluronic acid
 Peripheral nerves regenerate at 1mm/day
 Accelerated Wound Healing: reopening results in quicker healing 2nd time
around
 Contraction: centripetal movement of the whole thickness of surrounding
skin reducing scar
 Myofibroblasts: special Fibroblasts express smooth muscle and bundles of
actin connected through cellular fibronexus to ECM fibronectin,
communicate via gap junctions to pull edges of the wound
8 ABNORMALITIES
When burn-caused
contractions affect the
 Contracture (A minimization for wound’s size due to function of a joint it is
Myofibroblasts) called a Contracture
o The physical constriction or limitation of function as the result of  Most common sites:
Contraction (scars across joints, mouth, eyelid) Perineum and Trunk,
 Keloids: Beyond the Borders then Head and neck,
then Extremities.
o Excess deposition of collagen causes scar growth beyond the
border of the Original wound

15
10 Burns and wound healing

o Tx: XRT, steroids, silicone sheeting, pressure, excise, often

Refractory to Tx & but not preventable.
o Occur in specific areas such as: earlobes and sternum
 Hypertrophic Scar: confined within
o Excess collagen deposit causing raised scar remains within the
original wound confined
o Darker pigmented skin & flexor surfaces of upper torso
o Often occurs in burns or wounds that take a long time to heal,
sometimes preventable
o Can regress spontaneously
o Tx: steroids, silicone, pressure garments
o Surgical excision makes it worse
9 IMPEDIMENTS TO WOUND HEALING

 Bacteria>105/cm2 : Decreased O2 content, collagen lysis, prolonged

inflammation
 Devitalized Tissue & Foreign Body: Retards Granulation Tissue formation
and healing
 Cytotoxic drugs: 5FU, MTX, Cyclosporine, FK-506 can impair wound
healing. D-Penicillamine- inhibit collagen x-linking
 Chemotherapy: no effect after 14 days
 Radiation: Collagen synthesis abnormal, fibrosis of vessel
 Diabetes: impedes the early phase response
 Malnourishment: Albumin<3.0, Vit-C
 Smoking: vasoconstriction, atherosclerosis, carboxyhemoglobin, decreased
O2 delivery
 Steroids: inhibit macrophages, PMNs, Fibroblast collagen synthesis,
cytokines, and decreased wound tensile strength
 Vit A (25,000 IU QD) counteracts effect of steroids
 DENERVATION has NO EFFECT on Wound Healing
10 DISEASES ASSOC WITH ABNORMAL WOUND HEALING

 Osteogenesis Imperfecta: Type I Collagen defect

 Ehler-Danlos syndrome: Collagen disorder, 10 types
 Marfan Syndrome: fibrillin defect (collagen)
 Epidermolysis Bullosa: Excess fibroblasts Tx: phenytoin
 Scurvy: Vit C req. for proline hydroxylation

16
 MCQs 11

11 MCQS
1. Which type of Collagen is the primary type in wound healing
A. Type 1
B. Type 2
C. Type 3
D. Type 4

2. Platelet secretes ____ in vasoconstriction phase:

A. Collagen
B. ILKs
C. Thromboxane
D. Neutrophils

Answer Key  1A, 2C

17
 Objectives 1

SHOCK
1 OBJECTIVES

 To understand Physiology of sustaining blood pressure.

 To learn about the classifications of shock.
 To understand the consequences of the natural history of shock.
 To be able to diagnose and plan appropriate treatments for different types of
shock.
2 BLOOD PRESSURE REGUL ATION

Changes in many elements regulate BP and perfusion: 


1. Intravascular volume
2. Heart
3. Arteriolar bed
4. Capillary exchange network
5. Venules
6. Venous capacitance circuit
7. Large vessel patency
2.1 PERIPHERAL RESISTANCE

Figure 1

 Decreased peripheral resistance:

o Decreased arterial blood pressure (MAP = CO X PR)
 Increased peripheral resistance
o Decreased venous return 

o Decreased EDV

o Decreased SV

o Decreased CO (CO = HR X SV)

o Decreased arterial blood pressure (MAP=CO X PR)

Heart Rate X Stroke Volume ( intravascular volume,  EDV) = Cardiac Output

Cardiac Output X Peripheral Resistance = Arterial Pressure

18
2 Shock

CARDIAC OUTPUT ARTERIAL PRESSURE

Figure 2

2.2 EFFECTS OF INTRAVASCULAR VOLUME ON BP & PERFUSION  What maintains

blood pressure in our
 Alters mean blood pressure system and arteries is
o Decrease in intravascular volume=decreased BP the heart.
 Alters venous return to the heart
o Decrease in intravascular volume=
o Decreased venous return=

o Decreased end diastolic volume
o CO = HR x SV
o COXSVR=MAP

 How can intravascular volume be lost?
o Examples:
 Bleeding

 Failure to rehydrate

 Loss of third space fluids (sweating)
2.3 EFFECTS OF CARDIAC FUNCTION ON BP & PERFUSION CO = HR x SV

 Cardiac output is the result of: Bradycardia

o Heart rate MI (pump failure)
o Contractility Vasodilation: decreased
end-diastolic volume
o Loading conditions

 Examples of changes that can alter cardiac output:
o Heart rate (bradycardia or tachycardia)

o Contractility (MI or cardiomyopathy) i.e. pump failure

o Load (histamine release: vasodilation
2.4 EFFECTS OF THE RESISTANCE CIRCUIT (ARTERIOLAR BED)
ON BP & PERFUSION

 Decreases in arteriolar tone produce:

o Hypotension


19
 Blood Pressure Regulation 3

o Decreased perfusion to vital organs

 Increases in tone will prevent optimal cardiac performance (increased
afterload=decreased contractility)  What determine the
BP in the arterioles?
- Increase in the
 Further explanation: permeability and the
The heart delivers blood to all organs by the same mean arterial pressure. Because of
oncotic pressure.
that, the width of the arterioals is what determines blood flow to each organ. Arterioles
Oncotic pressure will
dilate and contract to alter their vascular radius depending on each organs requirement.
increase due to the
Arteriolar tone can be modulated by are regulated by complex substances and
presence of proteins in
mechanisms, but the most are:
the blood vessel which
 Vasoconstrictors:
lead to fluid shift from
1. Sympathatic tone extravascular to
2. Vassopressin intravascular space,
3. Endothelin leading to volume
 Vasodilators: expansion, this
1. Decreased organ perfusion physiological process
2. Nitric Oxide (NO) can be disturbed in case
3. Any decrease in inherits vasoconstriction regularly provided by the myogenic of sepsis, trauma or
activity and sympathetic stimulation. systemic inflammatory
response (SIR)
What is oncotic
pressure?
2.5 EFFECTS OF THE CAPILLARY EXCHANGE NETWORK ON BP & - It is the osmotic
PERFUSION pressure, which result
from the presence of
 Largest area of the vascular tree proteins in the blood
vessel.
 Site of exchange of nutrients, electrolytes and fluids
 Alterations in microvascular integrity (e.g., capillary leak syndrome) result in
loss of intravascular volume
 Blockage of or shunting away from small vessels leads to decreased tissue
perfusion
2.6 EFFECTS OF THE VENOUS CAPACITANCE CIRCUIT ON BP &
PERFUSION

 Portion of the circulatory system contains 80% of the intravascular volume


 Decrease in effective circulating blood volume and MAP caused by:
o Decreases in venous tone

o Increases in venous vascular capacitance

NORMAL INCREASED VENOUS CAPACITANCE

Decreased effective blood volume
Decreased MAP
Figure 3

20
4 Shock

2.7 EFFECTS OF LARGE VESSEL PATENCY ON BP & PERFUSION

 Obstruction of the systemic or pulmonic circuit will decrease ventricular

ejection and systemic perfusion
 Venous obstruction will decrease venous return
 Examples of obstructive shock:
o Massive pulmonary embolism
o Venous occlusion
VENOUS OBSTRUCTION Decreased effective blood volume,
Decreased MAP

Figure 4

3 SHOCK:

 Definition: It is the state of altered tissue perfusion severe enough to induce

derangements in normal cellular metabolic function. In short: low perfusion
that causes tissue hypoxia.
3.1 TYPES OF SHOCK:

o  More than one type may be present!

Type of Shock Clinical Causes Primary mechanism
1. Hypovolemic Volume loss Exogenous blood, plasma, fluid
or electrolyte loss
2. Cardiogenic Pump failure Myocardial infarction, cardiac
arrhythmias, heart failure
3. Distributive "shock that will  venous Septic shock, spinal shock,
result in vasodilatation > capacitance or autonomic blockade, drug
vasodilatation or leak > lead to arteriovenous overdose
the movement of the blood shunting “Neuorogenic, anaphylactic,
outside the vessel > decrease the septic"
end diastolic volume."
4. Obstructive Extra-cardiac Vena caval obstruction, cardiac
obstruction of tamponade, pulmonary
blood flow embolism, aortic compression or
dissection

3.2 SIGNS AND SYMPTOMS:

Clinical signs and symptoms of shock relate to decreased organ perfusion:

21
 SHOCK: 5

o Mental status changes: decreased cerebral perfusion

o Decreased urine output: decreased renal perfusion

o Cold clammy extremities:
 Decreased perfusion to the skin due to diverted blood flow
o EKG changes:
a. May indicate myocardial ischemia

b. May be primary event (cardiogenic shock) or due to decreased
myocardial perfusion due to shock from other causes
3.2.1 HEMODYNAMIC PARAMETERS THAT MAY INDICATE SHOCK:
 Heart rate: Initial tachycardia (attempt to increase CO)
 Rhythm: Regular and tachycardic
 Blood pressure: Low
 Cardiac output: Usually low
3.3 EFFECTS OF SHOCK AT THE ORGAN LEVEL   What happens to
the lung in systemic
inflammatory
 Kidney: Oliguric renal failure response (SIR)?
 Lung: Capillary leak associated with or caused by sepsis and infection Answer: ARDS (adult
 GI tract: Failure of intestinal barrier (sepsis, bleeding) respiratory distress
syndrome)
 Liver: Liver failure, which is a rare cause.
 What is ARDS?
Answer: it is a systemic
3.4 HEMODYNAMIC RESPONSE TO SHOCK: release of inflammatory
mediators, causing
 Mechanisms for restoring cardiovascular homeostasis inflammation,
1) Redistribution of blood flow: Attempt to preserve perfusion to vital hypoxemia and
organs frequently multiple
organ failure. And it may
2) Augmentation of cardiac output: Increased heart rate
Increased accompany many
peripheral resistance conditions, but most
3) Restoration of intravascular volume importantly: sepsis,
pancreatitis, and severe
3.4.1 REDISTRIBUTION OF BLOOD FLOW traumatic injury.

 The organ that will

contribute in
responding to shock
is the kidney, how?
- The kidneys are part of
the solution not the
problem when the body
responds to shock; it will
retain salt that will
( Because they are important for
catecholamine) maintain intravascular
volume.
Figure 5

22
6 Shock

Figure 6

4 TYPES OF SHOCK  How do you know if

it is cardiogenic or not?
4.1 CARDIOGENIC SHOCK: 1. SOB

2. Rest JVP?
 Caused by the progressive loss of myocardium 3. Lower limb edema
 Usually due to an acute myocardial infarction
 When the total amount of myocardium affected reaches a critical point,
myocardial function begins to deteriorate
 While stroke volume decreases, the heart rate increases in an effort to
maintain cardiac output (CO = SV x HR)
 But increased HR is limited and CO falls to levels that are inadequate to
support end-organ function
 Coronary perfusion decreases and this in turn causes progressive myocardial

ischemia with progression of myocardial injury

4.1.1 DECREASED CARDIAC FUNCTION

 -In cardiogenic
 Decreased ventricular function shock the volume is not
o Myocardial infarction the problem.
-The only shock that you
o Pericaridal tamponade
 DON’T give fluid is
o Tension pneumothorax cardiogenic because the
 Ineffective cardiac contraction pt. might develop
pulmonary edema (b\c
o Primary arrhythmias the ventricle is not
functioning, all volume
4.1.2 CLINICAL FINDINGS: will go to the RT
1. Hypotension ventricle then to lung)!
-The treatment will
2. Tachycardia depend on the cause.
3. Tachypnea
4. Oliguria

23
 Types of Shock 7

Figure 7

4.1.3 EVENTS IN CARDIOGENIC SHOCK

Figure 8

4.2 HYPOVOLEMIC SHOCK

 Decrease in intravascular blood volume → e.g. (hemorrhage. Vomiting,

diarrhea, fluid sequestration "intraluminal – bowel obstruction, intraperitoneal
– pancreatitis, interstitial – burns") → decrease in cardiac output and
tissue perfusion

24
8 Shock

 To treat it: replace volume + treat the underlying cause.

Figure 9

4.3 SEPTIC SHOCK

Figure 10

 To treat it: replace volume + give antibiotics.

4.4 SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS):

25
 Neurogenic Shock: 9

 The patients demonstrate a similar response as sepsis but WITHOUT

INFECTIVE AGENTS. It’s just an inflammatory process.
 The criteria are: (two or more to call it SIRS)
1) Temperature >38 or < 36 (in sepsis it could be hypothermia OR
hyperthermia!)
2) Heart rate >90
3) RR > 20 or a pco2 < 34 mmHg (4.3 kpa)
4) WBC > 12,000 0r < 4,000 with more than 10% bands
5 NEUROGENIC SHOCK:

 It is a shock that result from a high spinal cord injury (e.g Cervical spine
traumatic injury). The injury is at level T2 or above

 This will result in loss of sympathetic tone
 Loss of sympathetic tone will result in:
o Arterial and venous dilatation causing hypotension.
o Bradycardia as a result of unopposed vagal tone.
 The typical feature is hypotension with bradycardia (non- neurogenic patient
usually have 
tachycardia as a result of shock).
 Management of neurogenic shock:
1) Assessment of airway
2) Stabilization of the entire spine
3) Volume resuscitation
4) R/O other causes of shock
5) High dose corticosteroids
6 PRINCIPLES OF RESUSCITATION:

1. Maintain ventilation: ensure oxygen delivery

2. Enhance perfusion
3. Treat underlying cause

Figure 11: Treatment of shock enhancing perfusion/oxygen delivery:

7 SUMMARY:

1. Shock is an altered state of tissue perfusion severe enough to induce 


derangements in normal cellular function
2. Neuroendocrine*, hemodynamic and metabolic changes work together to
restore perfusion

26
10 Shock

3. Shock has many causes and often may be diagnosed using simple clinical
indicators
4. Generic classification of shock:
a. Circulatory shock:
i. Critical reduction in tissue perfusion results in organ dysfunction
and, if not treated, death.
ii. Usually accompanied by signs and symptoms:
a) Oliguria
b) Mental status changes
c) Weak thready pulse
d) Cool clammy limbs
b. Septic shock:
i. Hypotension
ii. Vasodilatation with warm limbs.

Figure 12: Diagnosing shock state based on hemodynamic parameters

5. Treatment of shock is primarily focused on restoring tissue perfusion

and oxygen delivery while eliminating the cause

27
 Cases 11

8 CASES

 Case 1: Circulatory Shock

10 y/o female fell off bike riding down a hill. Initially well but 4 hrs later complained of abdominal
pain and left shoulder pain.
 On examination:
o Vital signs (VS): BP 90/60, P 120 (tachycardic), RR 30 (tachypneic), T 100.1, O2 sat
95% (low)
o General (GEN): pale, anxious
o Lung: clear to auscultation
o Precordium (COR): tachycardic with murmur best heard at base
o Abdomen (ABD): diffuse tenderness without peritonitis or mass
 Labs: Hb 7.5 (low)
 Hemodynamics:
Central venous pressure Decreased
Cardiac output Decreased
Systemic vascular resistance Decreased

 Abdominal CT: splenic laceration with free peritoneal fluid

 Patient is in respiratory failure:

Splenic
Decreased
laceration Decreased Metabolic
O2 delivery,
with cardiac acidosis, Tachypnea
increased O2
hypovolemia output (CO) hypoxemia
demand
(blood loss)

 Treatment of respiratory failure:

1) Primary resuscitation
2) Oxygen
3) Mechanical ventilation if necessary

 Case 2: Septic Shock

15 y/o male with a 4 day history of abdominal pain, N/V and anorexia
 On examination:
o VS: BP 70/60 (low), P 130 (high), RR 28 (high), T102.4, O2 sat 99%
o GEN: moderate distress from abdominal pain
o COR: tachycardic
o ABD: diffuse tenderness w peritonitis
 Labs:
o WBC 19,600 (high), 90% segments
o Hb 14.2
 Hemodynamics:
Cardiac output Increased
Systemic vascular resistance Decreased

 Dx: perforated appendicitis

28
12 Shock

 Case 3: Neurogenic Shock

17 y/o male, diving into water
 On examination:
o VS: BP 90/60 (low), P 110 (high), RR 24 (high)
o Paralysis below C5
 Hemodynamics:
Central venous pressure Decreased
Cardiac output Decreased
Systemic vascular resistance Decreased

 Cervical X-ray: C5 fracture

 Case 4: Cardiogenic Shock

17 y/o male, training for track team

 On examination:
o VS: BP 70/50 (low), P 140 (high), RR 35 (high), O2 sat 88%

o Absent breath sounds in left lung field, distended neck veins
 Dx: tension pneumothorax

 Hemodynamics:
Central venous pressure Increased
Cardiac output Decreased
Systemic vascular resistance Normal Figure 13: Case 4

 Case 5: Capillary Leak Syndrome

3 y/o male, clothes ignited from roaster
 On examination:
o VS: BP 60/60 (low), P 170 (high), RR 35 (high), T102.4, O2 sat 89%
o GEN: moderate distress
o LUNG: tachypneic, clear to auscultation
o COR: tachycardic, regular
o SKIN: 60% TBSA partial and full thickness burn
 Hemodynamics:
Cardiac output Decreased
Figure 14: Case 5
Systemic vascular resistance Increased

 Dx: 60% of total body surface area (TBSA) burn; hypovolemic shock (loss of fluid into  What is capillary
interstitium, called “third spacing”) leak syndrome?
 Rx: MAINTAIN VENTILATION
1. Vasodilatation
Increased O2 Respiratory
2. A-V shunting
demand failure 3. Maldistribution of flow
Hyperventilati Repiratory
(sepsis,
on fatigue
(=acidosis, Death 4. Increased capillary
hypovolemia, hypoxia, permeability +
trauma etc) coma)
interstitial edema
5. Decreased oxygen
extraction
6. Primary defect of
oxygen utilization at
cellular level

29
 MCQs 13

9 MCQS

1. Which one of these parameters will appear first and can be diagnostic
for shock?
a. Hypotension
b. Bradycardia
c. Decreased tissue perfusion
d. Tachycardia
2. The most sensitive tissue to ischemia is:
a. Muscle
b. Nerve
c. Skin
d. Adipose tissue
e. Bone
3. Which one of the following does not cause hypovolemic shock?
a. Hemorrhage
b. Trauma
c. Surgery
d. Myocardial infarction
e. Burns
4. A 25 y/o driver sustained a car accident presented to the ER with flaccid
paralysis, bradycardia, and hypotension. The most likely diagnosis is:
a. Neurogenic shock
b. Cardiogenic shock
c. Hypovolemic shock
d. None of the Above
5. The commonest cause of the previous case is:
a. Massive external bleeding
b. Ischemic heart disease
c. Injury to the high thoracic spine
d. Internal bleeding

 Answers: 1:d, 2:b, 3:d, 4:a, 5:c 30

 Introduction 1

INTRAVENOUS FLUIDS
1 INTRODUCTION
Blood- based
products include:
 IV fluid is the giving of fluid and substances (electrolytes) directly into a vein. Whole blood, fresh
 Substances that may be infused intravenously: volume expanders frozen plasma,
(crystalloids and colloids), blood based products, blood substitutes & cryoprecipitate which is a
frozen blood product
medications prepared from plasma.
1.1 PHYSIOLOGY

 Water makes up around two thirds of our total body mass. To be exact, men
 Do not get confused:
are 60% water, whilst women are slightly less at 50-55%. 1 mEq/L = 1 mmol/L
 Total body fluid water is 60% of body weight (BW). 1 cc = 1 ml

Example:
A 70 kg man will contain about 42 liters, and a 70 kg woman will contain nearly 38 liters.
The reason of this difference between the sexes is that women contain an extra 5%
adipose tissue; the difference is only occasionally of clinical significance.

1.1.1 FACTORS THAT AFFECT OUR TOTAL BODY FLUID

 Age: the older you get, the more body fluids you lose.
 Gender: females have less total body fluid water.
 Lean body mass: (muscles): Increases total body water. (↑TBW)
 Weight: the higher the levels of fat in the body the lower the total body water
will be(↓ TBW)
 How to calculate TBW?
o Male sex TBW= BW× 0.6 / Female sex TBW= BW x 0.5
1.1.2 BODY FLUID COMPARTMENTS
 Intracellular volume: (40%) rich in water, the majority of our total body water
is in the intracellular compartment.
 Extra cellular volume: (20%) rich in water divided into:
o Interstitial space: contains 15% of water
o Intravascular space: contains 5% of water
o The intravascular compartment holds the smallest amount of water at
around 3 liters (further 2 liters of red blood cells makes up our total blood
volume)
o The intravascular space is the most important compartment for physicians
because:
 It is the compartment fluid is infused in
 It absorbs and loses fluid to the interstitial space or to the intracellular
compartment.
 Through this compartment almost all significant losses and gains
occur.
 We’ll see the electrolytes also if the patient is dehydrated by pricking
the vessel.

31
2 Intravenous Fluids

Example: How to measure fluid in different compartments?

 70 kg male: (70x 0.6) TBW= 42 L
 Intracellular volume = .66 x 42 = 28 L or .4 x 70 = 28
 Extracellular volume = .34 x 42 = 14 L or .2 x 70 = 14
 Interstitial volume = .66 x 14 = 9 L

1.1.3 FLUIDS SHIFT/INTAKE

 Water moves freely between the compartments
 We lose water through our renal and gastrointestinal tracts, and this can be
seen and measured. The water from our skin and respiratory tract cannot be
measured with ease, and makes up our insensible loss. It increases in
sickness, particularly when febrile.

Figure 1

1.1.4 BODY ELECTROLYTES CO MPARTMENTS  Normal electrolyte

 Intracellular volume includes: K+, Mg+, phosphate (HPO3-) values:
Serum Na+ = 135 – 147
 The main +ve intracellular electrolyte is K+/ the main –ve intracellular mmol/L
electrolyte is HPO3- Serum K+ = 3.5 – 5
 Extra cellular volume (intravascular) includes Na+, Cl-, Ca++, and albumin. mmol/L
-
 The main +ve extracellular electrolyte is Na+ / The main –ve extracellular Serum Cl = 98 – 108
mmol/L
electrolyte is Cl- -
Serum HCO3 = 20 – 28
mmol/L
+2
Serum Ca = 8.5-10.2
mg/dL (~2.2-2.6 mmol/L)

Figure 2: Normal values of electrolytes (know the main cations and anions)

32
 Introduction 3

1.1.5 OSMOTIC / ONCOTIC PRESSURE

 Gibbs – Donnan Equilibrium:

o It refers to the movement of chargeable particles through a semi

permeable membrane against its natural location to achieve equal
concentrations on either side of the semi permeable membrane. For
example, movement of Cl- from extra cellular space (natural location) to
intracellular space (unusual location) in case of hyperchloremic metabolic
acidosis because negatively charged proteins (natural location in
intravascular space) are large molecules that cannot cross the semi
permeable membrane for this equilibrium.
o The distribution of water throughout depends on:
 Size of the compartment available (the bigger the
size the more fluid it will get)
 Tonicity (mainly). Water balance is adjusted to maintain osmolality
at a constant throughout all three compartments.
 Oncotic pressure is generated by large molecules e.g.
plasma proteins (PP) and adds to the forces that retain water  Cations are
within the vascular space. positively charged ions
(e.g. Na+) due to loss of
o Sodium moves freely between the vascular and interstitial spaces, but is an electron (e-) and
actively extruded (forced out) from the intracellular space; therefore it is anions are negatively
the principle extracellular cation. charged ions (e.g. Cl-)
 It is also the cation that we most frequently administer by giving due to gain of an
electrone (e-)
normal saline (NaCl). When we do this, we increase extracellular
tonicity and water must move from the intracellular space to the
extracellular space to normalize osmolality
o Electrolytes are exchanged between compartments, if an electrolyte
increases in the blood, it will move to the interstitial or intracellular space.
o Some electrolytes move freely  they diffuse via gradients. But some
need active transportation e.g. Na+ moves freely extracellulary (between
the blood and interstitium), but needs active transport (Na/K pump) to
move intracellulary (because this is not its normal position)
 How to measure the osmolality of the blood:
o Its either you measure and add all active molecules, or  Because sodium is
o Multiply the amount of sodium in the blood by 2 and you add amount of the major extracellular
cation, the majority of
urea and glucose in blood  [(sodium x 2) + urea + glucose] extracellular anions will
o We measure it to know if the fluid is isotonic, hypotonic or hypertonic be equal to its
o In conditions such as hypernatremia, renal failure (raised urea) concentration.
or hyperglycemia, osmolality is raised.

33
4 Intravenous Fluids

2 TYPES OF IV FLUIDS

2.1.1 COLLOID SOLUTIONS

 They are fluids with high molecular weight, or contain protein. Used for volume
expanding (e.g. in hypotension), or protein replacement (e.g. when albumin is
low). They do not contain electrolytes. Examples: Dextran, hetastarch,
albumin…
 They tend to stay within the vascular space and increase intravascular
pressure.
 Colloids are used as a volume expander not for electrolyte imbalance or a
physiological condition, just for volume depletion (hypotension) or low albumin.
2.1.2 CRYSTALLOID SOLUTIONS
 Osmolality is the
 They’re IV fluids that contain varying concentrations of electrolytes (water and dissolution of a solute in
minerals e.g., sodium, potassium, calcium, chloride). whole blood measured in
kilograms.
 They are not given to a patient with hypoalbuminemia because they don’t Normal blood osmolality
contain proteins. = 280-303
 They come in different preparations and volumes. miliosmoles/kg
 It's important to know the crystalloid's osmolality  related to the blood's
 Crystalloid solutions are classified according to their tonicity into 3
categories:
1) Isotonic: almost equal tonicity to the plasma, such as:
 Normal saline: it is the commonly-used term for a solution of 0.9%
weight/volume of NaCl, about 300 mOsm/L or 9.0 g per liter.  Tonicity of a
solution Means effective
 1 liter of normal saline contains 154 mmol/L of Na and 154 osmolality in relation to
mmol/L of Cl only. plasma (=285
 Lactated Ringer's solution: 1 liter contains: 130 mmol/L of Na, 109 milliosmol/L).
mmol/L of Cl, 28 mmol/L of lactate, 4 mmol/L of K, 1.5 mmol/L of Ca
 Hartmann's solution: 1 liter contains: 131 mmol/L of Na, 111
mmol/L of Cl, 29 mmol/L of lactate, 5 mmol/L of K, 2 mmol/L of Ca
2) Hypotonic: have lesser tonicity than plasma, e.g. 2.5% dextrose
3) Hypertonic: have greater tonicity than plasma, e.g. D5 NaCl
Type of fluid* Sodium (mmol/L) Potassium Chloride Osmolarity
Plasma 136 -145 3.5 – 5.0 98 -105 280 - 300  Ringer’s lactate and
5% Dextrose 0 0 0 278 Hartmann’s are very
similar but not identical.
Dextrose 0.18% saline 30 0 30 283
The only difference is
0.9% “normal” saline 154 0 154 308 that Hartmann’s contains
0.45%”half normal” saline 77 0 77 154 131 mmol/L of Na and
Ringer’s contains 130
Ringer’s lactate 130 4 109 273 mmol/L.
Hartmann’s 131 5 111 275
Gelatin 4% 145 0 145 290
5% albumin 150 0 150 300
20% albumin - - - -
Hes 6% 130/0.4 154 0 154 308
Hes 10% 200/0.5 154 0 154 308
Hes 6% 450/0.6 154 0 154 308

34
 Fluid Requirements 5

3 FLUID REQUIREMENTS

 Fluid losses in disease and in health are those that can be seen and
measured, while insensible losses cannot be measured.
 Any fluid lost from the body is potentially in need of replacement, be it urine,
stool, or fluid from drains, or other tubes. If possible, measuring these losses
is a great help.
 The aim of fluid administration is the maintenance of organ perfusion by
keeping total body water at 55 - 60% - this is the euvolemic state.
 Hypovolemia, when total body water is deficient, is not compatible with
normal organ perfusion. Causes of hypovolemia include
o GI: diarrhea, vomiting, etc.
o Renal: diuresis
o Vascular: hemorrhage
o Skin burns
 Hypervolemia, when body water is in excess, is occasionally necessary for
organ perfusion, but is usually harmful. Causes of hypervolemia include:
o Heart /liver/kidney failure
o Iatrogenic
In order to assess how much fluid should be given to someone, we need to know
what their level of hydration is, what losses they may expect, and what gains they
may receive (oral intake: fluids, nutritional supplements, bowel preparations – or
IV intake: colloids & crystalloids, feeds, drugs); you have to calculate the
amount of fluid the person needs before giving him IV fluids.
o Normal adult requires approximately 35 cc/kg/d
3.1 HOW TO CALCULATE FLUID REQUIREMENTS

 Fluid requirements = normal requirement + amount of lost fluid per day +

insensible loss
o Normal fluid needed = body weight x 35
o You should know if the person has diarrhea or any disease to know how
much fluid he has lost.
 Fever increases insensible loss by 200 cc/day for each degree (C)
 Monitor abnormal GI loss e.g. NGT suctioning (nasogastric tube).
o Insensible water loss makes up about 500 ml a day. It is the amount of
fluid lost on a daily basis from the lungs, skin, respiratory tract, and water
excreted in the feces. The exact amount cannot be measured.

Figure 3: Fluid losses

35
6 Intravenous Fluids

3.1.1.1 HOW TO MEASURE HOW MUCH FLUID SHOULD BE GIVEN IN

AN HOUR
 There are 2 rules:
o Either you find out the normal fluid required and divide it by 24 hours.
o Or Apply the “4, 2, 1" rule.
 You give 4 cc/kg/hr for the first 10 kg
 You give 2 cc/kg/hr for the second 10 kg
 You give 1cc/kg/hr for each additional 10 kg

Example: How much fluid does a 100 kg male require?

 Daily requirement: 35 cc/kg  35x100 = 3500 cc/day
 IV fluid rate (per hour), there are 3 methods:
1) Divide 3500 by 24 = 140 cc/hr
2) “4, 2, 1” rule:
st
 1 10 kg x 4 = 40
nd
 2 10 kg x 2 = 20
rd
 3 10 kg x 1 = 10
th th th th
 4 10 kg x 1 = 10, 5 10 kg x 1 = 10, 6 10 kg x1 = 10,…. 10 kg x 1 = 10
 Total = 40 + 20 + (10 x 8) = 40 + 20 + 80 = 140 cc/hr
3) Using the “4, 2, 1” rule, we can conclude that: body weight + 40 = IVF rate
 100 + 40 = 140 cc/hr
 How does this work? According to 4, 2, 1 rule:
 You need 40 ml for first 10 kilograms, but you used 1 ml/kg = 1 x 10 = 10 ml
 40 – 10 = 30, so you need to add 30 ml
 You need 20 ml for second 10 kilograms, but you used 1 ml/kg = 1 x 10 = 10
ml  20 – 10 = 10, so you need to add 10 ml
 Total you need to add is 30 (for 1st 10 kg) + 10 (for 2nd 10 kg) = 40
 So body weight + 40 = fluid requirement as calculated by 4, 2, 1 rule

 This assumes no significant renal or cardiac disease and NPO [nil per os
(nothing by mouth)]
 This is the maintenance IVF rate; it must be adjusted (increased) for any
dehydration or ongoing fluid loss.
 Conversely, if the patient is taking fluids PO (by mouth), the IVF rate must be
decreased accordingly.
 Daily electrolytes, BUN, creatinine, input/output, and if possible, weight should
be monitored in patients receiving significant IVF. (BUN: blood urea nitrogen)
4 ELECTROLYTES REQUIREMENTS

4.1.1 SODIUM REQUIREMENT  Half-normal saline

Na+ required: 1-3 mEq/kg/day (0.45%) will result in
hyponatremia if given
 0.45% saline (half normal saline) contains 77 mEq NaCl per liter. rapidly or in excess
 0.45% saline is usually used as maintenance of IV fluid assuming there are no amounts.
Maintenance therapy
other volume or electrolyte issues. should be tailored to the
patient’s specific
requirements.

36
 Rules Of Fluid Replacement 7

Example 1:
 70 kg male requires 70 - 210 mEq NaCl in 2600 cc fluid per day.
 In such case, you give the patient half normal saline. Why?
o The patient needs 70 – 210 mEq NaCl in 2.6 L a day,
o The half normal saline contains 77 mEq NaCl per liter
o When you measure it: 77 x 2.6 = 200 mEq, It meets the daily requirement of the
patient.
o Unlike giving normal saline which contains 154 mEq NaCl per liter.
Example 2:
 Patient weighs 100 kg, requires100 to 300 mEq NaCl in 3500 cc /d.
 In such case, you give the patient half normal saline. Why?
o The patient needs 100 to 300 mEq NaCl in 3.5 L a day,
o The half normal saline contains 77 mEq NaCl per liter
o When you measure it: 3.5 L x 77 = 269.5 mEq, It meets the daily requirement of
the patient.
o Unlike giving normal saline which contains 154 mEq NaCl per liter.3.5x154 it
will be 539, it will exceed the amount needed.

4.1.2 POTASSIUM REQUIREMENT

K+ required: 1 mEq/kg/day
 K+ can be added to IV fluids. Remember this increases the osmolality load.
o 20 mEq/L is a common IVF additive.
 The potassium flow rate shouldn’t exceed 10-20 mmol/hour because it might
cause hyperkalemia.
 If significantly hypokalemia occurs, order separate K+ supplementation.
 Oral potassium supplementation is always preferred when feasible.
  The most important surgical abnormality is hypokalemia because they
always give fluids but not K+.

Example 1:
 70 kg male
o First you measure the amount of fluid the patient needs per day.
o Then you measure the amount of potassium the patient needs, which is 70
mEq/kg/day of K+.
o After that you’ll add the amount of K+ the patient needs to the fluid you chose to
give the patient.
o You’ll divide it into 20 mEq/L
o This will supply basal needs in most patients who are NPO.

5 RULES OF FLUID REPLACEMENT

 Someone with serious intravascular volume depletion, hypotension and

reduced cardiac output is in a shock, whether it was caused by blood loss
(e.g. hemorrhage), plasma loss (e.g. major burns), or water loss.
 The aim here is to restore intravascular volume with a fluid that remains in
the vascular compartment, and may even draw water from the intracellular
space into the blood system. A fluid with a high oncotic pressure would do this
job.
o Blood remains the fluid of choice to treat someone with blood loss.

37
8 Intravenous Fluids

o Colloid is the fluid of choice in resuscitation when blood loss is not

pronounced, or whilst waiting for blood.
o Any crystalloid will enter the vascular space, then distribute around the
other compartments. By containing sodium, the main extracellular cation,
saline will expand the interstitial and intravascular compartments more
than dextrose will, most of which will enter the intracellular space.
 The right treatment for blood loss is to replace it with blood. Giving 2 liters of
blood to someone will expand their intravascular compartment by 2 liters.
None of this fluid will escape across the blood vessel walls (in the short term
at least) and the other compartments are unaffected.
 Giving colloid into the vascular space results in an immediate expansion of the
intravascular compartment by 2 liters (like blood).
o Colloid does not escape from the vascular space, but does increase
oncotic pressure markedly causing water to be drawn into the
vascular space from the interstitial and intracellular reservoirs. Giving
colloid not only expands the vascular space itself, but does so by moving
water from other spaces
 Saline being a crystalloid, does not remain within the vascular space, but
will diffuse into the interstitial space. The sodium it carries will not enter the
intracellular space however, because of active sodium extrusion from the cell.
o Saline will cause immediate expansion of the intravascular volume,
followed by equilibration between the vascular and interstitial spaces,
the osmolality of which are equal, but are now slightly greater than that of
the intracellular space, due to the increased sodium load. This results in
water movement from the intracellular space in order to equalize
osmolality throughout all three compartments.
 5% Dextrose is isotonic to plasma. Giving 2 liters of 5% dextrose will cause
the immediate expansion of the vascular compartment but as its glucose
content is rapidly metabolized, the remaining water will distribute itself
between all compartments and very little will remain within the blood
space. For this simple reason, dextrose is not a fluid of resuscitation.
  In summary:
a. Replace plasma with colloid
b. Replace ECF (extra-cellular fluid) depletion with saline
c. Dextrose should be given in case of dehydration.
d. The only thing that goes intracellulary is the potassium.
Figure 4: Effects of different types of IV fluids

2L of blood: Stays in the intravascular compartment

38
 Abnormalities 9

2L of colloid: immediate expansion of intravascular

+ draws water from other compartments
space& increases oncotic pressure

Then: equilibration between the vascular and

2L of crystalloid: immediate expansion of vascular
interstitial spaces, and draws water from
compartment
intracellular space

Then: glucose content is rapidly metabolized,

2L of 5% dextrose: immediate expansion of vascular remaining water will distribute itself between all
compartment compartments and very little will remain within the
blood space

6 ABNORMALITIES

6.1 WATER

6.1.1 WATER EXCESS

 Causes:
o Inappropriate use of hypotonic solutions such as 0.5% water leading to
hypo-osmolar hyponatremia (iatrogenic)
o Syndrome of inappropriate ADH (anti diuretic hormone) secretion.
 Inappropriate secretion of ADH has many causes, such as:
malignant tumors, CNS diseases, pulmonary disorders (pneumonia,
lung abscess), medications, and severe stress e.g. major surgery)
 Signs and symptoms:
o Symptoms of water excess develop slowly and if not recognized and treat
ed promptly, they become evident by convulsions and coma due to
cerebral edema.
o Signs include: hypertension, tachycardia, raised JVP/ gallop, edema,
pleural effusions, pulmonary edema, ascites and organ failure.

39
10 Intravenous Fluids

Box: Antidiuretic Hormone (ADH):

 ADH is released from the posterior pituitary gland.
 It is secreted in response to high osmolality in plasma or in response to low
volume.
o ADH secretion is influenced by volume receptors so that hypovolemia stimulates
ADH secretion and water reabsorption. In the paradoxical situation where
hypovolemia is accompanied by a fall in osmolality, ADH secretion will increase
because the major stimulant is hypovolemia
 Role of ADH: to maintain normovolemia and the osmolality of plasma
o The principle mechanism by which osmolality is maintained: changes in ADH
secretion from the posterior pituitary.
 Anti-diuretic hormone secretion results in:
o Pure water reabsorption from the collecting duct of the nephron via a pathway
that involves the V2 receptor and aquaporin 2.
o It increases the urine’s concentration

 Diagnosis is established when urine sodium >20 mEq/L (in the absence of
renal failure, hypotension, and edema)
 Treatment:
o Water restriction by giving the patient <1 L/day, infusion of isotonic or
hypertonic saline solution and use of
o ADH- antagonist (Demeclocycline 300-600 mg b.i.d).
6.1.2 WATER DEFICIT:
 Third spacing is the
 The most encountered derangement of fluid balance in surgical patients is shift of fluid from the
hypovolemia. intravascular space to a
nonfunctional space, or
 Causes include: bleeding, third spacing , gastrointestinal losses, increase the loss of extracellular
insensible loss (normal ≈ 10ml/kg/day), and increase renal losses (normal ≈ fluid from the vascular to
500-1500 ml/day). other body
 Signs and symptoms: compartments.
o Symptoms: thirst, dryness, lethargy, and confusion.
o Signs:
 Dry tongue and mucous membranes, sunken eyes, dry skin, loss of
skin turgor, collapsed veins,
 postural hypotension, Tachycardia, absence of JVP at 45o
 Oliguria, organ failure
 Depressed level of consciousness, and coma
 Diagnosis: confirmed by increased serum sodium (>145mEq/L) and
increased serum osmolality (>300 mOsmol/L)
 Treatment:
o Bleeding should be replaced by IVF initially then by whole blood or
packed red cells depending on hemoglobin level. Each blood unit will
raise the hemoglobin level by 1 g.
o If fluid loss was caused by diarrhea or vomiting you give IVF (crystalloid
usually).
o If sodium is low, give a solution that contains sodium (e.g. 0.9% NaCl)
o If sodium is >145 mEq/L give 0.45% hypotonic saline solution
o If sodium is >160 mEq/L give D5% water cautiously and slowly (e.g. 1 liter
over 2-4 hours) in order not to cause water excess
o You should treat anything that causes further water loss.

40
 Abnormalities 11

 Third spacing replacement can be estimated within a range of 4-8

ml/kg/h.
 Gastrointestinal and intraoperative losses should be replaced 1 cc/cc
loss
o IVF maintenance can be roughly estimated by 4/2/1 rule.
6.2 SODIUM

6.2.1 HYPERNATREMIA
 It is established when serum sodium >145 mEq/L
 Causes :
1) Excessive sodium load (excessive normal saline (0.9%) or hypertonic
solutions e.g. 3% NaCl - >145 of Na)
2) Hyperaldosteronism; aldosterone promotes water & Na+ retention (rare)
3) Reduced water intake by fasting, nausea and vomiting, or reduced
consciousness as in Alzheimer’s patient/elderly (they forget to drink)
4) Increased water loss by sweating (pyrexia, hot environment), respiratory
tract loss (increased ventilation, administration of dry gases) or burns.
5) Inappropriate urinary water loss by diabetes insipidus (pituitary or
nephrogenic) or diabetes mellitus
6) Patients with CHF, cirrhosis, and nephrotic syndrome are prone to this
complication
 Symptoms: similar to water excess symptoms, includes coma, convulsions
and confusion.
 Treatment :
o Water restriction and ↓ sodium infusion in IVF (e.g. 0.45% NaCl or D5%
water).
6.2.2 HYPONATREMIA  Pseudo-
hyponatremia: low
 Causes: serum sodium
1) Hyperglycemia (it could be Pseudohyponatremia; diabetic) concentration resulting
 Corrected Na+ = BS mg/dl x 0.016 + P (Na) (BS = blood sugar) from volume
2) Excessive IV sodium-free fluid administration (hypotonic solutions) displacement by massive
hyperlipidemia or
3) Hyponatremia with volume overload “hypervolemic hyponatremia” hyperprotienemia or by
usually indicates impaired renal ability to excrete sodium. hyperglycemia.
 Treatment:
o Administering the calculated sodium needs in isotonic solution
o In severe hyponatremia (Na+ <120 mEq/L) you give a hypertonic solution
o Serum Na+ administration shouldn’t be given at a rate > 10-12 mEq/L/hr,
because rapid correction may cause permanent brain damage due to the
osmotic demyelination syndrome 
o Before treating hyponatremia, you should check if it’s true hyponatremia
or pseudohyponatremia by checking the glucose levels.
 The glucose levels should be corrected in case of pseudo-
hyponatremia, no further treatment is needed.
6.3 POTASSIUM

6.3.1 HYPERKALEMIA

41
12 Intravenous Fluids

 Causes:
o Increase K+ infusion in IVF
o Tissue injury, surgery
o Metabolic acidosis (causes a shift of potassium from intracellular space
into extracellular space)
o Renal failure ( excretion)
o Blood transfusion (RBCs contain high concentrations of K+)
o Hemodialysis
 Signs & symptoms: arrhythmia 
 Diagnosis: established by ↑ serum K+ >6 mEq/L and ECG changes
(bradycardia and peaked T wave)
 Treatment:
o Insulin: 10 IU (shifts K+ back into intracellular compartment) + glucose: 1
ampule of Dextrose 50% (prevent hypoglycemia from insulin) – over 15
minutes
o Calcium oxalate enemas (can also be given orally)
o Lasix 20-40 mg IV
o Dialysis (if needed)
6.3.2 HYPOKALEMIA
 Occurs when serum K+ <3 mEq/L
 The most common surgical abnormality.
 Causes:
1) Inadequate replacement (e.g. during surgery)
2) Diuretics (e.g. Lasix)
3) Metabolic alkalosis (shifts K+ to intracellular compartment)
4) Hyperaldosteronism (promotes K+ excretion in kidneys)
5) Gastrointestinal tract losses:
 Vomiting
 Gastric aspiration/drainage (the flow of gastric content into the
upper respiratory tract due to a ↓ antireflux reflex)
 Fistulae (an abnormal connection between an organ,
vessel, or intestine and another structure. It’s usually the result of
injury, surgery, infection or inflammation.)
 Diarrhea
 Ileus (disruption of the normal propulsive gastrointestinal track that
causes obstruction which prevents bowel contents, such as stool,
fluid and gas, from moving through the intestine, which becomes
distended)
 Intestinal obstruction
 Potassium-secreting villous adenomas
6) Urinary loss
7) Renal tubular disorders (e.g. Bartter syndrome, renal tubular acidosis,
amphotericin-induced tubular damage)
 Symptoms:  weakness and fatigue (most common), muscle cramps and
pain (severe cases), altered level of consciousness, arrhythmias
 Treatment: K+ replacement (KCl solution)

42
 Abnormalities 13

6.4 CALCIUM

6.4.1 HYPERCALCEMIA
 Causes: hyperparathyroidism and malignancy.
 Symptoms: confusion, weakness, lethargy, anorexia, vomiting, epigastric
abdominal pain (due to pancreatitis), and polyuria (due to nephrogenic
diabetes insipidus).
 Diagnosis is established by measuring the free Ca >10 mg/dl.
 Treatment includes normal saline infusion
o If Ca >14mg/dl with ECG changes: additional diuretics, calcitonin, and
mithramycin (antineoplastic antibiotic that has been discontinued) might
be necessary
6.4.2 HYPOCALCEMIA
 Causes: hypoparathyroidism after thyroid or parathyroid surgeries, other less
common causes include:
o pancreatitis (depletion of Ca due to saponification of fat),
o necrotizing fasciitis,
o high output GI fistula, and
o massive blood transfusion (citrate in the blood binds Ca)
o Low vitamin D
Figure 5: Carpopedal spasm
o Pseudo-hypocalcemia (low albumin and hyperventilation)
 Hypoalbuminemia; the relation between Ca++ and albumin is the
binding of the Ca++ to albumin which makes the calcium less free. In
hypoalbuminemia total calcium is  while ionized is unaffected.
 Hyperventilation  respiratory alkalosis   Ca binding &  free Ca
 Symptoms:
o Numbness and tingling sensation circumorally or at the finger-tips.
o Tetany and seizures may occur at a very low calcium level.
 Signs include tremor, hyperreflexia, carpopedal spasms and positive
Chvostek sign.
 Diagnosis: serum Ca < 8.5 mg/dl (2.1 mmol/L) Figure 6: Chvostek sign;
 Treatment: should start by treating the cause. Calcium supplementation with tapping the zygomatic arch
calcium gluconate or calcium carbonate IV or orally. Vitamin D causes the facial muscles to
twitch
supplementation especially in chronic cases.
6.5 MAGNESIUM

6.5.1 HYPERMAGNESEMIA
 Mostly occurs in association with renal failure, when Mg+ excretion is
impaired.
 The use of antacids containing Mg+ may aggravate hypermagnesaemia.
 Treatment includes rehydration and renal dialysis
 Hypermagnesemia and hypophosphatemia are all conditions of renal failure
6.5.2 HYPOMAGNESAEMIA
 Usually there are no symptoms but when you want to correct Ca or K levels
they don’t get corrected.

43
14 Intravenous Fluids

 Mg plays a role in the pumps and the muscular junctions

 When Mg decreases the Ca and K will decrease as well even though they
were in their normal levels.
 But when correcting the magnesium everything will go back to normal
 The majority of magnesium is intracellular with only <1% in the extracellular
space.
 It happens from inadequate replacement in depleted surgical patients with
major GI fistula and those on TPN.
 Magnesium is important for neuromuscular activities. (cannot correct K nor
Ca)
 In surgical patients hypomagnesaemia is a frequently missed common
electrolyte abnormality as it causes no major alerting symptoms.
6.6 PHOSPHATE

6.6.1 HYPERPHOSPHATEMIA
 Mostly associated with renal failure and hypocalcaemia due to
hypoparathyroidism, which reduces renal phosphate excretion.
6.6.2 HYPOPHOSPHATEMIA
 Causes:
o Inadequate intestinal absorption,
o Increased renal excretion,
o Hyperparathyroidism,
o Massive liver resection
o Inadequate replacement after recovery from significant starvation and
catabolism.
 Symptoms: muscle weakness and inadequate tissue oxygenation due to
reduced 2, 3- bisphosphoglycerate levels.
 Early recognition and replacement will improve these symptoms.

Mg and phosphate abnormalities occur with chronic diseases, before

replacing them check the renal system, caused all the time by renal failure

7 ACID BASE BALANCE

+
 Normal values:
When the H concentration increases, the pH value will decrease and blood pH = 7.36 – 7.4
+ +
will become acidic. If the H concentration decreases the blood will become H concentration = 36 –
alkaline. 40 mmol/L
PaCO2 ~ 40 mmHg
 Hydrogen ion (mainly intracellular) is generated in the body by: Bicarbonate con-
-
1) Protein and CHO metabolism (1 mEq/kg of body weight) centration [HCO3 ] = 20-
2) Predominant CO2 production 28, average 24 mmol/L
 Mechanisms to maintain the normal value of pH in the intracellular fluid:
1) Proteins which include hemoglobin : Protein buffers include basic group,
and acidic protein buffer groups, that act as hydrogen ion depletors or
donors to maintain the pH level at 7.4
2) Phosphate: when H concentrations increase, it binds to H ions and is
excreted in the urine with sodium
 Mechanisms to maintain the normal value of the PH in the extracellular fluid:
o The buffer system: bicarbonate/carbonic acid system:

44
 Acid Base Disorders 15

 pH levels depend on CO2 and HCO3 mainly

H+ + HCO3-  H2CO3  CO2 + H2O
 Hydrogen ions and the bicarbonate form carbonic acid which forms
CO2 and water under the enzyme carbonic anhydrase.
 So if hydrogen ions increase in the plasma, CO2 production will
increase therefore the pH will decrease.
 Respiratory compensation: In acidosis, pH changes will stimulate
the respiratory center in the brain stem  hyperventilation  PCO2
will decrease and the pH levels will get back to normal.
 Metabolic compensation: when acid accumulates: the kidneys
increase urinary excretion of acids and reabsorption of bicarbonate
(in the proximal tubules in the kidneys).
8 ACID BASE DISORDERS  Normal values for
anion gap vary according
8.1.1 METABOLIC ACIDOSIS to the source.

 Low pH due to H+ ions accumulation and HCO3 ions decrease

 Causes:

To know the cause of metabolic acidosis you have to calculate the anion gap:
 AG = Cations (Na + K) – Anions (Cl + HCO3)
 Normal value is 12 mmol (8-16)

o High anion gap (AG >16):

 Lactic acidosis caused by shock (any cause), severe hypoxemia,
severe hemorrhage/anemia, liver failure
 Diabetic ketoacidosis
 Acute or chronic renal failure
 Poisoning (ethylene glycol, methanol, salicylates)
 Vomiting, NGT:
Gastric secretions are
o Non-anion gap (AG = 8-12): rich in HCl. The
 Increased bicarbonate loss by diarrhea, intestinal fistulae, renal secretion of HCl by the
tubular acidosis (types I-IV) stomach usually
stimulates bicarbonate
8.1.2 METABOLIC ALKALOSIS secretion by the
pancreas.
 High HCO3  high pH
 Causes: (1) H+ ions loss (vomiting, NGT, Lasix) (2) Hypokalemia (3) HCO3  Diuretics cause
chloride depletion and by
retention. increased delivery of
sodium ions to the
If you lose K, you will get alkalosis. If you gain you will get acidosis. collecting duct, which
enhances potassium ion
8.1.3 RESPIRATORY ACIDOSIS and hydrogen ion
secretion
 Causes: (anything that causes hypoventilation)
o Common surgical causes of respiratory acidosis  Hypokalemia when
alone without hyper-
o Central respiratory depression
aldosteronism causes
o Opioid drugs only mild alkalosis
o Head injury or intracranial pathology
o Pulmonary disease
o Severe asthma
o COPD
o Severe chest infection

45
16 Intravenous Fluids

8.1.4 RESPIRATORY ALKALOSIS

 Causes: ( anything that causes hyperventilation):
o Pain
o Apprehension/hysterical hyperventilation
o Pneumonia
o Central nervous system disorders(meningitis, encephalopathy)
o Pulmonary embolism
o Septicemia
o Salicylate poisoning
o Liver failure

Type of A- B disorder Acute (Uncompensated) Chronic (Partially compensated)

PH PCO2 HCO3 PH PCO2 HCO3

Respiratory acidosis ↓↓ ↑↑ Normal ↓ ↑↑ ↑
Respiratory alkalosis ↑↑ ↓↓ Normal ↑ ↓↓ ↓
Metabolic acidosis ↓↓ Normal ↓↓ ↓ ↓ ↓
Metabolic alkalosis ↑↑ Normal ↑↑ ↑ ↑ ↑

9 MCQ’S

1) What is the composition of 0.9% Saline?

a) 130 mEq sodium, 109 mEq chloride, 28 mEq lactate.
b) 154 mEq sodium, 154 mEq chloride.
c) 513 mEq sodium, 513 mEq chloride.
d) 855 mEq sodium, 855 mEq chloride.
2) Which of the following is correct regarding the composition of the body fluid
compartments?
a) The major intracellular cation is sodium.
b) The major intracellular anions are proteins and phosphates.
c) The major extracellular cation is potassium.
d) The major extracellular anion is magnesium.

 Answers: 1:b, 2:b

46
 Introduction 1

BLOOD & BLOOD PRODUCTS

TRANSFUSION
1 INTRODUCTION
1.1 HISTORY OF TRANSFUSIONS
 Blood transfused in humans since mid-1600’s
 1828 – First successful transfusion
 1900 – Landsteiner described ABO groups
 1916 – First use of blood storage
 1939 – Levine described the Rh factor
1.2 OBJECTIVES
 Blood components
 Indications for transfusion
 Safe delivery
 Complications
1.3 BLOOD COMPONENTS 

 Prepared from whole blood collection

 Whole blood is separated by differential centrifugation
o Red Blood Cells (RBCs)
o Platelets
o Plasma
 Cryoprecipitate
 Others (include Plasma proteins—IV Ig, Coagulation Factors,
albumin, Anti-D, Growth Factors, Colloid volume expanders)
o WBCs
 Differential centrifugation
o First Centrifugation > Seperates RBCs from platelet rich plasma
o Second Centrifugation > Seperates platetlets from plasma

47
2 Blood & Blood Products Transfusion

2 TYPES OF BLOOD TRANSFUSIONS

Because of the high
risk of infections in blood
 Indication to use WBCs: (granulocyte) transfusion for patients with severe transfusions, we should
leukocytosis or immunocompromised who don’t respond to antibiotics not give blood if
 Important notes: unnecessary; instead,
we give colloids or
o Why do we need RBCs for anemic patients? Because RBCs have crystalloids (volume
Oxyegn carrier capacity “we notice shortness of breath and tachycardia expanders) to
in anemic patients”. compensate the volume
o Whole blood transfusion is excellent when it’s fresh, but if it’s frozen loss.
(storage) there will be risk of coagulopathy.
o Storage of whole blood hypocalcaemia (precipitate Ca+2) + affect Blood is only given
coagulation factors especially factor V & VIII.  when the Hb level is low
o In surgery, they order RBCs + plasma + platelets (to increase O carrying
o Platelets, fresh frozen plasma and cryoprecipitate are given to improve capacity) e.g. Anemia >
its earliest sign >
hemostasis. Resting tachycardia
o Before going through with the blood transfusion, we take a blood
sample from the donor to:
 Do screening test to avoid transmitted infection (viruses)
 Blood group ABO testing (do it in RBCs, whole blood but not in
plasma or platelets)
 Cross match test (Rh test) [If there is a Rh group antigen, it is (+ve),
if there is not then it is (-ve)]
2.1.1 WHOLE BLOOD
 Storage:
o 4° centigrade for up to 35 days, transported in 1-10 centigrade 
o With Mannitol, Adisol or Nutrisol, it lives up to 42 days
 Indications
o Massive Blood Loss / Trauma / Exchange Transfusion (thalassemia,
sickle cell anemia) - (patient needs volume expansion)
 Considerations
o Use filter as platelets and coagulation factors will not be active after 3-
5 days
o Donor and recipient must be ABO identical 
 Why should we consider filter in blood transfusion?
o To avoid any clot or debris and transmission of a virus
o We do it for whole blood, FFP and RBC.
o Platelets do not have to undergo filtering otherwise they will be
damaged.
o Filter size = 170 micro
o In case of immunocompromised patients or in severe infections, the
filter size is usually = 20-40 micro
2.1.2 RBC CONCENTRATE (PACKED) Packed cells should
 Storage never be given directly,
they must be diluted
o 4° for up to 42 days, can be frozen with saline (imagine
 Indications packed cells as a bag of
o Many indications—i.e. anemia, hypoxia, mild bleeding,..etc. honey which is
hyperosmolar)

48
 Types Of Blood Transfusions 3

 Considerations
o Recipient must not have antibodies to donor RBC’s (note: patients can
develop antibodies over time) > identical ABO
o Usual dose 10 cc/kg (will increase Hb by 2.5 gm/dl)
o Usually transfuse over 2-4 hours (slower for chronic anemia)
 Also, never dilate the cells with Ringer’s lactate. It has Ca+2 and that kills
the RBCs.
 Remember that the life span of RBCs depends on the preservative used.
2.1.3 PLATELETS
 Storage
o Up to 5 days at 20-24° (its half-life is 1-7 days)
 Indications
o Thrombocytopenia, Plt <15,000
o Bleeding and Plt <50,000 (because it increases volume expansion)
o Invasive procedure and Plt <50,000 (because it increases volume
expansion)
 Considerations
o Contain Leukocytes and cytokines
o 1 unit/10 kg of body weight increases platelet count by 5000-10000 
o Donor and recipient must be ABO identical
o Platelets are stored at room temperature, so no need to warm it.
(Unlike whole blood & RBCs, which we have to warm up to avoid
hypothermia)
o Platelets don’t need warming, filtering (it will inactivate it and damage
it) or ABO testing.
2.1.4 PLASMA AND FFP
 Contents—Coagulation Factors (1 unit/ml)
 Storage
 FFP:
o 12 months at 18° or colder
o We should give it to the patient in 2 hours when we order it because it
has a short half-life.
 Indications
o Coagulation factor deficiency, fibrinogen replacement, DIC, liver
disease, exchange transfusion, massive transfusion
 Considerations
o Plasma should be recipient RBC ABO compatible
o In children, should also be Rh compatible
o Usual dose is 20 cc/kg to raise coagulation factors approximately 20%
2.1.5 LEUKOCYTE REDUCTION FILTERS
 Used for prevention of transfusion reactions
 Filter used with RBCs, Platelets, FFP and Cryoprecipitate
 Other plasma proteins (albumin, colloid expanders, factors, etc.) do not
need filters
 NEVER use filters with stem cell/bone marrow infusions
 May reduce RBCs by 5-10%

49
4 Blood & Blood Products Transfusion

3 RBC TRANSFUSIONS

3.1 PREPARATIONS

 Typing
o Typing of RBCs for ABO and Rh are determined for both donor and
recipient
o If Rh antigen factor is present, it is (Rh +ve). If not, it is (–ve).
 Screening
o Screen RBCs for atypical antibodies
o Approximately 1-2% of patients have antibodies
o Viral screening 
 Crossmatching
o Donor cells and recipient serum are mixed and evaluated for
agglutination to prevent hemolysis reaction after the transfusion
o Duration: 30-45 minutes for the results to be ready
 In case of ER, we don’t have enough time to do cross matching, so we just
give the patient (O –ve)= universal donor.
3.2 ADMINISTRATION

 Before administering the blood, we should check the blood pack

for
o Patient’s name
o Hospital number
o ABO and Rh compatibility
o Expiration date
o Should be checked by 2 people in the operation room
 The most common cause of death after blood transfusion is ABO
incompatibility and the most common cause of that is a labeling
error.
 Dose
o Usual dose of 10 cc/kg infused over 2-4 hours (slowly) >> to avoid
massive blood transfusion
o Maximum dose of 15-20 cc/kg can be given to hemodynamically
stable patients
 Procedure
o Use IV line of size 20 gage (or larger) cannula to prevent hemolysis
and breakdown of RBCs, and we need to check if its working before
we use it on the patient.
o Warm the blood to prevent hypothermia > either by putting it in warm
water or by a warming machine
o May need Premedication (Tylenol and/or Benadryl) > first possible
complication is increase in temperature (hyperthermia) so we give this
medication to adjust it.
o Filter use—routinely leukodepleted
o Monitoring—VS q 15 minutes (vital signs every 15 minutes), clinical
status
o Do NOT mix with medications

50
 Transfusion Complications 5

4 TRANSFUSION COMPLICATIONS 

 Complications
o Rapid infusion may result in Pulmonary edema, hypothermia,
especially if it is not warmed
o Transfusion Reaction
o Transmitted diseases can be transmitted during blood transfusion
4.1 ACUTE TRANSFUSION REACTIONS

4.1.1 ACUTE HEMOLYTIC TRANSFUSION REACTIONS

 MOST important complication
 Occurs when incompatible RBCs (usually ABO or Rh) are transfused into a
recipient who has pre-formed antibodies
 Antibodies activate the complement system, causing intravascular
hemolysis > hemoglobinuria
 This hemolytic reaction can occur with as little as 1-2 cc of RBCs 
 Labeling error is the most common problem
 Can be fatal
 Symptoms occur within minutes of starting the transfusion and they
include:
o High fever/chills
o Hypotension
o Back/abdominal pain
o Oliguria
o Dyspnea
o Dark urine
o Pallor
 What to do? If an AHTR occurs 
o STOP TRANSFUSION
o ABCs
o Maintain IV access and run IVF (NS or LR)
o Monitor and maintain BP/pulse

51
6 Blood & Blood Products Transfusion

o Give diuretics
o Obtain blood and urine for transfusion reaction workup
o Send remaining blood back to Blood Bank
 Blood Bank Work-up of AHTR 
o Check paperwork to assure no errors
o Check plasma for hemoglobin
o Repeat crossmatch
o Repeat blood group typing
o Blood culture
 Monitoring in AHTR
o Monitor patient clinical status and vital signs
o Monitor renal status (BUN, creatinine)
o Monitor coagulation status (DIC panel– PT/PTT, fibrinogen, D-
dimer/FDP, Plt, Antithrombin-III)
o Monitor for signs of hemolysis (LDH, bili, haptoglobin)
4.1.2 FEBRILE NON-HEMOLYTIC TRANSFUSION REACTIONS
 Definition--Rise in patient temperature >1°C (associated with transfusion
without other fever precipitating factors)
 Occurs with approximately 1% of PRBC transfusions and approximately
20% of Plt transfusions
 What to do? If an FNHTR occurs
o STOP TRANSFUSION
o Use of Antipyretics—responds to Tylenol
o Use of Corticosteroids for severe reactions
o Use of Narcotics for shaking chills
 Future considerations:
o May prevent reaction with leukocyte filter
o Use single donor platelets
o Use fresh platelets
o Washed RBCs or platelets:
 PRBCs or platelets washed with saline
 Indicated to prevent recurrent or severe reactions
 Washed RBC’s must be used within 24 hours
 RBC dose may be decreased by 10-20% by washing
 In short, stop transfusion check ABO compatibility and papers, if there are
no precipitating facotrs, give Tylenol and continue the blood transfusion.
4.1.3 ALLERGIC NON-HEMOLYTIC REACTIONS
 Etiology
o May be due to plasma proteins or blood
preservatives/anticoagulants
 Presents with urticaria and wheezing
 Treatment 
o Mild reactions—Can be continued after Benadryl
o Severe reactions—Must STOP transfusion and may require steroids
or epinephrine
 Prevention—Premedication (Antihistamines)

52
 Transfusion Complications 7

4.1.4 TRANSFUSION RELATED ACUTE LUNG INJURY

 Clinical syndrome similar to ARDS
 Occurs 1-6 hours after receiving plasma-containing blood products
 Caused by WBC antibodies present in donor blood that result in pulmonary
leukostasis
 Treatment is supportive
 High mortality
 There will be damage to the alveoli by the donor’s WBCs and antibodies,
causing pulmonary leukocytosis. The lung will be white because of this
reaction.
4.1.5 COAGULOPATHY WITH MASSIVE TRANSFUSIONS  Blood can be
 Coagulopathy may occur after transfusion of massive amounts of blood returned to the blood
(trauma/surgery) – giving the patient 1 unit of blood volume within 2 hrs bank as long as it wasn’t
(unit of blood volume = 70 ml/kg) warm, whereas platelets
and FFP should be used
 Coagulopathy is caused by failure to replace plasma – stored blood has when they’re ordered
less coagulating factors, which leads to coagulopathy (so only order it when
[Thrombocytopenia due to decreased platelets number compared to the you need it).
increased blood vloume > causes more bleeding)
 Electrolyte abnormalities
o Due to citrate binding of Calcium (hypocalcemia)
o Also due to breakdown of stored RBCs
o May cause metabloic acidosis (electrolyte imbalance)
 When these complications occur, you should start supporting the platelets
(because they will decrease in number as well as the coagulation factors)
and replace it.
 In case of trauma or major surgery where there is active bleeding, large
amounts of blood will be transfused to the patient and as we said this will
lead to massive transfusion, which in turn will cause diluted platelets and
coagulation factors. So Platelets and Fresh Frozen Plasma should be
ordered from the blood bank to prevent these complications. They’re also
ordered if the patient is a known case of thrombocytopenia or coagulation
disorder.
4.1.6 BACTEREMIA
 More common and more severe with platelet transfusion (platelets are
stored at room temperature)
 Organisms
o Platelets—Gram (+) organisms, ie Staph/Strep
o RBCs—Yersinia, enterobacter
 Risk increases as blood products age (use fresh products for
immunocompromised)
4.2 CHRONIC TRANSFUSION REACTIONS
 Delayed, might take 2-20 days for the reaction to start
o Alloimmunization
o Transfusion Associated Graft Versus Host Disease (GVHD)
o Iron Overload
o Transfusion Transmitted Infection

53
8 Blood & Blood Products Transfusion

4.3 TRANSFUSION ASSOCIATED INFECTIONS 

 Hepatitis C
 Hepatitis B
 HIV
 CMV: CMV can be diminished by leukoreduction, which is indicated for
immunocompromised patients

5 SUMMARY

6 MCQS
1. RBCs can be stored at a temperature of:
a. 1c
b. 4 c
c. 10 c
d. 18 c

54
 MCQs 9

2. For a 70 kg patient, 1 unit of platelets transfusion increases platelets count by

approximately:
a. 500-1000
b. 5000-10000
c. 15000-20000
d. 25000-30000

3. Regarding disseminated intravascular coagulation:

a. Platelet count is normal
b. Coagulopathy profile is within normal
c. There is high platelet consumption
d. Cannot occur secondary to sepsis
e. Occurs if the patient loses 1.5 liter of blood

4. Standard screening tests on donors' blood include all the following

EXEPT:
a. Hepatitis C
b. Hepatitis B
c. Rubella
d. Syphilis

5. Blood transfusions may cause all of the following except:

a. Microcirculation thrombosis
b. Transmission of malaria
c. Allergic reaction
d. Bronchospasm
e. Increase platelets count

Answers  1;B , 2;B , 3;C , 4;D , 5;E

55
 Nutrition 1

NUTRITION
1 INTRODUCTION

 The best interference for a case of malnutrition is either medical or surgical.

About 30% of admitted patients, despite treatment, will not get better
because of malnutrition itself.

 WHAT IS NUTRITION? 

 It’s providing your body with the basic nutrition needed in order for it to
function properly. 
 If you do not take adequate amounts of minerals and macromolecules
(Carbohydrates + Proteins + fats), it will cause the body to function poorly,
and if the patient is already ill that makes it more specific. 
 The basal metabolic rate [BMR] increases tremendously during illness
[e.g. infections, malignancies, altered hormonal states, etc..]. In this state,
more energy is burnt than consumed [imbalance] making the body prone to
develop malnutrition. It affects all bodily systems. 
 (Imbalance = what’s lost is higher than what’s gained, same as in
starvation)
 In short, malnutrition is the condition that occurs when the body is not
being given enough nutrients. The most dangerous part of malnutrition is
when it involves protein loss. When you have a traumatic accident, for
example, a burnt patient, the body will try to consume protein as the main
source of calories. Glycogen stores will last for two days [~48hrs] after that;
fat starts to be consumed as the main source of energy instead.
2 TYPES OF MALNUTRITION

1. Kwashiorkor: adequate calories but not enough protein:

o Here, you get your calories from macromolecules other than proteins
[lipids-fat, and carbohydrates]
2. Marasmus: a condition of low calorie, and low [but not all the time] protein
state:
o Here, you have inadequate calories.
o Protein intake can be normal or low.
2.1 KW ASHIORKOR (PROTEIN MALNUTRITION):

 In liver cirrhosis patients, protein is not synthesized as it should be (they

have third space ascites). Protein is also lost in kidney disease [nephrotic
syndrome] patients and burnt patients.

2.1.1 CLINICAL MANIFESTATIONS OF KWASHIORKOR:

 Hypoalbuminia
 Peripheral edema
 Muscle atrophy
 Altered Immunity

56
2 NUTRITION

2.2 MARASMUS: NO PROTEIN, NO CARBOHYDRATE

 Usually seen in ICU patients, post major surgeries, cancer, and burn
patients.
2.2.1 CLINICAL MANIFESTATIONS OF MARASMUS:
 Very obvious sign in: Weight loss (very low BMI)
 Bradycharia
 Low body Temperature
 Dysphagia
 Anorexia
Mostly: in cancer patients, GIT diseases (Crohn's disease: thickening of the small
intestine), major surgery and alcoholism (high calories, zero nutrition).

Mixed Kwashiorkor Marasmus

 Depleted somatic and  Normal somatic  Depleted somatic

visceral proteins. proteins, depleted proteins, normal
 Patients appear visceral proteins. visceral proteins
cachectic and severely   Serum Albumin and (Weight).
malnourished. transferrin.  Normal Albumin and
 e.g. Chronic  Patients appear normal transferrin.
hypercatabolic patients or overweight.  Patients look thin and
and prolonged  Protein malnutrition malnourished.
starvation  e.g. Hypercatabolic  Protein-calorie
o Trauma critical care patients malnutrition
o Chronic diarrhea,  e.g. Patients with mild
chronic kidney to moderate
disease, trauma, starvation, common
burns, hemorrhage, severe burns, systemic
and liver cirrhosis infections, cancer ,
conditions in which
patients do not eat,
like in anorexia
nervosa

3 HOW CAN WE EVALUATE MALNOURISHED PATIENTS?

• First, look at the weight, BMI, fat and protein storage. Based on that, calculate
the losses.
• Remember, if someone loses more than 10% in the past 6 months, that’s a
severe sign of malnutrition (3% within a month = severe).
• Vitamin deficiency = severe malnutrition (comes after protein malnutrition)
• Basic energy expenditure: when you wake up doing nothing, that amount of
calories you require is basic energy (70% of your entire calorie requirement). It
depends on the patient’s weight and height.
• Calorie sources: carbohydrates, fat & protein. The average person will have
about 60 % from carbohydrates [glucose], 20-40 % of fat and15% from protein.
4 WHEN TO FEED?

57
 Nutrition 3

 24 to 48 hr for post-admission patients.

 > 7 days for NPO patients (TPN).
 1-2 weeks for pre-surgery patients.
 3rd day for post-surgery patients.
5 WHAT TO FEED? Note:
 Fat:
 Energy 25-30 kcl 1 gram = 9 cal

 CHO 55%   Protein:
 Protein 1-1.5 g/kg  1 gram = 4 cal

 Carbohydrates:
 Lipid 20% 0.5-1.5 g/kg 1 gram = 4 cal

 Electrolyte  Alcohol:
 Antioxidant 1 gram = 7 cal

Suppose you’re eating meat all day, or Carbohydrates... If you burn 1

gram of Carbs, it will give you 3-4 cal. If you burn protein, it’ll give you the
same thing. Which would be better to take? Do you prefer getting calories
from carbohydrates or protein? Let us see.
 Protein is only utilized in the body to build cells, enzymes, and muscle. Any
extra nutrients [protein in this case] will be converted through
gluconeogenesis, from amino acids to glucose. Glucose will be stored as
glycogen. So no matter how much protein you eat; it will be converted to
glucose. This way your body (kidney and liver primarily) will be working
harder. Therefore, it is not a very good idea to increase your protein intake
unless you are a body builder. Otherwise, it would be a waste of time and
effort.

6 WHAT ABOUT FLUIDS?

 If you take 45 ml, it will give you adequate fluid for every calorie you
consume.
 A very useful universal formula for patients with healthy kidneys:
o For first 10 kg, every kilogram will need 100 ml
o Second 10 kg, every kilogram will need 500 ml
o Third 10 kg will be around 900 ml
(It is very useful for children)

7 ROUTE OF ADMINISTRATION
 First, if the GI tract is functioning we use enteral route. If not (loss of
movement happens), you will end up giving them parenteral (IV). In IV,
there are two sub-routes:
o Peripheral line
o Central line (subclavian or jugular vein): the solution given is very high
in osmolarity in relation to the plasma (2000) [normally plasma
osmolarity is around 300]
 Enteral route: only if GIT is working (5 ways)
o Oral
o Naso-gastric tube
o Naso-duodenal
o Naso-jujenal [from the nose to the jujenum, bypassing the esophagus,

58
4 NUTRITION

stomach and duodenum]

o Directly into the stomach

7.1 EARLY ENTERAL NUTRITION AFTER BOWEL RESECTION

 Start oral diet within post-operative week, if hemodynamically &

clinically stable
o Sips of isotonic oral rehydration solution
o Small quantities of foods containing complex of CHO & protein (600-
1000kcal/d individualized)
o Limit oral intake if GI losses are high
 Tube feeding if intolerant to food items
o Polymeric enteric formulary  advance slowly
o Use of nasal or surgical placed gastric or SB feeding tubes
8 WHAT ARE THE COMPLIC ATIONS OF BOTH ENTERAL AND
PARENTERAL FEEDING?

Enteral feeding Parenteral feeding

• Aspiration • Catheter sepsis
• Pneumonia • Hyperglycemia 
• Diarrhea • Pneumothorax & hemothorax
• Electrolyte imbalance
• Azotemia
• Increase LFT 

8.1 WHO NEEDS PARENTERAL? Refeeding

syndrome is a
 When a patient is unable to feed himself for more than 5 days metabolic disturbance
 Intestinal obstruction that occurs as a result
 Major surgery of reinstitution of
 Short bowel syndrome nutrition to patients
who are starved or
 Before that, make sure that all electrolytes are balanced! Why? (Especially severely
K+ and phosphate) malnourished.

59
 Nutrition 5

 If he had low K+ and phosphate, and he’s given high Gl = major drop in K+
and Phosphate and he will die (Re-feeding syndrome)
8.2 WHY DON’T WE USE CENTRAL LINES?

Due to certain complications, which include infection, pneumothorax, and
catheter embolism.
 It’s avoided in severe necrotizing pancreatitis (only) because of the fistula
that will be formed in the intestine. So whatever is ingested is going to be
leaked out of the system.
 Also, in patients with nausea and vomiting issues, it will cause aspiration
pneumonia.
8.3 CENTRAL AND PARENTERAL NUTRITION

Central Nutrition Parenteral Nutrition

Peripheral Parenteral
Nutrition (PPN) can be
• Subclavian line • Peripheral line infused through central
• Long period • Short period < 14days line
• Hyperosmolar solution • Low osmolality
• Full requirement < 900 mOsm/L Central total
• Minimum volume • Min. requirement Parenteral Nutrition
(TPN) CANNOT
• Expensive • Large volume be infused through the
• More side effects • Thrombophlebitis peripheral line.

9 QUESTIONS TO BE ASKED
• Q: In which cases should we insert NG tube?
o Patients with dysphagia and stroke pt. (long term)
o In patients who need nutrition for more than 6 weeks, it will not be a good
idea; because it might cause ulceration and irritation.
• Q: What is the complication of using NG tubes?
o Aspiration pneumonia (since the pt. is not moving, the food will move on to
the lungs)

10 MCQS
1. All of the following are used to assess the nutritional status of the patient
except:
a. Platelet count
b. Lymphocyte count
c. Body weight
d. Serum albumin
e. Triceps skin fold
2. Which of the followings is (are) an indication(s) of nutritional support:
a. Anorexia nervosa
b. Intestinal fistula
c. Malignancy
d. All of the above
3. Metabolic changes after surgery include:
a. Decreased glycogen breakdown
b. Decreased lipolysis
c. Decreased gluconeogenesis
d. Decreased body weight

 Answers: 1;A , 2;D, 3;D

60
 Introduction 1

GENERAL COMPLICATIONS OF
SURGERY
1 INTRODUCTION

• All surgeons expect speedy, uneventful recovery

• Always recognized the risk of complications
• Affects result of surgery: poor scar, hernia
• Prolongs hospital stay and cost
• Increased morbidity/ mortality
• Medico-legal issues
1.1 METHODS OF REDUCING POST-OPERATIVE COMPLICATIONS:

• Good pre-operative evaluation

• Optimizing the general condition of patients: a surgeon should delay his
surgery until patients health status reaches optimality or relative
optimality, even if that means delaying surgery, especially when is not
a emergency surgery. So Medical problems and Nutritional issues
must be corrected before surgery.
• Minimizing preoperative hospital stay: reduces likelihood of
complications like hospital associated infections and DVT.
• Good surgical technique
• Early mobilization
1.2 PHASES OF POST-OPERATIVE CARE:

• Recovery room
• Surgical ward
• On discharge
1.3 COMPLICATIONS DEVELOPING IN THE RECOVERY ROOM:

• The complications in this stage are mostly due to cardiopulmonary

disease. These happen when patients are recovering from
anaesthesia, so Anaesthesiologists are people in charge of these
problems.
• Airway obstruction
• Acute pulmonary complications
• Cardio-vascular complications
• Fluid derangements
• Reactive haemorrhage is the most important post-operative complication in
the recovery room either: Slipped ligature or Dislodgement of clot 
1.4 “GENERAL” COMPLICATIONS:

• Nausea/ vomiting: this maybe due to effects of drugs given to the patients.
This usually isn't a significant problem, antiemetics can be given to stop
vomiting in sever cases.

61
2 General Complications of surgery

• Persistent hiccups: -gastric distension: gastrointestinal peristalsis can be

greatly reduced and as a result gas can build up in the stomach causing
gastric distension and irritation of the diaphragm (diaphragmatic irritation
causes hiccups). This can be corrected by decompressing the stomach
with a nasogastric tube. Otherwise, renal failure must be excluded.
• Headache - spinal anaesthesia
• IV site- bruising, haematoma, phlebitis, vein thrombosis, air embolism,
infection
2 PULMONARY COMPLICATIONS

• Largest single cause of post-op. morbidity

• 2nd most common cause of death in over 60 age
• Higher risk to patients with chronic pulmonary disease (COPD)
2.1 ATELACTASIS:

• Inability to breath deeply/ cough up secretions: happens in cases when

patient breath shallowly and don’t caugh. Secretions build up and collapse
airways. This is complicated by process like Paralysis of cilia (due to
anesthicts), impaired diaphragmatic movement, abdominal distension, pain
• Bronchus/bronchiole obstructed by secretions
• Distal alveolar space close (atelectasis), solidify
• Usually occurs within 24 hours
• Tachypnoea, tachycardia, mild fever (most common cause of increased
temperature after operation), ↓ breath sound on affected side, ↓PaO2 
• Chest X-ray- areas of opacification
• If left untreated: Infection- lobar or bronchopneumonia can develop
• Prophylaxis: stop smoking, physiotherapy for COPD
• Delay surgery if chest infection
• Treatment: encourage deep breathing/cough, mobilization, analgesia,
chest physiotherapy 
• If severe hypoxia develops- intubation, suction, bronchoscopy
2.2 PULMONARY INFECTION:

• Follows atelectasis, gastric aspiration

• Strep. pneumo., H. influenzae or gram negatives are the most common
causatives
• Pyrexia, tachypnoea, greenish sputum
• ↓ breath sounds, coarse crepitations, bronchial breath.
• Chest X-ray: patchy fluffy opacities
• Treatment: antibiotics, encourage to cough
• Severe cases: O2, bronchoscopy, ventilation
2.3 RESPIRATORY FAILURE:

• Definition: Inability to maintain normal PaO2 & PaCO2 levels

• Normal PaO2= 11.6 -13 kPa
• Resp. failure PaO2 < 6.7 kPa
• Central cyanosis
• ABG- key to early recognition

62
 Cardiac Complications: 3

• Treatment: Intubation and ventilation

2.4 ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS):

• Characterized by: Impaired oxygenation, diffuse lung opacification and lung

stiffness (↓ compliance)
• Signs: Tachypnoea, ↑ventilatory effort, confusion, hypoxia
• Causes: Systemic/lung sepsis, massive Blood transfusion, aspiration of
gastric contents
• Pathophysiology: Endotoxin activated leucocyte→ oxygen-derived free
radicals, cytokines & chemical ↑capillary permeability →interstitial &
alveolar oedema
• CXR- bilateral diffuse fluffy opacities
• Treatment is ventilation PEEP, treatment of sepsis, hypovolaemia
• Mortality: 50%
2.5 PLEURAL EFFUSION:

• Causes: usually happens after surgery only if the patient has another form
of pulmonary pathology like: collapse, consolidation, infarction, tumour
deposit.
• Also as a result in abdominal pathology: subphrenic abscess
• Approach: Small effusions left to reabsorb, while large effusions aspirated
for culture/ cytology.
2.6 PNEUMOTHORAX:

• Insertion of central venous line is the most common cause of post-operative

pneumothorax
• CXR after insertion central venous line is necessary to exclude this
complication. 
• Positive pressure ventilation- rupture of pre-existing bullae
• Drained by underwater seal
3 CARDIAC COMPLICATIONS:

• Likelihood of anaesthetic/surgery complications are increased in patients

with cardiovascular disease
• Severe aortic/mitral valve dis.- carefully monitor iv fluid administration
• Aortic stenosis impairs heart response to increased post-operative demand
• Whenever possible, treat these before surgery
3.1 MYOCARDIAL INFARCTION:

• Usually history of preceding cardiac disease

• Patients my experience Gripping chest pain.
• Sometimes hypotension is the only sign. This is greatly due to the
anaesthetics/post operative analgesics, where these drugs mask the other
symptoms of ischemia/MI.
• If ischemia is suspected: ECG changes, Cardiac enzymes should be
obtained, and Cardiologist should be consulted.
• 1/3rd postoperative MI are fatal

63
4 General Complications of surgery

3.2 ARRHYTHMIAS:

• Sinus tachycardia: hypovolaemia, hypotension, pain, fever, restlessness

• Sinus bradycardia: anaesthic agents, pharyngeal suction
• Atrial fibrillation may need medications
3.3 POST-OPERATIVE SHOCK:

• Hypovolaemic: Inadequate fluid replacement, bleeding

• Cardiogenic: acute MI, arrhythmias
• ↑pulse, ↓BP, sweating, pallor, vasoconstriction,↓ urine
• Septic:
o Early: hyperdynamic circulation, bounding pulse, fever, rigor and warm
extremity.
o Later: hypotension and peripheral vasoconstriction

3.4 CARDIAC FAILURE:

• Happens in context of Ischaemic or valvular diseases, arrythmia

• Causes: CF is commonly caused by excessive fluid administration in a
patient with limited Cardiac reserve.
• Signs: Progressive dyspnoea, hypoxaemia, and – diffuse pulmonary
congestion on x-ray
• Treatment:
o Avoid fluid overload
o CVP monitoring
o Diuretics, cardiac inotropes
o Cardiologist consultation
4 URINARY COMPLICATIONS:

• Associated with: Groin, pelvic, perineal surgery, operations under

spinal/epidural anaesthesia
• Causes: Pain, effect of anaesthetic drugs, lying/sitting position, BPH
• Males > females, especially when men have prostatic problems
• Signs: Palpable distended bladder
• Treatment: Catheterization
4.1 URINARY TRACT INFECTIONS:

• Most common nosocomial infection, including in postoperative patients.

• Pre-existing UTI, urinary retention, cathterization
• Frequency, dysuria, fever, flank tenederness
• Urine culture
• Treatment: Adequate hydration, urinary drainage, antibiotics
4.2 RENAL FAILURE:

• ARF: protracted inadequate renal perfusion

• Causes: Hypovolaemia (most common cause), sepsis, nephrotoxic drugs
like certain antibiotics

64
 Neurological Complications: 5

• Patients with pre-existing renal disease, jaundice are the most susceptible
• Prevention: adequate IV fluid, urine >0.5ml/kg/hr
• Treatment:
o replace fluid loss+ 500ml
o restrict dietary protein to <20Gm/day
o u/e monitoring, haemodialysis
• Polyuric phase: monitor of fluid intake and u/e
• Recovery 2-4 weeks
• Mortality up to 50%
5 NEUROLOGICAL COMPLICATIONS:

• Cerebrovascular accidents (CVA): sudden ↓ in BP during/ post surgery,

hypertensive patients. Carotid endarterectomy, cardiac surgery
• Psychiatric disturbence: elderly, dementia due to cerebral atrophy, use of
sedatives/ hypnotics
• Acute toxic confusion: sepsis, hypoxia, uraemia, electrolytes imbalance
• Sleep deprivation particularly in ICU
• Delirium tremens: agitation, tremors, hallucinations
6 DEEP VENOUS THROMBOSIS (DVT):

• Virchow’s triad: stasis, ↑coagulability, vessel wall injury

• Risk factors: old age, obesity, prolonged surgery, pelvic/ hip surg,
malignancy, past DVT, varicose veins, pregnancy, use of oral contraceptive
pills
• Presentation: painful swollen tender calf & fever.
• Diagnosis: Duplex ultrasonography
• Prevention: Compression stockings, mechanical compressions of calf
during surgery, subcutaneous heparin
• Treatment: iv bolus/ infusion heparin, LMWH, Warfarin for 3-6 months (INR
2-3 times normal)
7 PULMONARY EMBOLISM:

• Massive PE: severe chest pain, pallor & shock

• CP resuscitation, heparinization, CT angiography, streptokinase/ urokinase
( if 6 days post suregry)
• Small PE: chest pain, tachypnoea, haemoptysis
• CXR, ECG , V/Q scan, CT
• Haparinization
• Warfarin for 3-6 months
8 WOUND INFECTION:

• The most common complication

• Incidence 1% (clean) surgeries to 30% (dirty) casses
• Haematoma formation common before infection
• Manifests within 7 days of surgery
• Fever, tachycardia, increased pain at operation site
• Red, tender, swollen, discharging wound
• Remove few sutures to drain the wound

65
6 General Complications of surgery

• Antibiotics, if septicaemic
9 WOUND DEHISCENCE:

• Involves abdominal wall. Incidence <1%

• Partial (deep layer), Complete (deep+ skin)
• Serosanguinous discharge, evisceration
• Manifests within 2 weeks
• Risk factors: Obesity, resp. disease, infection, malnourishment, renal
failure, malignancy, diabetes, steroid use,& poor surg. Technique
• Re-suture under GA. Develops hernia later

66
 Introduction 1

SURGICAL INFECTIONS
1 INTRODUCTION Exotoxins: toxins
secreted by living
1.1 DEFINITION bacteria that act on
distant sites e.g. Cl.
 Infection is invasion of the body by pathogenic microorganisms and tetani toxin acts on the
nervous system
reaction of the host to organisms and their toxins.
 Surgical infections: Infections that require surgical intervention as a Endotoxins:
treatment or develop as a result of surgical procedure. structural molecules
released when the
o A major challenge bacteria is broken down
o Accounts for 1/3 of surgical patients
o Morbidity and mortality (e.g. septicemia due to post-op infection)
o Increased cost to healthcare (longer hospital stays)
1.2 PATHOGENESIS If a patient comes
with a wound that has
The interaction between microbes and host related factors. been there >6 hrs, the
wound was highly
 Microorganism related factors: contaminated, or the
a. Adequate dose surgeon was not able to
b. Virulence: pathogenic versus opportunistic organisms completely remove the
c. Pathogenicity: necrotic tissue, closing
the wound would create
i. Exotoxins: specific, soluble proteins, remote cytotoxic effect e.g. a suitable environment
Clostridium tetani, Streptococcus pyogenes for infection.
ii. Endotoxins: part of gram-negative bacterial wall,
lipopolysaccharides e.g. E. coli
iii. Resist phagocytosis i.e. by protective capsule e.g. Klebsiella
and Strep. pneumonia
 Host related factors 
a. Suitable environment e.g. hematoma, seroma, foreign body, closed
wound, septic technique, long surgery, inadequate drainage
b. Susceptible host
i. Skin/mucous membrane breach (surgery/trauma)
ii. Compromised immunity: cellular (phagocytes) or humoral
(antibodies) e.g. elderly, diabetes, drugs (corticosteroids,
chemotherapy), radiotherapy
1.3 CLINICAL FEATURES

1. Local: (apparent in superficial infections)

 Signs of inflammation: pain, heat, redness, swelling, loss of function.
 Can occur with, or progress to, systemic symptoms
2. Systemic: fever, chills, tachycardia
1.4 PRINCIPLES OF TREATMENT

1. Debridement: remove necrotic, injured tissue

2. Drainage: for abscess, or infected fluid
3. Excision: infection source (e.g. appendectomy)
4. Supportive measures:

67
2 Surgical Infections

a. Antibiotics
b. Immobilization (if in a limb)
c. Limb elevation (to avoid fluid collection)
1.5 MICROBIOLOGY

Organisms Properties, Common Infections & Treatment

1. Staphylococci • Inhabitants of skin
(Gram +ve) • Sensitive to penicillinase-resistant β-lactam antibiotics
• MRSA is resistant to penicillinase-resistant β-lactam antibiotics  MRSA: Methicillin-
resistant staphylococcus
• Infection characterized by suppuration (thick pus formation): aureus
o Staph. aureus: Surgical Site Infection (SSI), nosocomial, superficial
infections
o Staph. epidermidis: opportunistic e.g. wound (SSI), endocarditis
(especially with prosthetic valves)
• Rx: non-MRSA   cloxacillin, oxacillin  A patient 5 days
o MRSA = Vancomycin  post-appendectomy
presents with pain and
2. Streptococci • Aerobes/anaerobes
redness over the site of
(Gram +ve) • Flora of the mouth pharynx, bowel the wound associated
1. Streptococcus pyogenes (β hemolytic): 90% of infections e.g. with purulent discharge,
lymphangitis, cellulitis, rheumatic fever fever and chills. The
2. Strep. viridens: endocarditis, urinary infection most likely organism:
3. Enterococci: urinary infection, intra-abdominal infections E. coli
3. Gram –ve Rods • Most fall into the family Enterobacteriaceae
• Most are facultative anaerobic
a. Enterobacteriaceae Escherichia, Proteus, and Klebsiella
nd
• Susceptible to a broad variety of antibiotics e.g. 2 generation  An ICU patient,
intubated, and
cephalosporins
catheterized develops an
• Common in mixed surgical infections infection. Most likely
Enterobacter, Morganella, Providencia, and Serratia organism:
• Greater resistance to antibiotics Pseudomonas
rd
• Rx: 3 generation cephalosporins, extended-spectrum penicillins,
monobactam, carbapenem, aminoglycosides or quinolone
b. Pseudomonas, • Obligate aerobic gram –ve
Acinetobacter • Hospital-acquired : pneumonia, peritoneal cavity or severe soft
species tissue infections
rd
• Rx: ceftazidime (anti-pseudomonal 3 gen cephalosporin), cefepime
th
(4 gen cephalosporin), imipenem/cilastatin, meropenem,
ciprofloxacin, acylureidopenicillin, or an aminoglycoside
4. Anaerobes  Inhabitants of GIT (colon) & the mouth
 Most common: Bacteroides fragilis
(all ) • Rx: metronidazole, clindamycin, imipenem, meropenem,
ertapenem, the combinations ticarcillin/clavulanate,
ampicillin/sulbactam & piperacillin/tazobactam
5. Clostridia  Anaerobe, rod-shaped microorganisms
(Gram +ve)  Live in bowel & soil
• Produce exotoxin for pathogenicity
• Most important :
o Cl. perfringens, Cl. septicum: gas gangrene
o Cl. tetani: tetanus
o Cl. difficile: pseudomembranous colitis

68
 Specific Infections 3

2 SPECIFIC INFECTIONS  Pus appears with

superficial SSI if skin is
2.1 SURGICAL SITE INFECTIONS opened and with deep
SSI if superficial layer of
 38% of all surgical infections (very common ) muscle is exposed
 Definition:
o Infection within 30 days of operation
o Infection within 1 year if prosthetic device used (e.g. vascular graft,  In abdominal
artificial heart valve, or mesh for hernia repair) surgeries, the most
 Classification : common organisms
causing surgical
1. Superficial SSI: skin & subcutaneous plane (50%) infections are: B. fragilis
2. Deep SSI: subfascial and muscle plane (20%) & E. coli (can be a
3. Organ space SSI: intra-abdominal, other spaces (30%) mixed infection)
 Microbiology :
1. Staph. aureus is the most common organism
2. E coli, Enterococcus & other Enterobacteriaceae  deep infections  A patient who has
3. B. fragilis  intra-abdominal abscess undergone an ileostomy
 Risk factors: presents with signs of
o Patient-related: age, malnutrition, obesity, immunocompromised, infection.
o Surgery-related: poor surgical technique, prolonged surgery, Most likely organism:
preoperative shaving and type of surgery (clean/contaminated) E. coli
 Diagnosis: Management: Take a
swab for culture, AND
o Superficial SSI: erythema, edema, discharge and pain (take a swab THEN start empirical
of any discharge) antibiotics
o Deep SSI: no local signs, fever, pain, hypotension. Needs
investigation (e.g. CBC, blood & urine cultures, CXR, CT scan)
 Treatment: surgical / radiological intervention
 Prevention:
o Pre-op:
1. Treat pre-existing infection (if there is an active infection e.g.
UTI, delay surgery until infection resolves, unless surgical
emergency) 
2. Improve general nutrition
3. Shorter hospital stay (to avoid hospital acquired infections)
4. Pre-operative shower (with anti-septic wash to risk of
infection)
5. Hair removal (Surgical site should NOT be shaved the day
before the surgery. It’s recommended to shave it in the OR,
or use other methods of hair removal)
o Intra-operative:
1. Aseptic technique
2. Good surgical technique (e.g. do not
leave a hematoma or bleeders)
3. Normothermia
o Post-operative:
1. Wound dressing in 48-72 hours
2. Early drain removal
3. Blood sugar control

69
4 Surgical Infections

2.2 SOFT TISSUE INFECTIONS

2.2.1 ERYSIPELAS
 Erysipelas vs.
 Superficial spreading cellulitis & Cellulitis:
lymphangitis  (limbs to groin = spread
Both are skin infections
toward lymph nodes) that present as redness,
 Redness, sharply defined irregular border warmth and edema.
 Follows minor skin injuries Erysipelas: involves the
 Organism: Strep. pyogenes upper dermis &
 Rx: Penicillin, Erythromycin superficial lymphatics.
Therefore, lesions are
raised and sharply
2.2.2 CELLULITIS defined. It is more
 Inflammation of skin & subcutaneous common in children.
tissue Cellulitis: involves the
deeper dermis and
 Non-suppurative subcutaneous fat. It is
 Organism: Strep. pyogenes more common among
 Common sites: limbs young children & elderly.
 Affected area is red, hot & indurated
 Rx:
o Rest, limb elevation
o Penicillin, Erythromycin
o Fluocloxacillin (if staph. suspected)
2.2.3 ABSCESS
 Localized collection of pus Superficial abscess of the parotid,
 Superficial on the trunk, head and neck  caused by Staphylococcus
S. aureus, (less commonly streptococci) 
 In the axillae  gram-negative
 On the perineum  mixed aerobic &
anaerobic gram-ve
 Abscess may be mistaken for cellulitis
when located deep
 Rx: drainage, antibiotics
2.2.4 FURUNCLE & CARBUNCLE
 Furuncle: infection of hair follicle / sweat glands  Furuncle and
 Carbuncle: extension of furuncle into subcutaneous tissue carbuncle are both
caused by Staph. aureus
o Common in diabetics
o Sites: back, back of neck
o Rx:
 Drainage and antibiotics
 Control diabetes
2.2.5 NECROTIZING FASCIITIS
 Necrosis of superficial fascia, overlying
skin
 Risk factors: elderly, diabetic,
immunosuppressed

70
 Specific Infections 5

 Organism: “polymicrobial”  Streptococci, Staphylococci, Gram-ve rods &

anaerobes
 Sites:
o Limbs  An immune-
o Perineum (Fournier’s) compromised patient
presents with a small
o Abdominal wall (Meleny’s) area of cellulitis, severe
o Trunk (in elderly, diabetics, immunosuppressed) pain and fever post-op.
 Starts as cellulitis  edema  systemic toxicity  shock  On examination, patient
 Appears less extensive than actual necrosis  looks very ill and was
hypotensive.
 Investigation: aspiration, Gram’s stain, CT, MRI
Most likely Dx:
 Treatment: necrotizing fasciitis
o IV fluids
Differentiation from
o IV antibiotics (broad spectrum: ampicillin, cephalosporins, cellulitis: physical
clindamycin, metronidazole, aminoglycosides) findings do not
o Surgical: repeated debridement , dressings, skin grafting correspond to severe
pain
2.2.6 CLOSTRIDIAL MYONECROSIS (GAS GANGRENE) Most likely organism:
Streptococci
 Cl. Perfringens, Cl. Septicum, Cl. Novyi (exotoxins)
Management: immediate
 Risk factors: surgical debridement
o Bone trauma (i.e. open fractures)
o Large wounds of muscle (contaminated by soil, foreign body)
o Drug abusers
 Clinical picture:
o Pain, crepitus (air felt under skin), swelling, seropurulent discharge,
foul smell, myonecrosis  After debridement,
o Toxemia, tachycardia, ill looking the wound should be left
 Investigations: X-ray = gas in muscle and under skin open to allow healing
from the inside out, and
 Rx:
prevent bacteria from
o Antibiotics: Penicillin, clindamycin, metronidazole growing in their preferred
o Repeated debridement , drainage, amputation, hyperbaric anaerobic (closed)
oxygen environment.

2.2.7 TETANUS
 Organism: Cl. Tetani (produces neurotoxin)
 Risk factors: penetrating wound (rusty nail, thorn)
 Clinical picture:
o Trismus: first symptom; stiffness in neck & back
o Respiration & swallowing become progressively difficult
o Reflex convulsions along with tonic spasm
o Death by exhaustion, aspiration or asphyxiation
 Rx is prevention: wound debridement, IV antibiotics (penicillin)
o T toxoid: if previously immunized and booster taken >10 years ago
2.2.8 PSEUDOMEMBRANOUS COLITIS
 Organism: Cl. Difficile
 Overtakes normal flora in patients on
antibiotics 
 Clinical picture: watery diarrhea, abdominal
pain, fever

71
6 Surgical Infections

 Investigations:
o Sigmoidoscopy: membrane of exudates (pseudomembranes)
o Stool: culture and toxin assay
 Treatment :
o Stop offending antibiotic (e.g. clindamycin)
o Oral vancomycin/ metronidazole 
o Rehydration, isolate patient
2.3 BODY CAVITY INFECTIONS

Primary peritonitis Secondary peritonitis

Spontaneous Inflammation/ rupture of viscera
Streptococci, pneumococci  Polymicrobial
Children with ascites Peptic ulcer perforation, pancreatitis,
ruptured spleen, bladder, appendix,
diverticulitis
Haematogenous/ lymphatic spread Direct spread
Rx: antibiotics Investigations: blood, radiological
Treat the original cause

Drainage of liver abscess

Drainage of appendicular abscess

2.4 PROSTHETIC DEVICE-RELATED INFECTIONS

 Examples:
o Artificial valves and joints
o Peritoneal and hemodialysis catheters
o Vascular grafts
 Organism: Staphylococcus aureus
 Rx: Antibiotics, washing of prosthesis or removal
2.5 HOSPITAL-ACQUIRED INFECTIONS

 Definition: occurring within 48 hours of hospital admission, 3 days of

discharge or 30 days following an operation
 10% of patients admitted to hospitals
 Spent 2.5-times longer in hospital (UK)
 Highest prevalence in ICU
 Organism: Enterococcus, Pseudomonas, E coli, Staph. aureus
 Sites: Urinary , surgical wounds, respiratory tract, skin, blood, GIT

72
 Antibiotics 7

3 ANTIBIOTICS

3.1 CLASSES OF ANTIBIOTICS

Class Examples Coverage 

Penicillins Penicillin G, Piperacillin Gram +ve

Penicillins with β- Tazocin (piperacillin + tazobactam) Anti-pseudomonal

lactamase Methicillin, cloxacillin
inhibitors Anti-staphylococcal
st nd st nd rd
Cephalosporins Cephalexin 1 , Cefuroxime 2 , 1 & 2 gen.: Gram +ve cocci 3
rd
Ceftriaxone 3 gen.: Gram –ve rods

Carbapenems Imipenem, Meropenem Gram +ve, gram –ve & anaerobes

Monobactam Aztreonam Gram –ve, aerobic

Aminoglycosides Gentamycin, Amikacin Gram –ve rods e.g. E. coli

Fluoroquinolones Ciprofloxacin Gram +ve, Gram –ve, pseudomonas

Glycopeptides Vancomycin MRSA

Macrolides Erythromycin, Clarithromycin Erythro ≈ penicillin, Clarithro =

extended

3.2 ROLE OF ANTIBIOTICS

 Chemotherapeutic agents that act on organisms

o Therapeutic: To treat existing infection
o Prophylactic: To reduce the risk of wound infection
3.2.1 THERAPEUTIC USES
Pseudomembranous colitis Oral vancomycin/ metronidazole

Biliary-tract infection Cephalosporin or gentamycin

Peritonitis  Cephalosporin/ gentamycin + metronidazole/ clindamycin

Septicemia Aminoglycoside + ceftazidime, tazocin or imipenem

Septicemia due to vascular catheter Flucloxacillin/ vancomycin

Cellulitis Penicillin, erythromycin

3.2.2 PROPHYLACTIC USES

 Administration of antimicrobial(s) prior to surgical procedures to reduce the
number of microbes that enter the tissue or body cavity.
 Antibiotics are selected according to microbes likely to be present at the
surgical site.
 Surgical wound classification :

73
8 Surgical Infections

Class Site Infection Antibiotics?

I Clean Thyroid surgery, breast biopsy < 5% No

ID Graft/mesh used MUST

II Clean- Minimal contamination 11% Yes

contaminated e.g. Biliary, urinary or GI tract
surgery

III Contaminated Gross contamination 17% Yes

e.g. Bowel surgery

IV Dirty Surgery through established > 27% MUST

infection
e.g. Peritonitis

 Prophylaxis in class ID, II, III, IV

 Antibiotic is given just before patient sent for surgery
 Duration of antibiotic is controversial (one dose-24 hour regimen)
4 MCQS

1. To prevent infection developing in a lower limb wound sustained 8 hrs ago

In a road accident , the single most action is :
a. Adequate wound debridement
b. Application of topical antibiotic before Wound closure
c. Giving broad spectrum antibiotic
d. Immediate wound closure
2. A 34 y/o man had bacterial infection and treated with antibiotics. During his
course, he started to develop fever, which was associated with abdominal
pain and watery diarrhea. The most probable diagnosis is:
a. Food poisoning
b. Pseudomembranous colitis
c. Inflammatory bowel disease
d. None of the above
3. The first thing to do in treating the previous case is:
a. Start metronidazole
b. Start vancomycin
c. Isolation and rehydration
d. Stop the offending antibiotic

 Answers: 1:a, 2:b, 3:d

74
 table of contents 1

STERILIZATION
1 TABLE OF CONTENTS

 Evolution of Surgical Asepsis / Sterilization / Terminologies

 Methods of Sterilization
o Physical Methods
o Cool Chemical Methods
o Liquid Chemicals
o Other Methods
 Sterilization Processes
o Preparation of items before sterilization
o Steam Sterilization process
o Testing the Effectiveness of the Autoclave
o Storage of Sterile Packages
 Principles of Aseptic Techniques
2 EARLY CONCEPTS OF INFECTION/ASEPSIS AND
STERILIZATION

450 BC (Hippocrates)- Wine & boiled H2O used to irrigate wounds.

1450 BC (Moses)- Sterilization by fire.
200 AD (Galen)- Boiled the instruments in the care of wounded
gladiators (soldiers).
1545 (Fracastorious)- Proclaimed that diseases were spread: by direct contact,
by handling infected articles that infected people
handled previously & by airborne transmission.
1774 (Scheele)- Discovery of Chlorine.
1818 (Thenard)- Discovery of Hydrogen peroxide.
1837 (Schwan)- Beginning of sterilization by heat.
1847 (Semmelweis)- Used chloro-lime for puerperal sepsis prevention.
Introduced washing of hands between patients.
1850-1862 (Louis Pasteur)- Found out that heat can kill germs (Pasteurization) and
theorized that fermentation caused by particles of living
matter are so small that they could be carried freely in
the air.
1854 (Schroeder & Dusch)- Introduced the use of filters in sterilization of high
temperature pressure.
1859 (Wurtz)- Discovered Ethylene oxide.
1860 (Kuchenmeister)- Discovered Phenol as sterilizing agent.
1860 (Joseph Lister) - Advocated carbolic soaks, hand sprays, wound
dressings, sutures.
1867 (Lister)- Antiseptic principle in the practice of surgery. Discovery
of phenol for infection prevention after operation.

75
2 Sterilization

1876 (Koch R.)- Discovered bacillus anthracis as the cause of disease.

1879 (Chamberland)- The first autoclave was introduced.

1886 (Ernst Von Bergmann & Discovered steam sterilizer under pressure as it is known
associates)- today to kill heat resistant microorganisms.

1894 (Reinecke)- Sterilization action of 90% alcohol.

1894 (William Stewart Pioneered the widespread use of rubber gloves during
Halsted)- surgery.

1900- All sterilization equipment designed in USA & Europe.

1908 (Grossich)- Sterilization by Iodine tincture.

1927 (Schrader & Bossert)- Examination of sterilization action by Ethylene Oxide.

1929- EO gas as anti- bacterial agent was introduced.

1933 (Underwood C.)- Completion of high-pressure steam sterilizer.

1940- EO gas in industries & hospitals is used for sterilization.

1945-Gamma radiation- Introduced & used on commercial basis for the

sterilization.

1949 (Philips & Kaye)- Build up theory of E.O. gas sterilization.

1963 (Stone Hill)- Development of Glutaraldehyde (Cidex).

1980 - Antibiotics Are given before certain types of surgery to prevent

infection.

1993- Plasma Sterilizer was introduced.

1999- OPA Cidex was introduced.

3 TERMINOLOGIES

Sterilization  The process by which all living microorganisms both

pathogenic & non-pathogenic including spores are killed.

Sterile Absence of all microorganisms including bacteria, mold spores

and viruses.

Asepsis Freedom from infection or the absence of microorganisms

that cause diseases.

76
 Methods of Sterilization 3

Sepsis "Opposite of asepsis" Generalized reaction to pathogenic

microorganism, evident clinically by signs of inflammation &
systemic manifestation of febrile condition.

Aseptic Techniques Practices that restrict microorganisms in the environment, on

equipment, supplies & prevent the normal body flora from
contaminating the surgical wound. Methods by which
contamination with microorganisms is prevented.

Bactericidal Agents capable of killing or inactivating bacteria.

Antiseptics Substances that render microorganisms on living tissue

inactive by preventing growth. Combat sepsis. Disinfect body
surfaces, on skin & tissue & inhibit the growth of endogenous
bacteria.

Disinfection Any process, which renders inanimate objects free of

pathogenic bacteria.

Disinfectants Agents that kill all growing or vegetative forms of

microorganisms, thus completely eliminating inanimate
objects.

Contamination Introduction of microorganisms to a sterile field.

 The prevention of infection in health care areas is largely dependent on the
following There is no degree of
 Rigorous adherence to the principles of aseptic techniques by all personnel sterility.
who perform and assist in any invasive procedures on patients.  An item is either
 Sterility of all items directly used in such procedures. sterile or non-sterile; it
can never be relatively
 Disinfection of all surfaces and other items in the immediate environment. sterile. If you are not
 Take note: sure that this item is not
 Surgical instruments and heat sensitive items are sterilized by the method sterile, don't use it.
recommended by the manufacturer.
 No disposable items designed for sterile single use should be reprocessed.
 Sterilizing agent to be in contact with every part / surface of each item to be
sterilized for the specified period of time at the specified temperature.
4 METHODS OF STERILIZATION

 Physical Methods:
 Dry Heat-Hot air ovens, infra-red ovens (Not available in KKUH)
 Moist heat- Steam Autoclave- (Available in KKUH)
 Cool Chemical Methods:
 E.O. Sterilizer- (Available in KKUH)
 Plasma Sterilizer (Sterrad)- (Available in KKUH)
 Liquid Chemicals
 Other Methods

77
4 Sterilization

4.1 PHYSICAL METHOD

Moist heat, at a raised atmospheric pressure

 Steam sterilization is the most inexpensive and effective method of
sterilization. Steam under pressure permits permeation of moist heat to
porous substances by condensation and results in destruction of all
microbial life. Ex. Steam autoclave (steam under pressure)
 Usual method of sterilizing surgical instruments, dressing, drapes, swabs,
laps sponges and culture media.
1. Steam autoclave:
a. An autoclave is a closed chamber in which items or objects are
subjected to steam at high pressures and temperatures above
100ºC.
b. Types of autoclaves:
i. Downward Displacement Autoclave: Air is removed in two stages
and sterilization is effected by an atmosphere of pure steam.
Minimum exposure time is required for sterilizing instruments is
50 minutes at 131ºC or 60 minutes at 136ºC. (Not available in
KKUH)
ii. High Vacuum / High Pressure Autoclave: Air is removed by
powerful pump. Steam penetrates the load instantaneously and
very rapid sterilization of dressings, instruments, raytec swabs,
lap sponges, other surgical items & packs is possible in 15 to 40
minutes at 134ºC. (Available in KKUH)
c. Preparation of items BEFORE sterilization:
1) Decontamination (wash and decontaminate them)
2) Disassembly
3) Washing (wash them again)
4) Drying
5) Packing
6) Loading in sterilizer
2. Ultrasonic Washer: For delicate instruments like in vascular or
neurosurgery
3. Automated Washer: Washer & Dryer.
4.1.1 THE STEAM STERILIZATION PROCESS-5 DISTINCT PHASES 
1. PHASE I -The loading phase - in which the objects or items are packaged
and loaded in the sterilizer.
2. PHASE II -The heating phase - in which the steam is brought to the proper
temperature and allowed to penetrate around and through the objects in the
chamber.
3. PHASE III -The destroying phase or the time temperature cycle - in which
all microbial life is exposed to the killing effect of the steam.
4. PHASE IV -The drying and cooling phase - in which the objects are dried
and cooled “because if u touch it and it's still moist you’ll contaminate item”
, filtered air is introduced into the chamber, the door is opened and the
objects are removed and stored.

78
 Methods of Sterilization 5

5. PHASE V -The testing phase - in which the efficiency of the sterilization

process is checked. All mechanical parts of sterilizers, including gauges,
steam lines and drains, should be periodically checked by a competent
biomed engineer.
4.1.2 MAKING OF STERILE PACKAGES:
 Sterile packages / items should be left untouched and allowed to be cooled
before storage to avoid condensation inside the packs.
 Sterile packages must be handled as little as possible to reduce the risk of
contamination.
 Event Related Sterility - An item that has been properly cleaned, sterilized,
stored & handled will remain sterile unless it is opened or an event happens
that compromises sterility.
4.1.3 STORAGE OF STERILE PACKAGES: 
 Sterile packages should be stored on open shelves:
 The lowest shelf should be 8 inches off the floor.
 The highest shelf should be 18 inches from the ceiling.
 All shelves should be at least 2 inches from the walls.
 Sterile packages must be stored and issued in correct order.
 Sterile items are good for either 30 days or 6 months to a 1 year depending
solely on how the packages are wrapped and what type of wrappers are
used. When it’s process in the central supply department it should be with 2
wrappers> standard.
 This is called the shelf life which refers to the length of time a package
maybe considered sterile.
 Storage room must be subjected to regular adequate pest control to
prevent contamination from rodents, ants and cockroaches.
 Traffic is restricted to CSSD (Central Sterilization Supply Department)
personnel and trainees only.
4.1.4 CAUSES OF FAILURE TO DELIVER A STERILE LOAD: It is necessary to test
1. Faults in the autoclave: autoclaves regularly with
Geobacillus
a. Poor quality steam stearothermophilus,
b. Way it is operated which is one of the most
c. Failure to remove air and condensate heat tolerant species of
d. Faulty gauges and timings bacteria.
e. Leaking door seals If sterilization in an
2. Errors in loading: autoclave does not
a. Large packs destroy the Geobacilus
spores, the autoclave is
b. Excessive layers of wrapping materials not working properly.
c. Over packing
3. Recontamination after sterilization due to:
a. An inadequate air filter and leakage into the chamber
b. Wet or torn packs
c. Incorrect storage

79
6 Sterilization

4.1.5 METHODS OF TESTING EFFECTIVENES OF AUTOCLAVES:

 Bowie Dick test Pack- a pack with a chemical indicator both on the outside
and inside to verify that steam has penetrated the pack & to test air leaks.
 Mechanical- chart and gauges usually carried out by Biomed Engineer.
 Chemical- by the use of autoclave tapes, strips and card. A daily test in an
empty chamber using a heat sensitive tape. This is for high vacuum/high
pressure autoclaves.

Testing the effectiveness of steam autoclaves: 

 First- They run it empty for one cycle. (Dummy Run) – to warm up the machine.
Second- They put inside in the middle of the chamber, the Bowie Dick Test Pack and
run it again and finish the whole cycle. Oh high pressure- to test leaks and presence of
air. (Yellow turns black)
 Third- They load it with items and trays for sterilization ( little bit lower pressure). It is
done once daily.
 Fourth- Live Organism- done once in every Saturday morning in CSSD (Central
Sterilization Supply Department), KKUH

4.2 COLD (CHEMICAL) METHOD

4.2.1 ETHYLINE OXIDE (EO):

 Well established technique for sterilizing heat labile articles.
 Colorless gas at ordinary temperatures
 Has an odor similar to that of ether
 Has an inhalation toxicity similar to that of ammonia dioxide or fluorinated
hydrocarbons (Freon).
 In general, an exposure period of 4 to 7 hours is necessary for complete
E.O. sterilization. *Temperature for sterilizing is 21º C to 60º C (70º F to
140º F).
 Used for sterilizing vascular and bone grafts, delicate instruments, plastic
articles such as disposable syringes, surgical instruments such as
cystoscopes, catheters, bacteriological media and vaccines.

Advantages Disadvantages
•Used only if materials are heat sensitive •Lengthy process with long exposure and aeration
and unable to withstand sterilization by periods”7-8 hours” but it’s very effective also .
saturated steam under pressure. •Expensive and more complex process because after
•Easily available and effective against all sterilization we have to aerate the item to remove
types of microorganisms. residues of Co2.
•Penetrates through masses of dry •Produce serious burns on exposed skin if not
materials; does not require high immediately removed.
temperatures, humidity or pressures.
•Non- corrosive and non- damaging to •Insufficiently aerated materials can cause irritation,
burns of body tissues, hemolytic of blood and diluents
items.
used with EO cause damage to some plastics.
•Toxic and may cause Cancer. *Precautions should be
taken to protect personnel.

80
 Methods of Sterilization 7

4.2.2 PLASMA STERILIZATION:

Plasma Autoclave (Now replaces EO autoclave)
 Low Temperature Hydrogen Gas Sterilizers.
 Employs 1.8 ml. of 58 % hydrogen peroxide vaporized in a sterilization
chamber after a vacuum is created, the vapor is converted into plasma by
means of radio –frequency energy.
 Spore testing should be performed at the same interval as testing of other
sterilizers.
 Advantages of plasma sterilization include speed and safety of use, and the
process does not require aeration.
 Used for moisture and heat sensitive devices, such as cameras, scopes
and fiber-optic cables, microsurgical instruments , glass, ceramic & some
electrical equipment.
4.2.3 LIQUID (CHEMICAL) STERILIZATION:
 When used properly liquid chemo sterilizers can destroy all forms of
microbial life including bacterial, fungal spores, tubercle bacilli and viruses.
 Liquid chemicals can be used for sterilization when steam, gas or dry heat
is not indicated or available.
 Common liquid agents causing disinfection/sterilization:
o Aqueous Formaldehyde- Oldest chemo sterilizers known to destroy
spores; rarely used due to its pungent odor.
o 2% Aqueous Glutaraldehyde (Cidex)- Colorless liquid chemical with
pungent odor.
o OPA Cidex-(0.55% ortho-phthalaldehyde)-Clear, pale-blue liquid
(pH, 7.5), contains 0.55%the non-glutaraldehyde solution for
disinfection of flexible endoscopes and other medical devices.
o Alcohol- 70% Isopropyl Alcohol- Effective & rapidly acting
disinfectants. *Alcohol gel preparations today have been introduced
& long standing effect, fast in action & more users friendly.
o Chlorexidine- Useful skin antiseptic & highly active against
vegetative bacteria. Used in hand scrubbing .
o Hypochlorite- Broad spectrum chlorine disinfectant effective against
viruses, fungi, bacteria & spores. *Disinfectant of choice against
hepatitis B virus.
4.3 OTHER METHODS OF STERILIZAION

1. Gamma radiation:
a. Radioactive material, such as a Cobalt-60 source, emits radiation
(gamma rays).* Pure energy that is generally characterized by its
deep penetration & low dose rates.
b. Gamma Radiation effectively kills microorganisms throughout the
product and its packaging with very little temperature effect.
c. Used on commercial basis for the sterilization of a wide variety of
pre-packaged hospital items and devices.

81
8 Sterilization

d. Total sterilizing time is measured in days.

2. Flash sterilization:
a. Should be used in selected clinical situations & in a controlled
manner. *Use of flash sterilizer should be kept to a minimum & only
for emergent use.
b. Flash sterilization should be used only when there is insufficient
time to process by the preferred wrapped or container method, and
should not be used as a substitute for insufficient instrument
inventory.
c. Flash sterilization should not be used for implantable devices.
5 PRINCIPLES OF ASEPTIC TECHNIQUES

5.1.1 DEFINITION: All items used within

Aseptic techniques are sets of practices / procedures performed under careful, the sterile field must be
sterile.
controlled conditions in order to minimize contaminations of pathogens.
Scrubbed personnel
 Most strictly applied in the O.R. because of direct & extensive disruption should function within a
of skin & underlying tissues. sterile field.

 These practices ensure safe & effective ways in establishing & maintaining
sterile field in which surgery can be performed safely.
 Aseptic techniques help to prevent or minimize surgical site infection.
 Tears in barriers & expired sterilization dates are considered breaks in
sterility.
5.1.2 THE SURGICAL TEAM CONSISTS OF:
 Members are either:
o Sterile members or scrubbed personnel (work directly in the surgical
field.) e.g. Surgeons, Scrub nurse, O.R. Technician
o Non-sterile members or unscrubbed personnel, e.g. Anesthetists,
Circulating nurses, Anesthesia Technicians, X-Ray Technician and
students
 Surgical team members must wear the scrub suit attire with the surgical
cap, surgical face mask before performing surgical hand scrub.
 Surgical hand scrubbing should be performed prior to the donning of sterile
gown & sterile gloves.
5.1.3 SURGICAL HAND SCRUBBING: The sterility is limited
 Surgical Hand Scrub is performed before come in contact with sterile field. to the portions of the
gowns directly viewed by
 The first surgical hand scrub should be at least 5 minutes and the the scrubbed person.
subsequent hand scrub should be at least 2 to 3 minutes.
 Keep nails shorts. No rings & other jewelry, no artificial nails.
 Principle to be applied: “Fluid flows in the direction of gravity.” Hands are
held higher than elbows. Cuffs should be
considered unsterile due
5.1.4 DONNING OF GOWNS/STERILE GLOVES: to its tendency to collect
moisture & it is not an
a. Gown should not touch any unsterile parts. effective barrier.
b. Gloves outer side is not touched by bare hands. Therefore, cuff should
always be covered by
sterile gloves.

82
 Principles of Aseptic Techniques 9

 Scrub nurse may assist other personnel in donning sterile gown & sterile
gloves.
 Gowns are considered sterile only on the: 
1) Front of gown from chest to the level of the sterile field.
2) Sleeves of gown from 2 inches above the elbow to the cuff.
c. Areas of the gown considered non-sterile: 
1) Gown’s neckline
2) Under the arms
3) Shoulders
4) Back

5.1.5 SKIN PREPPING: It's better to use both

d. Surgical site is cleaned with appropriate antiseptics containing Iodine & Alcohol, starting
first with Iodine then
Povidone-Iodine 70%, Alcohol 70 % & Chlorexidine 0.5%. using Alcohol.
e. Apply antiseptic at the line of proposed incision site in concentric circles
moving towards the periphery.
f. Cotton tipped applicators with antiseptics are needed to clean the
umbilicus thoroughly.
g. Antimicrobial tincture or paint may be applied according to surgeon’s
preference.
5.1.6 SURGICAL DRAPES:
h. Surgical Drapes are sterile materials used to maintain the sterility of the
operation field, as they create a sterile field within them.
i. Surgical Drapes establish an aseptic barrier minimizing the passage of
microorganisms from non-sterile to sterile areas.
j. Sterile surgical drapes should be placed on the patient, parts of O.R.
table & equipment included in the sterile field, leaving only the incision
site exposed.
5.1.7 DRAPING PROCESS:
An inch safety margin
k. Only the scrubbed personnel should handle sterile drapes by cuffing the is usually considered
draping material over the gloved hand. standard on package
wrappers, whereas the
l. When draping, the surgical drapes should be compact, held higher than sterile boundary on a
the O.R. table & draped from the prepped incision site to the periphery. wrapper used to drape is
m. Tables are only sterile at the table level. at the table edge.
n. Once the drape is placed, it should not be moved or re-arranged & only
the top surface of the draped area is considered sterile.
5.1.8 STERILE WOUND DRESSING:
 Dressing material should only be opened during wound dressing time.
 Wound or surgical site should be cleaned & dried before application of the
dressing material.
 Dressing material should be applied before surgical drapes are removed to
avoid contamination of the incision.

83
10 Sterilization

5.1.9 GENERAL POINTS OF EMPHASIS: Edge of the bottle cap

is considered
 When opening the sterile items, unscrubbed personnel should open the contaminated once the
wrapper flap farthest away from them first and the nearest wrapper last to cap has been removed
prevent contamination by passing an unsterile arm over a sterile item. from the bottle.
 After a sterile package or container is opened, the edges are considered
unsterile. Fluid/solution should
 Either the entire bottle contents should be poured into the receptacle (Jug) be poured slowly to
or the remainder should be discarded. avoid splashing.
 Pouring should be done at the edge of the table & not at the middle. Splashing can cause
strike through and
 Contaminated items must be removed immediately from the sterile field. contamination of the
 Surgical patient’s operative site is the center of the sterile field & all the sterile field.
scrubbed personnel should remain close to this area without wandering
around the room. Movements can cause contamination of the sterile field.
 Surgical team should move only from sterile areas to sterile areas. If they
change positions, they should turn back to back or face to face and
maintain a safe distance close to the sterile field.
 When delivering sterile supplies onto the sterile field, never contact or
reach over any portion of the sterile area. Non-sterile items should not
cross above a sterile field.
 Non-sterile personnel should always face the sterile field on approach and The general margin of
should never walk between 2 sterile fields. safety is considered to
 O.R. personnel with colds & URTIs should avoid working inside the theater be a minimum of 12
or else wear double masks. inches.

6 MCQS

1. Which of the followings is correct regarding sterilization?

a. Chemical sterilization is the commonest type to be used
b. The scrub up team must keep hands above waist
c. Disinfection is considered enough for surgical instruments
d. Suspicion of organisms spread during an operation is not harmful
2. Which one of the following is the definition of sterilization:
a. The documentation of instrument after using then packing and
loading them.
b. The elimination of violable microorganisms including viruses ,
bacteria ,fungi except spores.
c. The process by which all living microorganisms both pathogenic &
non-pathogenic including spores are killed.
d. The universal precautions that is applied to all patients when there
is exposure of blood product
3. To avoid contamination of the surgical wound. The sterile wound
dressing pad should be applied:
a. After cleaning and drying the wound before removing the drape
b. After surgical drapes are removed
c. Before leaving the operating theater
d. Without cleaning and drying the surgical wound

Answer Key: 1;B , 2;C , 3;A

84
 Introduction 1

PRINCIPLES OF SURGICAL
ONCOLOGY
1 INTRODUCTION

1.1 TYPES OF TUMORS

1.1.1 BENIGN  The difference

 Encapsulated between metastasis
and direct invasion:
 No invasion (controlled growth)
 No metastasis - Direct invasion: tumor
enlarges to invade the
 Can be removed locally adjacent organ with
o In lipoma, we only have to resect it by simple excision, whereas in continuity of primary
liposarcoma, we have to remove the skin and adjacent tissue as well. tumor. (e.g. bladder
cancer goes to colon or
1.1.2 MALIGNANT uterus).

 Non-encapsulated - Metastasis: tumor

invades other organs
o Sometimes, there is a capsule but it’s a “false capsule”, meaning it’s a with discontinuity of
fibrous capsule from the same tissue. primary tumors.
 Usually does invade (uncontrolled growth)
 Metastasis
 Loss of contact inhibition 
o Normally, cells stop growing and reproducing once their plasma
membrane comes into contact with another. Cancer cells lack this
contact phenomenon. They continue to grow into other cells taking over
and often destroying the other cells, creating a tumor.
 Has two main types:
o Carcinoma
 Arises from epithelial tissue  Benign growth is
controlled whereas
 Ex: Adenocarcinoma of the stomach, transitional cell carcinoma of malignant growth is not.
the bladder, squamous cell carcinoma of the skin, follicular That's why it:
carcinoma of the thyroid. - can invade the same
o Sarcoma organ(non-
 Arises from connective tissue encapsulated), go to
 Ex: lipoma( Benign), liposarcoma ( Malignant), Fibroma(Benign) adjacent organs, or go
Fibrosarcoma ( Malignant), Myoma (Benign),myosarcoma to lymph or blood
- can metastasize e.g.
(Malignant), Rhabdomyosarcomas are tumors of the skeletal cancer in lung goes to
muscles, Leiomyosarcomas are smooth muscle sarcomas. brain, cancer of colon
goes to lung, cancer of
1.1.3 TERATOMA prostate goes to
vertebral column.
 Arises from the embryonic “totipotential cells”, which are capable of
developing into any variety of cells.
 Commonly found in germ cell areas (testes and ovaries)
 Could be benign or malignant
 Has the potential to produce new tissues in the organ affected

85
2 Principles of Surgical Oncology

 Ex: Dermoid ovarian cyst, a cystic teratoma that contains developmentally

mature skin, complete with hair follicles, sweat glands, bone and cartilage,
which are not normally found in the ovary.
1.1.4 HAMARTOMA
 Abnormal arrangement of normal tissue, “haphazardly arranged tissue” that
resembles a neoplasm.
 Benign
 Capable of producing complications
 Ex: Angiomyolipoma of the kidney, composed of blood vessels, smooth
muscle cells and fat.
2 GRADING AND STAGING

2.1.1 GRADING The cell usually

differentiates from being
 It describes the histological characteristics of cancer cells, mainly the cell a "blast" in the
layers (e.g. grade I, II, III…)  beginning to it becoming
a "cyte". The blast stage
 Grade of Differentiation describes the characteristics of cancer cells in
means it is still growing,
reference to their resemblance to the cell of origin  and if we see a "cyte",
o Well differentiated it’s closer in morphology
o Moderately differentiated to the mother cell.
o Poorly differentiated
 Indicates that the cancer is rapidly growing with no time for the cells
to be differentiated.
 Most of them are more susceptible to chemotherapy agents b\c
they’re weak due to the rapid development and growth.
o Anaplastic
 E.g.: if we found an enlarged lymph node but we did not know the
origin, we send it to the lab. If it it’s a well-differentiated tumor, the
pathologist will be able to identify the cell of origin.
 However, in poorly differentiated or anaplastic tumors, the
pathologist will not be able to identify the cell of origin, he will only
be able to confirm the malignancy.
2.1.2 STAGING
 Describes the primary tumor, the relation of the primary tumor with:
o The organ of origin
 Bladder cancer can go to the uterus, small intestines, peritoneum,
and rectum (local). Can also go to the liver, chest, brain
 E.g.: tumor in the stomach can go to the duodenum, tumor in
kidney can go to posterior abdominal wall, bladder cancer goes to
colon, uterus, lateral pelvic wall .
o The adjacent organs
o The distant organs and lymph nodes:
 In general, the organs that get metastasized the most are the liver,
lung and bone,
 But the brain is rarely metastasized due to presence of BBB and
can be metastasized from bronchogenic carcinoma.
 Types of Spread:

86
 Grading and Staging 3

1. Lymphatic
 Regional & distant lymph nodes
 E.g. Colon cancer manifesting as a lump in the neck
 Lump in the neck >> 1st sign of metastasis of cancer in the
colon, stomach and testes.
2. Hematogenous
 Common areas of metastasis: Liver, lung, bones
 Brain isn’t a common target of metastasis because of the
BBB that can block out the cancer cells. However, small-cell
lung cancer CAN metastasize to the brain. It spreads very
quickly and also produces hormones like ACTH from the
lung.
3. Transcoelomic
 Dissemination of malignant tumors throughout the peritoneal
(abdominal & pelvic) cavity
 E.g.” Krukenberg tumor”, stomach cancer metastasis to the
ovary, despite the lack of any anatomical relations between
both (lymph nodes nor blood vessels nor direct).
4. Intraperitoneal seeding during surgical manipulation
 Implantation e.g. needle tracks, wounds…
 Very rare
 Needle biopsy should be obtained for diagnosis

Local Invasion Black areas: Hot spots in bone False capsule

Cannonball Metastases

87
4 Principles of Surgical Oncology

 Types of Staging
o Classical staging:  There’s no mention
 Stage I and II confined to the organ of lymph nodes or
 III =direct invasion distant metastasis in the
 IV= metastasis classical staging. That’s
o TNM Classification is more specific: e.g. T1, No, Mo why the TNM
classification has been
 T – Tumor : T1,2,3…., Tis, Ta, Tb… added.
 N – Node : N0, 1, 2, 3 ….
 M – Metastasis : M0,1,2,3…
 Why do we stage malignant tumors?
o To decide the treatment
 Treatment for primary tumors is different from secondary ones
and localized is different from metastasis.
 E.g. you can’t tell the patient he has cancer in the kidney when
you don’t know if there’s metastasis to the liver. This way you
have exposed the patient to unnecessary treatment when
operated on (because there is no benefit of the operation, since
you didn’t check for metastasis)
o To plan the treatment
 Multimodality treatment
 Sometime they’re referred to the tumor board to plan the
treatment (surgery, radiotherapy, chemotherapy)
 Duration of treatment depends on the case
o To assess the prognosis
 E.g. if we have a patient with a localized kidney tumor and
another with a metastasized kidney tumor, the second patient
has poorer prognosis in comparison
 "Our expectations, according to Statistics but not necessarily
applied to the patient himself “. So when we talk about certain
tumors and its high percentage for bad prognosis, this is a
statistical study for a population. But when we talk for a person,
s/he has 50% of having bad or good prognosis.
 Remember that every organ has its own different staging (e.g. Duke
classification for colon cancer only)
3 PRESENTATION OF MALIGNANT TUMORS

 Asymptomatic (incidental finding)

 Symptoms related to the primary tumor  In the GIT, weight
o E.g. Bleeding per rectum or intestinal obstruction for colon cancer loss & cachexia
o Dysphagia for esophageal cancer depends on the level of
tumor, at which the food
o Hematuria for bladder tumor
is blocked. So it’s more
o Hemoptysis for lung cancer evident in the
 Symptoms related to the secondary tumors esophagus (highest
o E.g. 60 y/o female had sudden low back pain, after investigations, she level), than in the
was discovered to have breast cancer stomach and the colon
(lowest level).
o Hemoptysis- patient might have cancer in the kidney and the patient
doesn’t have any problem in urination (secondaries)
o Minimal fall > pathological fracture – discovered to have bone
metastasis

88
 Investigations 5

 Weight loss & Cachexia 

o Late manifestations of most malignant tumors (advanced stage) except
in GI and lung cancers (bronchogenic carcinoma)
 1st presentation comes from the secondary and not from the primary
Presentation of malignant tumors:
o Seizure > metastasis to brain
o Colon cancer > can present as bleeding per rectum – abdominal
distension – intestinal obstruction
o PE= enlarged liver: nodular, rough, smooth, hard.. (to know character of
pain)
4 INVESTIGATIONS

 Investigate for the primary tumor

o For primary we have to define histological features
o In 99% of the cases, we have to know the tissue diagnosis in order to
determine the tumor type
 Define the histology
 Define the local extension
 Depends on the site
 Investigate for the secondaries:
o Look for metastasis
o Usually liver, lung and bones
 Both will define the diagnosis & stage
o Accordingly, the treatment plan will be determined
o Treating Malignant tumors exposes the patient to major surgeries,
dangerous chemotherapy or troublesome radiotherapy. So make sure
that it is malignant then define the type of this tumor (each malignancy
has a specific way of treatment)
4.1.1 CYTOLOGY:
 Morphology of individual cells
 Many ways of obtaining it
o Exfoliative (fluid): urine – sputum the epithelial layer Multiplies and the
superficial cells fall down so try to collect & get benefit from it “without
any effort from doctor “as in sputum or urine sample”.
o Fluid aspiration: ascites, pleural fluid, cyst acidic fluid or plural effusion
draw out and send to cytology
o FNA: taking cells from solid tumors, Fine needle aspiration (FNA), very
common nowadays: in solid tissue and draw out cells, then stain the
cells on the slide and look under the microscope for any malignant cells.
4.1.2 BIOPSY
 Examination of the tissue
o Fine-needle aspiration
o Core biopsy
 E.g. Tru-cut: core of tissue removed for histological examination
 Usually done if the lump is apparent and distinct and localized
 Commonly done through endoscope
o Incisional

89
6 Principles of Surgical Oncology

 Removes a small accessible piece of the lesion for histological

examination (forceps, needle...)
 Many ways of obtaining it
 Like in ulcer, you take a small sample by a knife then send it
to histology
 Needle
 E.g. if having breast cancer for example under x-ray, US
or CT control
 Gastroscope
 If we suspect a gastric ulcer to be malignant OR
colonoscope
o Excisional:
 Complete removal of a discrete lesion without a wide margin
and without it being considered curative of the malignancy
 E.g. Remove breast lump for histology
 Sometimes, this cannot be done because the tumor is
disseminated or cannot be removed alone

 The difference between benign and malignant cells:

o Malignant cells are characterized by deeply stained nuclei (darker),
divided nuclei that are larger in size in comparison to the cytoplasm,
and the shape of the cells is not identical (polymorphism, the cells in
different stages of growth).
5 TUMOR MARKERS

 Substances present in the blood or tissue fluid in a concentration related to

the presence of a tumor
 Most markers are cells from normal cells or malignant cells (primitive)
o Most are non-specific

90
 Hormones and Cancer 7

o Important in diagnosis (general findings + tumor markers>> Dx)

 E.g. patient with testicular tumor "clinically" and was found to have a
high level of the tumor marker>> the patient has teratoma not
seminoma
o Important in follow up
 E.g. patient has testicular tumor and high α –fetoprotein,, after
removing the tumor, α –fetoprotein is decreased. If after 6 months,
the α –fetoprotein goes back up, that indicates recurrence of the
tumor.
o Important for screening
 The early detection, incidence of disease
 Males over 40 years old do PSA
 Mammography for carcinoma of the breast
 PAP smears for cervical carcinoma
 Others: CEA, α-fetoprotein, HCG
 Sometimes pathologists use histochemical stains for specific tumor markers
in tissue, and by this we can determine the type of tumor.
 Patients with high PSA, biopsy showed no indication of malignanacy > false
+ve
 Patient has malignancy but PSA level was normal > false –ve
 To detect relapses
6 HORMONES AND CANCER

 Hormones related to tumor growth:

o Usually sex hormones (testosterone, estrogen)
o They may have a relation to tumor growth
o Hormone receptors are involved
o The concept can be used in treatment
 E.g. In breast cancer, ask the histologist to find any estrogen
receptors. That will affect the treatment plan and prognosis. Also the
prostate needs testosterone to live, so if we block the testosterone
secretion by drugs, the tumor will stop growing
 Growth of the prostate and the malignant cells are dependent on the
testosterone. So we control the malignancy by either removing the
primary producing organ of the tumor, which is the testes, or
blocking one of these pathways.
o When tissue is taken from a cancerous breast and gets sent in to the
lab, we may find estrogen receptors which could be treated with
antiestrogen (Tamoxifen), thus decreasing the effect of estrogen on the
breast. This way we’re minimizing growth of the malignant cells.
 Hormones may be produced by tumors:
o Originally hormone producing organ e.g. adrenals (Cushing’s…)
o Originally non hormone producing organ e.g. lung (bronchogenic
carcinoma)

91
8 Principles of Surgical Oncology

7 MCQS
1. A patient comes with an enlarged cervical lymph node, which of the
following is unlikely to be the primary site?
a. Bronchus
b. Stomach
c. Colon
d. Mouth
e. Laryngopharynx

2. To detect hematogenous spread of a tumor, all the followings should

be done EXCEPT:
a. Chest radiograph
b. Cystoscopy
c. Abdominal CT
d. Bone scan

3. Which of the following tumors has the least potential of malignant

transformation?
a. Renal angiomyolipoma
b. Ovarian embryonic carcinoma
c. Osteosarcoma
d. Mesothelioma

Answers: 1:c, 2:b, 3:a

92
 Objectives of the Lecture 1

PRESENTATION AND
MANAGEMENT OF CARDIAC
SURGICAL DISEASES
1 OBJECTIVES OF THE LECTURE

 Overview of diseases of the heart, where surgery can play a role.

 Understanding of the Basic Principles of Cardiac Surgery.
 Information regarding pre-operative, operative and post-operative care in
cardiac surgery.

2 INTODUCTION

2.1 CARDIAC DISEASES

 Coronary Artery Disease

 Valvular Heart Diseases
 Congenital Heart Diseases
 Miscellaneous :
o Aortic Diseases
o Pericardial Disease
o Cardiac Tumors
o Trauma

2.2 MODES OF PRESENTATION OF CARDIAC DISEASES

 Chest pain
o IHD (Ischemic Heart Disease)
o Aortic disease:  Chest pain and
 Dissection Shortness of breath are
 Aneurism the most common
presentations of cardiac
 Shortness of Breath
patients.
 Palpitations
 Life threatening
 Peripheral Edema
causes of chest pain:
 Congestive Cardiac Failure IHD, Pulmonary
 Cyanosis and Clubbing in Congenital Defects Embolism, aortic
 Uncommon presentations dissection, tension
pneumothorax
o Pleural Effusion
o Hemoptysis

2.3 COMMON CARDIAC OPERATIONS

 Coronary Artery Bypass Grafting (CABG) (most common)
 Valve Replacement / Repair
 Repair of congenital defects like ventricular septal defect (VSD) or atrial
septal defect (ASD)
 Heart Transplantation

93
2 Presentation and Management of Cardiac Surgical Diseases

3 ISCHEMIC HEART DISEASE

3.1 CLINICAL MANIFESTATIONS:

 Asymptomatic
 Symptomatic:
o Angina pectoris: stable- unstable
o Myocardial infarction
o V.S.D., Ischemic mitral regurgitation, Ventricular aneurysm, Heart
failure, Conduction defects.

3.2 Risk factors:

1. Smoking
2. Diabetes mellitus
3. Hypertension
4. Hyperlipidemia
5. Hereditary factors.

3.3 LABORATORY INVESTIGATIONS:  Complications of IHD

 Routine investigations - Angiography is used to
decide the type of Rx:
 Cardiac enzymes
 E.C.G. 1- Medical
 Echocardiography 2- Angioplasty 80%
 Coronary angiography  3- Surgery 20%

3.4 INDICATIONS OF SURGERY: (2+3 Revascularization

therapy)
1. Failure of medical therapy or percutaneous intervention.
2. Left main coronary artery disease.
3. 3-vessel disease with left ventricular dysfunction; three coronary arteries  Percutaneous
are affected. intervention: angioplasty,
balloon dilatation and
4. Mechanical complications of myocardial infarction; include: stenting.
1. Tamponade .2. Wall rupture .3. Chordae tendinae rupture .4. Valve
weakening - Left main coronary
artery: this is the main
5. Associated valve disease; patient with IHD + valve problems = refer to stem of the left coronary
surgery. circulation. If the
blockage is before it
3.5 CORONARY CONDUITS: branches to left anterior
descending and
1. Arterial: Internal thoracic (mammary) artery circumferential artery
then its indicated for
2. Venous: Long saphenous vein. surgery.
3.6 TYPES OF SURGERY:
1. Conventional: the heart is stopped using the heart lung machine, and
cardioplegic arrest. The machine is used to maintain blood and oxygen
supply. Used in valvular and congenital cardiac surgeries (because we
have to open the heart)

94
 Valvular Heart Diseases 3

2. Off-pump (beating heart surgery); When working on the coronaries, we

don’t need to stop the heart because they’re external features. But we must Arterial grafts are
better than venous; they
stabilize the area. have longer patency (In
10 years, 95% arterial
grafts are patent, but
only 50% of veins
remain patent.
-Veins are normally
under low pressure, so if
they are used as
coronary grafts, they are
prone to high pressure
from the aorta and
Coronary Artery Bypass Grafting atherosclerosis.
The internal mammary
4 VALVULAR HEART DISEASES artery is preferred (it is a
smooth muscle artery,
as opposed to the radial
4.1 MITRAL STENOSIS: artery which is a
muscular artery and may
 Etiology: Rheumatic, Congenital undergo spasm).
 Investigations: E.C.G., X-ray chest, Echocardiography Venous graft's patency
 Indications for surgery: may be improved by
using antiplatelet
o Symptoms: exertional dyspnea, pulmonary hypertension, medication and statins.
hemoptysis But they are still not as
o Severe mitral stenosis: area less than 1 cm. patent as the internal
o Left atrial thrombus. mammary artery.
 Treatment:
o Medical
o Balloon valvuloplasty (dilatation in stenosis w/o regurgitation)
o Closed mitral commissurotomy (doesn’t need heart-lung machine)
o Open mitral commissurotomy (needs heart-lung machine)

4.2 MITRAL REGURGITATION:  Mitral and Aortic are

the most common
 Etiology: Rheumatic, Degenerative, Endocarditis, Ischemic, Traumatic diseased valves,
 Indications for surgery: sometimes the tricuspid
as well.
o Symptomatic
o Dilated left ventricle
o Diminished ejection fraction
 Treatment: 1.Medical 2.Mitral valve repair 3.Mitral valve replacement.

4.3 AORTIC STENOSIS:  Mitral valve

replacement.Open mitral
 Etiology: Rheumatic, Congenital, Degenerative. commissurotomy and
mitral valve replacement
 Indications for surgery: are the only surgical
o Symptoms (angina, shortness of breath, syncopal attacks) procedures in the
o Severe aortic stenosis treatment list
 Treatment: 1-Medical 2-Aortic valve replacement  Closed mitral
commissurotomy is a
4.4 AORTIC REGURGITATION: surgical procedure but it
is not preformed
anymore.

95
4 Presentation and Management of Cardiac Surgical Diseases

 Etiology: Rheumatic, Endocarditis, Connective tissue disorders, Aortic

dissection
 Indications for surgery:
o Symptomatic patients.
o Progressive left ventricular dilatation.

4.5 PROSTHETIC VALVES: TYPES, MERITS AND DEMERITS

1. Tissue Valves (Bio prosthesis)
a. No need to use long term anticoagulation.
b. Limited and unpredictable durability
c. When to use tissue valves?
i. Old patients
ii. Patient with contraindication to
anticoagulants i.e. bleeding disorders
iii. Non-compliant patients to
anticoagulants e.g. psychiatric patients
iv. Pregnant woman due to the teratogenic effect.
2. Mechanical Valves
a. Anticoagulation for life 
b. Prolonged durability

 Complications of prosthetic valves:

1. Thrombosis
2. Bleeding complications (1,2 Anticoagulant
related complications)
3. Infective endocarditis
4. Paravalvular leak
5. Degeneration of biological valves
5 THORACIC AORTIC DISE ASE
1. Thoracic aortic aneurysm
a. Symptoms are usually due to pressure on surrounding structures.
2. Aortic dissection:
a. Tear in the intima allowing blood to enter and flow in a false
channel.
b. There are 2 lumens separated by the dissecting membrane.

96
 Pericardial effusion 5

6 PERICARDIAL EFFUSION

 Progressive accumulation of fluid inside the pericardial cavity, may

compress the cardiac chambers.
 Etiology:
o Traumatic
o Pericarditis
o Malignancy
o Uremia, post irradiation
o Postoperative.
 Investigations:
o Plain x-ray chest
o Echocardiography
o CT scan
 Management:
o Treat the cause
o Aspiration
o Pericardiostomy (if the fluid is
not accessible)

7 CARDIOTHORACIC EMERGENCY
1. Chest pain (causes):
a. Myocardial ischemia
b. Pulmonary embolism
c. Aortic dissection
d. Tension pneumothorax
e. Rupture esophagus
2. Acute dyspnea (causes):
a. Myocardial infarction
b. Pulmonary embolism
c. Spontaneous pneumothorax
d. Bronchial asthma
e. F.B. (foreign body) aspiration
f. Stuck mechanical valve.
3. Chest trauma:
a. Flail chest
b. Traumatic hemo/pneumothorax
c. Hemopericardium

8 CONGENITAL HEART DISEASES

8.1 ACYANOTIC:

1. Patent ductus-arteriosus
2. Co-arctation of the aorta
3. Pulmonary stenosis
4. Atrial septal defect (ASD)
5. Ventricular septal defect (VSD)

97
6 Presentation and Management of Cardiac Surgical Diseases

8.2 CYANOTIC:
1. Tetralogy of Fallot (VSD, overriding aorta, pulmonary stenosis, RV
hypertrophy)
2. Transposition of the great vessels
3. Tricuspid atresia
4. Total anomalous venous drainage
5. Truncus arteriosus

9 BASIC PRINCIPLES OF CARDIAC SURGERY

1. Adequate Exposure
 Full or Partial Sternotomy / Thoracotomy / Robotic or Endoscopic
2. Bloodless Operative Field
 Suction and re-transfusion / Snaring or clamping of bleeding
vessels
3. Static Operative Target
 Cardiac Arrest / Ventricular Fibrillation / Mechanical Stabilizers
4. Preservation of body perfusion
 Use of Heart Lung Machine / Off-pump Techniques
5. Preservation of Myocardium
 Off-pump Techniques / Hypothermia / Cardiac Arrest with
cardioplegia

10 HEART LUNG MACHINE

 Components :
1) Roller pumps
2) Blood Reservoir (cardiotomy
reservoir)
3) Oxygenator
4) Heater-cooler unit
5) Tubing and Monitoring console
etc
 Limitation/Problems :
1) Requires full anticoagulation
2) Can cause micro embolism
3) Initiates Systemic Inflammatory Response

11 PREOPERATIVE ASSESSMENT

 Evaluation of patients referred for cardiac surgery aims to answer the

following questions:
o Is surgery appropriate for the condition?
o Is the patient fit to undergo the planned operation?
o Is there any comorbidities that may affect the operative
management?
 Approach:
1) History
2) Physical examination
3) Chest x-ray

98
 Summary& MCQs 7

4) E.C.G.
5) Laboratory investigations
 Pre-Operative Investigations for Cardiac Surgery
o Full Blood Count
o Blood Biochemistry
o ECG
o Chest X-ray
o Pulmonary Function Tests.  Carotid Duplex scan
and Peripheral Duplex
o Other test according to systemic review of patient scan:
o Echocardiography
To check if other vessels
o Angiography are affected too
o Carotid Duplex Scan
o Peripheral Duplex Scan
 Usual Duration of Stay in Hospital  This is for a standard
o One day before surgery non complicated case.
o 3-6 hours OR time
Duration may increase
o One day in ICU due to complications and
o 4-5 Days in Ward in older patients.
o Total 5-7 days

12 SUMMARY& MCQS

12.1 INDICATIONS OF CARDIAC SURGERY

IHD 1. Failure of medical therapy or percutaneous intervention.

2. Left main coronary artery disease
3. 3-vessel disease with left ventricular dysfunction
4. Mechanical complications of myocardial infarction.
5. Associated valve disease
Valvular heart Mitral stenosis
disease 1. When symptoms of severe SOB appear like: exertional dyspnea,
pulmonary hypertension, hemoptysis
2. Severe mitral stenosis : less than 1 cm opening
3. Left atrial thrombus

Mitral regurgitation
Significant shortness of breath : Symptomatic, dilated left ventricle,
diminished ejection fraction
Aortic stenosis
1. Symptoms (angina, shortness of breath, syncopaal attacks)
2. Severe aortic stenosis
Aortic regurgitation
1. Symptomatic patients
2. Progressive left ventricular dilatation
Thoracic aortic 1. Aortic aneurism
disease 2. Aortic dissection
Pericardial effusion Drainage by catheterization unless the fluid is not accessible

99
8 Presentation and Management of Cardiac Surgical Diseases

12.2 MCQS
1) For coronary artery bypass surgery, which one of the following conduits has
proved to be the best in long term patency?
a) Gastroepiploic artery
b) Internal mammary artery
c) Radial artery
d) Reversed saphenous vein

2) Which one of the following coronary arteries is the most commonly involved in
ischemic heart disease?
a) Left anterior descending artery (LAD)
b) Main coronary artery
c) Obtuse marginal branches
d) Right coronary artery
3) the most important pre-operative study in evaluating patients for coronary artery
bypass grafting that will serve as a road map for the surgeon is?
a) Cardiac catheterization
b) ECG
c) Thallium scan
d) trans-thoracic echocardiography

Answers: 1;B , 2;A , 3;A

100
 Overview: Structure and Development of the Lungs 1

PRESENTATION AND MANAGEMENT OF

COMMON THORACIC DISEASES
1 OVERVIEW: STRUCTURE AND DEVELOPMENT OF THE LUNGS

1.1 EMBRYOLOGY

 Bronchial system
 Alveolar system
1.2 ANATOMY

 Lobes and fissures:

o The right lung is divided into 3 lobes by the  Primary bronchi:
oblique and horizontal fissures. - Right primary bronchus
o The left lung is divided into 2 lobes by the is shorter, wider, and
oblique fissure more vertical than the
 Segments left primary bronchus.
Therefore, when foreign
 Blood supply: bodies are aspirated,
o Lungs don’t receive any vascular supply they often lodge in the
from the pulmonary vessels (pulmonary right main bronchus.
artery or vein)
o Blood is delivered to lung tissue via the bronchiole arteries
o Vessels evolve from aortic arch
o Travel along the bronchial tree
 Airways:  Bronchopulmonary
o Trachea, primary bronchi, secondary bronchi, tertiary bronchi out to 25 segments:
generations Each of the tertiary
o All comprised of hyaline cartilage bronchi serves a specific
o Trachea: bronchopulmonary
segments.. There are 10
 Begins where larynx ends (about C6) segments in the right
 10 cm long, half in neck, half in mediastinum lung and 8-10 segments
 20 U-shaped rings of hyaline cartilage, keeps lumen intact but not on the left and each
as brittle as bone have their own artery.
 Lined with epithelium and cilia, which work to keep foreign Each segment is a
discrete anatomical and
bodies/irritants away from lungs functional unit, so a
o Bronchioles: segment can be
 First level of airway surgically removed
surrounded by smooth without affecting the
function of the other
muscle; therefore can segments.
change diameter as in
bronco-constriction
and bronco-dilation
 Terminal bronchioles
 Respiratory
bronchioles
 3-8 orders Bronchopulmonary segments
o Alveoli

101
2 Presentation and Management of Common Thoracic Diseases

2 LUNG DISEASES

Congenital Infectious Tumors

 Agenesis • Lung Abscess  Malignant
 Hypoplasia • Bronchiectasis
 Cystic adenomatoid • Tuberculosis - Primary lung
malformation • Aspergillosis carcinoma
 Pulmonary sequestration • Hydatid cyst - Secondary lung
 Lobar emphysema carcinoma
 Bronchogenic cyst  Benign

2.1 CONGENITAL
CCAM:
 Agenesis: Presenting clinical
features include:
o Absence of the lungs respiratory distress and
 Hypoplasia: recurrent respiratory
o Incomplete development of the lungs infections. The usual
 Congenital Cystic Adenomatoid Malformation (CCAM): appearance of CCAM
on CXR is a mass
o A cystic area within the lung that stems from abnormal embryogenesis. containing air-filled cysts
Usually an entire lobe of lung is replaced by non-functioning cystic area of (Swiss cheese pattern),
abnormal lung tissue. Pulmonary
 Pulmonary Sequestration: Sequestration:
o It consists of a nonfunctioning mass of normal lung tissue that lacks normal Sequestrations are
communication with the airways, and often receives its own arterial blood classified anatomically
into intralobar and
supply from the systemic circulation (esp. thoracic aorta). Most of the time it extralobar. Usually
is located in the left lower lobe. Treated surgically to prevent infections. presents in adolescence
 Lobar Emphysema: or late childhood as
o Over-inflation of a pulmonary lobe (replacement of a whole lobe by bullae), repetitive chest
infections that fails to
which may compress the other remaining normal lobes. Air enters the lungs respond to medical
but cannot leave easily causing respiratory function to decrease. Treated treatment. It appears on
surgically (lobectomy) in serious cases to allow normal lung to inflate. CXR as an opaque
 Bronchogenic Cysts: mass. Diagnosed by
MRI/arteriography.
o They can be located:
 In the mediastinum most commonly attached to Lobar Emphysema:
trachea or below the carina (paratracheal or Diagnosed by
subcarinal) respiratory symptoms
and CXR, which shows
 Or within the lung parenchyma over-inflation of the
(intraparenchymal) affected lobe
o Clinical features: (radiolucency).
 They consist of semi-solid cartilaginous that secretes cheese like
material, which is prone to infections. It may also result in hemorrhage
and compression of the surrounding structures (i.e. trachea, aorta, and
esophagus) patient then complains of SOB, stridor, cough and
dysphagia.
 Could be asymptomatic found accidentally on CXE as a smooth
opacity.
 They may transform to malignant adenocarcinoma.

102
 Lung Diseases 3

o Treatment: surgical excision is done to confirm diagnosis, avoid

complications such as malignancy, rupture, infection, and compression on
vital organs.
2.2 INFECTIOUS

2.2.1 LUNG ABSCESS

Clinical Features of
 Causes: Lung Abscess:
o As a complication of pneumonia, bronchial obstruction (by tumor or - Gradual onset
inhaled foreign bodies esp. in children) bacteremia, and septic emboli. - Productive cough
 Clinical features: copious production of foul smelling sputum - High fever
 Investigations: - Night sweats
o CXR (air-fluid level)
- Weight loss & lethargy
o CT scan
- Chest pain (pleuritc)
 Treatment:
o Antibiotics
o Drainage: internal and external
o Pulmonary resection (surgical treatment)
 Indications:  Empyema= collection
1. Failure of medical treatment of pus in an anatomical
2. Giant abscess (>6 cm) cavity (e.g. pleural
3. Hemorrhage (patient presents with hemoptysis) empyema)
4. Inability to rule out carcinoma (e.g. a 65 y/o very ill smoker
can have lung cancer superimposed by abscess)
5. Rupture with resulting empyema
 Type of resections:
o Lobectomy (main) or bilobectomy (2 lobes)
o Pneumonectomy
2.2.2 BRONCHIECTATSIS Immotile Cilia
 Definition: Bronchial dilatation, usually affecting the lower lobes Syndrome:
 Cause: -Bilateral
o Congenital (i.e. cystic fibrosis and immotile cilia syndrome) -Lung transplant is
needed in old age
o Infection (repeated pulmonary infections and childhood infections)
o Obstruction (by tumors/ inhalation of foreign bodies)
 Clinical features:
o Cough mostly in morning with copious amounts of sputum
o Dyspnea
o Hemoptysis (50%)  Development of
o Clubbing (it is a chronic disease) childhood vaccinations
 Types: has reduced the
incidence of
o Cystic bronchiectasis due to
o Cylindrical whooping cough,
 Investigations: measles, and TB.
o Bronchogram (invasive)
o CT scan (more accurate)
o Bronchoscopy (not commonly used nowadays)
o CXR (cystic formation)

103
4 Presentation and Management of Common Thoracic Diseases

 Treatment:
o Medical:  E.g. a child inhales a
 Resolve most cases (bronchodilators, antibiotics, and physiotherapy foreign body  bronchial
with postural drainage) tree obstruction (> right
o Surgical indications:  main bronchus)  mom
explains that her child
 Failure of medical treatment was ok 6 months ago but
 Cystic dilatation (not cylindrical which is treated medically) now he has been getting
 Localized disease repetitive chest
 Not perfused (assessed by V/Q scan), most of cystic bronchiectasis infections/SOB/wheezing
are not perfused whereas most of cylindrical are perfused.  suspect foreign body
inhalation bronchiectasis
2.2.3 TUBERCULOSIS
 30,000 new cases occur annually in USA
 Cause:  Cystic? Localized?
o Pulmonary Non-perfused? >
o Extra-pulmonary Surgical
 Investigations: Cylindrical? Bilateral?
o CXR (more in apex) Perfused? > Medical
o AFB sputum culture (if positive confirms TB)
o Tuberculin skin test (latent TB)
o Bronchoscopy
o Chest CT scan (infiltration, abscess formation, lymph nodes)  Left bronchus
o Mediastinoscopy (caseating granuloma) syndrome:
 Treatment: Chronic condition that
o Medical: leads to unilateral post
 Effective in most cases TB lung destruction as a
o Surgical indications  result of
untreated/resistant TB.
 Failure of medical treatment
 Destroyed lobe or lung Fibrosisloss of
spaceloss of
 Pulmonary hemorrhage ventilation on left side 
 Persistent open cavity with positive sputum left lung is smaller,
 Persistent broncho-pulmonary fistula infective, and
bronchioectatic pulling
2.2.4 ASPERGILLOSIS the trachea towards it.

 Cause:  Don’t operate on

active open TB b/c of the
o Aspergillus fumigatues, Aspergillus niger risk of spread of
 Mode of Transmission infection. Manage them
o Inhalation of airborne conidia medically first for 4
o Contaminated water (during showering) weeks before surgery.
o Nosocomial infections (hospital fabrics and plastics)
o Esp. in immunocomprimsed individuals
 Forms:  Saprophytic
o Allergic (allergic bronchopulmonary aspergillosis) Aspergillosis:
o Saprophytic (aspergilloma/mycetoma) Characterized by Asp
o Invasive infection without tissue
 Clinical features invasion. The most
common underlying
o Aspergilloma/mycetoma causes are TB and
 Comes with a warning sign of hemoptysis sarcoidosis.
 At this stage, the doctor must act quickly because morbidity and
mortality are very high in these patients

104
 Lung Diseases 5

 Hemoptysis (patient with preexisting disease)

 Chronic productive cough
 Sometimes found accidentally on CXR
 Investigations:
o Skin test
o Sputum (fungal culture)
o Biopsy (invasive)
o CXR (radiolucent)
o CT scan (cavity with aspergilloma complex and
air crescent sign, DDx TB)
 Treatment:
o Medical (anti-fungal)
o Surgical indications:
 A significant aspergilloma (with serious clinical features)
 Hemoptysis
 Types of resection: depends on the affected side
 Segmentectomy
 Lobectomy (mainly)
 Pneumonectomy
2.2.5 HYDATID CYST  Transmission:
 Definition: Dog (definitive host) 
o Parasitic infestation by Echinococcus sheep (intermediate
granulosus (tapeworm) host) human by eating
raw sheep liver 
o Hosts: dogs, cats, and sheep (e.g. by eating enteric systemportal
raw contaminated sheep liver) systemliverIVC
 Clinical presentation: heart and
o Asymptomatic (accidentally found) lungssystemic!
o Symptoms are the result of compression by - The liver is the most
the cyst (e.g. dyspnea) common organ involved,
followed by the lungs
 Diagnosis (brain, bones, kidneys...
o Skin test (Casoni’s reaction) can also be involved)
o CXR
o CT scan (a chronic cyst will appear calcified
on CT)
o High echinococcus titers and other serologic  Hydatid cyst
tests layers:
o Routine blood work (nonspecific) 1. The outer pericyst,
 Treatment composed of host cells
that are formed as a
o Radical surgical excision (cyst reaction to the parasite
resection or partial affected organ (false layer).
resection) coupled with 2. The middle laminated
chemotherapy using albendazole membrane (external
and/or mebendazole before and layer of cyst)
after surgery. 3. The inner germinal
o If multiple cysts are present in multiple organs surgery becomes layer of cyst where the
impractical and chemotherapy is indicated. scolices are produced
and contained.
2+3 form the true wall of
the cyst

105
6 Presentation and Management of Common Thoracic Diseases

 Surgeon must be careful when doing this procedure, because each cyst contains millions of
scolex (highly infective) so if ruptured it’ll spill millions of scolex into surrounding cavities
which leads to the formation of new cysts!
 Injection of scoliodal agents such as hypertonic 20% saline is used during surgery to kill
scolex.
 Rupture of the cyst depends on the size of feeding bronchus, if it was big a small cyst can
get ruptured, but if the feeding bronchus was small, the cyst won’t rupture.

2.3 TUMORS

 Benign
 Malignant
o Primary
o Secondary
2.3.1 PRIMARY LUNG CARCINO MA
 Incidence:
o Worldwide, lung cancer is the most common cause of cancer death.
 Risk factor:
o Smoking (most important)
o Others: radiation, industrial chemicals, diet, genetic factors, asbestos,
and radon
 Pathology:
o Non-small cell carcinoma
 Adenocarcinoma
 Squamous cell carcinoma
 Large cell carcinoma
o Small cell carcinoma
 Classification: must differentiate between SCLC & NSLC because
treatment approach is completely different.
NSCLC SCLC
 Epithelial origin • Neuroendocrine origin  Definitions:
 75-80% • 20-25% - Horner’s syndrome:
1. Adenocarcinoma (40%) • Centrally located Characterized by the
o Peripherally located • Poor prognosis classic triad of miosis
partial ptosis, and loss
2. Squamous cell carcinoma (30%) • Patient usually presents with of hemifacial sweating
o Centrally located systemic disease (e.g. large (i.e., anhidrosis).
3. Large cell carcinoma (9%) mediastinal LAD) - SVC obstruction
o Peripherally located • Mostly discovered late when syndrome:
 Treatment:  tumor has already metastasized SOB most common
o Early: Surgery (+/- adjuvant • Treatment:  symptom and facial/arm
chemotherapy) swelling.
o NON-surgical (chemotherapy
o Intermediate: Neoadjuvant only +/- radiotherapy) - Pancoast tumor:
chemotherapy + surgery Superior sulcus tumor
o Late/metastasis: NON-surgical injury of C8 & T1
(chemo/radiotherapy + palliative causing shoulder pain
that radiates to arm
management)

106
 Lung Diseases 7

 Clinical Features:
o Asymptomatic  accidentally on CXR
o Symptomatic
 Lung manifestations (most commonly cough, hemoptysis, SOB...)
 General manifestations (loss of appetite, fever, weight loss, fatigue)
 Surrounding structures:
- Recurrent laryngeal nerve (e.g. hoarseness)
- Esophagus (dysphagia)
- C8, T1 nerve (arm pain/numbness)
- Sympathetic (esp. 1st sympathetic ganglion: Horner’s
syndrome)
- Pleural pain
- SVC obstruction syndrome
 Distal Para-neoplastic syndrome:
- PTH (hypercalcemia)
- ADH (hyponatermia)
- ACTH (Cushing’s syndrome)
- Hypertrophic pulmonary osteoarthropathy (Pain and swelling of
joints that doesn’t respond to medical treatment and improves
once tumor is resected)
 Investigations:
o CXR (find a previous CXR for comparison, if lesion is stable for more
than 2 years, it is most likely benign)
o Bronchoscopy (for central lesions as with squamous lung CA and
SCLC)
o Transthoracic needle aspiration (for peripheral masses, CT guided)
o CT scan (best modality for staging extent of metastasis) 
o MRI (poor modality in staging, its helpful to rule out involvement of
major structures in the apex: brachial plexus, vertebral column, and
spinal cord e.g. superior sulcus tumor)
 Staging:
NEW INTERNATIONAL REVISED STAGE GROUPING
 Lymph node
staging:
Stage 0 TIS
Stage IA T1, NO, MO N1  inside the lung
Stage IB T2, NO, MO N2  outside the lung
toward mediastinum
Stage IIA T1, N1, MO hilum
Stage IIB T2, N1, MO
N3 supraclavicular or
T3, NO, MO to the other side
Stage IIIA T1-3, N2, MO
T3, N1, MO
Stage IIIB T4, Any N, MO  Neoadjuvant
Any T, N3, MO chemotherapy:
Stage IV Any T, Any N, M1 Chemotherapy before
the surgery (to downsize
the tumor)
Adjuvant
 Management chemotherapy:
o Depends on: Chemotherapy after the
surgery

107
8 Presentation and Management of Common Thoracic Diseases

 Stage (tumor size, LN involvement, metastasis to liver, bone, and

brain) done by CT.
 Cell type
 Patient physical fitness (tumor might be of an early stage but the
patient has other comorbidities)
o NSCLC:
 Surgical (early stages) +/- adjuvant chemotherapy
 Neoadjuvant chemotherapy + surgery (intermediate)
 Radiotherapy and chemotherapy (late stages)
o SCLC:
 Chemotherapy (treatment of choice)
 Radiotherapy
 NON-surgical (because tumor is usually discovered late, when  Benign Vs.
metastasis is extensive and the patient develops systemic Malignant solitary
pulmonary nodules:
symptoms with massive mediastinal lymphadenopathy)
Benign 
2.3.2 SECONDARY LUNG CARCINOMA Age <50, nonsmoker,
size <2 cm, no growth
 Neoplasms that have spread from a primary lesion in another organ over 2 year period,
 Secondary lung tumors appear as solitary lung nodules (well-marginated, circular and regular
single mass <3 cm, intraparenchymal opacity) shaped, central
laminated/concentric
 Solitary Lung Nodule DDx: (coin lesions) calc.
o Primary Carcinoma
Malignant 
o Tuberculous Granuloma
Age >50, smoker, size
o Mixed tumor
>3cm, steady growth,
o °2 Carcinoma (metastatic) irregular nodule or
o Miscellaneous speculated margins,
 Hamartoma - Carcinoid stippled/eccentric calc.
o Age: hamartomas occur primarily in adults >50 y/o
o Sex: Males 3 times more likely than females  Hamartomas are the
o X-ray (usually peripherally located) most common type of
 Size: usually small <4cm in diameter, rounded benign lung tumors,
 Time: grows slowly accounting for 75% of all
benign lung tumors and
 Calcification: sometimes with varying patterns
most of them are
asymptomatic.
3 TRAUMA

 RTA (road traffic accidents)

 Fracture ribs (simple/complicated)  Traumatic
o Most common blunt thoracic injuries pneumothorax:
 Haemothorax: Can result from either
o Accumulation of blood in pleural cavity penetrating or non-
o Appears as radio-opacity on CXR. penetrating chest
trauma. Iatrogenic
o Cause is mostly traumatic pneumothorax is one of
 Pneumothorax the most common
 Flail chest: causes (e.g. during
o Fractures of several adjacent ribs in two or more places producing a transthoracic needle
aspiration procedure).
free unstable segment of chest wall that results in paradoxical Treat simple
movement. There is usually associated lung contusion. pneumothorax with a
 Lung contusion and ARDS (no surgery needed unless massive bleeding) chest drain if
large/symptomatic.

108
 Mediastinum 9

4 MEDIASTINUM

4.1 ANATOMY:

 Mediastinum is the space in the thoracic cavity between the lungs

 Boundaries 
o Superior: thoracic inlet
o Inferior: diaphragm
o Anterior: sternum and costal cartilages
o Posterior: thoracic spine
o Lateral: mediastinal pleura
 Divisions:
o Superior mediastinum (above the sternal angle)
o Inferior mediastinum (below the sternal angle) subdivided into: Anterior,
Middle, Posterior
 Access:
o Mediastenscopy
o Mediastenotomy
4.2 MEDIASTINAL MASS LESIONS:

Anterior Mediastinum Middle Mediastinum Posterior

Mediastinum
Neurogenic tumors
5 TS  Cysts  
a. Teratoma a. Pericardial cyst (E.g. dumbbell tumor
b. Thyroid (retrosternal b. Bronchogenic cyst of neurofibroma,
goiter) paravertebral mass…)
c. TB lymphadenitis
d. T cell lymphoma
e. Thymoma

4.2.1 THYMOMA
 Incidence:
o The commonest tumor of anterior mediastinum 
o Peak 40-60 y/o
o M: F (1:1) equally affected
 Pathology:
o Classification:
 Epithelial
 Lymphocytic
 Lymphoepithelial
 Spindle cell
o Benign Vs. malignant
o Stages: I, II, III, IV
 Clinical Features:
o Asymptomatic
o Symptomatic
 Mass effect  SVC syndrome, dysphagia, and cough…)

109
10 Presentation and Management of Common Thoracic Diseases

 Systemic effect  associated autoimmune disorders, most

commonly myasthenia gravis 40-50%
 Investigations:
o For all cases 
 CXR
 CT scan (can be indicative of malignancy)
 Biopsy
o For selected cases 
 Bronchoscopy, Esophagoscoy
 Angiogram
 Treatment:
o Benign  complete excision
o Malignant:
 Complete excision if possible
 If non-resectable (i.e. invasive and large)  Preoperative
(neoadjuvant) chemotherapy and/or radiotherapy may be used to
decrease the size and improve resectability or incomplete
resection.
5 CHEST WALL

 Deformities:  Thoracic outlet

o Pectus excavatum: caved-in or sunken appearance of the chest syndrome: compression
o Pectus carniatum: protrusion of the sternum & ribs (pigeon chest) at the sup thoracic outlet
 Infections (e.g. abscess, empyema, costochondritis…) placing pressure on
nerves and vessels
 Chest wall tumor: Those that grow on the ribs and sternum (>benign) passing through, with
 Thoracic outlet syndrome signs and symptoms
manifesting in arms and
5.1 PLEURA hands esp. pain.

 Spontaneous pneumothorax
 Pleural effusion: collection of fluid in the pleural cavity
 Empyema: collection of pus in the pleural cavity
 Mesothelioma: rare cancer, usually caused by asbestos exposure
5.1.1 PNEUMOTHORAX
 Definition: air in the normally airless pleural space
 Classification: Traumatic and non-traumatic (spontaneous)

Spontaneous Pneumothorax Tension Pneumothorax

- Life threatening condition.
 Primary/simple pneumothorax
- Accumulation of air under positive
- Occurs without any underlying lung
pressure in the pleural space
disease
collapses the ipsilateral lung and
- Spontaneous rupture of air-filled
shifts the mediastinum away.
sacs on the lungs causing escape of
air from the lung into pleural space Causes:
and lung collapse
1. Mechanical ventilation with
 Secondary/complicated
associated barotrauma
pneumothorax
2. CPR

110
 Chest wall 11

- As a complication of underlying lung 3. Trauma

disease, most commonly COPD
Clinical features:
Clinical features:
1. Hypotension and tachycardia
1. Sudden ipsilateral chest pain 2. Distended neck veins
2. Dyspnea and cough 3. Shift of trachea away
3. Decreased breath sounds over 4. Decreased breath sounds on
affected side affected side
4. Hyperresonance over the chest 5. Hyperresonance
5. Decreased tactile fremitus
Diagnosis: clinically (no time for
6. Mediastinal shift toward side of
CXR!)
pneumothorax
Treatment:
Diagnosis: CXR
Medical emergency!
Treatment:
 Primary spontaneous pneumothorax If tension isn’t relived patient is likely
- If small and patient is asymptomatic to die from hemodynamic
 compromise.
a. Observation (should resolve Immediately decompress the pleural
spontaneously in 10 days) reassess space via large-bore needle or chest
with CXR tube
b. Small chest tube may benefit some
patients
- If larger and/or patient is
symptomatic 
a. Administration of supplemental
oxygen
b. Chest tube insertion to allow air to be
released
 Secondary spontaneous
pneumothorax
a. Chest tube drainage

5.2 AIRW AY

 Congenital tracheal anomalies

 Tracheal stenosis: narrowing of the trachea that is caused by an injury or
birth defect.
 Tracheostomy
5.3 SURGERY

 Thoracotomy
 Thoracoscopy
 Sternotomy
 Analgesia

111
12 Presentation and Management of Common Thoracic Diseases

6 MCQS

1. Which one of the following thoracic diseases is treated by chest tube

insertion?
a. Caveating malignant lung mass
b. Cystic bronchiectasis
c. Large pneumothorax
d. Lung abscess

2. A 22 y/o female is referred for evaluation of 2-cm posterior mediastenal

mass discovered on routine chest radiograph. What is the most likely
diagnosis?
a. Bronchogenic cyst
b. Lymphoma
c. Neurogenic tumor
d. Thymoma
e. Adenocarcinoma

3. Which one of the following is the most common blunt chest injury?
a. Pneumothorax
b. Hemothorax
c. Sternal facture
d. Rib fracture
e. Pulmonary contusion

Answer key  1;C , 2;C , 3;D

112
 Introduction 1

PEDIATRIC UROLOGICAL
CONDITIONS
1 INTRODUCTION

 Most common anomalies of all organ systems

 10% of the population have some type of urogenital anomaly
 14:1000 births have an antenatal diagnosis of urogenital anomaly
 The antenatal diagnosis is done by ultrasound after 28 weeks of gestation
because at 24-28 weeks the urinary system starts to be clear on ultrasound
2 ANTENATAL HYDRONEPHROSIS (ANH)  Hydronephrosis is
dilation of the
2.1 INTRODUCTION: pelvicalyceal system.
Hydroureter: dilatation of
 This is hydronephrosis detected during pregnancy by ultrasound the ureter
 It is a condition which has a differential diagnosis and causes. It is not a Both renal pelvis and
diagnosis on its own! ureter:
hydroureteronephrosis
 Causes:
o Pelviureteric junction obstruction (41%)
o Ureterovesical junction obstruction (23%)
o Vesicoureteric reflux (7%)
o Duplication anomalies (13%)
o Posterior urethral valves (10 %)
o MCDK (Multicystic dysplastic kidney)
o Others (6%)
 Grades of ANH
o Specific details of grading are not important but you should know:
 Urine appears black on ultrasound
 Grade zero: normal kidney
 From I-IV: 1 is the simplest and 4 is the worst
 Grading depends on level of dilatation by ultrasound
o So if you see hydronephrosis in an antenatal ultrasound the
 diagnosis is: antenatal hydronephrosis
 the differential diagnosis is: (any of the below)
2.2 1ST DDX: PELVIURETERIC JUNCTION OBSTRUCTION (PUJO)

 Dilation of the renal pelvis due to obstruction at the junction between the
pelvis and ureter
 Because the obstruction is before the Ureter in these cases is usually not
affected
 So on Ultrasound the renal pelvis is dilated and the ureter is normal
 It is the most common cause of ANH
 Etiology: (theories): Segmental muscular attenuation, Angulation, True
Stenosis, Extrinsic compression, Crossing vessels; 20-30%.
 Associated findings:
o Reflux in 5-10%

113
2 Pediatric Urological Conditions

o Contralateral PUJO in 10%

o Contralateral agenesis in 5%
 Presentation:
o More in males and occurs in the left side more than the right
o Incidental in neonates by US or in infancy
o If the diagnosis is missed during pregnancy or early infancy the child
could come with symptoms like:
 UTI
 Pain
 Mass
 Hematuria
 Stones
 Investigations include ultrasound, renal scans and VCUG (voiding
cystourethrography)
 Indications of surgery:
o Symptomatic patients
o If the finding is incidental:
 Neonates: worsening pattern or reduced renal function
 Children: significant obstruction
2.3 2ND DDX: URETEROVESICAL JUNCTION OBSTRUCTION

 Also called megaureter or severely dilated ureter

 There is a narrow segment that causes the dilatation of the whole renal
system
 Could be bilateral or unilateral but it is mostly unilateral
 It is different from PUJO in that the ureterovesical junction obstruction has a
dilated ureter 

 Presentation:
o Male 3:1 female
o Left 3:1 Right
 Types:
o Obstructive non refluxing
o Obstructive refluxing
o Refluxing non obstructive
o Non refluxing non obstructive (adynamic ureter)
o Treatment:
 Obstruction: excision and reimplanting of the UVJ
 Reflux: according to the same line of reflux management

114
 Antenatal Hydronephrosis (ANH) 3

2.4 3 R D DDX: DUPLICATION ANOMALIES

2.4.1 RENAL AND URETERIC DUPLICATION

 Incidence is 1%, 1.6:1 F:M, 85% unilateral.
 Either two urethral buds meeting the meta-nephros or one ureteric bud that
bifurcates.
 Associated with: reflux 43%, renal dilatation 29%, ectopic insertion 3%,
infections and ureterocele.
 Duplication per se is of no clinical significance, but the associated anomalies
may require intervention

A: incomplete duplication
B: complete duplication

- Usually only one ureter comes

from each kidney to bladder: single
system.
- Duplication Anomalies: 2 ureters
coming from each kidney and going
to bladder.
- Incomplete Duplication: both
ureters meet in their way and one
ureter go to bladder.
- Complete Duplication: 2
duplications.

 Embryological view:
o Normally: One ureteral bud (early precursor of the ureter) meet future
kidney.
o In Incomplete (figure 1) ureteral duplication: Ureteral bud bifurcate into 2
after the generation they go to kidney as 2 ureters
o In complete (figure 2) ureteral duplication: 2 separate ureteral buds
come to meet metanephic kidney (future kidney)
o If the both ureters coming to kidney and no reflex or obstruction > no
harm to kidney but if there is obstruction as in uretrocele or ectopic ureter
or reflex that will be harmful

Figure 1 Figure 2

2.4.2 COMPLETE DUPLICATION FROM UPPER POLE OF KIDNEY TO

LOWER POLE OF BLADDER
 Here a principle called the Weiger-Meyer Law takes place which states:

115
4 Pediatric Urological Conditions

 The upper pole ureter (which drain the upper pole of the kidney) comes to
lower part of bladder and lower pole ureter coming to upper part of the
bladder

Figure 3

2.4.3 URETROCELE
 Commonest cause of urine retention in female infants 
 Cystic dilatation of the distal part of the ureter
o This will lead to obstruction and the whole ureter will get dilated
 Associated with duplication anomalies (figure 3)
 This can be confused with Uretrovesical junction obstruction but the
difference here is there is cystic dilatation which can be present in the bladder
 Sacculation of the terminal portion of the ureter has 2 types:
o Orthotopic
 Intravesical (inside bladder)
 Simple OR adult type ureterocele.
o Ectopic
 Start in bladder and extended outside the bladder
 Extravesical=duplex system OR infant type ureterocele.
o In ectopic ureterocele it involve the upper pole system.
Figure 4

 Presentation:
o Hydrouretronephrosis
o 7:1 F:M, 10% bilateral, ectopic : orthotopic 4:1

116
 Antenatal Hydronephrosis (ANH) 5

o Usually detected by Antenatal (U/S)  we use MCUG (micturating

cystourethrogram) to confirm the diagnosis  (figure 5)
o Symptoms include: urine retention, infection and presence of stones
o Intralabial mass:
 One of the differential diagnosis for an Intralabial mass in females is
a ureterocele
 Management:
o Needs urgent intervention
o Incision of ureterocele
o Upper pole heminephroectomy
o Excision of ureterocele and common sheath reimplant.

Cystic structure in bladder which is cystic dilation of distal part of ureter

MCUG, put catheter in bladder and use contrast if there is no abnormality the
whole bladder will be white. But in ureterocele we will see filling defect 

Figure 5

2.4.4 ECTOPIC URETER

 Ureter does not implant in the bladder and stays outside
 Most commonly associated with duplex system and with ureterocele.
 Clinical picture depend on: associated anomalies, site and sex of the patient.
 Can be:
o Simple ectopia: implanted in abnormal position

117
6 Pediatric Urological Conditions

o Ectopic ureter: it is completely outside the bladder

 Investigations include IVP, VCUG, cystoscopy
 Renal scan asses the function of both renal poles in case of duplication.
2.5 4TH DDX: VESICOURETERIC REFLUX (VUR)

 There is a normal anti-reflux mechanism between the bladder and the ureter
a “Flap Valve” which depends on: 
o Ureter has an Oblique course as it enters the bladder.
o Proper muscular attachments to provide fixation.
o Posterior support to enable its occlusion.
o Adequate submucosal length.
 The study to rule out reflux is MCUG and it is also used for grading:
o Normal: contrast in bladder
o Grade I: confined to ureter, contrast is in the distal part of the ureter
o Grade II: contrast reaches the kidney but there is no dilation
o Grade III: Mild dilation of the renal pelvis and ureter without loss of
calyces
o Grade IV: moderate dilation but there is loss of calyces
o Grade V: severe dilation and tortuous dilated ureter”

 Resolution of reflux: Over 3 year follow up:

o 87% of Grade 1
o 63% of Grade 2
o 53% of Grade 3
o 33% of Grade 4
 Management: The decision depends on :  Prophylactic dose:
o The chance of spontaneous resolution ( age and grade at presentation ) (1/3 of therapeutic dose
only at night (24h), long
o Breakthrough infection term)
o Renal scarring and renal function
o Compliance with medication
 Medical management:
o Patients with UTI (the most common presentation) and VUR is
suspected. 
 Continue on prophylactic antibiotics after treatment till the VCUG is
done.
o Patients for conservative management :

118
 Antenatal Hydronephrosis (ANH) 7

 Continue meticulously on prophylactic antibiotics and surveillance

with urine culture and sensitivity, U/S ,and DMSA (
dimercaptosuccinic acid) scan
2.6 5TH DDX: POSTERIOR URETHRAL VALVE (PUV)  Between anterior &
posterior urethra during
 Incomplete canalization of the posterior urethra embryologically there is
 1:5000 male infants. canalization from distal
to proximal and from
 Most common cause of urine retention in male infants. caudal to
 50% have renal impairment. cephalic leading to
 The bladder and the kidneys developed under high pressure and resistance. complete tube without
any narrowing,
 The more proximal the valve the more sever the condition
But in Posterior urethral
 Associated findings: valve incomplete
o Oligohydramnios : canalization of urethra
 low amount of Amniotic fluid and leave small
 No output of urine or little → Amniotic fluid membrane (posterior
 Low in Ultrasound because there is no secretion but there is urethral valve) which
cause obstruction
absorption.
 Obstruction of esophagus no absorption > Polyhydramnios.
o Bilateral renal dilatation 
o VUR: 40%
o Valve bladder → loss of its Function and become abnormal bladder
 The bladder is urogenic  because during pregnancy the
detrusor muscle is replaced by collagen so no contraction of muscle
occurs.
 Baby start voiding during 24th week of gestation → so in Posterior
urethral valve the baby will void against pressure so bladder will be
large and trabeculated and urogenic
o Renal impairment: in 30-50%, 25% of them will have renal transplantation
in the future
o The obstruction is not complete (narrowing or stenosis) because if its
complete “severe” the patient will die in utero
 Presentation:
o Antenatal (hydonephrosis)
o Urine retention
o UTI
o Poor urinary stream
o CRF; at late stage
 Investigations: Antenatal US, US, VCUG, Renal scan, renal function studies,
Urodynamic studies.
o MCUG: Posterior urethra dilated, normal anterior urethra ,bladder
trabeculated and elongated (christmas tree bladder)

119
8 Pediatric Urological Conditions

3 CONGENITAL ANOMALIES OF THE KIDNEY

3.1 ANOMALY OF POSITION, NUMBER AND ROTATION:

1. Simple ectopia:
 A kidney that is outside the renal fossa.
 Pelvic (commonest), lumbar, sacral.
2. Thoracic kidney. kidney in chest
3. Horseshoe kidney
 2 kidneys fused and connected together
 90% by the lower lobes
 10% upper lobes connected
 the connection is either fibrous band or
sometimes it’s parenchymal tissue
4. Unilateral renal agenesis.
5. Bilateral renal agenesis.
6. Crossed renal ectopia with no fusion.
7. Crossed renal ectopia with fusion.
Right to left ectopia
8. Malrotated kidney.
 Normal position of the kidney: retroperitoneal in flank area.
o Anywhere except this place is called ectopia
o Cross ectopia: kidney goes to other side

Horseshoe kidney

3.2 CYSTIC ABNORMALITIES:

1. Renal dysplasia
o Congenital unilateral multicystic kidney.
o Segmental and focal renal dysplasia.
o Renal dysplasia associated with congenital lower tract obstruction.
2. Congenital polycystic kidney disease:
o Infantile type
o Adult type
3. Simple cyst
4. Calyceal cyst
5. Peripelvic cyst
6. Perinephric cyst

120
 Prune belly syndrome 9

Figure: Multicystic dysplastic kidney

- One of the DDx of ANH
- Kidney is non functional
- The whole kidney replaced by cysts so
no nephrogenic tissue
- Multicystic: means multiple cysts
- Dysplastic: no renal tissue.
- Polycystic: kidney is large usually
bilateral

4 PRUNE BELLY SYNDROME

 Also called Eagle-Barrett Syndrome

 Consists of a triad of:
1. Absent abdominal wall muscles
 External oblique, Internal oblique,
Transverse abdominal muscles
 You can feel all the organs and you can
even see the bowel movement because the
muscle layer is either absent or thin
(hypopalstic).
2. Bilateral undescended testis
3. obstructive uropathy
 bilateral hydrouretronephrosis and large bladder
5 HYPOSPADIAS

 Abnormally located meatus which

contains the urethral opening
 The meatus usually opens in the tip of
the glans penis and if it opens anywhere
else it is considered an ectopic opening
o In hypospadias the opening is
towards the scrotum or ventral side
o In Epispadias the opening is
towards the abdomen or dorsal side
 Common ( 2%)
 Abnormal position of the EUM(external
urethral meatus ):
o Distal hypospadias: (from mid shaft
to Glans)
o Proximal hypospadias (from
proximal penile “proximal shaft” to
the perineal)
 Treatment:
o NO Circumcision 
o Absolute contraindication because dorsal urethral skin we will be needed
in repairing later on especially in proximal hypospadias

121
10 Pediatric Urological Conditions

o Age to repair:6 to 9 months

o Requires one stage repair
6 EPISPADIAS

 Very rare , Abnormal position of external urethral meatus in dorsal surface of

the penis

7 BLADDER EXSTROPHY

 Bladder has 3 walls: Anterior, lateral and posterior.

 Anterior wall consist of abdominal muscles and skin
 In bladder exstrophy the anterior wall is absent (no anterior abdominal wall,
no skin) so the lateral wall will be attached to skin to outside.
 the bladder is exposed to the outer environment
 We need to close bladder and to reconstruct abdomen
 Rare; 1:30000 live births with a 3:1 male : female ratio
 The results of improper development of anterior abdominal wall, pelvic girdle ,
and anterior wall of the bladder

122
 Urological Disorders 1

ADULT UROLOGICAL
DISORDERS
1 UROLOGICAL DISORDERS

1. Urinary Tract infections

2. Urolithiasis
3. Voiding dysfunction
4. Benign Prostatic Hyperplasia
1.1 URINARY TRACT INFECTIONS

1.1.1 INTRODUCTION Haematogenous

spread: e.g. tooth
Lower Urinary Tract (less morbid) Upper Urinary Tract
abscess > pyelonephritis
• Urethritis • Acute Pyelonephritis In the past, they used to
• Epididymitis/Orchitis • Chronic Pyelonephritis see more hematogenous
• Prostatitis • Renal Abscess spread like in TB>
• Cystitis Pyelonephritis & Renal Abscess can lead to secondary TB in kidney.
death. So, it’s a serious condition. -Adjacent invasion: e.g.
Diverticulum ruptured in
 Routes of UTI:  bladder >UTI.
o Ascending infection; 95%.
o Haematogenous spread.
o Adjacent invasion, imagine you have colon with diverticulum and
diverticulum would rapture in bladder so u will have UTI
o Lymphatics; rare.
1.2 URETHRITIS

Common in men; in young men usually the cause is STDs.

1.2.1 SYMPTOMS
 Urethral discharge
 LUTS in the form of dysuria
 Burning on urination
 Asymptomatic; 25% especially in women.
1.2.2 GONOCOCCAL VS. NON-GONOCOCCAL
 Diagnosis of the organism is established by :
o Incubation period: Gonococcal: 3-10 days vs. Non-gonococcal: 1-5 wks.
o Urethral swab; send it to be cultured to identify the proper antibiotics which
are affecting the organism.
o Serum marker & antigen: Chlamydia-specific ribosomal RNA (usually done
in chronic forms of disease)

123
2 ADULT UROLOGICAL DISORDERS

Gonorrhea Chlamydia
Organism Neisseria gonorrhea Chlamydia trachomatis
The most common
Organism Type Gram (-) diplococci Intracellular facultative organism nonspecific urethritis is
Incubation Period 3-10 days 1-5 weeks due to chlamydia.

Urethral Discharge Usually profuse, purulent Usually Scant

Asymptomatic 40%-60% 40%-60%
Carriers
Diagnostic Test Ligand chain reaction, Gram stain Polymerase/ligand chain reaction,
Culture Culture, Immunoassay
Treatment Ceftriaxone + Azithromycin or Ceftriaxone or Azithromycin
Doxycycline

1.3 EPIDIDYMITIS  Young male has

untreated urethritis, the
 Acute: Pain, swelling, of the epididymis <6wk. consequences  blood
 Chronic: Longstanding pain in the epididymis and testicle, usually no swelling. flows up to urethra 
goes to ejaculatory duct
 goes to epididymis.
 Young boy comes with bad testicular pain, must differentiate between 2 conditions:
Epididymitis is caused
1) Testicular torsion  urological emergency; patient should go to OR.
by retrograde ascent of
2) Epididymitis urinary pathogens from
the urethra and bladder,
via the ejaculatory ducts
 How can we differentiate b\w Epididymitis vs. Torsion? and vas deferens,
leading to colonization
Epididymitis Torsion and inflammation of the
epididymis.
Family Older patient Usually young boys, just reached
History Gradual onset adolescence
With urinary symptoms like burning Acute pain – sudden in onset
sensation – hematuria e.g patient may Usually without urinary symptoms  Cremasteric reflex is
elicited by lightly stroking
say doctor I had blood in urine for 2 the superior and medial
weeks now. (inner) part of the thigh.
Physical Inflammatory sign (redness-warmth and High raiding testis, testis is kidney- The normal response is
Examination swelling of the scrotum) shaped , bean-shape, Horizontal lie a contraction of
Loss of cremasteric reflex the cremaster
muscle that pulls up
U/S Because of infection > Hyperemia No blood flow the scrotum and testis on
Testicular Increased radiotracer uptake; Photopenia (white area) the side stroked.
Scan hyperscan photogenic (black)
Urine for Younger: N. gonorrhoeae or C.
 Examining a patient
Culture trachomatis with torsion is very
Older: E. coli (gram -ve rods) painful, but in
epididymitis, raising the
scrotum makes it better
because it increases
drainage  “Prehn's
sign”: pain relieved by
elevation of the testicle.

124
 Urological Disorders 3

Figure 1: Guidelines for Treatment

1.4 PROSTATITIS  The root of an

ascending infection may
Prostate: produces about 80% of the semen go through ejaculatory
 Syndrome that presents with inflammation ± infection of the prostate gland duct to prostate and
including: that’s why some people
get the infection.
o Dysuria, frequency
o Dysfunctional voiding -Difficult to treat because
of the capsule and
o Perineal pain configuration of prostate.
o Painful ejaculation So you may give patients
antibiotics for months.

Figure 2: It’s not required to know the categories of prostatitis. This table just shows that there’s more
than one type. Some are due to bacteria, and some are not due to bacteria. And we fail to isolate the
bacteria when doing urine culture

125
4 ADULT UROLOGICAL DISORDERS

1.4.1 ACUTE BACTERIAL PROSTATITIS  Acute bacterial

prostatitis: Patient should
 Rare get admitted b/c it’s a
 Acute pain serious problem. He may
 Irritative and obstructive voiding symptoms get hypotension 90/40
(urosepsis – septic
 Fever, chills, malaise, N/V shock)
 Perineal and suprapubic pain
It’s a rare clinical
 Tender swollen hot prostate emergency condition that
 Rx: antibiotics and urinary drainage maybe life threating 
BUT chronic prostatitis is
more common.

1.5 CYSTITIS  Cystitis is more

common in women than
 Signs and symptoms men, why?
o Dysuria, frequency, urgency, voiding of small urine volumes B\c women have shorter
o Suprapubic/lower abdominal pain urethras (4.5 cm). Some
o ± Hematuria of them are genetically
predisposed to bacteria
o No fever even if it’s severe as the lining of the
 Diagnosis bladder is more
o Dipstick: When nitrate is (+), it indicates an infection susceptible to E.coli.
o Urinalysis
o Urine culture; is the gold standard. It takes 2 days. Start treatment
before waiting for results b/c we know what are the commonest organisms.
 Treatment
o Usually treatment of UTI in women is just for 3 days, to avoid any effect on
normal bowel flora. In men, the treatment is usually for a week.

126
 Urological Disorders 5

Figure 3

1.6 PYELONEPHRITIS

 Definition: inflammation of the kidney and renal pelvis

 Signs and symptoms:
When will the patient
o Chills get fever? If the bacteria
o Fever has ascended and
o Costovertebral angle tenderness (flank pain) reached the kidney
o GI: Abdominal pain, N/V, and diarrhea (pyelonephritis)
o Gram -ve sepsis - mild flank pain -Some women will ignore
o Dysuria, frequency their feeling of dysuria
and they come to the ER
 Investigations: with urosepsis.
o Urine C&S (culture & sensitivity):+VE (80%)
o Enterobacteriaceae (E. coli), Enterococcus
o Urinalysis:↑ WBCs, RBCs,Bacteria
o Blood test for renal function: (±) ↑serum Creatinine  In culture, the most
common organism we
o CBC: Leukocytosis. see in pyelonephritis is
o Urine dipstick, microscopy: To get rapid results gram (-) rods E.Coli
o Imaging: To rule out any possible obstruction followed by
 IVP (Intravenous Pyelogram) enterococcus species.
 U/S
 CT

Pyelonephritis complicated by obstruction:

 Renal stones complicated by ovary cancer that is blocking the kidney; in this case, we have to
drain kidney. We don’t only give antibiotics b/c there is a collection of pus by putting the tube
in the kidney ”Nephrostomy Tube”, under local anesthesia> used in obstructive infective
kidney especially if patient is very sick.
 In U/S, we will see hydronephrosis; dilated kidney.
 Another option: If patient is better than the first example, we can do "Double J", which is a
tube placed inside the ureter during surgery to ensure drainage of urine from the kidney into
the bladder. Stent is temporary treatment to bypass the blockage > b/c if we manipulate the
stones, the patient may have bacteremia and die.

127
6 ADULT UROLOGICAL DISORDERS

Figure 4: Just a guideline.

2 UROLITHIASIS

2.1 INTRODUCTION  Cystinuria is an

autosomal recessive
 The condition associated with urinary calculi. disease: So it affects
o Common disease in Saudi Arabia children (it’s hard to tell if
o Egyptian mummies 4800 BC a child is drinking water).
o Prevalence of 2% to 3% And, in general, if not
treated, it can lead to
o Lifetime risk: Male : 20%, Female: 5-10% death b\c of the
o Recurrence rate 50% at 10 years complications like renal
 Risk factors: failure. When you do
o Intrinsic Factors transplantation for them:
new kidneys >the
 Genetics disease is gone
 Age (2Os-4Os); young people.
 Sex M>F
o Extrinsic Factors
 Anatomic
 Geography (mountainous, desert, tropics) abnormalities:
 Climate (July - October)
Presence of certain
 Water Intake abnormalities of the
 Diet (purines, oxalates, Na) urinary tract like
 Occupation (sedentary occupations) hydronephrosis or
 How do stones form? obstruction in the urinary
tract leads to stasis
o Supersaturated (patient doesn’t drink water) → solute will concentrate→ (stoppage) of the urine
Crystal Growth. and then the super-
o Aggregation of crystals →stone. saturation of minerals
 Most people have crystals in their urine, so why doesn’t everyone get that eventually leads to
formation of stones.
stones?
o Anatomic abnormalities.
o Modifiers of crystal formation: Inhibitors/promoters

128
 Urolithiasis 7

 Citrate, Mg, urinary proteins (nephrocalcin); are inhibitors for stone

formation.
 Oxalate; is a promoter for stone formation such as: coffee, chocolate
and soda drinks, except some of them which also contain citrate that
will inhibit stone formation
 Common stone types 
a) Calcium stones 75% (Ca Ox ) calcium oxalate
b) Uric acid stones; uric acid is found in animal protein & it’s the commonest
cause of radiolucent kidney stones.  The renal angle is
c) Cystine stones: Cystine is an amino acid. Remember them by COLA: very tender in
pyelonephritis, less
cystine, oxaline, lysine and arginine; the proximal tubules are unable to tender in renal stones
reabsorb these amino acids. All of them are water soluble except Cystine, and not tender in
that’s why it forms stones. appendicitis.
d) Struvite stones.
2.2 SIGNS AND SYMPTOMS  Taking History of
renal colic:
 Renal or ureteric colic
You have to memorize
 Frequency, dysuria the signs and symptoms.
 Hematuria Renal colic comes with
 GI symptoms: N/V, ileus, or diarrhea flank pain. So you should
 DDx : ask about PAIN which
o Gastroenteritis has 8-10 questions that
you should cover.
o Acute appendicitis
And when you take Hx of
o Colitis renal colic, you should
o Salpingitis form some differentials
 Restless  for flank pain such as:
o ↑HR, ↑BP -If pain is worse with
o Fever (If UTI) bowing and improves by
o Tender costovertebral angle lying down – MSK pain
-If the pain radiates to
2.3 INVESTIGATIONS right or left lower
quadrant – Renal stone
 Urinalysis : -Radiates to labia in
o RBCs women and to scrotum in
o WBCs men – Renal stone
o Bacteria -Pain when coughing –
Cholecystitis
o Crystals
 Imaging (table 1) -Pain with movement
and goes to leg –
o Plain Abdominal Films (KUB); shows only radiopaque stones. Prolapsed disk.
o Intravenous Pyelogram (IVP); shows radiolucent (uric acid stone) &
-If the pain comes after
radiopaque stones (calcium stones). eating – Cholecystitis
o Ultrasonography (U/S); shows hyperechoic stones + acoustic shadow. (and may also vomit)
o Computed Tomography (CT): The gold standard; most sensitive and -The pain is in the pre-
specific & shows the radiolucent stones. So it’s the first step. umbilicus then goes to
the right lower quadrant -
Appendicitis
-Young married female
with Hx of no period for 2
months – Ectopic
pregnancy

129
8 ADULT UROLOGICAL DISORDERS

KUB U/S

 The 3 normal
narrowings in the ureters
 Stenosis of
Ureteropelvic Junction
leads to stasis and
hydronephrosis.
 UPJ: Ureteropelvic
Junction

IVP: In case of high grade obstruction, you may stay 2 days without seeing any  UVJ: Ureterovesical
Junction.
findings.

CT

2.4 TREATMENT

1. Conservative:
a. Hydration
b. Analgesia
c. Antiemetics
d. Stones (<5mm ) >90% undergo spontaneous passage.
2. Indications for admission:
a. Renal Impairment
b. Refractory Pain
c. Pyelonephritis; patient has 3 mm stones with fever and chills>
pyelonephritis.
d. Intractable N/V; can’t take oral analgesia.

130
 Voiding Dysfunction 9

3. Shock Wave lithotripsy

(SWL): Good for kidney
stones and small stones;
potential injury to ovary.

4. Ureteroscopy: Breaks up
large stones by laser.

5. Percutaneous
Nephrolithotripsy (PNL):
For huge stones

6. Open surgery: Not used

anymore.
3 VOIDING DYSFUNCTION
Failure to store Failure to Empty
– Bladder Problems – Bladder Problems
– Overactivity: common in women or b/c of – Neurologic
spinal cord injury, stroke > loss of control by – Myogenic
causing damage to micturition inhibitory – Idiopathic
center.
– Hypersensitivity
– Outlet Problem – Outlet Problem
– Stress Incontinence: With pregnancies and – BPH: Benign Prostatic Hyperplasia
deliveries, the pelvic wall muscles is gone – Urethral Stricture
(?), the support is gone so with a little – Sphincter Dyssynergia
increase in abdominal pressure> leakage
– Sphincter Deficiency
– Combination – Combination

4 BENIGN PROSTATIC HYPERPLASIA

4.1 CLINICAL FEATURES:

 LUTS (Irritative/Obstructive)
 Poor bladder emptying
 Urinary retention
 Urinary tract infection

131
10 ADULT UROLOGICAL DISORDERS

 Hematuria
 Renal insufficiency
4.2 PHYSICAL EXAMINATION:

1. DRE (Digital rectal Examination) If it’s hard to palpable the nodules, it means
Cancer.
2. Focused neurologic exam
o Prostate Ca
o Rectal Ca
o Anal tone
o Neurologic problems
3. Abdomen: Distended bladder 
4.3 INVESTIGATIONS

1. Urinalysis, Culture
a. UTI
b. Hematuria
2. Serum Creatinine
3. Serum Prostate-Specific Antigen; it is elevated in prostatic cancer.
4. Flow rate
5. U/S (kidney, bladder and prostate).
4.4 MANAGEMENT

1. Medical therapy
a. α-Adrenergic Blockers; selective α1 blocker that opens the prostate.
i. Tamsulosin
ii. Alfuzosin
iii. Terazosin
b. Androgen Suppression; 5α reductase inhibitor > shrinks prostate 60% in
6 months
Figure 5: Endoscopy
i. Finasteride
2. Surgical Rx
a. Endoscopic (e.g. TURP, laser ablation, prostatic stent); Cut adenoma
that blocks the passage.

b. Open prostatectomy.

5 MCQS

1. A 13-year old boy presented to the Emergency Room with painful right scrotal
swelling. It was gradual in onset over the last 5 days. He gave history of Figure 6: Prostatectomy
dysuria and suprapubic pain for the last 2 weeks. The most common cause of
his symptoms is:
a. Epididymitis
b. Hydrocele
c. Testicular Torsion
d. Testicular Trauma

132
 MCQs 11

2. A 22-year old single male presented with dysuria and urethral discharge, 5
days after unprotected intercourse. On examination, there is erythema over his
urethral meatus with yellowish discharge. The most likely causative organism
for his presentation is:
a. Chlamydia trachomatis
b. Escherichia coli
c. Herpes simplex virus
d. Neisseria gonorrhea
3. A 65-year old diabetic woman presented with right flank pain and fever for 2
days. She has been complaining of dysuria and suprapubic pain for more than
one week. She is nauseated and had 3 episodes of vomiting. The most likely
diagnosis is:
a. Acute cholecystitis
b. Acute pyelonephritis
c. Pancreatitis
d. Renal colic
4. Irritative urinary tract symptoms include all of the following except:
a. Dysuria
b. Hesitancy
c. Frequency
d. Urgency
5. Main causative organism for UTI is:
a. E. Coli
b. Chlamydia
c. Proteus
d. Gonorrhea
6. The main symptoms of pyelonephritis are:
a. Fever
b. Flank pain
c. Chills
d. All of the above
7. The most common type of urinary tract stones is:
a. Calcium stones
b. Uric acid stones
c. Cystine stones
d. Struvite stones
8. All of the following are true about epididymitis except:
a. It takes days or weeks to develop
b. It can be diagnosed by US
c. Dysuria and pain are the main complaints
d. Testicular scan reveals ischemia of the testicles

 Answers: 1:a, 2:d, 3:b, 4:b, 5:a, 6:d, 7:a, 8:d

133
 Introduction and Classification 1

EMERGENCIES IN UROLOGY
1 INTRODUCTION AND CLASSIFICATION

 Require rapid diagnosis and immediate treatment.

 Compared to other surgical fields there are relatively few urological
emergencies
 Classification/topics
o Non-traumatic:
 Hematuria
 Renal colic
 Urinary retention
 Acute scrotum
 Priapism
o Traumatic:
 Renal trauma
 Uretral injury
 Bladder trauma
 Urethral injury
 External genital injury
2 NON-TRAUMATIC UROLOGICAL EMERGENCY

2.1 HEMATURIA

 Definition: blood in the urine

 Types:
o Gross
 Clinically visible/ emergency or urgency
 Up to 40% is malignancy
 1 ml of blood in 1 liter of urine is usually visible
o Microscopic
 Not visible
 Here the patient is told that he has Hematuria
 Not an emergency or urgency
 3 or more RBC/high power field
 Causes:
o They vary according to: patient age, presence of symptoms, presence of
risk factors for malignancies and the type (gross/microscopic)
o They could be:
1. Pre renal: SLE, Sickle cell disease, hemophilia, anticoagulants.
2. Renal: Tumor (benign or malignant), Renal stasis, Stone, TB,
Glumerulonephritis.
3. Post Renal: Tumor (bladder or ureter, Bilharzias, Prostate pathology,
urethral stricture, urethral polyp/tumor.
 History: Very important to diagnose 
o Chief complaint:
 Age: for example transitional cell carcinoma is not common in
children

134
2 Emergencies in Urology

 Residency: Bilharzias is common in Jizan

 Duration
 Occupation: Factories
 Painless:
 Usually transitional cell carcinoma (TCC) originating from the
urothelium of the bladder.
 Risk factors for TCC: Smoker, above 40, LUTS irritation, radiation to
the pelvis, bilharzias
 Painful: Stones, UTI, Trauma, Renal vein thrombosis
 Timing: helps in recognizing the site of the bleeding:
 Initial: urethra
 Terminal: bladder neck or triagone
 Total: rest of the bladder and upper tract
 Amount of bleeding, Clots and shape, trauma and history of bleeding
from other sites
o Associated urinary and other systemic symptoms
o History of bleeding disorders, infections, stones, TB, bilharzias.
o Family history of malignancy or hematological disease
o Drugs and colored foods and drinks
o SMOKING: asking about smoking is very crucial because it is known to
be a risk factor for bladder transitional cell carcinoma and renal cancer
 Management:
o Work up
 Full work up is mandatory
 History, examination (not much signs)
 Investigations: Single most important imaging method is CTU (CT
Urography) 
 3 way urethral catheter and wash out heavy bleeding
 Treat the underlying cause
2.2 RENAL COLIC

 The commonest urological emergency (in Saudi Arabia cases are seen daily)
 One of the commonest differentials associated with acute abdomen
 Characteristically: Sudden onset of severe pain in the flank
2.2.1 HISTORY OF PAIN: 
 Sudden onset, intermittent, relieved by analgesia & nothing aggravates it
 Colicky in nature
 Radiation
o The kidney and upper ureter are innervated from dermatomes T7-T9.
 In men the pain will radiate to the testicle because it embryological
originates from the same site and then the testicle descends
o Mid ureter: dermatome T10 > radiate to the iliac fossa
 If this happens in right side can be confused with appendicitis
o Distal ureter: dermatome T12> triagone of the bladder, posterior urethra,
scrotal skin, labia majora and lower abdomen
 Location may change from the flank to the groin SO the location of the pain is
not a food indicator of the location of the stone
 Patient is not comfortable and might be rolling around

135
 Non-Traumatic Urological Emergency 3

 Associated with nausea/vomiting

 Ureter stones:
o Sudden severe pain
o Urinary symptoms and suprapubic pain
 Remember that the pain of a renal colic is very painful, one of the worst a
human can experience
2.2.2 DIFFERENTIAL DIAGNOSIS
 Radiculitis (figure 1)
o Musculoskeletal pain that happens due to irritation of the nerve root in the
intervertebral foramen
o A common form of it is sciatica
o Irritation of the intercostals nerves (T7,8,9) can give a similar picture
o Usually aggravated by movement unlike stones that are relieved by
movement
o Radiates to lower limb if involving sciatic nerve roots
o History: back pain and predisposed mobility (carrying something heavy)
 Chest: Pneumonia and Myocardial infarction
 Abdomen: ruptured abdominal aortic aneurism, bowel obstruction, appendicitis, Figure 1

IBD, burst peptic ulcer and diverticulitis.

 Pelvis: Ectopic pregnancy and ovarian pathology (twisted cyst)
 Testicular torsion
2.2.3 WORK UP:
 History
 Examination:
o Patient wants to move around to find a comfortable position. This helps in
differentiating from appendicitis.
o Fever: indicates infection and needs extra hydration
 Investigations:
o Pregnancy test
o Mid stream urine: for Hematuria and urine analysis
o Urea and electrolytes: asses renal function
 Radiological investigation
o CT without contrast: (Figure 2)
 Imaging modality of choice 
 Greater specificity (95%) and sensitivity (97%) for diagnosing ureteric
stones
 Can identify other, non-stone causes of flank pain. Figure 2
 No need for contrast administration.
 Faster, taking just a few minutes
 the cost of CTU is equivalent to that of IVU
o Intravenous urogram (IVU): X-Ray and contrast before and after injection
o KUB: Plain X-ray of the kidney, ureter and bladder
o Renal ultrasound (RUS): not good for investigation stones
o MRI:
 Very accurate way of determining whether or not a stone is present
in the ureters
 Time consuming and expensive (not available in all hospital)

136
4 Emergencies in Urology

 Used for pregnant ladies (no radiation)

o In summary:
 CT without contrast is the module of choice in investigating a renal
colic in an emergency setting
 MRI is used for pregnant ladies only because it is time consuming
2.2.4 MANAGEMENT:
 Medical:
o Pain relief
 NSAID (IM, IV, Oral or suppository)
 Opiates analgesics (Morphine)
o Hyper hydration (IV-fluids and drinking water)
o Watchful waiting: 95% of stones measuring 5 mm or less will pass on
their own 
 Surgical
o Indications for surgery: 
1. To relieve obstruction and/or remove the stone
2. Pain that fails to respond to analgesia
3. Associated fever: kidney must be drained to reduce risk of
peylonephritis
4. Impairment in renal function because of the stone (causing uremia)
5. Obstruction is unrelieved for >4 weeks (Because after 4 weeks the
obstruction will cause necrosis)
6. Personal or occupational reasons: doctors or pilots
o Types of surgical intervention:
 Temporary relieve of obstruction:
 JJ stent from renal pelvis to bladder
 Percoetaneous nephrostomy tube
 Definitive treatment:
 Extracorporeal ShockWaves Lithotripsy (ESWL)
 Percoetaneous Nephrolithotomy (PCNL)
 Uretroscopy (commonly known as laser)
 Laparoscopic extraction (rare)
 Open surgery (rare)
2.3 URINARY RETENTION

2.3.1 ACUTE URINARY RETENTION

 Painful inability to void with relief of pain following drainage of the bladder by
catheterization
 More in Men than in Women
 Causes:
o Men:
 Benign prostatic enlargement due to hyperplasia is the most
common cause (usually in >40 years of age) 
 Carcinoma of the prostate
Figure 3
 Abscess in the prostate
 Urethral stricture
o Women:

137
 Non-Traumatic Urological Emergency 5

 Pelvic organ prolapsed (cystocele, rectocele, uterine prolapse)

 Urethral stricture or diverticulum
 Post surgery for stress incontinence
 Pelvis masses (e.g. Ovarian mass)
 Management:
o Initially: to relieve the pain!
 Urethral catheterization:
 Using a 3 way or Foley’s catheter (figure 3)
 Make sure to give adequate analgesia to prevent spasm
 Suprapubic catheter: (figure 4)
 Passed directly to the bladder through the skin Figure 4
 Used when urethra cannot be accessed (stricture)
o Definitive treatment: treat the underlying cause
2.3.2 CHRONIC URINARY RETENTION:
 Obstruction here develops slowly and the bladder is distended (stretched) very
gradually over weeks/months
 Pain is not a feature 
 Can be associated with:
o Reduced renal function or renal failure
o Upper tract dilation and hydronephrosis
 Presentation:
o Urinary dribbling
o Overflow incontinence (vesicle pressure exceed  Epididymitis is
inflammation of the
the urethral pressure
epididymis
o Palpable bladder with no pain
Orchitis is inflammation of
 Management: the Testicle
o In general it is more difficult that acute retention
Epididymo-orchitis is
because the cause is usually neurological inflammation of both
o Renal support and treat electrolyte imbalance
o Bladder drainage in a slow rate to avoid sudden
decompression (can cause Hematuria)
o Treatment of the underlying cause
2.4 ACUTE SCROTUM: Box 1
 Torsion of the spermatic cord
 Also known as scrotal pain or testicular pain  Torsion of the appendix testis
 Epididymitis
 Emergency situation requiring prompt evaluation, differential diagnosis, and  Epididymo-orchitis
potentially immediate surgical exploration  Inguinal hernia
 Differential diagnosis (Box 1)  Communicating hydrocele
 Hydrocele
o Epididymitis  Hydrocele of the cord
 Most common cause  Trauma/insect bite
 Can also be Epididymo-orchitis  Dermatologic lesion
 Inflammatory vasculitis
o Torsion of the spermatic cord: the most serious complication! (Henoch-Schonlein purpura)
 Idiopathic scrotal edema
 Tumor
 Spermatocele
 Non-urogenital pathology e.g.
adductor tendinitis

138
6 Emergencies in Urology

2.4.1 TORSION OF THE CORD 

 General consideration:
 Epidemiology
 Common among teenagers 12-18
 Possible in children and neonates
 Unlikely to occur after the age 25 years
 True surgical emergency of the highest order
 The testicular parenchyma will develop irreversible ischemic injury as soon
as 4 hours
 The twisting will lead to occlusion of venous return→ swelling and
blockage of arterial supply
 The longer the time of torsion → more ischemia Figure 5
 As duration of torsion increases the possibility of testicular salvage
decreases
 Anatomical variations: (figure 7)
A. Normal.
B. Bell clapper deformity. Tunica vaginalis surrounds the whole testicle
so it is very loose
C. Loose epididymal attachment to the Figure 6
testis
D. Torsed testis with transverse or
oblique lie
 Types: (not important)
 Extra-vaginal
 Intra-vaginal
 Presentation:
o Acute onset of scrotal pain
 Sharp and severe
 May be intermitting due to torsion then detorsion
o Majority have a history of prior episodes of severe, self limited scrotal
pain and swelling
o Nausea and vomiting due to the pain
o Referred to the Ipsilateral lower quadrant of the abdomen
o Children may present with abdominal pain.
 So any child that complains of severe abdominal pain may need to
have a genital examination
 Doctor mentioned a scenario: a mother brought her child to the
clinic and said “my son went to school and ate bad food and now he
has abdominal pain and nausea/vomiting” after further inspection the
child had Torsion of the cord.
o Dysuria and other bladder symptoms are usually absent (unlike
Epididymitis)
 Physical exam:
o Affected testis is high and lying transverse
o Acute swelling and scrotal edema or secondary hydrocele
o Absent cermasteric reflex(because the nerve is within the spermatic cord)
o Testis is tender and larger: the patient will not let you touch it
o Elevation of the scrotum causes MORE pain (unlike Epididymitis)
 Investigations:

139
 Non-Traumatic Urological Emergency 7

o Usually we do not need investigations because this is an emergency and

a high degree of suspicion is enough to send the patient to the OR
immediately
o Adjunctive tests aid in the deferential diagnosis
o Confirm the ABSENCE of torsion
o Tests used:
 Sound Doppler examination of the cord: high false positive and
false negatives
 Color Doppler ultrasound: (figure 8)
o Investigation of choice
o Done in the OR a lot of the time.
o Assessment of anatomy and determining the presence or
absence of blood flow.- to see the arterial blood supply of the
testis
o In the picture : in the left there is absence of blood supply ,
secondary hydrocele without arterial flow
o Sensitivity: 88.9% specificity of 98.8%
o Operator dependent.
Figure 7

 Radionuclide imaging: (figure 9)

o Assesses testicular blood flow
o Shows a photopenic area in cases of torsion
o False impression from hyperemia of scrotal wall
o Sensitivity of 90% and specificity of 89%
o Not helpful to determine a hydrocele or hematoma (does not
assess anatomy)
 Surgical exploration:
o Diagnostic and therapeutic 
o A scrotal incision is done and the affected site is examined first
  a needle prick is done and if there is no blood coming out
or black tissue it means it is dead
o The cord should be detorsed.
o Testes with marginal viability should be placed in warm and re-
Figure 8
examined after several minutes.
o A necrotic testis should be removed
o If the testis is to be preserved, it should be fixed
o The contra-lateral testis must be fixed to prevent subsequent
torsion
o Remember when there is a high possibility of testicular torsion from
history and examination → take the patient to the OR and do not wait 

140
8 Emergencies in Urology

2.4.2 EPIDIDYMO-ORCHITIS
 Presentation:
o Common in Saudi Arabia (can be a manifestation of Brucella)
o Indolent process causing little or no pain
o Usually gradual and not sudden and gets severe towards the end
o Scrotal swelling, erythema and pain.
o Dysuria and fever are common
o Patients with history of STD like gonorrhea or UTI
 Physical examination
o Localized epididymal tenderness
o Swollen and tender epididymis. Or massively swollen hemi-scrotum
o Cermasteric reflex is present. 
o Patient feels less pain when the scrotum is raised
 Urine analysis might show bacteruria and/or positive culture and WBC
 Management:
o Bed rest for 1-3 days
o Scrotal elevation with athletic supporter
o Parental or Oral antibiotics should be instituted when UTI is documented
or suspected
o AVOID urethral instrumentation to reduce risk of more infection. 
2.5 PRIAPISM

 Defined as a persistent erection of the penis for more than 4 hours that is not
related or accompanied by sexual desire
 Types of Priapism:
o Ischemic:
 Painful type
 Also called veno-occlusive or low flow
 Most common type
 Pathophysiology: thrombosis of the venous system causing
congestion and engorgement which leads to the erection
 Causes include:
 Hematological disease: Sickle cell 
 Malignancy that infiltrated the corpora cavernosa
 Drugs like prostaglandin injection
o Non-ischemic:
 Painless type
 Also called Arterial or high flow
 Pathophysiology: perineal trauma will cause an atriovenous fistula
which fills the corpora
 The persistence of Priapism will cause clotting which leads to healing by
fibrosis in the corpora and this will damage it and the patient will lose the ability
of erection
 Causes: 
o Primary (idiopathic) in 30-50% of the cases
o Secondary (as mentioned above): Drugs, trauma, pelvic malignancies,
hematological disease, neurological.
 Diagnosis:

141
 Traumatic Urological Emergencies 9

o Obvious from history!

 Erection for more than 4 hours
 Document if it is painful or not
 Previous history of Priapism
 Ask about predisposing factors and possible causes
o Examination:
 Erect penis that can be tender (in low flow) or not
 Characteristically the corpora cavernosa are rigid and the Glans is
flaccid
 Abdominal examination for evidence of malignancy
 Digital rectal exam: to examine the prostate and check for anal tone
(neurological assessment)
 Investigations:
o CBC
o Hemoglobin electrophoresis for SCD
o Urinalysis for toxicology
o Blood gases taken from either corpora
Variable Low flow (ischemic/occlusive) High-flow (non-ischemic/Fistula)
Blood color Dark blood Bright red blood (similar to arterial
blood at room temperature)
pH <7.25 (acidosis) =7.4 (normal)
pO2 <30 mmHg (hypoxia) >90 mmHg (normal)
pCo2 >60 mmHg (hypercapnia) <40 mmHg (normal)
o Color Doppler flow in cavernous arteries
 Ischemic: in flow is low or nonexistent
 Non-ischemic: inflow is normal to high
o Penile pudendal arteriography in cases of trauma
 Treatment:
o Depends on type of Priapism
o Conservative treatment should be tried first
 Ask the patient to climb the stairs to open venous channels
o Medical treatment: bicarbonates, high o2 and cold enema
o Surgical treatment: aspiration and saline wash of the corpora
o Treat the underlying cause
3 TRAUMATIC UROLOGICAL EMERGENCIES

3.1 RENAL TRAUMA

 The kidneys are relatively protected from traumatic injuries so a considerable

degree of force is usually required to injure a kidney.
 Mechanism and causes:
o Blunt trauma:
 Direct blow or acceleration/deceleration injuries
 Road traffic accidents, falls from heights, falls on flanks
o Penetrating trauma: knives, gunshots, iatrogenic (during operations)
3.1.1 RENAL IMAGING: 
 Modality of choice is contract enhanced CT. 

142
10 Emergencies in Urology

 Indications for renal imaging:

1. Macroscopic Hematuria
2. Penetrating chest, flank, and abdominal wounds
3. Microscopic [>5 red blood cells (RBCs) per high powered field] or dipstick
4. Hematuria in hypotensive patient (SBP <90mmHg )
5. A history of a rapid acceleration or deceleration
6. Any child with microscopic or dipstick Hematuria who has sustained
trauma – even < 5 RBC.
 Modalities available:
1. IVU:
a. widely replaced by CT scan with contrast
b. on table IVU: if patient is transferred immediately to the operating
table without having had a CT scan and a retroperitoneal
hematoma is found
c. done to see if the other kidney is functioning and/or exists because
the injured kidney might have to be removed
2. CT scan
a. Without contrast: does not allow accurate staging
b. With contrast: imaging modality of choice + other abdominal injuries
can be assessed 
3. Renal ultrasound
a. Advantages:
i. can certainly establish the presence of two kidneys
ii. the presence of a retroperitoneal hematoma
iii. power Doppler can identify the presence of blood flow in the
renal vessels
iv. To follow up on a hematoma after CT is done
b. Disadvantages:
i. Cannot accurately identify parenchymal tears, collecting
system injuries, or extravasations of urine until a later stage
when a urine collection has had time to accumulate.
3.1.2 STAGING:  (FIGURE 10)
 Grade I: flank pain + Hematuria with or without pericapsular hematoma, but no
evident kidney damage
 Grade II: injury to the cortex only of 1cm or less with hematoma
 Grade III: injury to the cortex and medulla without reaching the collecting
system with hematoma (more than 1cm)
 Grade IV: injury reaching to the collecting system OR thrombosis to the renal
vessels
o On IVU there will be extravasations of contrast and decreased filling
 Grade V: shattered kidney completely

143
 Traumatic Urological Emergencies 11

Figure 9

3.1.3 MANAGEMENT
A. Conservative
o Over 95% of blunt injuries
o 50% of renal stab injuries and 25% of gunshot wounds injury
o Needs a specialized center
o Includes:
 Wide bore IV lines to transfuse fluids
 IV antibiotics
 Bed rest
 Serial CBC and HCT
 Follow up US and/or CT
B. Surgical exploration (indications for surgery):
o Persistent bleeding: tachycardia and/or hypotension failing to respond to
appropriate fluid and blood replacement
o An expanding peri-renal hematoma after laparotomy
o Pulsatile peri-renal hematoma after laparotomy
3.2 URETRAL INJURIES

 The ureters are protected from external trauma by surrounding bony structures,
muscles and other organs therefore their injury is rare.
 Mechanisms and causes:
1. External trauma
 Rare because severe forced is required
 Can be blunt or penetrating
 Blunt external trauma severe enough to injure the ureters will usually
is associated with multiple other injuries.
 Penetrating knives or bullets to the abdomen may also damage the
ureter
2. Internal trauma
 More common but it is still uncommon
 Iatrogenic: causes by doctors during surgeries (hysterectomy,
oopherectomy, sigmoidcolectomy, urertoscopy, cesarean section,
laparoscopies and orthopedic operations
 Diagnosis:
o Requires high index of suspicion

144
12 Emergencies in Urology

o Usually diagnosed intra-operatively

o Late diagnosis: (these are suggestive of ureter injuries):
1. An ileus: presence of urine within the peritoneal cavity
2. Prolonged postoperative fever or overt urinary sepsis
3. Persistent drainage of fluid from abdominal or pelvic drains, from a
wound or the vagina.
4. Flank pain if the ureter has been ligated
5. An abdominal mass representing a urinoma
6. Vague abdominal pain
 Treatment options:
o JJ Stenting
o Primary closure of partial transaction of the ureter
o Direct ureter to ureter anastomosis
o Re-implantation of the ureter into the bladder using a psoas hitch or a
Boari flap
o Trans uretero-ureterostomy
o Auto-transplantation of the kidney into the pelvis
o Replacement of the ureter with ileum
o Permanent cutaneous ureterostomy
o Nephrectomy
3.3 BLADDER INJURIES

 Common in caesarean sections

 Causes:
o Iatrogenic
 Transurethral resection of bladder tumor (TURBT)
 Cystoscopic bladder biopsy
 Transurethral resection of prostate (TURP)
 Cystolitholapaxy
 Caesarean section, especially as an emergency
 Total hip replacement (very rare)
o Penetrating trauma to the lower abdomen or back
o Blunt pelvic trauma—in association with pelvic fracture or ‘minor’ trauma
in a drunkard patient
o Rapid deceleration injury seat belt injury with full bladder in the absence
of a pelvic fracture
o Spontaneous rupture after bladder augmentation
 Types of perforation:
o Intra-peritoneal perforation: the peritoneum overlying the bladder has
been breached along with the wall of the bladder allowing urine to escape
into the peritoneal cavity.
o Extra-peritoneal perforation: the peritoneum is intact and urine escapes
into the space around the bladder, but not into the peritoneal cavity.
 Presentation:
o Recognized intra-operatively
 The classic triad of symptoms and signs that are suggestive of a
bladder rupture :
1. Suprapubic pain and tenderness
2. Difficulty or inability in passing urine
3. Hematuria

145
 Traumatic Urological Emergencies 13

 Management:
o Extra-peritoneal:
 Bladder drainage +++++
 Open repair +++
o Intra peritoneal :
 Open repair…why?
 Unlikely to heal spontaneously.
 Usually large
 Leakage causes peritonitis
 Other organs are usually injured
3.4 URETHRAL INJURIES

3.4.1 ANTERIOR URETHRAL INJURIES

 Rare
 Mechanism:
o Majority are a result of straddle injuries in boys or men (jumping while
your legs are open)
o Direct injuries to the penis
o Penile fractures
o Inflating a catheter in the anterior urethra
o Penetrating injuries by guns or knives
 Symptoms and signs
o Blood at the end of the penis
o Difficulty in passing urine
o Frank Hematuria
o Hematoma around the site of rupture
o Swelling of the penis
 Diagnosis is by Retrograde Urethrography:
o Less filling means greater damage  Retrograde
 Contusion: no extravasations of fluid urethrogram: contrast is
 Partial rupture: extravasations of contrast with contrast present in the injected through the
urethra using a catheter
bladder and images are taken.
 Complete disruption: no filling of the posterior urethra or bladder
 Management:
1. Contusion
 Do nothing
 Small gauge catheter for one week
2. Partial Rupture of Anterior Urethra
 No urethral catheterization!!!!
 Majority can be managed by suprapubic urinary diversion for one
week
 Penetrating partial disruption (e.g., knife, gunshot wound), primary
(immediate) repair
3. Complete Rupture of Anterior Urethra.
 Unstable patient: a suprapubic catheter.
 Stable patient: the urethra may either be immediately repaired or a
suprapubic catheter is placed
o Penetrating Anterior Urethral Injuries are generally managed by surgical
debridement and repair

146
14 Emergencies in Urology

3.4.2 POSTERIOR URETHRAL INJURIES:

 Great majority of posterior urethral injuries occur in association with pelvic
fractures,
 10% to 20% have an associated bladder rupture
 Signs:
o Blood at the meatus, gross Hematuria, and perineal or scrotal bruising.
o High-riding prostate when examining by Digital rectal exam
 Classification of posterior urethral injuries
o type I:(rare ) stretch injury with intact urethra
o type II : (25%) partial tear but some continuity remains
o type III:(75%) complete tear with no evidence of continuity
o In women, partial rupture at the anterior position is the most common
urethral injury associated with pelvic fracture

 Management:
o Type 1 and type 2 are treated with Stenting with a urethral catheter
o Type 3:
 Patient is at varying risk of urethral stricture, urinary incontinence,
and erectile dysfunction (ED)
 Initial management with suprapubic cystotomy and attempting
primary repair at 7 to 10 days after injury.
3.5 EXTERNAL GENITAL INJURIES

 Penile fractures: during sexual intercourse

 Glans injury during circumcision
 Penile amputation and injury
 Scrotal injury
 Female external genital injury: in sports, crime or during vaginal labour

147
 MCQs 15

4 MCQS

1. A 12 year old boy presented to the ER department with sudden onset of severe
testicular pain with no history of trauma and no fever. What is the most likely
diagnosis?
A. Hydrocele
B. Testicular torsion
C. Tuberculosis Epididymitis
D. Varicocele
2. If the diagnosis is testicular torsion how would you further proceed with your
work up?
A. Take the patient to do a CT scan
B. Give the patient analgesia and ask him to return to you in 3 days
C. Take the patient to the OR immediately for surgical exploration
D. Administer antibiotics as testicular torsion is an infectious emergency
3. A 25 year-old male presented to the ER in a stable condition after a motor
vehicle accident. He complains of left flank pain. You suspect renal injury.
Which ONE of the following would be the best test to investigate renal injury?
A. CT scan Urography
B. Intravenous urography ( IVU )
C. MRI
D. Renal ultrasound
4. Which ONE of the following is an indication for a surgical intervention in
ureteric stones?
A. Gross Hematuria
B. If the stone is 6 millimetre in diameter
C. Impaired renal function due to obstruction
D. Stone in distal ureter

 Answers: 1;B , 2;C , 3;A , 4;C

148
 Renal Tumors 1

GENITOURINARY ONCOLOGY
1 RENAL TUMORS
 Onchocytoma is the
commonest benign
 Benign tumors of the kidney are rare tumor.
 All renal neoplasms should be regarded as potentially malignant
Most common kidney
 Renal cell carcinomas arise from the proximal tubule cells  cancer is renal cell
 Male: female ratio is approximately 2:1 carcinoma.
 Increased incidence seen in von Hippel-Lindau syndrome The commonest renal
 Pathologically may extend into renal vein and inferior vena cava cell carcinoma
o It could reach the heart histological subtype is
o Tumor thrombus could obstruct IVC and causes bilateral DVT. clear cell carcinoma
 Blood born spread can result in 'cannon ball' pulmonary metastases The renal cell
o The lungs are the commonest site for metastasis  carcinoma arising from
the collecting duct cells
is collecting duct
You can see multiple solid patches of lung metastasis
carcinoma of the kidney.
Familial papillary
cell carcinoma is
hereditary and runs in
families (all family
members should be
screened).

 Von Hippel-Lindau
"Cannon Ball" Metastases Syndrome:
 Genetic disease
1.1 CLINICAL FEATURES  Mutation: short arm of
chromosome 3 
 The commonest presentation is: incidental finding   CNS hemangio-
 10% present with classic triad* of blastomas, pheo-
chromocytomas,
1) Gross hematuria pancreas and kidney
2) Loin pain cysts, renal cell
3) Palpable mass carcinoma

This is usually a sign of advanced disease  Also associated with
 Other presentation include a pyrexia of unknown origin, hypertension adrenal gland
malignancies
 Polycythemia due to erythropoietin production
 Hypercalcemia due to production of a PTH-like hormone
1.1.1 PARANEOPLASTIC SYNDROME   ADH: Anti-diuretic
 A unique feature of renal cancer hormone
 EPO: Erythropoietin
 This is when the tumor starts secreting hormones e.g. ADH or EPO
 Treatment of this syndrome is by treating the underlying cause by surgical
removal, not symptomatic treatment.
 Other systemic manifestations of paraneoplastic syndrome include:
o Pyrexia of unknown origin (PUO)
o Hypertension
o Polycythemia (due to erythropoietin production)

149
2 Genitourinary Oncology

o Hypercalcaemia due to production of a PTH-like hormone

o Non-metastatic hepatic dysfunction called Stauffer’s syndrome,
characterized by elevated liver enzymes
 Remember: no liver metastasis, no jaundice
 All treated by surgical removal of kidney tumor EXCEPT hypercalcaemia,
which can be treated medically 
1.2 INVESTIGATIONS  If there is a
LOCALIZED tumor in
 Diagnosis can often be confirmed by renal ultrasound the heart, then we
 CT scanning allows assessment of renal vein and caval spread should treat it surgically.
o It is used for staging * Only if localized
 Echocardiogram (TEE) should be considered if clot in IVC extends above  When tumor
diaphragm thrombus extends above
diaphragm, survival rate
~20%

CT of the patient’s chest when he Solitary mass in the brain

White arrow shows a mass in
was first diagnosed with due to metastasis. Solitary
the right ventricle
intracardiac extension masses  surgical removed

When you find bilateral tumors, think of

familial syndromes like VHL

1.3 TREATMENT  Remember:

Kidney tumors are both
 Unless extensive metastatic disease, it invariably involves surgery radio-resistant and
 Surgical options usually involve a radical nephrectomy chemo-resistant, but
radio/chemo Rx
 Kidney approached through either a transabdominal or loin incision indicated in cases of
 Renal vein ligated early to reduce tumor propagation symptomatic bone
 Kidney and adjacent tissue (adrenal, perinephric fat) excised metastasis, in order to
 Lymph node dissection of no proven benefit relieve pain
o Remove only for lab purposes and staging
o Whether you remove them or not, patients will have recurrences
 Solitary (e.g. lung metastases) can occasionally be resected

150
 Renal Tumors 3

 Radiotherapy and chemotherapy have NO role

o Indicated in case of symptomatic bone metastasis to reduce pain
 Immunotherapy can help (performance status)
o Monoclonal antibodies, interferon, cytokine inhibitors
o Very cytotoxic
o Given only to patients with good performance status
o Not curable but it can prolong his life for 6-8 months
Open radical nephrectomy: This is a surgery that causes a big scar Gross Appearance and
that has to cut the muscles so the patient will suffer and feel pain Histopathology (Post-
with respiration Nephrectomy)

Laparoscopic nephrectomy: (GOLD STANDARD) Very clear, impacted cells

Advantages: 1. Shorter hospital stay 2. Less pain 3. Same results. with dark nuclei and clear
We use the groin incision to remove large tumors, because that way cytoplasm. This is the
we do not need to cut muscle, it is a muscle splitting incision. commonest histo-
pathological subtype 
For post-menopausal women who have undergone hysterectomy >
Transvaginal approach

 Staging of kidney
tumor includes:
1. Clinical staging by CT
scan
2. Pathological staging
 Grading system for
kidney cancer is called:
Fuhrman system

1.4 PROGNOSIS

 Early stage: 5 year survival is 95%

 Metastatic disease: 3-6 months average survival

151
4 Genitourinary Oncology

2 BLADDER TUMORS

2.1 PATHOLOGY
Squamous
carcinoma:
 Of all bladder carcinomas:
o 90% are transitional cell carcinomas (TCC)  Bad prognosis, in fact
the worst
o 5% are squamous carcinoma
 High risk groups
o 2% are adenocarcinomas (due to congenital fistulas; develops in the (chronic irritation):
dome of the bladder)
 Smokers*
 TCCs should be regarded a 'field change' disease with a spectrum of
 Chronic UTI
aggression
 80% of TCCs are superficial and well differentiated  Stones
o Above the muscle layer (muscularis propria)  Chronic indwelling
catheter
o Only 20% progress to muscle invasion
o Associated with good prognosis, but higher recurrence rate  Spinal cord injury
 20% of TCCs are high-grade and muscle invasive  Schistosomiasis*
o 50% have muscle invasion at time of presentation
o Associated with poor prognosis
2.2 ETIOLOGY

1. Occupational exposure
a. ~20% of transitional cell carcinomas are believed to result from
occupational factors
b. Chemical implicated - aniline dyes, chlorinated hydrocarbons
2. Cigarette smoking*
3. Analgesic abuse e.g. phenacitin
4. Pelvic irradiation - for carcinoma of the cervix
5. Schistosoma haematobium* associated with increased risk of squamous
carcinoma 
2.3 CLINICAL FEATURES  Painless gross
hematuria is considered
 80% present with painless hematuria to be cancer until proven
o Gross painless hematuria otherwise.
o Terminal hematuria
 Also present with treatment-resistant infection or bladder irritability and
sterile pyuria (DDx: TB)
2.4 INVESTIGATIONS (OF PAINLESS HEMATURIA)

1. Urinalysis
2. Ultrasound - bladder and kidneys
3. KUB - to exclude urinary tract calcification
4. Cystoscopy (a MUST in this case)
5. Urine Cytology
6. Consider IVU if no pathology identified (shows filling defect, or sometimes
hydronephrosis due to obstruction of the ureters, which is a bad sign
indicating progressive disease)

152
 Bladder Tumors 5

Bladder diverticulum causes stagnation of urine  chronic irritation. Diverticulum appears as a pouch.

2.5 PATHOLOGICAL STAGING  T2 and above needs

removing the whole
 Requires bladder muscle to be included in specimen bladder
 Staged according to depth of tumor invasion

Tis In-situ disease

Superficial

Ta Epithelium only  Grading:

T1 Lamina propria invasion  G1: Well differentiated
 G2: Moderately well
T2 Superficial muscle invasion differentiated
 G3: Poorly
Invasive

T3a Deep muscle invasion

differentiated
T3b Perivesical fat invasion

T4 Prostate or contiguous muscle

153
6 Genitourinary Oncology

2.5.1 CARCINOMA IN-SITU

 Carcinoma-in-situ is an aggressive disease
 Often associated with positive cytology 
 50% patients progress to muscle invasion 
 Consider immunotherapy
 If fails patient may need radical cystectomy
2.6 TREATMENT

2.6.1 SUPERFICIAL TCC Radical cystectomy:

removal of bladder,
 Requires transurethral resection and regular cystoscopic follow-up prostate, distal ureter
o To watch out for recurrence due to the high recurrence rate of and lymph nodes
superficial TCC * In females: also the
 Consider prophylactic chemotherapy if risk factor for recurrence or invasion uterus, cervix and
(e.g. high grade) anterior vaginal wall
o High risk: 1.Multiple tumors 2. Big tumors 3.Carcinoma in situ
 Consider immunotherapy
o BCG  = attenuated strain of Mycobacterium bovis
o Reduces risk of recurrence and progression
o 50-70% response rate recorded
o Occasionally associated with development of systemic
mycobacterial infection

Transurethral Resection of Bladder Tumor (TURBT)

2.6.2 INVASIVE TCC

 Radical cystectomy has an operative mortality of about 5%
 Urinary diversion achieved by:
o Ileal conduit
o Neo-bladder

154
 Prostate Tumors 7
Ileal conduit (incontinent)

 Local recurrence rates after surgery are approximately 15% and after
radiotherapy alone 50%
 Pre-operative radiotherapy is no better than surgery alone
 Adjuvant chemotherapy may have a role

Continent cutaneous reservoir

Orthotopic neobladder (continent)

3 PROSTATE TUMORS  Screening program

in North America: for
PROSTATE CANCER males above the age of
40 every year
 Commonest malignancy of male urogenital tract   PSA Test
o 8th most common tumor in in KSA  Digital Rectal Exam
 Rare before the age of 50 years If any of them positive
o Screening is recommended at age 40 this is an indication to
 Found at post-mortem in 50% of men older than 80 years take a biopsy.
o The patient usually dies from other causes (it will not kill the patient)
 5-10% of operations for benign disease reveal unsuspected prostate
cancer
3.1 PATHOLOGY  Malignant prostate
tumors usually arise in
 The tumors are adenocarcinomas  the peripheral zone,
 Arise in the peripheral zone of the gland  while benign prostate
hyperplasia (BPH) arises
 Spread through capsule into peri-neural spaces, bladder neck, pelvic wall in the transitional zone.
and rectum
 Lymphatic spread is common
 Hematogenous spread occurs to axial skeleton
 Tumors are graded by Gleeson classification
3.2 CLINICAL FEATURES

 Majority these days are picked up by screening

155
8 Genitourinary Oncology

 10% are incidental findings at TURP

 Remainder present with bone pain, cord compression or leuco-
erythroblastic anemia
 Renal failure can occur due to bilateral ureteric obstruction
3.3 DIAGNOSIS

 With locally advanced tumors diagnosis can be confirmed by rectal

examination
 Features include hard nodule or loss of central sulcus
 Transrectal biopsy should be performed
 Multiparametric MRI may be useful in the staging of the disease
 Bone scanning may detect the presence of metastases
 Unlikely to be abnormal if asymptomatic and PSA < 10 ng/ml
3.3.1 SERUM PROSTATE SPECIFIC ANTIGEN (PSA)
 Kallikrein-like protein produced by prostatic epithelial cells
 4 ng/ml is the upper limit of normal
 >10 ng/ml is highly suggestive of prostatic carcinoma
 Can be significantly raised in BPH
 Useful marker for monitoring response to treatment
3.3.2 STAGING

3.4 TREATMENT

 More men die with prostate cancer than from prostate cancer
 Treatment depends on stage of disease, patient's age and general fitness
 Treatment options are for:
o Local disease
 Observation (old men ≥ 80 with localized disease)
 Radical radiotherapy (prostate cancer is radiosensitive)
 Radical prostatectomy
o Locally advanced disease
 Radical radiotherapy
 Hormonal therapy
o Metastatic disease
 Hormonal therapy

156
 Prostate Tumors 9

3.4.1 HORMONAL THERAPY

 80-90% of prostate cancers are androgen dependent for their growth 
 Hormonal therapy involves androgen depletion
 Produces good palliation until tumors 'escape' from hormonal control
 Androgen depletion can be achieved by:
 Bilateral orchidectomy
 LHRH agonists (e.g. goseraline)
 Anti-androgens (e.g. cyproterone acetate, flutamide, biclutamide)
 Complete androgen blockade
Open/Laparoscopic/Robotic

Brachytherapy: internal radiotherapy, in which the radiation source is inside the body

157
10 Genitourinary Oncology

EBRT: External beam radiation therapy

4 TESTICULAR TUMORS

A disease of young men

 Commonest presentation: ipsilateral painless testicular swelling
 Commonest malignancy in young men 
 Highest incidence in Caucasians in northern Europe and USA
 Peak incidence for teratomas is 25 years and seminomas is 35 years 
 In those with disease localized to testis > 95% 5-year survival possible
 Risk factors include cryptorchidism, testicular maldescent, Klinefelter's
syndrome, and testicular torsion
4.1 CLASSIFICATIONS

 Seminomas (~50%)  Radiosensitive

 Non-Seminoma (~50%)  Radio-resistant
o Teratomas
o Yolk sac tumors
o Embryonal
o Mixed Germ cell tumor
4.2 INVESTIGATIONS

 Diagnosis can often be confirmed by testicular ultrasound

 Pathological diagnosis made by performing an inguinal orchidectomy
 Disease can be staged by thoraco-abdominal CT scanning
 Tumor markers are useful in staging and assessing response to treatment
o Alpha-fetoprotein (α-FP)
 Produced by yolk sac elements

158
 MCQs 11

 Not produced by seminomas

o Beta-human chorionic gonadotropin (β-hCG)
 Produced by trophoblastic elements
 Elevated levels seen in both teratomas and seminoma
o LDH
4.3 STAGE DEFINITION

Disease confined to testis

Stage I
Rising post-orchidectomy tumor marker
IM
Abdominal lymphadenopathy
Stage II
< 2 cm
A
2-5 cm
B
> 5 cm
C
Supra-diaphragmatic disease
Stage III

4.4 TREATMENT

4.4.1 SEMINOMA
 True or False:
 Seminomas are radiosensitive Radical orchiectomy is
 The overall cure rate for all stages of seminoma is approximately 90%. done within scrotum.
 Stage I and II disease treated by inguinal orchidectomy plus False. Done through the
o Radiotherapy to ipsilateral abdominal and pelvic nodes ('Dog leg') or groin.
o Surveillance
 Stage IIC and above treated with chemotherapy

4.4.2 NON-SEMINOMA
 Non-Seminoma are not radiosensitive
 Stage I disease treated by orchidectomy and surveillance vs. RPLVD vs.
chemo
 Chemotherapy (BEP = Bleomycin, Etopiside, Cisplatin) given to:
o Stage I patients who relapse
o Metastatic disease at presentation
5 MCQS

1) The most common presentation of renal tumors is:

a. Fever of unknown origin
b. Hypertension
c. Incidental finding
d. Hematuria

159
12 Genitourinary Oncology

2) Which of the following is the commonest malignancy in young men?

a. Lung
b. Testicular
c. Colon
d. Bone
3) Nephrouretroectomy is the treatment of choice in :
a. Transitional cell carcinoma of the renal pelvis
b. Renal cell carcinoma
c. Non-functioning pyelonephrotic disease
d. Non-functioning tuberculosis
e. Angiomyolipoma
4) Regarding cancer prostate all true except:
a. It’s a very common disease in the kingdom
b. The growth of the tumor can be affected by steroids
c. Usually treated by testosterone
d. Can be treated by estrogens
e. Can present with back pain
5) Benign prostatic hyperplasia all true except:
a. Is a disease of the young
b. Usually presents with hematuria
c. Can present with renal failure
d. Usually present with hydronephrosis
e. Can cause bladder stones

Answers: 1 = c, 2 = b, 3 = a, 4 = c, 5 = a

160
 Objectives 1

ACUTE ABDOMINAL PAIN IN

CHILDREN
1 OBJECTIVES

 Realize the impact of age

o Where/who are the history sources
 Recognize and interpret the
o important symptoms
o Important signs
2 HISTORY [THE IMPACT OF AGE]

 Less than 3-4 year

o Verbal expression
o Difficult to communicate
o Fear of strangers
 History sources
o Mother is the best source
o Social barrier less than what we expect
o Father is not very reliable
o Nurses are reliable
 Not always possible / available
 Important in ICU
 Other doctors
3 SYMPTOMS OF SURGICAL ABDOMEN

 Feeding
o Feeding well  healthy baby
o Poor feeding
 Sick baby  from any GI or systemic cause (ear infection)
 GI obstructed
 Pain
 Vomiting  sick baby
o Regurgitation is frequent in babies
 considered Pathological if associated with failure to gain weight,
respiratory infection
o Frequency
o Color
o Force
 Projectile  proximal obstruction
 Small amount after each feeds  regurgitation
 Bowel movement (BM)
o Frequency
 What is the normal for infant? 4 per day to once in 2-3 days
 Constipated, obstructed

161
2 Acute Abdominal Pain in Children

 Failure to pass meconium in the first 24-48hrs newborns,

Meconium is the
Meconium is 80% passed in the first 24 hrs, 95% in the 48hr. early feces (stool)
Greenish, sticky, dark passed by a newborn
o Consistency soon after birth, before
 Loose / watery  diarrhea the baby has started to
digest breast milk (or
 Firm & dry  constipation formula).
o Color
 Very pale  ?
 Black  Melena
 Bright red
 Upper & Lower GI Bleed is very rare in children. On the other hand anal
fissures are common.
 Crying baby
o Babies communicate their needs by crying
 Hungry
 Wet (Urinated)
o At >6 month  emotions they learn to cry for other reasons
 Want to be carried
 Want to play
o Baby who continue to cry, refuse feeding and dry  “irritable baby”
o pain
 Abdominal pain
 Other causes  Ear ache
o Non-crying baby with reasons can be worrisome  very sick
 Development
o Growth (height and weight)
 Chronic problems (Metabolic, Nutrition => gut health)
o Psychological
 Mental problem, chromosomal abnormalities
o Motor
 Syndrome
 Metabolic
4 RELAYED SYMPTOMS (BY PARENTS)

 External abnormality
o Anything that is not normal
 Swelling
 Abscess (swelled, red and tender abdomen)
 Mass (swelling and non-tender)
 Hernia (swelling that comes and goes in the inguinal region)
 Color changes
 Inflammation
 Rash
 Vascular malformation
o Mental changes
 ↓Responsiveness
 Sleepy
 Not interested in feeding

162
 Abdominal problems 3

 Indicates; sepsis, shock, CNS trauma, metabolic (O2,

Glucose, urea)
5 ABDOMINAL PROBLEMS

1. Vomiting
2. Constipated / diarrhea
3. Poor feeding
4. Abdominal distension
5. Palpable mass
6. Very dark or very pale colored stool
7. Jaundice
6 PHYSICAL EXAM

 Vital signs
o Fever
o RR, BP, HR, O2 Sat
o Babies usually have higher HR, RR. Lower BP. The younger the
child, higher the values
 Consciousness (crying)
o Crying baby not very sick (not critical)
o Unusually calm baby who doesn’t respond normally  sick
 Exam while crying
o Can’t hear the chest well
 Focus on inhalation
o Can’t examine abdomen well
 Examine while taking breath
 Keep hand on abdomen
o Can’t concentrate
 Parent are stressed  less time
 Never do a rectal examination on babies. It’s not helpful, it causes
anal fissures and it’s very painful.
 Otherwise it’s similar to adults
 A good history = a good logical story, Known major Predisposing factors 
 Describe the current problem  other risk factors  Symptoms of other
possible complications
7 INVISTGATIONS

 Due to the relative difficulties in taking a reliable history and performing an

accurate physical exam
 We tend to depend more on investigations in diagnosing the underlying
problems in infants
8 QUESTIONS

1. 5 weeks old boy brought to you by his parents because of

recurrent vomiting. Parents indicated that the baby vomits with
significant force all the milk he had ate completing the feed. Where do
you think is the level of obstruction?

163
4 Acute Abdominal Pain in Children

a) Esophagus
b) Middle ileum
c) Proximal colon
d) Pylorus

2. The child who is most likely to need a surgical consultation?

a) 1 month-old breast fed baby didn’t pass stool for 4 days

b) 5 day-old baby with fever , passing soft light yellow stool
c) 3 day-old baby didn’t pass meconium during the first 48 hours of life
d) 12 month-old baby didn’t pass frequent liquid stool for one day

3. 6 months old baby boy presented to emergency department with

history of possible swallowing of metallic object. The father said he
was not sure if the baby swallowed the object. The next most
appropriate is:

a) Perform an upper GI endoscopy

b) Perform a chest X-ray of the chest and upper abdomen
c) Perform a chest X-ray to the neck and chest, AP and lateral
d) Ask the mother about the incidence

 Answers: 1;D, 2;C , 3;D

164
 Inguinal Hernia 1

COMMON INGUINOSCROTAL
CONDITIONS IN CHILDREN
1 INGUINAL HERNIA
Umbilical hernia:
Intersection between
1.1 INTRODUCTION cranial fold, abdominal
wall, lateral fold. They
 Hernia is the protrusion of an organ or the fascia of an organ through the have to meet in the
wall of the cavity that normally contains it center – most of the
times they do not meet
 Inguinal Hernia: Extension of the perineum (and usually its contents – 100% resulting in a
small intestines) through the inguinal canal defect in the umbilicus >
 It has two subtypes: indirect (more common) and direct umbilical hernia
o An indirect inguinal hernia follows the tract through the inguinal  An incisional hernia
canal occurs when the defect
o A direct inguinal hernia usually occurs due to a defect or weakness is the result of an
in the transversalis fascia area of the Hesselbach triangle incompletely healed
surgical wound
 99% of groin hernias are indirect inguinal hernia
1.2 ANATOMY OF INGUINAL CANAL

 It extends from the deep inguinal ring which is the connection between
peritoneal cavity and the groin to the external ring.
 Boundaries:
o Anterior: External oblique muscle
o Posterior: Transversalis fascia
o Inferior wall (floor): Inguinal ligament
o Superior wall (roof): Internal oblique and transversus abdominis
 The deep ring is lateral to the inferior epigastric vessels.
o It is the LANDMARK to differentiate between direct and indirect
inguinal hernia
o This indicates an Indirect Inguinal Hernia
 If it’s plugged medial to the inferior epigastric vessels then it’s a direct
inguinal hernia
 It is difficult to differentiate between direct and indirect inguinal hernia
clinically
1.3 ETIOLOGY

 Extension of the prenium ( and usually its contents) through the inguinal
canal because of:
o Patent processes virginals: The embryological canal that the testes
descend through to the scrotum
o Congenital inguinal hernia: The processes virginals remains in open
communication with the peritoneal cavity.
o A loop of intestine may herniated through it into the scrotum.
o The opening may be:
 Incomplete

165
2 Common Inguinoscrotal Conditions in Children

 Complete

1.4 PRESENTATION

 The most common presentation is swelling " plugging " in the groin area
 Painless Inguinal swelling :
o Intermittent (appears and disappears) – the mother will tell you the
swelling comes and go
o The right side is affected more than the left side- more in males 
o The swelling disappear when lying down and appear when standing
up due to the effect of the gravity 
 In the hernia, swelling starts in the groin then descends to the scrotum
(opposite to hydrocele)
 There is thickness of the spermatic cord (felt in the groin area)
 Reducibility of the swelling 
1.5 TYPES

1. Simple: The swelling is reduced spontaneously without mechanical

enhancement
2. Complicated: The swelling is reduced by an expert hand only and not
spontaneously – also called Incarcerated hernia
3. Strangulated: The swelling does not get reduced + there is a decrease of
the blood supply to the herniated sac thus resulting in ischemia (this type is
painful)
1.6 COMPLICATIONS

1. Incarceration
2. Strangulation
3. Obstruction of the bowel
4. Testicular atrophy: Due to compression of the blood vessels
1.7 MANAGEMENT

 Simple non-complicated hernia

166
 Hydrocele 3

o If it was not complicated, we do herniotomy as soon as it is feasible.

 Incarcerated hernia
o +/- Sedation and analgesia
o Check to reduce it
o Urgent herniotomy
 Strangulated hernia (Emergent herniotomy in 24-48 hours)
o Irreducible hernia – urgent surgery" in a day or 2" to avoid
complications ".
o It’s irreducible because the hernia contains dead tissue, thus
stimulating inflammatory reaction around it.(So, you cannot push it
in).
o Compression in the testicular vessels decreases the blood flow to
the testis > atrophy " 
o What t is the danger of leaving hernias in females? ovary – not fixed
will be necrotic
 Obstructive type inguinal hernia: it irreducible, content of the hernia is
bowel (mainly small bowel), it cause obstruction of the bowel
 It’s different in
o How do patient with obstructive inguinal hernia will present? children than in adults.
 Abdominal distention
- In children, the inguinal
 Vomiting: (greenish. Why? Because the obstruction is distal hernia is indirect (so go
to the ampulla of vater (2nd part of duodenum), so the bile from the deep ring
will go to the bowel where there is obstruction which through the canal to the
prevents it from going down. Since it has to go somewhere, external ring)
the only way is up. - It’s fixed by separating
 Constipation – and maybe obstipation (complete obstruction the hernia sac from the
other content of the
of the bowel, no pass of stool and gas)  inguinal hernia which
o When you see patient with abdominal distention and growing bulge, differs between males
patient with obstructive inguinal hernia what will be the next step? and females.
EMERGENCY surgery, why? To avoid bowel ischemia - So you have to
o General rule for future doctors, never leave a patient with separate the sac from
obstructive bowel without intervention. the adjacent structure.
o How do they present? - In children, you have to
 SEVERE pain do simple high ligation at
the level of the deep ring
 Swelling and that is herniotomy.
 Redness of the Over lying skin (change the color of the over
-If any content is present
lying skin is a bad sign for any pts with hernia), why? It main in the hernia, you have
the hernia id strangulated subtype and need emergent to get it back to its
surgery (herniotomy). normal location.

2 HYDROCELE

 Hydrocele: Accumulation of fluid in the testes (( so it is a fluid filled sac

around the testis ))
 Types:
a. Incysted hydrocele: The fluid around the testicles is absorbed
b. Non-communicated hydrocele: The fluid stays around the testicles
and is not absorbed.(there was a tunnel then it was obliterated
c. Communicated hydrocele: The fluid flows back and forth between
the scrotum and the abdomen.( communication between abdominal
and scrotum, so you can squeeze the fluid back to the peritoneum
cavity )

167
4 Common Inguinoscrotal Conditions in Children

d. Hydrocele of the cord: The fluid is located in the spermatic cord,

between the scrotum and the abdomen.

2.1 ETIOLOGY

 Same as inguinal hernia: P atent processus vaginalis

 The opening is smaller than in inguinal hernia so only the fluid only comes
through
 Fluid may accumulate forming middle part of the processus vaginalis. (C)
 If the abdominal end of the processus vaginalis remains open but is too
small to permit herniation of intestine peritoneal fluid passes into the patent
processus vaginalis forming a hydrocele of the testis. (D)

2.2 PRESENTATION 

 Non reducible swelling

 Painless (asymptomatic), swollen testicle, which feels like a water balloon.
A hydrocele may occur on one or both sides.
 During a physical exam, the doctor usually finds an swollen scrotum that is
not tender. Often, the testicle cannot be felt because of the surrounding
fluid. The size of the fluid-filled sack can sometimes be increased and
decreased by pressure to the abdomen or the scrotum.
 If the size of the fluid collection varies, it is more likely to be associated with
an inguinal hernia.

168
 Undescended Testes 5

 The groin is not swelled as IH ( get above the swelling ) 

2.3 MANAGEMENT

 Hydroceles are usually not dangerous, and they are usually only treated
when they cause discomfort or embarrassment, or if they are large enough
to threaten the testicle's blood supply.
 The treatment is not urgent so we can wait until the 2nd year of age
because it may spontaneously get resolved. If not, we do surgery. 
 What the different between IH and hydrocele (both are common & in
children)?
o Hydrocele is a fluid full sac in the scrotum
o Etiology:
 It`s the same as of IH (persistent of patent processes
vaginalis), ppv: is the extension of the peritoneal out of the
abdominal cavity, enter through the deep ring, IC, and the
external ring.
 The open of the ppv is small in hyrocele, but in hernia it big
so allow abdominal content to go through it .
o If you can feel the testis it`s hernia, if u can`t feel it cuz of all fluid it
hydrocele.
 Why to different between them? Cuz if it is hydrocele you don`t need to fix it
right away, majority will disappear by itself, wait for 2 years if didn't
disappear enter to fix it.
Hydrocele Inguinal Hernia
Scrotal swelling Inguino-scrotal swelling
Not reducible Check reducibility 
+ve transillumination (not specific) May have +ve transillumination
The pt is fine & not irritable The pt is irritable

3 UNDESCENDED TESTES

3.1 INTRODUCTION

 Types:  Testis descend from

a. True undescended testes: Normally, testes descend from the the abdominal at the
genital ridge to the scrotum. If it stopped anywhere in the normal kidney level in the
pathway above the scrotum, it is called true undescended testes retroperitoneum,
“Retained testis”. descend to the inguinal
canal to the scrotum any
b. Ectopic: It stops anywhere rather than the normal pathway, most rest in this processes we
commonly in the superficial inguinal pouch. call it true Undesigning
c. Retractile: The testis descends normally at birth, but goes up again testis.
due to hyperactivity of the cremasteric muscle (cremasteric reflex). It
may be milked again though. It can also ascend in the inguinal
canal spontaneously.
 Normal phenomenon in children; the majority of them resolves.
 Incidence:
o At birth: 3-4%

169
6 Common Inguinoscrotal Conditions in Children

o At one year: 1%
o Pre-term: 30%
 It’s important to know the different types because each has a different
management.
3.2 PRESENTATION

 Empty scrotum
 The testis could be :
o Palpable : you can feel it in the groin area
o Not palpable ( it usually in the abdominal cavity )
o Non palpable Undesigning testis if u can't feel the testis in groin
what will be the next step?! 
 We expect the testis in abdomen > so to visualize the abdominal activity we
will do laparoscopy trying to search for testis.
 Laparoscopy can be diagnostic and therapeutic to bring the testis down to
scrotum.
3.3 DIAGNOSIS

 Imaging has no role unless the testis was not palpable

o In this case, we use MRA, MRI and US to determine the site of the  The most common
Dx method is the clinical
testis. picture and the mother’s
o The best imaging modality for Dx is MRA. fear.
o The gold standard tool for Dx and Rx is Laporoscopy. 
3.4 MANAGEMENT

 The retractile type does not need medical intervention. It usually returns to
its normal position at puberty because of the increased weight of the testes
and well development of the muscles.
 But the other types need surgical intervention:
o The treatment should be done at the age of 6-12 to give a chance
for spontaneous testicular descent after birth.  Orchiopexy: Fixation
o The reason we don’t wait 2,3 or 4 years is because fixation of the of testis in scrotum, we
place testis back to
testis will be affected by then. normal position to
o If it's palpable minimize cancer risk and
 Open orchiopexy: Small incision, same as hernia, in which to enhance the fertility!
open groin and search for testis.
o If it's non-palpable:
 Laparoscopy-assisted orchiopexy
 Two stages Fowler-Stephens orchiopexy If the testis is higher
 Other indications of surgery: (also considered possible complications) in the abdomen, we
o Abnormal fertility need to do a second
surgery. The procedure
o Testicular tumor is called the “Two
o Cosmetic/Social Stages Fowler-Stephens
o Trauma/Torsion Orchiopexy”.
 The higher the testes the worst the prognosis.
 Also, if it was bilateral the worst the prognosis.
 The most feared outcomes are infertility and malignancy (high risk at ages
20,30,40).

170
 Acute Scrotum 7

4 ACUTE SCROTUM

 Acute onset of pain in the scrotum

 Pediatric surgical emergency: It might lead to testicular loss
4.1 PRESENTATION

 Pain is the major feature; do not wait for swelling and redness.
 It may be associated with lower abdominal pain.
 It may also have an atypical presentation such as right flank pain
 They present with painful scrotum +/- swelling +/- redness.
 They present with sudden onset of scrotal pain that can progress to
swelling and redness which means the testis is necrotic. Pt can have
abdominal pain and N/V.
 Signs:
o Tenderness of testis
o High lying testis
o Maybe lying in horizontal plane
o Absent Cremasteric reflex (very specific)
 When the Hx and Ex suggest testicular torsion, the next step is emergent
scrotal exploration. Imp!!
 That’s because if we wait to do a Doppler ultrasound or nuclear scan we
will waste valuable time. Instead, we should take the boy to the OR and do
emergent scrotal exploration and untwist the testis.
 If it’s the left testis > untwist clockwise (fix contralateral testis)
 If it’s the the right testis > untwist counterclockwise
4.2 CAUSES

 Causes include:
o Torsion of appendages (commonest)
o Testicular Torsion
o Idiopathic scrotal edema
o Epididymo-orchitis
o Other conditions e.g. Incarcerated hernia, acute hydrocele, HSP,
trauma
4.2.1 TORSION OF APPENDAGES
 Embryological remnants of the mesonephric and mullerian duct system
occur as tiny (2-10 mm long) appendages of testis
 Appendix testes (hydatid of Morgagni), appendix epididymitis, etc..
 Peak age: 10-12 years
 Presentation:
o Pain at the upper part of the testis (more gradual onset), the rest of
the testis is not tender
o Blue dot sign (the most specific sign) and usually at the top of the
testis
o Swollen & red hemiscrotum appears on the 2nd day of onset of
pain. So, in this case, they are an early presentation whereas in
acute scrotum they present late.

171
8 Common Inguinoscrotal Conditions in Children

 Management:
o Conservative
o Operative: If torsion cannot be excluded
4.2.2 TESTICULAR TORSION
 Incidence: 1:4000
 Two peaks: Perinatal and peripibertal
 Symptoms:
o Lower abdominal pain and vomiting
o Hemiscrotal pain
o Swollen & red hemiscrotum
 Signs:
o Tender
o Absent Cremasteric reflex (most specific – 98%)
o Lies higher than contralateral testis
o Horizontal in position
 Investigations:
o Color Doppler US
o Radionuclide scan
o High clinical suspicion of torsion needs no investigation but needs
immediate intervention
 Management:
o Timing is critical 4-6 hours (risk of ischemia)
o Exploration if in doubt
o Untwist and assess viability
o Fix the other side
o If more than 12 hours it is likely to be non-viable (gangrenous) and
may need orchiectomy
4.2.3 IDIOPATHIC SCROTAL EDEMA
 Peak age: 4-5 years
 Presentation:
o Swelling & redness in scrotum
o Minimal pain
o Usually bilateral
o Samoan color is very pathognomonic
 Management
o Conservative: Self-limiting within 1-2 days

5 MCQS
1. Regarding the scrotal swellings:
a. Haemetocele is very common
b. Hydrocele could be inguinoscrotal
c. Solid epididymal swelling is usually tumor
d. Transluminant testicular mass is a tumor

172
 MCQs 9

e. Usually examined with the patient lying down

2. The first symptoms of strangulated Inguinal Hernia is:

a. Vomiting
b. Fever
c. Septic shock
d. Constipation
e. Pain
3. The following are important steps in the management of strangulated
hernia except:
a. Nasogastric tube
b. Antibiotics
c. Conservative treatment until obstruction is relieved
d. Intravenous fluids
e. Consent for possible bowel resection

 Answers: 1:B, 2:E, 3:C

173
 Inroduction 1

ACUTE ABDOMEN
1 INRODUCTION

1.1 DEFINITION

 Acute abdomen denotes any sudden onset, spontaneous non-traumatic

disorder in the abdominal area that requires urgent surgery in some cases
(most of them).
1.2 GENERAL APPROACH TO ACUTE ABDOMEN

 The standardized approach for all acute abdominal disorders is the (SOAP)
approach:
o Subjective– History Taking
o Objective - Physical Examination
o Assessment – Investigations
o Plan – Treatment (based on the final diagnosis)
 The approach is not that different from an elective case, except in patients
who are hemodynamically unstable and will go into shock, resuscitation
should be initiated first.
 Analgesia or painkillers are not preferable to be given until a diagnosis is
made.
2 HISTORY AND EXAMINATION

2.1 HISTORY

2.1.1 AGE
Mesenteric adenitis is
 Newborn child presents with acute abdominal pain; most likely, it is a general term for an
digestive disease (bowel atresia - congenital anomaly in which there is inflammation of a gland
incomplete development of the intestinal tract, typically with closures and or lymph node
“dead ends” that block flow through the intestines. or meconium ileus -
Obstruction of the intestine (ileus) due to overly thick meconium).
 Child who present with an acute abdominal pain, mesenteric adenitis is
suspected.
 12-year-old boy who present with an acute abdominal pain, appendicitis
is suspected.
 Elderly patient with acute abdominal pain, obstruction due to cancer or
acute diverticulitis is highly suspected.
2.1.2 PAIN
 Site
o Site will give an idea about what is the organ involved:
o Right upper quadrant  think about gall bladder or liver.
o Right lower quadrant most likely it is appendicitis.
o Left lower quadrant think about diverticulitis.
 Onset: Sudden or gradual
 Character

174
2 Acute Abdomen

o Dull “mild pain”

o Trooping “in wounds”
o Stabbing “ something in closed space like gallbladder and renal
colic”
o Compression ”MI”
o Burning “gastritis”
o Colicky in nature “bowel obstruction”
 Radiation
o Cholecystitis to the tip of the right shoulder.
o Pancreatitis to the back.
 Timing important to decide management
o Examples:
 Patient with pain in the right lower quadrant, most likely it is
appendicitis, if the patient reported that the pain started last
night, surgery is the likely choice of management
 If the same patient reported that he/she had this pain 4-5
days ago and the pain is getting worse then you diagnose
him/her with appendicular mass, the approach will be
conservative rather than surgical.
 Severity
o Pain scale from 1 to 10, 0 no pain \ 10 worst pain.
o Mild pain (0-4), moderate (5-7), severe (8-10).
o Acute abdomen is in the severe category.
 Relieving and aggravating factors
o Fatty food elicits biliary colic.
o Antacid for burning pain in the epigastrium, milk will temporarily
relieve the pain but after an hour, pain will become worse (milk
contain protein --> protein increase gastric acid secretions). Milk is a
temporal buffer.
 Progression.
 Associated symptoms: Nausea and vomiting with severe pain.
2.1.3 VOMITING
Superior mesenteric
 Hematemesis artery syndrome is
 Volume : small or large amount characterized by
 Projectile "force" In children usually due to pyloric stenosis In newborn due compression of the third
to congenital hypertrophy of pylorus. In adults, gastric outlet obstruction or transverse portion of
o Causes of gastric outlet obstruction : the duodenum between
 Scarring due to chronic peptic ulcer the aorta and the
 Gastric cancer obstructs the pylorus superior mesenteric
 Superior mesenteric artery syndrome artery. This results in
chronic, intermittent, or
 In bezoar psychiatric patient who eats foreign bodies e.g.
acute complete or partial
Hair forming a ball that obstructs the gastric
duodenal obstruction
 Frequent or occasional
 Does vomiting relieve the pain or not:
o Most of abdominal colic’s relieved by vomiting
 Content:
o Undigested food
o Digested food: greenish

175
 History and Examination 3

2.1.4 DEFECATION:
 It is important to ask about the bowel habits.
 Constipation for 2 days with acute abdominal pain means there's an
obstruction
o Ask them can they pass gases or not, if not it's called Obstipation
"complete bowel obstruction".
 Diarrhea with acute abdomen usually means infection; gastroenteritis
usually does not cause acute abdominal pain unless bowel perforation
happens.
o Salmonella lead to typhoid fever and typhoid fever can cause
gastroenteritis that lead to bowel perforation and acute abdominal
pain.
 Acute abdominal pain with severe diarrhea "mixed with blood"
o Ulcerative colitis
o Bowel ischemia
o Crohn's disease
2.1.5 FEVER
Peptic ulcer perforation
 Rigors with acute abdominal pain means Sepsis due to cholangitis is a hole in the wall often
leads to catastrophic
2.1.6 PAST HISTORY
consequences. Erosion of
 Similar episodes of UC or Crohn's disease but in less degree the gastro-intestinal wall
 Past abdominal surgery adhesion, bowel obstruction, bowel strangulation or by the ulcer leads to
ischemia spillage of stomach or
 Bowel obstruction due to hernia intestinal content into
the abdominal cavity.
 Peptic ulcer perforation
Perforation at the
 Gall stones Obstruction
anterior surface of the
o Acute cholecystitis (is a sudden inflammation of the gallbladder that stomach leads to acute
causes severe abdominal pain) peritonitis, initially
o Pancreatitis chemical and later
o Ascending cholangitis bacterial peritonitis. The
first sign is often sudden
2.2 EXAMINATION
intense abdominal pain
1. General look:
a. Lying on bed and they look ill and in pain, uncomfortable moving,
because they want to obtain a position that relieves them from
peritoneal irritation, sometimes they roll in bed in renal colic or
sometimes in acute cholecystitis when gallbladder get contracted
with stones
i. Anything related to stone make patient roll in bed
ii. Appendicitis dull aching pain that does not make patients roll
in bed
2. Vital signs: Important to see the hemodynamic state of the patient wither if
the patient is tachycardic, tachypenic or hypotensive, they must be treated
immediately or they will go into shock.
3. Head and neck
a. Check the eyes for jaundice. "jaundice+ fever+ abdominal pain to
diagnose cholangitis"

176
4 Acute Abdomen

b. JVP: in acute abdomen, patient will be hypovolemic hence the JVP

will disappear
c. Mucus membrane: sings of dryness
d. Lymph node may present with lymphadenopathy
4. Chest
a. Pleural effusion caused by pneumonia. In lower pneumonia or lobar
pneumonia you'll hear crackles and bronchial breathing
5. Abdomen
a. Inspection: distended, does not move with respiration because the
peritoneum contracting the muscles of the abdomen, might see
other signs (ex. In chronic liver disease...etc)
b. Palpation: start superficial away from the site of pain.
c. Percussion
i. Dullness fluid ascites
ii. Tympanic or tympanitic, drum-like sounds heard over air
filled structures during the abdominal examination which
suggest bowel obstruction
d. Auscultation:
i. Paralytic ileus because of infection, absence of bowel
sounds.
ii. Mechanical obstruction (bowel obstruction, UC,
strangulation, condition in which circulation of blood to a part
of the body is cut off by constriction, Enteritis) will lead to
hyperactive bowel sounds.
6. Rectal Examination
a. Trickling of exudates in the Douglas pouch
b. Between the rectum & uterus in female
c. Rectum & bladder in male
d. Pressing interiorly to see if there is tenderness
e. Look for blood & malena.
f. Any mass specially in elderly
7. Vaginal Examination
a. Ectopic pregnancy by moving the uterus “put your finger till you
reach cervix then you move the cervix” but more commonly you
inspect with speculum to check for pelvic inflammatory disease, it Normal spleen stores
manifests by exudates\ pus ”vaginal discharge” red blood cells and
i. Rule out salpingitis (infection and inflammation in the platelets, the cells that
help your blood clot, an
fallopian tubes).
enlarged spleen it
3 INVESTIGATIONS begins to filter normal
red blood cells as well as
1. Complete Blood Count: abnormal ones,
a. High WBC "Leukocytosis" more than 40,000 is a suggestive of reducing the number of
appendicitis healthy cells in your
b. Low hemoglobin indicates hemorrhage, UC, Ischemia, Ulcer, bloodstream. It also
anemia. traps too many
c. Platelet count, if the patient is thrombocytopenic because platelets. Eventually,
sometimes thrombocytopenia can happen due to severe sepsis also excess red blood cells
it is and platelets can clog
d. An indication of a problem that might prevent you from doing your spleen, interfering
with its normal
surgery or in splenomegaly.
functioning.

177
 Investigations 5

2. Electrolytes, BUN, Creatinine

a. In acute abdomen, there will be loss of fluid in and electrolytes will
decrease
b. Hypokalemia from upper GI cause (In vomiting you expect low
potassium)
c. Hyponatremia from lower GI cause (diarrhea)
d. BUN & Creatinine if elevated? In acute abdomen, hypovolemic pre-
renal azotemia, insufficient profusion to the kidney that will lead to
renal failure.
3. Liver Function Tests
a. If you suspect jaundice, biliary disease and cholangitis.
b. High bilirubin and high alkaline phosphatase are suggestive of
cholangitis.
c. High ALT and AST are suggestive of Hepatitis.
4. Serum Amylase
a. It will be high in pancreatitis but it will go down after 2-3 days, so
check lipase because it will persist high in pancreatitis.
5. Lactate:
a. (Product of anaerobic metabolism): if there is bowel ischemia.
6. Arterial blood gases [ABGs]
a. Reflex the respiratory and metabolic states.
b. Do it if ischemia is suspected, severe sepsis, metabolic acidosis and
before anesthesia.
7. Chest x-ray
a. Perforation of hollow viscous (commonly duodenal ulcer
perforation), see air under the diaphragm. Ask for upright chest x
ray
8. Abdominal X-Ray – KUB:
a. In bowel obstruction the abdomen will look distended in supine
position.
b. Other AXR is erect “upright” position to look for air fluid level, if more
than 3 it mean there's significant obstruction
c. In gastroenteritis you can see dilated loops of small or large bowel
but not necessary to have obstruction.
d. KUB- for renal stones.
9. Abdominal Ultrasound
a. Mainly used to rule out stones (gall bladder or renal), ascites,
pyelonephritis, polycystic ovarian disease.
10. Abdominal CT
a. To diagnose difficult echo vocal appendicitis (diagnosis of
appendicitis is commonly clinical), rule out pancreatitis, tumors and
bowel ischemia.
b. Angiography / Duplex Scanning:
c. If we suspect mesenteric ischemia so we can see the blood vessels
causes of ischemia (thrombus, embolus)
d. We usually do CT and angiography
e. CT to see the bowel
11. Angiography to see blood vessels
a. If they match no blood in the vessel and bowel is edematous this is
gangrene.

178
6 Acute Abdomen

b. Duplex: for peripheral Blood vessels.

4 DIAGNOSIS

 Acute Abdomen + Shock – Acute Pancreatitis/ Ruptured AAA (abdominal

aortic aneurysm) resuscitate & immediate surgery otherwise patient may
die in minutes.
 Generalized Peritonitis – Ruptured Viscus.
 Localized Peritonitis,
o Example: RLQ rebound tenderness means Acute Appendicitis.
 Bowel Obstruction (distention of the abdomen no movement during
respiration)
 Medical Causes [Lobar Pneumonia, Acute Inferior MI "if the patient have
epigastric pain and you think of MI you can rule it out by doing ECG or
Cardiac enzyme (troponin)"]
5 MANAGEMENT

 Immediate operation – Ruptured AAA

o (Amount of bleeding is huge so if you don’t stop it immediately
patient will die, do surgery immediately and stop it)
 Pre-operative preparation and urgent operation within 6 hours
o Because the condition can get worse if you operate immediately
(ruptured Viscus but preoperatively is hypotensive dehydrated, has
electrolyte abnormalities , quite septic , if you take him immediately
to operation he might die, to prevent mortality in such condition
resuscitate the patient and prepare them for surgery by giving fluids,
antibiotics (they do it in ICU usually).
 Urgent operation within 24 hours
o Especially in case of acute appendicitis
 Conservative treatment
o In acute (pancreatitis operation will worsen the condition - except
when there is pancreatic abscess or necrosis we operate on them)
o IBD
o Cholecystitis
 Observation
o Patients with sudden onset acute abdominal pain, tender on
examination but the diagnosis was not established yet. You should
observe them (check on them every 2-4 hours tell next day if they
have a disease it will manifest).
o E.g. early appendicitis, after 24 hours will be obvious
o If there is a follicle somewhere or ruptured Graafian follicle in the
ovary, next day they feel better then you can discharge the patient
at this step.
 Discharge
6 SCENARIOS &SUMMARY

6.1 SCENARIOS: (USE THE MNEMONIC SOAP)

179
 Scenarios &Summary 7

 Case 1:
A 35 year-old male presented to the ER with 2 days history of abdominal pain. He took antacids
but did not help him at all!

 Case 2:
A 55 year-old businessman presented to the ER with severe abdominal pain since 6 hours when
he felt something like a burst in his abdomen. He is known with PUD and H-pylori but he was not
taking his medications regularly

 Case 3:
A 73 year-old male developed atrial fibrillation while recovering from an acute MI in the medical
ward. The surgery team was consulted to evaluate a new onset of severe mid-abdominal pain

 Case 4:
A 54 year-old lady presented to the ER complaining of generalized abdominal pain associated
with vomiting, constipation for 2 days, and abdominal distention. She had an emergency
Cesarean Section for her 5th baby 5 years back

6.2 SUMMARY

 Acute abdomen is a sudden abdominal disorder that requires an urgent

operative intervention in some cases.
 Almost all acute abdominal events have a common general surgical
approach based on the mnemonic SOAP.
 We have applied this general approach to some case scenarios such as
acute appendicitis, perforated DU, acute mesenteric ischemia, and small
bowel obstruction.

180
 Achalasia 1

ESOPHAGEAL DISEASES
1 ACHALASIA

 Uncommon disease of esophageal motility disorder.

 Characterized by degeneration of the myenteric neurons that innervate
LES and esophageal body.
 Pathogenesis: autoimmune, familial, viral.

1.1 PRESENTATION

 Most commonly presents in patients between the ages of 25 and 60 years.

 Equal male-to-female gender distribution.
 Symptoms:
a. Dysphagia to solids and liquids is the (most common; 90% of patients).
b. Regurgitation (2nd most common; 60% of patients).
 Nocturnal regurgitation of esophageal contents can lead to night-time
cough and aspiration.
c. Weight loss occurs in end-stage disease.
d. Chest pain (20% to 60% of patients).
e. Heartburn (30% of achalasia patients).
 May be related to direct irritation of the esophageal lining by retained
food, pills, or acidic by-products of bacterial metabolism of retained
food.

1.2 DIAGNOSIS

 CXR: may show air-fluid level.

 Barium study: quite dilated, and an air-fluid level may be secondary to
retained secretions.
o The classic finding is a gradual tapering at the end of the esophagus,
similar to a bird's beak (rat tail).
 Upper endoscopy is the next diagnostic test in a patient with dysphagia or
suspected achalasia (to rule out tumors).
o Findings can include:
 Dilated esophagus with retained food or secretions.
 Normal in as many as 44% of patients with achalasia.
o Difficulty traversing the GEJ should raise suspicion for pseudoachalasia
due to neoplastic infiltration of the distal esophagus.
 Esophageal manometry (highest sensitivity for the diagnosis of achalasia):
o Aperistalsis of the distal esophageal body.
“Bird’s beak” or “rat’s
o Incomplete or absent LES relaxation (Hypertensive LES). tail” on barium study
o Manometric variants of achalasia exist.

181
2 Esophageal Diseases

 The best known is vigorous achalasia –may represent an early

stage-, defined by the presence of normal to high amplitude
esophageal body contractions in the presence of a non-relaxing
LES.

1.2.1 SECONDARY ACHALASIA

 Chagas' disease is a parasitic infection caused by Trypanosoma cruzi
which can cause secondary achalasia.
 The most concerning secondary etiology is cancer, which can present as Barium study
achalasia through mechanical obstruction of the GEJ.
 Post fundoplication (surgery done for treatment of GERD patients):
achalasia caused by mechanical obstruction of the GEJ by the
fundoplication or diaphragmatic crural closure.
 Bariatric surgery using a gastric band device which constricts the proximal
stomach a few centimeters below the LES.
 Some types of surgery could cause achalasia by reducing the LES
diameter.

1.3 TREATMENT

 The primary therapeutic goal in achalasia is to reduce the LES basal

pressure. Dilation and tapering on
 Treatment options include barium study
o Medical therapy: Nifedipine, Isosorbide dinitrate.
o Botulinum toxin injection: block the release of acetylcholine; limited
value.
o Pneumatic dilation: blindly rupture the muscle fibers while leaving the
mucosa intact.
o Surgical myotomy (+ partial fundoplication).
 Symptomatic relief, particularly relief of dysphagia, is accepted as the
primary desired outcome.

1.3.1 MEDICAL THERAPY

Inconvenient, only modestly effective, and frequently associated with side
effects.
It is reserved for patients who are awaiting or unable to tolerate more
invasive treatment modalities.
Pharmacologic therapies attempt to decrease the LES pressure by causing smooth
muscle relaxation.
 Nitrates were first recognized as an effective treatment of achalasia.
o Systemic vasodilatory effects and headaches limit their tolerability by
patients.

182
 Achalasia 3

 Calcium channel antagonists have a better side-effect profile when

compared with nitrates.
o 30% of patients report adverse side effects including peripheral edema,
hypotension, and headache.

1.3.2 BOTULINUM INJECTION

 Injected into the LES targets the excitatory, acetylcholine-releasing neurons
that generate LES basal muscle tone.
 Easy to administer and associated with relatively few side effects.
It is apparent that, with repeated injections, the response rates reported are
similar or lower to that achieved with the initial injection; not very effective.
 Response rates at 1 month following administration average 78%, By 6
months, the clinical response rate drops to 58% and by 12 months to 49%
Given the limitations of the efficacy and durability of response, botulinum
toxin is generally reserved for use in patients who are not candidates for
more invasive treatments.
1.3.3 PNEUMATIC DILATATION
 Pneumatic dilation remains one of the most effective first-line therapies for
achalasia.
 Long-term follow-up studies reported significant symptom relapse of
50% at 10 years.
 Complications of pneumatic dilation:
o Gastroesophageal reflux 25-35%.
o Esophageal perforation 3 %.

1.3.4 SURGERY
 Standard management
 Success rates >90% - with hospital stays averaging only a few days.
 Acid exposure is a known complication of surgical intervention for achalasia
(reflux esophagitis).
 Even with a successful myotomy, it is expected that patients will have some
degree of dysphagia as a consequence of esophageal peristaltic
dysfunction.
 Delayed recurrence of postoperative dysphagia is most commonly caused
by development of a recurrent high pressure zone at the LES or a peptic
stricture complicating acid reflux.
 Laparoscopic Heller myotomy demonstrated excellent results, with 98% of
patients reporting symptomatic improvement at 5.3 years.
 Several retrospective and prospective studies have reported superior
success rates for surgery when compared with pneumatic dilation

183
4 Esophageal Diseases

1.3.5 REFRACTORY ACHALASIA

 In patients with achalasia that is refractory to therapy with Heller myotomy,
options are limited.
 Although esophagectomy is considered in patients with marked dilation and
sigmoid deformity, such patients may respond to Heller myotomy.

1.4 COMPLICATIONS

 The primary complications of achalasia are related to the functional

obstruction rendered by the non-relaxing LES and include progressive
malnutrition and aspiration.
 Uncommon but important secondary complications of achalasia include the
formation of epiphrenic diverticula and esophageal cancer.
 There is an established link between achalasia and esophageal cancer,
most commonly SQUAMOUS CELL CARCINOMA.
o The overall prevalence of esophageal cancer in achalasia is
approximately 3% with an incidence of approximately 197 cases per
100,000 persons per year.

2 ESOPHAGEAL DIVERTICULA

 Causes: Most diverticula are a result of a primary motor disturbance or an

abnormality of the UES (upper esophageal sphincter) or LES (lower
esophageal sphincter).
 Site: Can occur in several places along the esophagus. The three most
common sites of occurrence are:
o Pharyngoesophageal (Zenker's).
o Parabronchial (mid-esophageal) .
o Epiphrenic.
 True vs. False:
o True diverticula involve all layers of the esophageal wall, including
mucosa, submucosa, and muscularis.
 Traction, or true, diverticula result from external inflammatory
mediastinal lymph nodes adhering to the esophagus.
o A false diverticulum consists of mucosa and submucosa only.
 Pulsion diverticula are false diverticula that occur because of
elevated intraluminal pressures generated from abnormal motility
disorders.
 Zenker's diverticulum and an epiphrenic diverticulum fall under the
category of false, pulsion diverticula.

2.1 PHARYNGOESOPHAGEAL (ZENKER'S) DIVERTICULUM

 Most common esophageal diverticulum found today.

 It usually presents in older patients in the 7th decade of life.
 Found herniating into Killian's triangle, between the oblique fibers of the
thyropharyngeus muscle and the horizontal fibers of the cricopharyngeus
muscle.

184
 Diffuse Esophageal Spasm 5

Barium esophagaram

Figure 1: Killian's Triangle

 Symptoms:
o Sticking in the throat (common).
o Nagging cough .
o Excessive salivation. Signs of progressive disease
o Intermittent dysphagia .
o Regurgitation of foul-smelling, undigested material (common as the sac
increases in size, because of fermentation of food).
o Halitosis (bad mouth smell).
o Voice changes.
Especially common in elderly
o Retrosternal pain.
o Respiratory infections .
 Complications: the most serious complication from an untreated Zenker's
diverticulum is aspiration pneumonia or lung abscess.
 Diagnosis: is made by barium esophagram ONLY
o Neither esophageal manometry nor endoscopy is needed to make a
diagnosis of Zenker's diverticulum.
 Treatment:
o Surgical or endoscopic repair of a Zenker's diverticulum is the gold
standard of treatment.
o Open repair involve:
 Myotomy of the proximal and distal thyropharyngeus and
cricopharyngeus muscles.
 Diverticulectomy or diverticulopexy are performed through an
incision in the left neck.
o An alternative to open surgical repair is the endoscopic Dohlman
procedure.
o Endoscopic division of the common wall between the esophagus and
the diverticulum using a laser or stapler has also been successful.

3 DIFFUSE ESOPHAGEAL SPASM

 Pathology:

185
6 Esophageal Diseases

o The esophageal contractions are repetitive, simultaneous, and of high

amplitude.
o DES is a hypermotility disorder of the esophagus (non-peristalsis
disorder).
o The basic pathology is related to a motor abnormality of the esophageal
body that is most notable in the lower two thirds of the esophagus.
 Clinical presentation:
o Is seen most often in women and is often found in patients with multiple
complaints.
o Typically: chest pain and dysphagia
 Patients will complain of a squeezing pressure in the chest that may
radiate to the jaw, arms, and upper back (could be misdiagnosed as
angina pectoris).
 May be related to: eating or exertion.
 Aggravating: heightened emotional stress, acid reflux, cold liquids.
o Regurgitation of esophageal contents and saliva is common (but NOT
acid reflux).
o Associated with: Irritable bowel syndrome (IBS) and pyloric spasm.
o Triggers: GI problems e.g. gallstones, peptic ulcer disease (PUD), and Corkscrew appearance
pancreatitis.
 Diagnosis: esophagram and manometric studies.
 Treatment:
o The mainstay of treatment for DES is NON-SURGICAL, and
pharmacologic or endoscopic intervention is preferred.
o Surgery is reserved for patients with recurrent incapacitating episodes
of dysphagia and chest pain who do not respond to medical treatment.

4 CAUSTIC INJURY

The best cure for this condition is an ounce of prevention

 In children: ingestion is accidental and in small quantities.
 In teenagers and adults: ingestion usually is deliberate during suicide
attempts, and in much larger quantities.
 Alkali ingestion is more common than acid ingestion because of its lack of
immediate symptoms.
 Alkali ingestion is more devastating and almost always lead to significant
destruction of the esophagus.
Three Phases Of Tissue Injury From Alkali Ingestion
Phase Of Tissue Injury Onset Duration Inflammatory Response

1 Acute necrosis 1-4 days 1-4 days Coagulation of intracellular proteins

Inflammation

2 Ulceration and granulation 3-5 days 3-12 days Tissue sloughing

Granulation of ulcerated tissue bed

3 Cicatrization and scarring 3 weeks 1-6 mo Adhesion formation

Scarring

186
 Caustic Injury 7

 Symptoms:

Phase I Patients may complain of oral and substernal pain, hypersalivation,

odynophagia and dysphagia, hematemesis, and vomiting.
Phase II These symptoms may disappear.
Phase III Dysphagia reappears as fibrosis and scarring begin to narrow the
esophagus.

o Symptoms of respiratory distress, such as hoarseness, stridor, and

dyspnea, suggest upper airway edema and are usually worse with acid
ingestion.
o Pain in the back and chest may indicate a perforation of the mediastinal
esophagus, whereas abdominal pain may indicate abdominal visceral
perforation.
 Diagnosis:
1) Physical exam:
a. Specifically evaluating the mouth, airway, chest, and abdomen.
b. Careful inspection of the lips, palate, pharynx, and larynx is done.
c. The abdomen is examined for signs of perforation.
2) Early endoscopy is recommended 12 to 24 hours after ingestion to
identify the grade of the burn.
3) Serial chest and abdominal radiographs are indicated to follow patients
with questionable chest and abdominal exams.
Degree of Burn Endoscopic Evaluation Treatment
First Degree Mucosal hyperemia 48-hr observation
Edema Acid suppression
Second Degree Limited hemorrhage Aggressive IV resuscitation
Exudates IV antibiotics
Ulceration Acid suppression
Pseudomembrane formation
Third Degree Mucosal sloughing Inhaled steroids
Deep ulceration Fiberoptic intubation (if needed)
Massive hemorrhage
Complete luminal obstruction
Charring
Perforation

 Management (of the acute phase):

o Goal: limiting and identifying the extent of the injury.
o It begins with neutralization of the ingested substance.
o Alkalis (including lye) are neutralized with half-strength vinegar or citrus
juice (we give them an acids to compensate alkaline solution)
o Acids are neutralized with milk, egg whites, or antacids.

187
8 Esophageal Diseases

o Emetics and sodium bicarbonate need to be avoided because they can

increase the chance of perforation.

First degree burns Second and third degree burns

 48 hours of observation is indicated.  Resuscitation is aggressively pursued.
 Oral nutrition can be resumed when a  The patient is monitored in the intensive
patient can painlessly swallow saliva. care unit.
 A repeat endoscopy and barium  Kept (NPO) with IV fluids. IV antibiotics and
esophagram are done in follow-up at a proton pump inhibitor are started.
intervals of 1, 2, and 8 months.  Fiberoptic intubation may be needed and
must be available.

5 ESOPHAGEAL PERFORATION

 Perforation of the esophagus is a surgical emergency.

 Early detection and surgical repair within the first 24 hours results in 80% to
90% survival.
 After 24 hours, survival decreases to less than 50%.
 Causes:
o Forceful vomiting “Boerhaave's syndrome” (15%) .
o Foreign body ingestion (14%) .
o Trauma (10%).
o Endoscopic instrumentation for a diagnostic or therapeutic procedure
(Majority).

5.1 SIGNS AND SYMPTOMS

 Patients with esophageal perforation mainly come with fever & dysphagia.
o Severe dysphagia, the patient is unable to swallow his saliva.
 Pain: neck, substernal, or epigastriac.
 +/- Vomiting or hematemesis.
 Cervical perforations:
o May present with neck ache and stiffness due to contamination of the
prevertebral space.
o Could cause subcutaneous emphysema .
 Thoracic perforations:
o Present with shortness of breath and retrosternal chest pain lateralizing
to the side of perforation.
o Could cause pneumothorax.
 Abdominal perforations: present with epigastric pain that radiates to the
back if the perforation is posterior .
 History: trauma, advanced esophageal cancer, violent wretching (as seen
in Boerhaave's syndrome), swallowing of a foreign body, or recent
instrumentation.
 On examination:
o Patient may present with tachypnea, tachycardia, and a low-grade fever
but have no other overt signs of perforation.
o Subcutaneous air in the neck or chest, shallow decreased breath
sounds, or a tender abdomen are all suggestive of perforation.

188
 Esophageal Perforation 9

 With increased mediastinal and pleural contamination, patients progress

toward hemodynamic instability (shock).

5.2 DIAGNOSIS

 Lab:  WBC count and  salivary amylase in the blood or pleural fluid.
 Chest x-ray: may demonstrate a hydropneumothorax.
 Contrast esophagram: done using barium for a suspected thoracic
perforation and Gastrografin is used for an abdominal perforation.
o Most perforations are found above the GEJ on the left lateral wall of the
esophagus which results in a 10% false-negative rate in the contrast
esophagram if the patient is not placed in the lateral decubitus position.
 Chest CT: shows mediastinal air and fluid at the site of perforation.

5.3 TREATMENT

 A surgical endoscopy needs to be performed if the esophagram is negative

or if operative intervention is planned.
o Mucosal injury is suggested if blood, mucosal hematoma, or a flap is
seen or if the esophagus is difficult to insufflate.

189
10 Esophageal Diseases

 Patients with an esophageal perforation can progress rapidly to

hemodynamic instability and shock.
 If perforation is suspected:
o Resuscitation with placement of large-bore peripheral IV catheters, a
urinary catheter, and a secure airway, before the patient is sent for
diagnostic testing.
o IV fluids and broad-spectrum antibiotics are started immediately, and
the patient is monitored in an ICU.
o The patient is kept NPO, and nutritional access needs are assessed.
Surgery is not indicated for every patient with a perforation of the esophagus
 Management is dependent on several variables: stability of the patient,
extent of contamination, degree of inflammation, underlying esophageal
disease, and location of perforation.
 The most critical variable that determines the surgical management of an
esophageal perforation is the degree of inflammation surrounding the
perforation.
o When patients present within 24 hours of perforation, inflammation is
generally minimal, and primary surgical repair is recommended.
o With time, inflammation progresses, and tissues become friable and
may not be amenable to primary repair.
 The final variable to consider in the surgical management of esophageal
perforations is the location of the perforation.

Hamman's sign (a.k.a.

Hamman's crunch) is a
“mediastinal crunch” heard
upon auscultation in the
setting of mediastinal
emphysema (air in the
mediastinum). With each
heartbeat, the air is displaced
creating this auscultatory
finding.

190
 Gastroesophageal Reflux Disease 11

6 GASTROESOPHAGEAL REFLUX DISEASE

 Definition:
o Symptoms OR mucosal damage produced by the abnormal reflux of
gastric contents into the esophagus.
o Often chronic and relapsing.
o May see complications of GERD in patients who lack typical symptoms.
 Pathology:
o LES has the primary role of preventing reflux of the gastric contents into
the esophagus.
o GERD may occur when the pressure of the high-pressure zone in the
distal esophagus is too low to prevent gastric contents from entering the
esophagus (when the LES is NOT contracting well).
o GERD is often associated with a hiatal hernia:
Type I The most common. Also called “sliding” hernia.
Gastroesophageal junction is above the diaphragm.
Type II Referred to as paraesophageal hernias. May be associated with GERD.
GE junction is normal in position BUT part of the stomach herniated
above the diaphragm.
Type III Referred to as paraesophageal hernias. May be associated with GERD.
GE junction is above the diaphragm and part of stomach too.
Type IV Another organ is herniated into the chest e.g. spleen, colon.
Types of hiatus hernia

191
12 Esophageal Diseases

 Epidemiology:
o About 44% of the US adult population have heartburn at least once a
month.
o 14% of Americans have symptoms weekly.
o 7% have symptoms daily.

6.1 SYMPTOMS

Classic GERD Complicated GERD

Substernal burning and or regurgitation Dysphagia
Postprandial Odynophagia: Retrosternal pain w/swallowing
Aggravated by change of position Bleeding
Prompt relief by antacid
Extra-esophageal
Pulmonary ENT
Asthma Hoarseness (dysphonia)
Aspiration pneumonia Laryngitis
Chronic bronchitis Pharyngitis
Pulmonary fibrosis Chronic cough
Other Sinusitis
Chest pain Subglottic stenosis
Dental erosion Laryngeal cancer

6.2 DIAGNOSIS & TREATMENT

6.2.1 DIAGNOSIS
 Barium swallow (to confirm the diagnosis).
 Endoscopy (important to see the complication of GERD).
 Ambulatory pH monitoring (the gold standard and most accurate).
 Esophageal manometry.
 Bravo capsule is a capsule that receive the PH massages for 24 hours.

6.2.2 TREATMENT
 Lifestyle Modifications (most important)
o Elevate head of bed 4-6 inches.
o Avoid eating within 2-3 hours of bedtime.
o Lose weight if overweight.
o Stop smoking.
o Modify diet:
 Eat more frequent but smaller meals.
 Avoid fatty/fried food, peppermint, chocolate, alcohol, carbonated
beverages, coffee and tea.
o OTC medications prn (as needed).
 Acid Suppression Therapy
o H2-Receptor Antagonists (H2RAs)
 Cimetidine (Tagamet®), Ranitidine (Zantac®), Famotidine
(Pepcid®), Nizatidine (Axid®).
o Proton Pump Inhibitors (PPIs)

192
 Barrett’s Esophagus 13

Omeprazole (Prilosec®), Lansoprazole (Prevacid®), Rabeprazole

(Aciphex®), Pantoprazole (Protonix®), Esomeprazole (Nexium ®)
 Anti-Reflux Surgery: Indications:
o Failed medical management.
o Patient’s choice (opt for surgery despite successful medical
management, due to life style considerations including age, time or
expense of medications, etc).
o Complications of GERD (e.g. Barrett's esophagus; grade III or IV
esophagitis).
o Medical complications attributable to a large hiatal hernia (e.g. bleeding,
dysphagia).
o “Atypical" symptoms (asthma, hoarseness, cough, chest pain,
aspiration) and reflux documented on 24 hour pH monitoring.
 Endoscopic Antireflux Therapies:
o Radiofrequency energy delivered to the LES
 Stretta procedure.
o Suture ligation of the cardia
 Endoscopic plication.
o Submucosal implantation of inert material in the region of the lower
esophageal sphincter
 Enteryx.

Summary of GERD:
 It is due to low LES pressure that allows the reflux of gastric acids into the esophagus.
 Symptoms of GERD: 1) sore throat (2) epigastric pain (3) sub-sternal burning (4) hoarseness
o Mainly occur post-prandial and with change of position.
o Relieved by anti-acids.
 Diagnosis:
o Barium swallow to confirm the diagnosis.
o Endoscopy for complications.
o PH monitor is the most accurate.
 Chronic GERD mainly followed by Barrett’s esophagus which is a pre-malignant sign.

7 BARRETT’S ESOPHAGUS

 Definition & pathology:  Barrett’s esophagus

o Barrett's esophagus is a condition in which intestinal, columnar predisposes to
epithelium replaces the stratified squamous epithelium that normally adenocarcinoma NOT
lines the distal esophagus. squamous cell
carcinoma of the
o Chronic gastroesophageal reflux is the factor that both injures the esophagus.
squamous epithelium and promotes repair through columnar
metaplasia.
o Ten percent (10%) of patients with GERD develop Barrett's
esophagus.
o Although these metaplastic cells may be more resistant to injury from
reflux, they also are more prone to malignancy (Barrett’s esophagus is
pre-malignant sign ) .
o With continued exposure to the reflux disease, metaplastic cells
undergo cellular transformation to low- and high-grade dysplasia
o Dysplastic cells may evolve to cancer:

193
14 Esophageal Diseases

 Low grade dysplasia only affecting mucosa and has a risk of

cancer.
 High grade dysplasia the patient for sure has carcinoma in situ.
o 40-fold increase in risk for developing esophageal carcinoma in
patients with Barrett's esophagus.
 Epidemiology:
o 70% of patients are men aged 55 to 63 years.
o Men have a 15-fold increased incidence over women of
adenocarcinoma of the esophagus, but women with Barrett's
esophagus are increasing in number as the differences in the Western
lifestyle between men and women diminish.
 Clinical presentation:
o Many are asymptomatic.
o Most patients present with symptoms of GERD: heartburn,
regurgitation, acid or bitter taste in the mouth, excessive belching, and
indigestion.
o Recurrent respiratory infections, adult asthma, and infections in the
head and neck also are common complaints.
 Diagnosis:
o The diagnosis of BE is made by endoscopy and pathology. 
o The presence of any endoscopically visible segment of columnar
mucosa within the esophagus that on pathology identifies intestinal
metaplasia defines BE.
 Treatment:
o Surveillance:
 Yearly surveillance endoscopy is recommended in all patients with
a diagnosis of Barrett's esophagus.
 For patients with low-grade dysplasia, surveillance endoscopy is
performed at 6-month intervals for the first year and then yearly
thereafter if there has been no change.
 Patients undergoing surveillance are placed on acid suppression
medication and monitored for changes in their reflux symptoms.
o Anti-reflux surgery (controversial):
Columnar mucosa in
 Those in favor of surgery argue that medical therapy and distal esophagus
endoscopic surveillance may treat the symptoms but fail to address
the problem.
 The problem is the functional impairment of the LES that leads to
chronic reflux and metaplastic transformation of the lower
esophageal mucosa.
 Surgery renders the LES competent and restores the barrier to
reflux.
 Studies have demonstrated regression of metaplasia to normal
mucosa up to 57% of the time in patients who have undergone anti-
reflux surgery.
o Photodynamic therapy (PDT) is the most common ablative method
used to treat BE.
o Endoscopic mucosal resection (EMR) is gaining favor for the treatment
of Barrett's esophagus with low-grade dysplasia.
o Esophageal resection for Barrett's esophagus is recommended only for
patients in whom high-grade dysplasia is found.

194
 Carcinoma of the Esophagus 15

Pathologic data on surgical specimens demonstrate a 40% risk for

adenocarcinoma within a focus of high-grade dysplasia.

8 CARCINOMA OF THE ESOPHAGUS

 Esophageal cancer is the fastest growing cancer in the western countries.

 Squamous cell carcinoma still accounts for most esophageal cancers
diagnosed.
o Arises from the squamous mucosa (native to esophagus), found in
upper and middle third 70% of the time.
 In the US: adenocarcinoma in 70% of patients presenting with esophageal
cancer.
o Esophageal adenocarcinoma now 70% of all esophageal carcinomas
diagnosed in Western countries. There are a number of factors that are
responsible for this shift in cell type:
 Increasing incidence of GERD.
 Western diet.
 Increased use of acid-suppression medications.
 Intake of caffeine, fats, and acidic and spicy foods all lead to
decreased tone in the LES and an increase in reflux.
 The 5-year survival rate: 70% with polypoid lesions and 15% with
advanced tumors.
 Risk factors:
o Smoking and alcohol both increase the risk for foregut cancers by 5-fold
(combined).
o Food additives: nitrosamines (pickled and smoked foods).
o Long-term ingestion of hot liquids.
o Caustic ingestion, achalasia, bulimia, tylosis (an inherited autosomal
dominant trait), Plummer-Vinson syndrome, external-beam radiation,
and esophageal diverticula all have known associations with squamous
cell cancer.
 Symptoms:
o Early-stage cancers: asymptomatic or mimic symptoms of GERD.
o Most patients with esophageal cancer present with dysphagia and
weight loss.
 Because of the distensibility of the esophagus, a mass can obstruct
two thirds of the lumen before symptoms of dysphagia are noted.
o Choking, coughing, and aspiration from a tracheoesophageal fistula
(signs of advanced disease).
o Hoarseness and vocal cord paralysis from direct invasion into the
recurrent laryngeal nerve (signs of advanced disease).
o Systemic metastases to liver, bone, and lung can present with jaundice,
excessive pain, and respiratory symptoms.
 Diagnosis:
1. Esophagram:
 A barium esophagram is recommended for any patient presenting
with dysphagia.
 differentiate intraluminal from intramural lesions.
Barium esophagram

195
16 Esophageal Diseases

 discriminate between intrinsic (from a mass protruding into the

lumen) and extrinsic (from compression of a structures outside the
esophagus).
 The classic finding of an apple-core lesion.
 Not specific for cancer, but good first test to perform in patients
presenting with dysphagia and a suspicion of esophageal cancer.
2. Endoscopy:
 The diagnosis of esophageal cancer is made best from an
endoscopic biopsy.
 Any patient undergoing surgery for esophageal cancer must have
an endoscopy before entering the operating room for a definitive
resection.
3. CT scan: of the chest and abdomen is important to assess the length of
the tumor, thickness of the esophagus and stomach, regional lymph
node status and distant disease to the liver and lungs.
4. PET scan:
 Evaluates the primary mass, regional lymph nodes, and distant
disease.
 Its sensitivity and specificity slightly exceed those of CT; however,
they remain low for definitive staging.
5. Endoscopic ultrasound (EUS) is the most critical component of
esophageal cancer staging .
 The information obtained from EUS will help guide both medical
and surgical therapy.
 Biopsy samples can be obtained of the mass and lymph nodes in
the paratracheal, subcarinal, paraesophageal, celiac region.
 Treatment:
1. Chemotherpay.
2. Radiation therapy.
3. Chemo-radiotherapy.
4. Surgical resection.

9 LEIOMYOMA

 Leiomyomas constitute 60% of all benign esophageal tumors.

 Found in men ≥ women and tend to present in the 4th & 5th decades.
 80% are found in the distal 2/3 of the esophagus.
 Usually solitary and remain intramural, causing symptoms as they enlarge
 Recently, they have been classified as a gastrointestinal stromal tumor
(GIST).
o GIST tumors are the most common mesenchymal tumors of the
gastrointestinal tract and can be benign or malignant.
o Nearly all GIST tumors occur from mutations of the c-KIT oncogene,
which codes for the expression of c-KIT (CD117).
 All leiomyomas are benign. Malignant transformation is rare .
 Clinical presentation:
o Many leiomyomas are asymptomatic.
o Dysphagia and pain are the most common symptoms and can result
from even the smallest tumors.

196
 MCQs 17

 Diagnosis:
o CXR: not helpful.
o Barium esophagram: leiomyoma has a characteristic appearance
(smooth filling defect).
o Endoscopy: extrinsic compression is seen, and the overlying mucosa is
noted to be intact.
o Endoscopic ultrasound (EUS): hypoechoic mass in the submucosa or
muscularis propria.

 Treatment:
o Leiomyomas are slow-growing tumors with rare malignant potential that
will continue to grow and become progressively symptomatic with time.
o Although observation is acceptable in patients with small (<2 cm)
asymptomatic tumors or other significant co-morbid conditions, in most
patients, surgical resection is advocated.
o Surgical enucleation of the tumor remains the standard of care
(thoracotomy or with video or robotic assistance).
o The mortality rate is less than 2%, and success in relieving dysphagia
approaches 100%.

10 MCQS
1. The gold standard investigation for GERD is:
A) Ambulatory pH monitoring
B) Barium swallow
C) Endoscopy
D) Clinical picture

2. Hiatus hernia:
A) Reflux is not seen in paraesophageal type
B) Dysphagia is the commonest symptom of sliding type
C) Paraesophageal type is treated medically
D) The gastroesophageal junction is intraabdominal in sliding type

197
18 Esophageal Diseases

3. Achalasia's usual investigating tools & equipment ... all except:

A) Radionucleotide
B) MRI
C) Endoscopy
D) Barium swallow

4. Most common site for squamous cell carcinoma of the esophagus is:
A) Upper 1/3
B) Middle 1/3
C) Lower 1/3
D) Site of esophageal reflux

5. Barrett’s esophagus:
A) Transforms into adenocarcinoma in 10% of cases
6. What is not true about leiomyoma of the esophagus?
A) 10% are multiple
B) They are due to mutation in c kit oncogene
C) They arise from the mucosa of esophagus
D) Most common site of origin is the middle 1/3 of esophagus

7. 10. Weight loss comes earlier with:

A) Colon cancer
B) Prostatic cancer
C) Esophageal cancer
D) Hepatoma

8. 70 year old male newly diagnosed with pharyngoesophageal (zenker's)

diverticulum, which one of the following most likely the presenting
symptoms?
A) Abdominal pain
B) Haematemesis
C) Halitosis
D) Vomiting

9. 55 year old newly diagnosed with diffuse esophageal spasm, his

presenting history may include one of the following?
A) Abdominal pain
B) Chest pain and dysphagia
C) Haematemesis
D) Recurrent vomiting

 Answers: 1;A, 2;A, 3;B (Source: bestpractice.bmj.com), 4;A (Source: Wikipedia), 5;A, 6;D, 7;C,
8;C, 9;B

198
 Objectives 1

ESOPHAGEAL DISEASES:
CASES
1 OBJECTIVES

 Understand the history related to common esophageal diseases such as

GERD.
 Understand the symptoms and signs of esophageal perforation.
 Understand the symptoms and signs of esophageal motility disorder.

2 CASE 1

Part 1:
A 50 year old male presented to you in the clinic with history of heartburn and
hoarseness.
He is obese and a smoker.
Examination was unremarkable.

 What else would you like to ask about in the history?

 What are the symptoms of:
o Classic GERD?
o Complicated GERD?
 What are the extra-esophageal manifestations of GERD?
 What is your next step in management?

Part 2:
Barium-swallow report:
- No stricture or tumor.
- Small hiatus hernia.
- Evidence of reflux of the contrast.

 What are the types of hiatus hernia?

 What other tests & procedures can aid in the diagnosis? And what is their
diagnostic value?

Part 3:
Biopsy was done.
Pathology report: esophagitis with intestinal, columnar epithelium replaces the stratified
squamous epithelium (metaplasia) consistent with Barrett's Esophagus. No evidence of
dysplasia.

 What is the next step in management?

 What are the indications of surgery?

199
2 Esophageal Diseases: Cases

Part 4:
You advise the patient to: Reduce weight and quit smoking, and schedule follow up
endoscopy.
Started the patient on: Nexium 40 mg OD

3 months later, you did endoscopy for the patient. 6 hour post endoscopy patient started
to complain of: chest pain & fever.

 What else would you like to ask about in the history?

 What is the next step in management?

 What is the treatment?

Part 5:
6 years later, he presented to your clinic complaining of: Dysphagia & weight loss.

 What else would you like to ask about in the history?

 Make a list of differential diagnoses.
 How are you going to manage this patient?

200
 Case 2 3

Part 6:
The biopsy from the endoscopy revealed: adenocarcinoma.

 What are the treatment options?

3 CASE 2

Part 1:
24 years old, healthy, presented to your clinic complaining of: Dysphagia.

 How will you manage this patient?

201
4 Esophageal Diseases: Cases

Part 2:
His manometry consistent with Achalasia.
Endoscopy showed:
- Dilated esophagus.
- Retained food particles.

 How will you treat this patient?

4 CASE 3

70 years old male, his wife bring him to your clinic because of:
- Bad breath.
- Chronic cough especially after eating.

 How will you manage this patient?

 What is the cause of esophageal diverticula?

 What are the different types of esophageal diverticula?
 What are the most common sites?

202
 Introduction 1

GASTRIC AND DUODENAL

DISEASES
1 INTRODUCTION

 The duodenum is divided into 4 parts, which are closely applied to the head of
the pancreas.
 The 1st part of the Duodenum:
o 5 cm in length
o Most common site for peptic ulceration to occur
o Begins at the pylorus
o Runs upward and backward on the transpyloric plane at the level of the
first lumbar vertebra Superior Mesenteric
o The relations of this part are as follows: Artery Syndrome: The
 Anteriorly: The quadrate lobe of the liver and the gallbladder rd
obstruction of the 3 part
 Posteriorly: The lesser sac (first inch only), the gastroduodenal of the duodenum by the
superior mesenteric
artery (that's why posterior ulcers bleed ), the bile duct and portal artery
vein, and the inferior vena
 Superiorly: The entrance into the lesser sac (the epiploic foramen)
 Inferiorly: The head of the pancreas
2 DISEASES OF THE STOM ACH AND DUODENUM

2.1 PEPTIC ULCER

 Most common cause of abdominal pain related to the stomach and the
duodenum 
 Sites:
o Esophagus
o Stomach
o Duodenum
o Jejunum (following a gastrojejunostomy)
o Ileum (in relation to ectopic gastric mucosa in Meckel’s diverticulum)
 Men are affected three times as often as women 
 Duodenal ulcers are ten times more common than gastric ulcers in young
patients 
 In the older age groups the frequency is about equal 
 Clinical presentation:
o Pain
o Bleeding
o Perforation
o Obstruction
2.1.1 DUODENAL ULCER
 95% occur in the duodenal bulb (2 cm), the first part of the duodenum 
 They may be acute (ulcers with a history of less than 3 months with no
evidence of fibrosis) or chronic
 Common in young and middle-aged males

203
2 Gastric And Duodenal Diseases

 Normal or increased acid secretion

 90% caused by Helicobacter Pylori (GNCB aerophilic)
 Clinical Features:
o Well-localized epigastric pain (mid-day, noon and night)
o Pain when hungry, and is relieved by food 
 Diagnosis:
1. EGD (Esophageogastroduodenoscopy)
2. Gastric analysis:
 Basal vs. Maximal (not practical and isn’t used nowadays)
3. Gastrin serum levels:
 Severe or Refractory (Done if Zollinger-Ellison Syndrome is
suspected or the treatment was not effective) 
4. Contrast meal
 Used when either endoscopy is contraindicated or complications
of the ulcer have occurred 
 Before doing all the tests, you must first treat the patient if you suspect
duodenal ulcer for at least 6 weeks 
 Treatment:
1. Medical Treatment (80% in 6 weeks)
 H2 antagonist (e.g. Zantac) – control acid secretion
 Proton pump inhibitors (e.g. Omeprazol)
 Antibiotics (e.g. Amoxicillin): For H. Pylori eradication
2. Surgical Treatment [It has been limited to patients in whom
complications have occurred or to block hormonal stimulation]
 Vagotomy
 Antrectomy and vagotomy
 Subtotal gastrectomy
2.1.2 GASTRIC ULCER
 95% occur along the lesser curvature in the distal half of the stomach 
 Gastric ulcers generally run a chronic course
 Common in 40-60 year old males (Gastric ulcer is more prevalent with older
age)
 Gastric ulcers may develop into malignancy much more often than duodenal
ulcers
 Types:
1. In Incisura Angularis with normal acid
2. Prepyloric and DU with high acid - Most common type
3. In the Antrum due to NSAIDs
4. At the Gastroesophageal Junction (GEJ)
 Clinical Features:
1. Epigastric pain
2. The pain occurs during eating and is relieved by vomiting (Patient might
lose weight) (very  to help differentiate from duodenal)
 Diagnosis:
o EGD with biopsy (Biopsy is important here to exclude malignancy)
o Contrast swallow (Filling defect)
 Treatment:
o Medical Treatment:

204
 Diseases of the Stomach and Duodenum 3

 Not common
 Eradication of H. Pylori
o Surgical Treatment: Usually done to make sure that the ulcer does not
develop into cancer 
 Complications of surgical treatment for peptic ulcers:
1. Early complications: Leakage, bleeding and retention
2. Late complications:
A. Recurrent ulcer (marginal, stomal or anastomotic ulcers)  Dumping
Syndrome:
B. Gastrojejunocolic and gastrocolic fistula
C. Dumping syndrome  A condition where the
ingested food bypasses
 There is no pylorus due to surgery, so the food will go to the the stomach too rapidly
small bowel directly due to eating food with osmotic and enters the small
potential intestine largely
 Patient will suffer from fainting and sweating undigested. It happens
when the upper end of
 Early dumping the small intestine, the
 Late dumping is caused by hypoglycemia duodenum, expands too
 Late dumping occurs 1-3 hours after a meal. The quickly due to the
pathogenesis is thought to be related to the early presence of
hyperosmolar food from
development of hyperinsulinemic (reactive) hypoglycaemia. the stomach.
 Advise the patient to eat less sugar or give him acarbose
Clinical presentation:
D. Alkaline gastritis
E. Anemia  - Tachycardia
 Iron deficiency - Flushing
 Vit. B12 deficiency (Pernicious anemia) - Sweating
F. Postvagotomy diarrhea
- Colicky pain
G. Chronic gastroparesis
H. Pylroic obstruction/ stenosis - Hypoglycemia and may
 Complications of Peptics ulcers: lead to fainting (seen
more in late dumping)
o Pyloric obstruction:
 Dull epigastric pain & projectile vomiting of large volumes of
undigested food matter
 Could be due to stricture formation
 Medical treatment (must make sure pt is taking their medication
even if the pain stops)  Beeding site in
 Surgical treatment duodenal ulcers:
1. Remove and anastomose When bleeding (upper
2. Bypass GI, presents with
vomiting blood) is seen,
o Perforation:
we suspect the ulcer to
 Occurs in acute ulcers (duodenal mostly) be in the posterior wall of
 On the anterior wall of the duodenum (duodenal ulcer) the 1st part of the
 Anterior ulcers cause perforation , whereas posterior ulcers duodenum. Perforation
cause bleeding  occurs in the anterior
wall’s ulcer, bleeding
 High risk: Female, old age, gastric ulcer more commonly occurs
 Acute onset of severe unremitting epigastric pain in the posterior ulcer
 Diagnosis: X-ray will demonstrate free air under the diaphragm mainly due to the
[which means air in the peritoneum indicating that there is Gastroduodenal artery
that lies behind the 1st
perforation of the viscus] (85%) and fill 400 cc of air by the
part of the duodenum.
Nasogastric tube (NGT) [Never do gastroscopy]
 Treatment: NGT, ABS, Surgery

205
4 Gastric And Duodenal Diseases

2.2 ZOLLINGER-ELLISON SYNDROME (GASTRINOMA)

 Peptic ulcer disease (often severe) in 95%

 Gastric hypersecretion + very high no. of ulcers + gastroma
 Elevated serum gastrin
 Single one is usually malignant
 Multiple is benign (MEN 1)
 Diagnosis:
o Gastrin levels more than 500 pg/ml 
o CT Scan, somatostatin scan
o Portal vein blood sample
 Presentation: Diarrhea (steatorrhea due to the inactivation of the pancreatic
lipase) and severe persistent epigastric pain
 Treatment:
1. Medical treatment: Acid control (massive dose of PPI) 
2. Surgical treatment: Distal hemi-gastrectomy and ulcer excision
2.3 UPPER GASTROINTESTINAL BLEEDING
Management:
 Presentation: 1. Resuscitation
o Hematemesis 2. Detection and
o Melena endoscopic treatment
o Hematochezia [Occurs very rarely] (If the cause is an
ulcer we can either
 Causes of massive upper gastrointestinal hemorrhage: put a clip on it, burn
Common causes Uncommon causes 5% it, use a rubber band
or injection of a
Peptic ulcer  45% Gastric carcinoma sclerosing agent to
Esophagitis form a clot and stop
Duodenal ulcer 25%
Pancreatitis the bleeding)
Gastric ulcer 20% 3. Surgical
Esophageal varices 20% Hemobilia management
Gastritis 20% Duodenal diverticulum
Mallory-Weiss syndrome 10%

2.4 MALLORY-W EISS SYNDROME

 Usually caused by severe retching, coughing, or forceful vomiting 

 10% of Upper Gastrointestinal Bleeding (UGIB) cases
 1-4cm longitudinal tear in gastric mucosa at esophageal-gastric junction
(most common site) 
 EGD is done to confirm diagnosis
 90% of bleeding stops spontaneously:
- By cold gastric wash (To induce vasospasm to stop the bleeding)
- If it doesn’t stop, we perform EGD
- If the tear is small, we can burn it (cautery). If not, it will need surgical
intervention.
2.5 STRESS GASTRODUODENITIS, STRESS ULCER & ACUTE
HEMORRHAEGIC GASTRITIS

 Stress ulcer: Ulcer due to shock or sepsis

206
 Diseases of the Stomach and Duodenum 5

 Curling’s ulcer: Ulcer due to burns

 Cushing’s ulcer: Ulcer due to the presence of a CNS tumor or injury (more to
perforate, high acid production)
 Acute Hemorrhagic Gastritis
2.6 GASTRIC POLYPS

 Incidental finding
 Type of Gastric polyps:  If found through
1. Hyperplastic – treat with Omeprazole endoscopy, remove the
2. Adenomatous (Premalignant) – most serious polyp. If the polyp is
3. Inflammatory found to be
 Affects distal part of the stomach adenomatous, we do
further investigations.
 Presentation: Anemia
 EGD to R/O malignancy
 You have to resect the adenomatous type due to its malignant potential
2.7 GASTRIC LEIOMYOMAS

 Incidental finding
 Benign smooth muscle tumor
 Common submucosal growth
 90% asymptomatic, less than 1% present with massive bleeding
 Diagnosis: EGD and CT scan (bulging mass in the mucosa on endoscopy)
 Never take biopsy (the capsule will break) 
 Surgical wide excision
2.8 MENETRIER’S DISEASE

 Giant hypertrophy of the gastric rugae (thick rugae)  Mucosal hypertrophy

may lead to abnormally
 Presents with hypoproteinemia large secretion of
 Diarrhea, edema and weight loss protein-rich mucus and
 Treatment: acid (This over-secretion
o Atropine (to reduce the secretion) contributes to symptoms
of epigastric pain and
o Omeprazole hypoproteinaemia).
o H. Pylori eradication
o If the patient still has symptoms we perform a gastrectomy (rarely so)
2.9 PROLAPSE OF THE GASTRIC MUCOSA

 Occasionally accompanies small gastric ulcer

 Presentation: Vomiting and abdominal pain
 X-Ray: Antral folds into duodenum (Double ring on X-ray) [not well defined]
 Treatment: Antrectomy with Billroth 1
2.10 GASTRIC VOLVULUS 

 Benign disease, but lethal (can lead to death)

 Types:
1. Its longitudinal axis (Organoaxial volvulus):
o More common

207
6 Gastric And Duodenal Diseases

o Associated with HH (hiatal hernia)

2. Transverse (Mesenterioaxial volvulus):
o Line drawn from the mid lesser curvature to the mid greater
curvature - Associated with vomiting (obstruction)
 Presentation: Severe abdominal (epigastric) pain and Brochardt’s triad

Brochardt’s Triad 

 Vomiting followed by retching and then inability to vomit

 Epigastric distention
 Inability to pass a nasogastric tube
 Diagnosis: Confirmed by a Ground Glass appearance on X-Ray
 If diagnosed, we should immediately take him to the OR

2.11 GASTRIC DIVERTICULA

 Uncommon
 Asymptomatic
 Weight loss, diarrhea
 It causes anemia
 Diagnosis: EGD, X-Ray
 Surgery
2.12 DUODENAL DIVERTICULA

 Affects 20% of the population

 Asymptomatic – incidental finding  2nd part of the
duodenum is the most
 90% in the medial aspect of the duodenum common site for
 Rare before 40 years of age diverticulum formation in
 Most are solitary and 2.5 cm peri-ampullary of vater the GI tract.
 It can cause obstruction, bleeding and inflammation
 If it’s asymptomatic, we leave it. If there is superficial cancer, we excise it.
2.13 BEZOAR

 Retained concretions of indigestible foreign material in the stomach (foreign

body in the stomach)
 Types:
1. Trichobezoars: Formed from hair
2. Phytobezoars: Indigestible plant material
 Presentation: Obstruction
 Diagnosis: EGD, X-Ray
 Treatment: Surgical removal
2.14 BENIGN DUODENAL TUMORS

 Brunner’s gland adenomas

 Carcinoid tumors
 Heterotopic gastric mucosa
 Villous adenomas

208
 MCQs 7

2.15 SUPERIOR MESENTERIC ARTERY OBSTRUCTION OF THE

DUODENUM
 Fat is the only thing
that lies between the
duodenum and the SMA.
 Obstruction of the third portion of the duodenum leads to compression of the So when a person is
superior mesenteric artery (SMA) and Aorta cachexic and chronically
 Appears after rapid weight loss following injury ill, the fat will diminish
and this will bring the
 Distance between two vessels is 10-20 mm duodenum and SMA
 Proximal bowel obstruction symptoms and signs (Vomiting) closer to each other,
 Diagnosis: CT Scan leading to the
obstruction.
 Treatment: Bypass surgery
2.16 REGIONAL ENTERITIS OF THE STOMACH & DUODENUM

 Food poisoning  Three emergencies

that need immediate
 Presentation: Pain and diarrhea intervention:
 Clinical diagnosis 1. Gastric volvulus
 Observation of the patient 2. Superior mesenteric
artery syndrome
3 MCQS 3. Mesenteric thrombosis
- E.g. history of Atrial
fibrillation; will cause
1. Features of Dumping syndrome include all of the following except: embolization
a. Tachycardia - Severe pain, do CT
b. Sweating
c. Palpitations
d. Constipation
e. Diarrhea

2. Regarding the treatment of duodenal ulcers:

a. Most duodenal ulcers are treated medically with no need for surgical
intervention
b. Arteriography in bleeding ulcers is a useful diagnostic modality but has no
place in therapy
c. Endoscopy in bleeding ulcers is a useful diagnostic modality but has no
place in therapy
d. When a vagotomy is performed only one vagus should be divided in order to
preserve the pyloric function
e. A Billroth 2 gastrectomy is more physiological and anatomical than highly
selective vagotomy

3. Which one of the following statements is true about Mallory-Weiss

syndrome:
a. It is caused by H. Pylori organism infection
b. It is a 1-4 cm longitudinal tear in gastric mucosa at EGJ
c. It causes 80% of upper GI bleeding
d. 5% of the bleeding stops spontaneously

 Answer key: 1;D , 2;A , 3;B

209
 Outline 1

INFLAMMATORY BOWEL
DISEASE
1 OUTLINE

 What is the Disease?

 Epidemiology
 Pathophysiology
 Ulcerative Colitis
 Crohn’s Disease
2 INFLAMMATORY BOWEL DISEASE  Some patients have
(undetermined colitis): if
2.1 TWO CHRONIC DISEASES THAT CAUSE ULCERATION & the inflammation is in the
large bowel and we do
INFLAMMATION OF THE INTESTINES not know whether it is
UC or CD 
 Ulcerative Colitis
 Crohn's Disease.
 They have some features in common but there are some important
differences
 20% of patients have clinical pictures that fall in between (indeterminate
colitis)
2.2 EPIDEMIOLOGY

 Most numbers are North American

 Increasingly diagnosed in Saudi Arabia
 It increased in the last decade due to improvement of the diagnostic
methods and changing lifestyle

210
2 Inflammatory Bowel Disease

2.3 PATHOPHYSIOLOGY

 Unclear
 A number of factors may be involved: 
o Host Factors
o Environmental Factors
2.3.1 HOST FACTORS
 Genetics (Twins, Relatives, & children)  not very clear but we believe that
the risk increase for relatives, if a family member has it.
 Obesity ( increases the risk of IBD )
 Appendectomy ( decreases the risk of IBD )
2.3.2 ENVIRONMENTAL FACTORS
 Smoking ( protective against UC but it increases the incidence of CD )
 Infection
 Oral Contraception
2.3.3 CURRENT THEORY: 
 There is a genetic defect that affects the immune system, so that it attacks
the bowel wall in response to stimulation by an offending antigen, like a
bacteria, a virus, or a protein in the food
3 ULCERATIVE COLITIS

 An inflammatory disease of the large intestine 

 Recurring and continuous Inflammation and ulceration of the mucosa of
the large intestine 
 Almost always involve the rectum and extend proximally 
 NB : if the rectum is free of inflammation consider other diagnoses than UC
 It extends in a continuous fashion
 40-50% of patients have disease limited to the rectum and rectosigmoid
 30-40% of patients have disease extending beyond the sigmoid
 20% of patients have a total colitis
3.1 MACROSCOPIC APPEARANCE 

 Erythematous mucosa, has a granular surface, looks like sand paper

 In more severe diseases hemorrhagic, edematous and ulcerated
 In fulminant disease a toxic colitis or a toxic megacolon may develop

211
 Ulcerative Colitis 3

3.2 MICROSCOPIC APPEARANCE 

 Crypt abscesses
 Branching of crypts
 Atrophy of glands
 Loss of mucin in goblet cells
3.3 ULCERATIVE COLITIS PRESENTATION

3.3.1 THE MAJOR SYMPTOMS OF UC ARE:

 Diarrhea (4 to more than 10)
 Rectal bleeding
 Tenesmus ( painful passing of the mucus ) & Passage of mucus
 Crampy abdominal pain & Fever
 Exam is often normal unless complications occur.
3.4 ULCERATIVE COLITIS COMPLICATIONS

 Hemorrhage: if it’s too much, we need surgical intervention to stop it

 Toxic megacolon
 Perforation
 Stricture ( due to the fibrosis )
 Cancer ( late stages )  so IBD patients need special programs for
screening: the screening is biopsy taking – endoscopy is not enough 

3.5 EXTRA-INTESTINAL MANIFESTATIONS 

 Uveitis and Episcleritis
 Erythema Nodosum and Pyoderma Gangrenosum
 Arthritis
 Ankylosing Spondylitis
 Sclerosing cholangitis
3.6 ULCERATIVE COLITIS TREATMENT

 Mainly medical treatment but if it fails we use surgical treatment

3.6.1 SURGICAL TREATMENT
 Failure of medical management
 Treating complications
 Prophylaxis for cancer
 Cure after colectomy

212
4 Inflammatory Bowel Disease

4 CROHN’S DISEASE
 Research shows a
possible link between
 An inflammatory disease that affects any part of the GI tract  Mycobacterium
 80% Small bowel Paratuberculosis and
 50 % ileocolitis Crohn’s Disease
 20 % colon
 30% perianal disease
 UGI < 5 %
 Recurring transmural Inflammation of the bowel 
 About 80% have small bowel involvement, mostly the terminal ileum 
 Characterized by skip lesions 
 30-40% of patients have small bowel disease alone
 40-55% of patients have both small and large intestines disease
 15-25% of patients have colitis alone

213
 Crohn’s Disease 5

4.1 MACROSCOPIC APPEARANCE

 Mild disease has aphthus or small superfecial ulcers

 In more severe diseases there is the characteristic cobblestone
appearance 
 Thickening of the bowel wall with creeping fat 

4.2 MICROSCOPIC APPEARANCE

 Transmural inflammation 
 Focal ulcerations
 Acute and chronic inflammation
 Granulomas may be noted in up to 30% of patients
4.3 CROHN’S DISEASE PRESENTATION

4.3.1 THE MAJOR PRESENTATIONS OF CD ARE

 Crampy abdominal pain 
 Diarrhea ( rarely accompanied with blood (( less than UC )) )
 Weight loss
 Colitis and Perianal disease (If a patient presents with a perianal disease
that resists treatment then consider CD)
 Duodenal Disease
4.4 CROHN’S DISEASE COMPLICATIONS

 Phlegmons ( inflammatory mass ) & abcesses

 Fistulas
 Stricture
 Malabsorption
 Perianal disease
 Cancer risk

214
6 Inflammatory Bowel Disease

4.5 EXTRA-INTESTINAL MANIFESTATIONS 

 Uveitis and Episcleritis

 Erythema Nodosum and Pyoderma Gangrenosum
 Sclerosing cholangitis
 Renal stones
 Gall stones
 Amyloidosis
4.6 CROHN’S DISEASE TREATMENT

 Mainly medical treatment

4.6.1 MEDICAL TREATMENT
 Oral 5-aminosalicylates (sulfasalazine)
 Antibiotics (Cipro, Metronidazole) 
 Glucocorticoids (Prednisone)
 Immunomodulators(Azathioprine)
 Biologic therapies (infliximab)
4.6.2 SURGICAL TREATMENT
 Failure of medical management
 Treating complications
 Not a Cure 

5 MCQS
A 22 y/o male presents to the clinic complaining of abdominal pain, diarrhea,
and weight loss lasting for one month. He gave a history of occasional occult
bleeding in stool. The most likely diagnosis is:
A. Crohn's disease
B. Peptic ulcer
C. Incarcerated hernia
D. Intestinal obstruction

Features of the previous diagnosis include all the followings EXCEPT:

A. Mucosal ulceration separated by normal mucosa
B. All cases should be treated surgically
C. The most common site is the ilium
D. Development of fistulae is a known complication

Crypt abscesses are a feature of:

A. Crohn’s Disease
B. Ulcerative Colitis
C. Colon cancer
D. Both A & B

215
 MCQs 7

Transmural inflammation of the colon is seen in:

A. Crohn’s Disease
B. Ulcerative Colitis
C. Colon cancer
D. Both A & B

UC Crohn’s disease
Blood in stool Yes Occasionally
Mucus Yes Occasionally
Systemic Occasionally Frequently
symptoms
Pain Occasionally Frequently
Abdominal mass Rarely Yes
Perineal disease No Frequently
Fistulas No Yes
Small Intestine No Frequently
Obstruction
Colonic Rarely Frequently
Obstruction
Responce to No Yes
Antibiotc
Recurrance after No Yes
surgery
Rectal Sparing Rarely Frequently
Continuous Yes Occasionally
Disease
Cobblestoning No Yes
Granuloma on No Occasionally
Biopsy

 Answer Key 1;A , 2;B , 3;B , 4;A

216
 Overview: Anatomy and Physiology 1

ANORECTAL CONDITIONS
1 OVERVIEW: ANATOMY AND PHYSIOLOGY

 The anal canal is approximately 3-4 cm long and extends from the
anorectal junction (dentate/pectinate line) to the anal verge
 Blood supply 
a. The superior rectal (a branch from the inferior mesenteric artery)
b. The middle rectal (a branch from the internal iliac artery)
c. The inferior rectal artery (a branch from the internal pudendal artery)
 Venous drainage 
a. The superior rectal (to the portal system by the inferior mesenteric
vein)
b. The middle and the inferior rectal veins (to the systemic circulation
by the internal iliac and pudendal vein)
 The physiology of anal continence is the result of complex interactions
between sensory, involuntary and voluntary motor functions
 The dentate line is the transitional zone from columnar rectal epithelium
and the squamous anal epithelium
- Above the line: endodermal origin, lined by columnar rectal epithelium,
no sensation of pain except in ischemic cases, it’s only sensitive to
stretch
- Below the line: anodermal origin, lined be squamous anal epithelium,
sensitive to pain, richly innervated by somatic sensory nerves.
Pathologic conditions that arise below the level of the dentate line
cause severe pain.
 Internal anal sphincter  involuntary sphincter of smooth muscle,
autonomic innervation, controls gas and liquid stool.
 External anal sphincter  striated voluntary muscle, controls solid stool

2 ANORECTAL ABSCESSES AND FISTULA-IN-ANO

 Both abscess and fistula-in-ano can be considered simultaneously

 The abscess is an acute manifestation, & the fistula is a chronic condition
 Most surgeons’ reputations reportedly have been impugned because of
problems with fistula operations than from other operative procedure

217
2
Anorectal Conditions

2.1 ETIOLOGY

NON-SPECIFIC SPECIFIC

√ Crypto-glandular in origin 90% √ Crohn’s disease (most

 Crypto-glandular hypothesis states that infection important; very tough to
of anal glands associated with anal crypts is the treat)
primary cause of anal fistula & abscess √ Ulcerative colitis
 In the dentate line there are about 9-15 glands √ TB
inside the crypt, which secrete through ducts. √ Actinomycosis
 In case of obstruction → accumulation of √ Carcinoma
secretion & inflammation → causing abscess √ Trauma
and anal fistula √ Radiation
 An anal fistula is an abnormal connection √ Lymphoma, leukemia
between the epithelialized surface of the anal √ Foreign body
canal and (usually) the perianal skin √ Pelvic inflammation
 Anal fistulae originate from the anal glands,
which are located between the two layers of the
anal sphincters, which drain into the anal canal. If
the outlet of these glands becomes blocked, an
abscess can form which eventually point to the
skin surface. The tract formed by this process is
the fistula.

2.2 CLINICAL PRESENTATION

 Abscess (acute) 
o Patient presents with constant throbbing perianal pain and
systemic manifestations as fever if it becomes infected
 Anal fistulae (chronic)
o Patient most likely has a history of abscess, pus discharge
(bloody/purulent), pruritus ani, perianal discomfort
2.3 DIAGNOSIS

 Done by examination, either in an outpatient setting or under anesthesia

(EUA: examination under anesthesia)
2.4 CLASSIFICATION OF ABSCESSES (ACUTE PHASE)

1. Ischiorectal/ischioanal (most common) 

2. Intersphincteric abscess
3. Perianal abscess
4. Supralevator/pelvirectal abscess (rare, difficult to diagnosis; caused by
inflammation or a disease of the pelvis)

218
 Anorectal Abscesses And Fistula-in-ano 3

 The process of
abscess drainage results
in the formation of a
communication between
the skin and anal canal.
Therefore, 50% of
abscesses will form a
fistula (patient presents
after few months from
2.5 TREATMENT OF ABSCESSES drainage with discharge)

2.5.1 INCISION AND DRAINAGE

 Prompt surgical drainage to prevent permanent fistula formation
 Determine the most tender point: a 2 cm area of skin is injected with local
freezing
All fistulae open into
 Elliptical or cruciate incision the dentate line except
 Drainage of pus & destroying all loculations traumatic fistulae, which
are difficult to treat
2.5.2 ANTIBIOTICS
 Alone: has NO role in the primary treatment of an abscess
 Except in certain groups of people: 
- Immunocomprised
- Patients with valvular disease
- Diabetics Parks Classification
of Fistula-in-ano:
- Extensively diseased patients
- Associated with systemic manifestations 1. Intersphincteric
fistulas: simple low tract,
high blind tract, and high
2.6 CLASSIFICATION OF FISTULAE (CHORNIC PHASE)
tract with rectal opening,
rectal opening without a
1. Intersphincteric: via the internal sphincter to the intersphincteric space and perineal opening,
then to perineum extrarectal extension,
and secondary to pelvic
2. Transsphincteric: low, via the internal & external sphincters into the disease.
ischiorectal fossa and then to the perineum 2. Transsphincteric
3. Suprasphincteric: via the intersphincteric space superiorly to above the fistulas: uncomplicated,
puborectalis muscle into the ischiorectal fossa and then to the perineum high blind tract

4. Extrasphincteric (traumatic), as in gunshot wounds: from the perianal skin 3. Suprasphenctric

fistulas: uncomplicated,
→ levator ani muscles → rectal wall i.e. no specific relation to sphincters. high blind tract
4. Extrasphincteric
fistulas: secondary to
anal fistula, secondary to
trauma, secondary to
anorectal disease,
caused by pelvic
inflammation

219
4
Anorectal Conditions

2.7 EVALUATION OF ANAL FISTULA

 An accurate pre-operative evaluation is very important

 Management depends on muscles involvement
 Five essential points of a clinical examination of an anal fistula:
√ Location of the internal opening
√ Location of the external opening
√ Location of the primary tract
√ Location of any secondary tracts
√ Determination of presence/absence of underlying disease
 Digital examination is up to 79%, 84%, and 71% accurate in defining the
internal opening, primary track and secondary track, respectively.
 Resting anal tone & voluntary anal contraction before operation should be
determined
 Intersphincteric tracks tend to open externally near the anal verge while
transsphincteric and more complicated fistulas tend to open further away
from the anal verge
 Gentle use of probes along the dentate line or through the external
opening may be useful in locating internal openings
 Injection of hydrogen peroxide via the external opening into the track may
help locate the internal opening and outline the fistula tract course. This
may be useful to help delineate missed internal openings. 

2.7.1 GOODSALL’S RULE 

 With the patient in knee-chest position, an imaginary horizontal line is
drawn at the level of the anus, parallel to the floor.
 For an external opening located:
o Anterior to this line: the tract passes radially straight towards the
internal opening (i.e. 9 to 3 o’clock position)
o Posterior to this line: the fistulae tract is curved around & internal
opening is in a frank midline position (i.e. to 6 o’clock position)

220
 Anorectal Abscesses And Fistula-in-ano 5

2.8 INVESTIGATIONS

 Fistulography
o Involves injection of contrast via the internal opening
o The accuracy rate is 16-48%
 Abscesses &
 Endoanal/Endorectal US: fistulas are usually seen
o Involves passage of 7-10 MHz transducer into the anal canal to help as hypo-echoic perirectal
defects. Sometimes,
define muscular anatomy and differentiating intersphincteric from fistulous tracts can’t be
transsphincteric lesions easily recognized with
o 50% better than physical examination alone, 94% accuracy rate US. In order to aid
identifying these tracts,
o A standard water filled balloon transducer can help evaluate the rectal hydrogen peroxide can
wall for any suprasphincteric extension be injected into the
external opening making
 CT scan the tract course visible
 MRI (the best modality)
o Findings show 80-90% concordance with operative findings when
observing primary tracts course & secondary extensions
o MRI is becoming the study of choice when evaluating complex fistulae
o It has been shown to improve recurrence rates by providing
information on otherwise unknown extensions

2.9 TREATMENT

 Goals of therapy:
o Cure with lowest possible recurrence rate  To treat any fistula,
o Minimal, if any, alteration in continence in the shortest period must identify the external
opening by inspection
 The principles are: and the internal opening
o Identification of primary opening according to goodall’s
rule.
o Relationship to puborectalis muscle
o Least amount of muscle should be divided
o Side tracts should be sought
o Presence of underlying disease

2.9.1 FISTULOTOMY/FISTULECTOMY
 The gold standard
 Considerations:
o Age, sex, location, type of fistula, previous anorectal surgery, anal
manometer
 Complication: Incontinence (by cutting the anal sphincter muscle)

 FISTULECTOMY:
o Going around the tract, excising it completely and then close
o Complete fistulectomy creates larger wounds that take longer to heal &
offers no recurrence advantage over fistulotomy

221
6
Anorectal Conditions

 FISTULOTOMY (laying open technique):

o Fistulous tract is merely laid open to heal
o Useful for 85-95% of primary fistulae i.e. submucosal, intersphincteric &
low transsphincteric.
o A probe is passed into the tract through internal & external openings
o Overlying skin, subcutaneous tissue, and internal sphincter are divided,
thereby opening the entire fibrous tract
o At low anal levels, the internal sphincter & subcutaneous external
sphincter can be divided at right angles to the underlying fibers without
affecting continence
o Curettage is performed to remove granulation tissue in the tract base
o Marsupialization of the edges speeds up healing
o Opening the wound out on the perianal skin for 1-2 cm adjacent to the
external opening with local excision of skin promotes internal healing
before external closure
o Perform a biopsy on any firm or suggestive tissue

2.9.2 SETONS
 Placement of a seton which can be made from large silk sutures, silastic
 Every time the patient
vessel markers, or rubber bands that are threaded through the fistula tract
goes to the washroom,
 Most patients prefer this method to avoid incontinence he/she pulls the Seton till
 It takes 6-8 weeks or more he/she can’t bear the
 Setons purposes: pain (slipping it through
his/her hand)
1. Visual identification of the amount of sphincter muscle involved (as
markers for better postoperative assessment by outlining the track)
2. Cutting seton (silk)  applied tightly to cut slowly though the tract
3. Drainage seton (rubber)  applied loosely to serve as drains
4. Fibrosis induced by the seton prevents separation of the ends of the
anal sphincter muscle when fistulotomy is subsequently performed
 A seton can be placed alone, combined with fistulotomy or in a staged  In females, NEVER
cut anterior fistulae,
fashion. It is useful in these situations: they’re located in a weak
o Complex/high fistulae (i.e. high transsphincteric, suprasphincteric, muscle where cutting
may lead to incontinence.
extrasphincteric) Therefore, the seton
o Multiple fistulas technique is useful here.
o Recurrent fistula after previous fistulotomy
o Anterior fistula in female patients
o Poor preoperative sphincter pressures
o Crohn’s disease (IBD)
o Immunosuppressed patients
o Extensive scarring
o Crazy fistula
o Lazy sphincter

222
 Anorectal Abscesses And Fistula-in-ano 7

2.9.3 ANAL FISTULA PLUG

 Suturable bioprosthetic plug was fashioned to seal and close the primary
opening of fistulae tracts
 Made of porcine small intestine submucosa
2.9.4 MUCOSAL ADVANCEMENT FLAP
 Reserved for use in patients with chronic complex high fistulae, but is
indicated for the same disease processes as Seton use.
 Technique:
o Involves total fistulectomy with removal of the primary & secondary
tracts, excision of the internal opening, and closure of the rectal defect
with a mucosal advancement flap
o A rectal mucomuscular flap with a wide proximal base (2 times the
apex width) is raised.
o Curettage of the external portion of the tract, as opposed to
fistulectomy or excision
o The internal muscle defect is closed with an absorbable suture, and
flap is sewn down over the internal opening so that its suture line
doesn’t overlap the muscular repair.
 Advantages 
o Reduced healing time
o No additional sphincter damage
o No deformity of the anal canal
o One stage procedure if primary healing is achieved
 Disadvantages 
o Poor success in Crohn’s or acute infection

2.10 CAUSES OF RECURRENCE:

1. Failure to identify the primary internal orifice  Rectovaginal

2. Lateral or upward extensions Fistulas:
3. Failure to open fistulous tract Constitute 5% of all
anorectal fistulas, most
4. Premature closure of wound commonly due to
5. Etiology obstetric trauma.
6. Surgeon performing the procedure Diagnosed by endorectal
US, transvaginal US, and
methylene blue enema to
2.11 CAUSES OF INCONTINENCE: confirm the diagnosis.

1. 27% overall risk

2. Division of anorectal muscles
3. Severance of motor nerve to sphincter mechanism
4. Prolonged packing after surgery
5. Previous operation
6. Female

223
8
Anorectal Conditions

3 HEMORRHOIDS

3.1 ANATOMY AND CLASSIFICATION

 Vascular cushions located in the anal canal covered by mucosa

 Most hemorrhoids appear in the following sites: 
1. Right anterior (11 O’clock)
2. Right posterior (7 O’ clock)
3. Left lateral (3 O’ clock)
 Classification (according to their relation to the dentate line):
1. Internal hemorrhoids  those originating above the dentate line
2. External hemorrhoids  those originating below the dentate line
3.2 PATHOPHYSIOLOGY

 They represent engorgement or enlargement of the normal fibrovascular

cushions lining the anal canal. (They’re not varicosities)
 Chronic straining secondary to constipation or occasionally diarrhea
 Fibrovascular cushions lose their attachment to the underlying rectal wall
 Prolapse of internal hemorrhoidal tissue through the anal canal
 The overlying mucosa becomes more friable and the vasculature increases.
 With overlying thinning of the mucosa and vascular engorgement, subsequent
rectal bleeding occurs
3.3 CLASSIFICATION

 Internal hemorrhoids are classified by history (level of prolapse) and not

by physical examination 
1. Grade 1  bleeding without prolapse
2. Grade 2  prolapse with spontaneous reduction
3. Grade 3  prolapse with manual reduction
4. Grade 4  incarcerated, irreducible prolapse
3.4 SYMPTOMS

 Internal hemorrhoids
 Bright blood per rectum  with or following bowel movements, is
almost universally bright red, and very commonly drips into the toilet
water
 Blood may also be seen while wiping after defecation
 As a prolapsing anal mass  prolapse usually occurs in association
with a bowel movement, during walking or heavy lifting as a result of
increased intra-abdominal pressure
 Extreme pain, bleeding and occasionally signs of systemic illness in
case of strangulation
 External hemorrhoid appears as a painful skin tag (necrotic old external
hemorrhoid) that doesn’t bleed or prolapses
3.5 PHYSICAL EXAMINATION:

 Position: left lateral decubitus (lithotomy) position

224
 Hemorrhoids 9

 Inspection:
- Any rashes, condylomata, or eczematous lesions.
- External sphincter function
- Any abscesses, fissures or fistulae
 Palpation:
- Gentle digital examination
- Lubricated finger should be gently inserted into the anal canal while
asking the patient to bear down
- The resting tone of the anal canal should be ascertained as well as the
voluntary contraction of the puborectalis and external anal sphincter.
- Masses should be noted as well as any areas of tenderness.
(Abdominal masses that may increase intraabdominal pressure)
- Internal hemorrhoids are generally not palpable on digital examination.
 Anoscopic examination:
- Anoscopy is mandatory to notice any impalpable mucosal changes
- The side viewing anoscope should be inserted with the open portion in
the right anterior then right posterior and finally the left lateral position
- Hemorrhoidal bundles will appear as bulging mucosa and anoderm
within the open portion of the anoscope.

3.6 EVALUATION OF RECTAL BLEEDING

 Must rule out cancer

 Patients are divided into 2 categories: 
1. Low risk group
o A young individual with bleeding associated with hemorrhoidal
disease without other systemic symptoms and no family history 
Anoscopy and rigid sigmoidoscopy (1st 25cm of rectum and colon)
2. High risk group
o An older individual, with either a family history of colorectal
cancer, or change in bowel habits  complete colonoscopy
should be performed to rule out proximal neoplasia

3.7 TREATMENT

 Varies from simple reassurance to operative hemorrhoidectomy.

 90% of cases conservative only (constipation treatment and banding),
10% require surgery
 Treatments are classified into three categories:
1. Dietary and lifestyle modification.
2. Non-operative/office procedures.
3. Operative hemorrhoidectomy.
3.7.1 DIETARY AND LIFESTYLE MODIFICATIONS
 The main goal of this treatment is to minimize straining at stool.
 Achieved by increasing fluid and fiber in the diet, recommending exercise,
and perhaps adding fiber agents to the diet such as psyllium.
 If necessary, stool softeners may be added.

225
10
Anorectal Conditions

3.7.2 OFFICE PROCEDURES

1. Rubber band ligation
o For grade I or grade II hemorrhoids &, in some circumstances, Grade III
o Complications include bleeding, pain, thrombosis and life threatening
perineal sepsis.
o Successful in two-thirds to three quarters of all individuals with first and
second-degree hemorrhoids.
o Only used for internal hemorrhoids
o Never done in external ones because its very painful (so we just do an
incision, evacuate the clot, and then close it under local anesthesia)
2. Infrared coagulation
o Generates infrared radiation, which coagulates tissue protein and
evaporates water from cells.
o Most beneficial in Grade I and small Grade II hemorrhoids.
3. Bicep electrocoagulation
o It works, in theory, similar to photocoagulation or to rubber banding.
o The probe must be left in place for ten minutes.
o Poor patient tolerance minimized the effect of this procedure.
4. Sclerotherapy
o Injection of an irritating material into the submucosa in order to
decrease vascularity and increase fibrosis.
o Injecting agents have traditionally been phenol in oil, sodium morrhuate,
or quinine urea.
3.7.3 SURGICAL TREATMENT OF HEMORRHOIDS
HEMORRHOIDECTOMY
 The triangular shaped hemorrhoid is excised down to the underlying
sphincter muscle, and the wound can be closed or left open
 Stapled hemorrhoidectomy has been developed as an alternative to
standard hemorrhoidectomy
IN SUMMARY:
 Grade I and II  lifestyle modification
- Diet: increase fiber intake and drink lots of water.
- Supplement fibers and laxatives if he/she constipated
- Never squeeze or strain
- Office treatment
 Grade III  lifestyle modification with banding and if failed, do surgery
 Grade IV  Immediate surgical intervention
4 ANAL FISSURES

4.1 INTRODUCTION
 Anal fissures are the
most common cause of
 A tear in the anal canal extending from just below the dentate line to the severe localized
anal verge. anorectal pain. They’re
 Most commonly in young and middle age adults. almost always on the
 Cardinal symptom is PAIN during & for minutes to hours after defecation posteroanterior plane.
Multiple fissures may be
 Bright red blood is common but minimal due to Crohn’s disease.

226
 Anal Fissures 11

 Over 90% of anal fissures are located in the posterior midline 

 Almost all the rest located in the anterior midline.
 The acute fissure is a "mere simple crack" in the anoderm.
 The chronic fissure appears with the following signs:
1. Distal sentinel tag
2. Proximal hypertrophied anal papilla
3. Fibrotic edges of the fissure
4. Exposed internal sphincter fibers in the base of the fissure
4.2 ETIOLOGY AND PATHOGENESIS
 In simple words,
 The initiating factor is trauma, typically overstretching of the anoderm by a Constipation  straining
large hard stool (constipation)  pressure 
hypertrophy of the anal
 The proposed explanation for the posterior midline predominance is a lack sphincter  increased
of tissue support and maximal stretching at this site. pressure inside lumen 
 Failure to heal is 2ndry to poor perfusion of the anoderm in the post midline. decreased blood supply
 Posterior midline ischemia is the result of arterial anatomy and internal anal  ischemia  traumatic
bowel movement
sphincter hypertonicity. sloughing  fissure
4.3 TREATMENT - Pain causes them not to
want to defecate
 90% of acute fissures settle with conservative management, in those that increasing constipation
causing more physical
don’t surgery can be done (a lateral internal sphinecterotomy) trauma and a cycle occur
 Correcting constipation (keeping bowel movements atraumatic)
- Warm baths (sitz baths) and a high fiber diet to achieve soft bulky stools
allow approximately 50% of acute anal fissures to heal within 3 weeks.
- Stool softeners and fiber supplements are reasonable additions.
- Recurrence is common, in the range of 30-70%, but can be reduced to
15-20% by maintaining a high fiber diet
 ACUTE FISSURE: (Topical application)
1. Nitroglycerin
o Topical application of nitroglycerin, a nitric oxide donor, causes a
transient lowering of resting anal pressure (relaxing internal
sphincter) and an increase in anodermal blood flow (vasodilator)  Topical
o A 92% healing rate within 2 weeks for acute fissures treated with application
application of 0.2% glyceryl trinitrate ointment t.i.d. vasodilationincrease
blood supplyhelp
2. Calcium channel blockers healing of fissure
o Topical calcium channel blockers (2% diltiazem, 0.3% nifedipine)
o Heal 65-95% of fissures.
o The most common side effects are headache, flushing, and
symptomatic hypotension.

 CHRONIC FISSURE:
1. Topical Nitroglycerin: At eight weeks healing was observed in 68% of  LIS: is based on
the GTN cutting a small portion of
2. Botulinum Toxin: Botulinum toxin has been injected into the external the internal sphincter,
relaxing the muscle and
and internal sphincters and, with short term follow up, healing rates of increasing blood supply
80% have been achieved. to allow the fissure to
3. Internal Sphincterotomy: lateral internal sphincterotomy (LIS) achieves heal, 5% risk of
healing in over 95% within several weeks incontinence.

227
12
Anorectal Conditions

4. Anal dilatation
 Chronic fissures are unlikely to heal with warm baths & a high fiber diet.
5 MCQS

1. The commonest site for anal fissure is:

a. anterior
b. lateral
c. posterior
d. right posterior
2. The cardinal symptom of anal fissure is:
a. bleeding
b. itching
c. pain
d. skin tag
3. The anatomical location of hemorrhoids is:
a. left anterior ,left posterior and right lateral
b. left lateral, right anterior and right posterior
c. right anterior, right posterior and left anterior
d. right lateral, right anterior and left lateral
4. The following symptoms are common in anal problems, except:
a. Perianal discharge
b. Perianal itching and irritation
c. Pain
d. Nausea and vomiting
5. The proper treatment of a patient with a peri-anal abscess is;
a. Incision and drainage as soon as fluctuation develops
b. Incision and drainage with excision of the internal opening
c. Prompt incision and drainage
d. Use of antibiotics and sitz bath

 Answer key: 1;C , 2;C , 3;B, 4;D, 5;C

228
 Introduction 1

COLORECTAL CANCER
1 INTRODUCTION

1.1 DEFINITIONS:

• Colon = large bowel = large intestine

• Rectum - terminal portion of the colon
• Polyp: is a descriptive term used to describe any mass of tissue that bulges
or projects outwards. Colonic polyps are mostly benign outgrowths.
• Adenoma - type of polyp and has chance to develop cancer but not all.
• Cancer - malignant growth; invasive (invades the basement membrane)
• Stage is an estimate to determine how large has the tumor grown.
• Primary - the original tumor, where it started.
• Metastases - where the tumor has spread to.
1.2 COLON AND RECTUM ANATOMY AND CANCER SIGNIFICANCE:

 The management and the

characteristics of colon and
rectal cancers are
completely different
 Cancer Development:
o Most cancers are
acquired (sporadic), but
some small percentage
of cases arise from
inherited diseases.
o Most cancers begin as
adenomatous polyps,
however only a tiny
percentage of
adenomas become
cancers (1 – 9%
become malignant)

1.3 POLYPS:

 Non-neoplastic polyps:
o The majority of polyps are non-neoplastic accounting for more than
90% of polyps are benign.
o These arise as a result of inflammation or improper maturation. These
include:
 Hyperplastic polyps (most commonly seen)
 Hamartomatous polyps (Juvenile & Peutz-Jeghers polyps)
 Inflammatory polyps
 Lymphoid polyps
 Neoplastic polyps:

229
2 Colorectal Cancer

 Account for less than 10% of polyps and these are dysplastic polyps
that have malignant potential.
 Adenoma
 Adenomatous Polyps (adenomas):
o Occur mainly in large bowel.
o Sporadic and familial
o Vary from small pedunculated to large sessile.
o Epithelium proliferation and dysplysia
o Divided into:
 Tubular adenoma: less than 25% villous architecture
 Villous adenoma villous architecture over 50%
 Tubulovillous adenoma: villous architecture between 25 and 50%.
1.4 CANCER SEQUENCE:

 The transformation from benign polyps to cancer takes from 7 - 10 years

 The transformation risk into cancer is based on:
o Size of polyp
o the histologic subtype of the polyp. They are organized in descending
order for cancer development risk: Villus, Tubuloviilus, Tubular polyps
o Severity of epithelial dysplasia
o Number of polyps, with multiple polyps holding a greater risk of
developing cancer
 The transformation from normal mucosa to cancer undergoes some
important steps as the following:

2 EPIDEMIOLOGY OF CRC:

 3th most common malignancy worldwide.

 Most common in Saudi males.
 Second to lung cancer as a cause of cancer death
 21,500 new cases, 8900 will die (2008)

230
 Clincal presentation: 3

 Risk of CRC – women 1/16 , men 1/14

 Median age of diagnosis was 60 according to the Saudi Cancer registry
reports.
2.1 EFFECT OF AGE ON THE INCIDENCE OF COLORECTAL
CANCER AND COLORECTAL POLYPS:

 As seen on the graph, the incidence of CRC increases tremendously after

the age of 50.
 Colonoscopy is advised to be performed at the age of 50 for people with no
significant risk factors, and should be performed at a younger age if the
person has risk factors.
 Colonoscopy can detect and remove adenomas and thus prevent cancer
occurrence.
2.2 CLASSIFICATION OF COLORECTAL CARCINOMA: Hereditary colorectal
cancer syndromes are a
1. Adenocarcinoma (>95%) group of syndromes
2. Carcinoid include hereditary non-
polyposis colorectal
3. Lymphoma
cancer (HNPCC)
4. Sarcoma syndrome and Familial
5. Squamous cell carcinoma adenomatous polyposis
(FAP). In typical FAP,
2.3 RISK FACTORS: numerous colonic
adenomas appear
 Medical and Family history: (relative risks are extra info) during childhood.
Symptoms appear at a
o Hereditary colorectal cancer syndromes very early age and
o Personal history: previous polyps (relative risk of 3.5 to 6), occurrence colonic cancer occurs in
of previous CRC (relative risk of 2 in the first two years) 90 percent of untreated
o Family history: a first-degree family member doubles risk. Further detail individuals by age 45.
These patients will have
to follow, so when a member of a family is diagnosed with colorectal
to undergo prophylactic
cancer, it is recommended to screen other members at 10 years colectomy.
younger from their relative’s age of diagnosis.
 Inflammatory bowel disease (mainly for cases of disease that extensively
involve the colon and pancolitis, these conditions hold a relative risk of  Hematochezia is
around 2.6 – 2.8) more often caused by
rectal than colon cancer.
 Other: Diet, nutrients, smoking, alcohol consumption Iron deficiency anemia
is from unrecognized
2.4 COLORECTAL CANCER RISK BASED ON FAMILY HISTORY: blood loss and is more
common with right sided
 General population “ sporadic “ 6% CRCs and is frequently
 One 1st degree CRC 2-3X* (12-18%) associated with a
delayed diagnostic
 Two 1st degree CRC 3-4X* evaluation.
 One 1st degree CRC < 50 y 3-4* Abdominal pains is
 One 2nd or 3rd CRC 1.5X caused by partial
 Two 2nd degree CRC 2-3X* obstruction, peritoneal
 One first degree with polyp 2X* dissemination, or
intestinal perforation
leading to generalized
3 CLINCAL PRESENTATION: peritonitis.

 Bleeding (melena/hematochezia) - gross, occult, anemia.

231
4 Colorectal Cancer

 Change in bowel habit – pain, diarrhea, constipation, alternating pattern

 Abdominal pains.
 Obstruction
 Change in caliber of the stools
 Weight loss
 Abdominal mass
 Asymptomatic.
 Some symptoms give clues on the location of the tumor:  Obstruction is more
common with left sided
 Sigmoid colon: obstruction and change in bowel habits. lesions, because fecal
 Rectum: bleeding and tenesmus contents are liquid in the
 Cecum: pain and melena proximal colon and the
 Metastasis: weight loss. lumen caliber is larger,
and they are therefore
 Notes on Clinical Presentation: less likely to be
o Symptoms of CRC are typically due to growth of the tumor into the associated with
lumen or adjacent structures. As a result, symptomatic presentation is obstructive symptoms.
often a manifestation of relatively advanced CRC. CRC is the most
common cause of bowel
o In a series of Meta analyses: the previous first three symptoms were the obstruction in the elderly.
most common upon presentation.
o Sensitivity of individual symptoms for the diagnosis of CRC was poor,
but Dr.AlKhayal mentioned it in the lecture and I thought I should add it
4 DIAGNOSIS  Synchronous lesions:
defined as two or more
 General: Complete history and physical examination including a DRE distinct primary tumors
 Endoscopic: (identify primary, synchronous lesions) separated by normal
bowel and not due to
 Flexible sigmoidoscopy direct extension or
 Colonoscopy “ to rule out other lesions“ metastasis. In other
words: two or more
4.1 STAGING: cancers occurring at the
same time.
 Endorectal ultrasound (rectal cancer) Colonoscopy “ to rule
 Chest x-ray (metastases) out other lesions “: it is
the most accurate
 Liver ultrasound (metastases) diagnostic test in
 Abdominal CT scan (metastases) symptomatic individuals,
 Barium Enema: may show apple-core lesion as since it can localize and
seen with this Double contrast barium enema of biopsy lesions throughout
the large bowel, detect
the descending colon. synchronous neoplasms,
 When colorectal cancer is diagnosed, it is almost and remove polyps.
protocol to perform CT scans of the chest,
abdomen, and pelvis to detect or rule out any
metastasis.
 Extra notes on Cancer spread:
o CRC can spread by lymphatic and hematogenous dissemination, as
well as by contiguous and transperitoneal routes.
o The most common metastatic sites are the regional lymph nodes, liver,
lungs, and peritoneum.
o Because the venous drainage of the intestinal tract is via the portal
system, the first site of hematogenous dissemination is usually liver,
followed by lungs, bone, and many other sites, including brain.

232
 Therapy: 5

o Tumors arising in the distal rectum may metastasize initially to the lungs
because the inferior rectal vein drains into the inferior vena cava rather
than into the portal venous system.
4.2 BLOODWORK

 CBC, electrolytes, and other function tests

 CEA (CarcinoEmbryonic Antigen) is a known protein molecule that is
produced in high levels by CRC cells.
 It is not a specific marker, and can be elevated in many benign conditions
like smoking! and other malignant cases like pancreatic cancer; therefore,
can never be used as a screening test. However, CEA maybe used as a
prognostic factor for evaluation of CRC management. 
5 THERAPY:

 Surgery is the most important variable in the treatment of colorectal cancer


 Radiation and chemotherapy alone cannot cure any stage of colorectal
cancer
 The site of tumor dictates the basic procedure
5.1 TREATMENT INDICATIONS FOR DIFFERENT STAGES 

 Stage I and II: surgery

 High risk stage II and stage III: surgery + chemo/radiotherapy
 Stage IV: chemotherapy ± Surgery, depending on withier or not the tumor is
resectable and on other factors.
5.2 PREOPERATIVE PREPARATION:

 Evaluation of medical problems. This is important especially for patients

who have cardiopulmonary disease, as these patients must be evaluated
by concerned specialists.
 Mechanical bowel preparation (bowel cleansing by laxatives)
o Colyte, Oral fleet
 IV antibiotics
 DVT prevention: Heparin shots, Compression stockings
 Foley catheter
 Epidural catheter
5.3 PRINCIPLES OF SURGERY:

 Examine the entire abdomen

 Remove the appropriate segment of the colon with adequate margins
 Remove the corresponding lymph nodes: a minimum of 12 lymph nodes
have to be removed in a proper colectomy. 
 Open vs laparoscopic approach
 The types of colectomies can been seen on this figure:

233
6 Colorectal Cancer

5.4 OSTOMY INSERTION:

 The intestine is brought out through a hole in the abdominal wall

 Colostomy (colon on the skin)
 Permanent when the rectum is removed
 Temporary when it is unsafe to make a join
 Ileostomy (ileum on the skin)
 Temporary when the join needs time to heal
5.5 RECOVERY:

 Surgery 2 to 4 hours
 Hospital stay 4 to 10 days
o IV, urine catheter, compression stockings, intravenous pain killers, blood
thinner
o Discharge when ambulating, eating, bowel function, good pain control
o Recovery 4 weeks
5.6 FOLLOW UP:

 Office visit every 3 months for two years then every 6 months for 3 years
 Regular blood work (CEA)
 Colonoscopy at year 1 and 4 and every 5 years
 CT scan yearly
 Some points on CEA:
o CEA is used to detect the prognosis: higher CEA levels indicate a
worse prognosis.
o It is used to detect recurrence: (CEA levels are usually around 2.5 – 5
ng/ml).
o If CEA was 50, then after surgery it goes back to 5, then after some
time it rises to 50 again. Here we suspect recurrence.
o If CEA was 100 and after a surgery it is still 100 it can indicates 2 things
A) There is another mass, i.e. metastasis and it hasn’t been removed or
B) the initial mass was not excised properly.

234
 Therapy: 7

5.7 STAGING:  (VERY IMPORTANT)

 Staging of CRC is now achieved by using the TNM classification and not
the modified Duke classification, as studies have shown that the 2010
modification of the TNM classification had better results. 
 How far into the wall has it grown?
o T stage:
 Tis – invasion of mucosa only
 T1 – Invasion of submucosa
 T2 – Invasion of muscularis propria
 T3 – Full thickness/perirectal fat
 T4 – Invasion into adjacent organs.
 Take note that adjacent organs does not mean distant metastasis, as that
is a different component in the score. Adjacent organs mean structures like:
the urinary bladder, uterus, and even the abdominal wall.
 2. Is it growing in other places?
o N stage: lymph node involvement, M stage: presence of metastasis
 N1 – 1-3 lymph nodes
 N2 - >4 lymph nodes
 N3 – distant lymph nodes
 M1 – Distant organ (mostly to the liver, lung)
5.8 TNM STAGING:

 Stage 0 – Tis tumors

o Invasion of mucosa
 Stage 1 – T1 and T2 tumors
o Invasion of sub mucosa & muscularis propria
 Stage 2 – T3 and T4 tumors
o Invasion of full thickness & adjecent organ
 Stage 3 – Any lymph node involvement 
 Stage 4 – Distant metastases
5.9 WHO GETS ADDITIONAL THERAPY?

 COLON
o All stage 3 patients (positive nodes) - chemotherapy
o High risk stage 2 patients. These patients include: Cancers with the
mucinous subtype, patients with bowl obstructions; perforation, and who
have undergone resection with less than 12 resected nodes.
 RECTUM
o All stage 2 and stage 3 patients should get radiation and chemotherapy.
o Note: in the rectum there are no serosa layer so the stage 2 patients
should receive chemotherapy
 Survival and TNM staging:
o STAGE 5-Year Survival
1 90%
2 80%^
3 27-69%*
4 8%
^for T3N0 tumors

235
8 Colorectal Cancer

*depends on # of nodes involved

6 SUMMARY:

 Common Cancer
 Can be prevented through screening and resection of polyps
 Surgery is the primary treatment
 Slow but steady improvement in survival

7 MCQS:

1) How should a patient who had Dukes C colon cancer two years previously
be followed for recurrence of liver metastasis?
A. liver enzymes
B. CEA
C. U/S
D. CT
E. Radionuclide imaging

2) An 80-year-old man is admitted to the hospital complaining of nausea,

abdominal pain, distention, and diarrhea. A cautiously performed transanal
contrast study reveals an “apple core” configuration in the rectosigmoid.
Appropriate management at this time would include:
a) Colonoscopic decompression and rectal tube placement
b) Saline enemas and digital disimpaction of fecal matter from the rectum
c) Colon resection and proximal colostomy
d) Oral administration of metronidazole and checking a Clostridium difficile
titer
e) Evaluation of an electrocardiogram and obtaining an angiogram to evaluate
for colonic mesenteric ischemia

3) Correct statements regarding carcinoembryonic antigen (CEA) and

colorectal tumors include which of the following?
a) Elevated CEA is indicative of a tumor of gastrointestinal origin
b) A low CEA level after resection of a colon tumor is a poor marker of
disease control
c) Ninety percent of colorectal tumors produce CEA
d) There is a high likelihood of liver involvement if the CEA level is high
(greater than 100 ng/mL)
e) CEA levels are unusually low in cigarette smokers

4) A definite increased risk of colon cancer is associated with:

a) Diet high in fiber.
b) Diet low in animal fat and protein.
c) Diet low in fiber.
d) Ulcerative Colitis
e) Prior cholecystectomy.

5) A 52 year-old female diagnosed to have sigmoid cancer invading the

uterus with no evidence of metastasis based on CT scan and colonoscopy,
she underwent sigmoidoctomy and hysterectomy, the histopathology report

236
 MCQs: 9

revealed invasive moderately differentiated adenocarcinoma involving the

entire bowel wall and invading the myometrium, perinural and
lymphovascular invasion, 6 out of 15 lymph nodes were positive for
metastasis. The TNM classification for this patient will be:
a) T3 N1 M0
b) T3 N2 M1
c) T4 N2 M0
d) T4 N2 M1

6) For the above patient, she recovered well from surgery and visited you in
clinic. The action that should be taken at this stage is?
a) Referral to medical oncology for adjuvant chemotherapy
b) Referral to radiation oncology for adjuvant radiotherapy
c) Referral to medical radiation oncology for both chemo-radiation
d) Referral to medical oncology for surveillance only

7) A 39 year-old male presented to the clinic for medical checkup because of

significant family history of colon cancer, detailed family history revealed
that three of his second degree relatives were diagnosed with colon cancer
at age of 50, you counseled him for screening because:
a) He as average risk
b) He as double risk
c) He has 5 times greater risk
d) He has 10 times greater risk

8) Which one of the following factors is most likely to be associated with

development of colorectal cancer?
a) Increase Calcium intake
b) Increase fat intake
c) Smoking
d) History of Colonic polyps

Answer key: 1;B , 2; C , 3;D , 4;D , 5;C , 6;C , 7; , 8;D

237
 introduction 1

CHOLELITHIASIS
1 INTRODUCTION
Biliary colic is
produced by migration
 Cholelithiasis is the presence of gallstones in the gallbladder. of a gallstone into the
 Presentation and complications: opening of the cystic
o May remain asymptomatic for decades. duct that may block the
o May cause biliary colic type of pain . outflow of bile during
gallbladder contraction.
o May lead to Cholangitis  This results in increase
o May lead to choledocholithiasis  in the gallbladder’s wall
o May lead to cholecystitis. tension and produces
this pain.
2 ANATOMY
cholangitis is
infection of the biliary
tree.

Choledocholithiasis is
the presence of a
gallstone in the common
bile duct.

 The porta hepatis or hepatoduedenal ligament contains the portal vein,

hepatic artery and bile. 
3 PATHOPHYSIOLOGY  Infections result in
an increase in billiary
 There are different types of stones: cholesterol stones which are the most calcium as well as an
common, pigment stones, and mixed. increase in B-
glucuronidase, which
 They are formed by crystallization of bile. The bile consists of lethicin, bile
converts conjugated
acids, and phospholipids in a fine balance. bilirubin to the
 The solubility of cholesterol in bile depends on the concentration of lethicin, unconjugated form. The
bile salts and cholesterol. Lethicin and cholesterol are insoluble aqueous calcium binds to
solutions but dissolve in bile salt-lethicin micelles. unconjugated bilirubin
 Failure of the liver to maintain a micellar liquid can be caused by increase and precipitate to form
in the concentration of cholesterol or decrease in the calcium bilirubinate
stones.
 Concentration of bile salts or lethicin; either way it can result in cholesterol
stone formation.

238
2 Billary colic and cholecystitis

 Conversely, increasing the biliary concentration of lethicin and bile salts

should hinder cholesterol stone formation.
 Normal bile (normally 1 Liter/day) contains glucaro-1,4-lactone, which
inhibit the conversion of conjugated to unconjugated bilirubin, and thus stop
the formation of calcium bilirubinate stones.
 Impaired motility can predispose to stones.
 Sludge is crystals without stones. It may be a first step in formation of
stones, or independent of their formation. It can be found on Ultrasound.

 Pigment stones (15%):

o Pure pigment (bilirubin) stones:
 Associated with diseases that increase RBC destruction, such
as sickle cell anemia or spherocytosis.
o Calcium bilirubinate stones:
 In cirrhotic patients, and parasitic infections.
4 EPIDEMIOLOGY, CAUSES AND RISK FACTORS

 US: affected by race, ethnicity, sex, medical conditions, fertility.

 20 million people have cholelithiasis.
 Every year 1-2% of people develop them.
 Internationally: 20% of women get it and 14% of men.
4.1 RACE

 Highest in fair skinned people of Northern European descent and in

Hispanic populations.
 High in Pima Indians (75% of elderly).
 Asians with stones are more likely to have pigmented stones than other
populations.

239
 presentation 3

4.2 AGE

 It is uncommon for children to have gallstones. If they do, it’s more likely
that they have congenital anomalies, biliary anomalies, or hemolytic
pigment stones.
 Incidence of GS increases with age 1-3% per year.
 In patients over 60 years old, the prevalence of developing gallbladder
stone in men is 12.9% and 22.4% in women.
4.3 GENDER

 More common in women. Etiology may be secondary to variations in

estrogen causing increased cholesterol secretion, and progesterone
causing bile stasis.
 Pregnant women are more likely to have symptoms.
 Women with multiple pregnancies are at higher risk.
 Women who are on oral contraceptives, or estrogen replacement treatment
are at higher risk.
 To sum it up, these are the factors that cause and increase the risk of
getting stones:
o Fair skinned people
o Females
o Fertile
o People on a high fat diet and obese people.
o People with a family history.
o Rapid weight loss, TPN (total parenteral nutrition), ileal disease, NPO
o Old people.
o People who drink alcohol.
o Diabetics and hemolytics have more complications.
5 PRESENTATION

5.1 HISTORY
 Differential
diagnosis:
 There are 3 clinical stages:
Asymptomatic, symptomatic, and with complications (cholecystitis,  AAA (abdominal
cholangitis, Common bile duct stones). aortic aneurysm)
 Most cases (60-80%) are asymptomatic; such cases are discovered  Appendicitis
 Cholangitis,
accidently by abdominal sonar. cholelithiasis
 Every year 1-3% of patients develop symptoms.  Diverticulitis
 60-80% of patients are asymptomatic, 40 -20% develop symptomats,  Gastroenteritis,
around 20% of the Symptomatic patients will develop complications. hepatitis
 IBD, MI, SBO (small
 Most patients develop symptoms before complications but sometimes the
bowl obstruction)
patient might develop the complications without having any previous  Pancreatitis, renal
symptoms. colic, pneumonia
 Once symptoms occur, severe symptoms develop in 3-9% of the cases,
with complications in 1-3% per year, and a cholecystectomy rate of 3-8%
per year.
 Patients who have small stones are more prone to develop symptoms.
 Asymptomatic GS are not associated with fatalities.

240
4 Billary colic and cholecystitis

 Morbidity and mortality are associated only with symptomatic patients.

 Symptoms include :
o Severe Epigastric colicky pain, located in the Right upper quadrant, that
lasts for 1 to 5 hours, and wakes the patient up from his sleep at night.
o Classically the pain is in the Right upper quadrant, however visceral
pain and gallbladder wall distension may be only in the epigastric area.
o A gallstone may impact in the neck of gall bladder or in the cystic duct
giving biliary pain or cholecystitis >> Biliary pain usually occurs in the
epigastrium and right hypochondrium (RUQ).
o Other symptoms are related to the site of movement of the stone.
 Indigestion, bloating, and fatty food intolerance occur in similar frequencies
in patients without gallstones, and are not cured with cholecystectomy.

5.2 PHYSICAL EXAMINATION  Murphy’s sign: A

sign of gallbladder
 Vital signs and physical findings in asymptomatic cholelithiasis are diseases consisting of
completely normal. pain on taking a deep
breath when the
 Fever, tachycardia, Murphy’s sign  and hypotension alert you to more
examiner’s fingers are
serious infections, including cholangitis, cholecystitis. on approximate location
of the gallbladder.
6 INVESTIGATIONS

6.1 LABORATORY STUDIES

 Lab results in asymptomatic patients and patients with biliary colic should
be normal.
 WBC, elevated LFTS may be helpful in diagnosis of acute cholecystitis, but
normal values do not rule it out.
 Elevated WBC is expected but not reliable.
 ALT, AST, AP more suggestive of CBD stones
 Amylase elevation may be GS pancreatitis
6.2 IMAGING STUDIES  A Study examined
the utility of labs with
 U/S and Hida are the best. Plain x-rays, CT scans ERCP are adjuncts. cholethiasis diagnosed
 X-rays: with HIDA, and showed
o 15% stones are radiopaque, porcelain GB may be seen. no difference in WBC,
o Will show air in biliary tree and emphysematous GB wall. AST, ALT Bili, & Alk
Phos, in patients
 CT: IT IS THE BEST IMAGING EXAMINATION: diagnosed & those
o Used for complications, ductal dilatation, surrounding organs. without.
o Misses 20% of GS.
o Done if diagnosis is uncertain. In a retrospective study,
only 60% of patients with
 Ultrasound: IT IS THE FIRST IMAGING TEST YOU DO: cholecytitis had a WBC
o It is 95% sensitive for stones greater than 11,000. A
o It is 80% specific for cholecystitis. WBC greater than
o It is 98% sensitive and specific for simple stones. 15,000 may indicate
perforation or gangrene.
o Sometimes it might show Wall thickening (2-4mm), might be false
positives!
o Distension
o Pericholecystic fluid, sonographic Murphy’s.

241
 complications 5

o If it showed Dilated CBD (7-8mm) , this indicates the presence of an

obstruction.
 Hida scan:
o Documents cystic duct patency.
o 94% sensitive, 85% specific
o GB should be visualized in 30 min.
o If GB is visualized later, it may point to chronic cholecystitis.
o CBD obstruction appears as non visualization of small intestine.
o False positives, high bilirubin.
 ERCP (Endoscopic retrograde cholangiopancreatography):
o ERCP is diagnostic and therapeutic.
o It provides radiographic and endoscopic visualization of biliary tree.
o Done when CBD is dilated and LFTs are elevated.
o Complications include bleeding, perforation, pancreatitis, and
cholangitis.
o ERCP needs: endoscope + fluoroscopy (X-ray and contrast and
guide wire) 
o If a patient presented with jaundice, you admit him for ERCP. 

7 COMPLICATIONS  Gangrenous
cholecystitis is the most
7.1 CHOLYCYSTITIS common complication of
cholecystitis, particularly
in older patients,
 It’s an inflammation of the gallbladder secondary to calculi. diabetics, or those who
 Characterized by: delay seeking therapy.
o Continuous pain. Associated inflammation
o Fever. leads to ischemic
o High WBC count due to inflammation. necrosis of the wall, with
o Murphy’s sign on examination. or without associated
cystic artery thrombosis.
o Distended gall bladder and thickening of the wall on Ultrasound due to
inflammation.
 How to manage this patient?
o The patient should be admitted to the hospital
o Stabilized
o Given IV antibiotics and analgesics.
o If the patient responded to the treatment, elective cholecystectomy is
done after 6 weeks so that the inflammatory process cools down.
o Urgent surgery is required only if the patient did not respond to the
treatment because gangrenous cholecystits may develop.
7.2 OBSTRUCTIVE JAUNDICE  Stones that block the
ampulla of Vater may
 When obstructive jaundice occurs it means that one of the stones moved block pancreatic
down to the common bile duct and caused an obstruction which will secretions and
predispose the patient to
obstruct the flow of bile from the liver to the small bowel.
Pancreatitis, as gall
 It can also be a mass that’s causing the obstruction. stones are the most
important risk factor for
Pancreatitis

242
6 Billary colic and cholecystitis

7.2.1 SYMPTOMS AND SIGNS  The whiter your skin

is the less bilirubin you
 Jaundice: need to develop
o Look for it in the sclera (specially dark skinned people and during the jaundice.
sun light), skin and mucosa The darker your skin is
o The bilirubin level in the blood is at least double the normal (Upper the more bilirubin you
need to develop
normal level is 17 mmol)  jaundice.
 Pale stool
 Dark urine
 Itching (due to accumulation of bile salts under the skin) 
7.2.2 DIFFERENTIAL DIAGNOSIS  When you take
 Painless obstructive jaundice with significant weight loss might be cancer history of a patient with
jaundice it is important to
(obstruction develops gradually) ask about eye or skin
It could be: discoloration, pale stool,
o Head of pancreas cancer dark urine, any itching.
o ampulla of Vater cancer
o Distal CBD cancer
7.2.3 MANAGEMENT  Both benign tumors
 Stone removal: and hamartomas are
composed of normal
o To relieve obstructive jaundice: admit the patient for ERCP: First
cells in excessive
shpincterotomy is done to widen the diameter of the sphincter of Oddi quantities, but benign
then take the stone out by the basket. tumors have a normal
o After doing ERCP we wait for one day before removing the gall bladder arrangement whereas
(cholecystectomy) to make sure the patient didn’t develop pancreatitis. hamartomas have an
abnormal arrangement
7.3 CHOLYNGITIS of cells.

 It’s the inflammation of biliary tree. In involuting

hemangioma, the deeper
 Charcot’s triad: (it’s diagnostic)  they go the bluer they
1. Fever become, whereas the
2. Jaundice more superficial the
3. Right upper quadrant pain RUQ more cherry red they get.
 If patient was hypotensive send him to the ICU for ionotrops 
 Treatment: ERCP

7.4 OTHERS

 Sepsis
 Pancreatitis
 Perforation (10%)
 GS ileus (mortality 20% as diagnosis difficult).
 Hepatitis
 Choledocholithiasis

243
 management 7

8 MANAGEMENT The severity of signs

and symptoms
 Historically cholecystits was operated on emergently which increased /complications determine
mortality. if this patient should do
 Surgical consult is appropriate, and depending on the institution, either the surgery electively or
medicine or surgery may admit the patients for care. operate now.
 Get GI doctor involved early if suspect CBD obstruction
8.1 EMERGENCY DEPARTMENT CARE
Patients with acute
cholycystitis Admit
 GB colic is suspected in patients with RUQ pain of less than 4-6h duration
and radiating to back. Evaluate patient
 Acute cholecystits is suspected in those with longer duration of pain, with or -Pain for 24-48 hours :
without fever. Elderly and diabetics should be diagnosed as soon as operate
possible because it might proceed to sepsis. -Pain for more than 48
 If a patient presents with acute cholycysitis and hypotension, he must be hours  IV
admitted to the ICU and given ionotrops and then the obstruction must be antibioticsStabilize the
patient  then operate
relieved. 
 After assessment of ABCs, standard IV, pulse oximetry, EKG, and -Why? Because
operating on a patient
monitoring must be performed. Also, culture should be included if the while the gallbladder is
patient is febrile.  acutely inflamed has
 The primary goal of the emergency department care is to diagnose acute been shown to have
cholecystitis with labs, US, and or Hida. Once diagnosed, hospitalization is more complications.
usually necessary. Although Some are treated as OP.
 In patients who are unstable or in severe pain, a bedside US should be
considered to exclude AAA and to asses in diagnosing acute cholecystitis.
 Volume should be replaced with IVF, NPO, +/- NGT.
 Administer pain control early. A courtesy call to surgery may give them time
to examine without narcotics.
8.2 MEDICATIONS

 Anticholinergics such as Bentyl (dicyclomine hydrochloride) to decrease GB

and biliary tree tone. (20mg IM q4-6).
 Demerol 25-75mg IV/IM q3
 Antiemetics (phenergan, compazine).
 Antibiotics (Zosyn 3.375g IV q6) need to cover Ecoli (39%),
Klebsiella(54%), Enterobacter(34%), enterococci, group D strep.

8.3 FURTHER INPATIENT CARE

 Cholecystectomy can be performed after the first 24-48h or after the

inflammation has subsided. Unstable patients may need more urgent
interventions with ERCP, percutaneous drainage, or cholecystectomy. 
 Laparoscopic cholecystectomy is very effective but it has few complications
(4%). 5% convert to open. In acute setting up to 50% open.

8.4 FURTHER OUTPATIENT CARE

 Afebrile, normal VS

244
8 Billary colic and cholecystitis

 Minimal pain and tenderness.

 No markedly abnormal labs, normal CBD, no pericholecystic fluid.
 No underlying medical problems.
 Next day follow-up visit.
 Discharge on oral antibiotics, pain meds
9 PROGNOSIS

 Uncomplicated cholecystitis has a low mortality.

 The mortality rate for emphysematous GB is 15%
 Perforation of GB occurs in 3-15% of patients with a mortality rate up to
60%
 Gangrenous GB has a mortality rate up to 25%
10 MCQS

1. A 73-year old previously healthy man presents to the emergency room

with several days of jaundice followed by 12 hours of RUQ pain and
fever. He is mildly hypotensive. CT scan of the abdomen revealed
dilation of the biliary tree.
 What is the most likely diagnosis?
Answer: Cholyangitis
 Management includes which of the following?
A. Laproscopic cholecystectomy.
B. Open cholecystectomy and T tube replacement.
C. Open cholecystectomy and choledochojejunostomy.
D. Fluid resuscitation, antibiotics, and ERCP.
E. Fluid resuscitation and hepatitis serologies.

2. What is the most common cause of chronic pancreatitis?

A. Gall stones
B. Alcohol
Answer: A (80%) gall stones is the cause either in acute or chronic
pancreatitis.

3. How much bile is produced by the liver?

A. 100 – 200 ml/day
B. 300-400 ml/day
C. 500-1000 ml/day ( 1Liter)

4. In Endoscopic ERCP, stone extraction from the common bile duct

(CBD) is NOT possible in all of the following except:
A. Multiple stones in CBD
B. Intrahepatic stone
C. Multiple gall stones
D. Pt has CBD stone with prior gastrectomy

245
 MCQs 9

5. What is the correct procedure to do in the following cases?

Q5:
 A patient had CBD stones but he had prior gastrectomy (or post gastric
B1: an operation in
resection B2 “Billroth's operation II”). which the pylorus is
Answer: No gastric --> we cannot reach the duodenum --> never do ERCP removed and the distal
So open the abdomen --> open the CBD and extract the stones stomach is anastomosed
(intraoperative cholangiogram). directly to the
duodenum.
 Patient had post gastric resection B1 “Billroth's operation I”?
Answer: We can do ERCP because duodenum is still open B2: an operation in
which the greater
curvature of the stomach
6. A patient presented to the ER with abdominal pain, elevated WBCs is connected to the first
and increased serum amylase. part of the jejunum in a
What is the most likely diagnosis? side-to-side manner.
Answer: Acute pancreatitis This often follows
resection of the lower
part of the stomach
7. A 45 Y/O obese female with cholelithiasis, presents to the ER (antrum). The
complaining of N/V & severe continuous abdominal pain, high grade antrectomy (resection of
fever, slightly elevated WBC (12,000), & increased serum amylase. the stomach antrum) is
not part of the originally
What is the most likely Diagnosis? described procedure.
Answer: Acute Pancreatitis The surgical procedure
is called
8. A 70 years old male came with progressive painless jaundice. gastrojejunostomy.
What are the Differential diagnosis?
Answer: It could be:
 Head of pancreas cancer
 ampulla of Vater cancer
 Distal CBD cancer

9. A 70 years old male with progressive painless jaundice is referred to

your clinic. You order LFT that shows abnormal pattern of obstruction
jaundice, US shows dilated CBD 2 cm.
Which procedure do you suggest?
A. ERCP
B. Laparoscopic Cholecystectomy
C. Modified barium swallow
D. Laparoscopic abdominal exploration
E. Upper GI endoscopy

10. A patient came to you complaining of chronic nausea and mild right
upper quadrant pain; you suspect the cause of his symptoms is gall
stones.
What is the first image study in this case?
Answer: US
What is the best image study in this case?
Answer: CT

246
10 Billary colic and cholecystitis

11. Which of the following structures is in not found in the

hepatodeudenal ligament?
A. Hepatic vein
B. Hepatic artery
C. CBD

12. Which of the following is not an ultrasonic finding in acute

cholecystitis?
A. Sonographic Murphy’s sign
B. Pericholecystic fluid
C. Gall bladder wall thickening more than 6 mm
D. Absence of gall stones

13. Signs and symptoms of acute cholecystitis usually include all of the
following except:
A. Jaundice
B. RUQ pain
C. Fever
D. Elevated WBC count
E. Nausea and vomiting

14. In obstructive jaundice, LFTs usually shows:

A. Elevated indirect bilirubin and alkaline phosphatase
B. Elevated indirect bilirubin and GGT
C. Elevated direct bilirubin and alkaline phosphatase
D. Elevated direct bilirubin and ALT
E. Elevated direct bilirubin and AST

15. Prolonged PT (INR) in obstructive jaundice is due to decreased

absorption of:
A. Vitamin A
B. Vitamin D
C. Vitamin E
D. Vitamin K
E. Calcium

16. In acute cholecystitis, HIDA scan shows

A. Distended gallbladder
B. Contracted gallbladder
C. Non-filling of gallbladder
D. Dilated common bile duct
E. Bile leak

17. Bile contains all of the following except:

A. Bile salts
B. CCK
C. Bile pigments
D. Cholesterol
E. Phospholipids

247
 MCQs 11

18. Bile secretion is increased by:

A. Vagus
B. Fasting
C. Sympathetic stimulation
D. Adrenaline
E. Octreotides

19. Risk factors for gallstones include all of the following except:
A. Obesity
B. Contraceptive pills
C. Sickle cell anemia
D. High protein diet
E. Rapid weight loss

20. Which of the following can be diagnostic and therapeutic for common
bile duct stones:
A. US
B. CT scan
C. HIDA scan
D. ERCP
E. MRCP

21. A 25 Years old lady presented to ER with 2 days history of right upper
quadrant pain and fever. She has no Murphy's sign and WBC count is
7. The best management will be
A. PO Analgesia
B. IV analgesia
C. Admission and start IV antibiotics
D. Admission and start PO antibiotics
E. IV antibiotics and follow up in clinic

22. The following are indications for cholecystectomy in asymptomatic

gall bladder stone patients except:
A. Diabetes
B. During surgery
C. Stone 4 cm in size
D. Ischemic heart disease
E. Hemolytic anemia

 Answer Key: 1=D, 2=A, 3=C, 4=A, 9=A, 11=A, 12=D, 13=A, 14=C, 15=D, 16=C, 17=B, 18=A,
19=D, 20=D, 21=C, 22=D

248
 Introduction 1

PORTAL HYPERTENSION
1 INTRODUCTION

Portal hypertension (defined as hydrostatic pressure >5 mmHg) results initially

from obstruction to portal venous outflow. Obstruction may occur at a presinusoidal
(portal vein thrombosis, portal fibrosis, or infiltrative lesions), sinusoidal (cirrhosis),
or postsinusoidal (veno-occlusive disease, Budd Chiari syndrome) level. Cirrhosis
is the most common cause of portal hypertension; in these patients, elevated portal
pressure results from both increased resistance to outflow through distorted
hepatic sinusoids, and enhanced portal inflow due to splanchnic arteriolar
vasodilation.
1.1 CAUSES:  Varices develop in
order to decompress the
Causes of Portal hypertension can be classified as: hypertensive portal vein
and return blood to the
 Cirrhotic (definition) systemic circulation.
 Non-cirrhotic: most important non-cirrohtic causes are: shistosomaiasis and They are seen when the
pressure gradient
splenic vein thrombosis (mainly caused by hypercoaguable state and between the portal and
pancreatitis) hepatic veins rises above
12 mmHg; patients with
1.2 SYMPTOMS OF PORTAL HYPERTENSION lower values do not form
varices and do not bleed.
 Asymptomatic: portal hypertension is asymptomatic until complications
develop, where patients present according to the ongoing pathological
process. These complications are in the form of:
 Gastroesophageal varices
 Ascites
 The risk of Esophgeal
 Splenomegaly: can sometimes cause dull abdominal pain. Varecies development
 Underlying disease can be predicted by the
Child-Pugh score,
2 VARECIAL BLEEDING calculated by computing
different values for
 Approximately one-third of all patients with varices will develop variceal certain conditions like:
hemorrhage presence of Ascites,
encephalopathy, bilirubin
 A major cause of morbidity and mortality in patients with cirrhosis.  Veins and albumin levels, and
don't have much smooth muscles and as a result do not go into spasm other factors.
once they bleed. With this lack of smooth muscle and engorgement of the  Red wale signs are
esophageal veins with, varecies tend to bleed profoundly, when they longitudinal red streaks
seen in endoscopies on
rupture. varices that resemble red
corduroy wales. See
2.1 PREVENTION OF VARECIAL BLEED below>


AASLD RECOMMENDATIONS — Recommendations for prevention of
variceal bleeding have been issued by the American Association for the
Study of Liver Diseases
 These Recommendations are as follows:
 No treatment is given to people who haven’t developed Cirrhosis.

249
2 Portal Hypertension

o In patients who have compensated cirrhosis and small varices that have
not bled but have criteria for increased risk of hemorrhage (Child B/C or
presence of red wale marks on varices), nonselective beta blockers
o In patients with medium/large varices that have not bled, nonselective
beta blockers (propranolol or nadolol) is recommended or undergo EVL
o In patients who receive beta-blockers, a follow-up EGD is not
necessary.
o If a patient is treated with EVL, it should be repeated until the varices
are obliterated. EGD should performed one to three months after
obliteration and then every 6 to 12 months to check for variceal
recurrence.
3 TREATMENT OF ACTIVE VARECIAL BLEED The principal
complications that cause
3.1 PRIMARY GOALS death are aspiration
pneumonia, sepsis
There are three primary goals of management during the active bleeding episode: (antibiotic
administration), acute-on-
1.  ABCs, especially hemodynamic resuscitation: this is achieved by two chronic liver failure,
large bore peripheral lines, where fluids or blood should be administered. hepatic encephalopathy
(lactulose and treatment
In some cases, clotting factors/platelets might be needed due to the of other precipitating
massive blood transfusion and exhausted clotting factors/platelets. factors), and renal failure
2. Prevention and treatment of complications (careful fluid balancing
o Prophylactic antibiotics, preferably before endoscopy (although and avoid giving
nephrotoxic substances)
effectiveness has also been demonstrated when given after). Suggest
intravenous ceftriaxone (1 g IV) or Cipro (400 mg IV BID) About 20%  Vasoactive
of patients with varecial bleeding will have a infection. Most commonly substances agents
directly constricts
a UTI, but other more serious conditions like a respiratory infection or mesenteric arterioles and
peritonitis may develop. decreases portal venous
inflow, thereby reducing
3. Arresting Varecial bleeding: portal pressure.
o Vasoactive substances: Suggest terlipressin in countries where it is However, Terlipressin is
the only pharmacological
available and somatostatin or octreotide (50 mcg bolus followed by 50 agent shown to reduce
mcg/hour by intravenous infusion) where terlipressin is unavailable. mortality in compared to
placebo.
o  Endoscopic treatment: is the treatment of choice, where it can be
diagnostic and also therapeutic. Endoscopic therapy can either be
Endoscopic variceal ligation (EVL) or Endoscopic scelotherapy.
o If the patient’s bleeding is still not controlled, Surgery mostly in the form  EVL should be
performed as soon as
of TIPS is usually performed. possible. It involves the
placement of rubber
3.2 SALVAGE TREATMENT bands around a portion
of oesophageal mucosa
 TIPS (transjugular intrahepatic portosystemic shunt) used primarily as a that contains the varix.
salvage therapy in patients with recurrent variceal bleeding despite an EVL is superior to
sclerotherapy in general,
adequate trial of endoscopic and pharmacologic treatment (usually defined
but sclerotherapy maybe
as two failed attempts of endoscopic treatment) used in cases when
 The best candidates for surgery are patients with well preserved liver esophageal visualization
function who fail emergent endoscopic treatment and have no is limited due the
complications from the bleeding or endoscopy. bleeding mainly because
scleortherapy is quicker
 The choice of surgery usually depends upon the availability, training, and and provides better
expertise of the surgeon. visualization of the
esophagus.

250
 Treatment of Active Varecial Bleed 3

 Although a selective shunt has some physiologic advantages, it may

significantly exacerbate marked ascites. Thus, a portacaval shunt would be
preferable in patients with marked ascites
3.3 PORTAL HYPERTENSION OPERATIONS

A. Shunt Surgery:
Definition: Transjugular intrahepatic portosystemic shunts (TIPS) involve
creation of a low-resistance channel between the hepatic vein and the
intrahepatic portion of the portal vein (usually the right branch) using
angiographic techniques. The tract is kept patent by deployment of an
expandable metal stent across it, thereby allowing blood to return to the
systemic circulation. Portosystemic shunts are classified as nonselective,
selective, and partial, depending on how much hepatic portal flow is
preserved.
o Types of shunts:
1. Nonselective — those that decompress the entire portal tree, such
as portacaval shunts
2. Selective — those that compartmentalize the portal tree into a
decompressed variceal system while maintaining sinusoidal

251
4 Portal Hypertension

perfusion via a hypertensive superior mesenteric-portal

compartment, such as a distal splenorenal shunt
3. Partial — those that incompletely decompress the entire portal tree
and thereby also maintain some hepatic perfusion
B. Nonshunt operations generally include either esophageal transection (in
which the distal esophagus is transected and then stapled back together
after varices have been ligated) or devascularization of the
gastroesophageal junction (Sugiura procedure).
3.4 GENERAL OUTLINE OF VARECIAL BLEEDING TREATMENT

 Maintain a hemoglobin level of approximately 8 g/dL. A threshold above

this may actually increase mortality.
 Pharmacologic therapy (somatostatin or its analogue octreotide) should
start as soon as bleeding is suspected and continue for 3-5 days after
confirmation.
 Short-term (maximum seven days) antibiotic prophylaxis should be
instituted in any patient with cirrhosis and GI hemorrhage.
 Upper endoscopy, performed within 12 hours, should be used to make the
diagnosis and to treat variceal hemorrhage either with endoscopic variceal
ligation or sclerotherapy.
 TIPS is indicated in patients in whom hemorrhage from esophageal varices
cannot be controlled or in whom bleeding recurs despite combined
pharmacological and endoscopic therapy.
 Balloon tamponade should be used as a temporizing measure (maximum
24 hours) in patients with uncontrollable bleeding for whom a more
definitive therapy (eg, TIPS or endoscopic therapy) is planned.
  Note: Dr.Mazen mentioned that Proton pump inhibitors should be added
even in cases with known Liver disease. The rationale behind this is A) that
peptic ulcer bleeding hasn’t been ruled out and B) decreased acid secretion
may help in the healing of these gastrointestinal bleeds. I did not know
where to add this point, so I did here.

252
 Ascites: 5

2 ASCITES:

 Cirrhosis is the most common cause of ascites in the United States,

accounting for approximately 8%5
 Ascites is the most common complication of cirrhosis
 Fluid leaks from the surface of the liver and intestine.
 Factors responsible: portal hypertension, decreased ability of the blood
vessels to retain fluid, fluid retention by the kidneys, and alterations in
various hormones and chemicals that regulate bodily fluids
2.1 TREATMENT OF ASCITES:

 Dietary sodium restriction is a central component, 2000 mg / day

 Patients should be instructed to avoid NSAIDs, which can cause sodium
retention and affect renal function
 Fluid restriction is equivocal and not strongly recommended
 Diuretic therapy, a single morning oral doses of spironolactone and
furosemide, beginning with 100 mg and 40 mg
 Serial therapeutic paracentesis and TIPS are usually reserved for patients
with refractory ascites.
 Peritoneovenous shunts (LeVeen or Denver) or surgical portosystemic
shunts have very limited indications
2.2 COMPLICATIONS OF ASCITES:

 Spontaneous bacterial peritonitis: (SBP) is an infection of preexisting ascitic

fluid without evidence for an intra-abdominal secondary source such as a
perforated viscus
 The diagnosis is established by:
o positive ascitic fluid bacterial culture, and/or
o elevated ascitic fluid absolute polymorphonuclear leukocyte (PMN)
count (≥250 cells/mm3)
3 PORTAL VEIN THROMBOSIS
Causes:
 Can be picked up Ultrasound with Doppler flow studies, CT scanning, and
magnetic resonance angiography
 UGD should be performed to establish wither varices are present
 In cases of detected acute thrombosis (e.g. pancreatitis) Anticoagulation
therapy for at least three months starting with low molecular weight heparin
and shifting to oral anticoagulation as soon as the patient's condition has
stabilized.
 Anticoagulation should be continued long-term in patients with acute portal
vein thrombosis who have a permanent thrombotic risk factor that is not
correctable.

253
6 Portal Hypertension

3.1 BLEEDING FROM PORTAL VEIN THROMBOSIS:

 Gastric fundal varices: endoscopic variceal obturation using tissue

adhesives such as cyanoacrylate is preferred, where available. Otherwise,
endoscopic variceal ligation is an option.
 Splenectomy is curative for cases of splenic vein thrombosis and
gastric varices formation.
 TIPS should be considered in patients in whom hemorrhage from fundal
varices cannot be controlled or in cirrhosis whom bleeding recurs despite
combined pharmacological and endoscopic therapy.

254
 Acute Pancreatitis 1

PANCREATIC DISEASES
 1 ACUTE PANCREATITIS

1.1 DEFINITION  The most important

enzymes for protein
Acute non-bacterial inflammation caused by activation of pancreatic enzymes and digestion are trypsin,
auto-digestion of the pancreas by its own enzymes.  chymotrypsin, and
carboxypolypetidase.
1.2 ETIOLOGY These enzymes are not
in the active form until
they reach the
1. Gall stones (most common) : duodenum. Trypsin is
a. Small stones can lodge in the Ampulla of Vater and block both the activated (from its
common bile duct (CBD) & pancreatic duct precursor: trypsinogen)
by an enzyme called
b. Small stones eventually pass and can be found in stool enterokinase that is
2. Alcohol (2nd most common) : underlying mechanisms are still unclear, but secreted from the
intestinal mucosa when
2 effects are proposed to be involved: chyme enters the
a. Direct toxic effect on pancreatic cells intestine. Trypsin then
b. Transient ischemia (cutaneous vasodilation → blood diverted away cleaves the other two
enzymes and
from splanchnic circulation → pancreatic ischemia) trypsonigen into their
3. Hypercalcemia: Ca++ activates enzymes active forms.
a. Excessive calcium causes:
i. Deposition of Ca in soft tissues leading to obstruction of the  Antitrypsin is a
pancreatic duct substance secreted from
ii. Trypsinogen activation before it reaches the intestines the pancreatic acini that
prevents the activation
b. With severe inflammation: Ca++ + fat = saponification (soap of trypsin and
formation) → serum Ca++ will be depleted in the process (low- subsequently the other
enzymes, which
normal serum Ca++ levels) prevents auto digestion
4. Hyperlipidemia of the pancreas itself.
a. Mechanism unclear. When the duct gets
obstructed or pancreatic
b. Could be a cause: Elevations greater than 1,000 mg/dL can lead to cells gets damaged
pancreatitis lysosomal enzymes
activate trypsin. This is
c. Could be a result: TG serum levels increase with inflammatory initially controlled by
processes– but the elevation will be moderate (<1000 mg/dL) antitrypsin, but its
quantities are soon
5. Familial (rare)
overwhelmed by the
6. Iatrogenic amount of activated
a. Drugs: diuretics (lasix and thiazides), HRT (hormone replacement enzymes, until these
enzymes digest the
therapy)/OCP (oral contraceptive pill), azathioprine, and steroids pancreas and cause the
b. ERCP (endoscopic retrograde cholangiopancreatography): condition of acute
pancreatitis.
 Pressure with duct cannulation or contrast injection
7. Obstruction (1%): tumor at Ampulla of Vater
8. Viral infection: Coxiella, mumps
9. Trauma
10. Scorpion bite
11. Idiopathic

255
2 Pancreatic Diseases

1.3 CLINICAL MANIFESTATIONS

1.3.1 HISTORY
 Courvoisier sign: is
 Acute epigastric pain, radiating to back (pancreas is a retroperitoneal case of painless jaundice
and a palpable
organ) gallbladder. It is not
o Patient will be leaning forward ( pain as pancreas moves away caused by stones but
from the nerves) most often by
malignancies like
 Nausea & vomiting pancreatic cancer and
 Previous attacks (untreated underlying disease e.g. gall stones) cholingeocarcinoma.

 Symptoms of underlying cause e.g. gall stones

 Shock in acute
1.3.2 EXAMINATION pancreatitis can be
attributed to a few
 Hypotension,  peripheral resistance, tachycardia & fever factors: (a) Massive
 Dehydration – can progress to → shock exudation and
hemorrhage in the
 Epigastric tenderness retroperitoneal space
 Pleural effusion “sympathetic effusion” (Left lower lobe) (b) Release of a number
of vasodilators, like
Hemorrhagic pancreatitis: bradykinin and PAF and
in the systemic
 Grey Turner sign: bruising of the flanks; sign of retroperitoneal hemorrhage circulation
 Cullen’s sign: superficial edema and bruising in the subcutaneous fatty (c) The ileus which
causes the accumulation
tissue around the umbilicus – indicating pancreatic necrosis &
of fluid in the intestine
retroperitoneal bleeding
Figure 1: Grey Turner's Sign Figure 2: Cullen's Sign

 Amylase:
 It goes up quickly &
down quickly.
 Secreted everywhere in
1.3.3 LAB TESTS the GI, and in the
ovaries and fallopian
 ↑ WBC tubes.
 ↑ Amylase (most sensitive; shorter t1/2): >1000  Elevated in GI
diseases & ectopic
 ↑ Lipase (more specific than amylase) pregnancy.
 Serum calcium & lipids (see section 1.2)  >1000 elevation occurs
only with pancreatitis.
1.3.4 RADIOLOGY
 Plain erect chest & abdominal X-ray:

256
 Acute Pancreatitis 3

o Sentinel loop: 1-2 inflamed bowel loops dilated around pancreas

causing ileus (painful obstruction); localized peritonitis causing
localized ileus
 CT scan (BEST): Phlegmon; edematous, inflamed pancreas, “dirty
mesentery”

1.3.5 RANSON’S CRITERIA 

Assess severity & prognosis
1. On admission
a. Age >55 years
b. WBC > 16,000
c. Glucose >11 mmol/L (x 18 = 198 mg/dL) (no insulin secretion)
d. AST >250
AXR: Sentinel loop
e. LDH >350
2. 36-48 hours after admission
a. Urea >8 mg/dL (dehydration)
b. Hematocrit: >10% decrease (hemorrhage)
c. Fluid sequestration >6 L (patient needed 6 L of fluid)
d. PO2 <60
e. Base deficit >4 (acidosis)
f. Serum calcium <8 mg/dL (saponification)

1.4 MANAGEMENT 

 Acute pancreatitis is the only acute abdomen emergency that DOESN’T NEED
SURGERY
 Most important: IV FLUID REPLACEMENT
o Patients lose a lot of fluid (~3-4 L) to the interstitium “3rd spacing” =
massive edema +/- retroperitoneal bleeding (due to vessel wall
digestion be activated enzymes), leading to hypovolemia →
replace fluid with normal saline or Ringer’s lactate
 Then:
a) Rest the patient: Analgesics
b) Rest the bowel: Nasogastric tube
c) Rest the pancreas: NPO (Nil per Os: nothing by mouth)
 Do not administer antibiotics
 90% will improve with conservative management; surgery rarely indicated
(only to debride necrotic tissue in advanced stages “necrosectomy”) CT scan: Phlegmon

1.5 COMPLICATIONS

The only indications for antibiotics  (+/- surgery, if no improvement w/antibiotics):

1. Necrosis
2. Infected necrosis
3. Abscess
4. Pseudocyst

257
4 Pancreatic Diseases

Figure 3: Infected Necrosis (gas formation) Figure 4: Pseudocyst

2 PSEUDOCYST

“Failure of pancreas to recover/recurrence of symptoms”

 A collection of amylase-rich fluid enclosed in a wall of fibrous or granulation
tissue (not epithelium) that develops following an acute pancreatitis attack
(>4 wks from onset)
 50% are found to have a communication with the main pancreatic duct.
2.1.1 PRESENTATION
 Abdominal pain
 Pressure symptoms e.g.
o Stomach: nausea
o Bile duct: obstructive jaundice
 Epigastric mass

2.1.2 INVESTIGATIONS
 ↑ Lipase/WBC
 CT scan (BEST)

2.1.3 COMPLICATIONS
 Infection --→ abscess
 Rupture → pancreatic ascites
 Bleeding (erode the vessels, esp. gastroduodenal artery)

2.1.4 MANAGEMENT
 Observe for 6-12 weeks (50% resolve spontaneously) then repeat CT scan
 Surgery (drainage) indications:
o Infection (external)
o Symptomatic (internal)
o > 5 cm (internal)

258
 Chronic pancreatitis 5

3 CHRONIC PANCREATITIS

Chronic pancreatitis is a progressive inflammatory disease of the pancreas causing

fibrosis and loss of endocrine & exocrine functions of the pancreas.
Most common cause: Chronic alcoholism
3.1.1 SIGNS & SYMPTOMS:
 Abdominal pain
 Malabsorption
 Diabetes

3.1.2 DIAGNOSIS:
 Lipase & amylase: usually normal
 ↑ Glucose
 Abdominal x-ray: calcification, stones
 CT scan: calcifications, atrophy, dilated ducts

3.1.3 COMPLICATIONS:
 Biliary obstruction (due to fibrosis of the head of the pancreas)
 Pseudocyst (due to rupture of a stricture)
 Carcinoma (due to repeated inflammation)
 Splenic vein thrombosis (lies on top of the pancreas)

3.1.4 TREATMENT:
 Pancreatic enzymes (for malabsorption)
 Insulin (for diabetes)
 Analgesics (narcotics) or celiac block (injection of analgesics)
 Surgery
o Pancreaticojejunostomy (pancreatic duct drainage procedure to
decompress the dilated pancreatic duct)—most common procedure
 Bypasses pancreatic duct & relieves pain
o Pancreatic resection (last resort; will lead to “brittle diabetes” which
is unstable diabetes with recurrent swings in glucose levels)

4 PANCREATIC ADENOCARCINOMA

 3rd leading cause of cancer death in men aged 35-55 years

4.1.1 RISK FACTORS

 Most important: smoking 
 Fatty food
 Remote gastrectomy
 Race: Black
 Chronic pancreatitis

259
6 Pancreatic Diseases

 Polyposis syndromes
 Family history
 Cholecystectomy

4.1.2 PRESENTATION  Jaundice + fever =

cholangitis
Arise most commonly in the head of the pancreas (70%) → present w/jaundice
Other (tail, body) usually presents late w/metastases.  Cholangitis:
inflammation of the
 Weight loss biliary tree. It is a
medical emergency.
 Deep seated pain  Obstruction of the
 Back pain (sign of retroperitoneal invasion) biliary duct by a
pancreatic head tumor
 Gastric outlet obstruction promotes infection,
leading to cholangitis.
Physical examination:
 Jaundice
 Hepatomegaly
 Palpable gallbladder (distended GB due to obstruction)
 Succession splash (gastric outlet obstruction)

4.1.3 INVESTIGATIONS
 Lab
o ↑ WBC (w/cholangitis)
o CA 19-9 >100 (tumor marker)
 Imaging: double-duct sign (dilated bile duct & pancreatic duct) on U/S & CT
o U/S: dilated bile duct
o ERCP (esp. cholangitis)
o CT scan (BEST)

4.1.4 TREATMENT
 Treatment is surgical
o Assess resectability (rule out local invasion & distant metastases)
o Whipple’s resection (pancreatectomy)
o Palliative biliary & gastric drainage
POOR LONG TERM SURVIVAL

260
 MCQs 7

5 MCQs

1. The most specific blood test in diagnosing acute pancreatitis is:

a. Serum amylase
b. Urinary amylase
c. Serum lipase
d. CA 19-9
e. CEA
2. The most important step in the management of acute pancreatitis is :
a. IV fluids
b. Antibiotics
c. NG tube
d. ERCP
e. Pain medications
3. Ranson's criteria include the following except:
a. WBC
b. Age
c. Serum glucose
d. LDH
e. Serum Lipase
4. The following are causes of acute pancreatitis except:
a. Alcohol
b. Gall stones
c. Trauma
d. Viral infections
e. Hypocalcemia
5. The most important factor in pancreatic adenocarcinoma is :
a. Alcohol
b. Smoking
c. Chronic pancreatitis
d. Diabetes
e. Gastrectomy
6. Pancreatic pseudocyst might be complicated with all of the following
except:
a. Malignant transformation
b. Rupture
c. Bleeding
d. Jaundice
e. Infection
7. Symptoms of chronic pancreatitis include all of the following except:
a. Diabetes
b. Constipation
c. Diarrhea
d. Abdominal pain
8. Which of the following is most helpful in diagnosing pancreatic
adenocarcinoma:
a. CA 125
b. Serum amylase
c. CEA
d. CA 19-9

261
8 Pancreatic Diseases

9. Pain in chronic pancreatitis could be improved with, except:

a. Antibiotics
b. Narcotics
c. Celiac block
d. Surgical drainage
e. Pancreatectomy
10. Pancreatic adenocarcinoma can present with, except:
a. Hematemesis
b. Jaundice
c. Abdominal pain
d. Abdominal mass
e. Weight loss

Answers: 1:c, 2:a, 3:e, 4:e, 5:b, 6:a, 7:b, 8:e, 9:a, 10:a 262
 Overview: Anatomy of the Skin 1

SUPERFICIAL LUMPS
1 OVERVIEW: ANATOMY OF THE SKIN

 SKIN ANATOMY:
o Epidermis  openings of glands
o Papillary dermis  basal cell layer
o Dermis  contains sweat and sebaceous glands
2 BENIGN SKIN LUMPS

2.1 PAPILLOMA (W ART):

 Pedunculated =
attached by a
 Finger-like projections of all skin layers peduncle/stalk
 Usually infective (papilloma virus)
 Pedunculated or sessile
 Treatment:
o Cauterization  if small or multiple
o Excision  if large or sessile
 Sessile= attached
directly by its base
2.2 SCARS: without a stalk

 A scar is considered a fibrous tissue proliferation

following:
o Trauma
o Surgery
o Infection
 It is usually flat
2.3 HYPERTROPHIC SCAR

 Excessive fibrous tissue in a scar

 Confined to the scar 
 No neovascularization
 Wound infection is an important factor
 Clinically:
o Raised
o Non tender swelling
o Not itchy
 It my regress gradually in six months
 Does not recur after excision
2.4 KELOID

 Excessive fibrous and collagen tissue with neovascular

proliferation in a scar (enabling it to continue to grow and
extend)
 Usually extends beyond the original scar 
 Clinically:
o Initially raised

263
2
Superficial Lumps

o Pink and tender

o Itchy and may ulcerate
 More common in dark skinned people
 Progressive vs. non-progressive
 Acquired vs. spontaneous
 Keloids can recur after excision
 Treatment:
o Injection (hyaluronidase, steroids etc.)
o Excision and grafting
2.5 PYOGENIC GRANULOMA
 In pyogenic
granuloma, patient
 Excessive granulation tissue growth in ulcers complains of a rapidly
 Clinically: growing lump on skin,
o Firm and bright which bleeds easily.
o Red swelling that bleed on touch
o Recurrent bleeding when exposed to minor trauma
 Treatment:
o Cauterization (if small)
o Excision (if large)
2.6 HAEMANGIOMA

 A developmental malformation of blood vessels rather

than a tumor
 Types: capillary, cavernous, arterial
 It commonly occurs in skin and sub-cutaneous tissue
but can occur in other organs e.g. lips, tongue, liver,
and brain may be affected
3 MALIGNANT SKIN TUMORS

3.1 BASAL CELL CARCINOMA

 Ulcerated tumor of basal cell layer of skin

 Middle aged white tropical males (Australia) (high
UV light exposure)
 Common in face (triangle of face: nose, forehead,
and eyelids)
 Low grade and slowly growing tumor (years)
 Clinically:
o Rolled-in edges (inverted) with attempts of
healing 
o Floor shows an unhealthy granulation with a scab
o The base is indurated and may be fixed to bone
o Spreads locally (usually no lymph nodes metastases)
 Treatment:
o Radio-therapy & surgery

264
 Malignant Skin Tumors 3

3.2 SQUAMOUS CELL CARCINOMA (EPITHELIOMA)

 Arise from squamous cell layer of skin or mucus

membrane
 It may arise from metaplasia of columnar epithelium due
to chronic irritation (gall bladder, bronchus, stomach etc.)
 It can occur anywhere in the body
 Males are more affected than females
 More malignant and rapidly growing than BCC
 Clinically:
o Edges are rolled out (everted) 
o Spreads: locally, lymph nodes, and blood
 Treatment:
o Radio-therapy and surgery
3.3 MARJOLIN ULCER

 It is a low grade squamous cell carcinoma arising in chronically inflamed

ulcers or scars
 Treatment:
o Radiotherapy and surgery
3.4 NAVEUS (MOLE)

 A localized cutaneous malformation This picture shows a

patient who started to
 Includes moles and birth marks develop marjolin ulcer on
 They may present at birth, or even later in life top of his 20 years old
 Types: burn scar.
o Junctional, intradermal, compound, blue naveus
o Juvenile and freckle
 Evidences of malignant change: 
 Junctional=located in
o Increase in size dermo-epithelial junction,
o Change to irregular edge may turn into
o Change in thickness malignancy.
o Change in color (deepening in color) Compound=located in
o Change in surrounding tissue both dermis and junction,
o Symptoms e.g. itching, bleeding discharge may turn into
malignancy.
o Lymphadenopathy
o Microscopic evidence Intradermal=located
mostly in dermis, has no
malignancy potential.
3.5 MALIGNANT MELANOMA

 It’s a rare but most rapidly

infiltrating skin tumor
 90% of the time it arises
from a pre-existing naevus
 10% De-novo

 Metastasis:
o Local and satellite nodules

265
4
Superficial Lumps

o Lymphatic (early metastasis to LN)

o Blood (liver, lung, bone etc.)
4 SKIN CYSTS

4.1 IMPLANTATION DERMOID

 It is a post-traumatic dermoid
 Commonly in fingers and hands of farmers and tailors 
 Tense, may be hard tender swelling
 Attached to skin which may be scarred
 Contains desquamated epithelial cells
 Pain and ulceration may occur following repeated trauma
 Treatment:
o Excision is curative
4.2 SEBACEOUS CYST  Sebaceous cysts
have two important
 It is a retention cyst due to blockage of its duct features:
1. Skin adherence
 Lined by squamous epithelium and contains sebum 2. Punctum
and desquamated epithelium
 Commonly in scalp, face, scrotum and vulva (NEVER
in palm and sole) 
 Clinically: 
o Spherical, cystic or tense swelling, attached to
skin with punctum (very diagnostic) that may discharge sebum upon
squeezing
o Indentation and fluctuation tests may be positive but
transillumination test is negative (opaque fluid)
 Complications:
o Cosmetic
o Infection
o Ulceration
o Cock peculiar tumor (granuloma due to ulceration)
o Sebaceous horn (inspissated secreted sebum)
 Treatment:
o Excision (uninfected cyst)
o Drainage followed by excision (infected)
5 SUBCUTANEOUS LUMPS

 Cystic swellings:
o Congenital:
o Dermoid cyst
o Cystic hygroma
o Haemangioma
o Aquired:
 Parasitic
 Haematoma
 Abscess

266
 Subcutaneous Lumps 5

 Solid swellings:
o Commonly benign: Schwanoma, neurofibroma, lipoma
o Rarely malignant
5.1 DERMOID CYST

 Clinically four variants:

o Sequestration dermoid
o Implantation dermoid
o Tubulo-dermoid
o Terato-dermoid
5.1.1 SEQUESTRATION DERMOID
 It is a true congenital cyst (c.f. implantation dermoid)
 Ectodermal tissue buried in mesoderm forming a cyst
lined by squamous epithelium and contains paste-like
desquamated epithelium
 Common at lines of embryonic fusion sites 
o Midline: neck and root of nose
o Scalp
o Inner or outer angles of eyes
 Clinical features: 
o Painless, spherical, cystic mass
o Smooth surface
o Not attached to skin (c.f. sebaceous cyst)
o No punctum (c.f. sebaceous cyst)
o Not compressible (c.f. meningocele)
o Cough impulse and bone indentation (scalp)
o Transillumination test? positive
5.1.2 TUBULO-DERMOID:
 Cystic swelling arising from the non-obliterated part of congenital duct or
tube which fills up by secretions of lining epithelium
 Examples:
o Thyroglossal cyst (remnant of thyroglossal duct)
 Most common midline neck swelling and usually presents as a
painless, rounded cystic lump, which moves on swallowing or
protruding the tongue.
o Post-anal dermoid (remnant of neuro-enteric canal)
o Epindymal cyst tin brain (remnant of neuro-ectoderm canal)
5.1.3 TERATO-DERMOID:
 Cystic swelling arising from totipotent cells with ectodermal
preponderance
o Ovary; ovarian cyst
o Testes; teratoma
o Mediastinum
o Retroperitoneum
o Pre-sacral area

267
6
Superficial Lumps

 They usually contain derivatives of mesoderm (cartilage, bone, hair,

cheesy material)
5.2 CYSTIC HYGROMA  This picture shows
thyroglossal cyst, which
 A congenital malformation affecting lymphatic channels characteristically moves
 Clinically: with tongue protrusion.
o it appears early, multilocular, filled with clear fluid
(transillumination positive)
 Lined by columnar epithelium
 Common in: neck, axilla, groin, mediastinum and tongue

5.3 BRANCHIAL CYST

 A congenital cyst in persistent cervical sinus

 Located below angle of mandible, behind mid
sternocleomastoid muscle
 Clinically:
o Tense, distinct edges, positive fluctuation and
negative transillumination
 Contains cholesterol crystals (diagnostic)
 Differential diagnosis:
o Cold abscess, dermoid cyst, plunging ranula, cystic hygroma
o Carotid body tumor, lymph node, submandibular gland
5.4 GANGLION

 A cystic swelling of synovial membrane of tendon or

capsule in small joints
 Myxomatous degeneration
 May be communicating
 Common sites: 
o Dorsum of wrist
o Dorsum of foot and ankle
o Palmar aspect of wrist and fingers
 Clinically:
o Slowly growing lump
o Common in females
o Spherical, firm, cystic swelling
o Mobile across tendon axis but limited along longitudinal axis
 Treatment:
o Excision
5.5 LIPOMA

 Benign tumor of adipose tissue

 The most common benign tumor in subcutaneous tissue 
 Common in trunk, neck and limbs
 Encapsulated vs. diffuse

268
 Subcutaneous Lumps 7

 May be mixed e.g. fibrolipma, neurolipoma (with neural tissue), and

haemangioma-lipoma (with vascular tissue)
 Dercum’s disease = multiple lipomatosis
 Clinically:
o Painless, soft and lobulated lump.
o Well-defined edges and skin is free.
o Slipping sign positive.
o Freely mobile.
o Fluctuation test is negative.
o Tranillumination test is negative.
 Complications:
o Necrosis, calcification, hemorrhage, infection, and rarely malignancy
 Treatment:
o Small symptomatic  reassurance only
o Symptomatic  surgical excision (if encapsulated) or liposuction (if
diffuse)
5.6 NEUROFIBROMA

 Tumor of nerve connective tissue (not necrosis)

 Types:
o Localized or solitary NF
o Generalized multiple neurofibromatosis type 1 (Von-Recklinghausen’s
disease)
o Plexiform NF
o Elephantiasis NF
o Cutaneous NF
 Clinically:
o Encapsulated, rounded or elliptical swelling
o Smooth, firm with well defined edges
o Tenderness and parasthesia may be present
o Mobility may be diminished along nerve-axis
 Treatment:
o Excision
5.7 MULTIPLE NEUROFIBROMATOSIS (VON-RECKLINGHAUSEN’S
DISEASE)

o Inherited as an autosomal disease

o More common in males
o Multiple tumors with Café-au-leit spots
o Peripheral and cranial nerves maybe affected
o May be associated with other tumors (e.g. endocrine)

269
8
Superficial Lumps

6 MCQS

1. The finger like projections of connective tissue core that is lined with an
epithelium is called:
A. Fibroma
B. Papilloma
C. Lipoma
D. Ganglion

2. The most common midline single neck swelling is:

A. Pharyngeal pouch
B. Dermoid cyst
C. Laryngocele
D. Thyroglossal cyst

3. Basal cell carcinoma:

A. Metastasize very quickly
B. Aggressive tumor that grows rapidly
C. Surgery is the best treatment for local lesions
D. A tumor of infancy

4. All of the following are common sites of squamous cell carcinoma, except:
A. Neck
B. Back of the hand
C. Lower lip
D. Lower back

5. A 40 years old male presented with 10x10 cm, soft non-compressible,

mobile mass that was not attached to the skin. The most likely diagnosis is:
A. carbuncle
B. hemangioma
C. Lipoma
D. Dermoid cyst

6. Marjolin ulcer:
A. Is a type of basal cell carcinoma
B. Is a type of squamous cell carcinoma
C. Is a type of melanoma
D. Is a type of an ulcer in a dysplastic navus

 Answers: 1=B, 2=D, 3=C, 4=D, 5=C, 6=B

270
 Right Upper Quadrant Mass 1

ABDOMINAL MASSES AND

HERNIAS
1 RIGHT UPPER QUADRANT MASS

1.1 HEPATIC MASSES:

 Congestive heart failure

 Macronodular cirrhosis
 Hepatitis
 Hepatoma or secondary carcinoma
 Hydatid cyst
 Liver abscess
 Riedel’s lobe: an extension of the right lobe down below the costal margin
along the anterior axillary line
1.1.1 PHYSICAL SIGNS
 Can’t go above it, and moves with respiration
 Dull to percussion up to the level of the 8th rib in the midaxillary line
 Edge: Sharp or rounded
 Surface: Smooth or irregular
1.2 GALLBLADDER MASSES

 Mucocele: Containing Mucus

 Empyema: Containing pus
 Courvoisier law:
o If the gallbladder is palpable and the patient is jaundiced, the
obstruction of the common bile duct causing the jaundice is unlikely to
be a stone because the previous inflammation will have made the
gallbladder thick and non-distensible
1.2.1 PHYSICAL SIGNS
 Moves with respiration
 Not dull because it is covered by the colon
 It can be balloted i.e. felt bimanually
2 LEFT UPPER QUADRANT MASSES

2.1 SPLEEN

 Typhoid
 Tuberculosis
 Syphilis
 Glandular fever
 Malaria
 Ka lazar

271
2 Abdominal Masses and Hernias

 Myeloid and lymphatic leukemia

 Spherocytosis
 Thrombocytopenia purpura
 Portal hypertension
 True solitary cyst
 Hydatid cyst
 Lymphoma
2.1.1 PHYSICAL SIGNS
 Appears from below the costal margin and enlarges towards the umbilicus
 Firm, smooth and has a defined notch on its upper edge
 Cannot get above it, and dull on percussion
2.2 ENLARGED LEFT KIDNEY

3 EPIGASTRIC MASSES

3.1 CARCINOMA OF THE STOMACH

 Abdominal pain/mass
 Indigestion
 Loss of weight and appetite
3.1.1 PHYSICAL FINDINGS
 When palpable it is hard and irregular and disappears below the costal
margin i.e. cannot go above it
 Moves with respiration
3.2 PANCREATIC PSEUDOCUST

 Collection of pancreatic secretion, caused by pancreatitis, on the surface of

the pancreas or in part of the whole lesser sac.
 There is history of acute pancreatitis followed by epigastric fullness, pain,
nausea and sometimes vomiting.
3.2.1 PHYSICAL FINDINGS
 Firm mass in the epigastric region with indistinct lower edge.
 The upper limit is not palpable.
 Usually resonant because it is covered by the stomach
 Moves very slightly with respiration
4 RIGHT ILIAC FOSSA MASSES

4.1 APPENDICULAR MASS

 Central abdominal pain shifting to the right iliac fossa associated with
nausea, vomiting and loss of appetite
 Physical finidings:
o Tender indistinct mass, dull to percussion and fixed to the right iliac
fossa posteriorly

272
 Left Iliac Fossa Masses 3

4.2 APPENDICULAR ABSCESS

 As for appendicitis with additional symptoms of an abscess such as fever,

rigors, sweating and increased local pain
 Physical findings:
o A tender mass which in its late stages may fluctuate and be associated
with edema and reddening of the overlying skin
4.3 TUBERCULOSIS

 Inflamed ileocecal lymph nodes, parts of and the terminal ileum and the
cecum
 Vague chronic central pain for months
 General ill health and weight loss
 The pain eventually becomes intense and settles in the iliac fossa
 Physical findings:
o The mass is firm, distinct and hard
o It is not tender and does not resolve with observation
4.4 CHRON’S DISEASE

 Recurrent episodes of pain in the right iliac fossa, malaise, loss of wight
and episodes of diarrhea and melena
 Physical findings:
o The elongated terminal ileum forms an elongated sausage-shaped
mass which is rubbery and tender
4.5 PSOAS ABSCESS

 General ill feeling for months, night sweats and weight loss
 Physical findings:
o Soft, tender, dull and compressible
o There may be fullness in the lumbar region
o The swelling extends below the groin and it may be possible to empty
the swelling
4.6 OTHERS

 Cecal carcinoma
 Actinomycosis
 Ruptured epigastric artery
 Iliac lymphadenopathy
 Iliac artery aneurysm
5 LEFT ILIAC FOSSA MASSES

5.1 DIVERTICULITIS

 Recurrent lower abdominal pain and chronic constipation for years

 The acute episodes starts suddenly with severe pain, nausea, loss of
appetite and constipation

273
4 Abdominal Masses and Hernias

 Physical finding:
o Tender indistinct mass, with sings of general or local peritonitis
5.2 CARCINOMA OF THE SIGMOID COLON

 General cachexia
 Lower abdominal pain associated with rectal bleeding
 Change in bowel habits and sometimes intestinal obstruction
 Physcial findings:
o Hard mass, non tender
o May be mobile or fixed
o The colon above the mass may be distended with indentable feces
5.3 OTHERS

 Chron’s disease
 Psoas abscess
 Same masses of the right iliac fossa
6 HYPOGASTRIC MASSES

6.1 URINARY BLADDER

 Acute retention: the bladder is full and tender

 Chronic retention: Painless
 History of prostatism
 Physical findings
o Arises out of the pelvis and so it has no lower edge
o Not mobile and dull to percussion
o Direct pressure often produces a desire to micturate
6.2 PREGNANT UTERUS

 The uterus enlarges to the xiphisternum by the 36th week of pregnancy, at

this stage the fetus is palpable
 A pregnant uterus is smooth, firm and dull
6.3 FIBROIDS

 They cause irregular and heavy periods, disturbed micturation, lower

abdominal pain and backache
 Physical findings:
o Arises out of the pelvis and so the lower edge is not palpable
o Firm or hard, moves slightly in transverse direction and dull on
percussion
7 ABDOMINAL HERNIA

7.1 DEFINITION

 An abnormal protrusion of intra-abdominal contents through a defect in the

abdominal wall.

274
 Abdominal Hernia 5

 Protrusion of a viscus or part of it through an opening in the wall of its

containing cavity
7.2 ETIOLOGY

7.2.1 CONGENITAL DEFECTS:

 Indirect inguinal hernia, umbilical hernia
 Patent processus vaginalis: almost always causes indirect inguinal hernia
7.2.2 ACQUIRED
 Loss of tissue strength and elasticity, due to aging or repetitive stress:
o hiatal hernia
 Operative Trauma, in which normal tissue strength is altered surgically:
o incisional hernia
 Increased intra-abdominal pressure:
o Heavy lifting
o Coughing, asthma, and COPD
o Straining at defecation or urination (e.g. Benign prostatic hypertrophy,
constipation, colon/rectal cancer)
o Multiparity (Multiple pregnancies)
o Ascites and abdominal distension
o Obesity
7.3 COMPOSITION

 The sac: diverticulum of peritoneum

consisting of a mouth, neck, body and
fundus
 The body: varies in sice snd is not
necessarily occupied
 The coverings: derived from the layers of the
abdominal wall
 The contents: may be omentum, bowel,
ovary, bladder… etc.

7.4 COMMON CLINICAL PRESENTATION OF ABDOMINAL WALL

HERNIA

 Swelling
 Reduction
 site
7.5 ABDOMINAL WALL SITES

 Mid-line
 Umbilical area
 Inguinal region
 Femoral canal
 Para-median lineObturator

275
6 Abdominal Masses and Hernias

 Lumber area
 Obturator foramen
 Incisional or scar line
7.6 CLASSIFICATION

7.6.1 REDUCIBLE:
 The contents of the sac are reduced spontaneously or manually
7.6.2 IRREDUCIBLE
 The contents remain constantly outside
7.6.2.1 INCARCERATED
 Trapped or imprisoned
 Initially it is reducible, then it becomes irreducible  cannot be reduced
(either spontaneously or manually).
 Does not denote obstruction
 Blood supply remains intact
 Nausea, vomiting, and symptoms of bowel obstruction (possible).
7.6.2.2 OBSTRUCTED
 Contains obstructed intestine
 Small intestine obstruction presents with pallor and vomiting
 Large intestine obstruction presents with distention and constipation
 Blood supply remains intact
7.6.2.3 STRANGULATED
 A surgical emergency
 Likely in hernias with narrow necks
 Blood supply is seriously impaired rendering the contents ischemic 
 Gangrene may occur within 5-6 hours after the inset of symptoms
 Symptoms of an incarcerated hernia present combined with a toxic
appearance.
 Strangulation is probable if pain and tenderness of an incarcerated hernia
persist after reduction.
 The femoral hernia is the most liable to strangulation due to its narrow neck
and its rigid surroundings 
 The constricting agents that compress the blood supply are: (In order of
frequency)
o The Neck
o External ring in children
o Adhesions with the sac (rare)
 Symptoms
o Sudden pain over the hernia
o Nausea and vomiting
 Signs
o Tense and tender
o Absent cough impulse (non expansile) 

276
 Inguinal Hernia 7

7.6.2.4 INFLAMED
 Rare
 Due to inflammation on the sac contents, e.g. acute appendicitis or
salpingitis
8 INGUINAL HERNIA

 The most common form of hernia in both sexes

 Subdivided into direct and indirect
 In adult males it is most commonly indirect
8.1 SURGICAL ANATOMY

 Superficial ring: triangular aperture in the external oblique aponeurosis 1.25

cm above the pubic tubercle
 Deep ring: U-shaped condensation of the transversalis fascia 1.25 cm
above the inguinal ligament
 The inguinal canal:
o In infants the two triangular aperture are superimposed and the canal is
slightly oblique
o In adults it is 3.75-4 cm long
o In females, it contains the round ligament of the uterus Contains the
spermatic cord and round ligament of the uterus
o In males, it contains
 The ilioingunal nerve
 The spermatic cord and its
contents, which are
 Genital branch of the
genitofemoral nerve
 Testicular artery
 Pampiniform plexus of
veins
 Cremasteric muscle
fibers
 Cremasteric vessels
 Vas deferens
o Boundaries of the inguinal canal
 Anteriorly: external oblique aponeurosis
 Posteriorly: facia transversalis and conjoined tendon
 Superiorly: internal oblique aponeurosis
 Inferiorly: inguinal ligament

277
8 Abdominal Masses and Hernias

8.2 INDIRECT (OBLIQUE) INGUINAL HERNIA

 Most common of all forms at all age groups

 The male: female ratio is 20:1
 Travels down the inguinal canal on the outer side of the spermatic cord
 Its neck lies lateral to the inferior epigastric vessels
 Can be due to a congenital lesion i.e patent processus vaginalis
 Strangulation is common, but less than in femoral hernia
 Seen in young patients
 In adult males
o Mostly on the right side because of delayed decent of the right testicle
o 12% bilateral
8.3 DIRECT INGUINAL HERNIA

 Comes out forward via the posterior wall of the inguinal cana, at
Hasselbach’s (i.e. ingunal) triangle due to a defect of weekness of the facia
transversalis
 Always acquired, never congenital 
 Pantaloon
 It has a wide neck and therefore there is no hazard of strangulation  (Saddlebag) hernia is the
 The neck is medial to the inferior epigastric vessels simultaneous occurrence
 Does not attain a large size of a direct and an
indirect hernia. 
8.4 CLINICAL PRESENTATION OF INGUINAL HERNIA It causes two bulges
(medial and lateral) that
straddle the inferior
 Groin pain referred to the testicle epigastric vessels
 Cough impulse (Expensile) 
 A large hernia causes dragging pain Hasselbach’s triangle is
bounded by: 
 Presents as a swelling or fullness at the hernia site
-Inguinal ligament
 Aching sensation (radiates into the area of the hernia) inferiorly
 No true pain or tenderness upon examination -Inferior epigastric artery
 Enlarges with increasing intra-abdominal pressure and/or standing laterally
-Lateral border of rectus
8.5 DIFFERENTIAL DIAGNOSIS muscle medially

 Hydrocele

278
 Femoral Hernia 9

 Encysted hydrocele of the cord

 Varicocele
 Epididymoorchitis
 Testicular torsion
 Undescended testis
 Ectopic testis
 Testicular tumor
 Pseudohernia
 Femoral artery aneurysm
 Saphena varix (dilation of the saphenous vein at it’s junction with the
femoral vein in the groin)
 Spermatic cord lipoma
 Inguinal lymphadenopathy
 Psoas abscess
 Cutaneous lesions, e.g. sebaceous cyst, skin tumor
8.6 TREATMENT OF INGUINAL HERNIA  In adults, we do
herniotomy and
 Surgical repair: open vs laproscopic herniorrhaphy (repair)
because the problem is
8.7 ESSENTIAL STEPS FOR THE INGUINAL HERNIA REPAIR due to weakness.
In children, we do
 Complete division of the external oblique aponeurosis and the transversalis herniotomy only;
fascia because the problem is
 Differentiation between indirect and direct defects congenital, not muscle
weakness.
 Isolation of the spermatic cord
 Ligation and removal of the sac at the deep inguinal ring flush with
peritoneum
 Oblique reconstruction of the inguinal canal with an anterior and posterior
wall and an internal and external ring
9 FEMORAL HERNIA

 Commonly affecting females 

 Most liable to strangulation
 The hernia descends vertically to the saphenous opening
 Surgical anatomy
o Boundaries of the femoral sheath
 Anteriorly: inguinal ligament
 Posteriorly: Iliopectineal ligament, pubic bone and pectineus
muscle fascia
 Medially: lacunar ligament
 Laterally: femoral nerve
o The femoral canal
 The most medial compartment of the femoral sheath
 Extends from the femoral ring to the saphenous opening
 1.25 cm long and 1.25 cm wide at the base
 Contains fat, lymphatic vessels and the lymph node of
Cloquet

279
10 Abdominal Masses and Hernias

 Differential diagnosis
o Inguinal hernia
o Inguinal hernias are located above and medial to the inguinal
ligament and pubic tubercle, whereas femoral hernias are located
below and lateral to the inguinal ligament and pubic tubercle 
o Saphena varix
o Femoral lymphadenopathy
o Femoral artery aneurysm
o Psoas abscess
 Complications: Strangulation due to a narrow unyielding femoral ring
 Treatment: Surgical repair
10 UMBILICAL AND PARAUMBILICAL HERNIA

 Umbilical hernia is seen in infants and children

 The female: male ratio is 20:1
 PUH affects adults. The defect is either supra or infraumbilical through the
linea alba
 When enlarged, it becomes rounded or oval shaped
 May contain omentum, small intestine or transverse colon
 Etiology
o Obesity
o Flabbiness of the abdominal muscles
o Multiparity
 Clinical Features
o Irreducibility in PUH is due to omental adhesions within the sac
o Pain may be colicky due to parital or complete intestinal obstruction
 Treatment: Open (Mayo’s repair) or laproscopic repair (if the defect is more
than 4 cm)
11 INCISIONAL HERNIA

 Occurs in surgical scars and it has no actual neck (or its neck is wide), so it
does not lead to complications
 Causes
o Mechanical factors (increase in intraabdominal pressure
postoperatively)
 Prolonged ilius
 Chronic cough

280
 Epigastric hernia 11

 Repeated vomiting
 Lifting heavy objects in the immediate postoperative period
o Patient factors
 Infection
 Malnutrition
 Diabetes and chronic illness
 Steroid treatment
o Technical factors
 Too much tension on closure, or closure with absorbable
sutures
 Ischemia
 Clinical features: swelling at the scar associated sometimes with pain
 Treatment: Open or laparoscopic repair
12 EPIGASTRIC HERNIA

 Due to a defect in the linea alba between the xiphoid process and the
umbilicus
 Starts as a protrusion of the extraperitoneal fat at the site where a small
blood vessel pierces the linea alba
 If the protrusion enlarges, it drags a pouch of peritoneum after it
 Clinical features
o May be asymptomatic or painful, either locally or simulates peptic
ulcer pain
 Treatment: Mayo’s repair
13 RARE EXTERNAL HERNIAS

13.1 SPIGELIAN HERNIA

 Occurs at the space between the semilunar line and the lateral adge of the
rectus muscle (Inferior to the arcuate line)
 The posterior recuts sheath is lacking which contributes to the inherent
weakness in this ares
 Preoperative diagnosis is correct in only 50% of patients
 US and CT scan are helpful to confirm the diagnosis
 Approximation of the tissues adjacent to the defect with interrupted sutures
is curative. If the defect is large, it can be covered with mesh

281
12 Abdominal Masses and Hernias

13.2 LUMBAR HERNIAS

 Secondary lumbar
hernia develops as a
 Broad bulging hernias result of trauma, mostly
 Usually don’t get incarcerated surgical (e.g. renal
 Petit’s hernia surgery) or infection.
o Occurs in the inferior lumbar triangle which has the following Lumbar hernias were
boundaries encountered relatively
 Laterally: external oblique muscle frequently in the past in
cases of spinal
 Medially: latissimus dorsi tuberculosis with
 Inferiorly: iliac crest paraspinal abscesses
 Grynfeltt’s hernia
o Less common
o Occurs in the superior lumbar triangle which is bounded:
 Superiorly: inferior margin of the 12th rib
 Medially: sacrospinalis muscle
 Laterally: internal oblique muscle
13.3 OBTURATOR HERNIA

 The obturator canal is covered by a membrane pierced by the obturator

nerve and vessels. Weakening of the obturator membrane and
enlargement of the canal may result in the formation of a hernia sac. Which
can lead to intestinal herniation and obstruction
 Presentation could be with evidence of compression of the obturator nerve
leading to pain in the medial aspect of the thigh
 Treated by surgery
13.4 SLIDING HERNIA

 It is a hernia in which part of the posterior wall

of the sac is formed by a viscus
(intraabdominal organ), e.g. sigmoid colon,
cecum, ovary or portion of the bladder
 The wall of the hernial sac, rather than being
formed completely by peritoneum, is in part
formed by a retroperitoneal structure
 Bladder slides posterio-medially (PM) and the
colon posterio-lateral (PL)
13.5 OTHER

1. Richter’s hernia
a. It is a hernia at ant site in which only part of the circumference of the
bowel (usually jejunum) is involved
b. Only one side of the bowel wall is trapped in the hernia, rather than
the entire loop of bowel.
c. Does not usually obstruct but can strangulate or become
incarcerated 
d. This is especially dangerous because the incarcerated portion of
bowel can necrose and perforate in the absence of obstructive
symptoms.

282
 Methods of Hernia Repair 13

2. Littre’s Hernia
a. Any groin hernia that contains a Meckel’s Diverticulum,
b. Rare.
c. Usually incarcerated or strangulated
d. If the diverticulum is symptomatic or strangulated, it is mandatory to
excise it at the time of repair.
3. Divarication (Separation) of the recti abdominis (Diastasis recti)
a. Only a facial weakness, not a true hernia 
b. Seen more in elederly multiparous patients
c. A gap in the linea albe (medial margin of the recti) seen on straining
through which the abdominal contents bulge.
d. No treatment is necessary 
4. Perineal Hernias
a. Occur in the pelvic floor usually after surgical procedures such as an
abdominoperineal resection.
5. Peri- or para-stomal Hernia
a. Hernia adjacent to an ostomy “e.g. colostomy”.
6. Amyand’s Hernia
a. Hernia sac containing a ruptured appendix.
7. Hesselbach’s Hernia
a. Hernia under the inguinal ligament lateral to femoral vessels.
8. Cooper’s Hernia
a. Hernia through the femoral canal & tracking into the scrotum or labia
majus.
14 METHODS OF HERNIA REPAIR

14.1 OPEN TECHNIQUE (HERNIOTOMY AND REPAIR)

 Bassini repair
 Draning
 Shouldice
 McVay (Cooper’s ligament repair)
 Mesh (i.e. hernioplasty)
14.2 LAPAROSCOPIC REPAIT

 Two types
o TAPP (transabdominal preperitoneal) repair
o TEP (totally extraperitoneal) repair
 Indicated in only two conditions: 

283
14 Abdominal Masses and Hernias

o Bilateral hernia
o Recurrent hernia

15 HISTORY 
15.1 LUMP

 duration, first symptoms, associated symptoms, progression, persistent

,other sites ,cause
 Does it reduce on lying down?
 Has there been an episode of pain in the swelling?
 Has there been an episode of abdominal pain?
 Does the patient have any febrile symptoms?
15.2 HISTORY OF RECTAL BLEEDING

 Causes of increase of intrabdominal pressure.

 Previous surgeries?

16 PHYSICAL EXAM 
 Examine the patient in the standing and supine positions.
 Examine the patient from the front
Inspection
 lump: site shape
 scrotum: does it extend to the scrotum
Palpation
 Ask the patient about pain before you palpate
 Can you go above it
 Can you palpate the testis
 If it is a hernia  type
 Define pubic tubercle
Feel from the sides
 Aim to examine the lump.
 Tenderness, temperature, size ,shape, site, composition
 Reducible. Ask the pts if you couldn’t
 Controlled when you pressure over deep inguinal ring.
 Expensile cough impulse.
 Direction of reappearance.
Investigations
 CBC
 Leukocytosis may occur with strangulation.
 Electrolytes, BUN, creatinine levels :
 Assess the hydration status of the patient with nausea and vomiting.
 Urinalysis: narrowing the differential diagnosis of genitourinary causes of
groin pain.

284
 MCQs 15

 Imaging studies:
o Imaging studies are not required in the normal workup of a hernia.
o Ultrasonography. (obese)
o If an incarcerated or strangulated hernia is suspected:
 Flat and upright abdominal films to diagnose a small bowel
obstruction.
17 MCQS

1. Which of the following is true regarding femoral hernia?

a. Commonly seen in children.
b. It is the commonest hernia seen in females
c. usually presents with inguinal swelling
d. it is liable for complications
e. usually treated conservatively

2. The most common cause of an enlarged lymph node in the femoral

triangle
is
a. Tuberculosis lymphadenitis
b. Brucella
c. Neoplastic
d. Nonspecific lymphdenitis
e. Sarcoidosis

3. The first symptoms of strangulated Inguinal Hernia is:

a. Vomiting
b. Fever
c. Septic shock
d. Constipation
e. Pain

4. Inguinal Hernia:
a. Is more common in girls.
b. Hernioraphy is the treatment of choice.
c. Ultrasound is required to diagnose it.
d. Hernia sac may contain ovary, appendix, or omentum.
e. Direct inguinal hernia is more common than indirect.

5. Patent processus vaginalis results in:

a- indirect inguinal hernia
b- direct inguinal hernia
c- femoral hernia
d- umbilical hernia

6. The following are important steps in the management of strangulated

hernia except:
a. Nasogastric tube
b. Antibiotics
c. Conservative treatment till obstruction is relieved

285
16 Abdominal Masses and Hernias

d. Intravenous fluids
e. Consent for possible bowel resection

7. All of the followings are external hernias except:

a. Obturator hernia
b. Hiatal hernia
c. Femoral hernia
d. Lumbar hernia

8. The differential diagnosis of an inguinal swelling could include all of

the followings except:
a. Lipoma of the cord
b. Indirect inguinal hernia
c. Encysted hydrocele
d. Undescended testis
e. Varicocele

9. A 41 y/o woman is a known case of femoral hernia and was scheduled

to be operated later. She presented in the ER with severe pain over
the hernia and fever. On examination, the hernia was tense and
tender, and the cough impulse was negative. The diagnosis is:
a. Inflamed hernia
b. Strangulated hernia
c. Obstructed hernia
d. Incarcerated hernia

10. Boundaries of Hesselbach's triangle include all the followings

EXCEPT:
a. Lateral border of rectus muscle
b. Inferior epigastric artery
c. External iliac artery
d. Inguinal ligament

11. Which one of the following clinical future helps to differentiate

between inguinal hernia and hydrocele in children?
a. Reducibility
b. Scrotal swelling
c. Tenderness
d. Transillumination

 Answer Key  1D, 2D, 3E, 4D, 5A, 6C, 7B, 8E, 9B, 10C, 11A

286
 Mechanisms and Patterns of Injury 1

INTRODUCTION TO TRAUMA
1 MECHANISMS AND PATTERNS OF INJURY 
1.1 BLUNT INJURY

Classified into:
1. High-energy transfer (e.g. Car Accident).
2. Low energy transfer (e.g. Fall from a bicycle).
 Associated with multiple widely distributed injuries because the energy is
transferred over a wider area during blunt trauma.
1.2 PENETRATING INJURY

Classified into:
1. Stab wound.
2. Gunshot wound.
3. Shotgun.
 Damage is localized to the path of the bullet or knife.
2 PRE-HOSPITAL CARE

The objective of pre-hospital care is to prevent further injury, initiate resuscitation

and transport the patient safely and rapidly to the most appropriate hospital.
 Most important things in pre hospital care:
o Airway control.
o Fluid resuscitation.
 Transportation either by:
o Ground Ambulance, or
o Helicopter.
Initial evaluation and resuscitation of the injured patient in the ER is done using
Primary survey and secondary survey.

3 PRIMARY SURVEY “ T H E M O S T IM P OR T A N T”   The golden hour:

it’s the first hours of the
 The goal of primary survey is to identify and treat conditions that constitute patient arrival to the ER.
an immediate threat to life.
 Advanced trauma life support (ATLS) provides a structured approach to
the trauma patient with standard Algorithms of care.
 It emphasizes the “golden hour” concept that timely prioritized
interventions are necessary to prevent death.
 The ATLS Course refers to the primary survey as assessment of the “ABC”
(Airway with cervical spine protection, Breathing and Circulation). 
 Although the concepts within primary survey are presented in a sequential
fashion in reality they often proceed simultaneously. In details:

287
2 Introduction to Trauma

3.1 AIRW AY MANAGEMENT WITH CERVICAL SPINE PROTECTION

I. Conscious patient who do not show tachypnea and have normal voice do
not require early attention to the airway. (So you proceed to the next step!)
II. Patients with penetrating neck injuries and:
 An expanding hematoma.
 Evidence of chemical or thermal injuries to mouth, nares or hypopharynx.
 Extensive subcutaneous air in the neck.
 Complex maxillofacial trauma.
 Airway bleeding.
o In these cases elective intubation should be performed. These
patients may initially have a satisfactory airway but they may become
obstructed if soft tissue swelling, hematoma formation, or edema
progress.
III. Establishment of a definitive airway, immediate intubation, (i.e.
endotracheal intubation) is indicated in:
 Patients with apnea.
 Inability to protect the airway due to altered mental status.
 Impending airway compromise due to inhalation injury.
 Hematoma.
 Facial bleeding.
 Soft tissue swelling or aspiration.
 Inability to maintain oxygenation.
: Altered mental status is the most common indication for intubation in the ER for
traumatic patients.
3.1.1 OPTIONS FOR ENDOTRACHEAL INTUBATION INCLUDE:
3.1.1.1 NASOTRACHEAL INTUBATION:
It can be accomplished only in patients who are breathing spontaneously. The
primary application for this technique in Emergency Department (ED) is in those
patients requiring emergent airway support in whom chemical paralysis cannot be
used.
It is contraindicated in extensive maxillofacial injuries. Why? It may cause
further injury.
3.1.1.2 OROTRACHEAL INTUBATION:
It is the most common technique used to establish a definitive airway.
 Because all patients are presumed to have cervical spine injuries, manual
in-line cervical immobilization is essential especially in unconscious
patients in which we must protect the cervical spine.
 Correct endotracheal placement is verified with:
o Direct laryngoscopy, you see the tube heading to the vocal cords.
o Capnography, if you connect the patient on a ventilator you will see
high CO2, at least it’s in the trachea.
o Clinically: Audibility of bilateral breath sounds, by auscultation.
o And finally Chest X-Ray, only if the patient is stable.

288
 Primary Survey “the most important” 3

3.1.1.3 SURGICAL ROUTES:

3.1.1.3.1 CRICOTHYROIDOTOMY:
Patients in whom attempts at intubation have failed or who are precluded from
intubation due to extensive facial injuries .
It has no complications that affect the vessels because you go to the laryngeal
membrane directly (no stenosis).
3.1.1.3.2 EMERGENT TRACHEOSTOMY:
Is indicated in a patient with extensive laryngeal injury
It may cause complications that damage the vessels (stenosis).
3.2 BREATHING AND VENTILATION

Once a secure airway is obtained, adequate oxygenation and ventilation must be

assured. All injured patients should receive supplemental oxygen and be
monitored by pulse oximetry.
The following conditions constitute an immediate threat to life due to inadequate
ventilation and should be recognized during the primary survey. The main 3
conditions that you must take care of are :
1. Tension pneumothorax
2. Open pneumothorax
3. Flail chest with underlying pulmonary contusion
3.2.1 TENSION PNEUMOTHORAX
Tension pneumothorax is the accumulation of air in the pleural cavity with lung
making a one-way valve, allowing the air to enter without going out.
Diagnosis: Respiratory distress and hypotension in combination with any of the
following physical signs in patients with chest trauma:
 Tracheal deviation away from the affected side (e.g accumulation of air in
the right lung will deviate the trachea to the left side).  If there is a tension
 Lack or decreased breath sounds on the affected side.  pneumothorax on the
 Subcutaneous emphysema on the affected side. right side, this will push
the mediastinum to the
 Distended neck veins due to impendence of superior vena cava, but the left and kink the SVC
neck veins may be flat due to systemic hypovolemia. which lead to congestion
of the face and upper
1. In cases of tension pneumothorax, the parenchymal tear in the lung act limbs and distension of
as a one-way valve, with each inhalation allowing additional air to neck veins b/c there is
accumulate in the pleural space. obstruction of venous
return. This condition is
2. The normally negative intrapleural pressure becomes positive which known as “Superior
depresses the ipsilateral hemidiapgragm and shift the mediastinal Vena Cava Syndrome"
structures into the contralateral part of the chest. But if the patient is
hypovolemic, the veins
3. Subsequently the contralateral lung is compressed and the heart will not distend.
rotates about the superior and inferior vena cava, this decreases
venous return and ultimately decreases cardiac output, which results in
an immediate cardiovascular collapse.

289
4 Introduction to Trauma

Treatment:
 Immediate needle thoracostomy decompression with a 14-gauge
angiocatheter in the second intercostal space in the midclavicular line.
 Tube thoracostomy (chest tube) in the fifth intercostal space in the
midaxillary line immediately in the emergency department before the chest
radiograph.
3.2.2 OPEN PNEUMOTHORAX (OR SUCKING CHEST WOUND)
This occurs with full-thickness loss of the chest wall, permitting free communication
between the pleural space and the outer atmosphere.
This compromises ventilation due to equilibration of atmospheric and pleural
pressures, which prevents lung inflation and alveolar ventilation and result in
hypoxia and hypercarbia (↑CO2).
Treatment:
 Closure of the chest wall defect if it’s small and tube thoracostomy if it’s
large defect.
3.2.3 FLAIL CHEST
 It occurs when three or more contiguous ribs are fractured in at least two
locations
 Paradoxical movement of this free-floating segment of chest wall. 
 Rarely the additional work of breathing and chest wall pain caused by the
flail segment is sufficient to compromise ventilation.
 Resultant hypoventilation and hypoxemia may require intubation and
mechanical ventilation.
 Most of the time flail chest it associated with contusion of the lung
parenchyma.

  It occurs when multiple adjacent ribs are broken in multiple places,

separating a segment, so a part of the chest wall moves independently.
 The number of ribs that must be broken varies by differing definitions: some
sources say at least two adjacent ribs are broken in at least two places,
some require three or more ribs in two or more places.
 The flail segment moves in the opposite direction as the rest of the chest
wall: because of the ambient pressure in comparison to the pressure inside
the lungs, it goes in while the rest of the chest is moving out, and vice
versa.
 This so-called "paradoxical motion" can increase the work and pain
involved in breathing.
3.3 CIRCULATION WITH HEMORRHAGE CONTROL Diagrams depicting the
paradoxical motion observed
during respiration with a flail
I. Blood pressure and pulse should be measured manually at least every 5 segment
minutes for patient with significant blood loss until normal vital signs values
are restored.
II. Two peripheral catheters, 15- 16 gauge or larger in adults.
III. Fluid resuscitation. We start with crystalloids like normal saline or ringer’s
lactate but ringer’s is better. Normal saline contains large amount of Cl-

290
 Primary Survey “the most important” 5

which can lead to hyperchloremic metabolic acidosis and the patient is

already has metabolic acidosis.
IV. Blood should be drawn simultaneously and send for measurement of
hematocrit level, as well as for typing and cross-matching for possible blood
transfusion in patient with evidence of hypovolemia.
V. If peripheral angiocatheter access is difficult, saphenous vein cutdown at
the ankle provide excellent access.
VI. Additional venous access through femoral or subclavian vein (can be used
for central venous pressure (CVP) measurement).
VII. Intraosseous needle can be placed in the proximal tibia (preferred) or distal
femur of an unfractured extremity for fluid resuscitation in patient under 6
years of age.
VIII. External control of hemorrhage should be achieved promptly while
circulating volume is restored. Manual compression of open wounds with
ongoing bleeding should be done with single 4 x 4 gauze and a gloved
hand. Blind clamping of bleeding vessels should be avoided because
you may damage the vessels. 
 During the circulation section of the primary survey FOUR life-threatening
injuries must be identified:
a. Massive hemothorax “bleeding in the thorax”
b. Cardiac tamponade “bleeding in the myocardium”
c. Massive hemoperitoneum “bleeding in the abdomen”
d. Mechanically unstable pelvic fracture “bleeding in the pelvis”
 Those are the causes of massive hypotension in traumatic patients.
 If the patient has hypotension and you couldn’t find a source of bleeding when
looking in the abdomen and chest. Think of cardiac tamponade, as it is very
commonly missed. 
 THREE critical tools used to differentiate these in multisystem trauma patient
a. Chest radiograph
b. Pelvis radiograph
c. Focused Abdominal Sonography for Trauma (FAST)
 The FAST is performed as part of the initial evaluation of the trauma
patient in the emergency center. It consists of four separate views of
four anatomic areas:
1. The right upper abdomen (Morison's space between liver and
right kidney).
2. The left upper abdomen (perisplenic and left perirenal areas).
3. Suprapubic region (perivesical area).
4. Subxyphoid region (pericardium).
3.3.1 IMMEDIATE TREATMENT:
3.3.1.1 MASSIVE HEMOTHORAX
 Clinically, if you listen to the chest there will be no breathing sounds on the
affected side.
 Tube thoracostomy to facilitate lung re-expansion.
 Massive hemothorax (if the tube drain >1500 ml).
 If blood is seen it’s an indication for operative intervention.

291
6 Introduction to Trauma

3.3.1.2 CARDIAC TAMPONADE

 Pericardial drain under ultrasound guidance.
 Followed by operative intervention.
3.3.1.3 MECHANICALLY UNSTABLE PELVIS FRACTURE
 Pelvis fracture.
 Immediate external fixation.
3.3.1.4 MASSIVE HEMOPERITONEUM WITH HEMODYNAMIC
UNSTABILITY
 Fluid resuscitation
 Immediate surgical intervention with shock patients
3.3.1.4.1 SHOCK CLASSIFICATION AND INITIAL FLUID RESUSCITATION
Classic signs and symptoms of shock: are tachycardia, hypotension,
tachypnea, mental status changes, diaphoresis and pallor. The quantity of acute
blood loss correlates with physiologic abnormalities.
1. Tachycardia is often the earliest sign of ongoing bleeding. And it is not
reliable in old patients or patients on beta-blockers.
2. Hypotension is not reliable early sign of hypovolemia, because blood
volume must decrease by >30% before hypotension occurs.

Signs and Symptoms of Advancing Stages of Hemorrhagic Shock 

Class I Class II Class III Class IV

Blood loss (ml) Up to 750 750 – 1500 1500 – 2000 > 2000
Blood loss (% BV) Up to 15% 15 – 30% 30 – 40% >40 %
Pulse Rate <100 >100 >120 >140
Blood Pressure (mmHg) Normal Normal Decreased Decreased
Pulse Pressure Normal or Decreased Decreased Decreased
Increased
Respiratory Rate 14 – 20 20 – 30 30 – 40 > 35
Urine Output (ml/hr) >3 20 – 30 5 – 15 Negligible
“Anuria”

CNS/Mental Status Slightly anxious Mildly anxious Anxious and Confused and
confused Lethargic

 Fluid resuscitation begins with a 2 L (Adult) or 20 ml/kg (child) IV bolus of

isotonic crystalloid, typically Ringers’s Lactate.
 For persistent hypotension, this is repeated once in an adult and twice in a
child before red blood cells (RBCs) are administered.
 Urine output is a quantitative reliable indicator of organ perfusion. Adequate
urine output is 0.5 ml/kg per hour in an adult, and 1 ml/kg per hour in a
child. 

292
 Secondary Survey 7

 Based on the initial response to fluid resuscitation, hypovolemic injured

patients can be separated into three broad categories:
1. Responders “BP will stabilize”
2. Transient responders “BP will improve and then it will fall down again
which means there an active bleeding”
3. Non-responders “which means there is a major bleeding that you can’t
control by resuscitation.”
Before you go to the secondary survey you have to make sure that there is no life
threatening condition is missed.
4 SECONDARY SURVEY

 Once the immediate threats to life have been addressed, a thorough

history is obtained and the patient is examined from top to toe to ensure
that no wound, bruise or swelling is missed.
 The back and spine are examined with the patient “log-rolled”, looking
specifically for localized tenderness, swelling, bruising or a “step”.
 The perineum is examined and a rectal examination is performed to
evaluate for sphincter tone, presence of blood, rectal perforation, or high
riding prostate, this is particularly critical in patients with suspected spinal
cord injury, pelvic fracture, or transpelvic gunshot wounds. 
 Vaginal examination with speculum should be performed in women with
pelvic fractures to exclude an open fracture.
 In edition to physical examination the following should be done:
1. Continuous vital signs monitoring.
2. Central venous pressure (CVP) Monitoring.
3. ECG Monitoring.
4. Nasogastric Tube Placement, which is contraindicated in complex
maxillofacial injury or fractures of the base of the skull and should be
passed orally.
o It evaluates the stomach content for blood, which may suggest
gastro- duodenal injury.
o If it passed to the chest it may suggest diaphragmatic injury.
5. Foley Catheter Placement:
o To monitor the urine output-Foley Catheter placement should be
deferred after urological evaluation in patients with signs of urethral
injury (Blood at the meatus, perineal or scrotal hematoma, or a
high riding prostate on the PR exam.).
6. Repeat FAST as needed.
7. Laboratory Measurement.
8. Radiographs:
o Selective radiography and laboratory tests are done early after the
primary survey.
o For patients with severe blunt trauma the following radiograph
should be done:
1. Lateral Cervical Spine X-R
2. Chest X-R
3. Pelvis X-R

293
8 Introduction to Trauma

o For patients with truncal gunshots wound, anteriorposterior and

lateral radiographs of the chest and abdomen should be done with
marking the entrance and exit sites with metallic clips or stables.
o In critically injured patient we obtain blood sample for:
1. Type and Cross- Matching.
2. Complete Blood Count
3. Blood Chemistry
4. Coagulation Studies
5. Lactate Level
6. Arterial Blood Gas Analysis “ABG”
5 MCQS
1. Which of the following is true concerning traumatic pneumothorax:
a. Needle aspiration is the treatment of choice
b. The commonest type of chest injury
c. Definitive treatment by intercostals tube drainage
d. The main factor causing respiratory distress in flail chest
e. Present with stridor

2. Two hours post Rt subclavian central venous catheter insertion, patient

started to complain of Rt sided chest pain, shortness of breath, taccypnea,
and he is tacchycardic. There is decrease air entry to the Rt side. The most
likely diagnosis is:
a. Hemothorax
b. Air embolism
c. Line was inserted in the artery
d. Pneumothorax



3. The proper management of the previous patient is:
a. Chest tube
b. Removal of the line
c. Intubation
d. Aspiration of the gas from the line

4. Immediate life-saving attention is required for a trauma victim who suffers

any of the following conditions except:
a. Airway obstruction
b. Fracture of the femoral shaft
c. Massive flail chest
d. Open pneumothorax
e. Tension pneumothorax


5. The most common chest injury is:

a. Pneumothorax
b. Hemothorax
c. Sternal fracture
d. Rib fracture
e. Pulmonary contusion

294
 MCQs 9

6. In laparoscopic procedures:
a. CO is used for insufflation
b. The umbilical trocar is commonly used for the camera
c. Bowel perforation occurs more commonly with the open method for
trocar
 insertion
d. Diathermy is not used because of risk of explosion
e. The pressure in the abdomen can be raised safely up to 35mmHg

 

7. The following are adverse prognostic factors in head injury except:
a. Hypertension.
b. Poor Glasgow Coma Score on admission.
c. Hypotension.
d. Age > 65 years.
e. Non of the above

8. The Glasgow coma scale (GCS) is dependent upon the following except:
a. Response to speech
b. Response to pain
c. Response of the pupils
d. Best response
e. Response of the patient

9. Severe head injury is defined as Glasgow Coma Score (GCS) of:

a. 3
b. 3-9
c. 10
d. 11-12
e. 13-15

10. The outcome of head injuries:

a. Depends upon the severity of head injury
b. Most of minor head injured are able to return to work
c. Only about a third of severe head injured make good recovery
d. All the above
e. None of the above

11. The adverse prognostic factors for the development of acute subdural
haematoma include the following except:
a. Old age
b. Young age
c. Chronic alcoholism
d. Skull fracture
e. Anticoagulation therap

12. The source of bleeding in the subdural space are all true except:
a. Bridging veins into the superior sagittal sinus.
b. Bridging vein of Labbe
c. Cerebral contusion
d. Sinus bleeding
e. Fracture haematoma

295
10 Introduction to Trauma




13. Extradural haematoma, (the following are correct except):
a. Is more common than acute subdural haematoma
b. Is more often associated with vault skull fracture
c. Is caused by rupture of bridging veins
d. Is more likely to expand
e. Is more likely to be arterial in origin

14. Mortality from trauma occurs mostly:

a. Immediately at the scene
b. During the first hour from the accident
c. After admission to the hospital
d. In the intensive care unit (ICU)
e. Just before discharge from the hospital

15. Which one of the following is a life threatening injury

a. Pneumothorax
b. Hemothorax
c. Head injury
d. Fractured ribs
e. Compound fracture of the leg

16. Paradoxical breathing is associated with:

a. Bilateral ribs fracture
b. Massive hemothorax
c. Tension pneumothorax
d. Hypoxemia
e. Pulmonary contusion

17. A polytraumatized patient who arrives to the emergency department alive

but unconscious is best managed by:
a. Adrenalin infusion
b. Blood transfusion
c. Cardiopulmonary compressions
d. Endotracheal intubation
e. Intravenous fluids resuscitation

18. In hemodynamically stable trauma patient, intraabdominal injury is best

assessed by:
a. Clinical abdominal examination
b. CT scan
c. Diagnostic peritoneal lavage (DPL)
d. Four quadrants peritoneal tapping

19. The best method to stop continuous bleeding from pelvic fracture is by:
a. Applying mass trousers
b. Insertion of external fixators
c. Internal fixation
d. Internal pelvic packing

 Answers: 1:d, 2:a, 3:a, 4:b, 5:d, 6:b, 7:e, 8:c, 9:b, 10:d, 11:b, 12:e, 13:c, 14:b, 15:c, 16:a, 17:d, 18:b, 19:b.
296
 Introduction 1

TRAUMA CARE
1 INTRODUCTION

1.1 COURSE OBJECTIVES

 Importance of Trauma Care

 Principles of primary and secondary assessments.
 Establish management priorities
1.2 THE NEED

 The leading cause of death in the first four decades of life

 More than 5 million trauma-related deaths each year worldwide.
 Motor vehicle crashes cause over 1 million deaths per year. (we don't call it
accidents b/c it's preventable)
 Injury accounts for 12% of the world’s burden of disease.
1.3 TRIMODAL DEATH DISTRIBUTION

Immediate: you have

to prevent it (seatbelt)!
- Early: Get the patient to
the hospital (golden
hour)
- Late: complications e.g.
infection, multi-organ
failure

2 ADVANCED TRAUMA LIFE SUPPORT CONCEPT (ATLS)

 ABCDE approach to evaluation and treatment

 Treat greatest threat to life first
 Definitive diagnosis not immediately important
 Time is of the essence
 Do no further harm

297
2 Trauma Care

2.1 ABCDE APPROACH 

 Airway with c-spine protection

 Breathing / ventilation / oxygenation
 Circulation: stop the bleeding!
 Disability / neurological status
 Expose / Environment / body temperature
2.2 INITIAL ASSESMENT AND MANAGEMENT

 Primary survey and resuscitation of vital functions are done simultaneously

using a team approach.
2.2.1 QUICK ASSESSMENT 
What is a quick, simple way to assess a patient in 10 seconds?
 Identify yourself
 Ask the patient his or her name
 Ask the patient what happened
An appropriate response to the previous question confirms the following:
 Patent’s Airway
 Sufficient air reserve to permit speech
 Sufficient perfusion to permit cerebration
 Clear sensorium
2.3 ADVANCED TRAUMA LIFE SUPPORT OBJECTIVES

 Apply principles of primary and secondary surveys

 Identify management priorities
 Institute appropriate resuscitation and monitoring procedures
 Recognize the value of the patient history and biomechanics of injury
 Anticipate and manage pitfalls

298
 Primary Survey 3

2.4 STANDARD PRECAUTIONS

 Cap
 Gown
 Gloves
 Mask
 Shoe covers
 Goggles / face shield
3 PRIMARY SURVEY 

The priorities are the same for all patients

 Airway with c-spine protection
 Breathing with adequate oxygenation
 Circulation with hemorrhage control
 Disability
 Exposure / Environment
Special Considerations
 Trauma in the elderly
 Pediatric trauma
 Trauma in pregnancy
3.1 AIRW AY 

 Establish patent airway and protect c-spine

 Basic Airway Techniques:
1. Chin-lift Maneuver
2. Jaw-thrust Maneuver

Chin-lift Maneuver

Jaw-thrust Maneuver

299
4 Trauma Care

 Advanced Airway Techniques: orotracheal intubation

 Pitfalls (Unexpected difficulties):
o Occult airway injury
o Progressive loss of airway
o Equipment failure
o Inability to intubate
3.2 BREATHING

Assess and ensure adequate oxygenation and ventilation 

 Respiratory rate
 Chest movement
 Air entry
 Oxygen saturation
 Pitfalls (Unexpected difficulties):
o Airway versus ventilation problem?
 latrogenic pneumothorax or tension pneumothorax
3.2.1 THE IMMEDIATE LIFE THREATENING INJURIES
 Laryngeotracheal injury / Airway obstruction
 Tension pneumothorax
 Open pneumothorax
 Flail chest and pulmonary contusion
 Massive hemothorax (> 1.5 L) 
 Cardiac tamponade
3.2.2 MANAGEMENT 
 Where to insert chest tube?
o 5th intercostal space, anterior to the mid axillary line.
 How to manage tension pneumothorax?
o Needle to the 2nd intercostal space at the mid axillary line (needle
thoracostomy) followed by Chest tube!
 How to manage open pneumothorax?
o Placement of dressing secured on 3 sides to create (flutter-valve)
because securing on 4 sides will cause tension pneumothorax, a chest
tube distant from injury must then be placed.
 How to manage hemothorax?
o Chest tube, if the bleeding didn't stop, the patient must be taken to the
OR
 How to manage cardiac tamponade in trauma?
o Heart injured, needle pericardiocentasis or pericardial window can be
immediately life-saving. Thoracostomy is the definitive treatment with
repair of injury
3.3 CIRCULATION 

 Level of consciousness
 Skin color and temperature
 Pulse rate and character

300
 Primary Survey 5

3.3.1 CIRCULATORY MANAGEMENT:

 Control hemorrhage
 Restore volume
 Reassess patient
 Lethal triad: [ Hypothermia, Coagulopathy and Acidosis ] 
 Pitfalls (Unexpected difficulties):
o Elderly
o Children
o Athletes
o Medications
3.3.2 WHAT ARE THE CAUSES OF HYPOTENSION IN TRAUMA? 
 Bleeding in the chest - Dx: by Examination & X-ray
 bleeding in the abdomen - Dx: Fast , DPL, abdominal distention
 Bleeding in the pelvis - pelvis is moving with hypotension!
 External bleeding
 bleeding at the site of trauma
3.4 DISABILITY 

 Baseline neurologic evaluation

 Glasgow Coma Scale Score
 Pupillary response
 Observe for neurologic deterioration

3.5 EXPOSURE / ENVIRONMENT 

 Completely undress the patient

 Prevent hypothermia
 Check for missed injuries

301
6 Trauma Care

4 RESUSCITATION

 Protect and secure airway

 Ventilate and oxygenate
 Stop the bleeding!
 Vigorous shock therapy
 Protect from hypothermia
5 ADJUNCTS TO PRIMARY SURVEY

 X-rays to any trauma patient:

o C-spine x-ray
o Chest x-ray
o Pelvic x-ray
 Diagnostic Tools:
o FAST (Focused Assessment with Sonography for Trauma)
o DPL (diagnostic peritoneal lavage)
 Consider Early Transfer
o Use time before transfer for resuscitation
o Do not delay transfer for diagnostic tests
 Primary survey should take 10 – 20 minutes

6 SECONDARY SURVEY 

 The complete history and physical examination.

When do I start the secondary survey?
 Primary survey is completed
 ABCDEs are reassessed
 Vital functions are returning to normal
6.1 COMPONENTS OF THE SECONDARY SURVEY:

 History: Allergies, Medications, Past illnesses, Last meal, Events /

Environment / Mechanism.
 Physical exam: Head to toe
 Complete neurologic exam
 Special diagnostic tests
 Reevaluation
6.1.1 HEAD

302
 Secondary Survey 7

 External exam
 Scalp palpation
 Comprehensive eye and ear exam
 Including visual acuity
Pitfalls:
 Unconsciousness
 Periorbital edema
 Occluded auditory canal
6.1.2 MAXILLOFACIAL
 Bony crepitus
 Deformity
 Malocclusion
Pitfalls:
 Potential airway obstruction
 Cribriform plate fracture
 Frequently missed
6.1.3 NECK (SOFT TISSUES)
 Mechanism: Blunt vs penetrating
 Symptoms: Airway obstruction, hoarseness
 Findings: Crepitus, hematoma, stridor, bruit
Pitfalls:
 Delayed symptoms and signs
 Progressive airway obstruction
 Occult injuries
6.1.4 CHEST
 Inspect
 Palpate
 Percuss
 Auscultate
 X-rays
Potential life threatening injuries:
 Blunt cardiac injury
 Traumatic aortic disruption
 Blunt esophageal rupture
 Traumatic diaphragmatic injury
6.1.5 ABDOMEN
 Inspect / Auscultate
 Palpate / Percuss
 Reevaluate
 Special studies
Pitfalls:

303
8 Trauma Care

 Hollow viscous injury

 Retroperitoneal injury
6.1.5.1 INDICATIONS FOR LAPAROTOMY – BLUNT TRAUMA:
 Hemodynamically abnormal with suspected abdominal injury (DPL /FAST)
 Free air
 Diaphragmatic rupture
 Peritonitis
 Positive CT
6.1.5.2 INDICATIONS FOR LAPAROTOMY – PENETRATING TRAUMA:
 Hemodynamically abnormal
 Peritonitis
 Evisceration
 Positive DPL, FAST, or CT
6.1.6 PERINEUM
 Contusions, hematomas, lacerations, urethral blood
6.1.7 RECTUM
 Sphincter tone, high-riding prostate, pelvic fracture, rectal wall integrity,
blood
6.1.8 VAGINA
 Blood, lacerations, Urethral injury, Pregnancy
6.1.9 PELVIS
 Pain on palpation
 Leg length unequal
 Instability
 X-rays as needed
Pitfalls:
 Excessive pelvic manipulation
 Underestimating pelvic blood loss

6.1.10 EXTREMITIES
 Contusion, deformity
 Pain
 Perfusion
 Peripheral neurovascular status
 X-rays as needed
6.1.11 MUSCULOSKELETAL
 Potential blood loss
 Missed fractures
 Soft tissue or ligamentous injury

304
 Pain Mangment 9

 Compartment syndrome (especially with altered sensorium / hypotension)

6.1.12 NEUROLOGICAL EXAM
 Brain
o GCS
o Pupil size and reaction
o Lateralizing signs
o Frequent reevaluation
o Prevent secondary brain injury (Early neurosurgical consult)
 Spinal Assessment Early neurosurgical
o Whole spine consult
o Tenderness and swelling
o Complete motor and sensory exams
o Reflexes Altered sensorium
o Imaging studies - Inability to cooperate
 Spine and Cord: Conduct an in-depth evaluation of the patient’s spine and with clinical exam
spinal cord
6.2 ADJUNCTS TO SECONDARY SURVEY Early neurosurgical
orthopedic consult
 Special Diagnostic Tests as Indicated
Pitfalls:
 Patient deterioration
 Delay of transfer
 Deterioration during transfer
 Poor communication
6.3 HOW TO MINIMIZE MISSED INJURIES?

 High index of suspicion

 Frequent reevaluation and monitoring
7 PAIN MANGMENT

 Relief of pain / anxiety as appropriate

 Administer intravenously
 Careful monitoring is essential
8 TRANSFER

Which patients do I transfer to a higher level of care?

 Those whose injuries exceed institutional capabilities:
1. Multisystem or complex injuries
2. Patients with comorbidity or age extremes
When should the transfer occur?
 As soon as possible after stabilization
Which patients do I transfer to a higher level of care?
 Airway and ventilatory control

305
10 Trauma Care

 Hemorrhage control
8.1 TRANSFER TO DEFINITIVE CARE

306
 Overview 1

SPECIFIC ORGAN ABDOMINAL

TRAUMA
1 OVERVIEW

 Trauma is a major cause of death after IHD and malignancies.

 Trauma is considered the leading cause of death in the young population
with ages that vary between 1 and 35 years.
 If trauma didn’t cause death, it can cause any type of disability for a large
group of people per minute.
 Trauma care account up to 7% of all hospital care which is a big budget.

There is no specific organ trauma, so abdominal trauma comes with multiple

traumas.

1.1 ROAD TRAFFIC ACCIDENTS

 Road traffic accident (RTA) is one of the good examples of trauma and it
is the most common trauma.
 RTA is the third leading cause of death after IHD and cancer.
 How to reduce trauma due to RTA?
o Roads should be in a good shape.
o Every person should make a complete check up for his car every
once in a while, such as: breaks, water the car, wheels... etc.
o Drivers should follow the rules which include: wearing the seat belt,
not to drive while person is drunk or on drugs, follow the road signs,
not to exceed the assigned speed and so on.
o Medical care: there should be very good equipments/machines at the
ERs with qualified staff.
2 TYPES OF TRAUMA Blunt trauma: injury
incurred when the
 There are different types of traumas; the types are classified according to human body hits or is hit
the Mechanism of trauma. by a large outside object
(as a car).
 A patient can either get one of these types or a combination of them.
 Types of trauma: Blast trauma: injury
caused by the explosion
o Blunt trauma: Road traffic accident is the major cause of blunt of a bomb (especially in
trauma. enclosed spaces)
o Penetrating
o Burns
o Blast
3 ABDOMINAL TRAUMA

 The majority of abdominal injuries are due to blunt abdominal trauma (90%)
secondary to high speed automobile accidents.

307
2 Specific Organ Abdominal Trauma

3.1 ANATOMICAL REGIONS OF THE ABDOMEN

 Peritoneum:
o Intra thoracic abdomen:
It is under the costal margin. Contains the liver, spleen, stomach,
and pancreas.
It is hard to examine it.
o True abdomen:
It can be clinically examined.
 Retroperitoneal:
o Pancreas & Duodenum
o Bowel
o Vascular( IVC , aorta )
o Kidneys, ureter
o Pelvic abdomen: bladder, female genital system
o It is not accessible during physical examination, investigations are
needed.

3.2 TYPES OF THE ABDOMINAL TRAUMA

 Blunt abdominal trauma: ( take about 90 % of trauma )
o Sometimes doctors miss such cases because a patient with a blunt
abdominal trauma can come walking to the ER. Some doctors take
superficial history and physical examination and let the patient go
home without admitting him. At the mean time, the patient would be
bleeding slowly from the inside and in an hour he would collapse.
Patients who come to the ER because of trauma should be
examined from head to toe whether they came walking and
conscious or not.
 Penetrating abdominal trauma: It is to diagnose and manage.
3.3 MANAGEMENT OF TRAUMA PATIENTS
 The primary management of abdominal trauma is determination that an
intra abdominal injury exists and operative intervention is required.
 Many deaths would have been preventable if there wasn’t a failure in
managing the abdominal injuries.
 Causes of the failure of management includes:
1- Delay in ambulance to arrive, traffic jam, wrong place of hospitals,
no good qualified hospital, and non well equipped hospitals.
2- Many patients die because doctors don’t do ABC
 When you receive a trauma case always assume that there is injury even if
the patient came walking to you until proven otherwise by history clinical
presentation and investigations.

308
 Abdominal Trauma 3

3.3.1 PRIMARY SURVEY

 The resuscitation & Management priorities of patient with major abdominal
trauma are:
1) ABCDE of emergencies (must be done to all trauma patients):
 Airway: intubation if the airway is damaged.
 Breathing: if breath sounds were absent, insert a chest tube
immediately. No O2 for 15 minutes will cause a disability.
 Circulation: If there was bleeding (hemorrhage), control should
be initiated. Give IV fluids (usually crystalloids and normal
saline) and control the bleeding.
 Disabilities
 Exposure: cut the clothes.
2) Usage of Nasogastric tube. It is contraindicated if there was bleeding
from the nose or mouth.
3) Usage of urinary catheter to monitor the output and input. It is
contraindicated If there was bleeding from the urethra.

3.3.2 SECONDARY SURVEY

 History: History is taken from the patient himself, if he was conscious, if not
it is taken from the person who attended or the paramedic.
o Blunt trauma
o Penetrating trauma  immediately to surgery
 Physical examination: General and abdominal examination
 Sometimes there is no time for Secondary survey.
 Abdominal Examination: Inspection, Palpation, Percussion, Auscultation,
Rectal Examination, and Vaginal Examination.

3.3.2.1 INVESTIGATIONS:
 Blood Tests
 Radiological Studies (Plain abdominal X-ray , CXR)
 Diagnostic Peritoneal Lavage (DPL):
o Indicated when the patient is in a shock or suffering from abdominal
distention.
o It is extremely reliable; it can determine the presence of blood in the
peritoneal cavity up to 98% of the cases.
o When positive take the patient to the OR immediately.
o If the results weren’t so accurate and clear, insert a liter of saline and
if fresh blood appears then it is positive.
 If the patient is stable you do:
o USG abdomen
o CT abdomen
o Peritoneoscopy (diagnostic laparoscopy)

309
4 Specific Organ Abdominal Trauma

3.3.3 INDICATIONS FOR SURGERY- LAPROTOMY

1. If there were any signs of peritoneal injury such as tenderness, distention,
guarding, bruising and so.
2. Unexplained shock (If you give a lot of fluid but your patient is still in a
shock).
3. Evisceration of viscus (If the bowel was out).
4. Positive DPL – diagnostic peritoneal lavage.
5. Determination of finding: During routine follow up on investigations.
a. Sometimes you need to admit the patient for observation or admit
them to the ER for 6 hours then signs will start to appear.
b. Ex: Patient came conscious with injury for conservative therapy to
the ER and got admitted, after 4-6 hours he went into a shock.
4 SPECIFIC ORGAN TRAUM A

 Peritoneal:
o Liver: protected by ribs.
o Spleen: it is a mobile organ.
o Kidneys: in the retroperitoneal, it is not easy to injure so if it was
injured it will be a severe trauma.
o Bowel
 Retroperitoneal:
o Pancreas & Duodenum
o Bowel
o Vascular( IVC , aorta )
o Kidneys, ureter
 Geneto-urinary system:
o Urinary bladder, urethera (it is easy to diagnose if there was a
fracture in the pelvis)
o Female reproductive system
4.1 LIVER TRAUMA If you found a gunshot or
a stab in the fifth
 th
Liver is the largest organ in the abdominal cavity “5 intercostal space” intercostal space,
 Any trauma under the nipple we expect liver; it means the liver is injured. assume that the liver is
injured.
 Most commonly injured organs in all patients with abdominal Trauma.
 Commonest organ injured in case of penetrating trauma.

4.1.1 MECHANISM OF INJURY

 In blunt trauma:
 Hepatic injuries result from direct blows
 compression between the lower ribs on right side and the spine
 Shearing at fixed points secondary to deceleration.
 Any penetrating gunshot, stab or shotgun wound below the right
nipple on right upper quadrant of the abdomen is also likely to
cause a hepatic injury.

310
 Specific Organ Trauma 5

4.1.2 DIAGNOSIS AND INVESTIGATIONS

 Clinical manifestations:
o Often made at laparotomy in patients presenting with penetrating
injuries requiring immediate Surgery or in shock.
o Blunt Trauma: patients who remain in a shock or present with
abdominal rigidity, you do no further investigation and you take him
to the OR immediately.
 Investigations:
o Diagnostic peritoneal lavage (DPL)
o CT Scan abdomen: used to diagnose intra peritoneal injuries in
stable patients after blunt trauma

Figure: Gunshot below the nipple, Right side hemothorax,

grade 3. The patient is stable; there is no blood in the
peritoneal cavity. In this case the patient will go with
conservative management, if he bleeds, he must be taken
to the OR and if there was another injury take him to the
OR and deal with all the injuries.

4.1.3 MANAGEMENT
 When the patient comes to ER, the initiate management should be uniform:
 ABCDE: regardless what injury you have.
 Non-operative approach:
o Not all patients with liver injury need operation. It is determined by
CT scan.
o The criteria for non-operative approach is:
 Simple hepatic laceration Or intra hepatic hematoma
 No evidence of active bleeding
 Intra peritoneal blood loss less than 250 ml
 Absence of other Intra peritoneal injuries “ spleen , bladder,..”
that requires surgery
 Operative approach:

311
6 Specific Organ Abdominal Trauma

o Persistent hypotension, despite adequate volume replacement,

 The Pringle
suggests ongoing blood loss and mandates immediate operative maneuver is a surgical
intervention maneuver used in some
abdominal operations. A
o Classification: This classification is based on operative findings large hemostat is used to
and management. So hepatic injury is classified into: clamp the
a. Grade 1: Simple injuries – non bleeding. Conservative treatment hepatoduodenal
ligament interrupting the
if no bleeding or other injuries. flow of blood through the
b. Grade 2: Simple injuries managed by superficial suture alone if hepatic artery and the
portal vein and thus
you opened the patient. Conservative treatment if no bleeding or helping to control
other injuries. bleeding from the liver.
c. Grade 3: Major Intra parenchymal with active bleeding but not
requiring inflow occlusion (Pringle maneuver) to control
hemorrhage. Some of the patients go for conservative treatment
others go for OR.
d. Grade 4: Extensive Intra parenchymal injury with major active
bleeding requiring inflow occlusion for haemostatic control.
Needs operation and do Pringle manoeuvre.
e. Grade 5: Juxtahepatic venous injury (injuries to retrohepatic
cava or main hepatic veins) portal vein injury. Patients in this
grade are less likely to survive
o All patients undergoing laparotomy for trauma should be explored
through midline incision (from xiphisternum to pubic” around the
umbilicus go up or down) because you do not know where is the
lesion.
o Management according to classification: Figure:
a. Grades 1 & 2: Simple injuries can be managed by any one of Finger fraction: the injury
in the liver is small, you
variety of methods: if we open it simple suture, electrocautery, will open the liver
tropical hemostatic agents, etc. Does not require drainage. according to the injury,
b. Grade 3: Major intra-parenchymal injuries with active bleeding start ligating the blood
vessels then ligating the
can be managed best by Finger Fracturing the hepatic ducts. Then omental
parenchyma and ligating or repairing lacerated blood vessels & packing: put omentum in
between and suture it
bile ducts under direct vision because it will cause
c. Grade 4: Extensive intraparenchynal injuries with major rapid hemostasis.
blood loss require occlusion of portal trial to control hemorrhage.
It might need liver resection, lobe resection, and ligation of
intrahepatic artery. It is rarely saved.

312
 Specific Organ Trauma 7

Summary:
 Simple techniques: Simple techniques include drainage only of non-bleeding injuries,
application of fibrin glue, sutures “hepatorrhaphy” and application of surgical (I & II).
 Advanced techniques: Advanced Techniques of Repair (III & IV) all performed with Pringle
Maneuver in place
 Types of repair:
1) Extensive hepatorrhaply
2) Hepatotomy with selective vascular ligation
3) Omental pack
4) Resectional debridement with selective vascular ligation
5) Resection
6) Selective Hepatic Artery Ligation “remember liver is regenerate”
7) Peri-hepatic packing: If you can’t deal with a patient, just pack the patient and send
him to a center where he will be treated. Also, if you did what you have to do but
the bleeding didn’t stop, pack your patient and send him to another hospital.

4.1.4 COMPLICATIONS AND MORTALITY

 Recurrent bleeding
 Hematobilia: blood will go to the bile duct and the patient will bleed per
rectum.
 Perihepatic abscess then Biliary Fistula later on.
 Billiary Fistula
 Intrahepatic Haematoma
 Pulmonary Complications
 Coagulopathy: because of a lot of blood transfusion.

4.2 SPLENIC TRAUMA

4.2.1 GENERAL CONSIDERATIONS

 The spleen remains the most commonly injured organ in patients who have
suffered blunt abdominal trauma
 Involved frequently in penetrating wounds of the left lower chest and upper
abdomen.
 Management of the injured spleen has changed radically over the past
decade.
 The spleen is now recognized as an important immunological factory as
well as a reticuloendothelial filter. The problem is when spleen has a
disease; splenomegaly;- malaria, portal hypertension makes it more
susceptible to be damaged from simple trauma and you will find the patient
collapsed.
 Although the risk of over whelming post- splenctomy sepsis (OPSS) is
greatest in children less than 2 years, recognition of OPSS has stimulated
efforts to (Conserve spleen) by splenorrhaphy (either by repair or leave
according to grade).

313
8 Specific Organ Abdominal Trauma

4.2.2 MECHANISM OF INJURY

 Commonly injured in patients with blunt abdominal trauma because of its
mobility.
 Most civilian stab wounds and gunshot wounds cause simple lacerations
through injuries.
 It is of interest that 2% of patients who are undergoing a surgery in the LUQ
of the abdomen can get injured in the spleen by the surgeon causing a
small injury by any of the surgical equipment being used by the doctor
using or the assistant.

4.2.3 CLASSIFICATIONS
 The Magnitude of splenic disruption depends on the patient’s age, injury
mechanism and presence of underlying disease.
 Splenic injury has been classified according to its pathological anatomy
into:
o Grade I: Subcapsular hematoma.
o Grade II: Sub segmental parenchgmal injury.
o Grade III: Segmental devitalization (part of it)
o Grade IV: Polar disruption (complete pole)
o Grade V: Shattered or devascularized organ (autosplenectomy),
Patient is in a shock but he can survive because of the blood
supply.

4.2.4 DIAGNOSIS AND INVESTIGATIONS  Kehri’s sign is the

 History occurrence of acute pain
in the tip of the shoulder
 Physical examination: due to the presence of
o Sign & symptom: if you find any of these, you presume spleen and blood or other irritants in
kidney injury: the peritoneal cavity
when a person is lying
 LUQ bruising or abrasion down and the legs are
 Left lower ribs fracture on CXR elevated.
 Kehri's sign : shoulder tip pain (L shoulder)
 Balance's sign : LUQ mass (hematoma)
 Radiological:
o CXR ” very important in case of spleen injury “
o Plain abdominal X-Ray
o CT Scan: it is the most important investigation in spleen injury.
(Done if the patient is stable)
o Angiography: it is very important for grading. It can be used for
diagnosis and a therapeutically. Done if the patient is stable.
o Picture -1-: it shows grade 1 hematoma – patient is stable so go
with conservative therapy.

314
 Specific Organ Trauma 9

Image showing a grade 2 – laceration but the wall is not

disrupted. Go with conservative therapy.

4.2.5 TREATMENT
 ABCDE
 Non-operative approach:
o Widely practiced in pediatric trauma
o criteria for non-operative approach :
o Haemodynamically stable children / adult (not in a shock)
o Those patients who do not have any peritoneal findings at any time
(no rigidity, no tenderness, just bruising).
o Those who did not need more than two units of blood (more than 2
go to OR)
 Operative approach:
o Decision to perform splenctomy or splenorraphy is usually made after
assessment & grading the splenic injury
o Contra indication for splenic salvage: ( perform splenoctomy)
o The patient has protracted hypotension (Everything is done but
there is no response and the patient is still bleeding)
o Undue delay is anticipated in attempting repair the spleen (if we put
a needle patient will bleed)
o The patient has other severe injuries (in the liver, bowel, or bladder)

315
10 Specific Organ Abdominal Trauma

4.2.6 COMPLICATIONS OF SURGERY

 Early complications occur such as:
o Bleeding.
o Acute gastric distention.
o Gastric necrosis (short gastric vessels are close to each other so
when you ligate them, it might lead to necrosis.)
o Recurrent splenic bed bleeding.
o Pancreatitis (remember the tail of pancreas ends at the pelvis of the
spleen)
o Subpherinic abscess
 Late complications occur such as:
o Thrombocytosis
o OPSS (1 – 6 Week)
o DVT

4.3 RENAL TRAUMA

4.3.1 GENERAL CONSIDERATIONS

 The commonest organ prone to injury in the urinary system.
 If contusion occurs, it can be treated by conservative therapy.
 If hematuria is present, it means there is a poor indicator of severe renal
injury (complete or partial kidney damage)

4.3.2 DIAGNOSIS: MEASUREMENT OF MEAN ARTERIAL PRESSURE

 Symptoms and signs ( 3 Fs) :
o Flank abrasion
o Fracture of the ribs
o Fracture vertebral transverse process
 Investigation: Intravenous urography (IVU) + CT scan.

4.3.3 MANAGEMENT
 For minor injuries such as hematoma: US scan, percutanous drainage,
antibiotic usage.
 For severe injuries: partial nephroctomy or total nephroctomy.

5 MCQS

1. In abdominal injuries, the most informative initial investigation is:

A. CT
B. Ultrasound
C. Diagnostic peritoneal lavage
D. Abdominal x-ray

316
 MCQs 11

2. Blunt trauma to the abdomen most commonly injures which of the

following organs?
A. Liver
B. Kidney
C. Spleen
D. Intestine
E. Pancreas

Explanation: The diagnosis of injuries resulting from blunt abdominal

trauma is difficult; injuries are often masked by associated injuries. Thus,
trauma to the head or chest, together with fractures, frequently conceals
intraabdominal injury. Apparently trivial injuries may rupture abdominal
viscera in spite of the protection offered by the rib cage. The structures
most likely to be damaged in blunt abdominal trauma are, in order of
frequency, the spleen, kidney, intestine, liver, abdominal wall, mesentery,
pancreas, and diaphragm.
Abdominal paracentesis is a rapid, sensitive diagnostic test for patients
with suspected intraabdominal injury and may be extremely helpful in the
management of patients with associated head, thoracic, or pelvic trauma
in whom signs and symptoms of the abdominal injuries may be masked or
overlooked. Abdominal CT scans, which should be done promptly and
rapidly, are being used more frequently to evaluate these injuries.

3. Which of the following conditions is most likely to follow a compression-

type abdominal injury?
A. Renal vascular injury
B. Superior mesenteric thrombosis
C. Mesenteric vascular injury
D. Avulsion of the splenic pedicle
E. Diaphragmatic hernia
Explanation: In the rapid deceleration injury associated with
automobile crashes, the abdominal viscera tend to continue moving
anteriorly after the body wall has been stopped. These organs exert
great stress upon the structures anchoring them to the
retroperitoneum. Intestinal loops stretch and may tear their
mesenteric attachments, injuring and thrombosing the superior
mesenteric artery; kidneys and spleen may similarly shear their
vascular pedicles. In these injuries, however, ordinarily the
intraabdominal pressure does not rise excessively and diaphragmatic
hernia is not likely. Diaphragmatic hernia is primarily associated with
compression-type abdominal or thoracic injuries that increase
intraabdominal or intrathoracic pressure sufficiently to tear the central
portion of the diaphragm.

317
 Introduction 1

RAISED INTRACRANIAL
PRESSURE
1 INTRODUCTION

 The skull is like a rigid box that doesn’t allow any expansions.
o It contains: the brain (volume measured is 1400 ml), meninges, vessels,
blood (volume measured is 75 ml), and CSF (volume measured 75 –
100ml). Water, blood, and CSF are incompressible.
 The pressure in the skull is called the Intra-cranial pressure (ICP). The ICP
must stay balanced in order for the survival of the brain.
2 BASIC PRINCIPLES OF ICP

2.1 MONRO-KELLIE DOCTRINE

Doctrine means a
particulate system of
 This principle states that any change in the brain’s volume is associated with a principles taught of
change in CSF or blood volume. advocated.
 When the volume of the brain increases, the other components will have to
compensate. CSF will decrease and vasoconstriction will occur in order to
decrease the blood volume.

2.2 VOLUME – PRESSURE CURVE

 Increase in the volume of one

compartment will lead to change
in the volume of the other ones.
 When the blood volume increases, the
ICP will increase but the cranium’s
components’ accommodation will keep
it balanced until a certain level where
even a small increase in the volume
can take the curve over and will no
longer be able to accommodate leaving
the ICP with a sudden increase. At this
point, symptoms such as headache,
nausea, vomiting, numbness and weakness will start to occur.
 Assume that brain develops a tumor. Depending on how fast the tumor grows,
the pressure will either increase slowly and be tolerated, or massively (ex,
sudden hemorrhage) and lead to comatose.
 Example 1: A patient came to the ER complaining from headaches. He was
conscious when the doctor talked to him and examined him. Few minutes later
he collapsed and went into a coma. In this case, the patient was at the at edge
of the pressure - volume curve

318
2 Raised Intracranial Pressure

 Example 2: A patient with a brain tumor that grows 1 mm yearly, his brain will
have enough time to accommodate, CSF will get a lot of time to change its
absorption and production pattern, and the blood flow will change and has a lot
of time to accommodate. Unlike a sudden change which isn’t tolerated well.

2.3 ICP WAVEFORM

 Any pressure has a waveform.

 The ICP waveform corresponds to the cardiac waveform. So when systole
occurs, there will be a rise in the ICP waveform. It gives the brain pulsation and
this pulsation is what forms the ICP. Pulsation of heart is transmitted into the
great vessel then into the internal carotid artery and into the brain.

2.4 NORMAL ICP VALUES

 Because children
have softer bones, their
ICP value is lower.
Infants have lesser ICP
= 1.5 – 6 because their
bones haven’t united yet.
up)

3 CEREBRAL PERFUSION PRESSURE

 Cerebral perfusion pressure is the pressure coming from the blood rushing into
the brain.
 It has a very wide range between 50 and 140 mmHg
 In trauma cases, it is preferred to keep cerebral perfusion pressure around 70.
 The brain only dysfunctions at a very high extreme pressure or very low
extreme pressure.

3.1 CEREBRAL AUTOREGULATION

 It is the ability of cerebral vessels to maintain cerebral perfusion within strictly

determined limits.
 Mechanisms of cerebral auto-regulation:
o A rise in the systolic blood pressure will cause constriction of cerebral
arteries.
o A drop in the systolic blood pressure will cause cerebral vessels to dilate
for accommodation.
o This will help keep the person conscious and able to judge.
o Example: someone got dehydrated; s/he will still be able to go drink water.
But if the brain collapsed, one won’t be able to protect him/her self.

319
 Cerebral Perfusion Pressure 3

 If there is a repetitive increase in the pressure such as hypertension, the brain

vessels will start to develop small aneurisms. They’re very tiny aneurisms that
develop on the small arterioles and at some point they rupture and cause
hypertensive hemorrhage to the brain.
o Loss of auto regulation will cause changes in cerebral blood flow with
changes in the BP levels.
 Increase of pressure will constantly increase the blood flow pressure.
When it reaches to an extreme abnormal state, the auto regulation
will then fail.
 Example:. 25:25 , 50:50. 75: blood flow pressure remains constant.
 Disrupted auto-regulation: BBB or vessels badly affected like bad hematoma or
bad contusion of brain. In that area, increased pressure will increase flow and
this area can bleed inside.

3.2 MEASUREMENT OF CPP  MAP = mean arterial

pressure and it’s the
 The heart pumps the blood with pressure into the brain. The brain has its own blood coming from the
pressure. The pressure that goes into the brain has to be the average pressure body to the brain.
in the head subtracted from the average of the blood’s pressure.
CPP = MAP – ICP

3.2.1 MEASUREMENT OF MEAN ARTERIAL PRESSURE

 The systolic heart beats over the diastolic heart beats divided by 3.
 You can find out by using the blood pressure cuff and connecting it to a monitor
in the ICU where it will show the results there.

3.2.2 MEASUREMENT OF ICP

 It is measured by inserting a catheter into the head.
 ICP can be adjusted by giving fluids or medications that can increase the
pressure and by this the cerebral perfusion pressure can be maintained.
 Example: if a MAP of someone was = 85. And the ICP was = 15

320
4 Raised Intracranial Pressure

Measure the CPP = 85 -15 = 70.

(Recommended to keep it above 70 in head injuries)
 In a case of trauma with bad head injury:
ICP and MAP must be measured, CPP must be around 70. If it was around
40 then BP must be increased or ICP must be decreased.
 If ICP goes up, how does the brain get perfusion? Process of auto-regulation.

4 RAISED ICP

Any abnormal contents such as masses, tumors or hematoma will cause an

increase in the pressure which will affect the brain.
4.1 CAUSES OF RAISED ICP

 Vitamin D  is an Acronym to remember the causes of raised ICP:

Vascular, Infection, Trauma, Autoimmune, Metabolic, Endocrine,
Neoplastic, Drugs
 ICP causes can be classified in several ways. It can be classified according to
the structures over there. If the problem was in the brain causes can be tumor,
traumatic contusion, CSF obstruction, obstructive hydrocephalus, thrombosis…
etc
 Or classified according to major pathological criteria: infection, trauma, and
tumor.

4.2 SIGNS AND SYMPTOMS

 Vomiting
 Headaches:
o Characteristics of the headache:
 Early morning headaches. It is very characteristic. Once the
patient wakes up with a really bad headache, when he’s in his
best situation. What happens? Patient was laying flat during
sleeping which will increase venous return and the amount of

321
 Raised ICP 5

blood reaching the brain will increase. But when the patient is
sitting upright, gravity will take blood down and ICP will
decrease.
 Throbbing / Bursting
 It increases with sneezing and coughing. Coughing and
sneezing will increase intrathroacic pressure which will keep the
blood from coming down and this will increase the ICP
 Papilledema:
o It’s important to examine the fundus in patients with raised ICP.
o This symptom is reliable but may take several days to develop.
 Therefore when a patient comes to the ER with raised ICP,
he is not examined for papilleodema first.
o It can be associated with fundal hemorrhage and this indicates
acute and severe rise in ICP.
o It happens only with chronic problems like with growing brain tumor.

o When you look into the eye

you’ll find a blurred optic disk
because the venous return
from the eye that’s supposed to
go to the head, wants to go but
it’s finding very high pressure
so it becomes congested.
o Thick congested veins cause
edema.

o Increase pressure in brain  veins within optic nerve become

congested  whole optic nerve head becomes congested.
o Very large tortures veins , elevated and floored optic disk margin
can be seen.

 In Neurological exam the most common signs:

o Hemiplegia (any weakness)
o Cranial nerve deficit
o Pupillary dilation:
 It is one of the earliest signs that occur and it is very
characteristic.
 The pupil dilates or constricts based on the Occulomotor
nerve that comes from the midbrain in the brainstem (figure
-1-), just next to the temporal lobe.
 So if the temporal lobe is pushed, it compresses the nerve.
In the beginning of herniation, this nerve will be affected.

322
6 Raised Intracranial Pressure

 If there is a mass compressing the 3rd nerve  ipsilateral

pupil dilation and contralateral hemiplasia ”weakness” will
occur.

Figure 1: Coronal cut MRI shows u the Figure 2: This pathological picture
same thing shows Cingulate herniation
(subfalcine herniation), central
herniation, and some Uncal
herniation. Blood in temporal area,
basal ganglia, frontal area.

Figure 3 Figure 4: Tonsillar herniation, tonsil

comes down from foramen magnum

 Systemic: reaction to increased ICP:

o Raised BP (recall: CPP=MAP-ICP) blood is pumping so high to
compensate (you rise MAP by rising systolic BP) if you drop his Bp
you Kill him.
o When you have a raised ICP, if you increase the ICP how to
maintain a good CPP? By increasing MAP.
o Respiratory change:
 Cheyne-Stokes breathing: not seen in every case
 Oscillating periods of apnea-tachypnea.
 A lot of pressure on the brainstem (stop breathing 
suddenly breathing fast  again suddenly stop
breathing...Etc).

323
 Raised ICP 7

 Raised ICP in infants results in: skull here isn’t fully developed yet so it can
accommodate:
o Widened sutures
o Increased Head circumference
o Dilated head veins
o “Sun set” eyes “his eyes always looking down” pushed down
o Tense and bulging fontanels (normally flat and sunken except if he
cries it bulge and come flat again)
o Head is to large
o A lots of Dilated veins

4.2.1 KERNOHAN’S NOTCH

 Simply, when there is a huge growing right side hematoma it will push the
whole brain stem to the opposite side (it will push the whole brainstem against
the contralateral tentorium) and that may cause ipsilateral weakness and
contra-lateral dilated pupil.
 Don’t take any patient to the OR room unless we do a CT to make sure.
 This sign is used to clinically estimate the side of bleeding.
 CT scan is done to know the exact location of the bleeding.

4.3 GLASGOW COMA SCORE

 It is very important for the assessment of the severity of coma.(so will be easier
to estimate prognosis)
 It relies on 3 things: the ability to open the eyes, verbal responses and motor
responses.
 If a patient’s GCS was 3 (which is the lowest), he might die within days.
 If a patient’s was GCS 14, he should be admitted to the hospital for 2 days then
leave.
 When it comes to head injury there is a classification of GCS:
o Mild GCS= 13 – 15
o Moderate GCS= 9 – 12
o Severe GCS= 3 – 8
o The lowest number in GCS is 3 and the highest number is 15

324
8 Raised Intracranial Pressure

4.4 RAISED ICP AND BRAIN HERNIATIONS Hemiplegia means

total paralysis of the arm,
 Most of our body organs contain water. If you try to compress an organ that is leg, trunk of the same
full of water, this organ is going to shift. And this is what happens in case of side of the body.
raised ICP. Tentorium is a
membranous cover of
 When ICP increases, the brain goes under so much pressure that it will go to cerebellum the process
least resistance part in the brain and go out through it  brain herniations. of the dura mater
supporting the occipital
 If there was a severe brain compression, the brain is going to shift and go lobes and covering the
through an opening such as foramen magnum which will compress the cerebellum
respiratory center in the brain stem and cause a fatal problem.

4.4.1 TYPES OF BRAIN HERNIATIONS

 Uncal herniation: It is the most common clinically seen type of brain hernias.
Uncus is the most medial part of the temporal lobe. It’s the part that is going to
be herniated. If there’s an increased ICP, the uncus goes above the
tentorium and compresses the brainstem, causing dilated pupil “3rd cranial
nerve affected”, coma state and hemiaplagia.
 Central herniation: If there was a hematoma or mass that compresses the
upper part, it will push the whole brain down through the tentorial opening.
 Tonsillar herniation: This type is fatal. If there was massive increase in the
ICP especially that around the cerebellum, the tonsil will come down through
the foramen magnum and will compress the lower medulla where the centre of
respiration lays and the patient will stop breathing.
 Cingulate herniation: subfalcine herniation, it’s when the left side of the brain
is compressed and pushes the right side then goes under the falx cerebri to
other side.
 Outside herniation: If there was a skull fracture and the pressure inside was
so huge so the brain will look for the easiest way to be out.

A. Cingulate herniation
B. Uncal herniation
C. Central herniation
D. Outside herniation
E. Tonsillar herniation

4.5 INVESTIGATIONS

 If a patient came with headache and vomiting, check for Papilledema and do
an urgent CT to the head.
 Lumbar Puncture is contraindicated until you do at least the CT (because if you
take the CSF from the back and there was high pressure in the brain, it will

325
 Raised ICP 9

cause tonsil herniation which will kill the patient because he won’t be able to
breathe.)
 If also has fever, you start by checking for Papilledema and do a CT before
doing Lumbar puncture to rule out meningitis.

4.6 TREATMENT  Mannitol is an

osmotic diuretic, goes
 General measures: into the blood, makes the
o To increase the venous return, elevate the Head (30 degrees) to blood very light and will
suck fluids
help with VR
o No neck compression to relief veins
o Give Mannitol for patients who have decreased LOC (or
Furosemide) it will increase osmotic pressure in vessel & suck fluid
from intracellular.
o Steroids (Dexamethazone) only for tumors (a lot of edema around of
tumor, it can be controlled by giving dexamethazone).
o Hyperventilation: controlled to PCO2 35-40 mmHg a lot of
hyperventilation  wash out CO2  shrink blood vessels (decrease
the amount of blood reaching brain) a CO2 is a very potent
vasodilator so you want to decrease the amount CO2 so the blood
vessels will go down and ICP will go down, a controlled
hyperventilation.
o Sedation, muscle relaxants decrease metabolic rate
o Hypothermia decrease metabolic rate
o Barbiturates: terminal option  you put the brain in complete
relaxation.
 Specific treatment: Depends on the cause of raised ICP:
 Vascular - SAH / ICH
 Infection/Abscess:
Rounded space
In IV drug abusers or immune suppressed patients, with sinusitis.
Sustained infection, that when you give contrast  enhanced
picture (big collection of pus)

 Trauma:

326
10 Raised Intracranial Pressure

Localized: * Epidural Hematoma * Subdural Hematoma,

compress brain, subfalcine herniation + temporal herniation.
Diffuse: Severe shaking of head  cut of Fx  Salt and pepper
appearance of blood scattered around in brain
 Tumor: midline shift to other side, edema around it (Meningioma,
Glioblastoma Multiformi). (you dissect the tumor)
 Hydrocephalus: Treated with shunt, ventricles enlarged, diffusion of
CSF into brain substance.
 ICP can be monitored by inserting a catheter in the right ventricle of the brain
substance to give pressure and suck fluid.

 Case:
A 20 year old man presented to the ER unconscious with BP of 75/30, HR of 125 bpm, and with a
right hemiplegia caused by a motor vehicle crash as unrestrained driver.
1. What are the differential diagnoses?
a. Intracranial bleeding (he’s unconscious, with right hemiplegia)
b. Hematoma in the brain (that’s why he is with hemiplegia and he is bleeding somewhere in
the body and because of that he is hypotensive and unconscious and he has high HR)
2. How to deal with him in the emergency?
st
a. 1 ABC:
A. Check airway  endotracheal intubation (the first thing done for unconscious patient,
because if his airway was blocked he will die within seconds)
B. Breathing  chest tube (if tube was inserted and the patient’s lungs were not inflated, he
might have pneumothorax, and this will kill him in a minute)
C.Circulation  stop the external bleeding but after giving I.V fluids. (Brain needs fluids so
fluids must be replaced)
nd
b. 2 insert 2 large I.V lines to start fluid, blood.
rd
c. 3 C.T: to find out why he is unconscious.

327
 MCQs 11

5 MCQS

1. The Glasgow coma scale (GCS) is dependent upon the following except:
A. Response to speech
B. Response to pain
C. Response of the pupils
D. Best response
E. Response of the patient

2. Severe head injury is defined as Glasgow coma score of:

A. 3
B. 3-9
C. 10
D. 11-12

3. Which of the following statements regarding the Glasgow coma scale is

true?
A. It serves as a scale to assess the long-term sequelae of head trauma
B. A high score correlates with a high mortality
C. It includes measurement of intracranial pressure
D. It includes measurement of papillary reflexes
E. It includes measurement of verbal response
Explanation:The Glasgow coma scale was developed to enable an initial
assessment of the severity of head trauma. It is now also used to
standardize serial neurologic examinations in the early postinjury
period. It measures the level of consciousness using three parameters:
verbal response (5 points), motor response (6 points),
and eye opening (4 points). The score is the sum of the highest number
achieved in each category. The fully oriented and alert patient will
receive a maximum score of 15. A score of less than 5 is associated with
a mortality of over 50%.

4. An acute increase in intracranial pressure is characterized by which of the

following clinical findings?
A. Respiratory irregularities
B. Decreased blood pressure
C. Tachycardia
D. Papilledema
E. Compression of the fifth cranial nerve.
Explanation: The onset of irregular respirations, bradycardia, and finally
increased blood pressure with increasing intracranial pressure (ICP) is
termed the Cushing response. These physiologic alterations are caused
by brainstem compression. Slow rises in ICP are, by contrast,

328
12 Raised Intracranial Pressure

autoregulated by the brain’s compensatory mechanisms and lead to a

late onset of neurologic sequelae. A mass lesion is more apt to
compromise local cerebral blood flow and increase cerebral edema and
ICP. The vector of the mass effect may lead to herniation of brain
parenchyma through the tentorial incisura or foramen magnum with
resultant brainstem compression. Herniation usually causes
compression of the third cranial nerve and thus leads to a fixed and
dilated pupil on that side. Papilledema is a finding with chronic
increases in ICP.

329
 Hydrocephalus 1

COMMON CONGENITAL
NEUROSURGICAL DISEASES
1 HYDROCEPHALUS
 Hydrocephalus
1.1 DEFINITION It is an accumulation of
CSF within the cerebral
ventricle and is usually
 Hydro; water and cephalus; head associated withaltered
 Hydrocephalus is an increase in the CSF, associated with increased ICP. ICP
 Ventriculomegaly secondary to cortical atrophy; aka hydrocephalus The pressure is usually
exvacuo high, and sometimes
normal, but rarely low
1.2 CAUSES (negative pressure
hydrocephalus)
 Overproduction of CSF (Tumor of the choroid plexus) When the ventricles
 Obstruction of CSF flow are large but the patient
 Under absorption of CSF into the blood stream (leads to accumulation of is asymptomatic, that is
not hydrocephalus; it’s
CSF) (When the way to the arachnid granulations is obstructed 
just hydrocephalus ex
Examples: Post meningitic lesions and post hemorrhagic lesions. vacuo “old name” or
ventriculomegaly. So
1.3 PHYSIOLOGY when you see large
ventricles, it does not
 Total volume of CSF in the ventricles varies from 5-15 ml in neonates to indicate hydrocephalus
150 ml in adults. (Depends on age and weight) UNLESS there are
symptoms of pressure
 Produced by choroid plexus and the extracellular fluid of the brain. changes of the brain.
 Rate of production is 0.3-0.4 ml/minute.
 Only very high ICP will reduce CSF production; usually at the point when
brain perfusion is affected.
 CSF is produced by
the choroid plexus of the
ventricles
 A tumor of the plexus
can increase CSF
production
 Everyday the plexus
produces 500ml of CSF

330
2 Common Congenital Neurosurgical Diseases

Figure 1: Coronal view of the brain

1. Both lateral ventricles will drain CSF into 3rd ventricle through the foramen of Monro IMP Rate of CSF
2. From 3rd ventricle the CSF will pass to the 4th ventricle in the posterior fossa through the production is 0.3-0.4
aqueduct of Sylvius IMP ml/minute →
3. From 4th ventricle CSF circulates around the brain then passes through the three apertures 500 ml CSF/day – 150
(median foramen of Magendie & 2 lateral foramina of Luschka) to circulate around the brain, ml in the CNS → 350
spinal cord and in central canal of spinal cord. CSF absorbed every
Figure 2: This small cut section at the level of superior sagittal sinus (which is one of the dural day.
venous sinuses of brain) shows the arachnoid granulations, which are an extension of the It is a process of active
arachnoid. CSF drains into the arachnoid granulations (villi), then through the core of the villi formation and it does not
into the venous circulation. stop it
So CSF circulates within ventricles then around the brain then it is reabsorbed in the It may be affected by ↑
cerebral ventricles. ICP BUT it does not stop
it
If there is any problem
affecting absorption or
Figure 3:
the pathway of CSF →
Shows the communication between the
accumulation of
ventricles
CSF and ↑ ICP (which
2 lateral ventricles inside cerebral
decreases CSF
hemisphere - they have a frontal horn,
production)
occipital horn & temporal horn
Both communicate through foramen of
Monro> 3rd ventricle> cerebral
aqueduct> 4th ventricle

1.4 EPIDEMIOLOGY

 The overall incidence of infantile hydrocephalus is 1/1000 live birth and

2/1000 in some countries like Africa and India * It is not a common disease
1.5 TYPES OF HYDROCEPHALUS

1.5.1 COMMUNICATING:
 All ventricles are dilated
 Overproduction or under absorption of CSF
 No obstruction in the pathway of CSF within the ventricles (the ventricles
can communicate with each other)
1.5.2 NON-COMMUNICATING:
 Partial dilatation
 Blockage of the flow of CSF
 Obstruction within ventricles or the pathway of CSF (obstruction to the CSF
flow at the foramen of Monro, the third ventricle, the aqueduct of Sylvius,
the fourth ventricle, or the foramina of Magendie or Luschka.)
 Congenital, since birth
 Acquired, develops after birth as a result of injury, tumors or meningitis.

331
 Hydrocephalus 3

1.6 ETIOLOGY
 Important 3 causes
of communicating
1.6.1 CONGENITAL (PRIMARY) hydrocephalus:
 Aqueductal anomalies Most common cause of congenital hydrocephalus - Post-hemorrhagic
- Post-meningitic
 Dandy Walker malformation associated with meningomyelocele - Post-traumatic
o Atreisa of the foramen of Magendie or Luschka 3 posts for acquired
 Chiari II malformation causes!

 Myleomeningocele Remember that the

 Intrauterine viral infection (CMV, mumps, rubella, varicella) cause of acquired
 Toxoplasmosis hydrocephalus is usually
outside the ventricles.
 Congenital tumors
 Vein of Galen aneurysms
 Chromosomal anomalies (Trisomy 13 and 18)
 Congenital or primary hydrocephalus. (idiopathic; no known reason)
1.6.1.1 AQUEDUCTAL ANOMALIES
 Aqueduct is the passage of CSF between the 3rd & 4th ventricles-passes in
the midbrain
 It is still know as aqueductal stenosis, however by definition, the correct
term is
 “aqueductal atresia“ because no aqueduct is found in most of cases - but in
some cases
 (who develop hydrocephalus late in their childhood) it allows a small
amount of CSF to
 pass through so it is usually called stenosis
1.6.1.2 DANDY WALKER MALFORMATION (LARGE DANDY WALKER
CYST)
 Dandy-Walker
malformation is
 By definition it is congenital hypoplasia or even aplasia of cerebellum characterized by
associated with formation of a large CSF cavity within the posterior fossa agenesis or hypoplasia
due to the obstruction of CSF flow by a large cyst (which doesn’t allow CSF of the cerebellar vermis,
cystic dilatation of the
to pass from the 4th ventricle and circulate around the brain) fourth ventricle, and
 There are different types of Dandy Walker cyst according to the volume of enlargement of the
cerebellum that’s involved posterior fossa
 Most of cases of Dandy Walker malformation are associated with
Presentation:
hydrocephalus Incoordination, ataxia,
 In short: large CSF cyst on posterior fossa due to agenesis of the nystagmus
cerebellum that communicates with the 4th ventricle, and causes
hydrocephalus.
1.6.1.3 VEIN OF GALEN ANEURYSMS
 A large vascular malformation where there is a direct communication
between the arterial system and venous system (shunting), leading to
dilatation of the Vein of Galen (one of the deep venous structures in the
brain) and to obstructive hydrocephalus.
 What is the clinical manifestation for such cases in neonates?
o 1st and most important is heart failure (the size of the arteriovenous
shunt that can steal 80% or more of the cardiac output), then

332
4 Common Congenital Neurosurgical Diseases

symptoms of hydrocephalus (developmental delay, seizures,

headaches)
 Rx: treat the cause, which is the aneurysm (stop passage of blood from
artery to vein by embolization) - and no need for shunt to treat the
hydrocephalus
o Also shunts can burst the aneurysms and cause fatal hemorrhage
1.6.2 ACQUIRED (SECONDARY)
 Normal pressure
 Most cases
hydrocephalus (NPH)
 Germinal plate hemorrhage: “immature blood vessel walls” -Usually in elderly,
o Leads to intracranial hemorrhage in premature babies <1500 gm -Presents with dementia-
(30%-40%) like symptoms
 Subarachnoid hemorrhage: -Patient’s family
complain of patient’s
o Due to trauma memory loss
 Post-meningitis: -It is treatable
o 1% of survivors of bacterial meningitis -Investigate with CT and
o More in neonates MRI  you’ll see
o Especially G-ve organisms (i.e. E. coli). ventricular dilatation
o Rare but important, postnatal cysticercosis. more than cortical
atrophy
 Tumors. (Most common cause)
 SAH. (Subaeachnoid Hemorrhage)
 Severe TBI (Traumatic Brain Injury)

Dandy Walker malformation

Congenital or primary hydrocephalus Vein of Galen aneurysms

333
 Hydrocephalus 5

1.7 CLINICAL FEATURES

1.7.1 INFANTS & YOUNG CHILDREN:

 Increasing head circumference. (Scalp bones are still soft. So the head
circumference increases abnormally – not according to curve of growth)
 Irritability, lethargy, poor feeding, and vomiting. (Leads to delayed
development)
 Bulging anterior fontanelle. (Wide, full and tense)
 Widened cranial sutures.
 McEwen's cracked pot sign with cranial percussion.  (sounds like you’re
tapping on a cracked pot)
 Scalp vein dilation (collateral venous drainage).
 Sunset sign (downward deviation of the eyes). 
o not only infants but also in children and sometimes adults
 Epidsodic bradycardia and apnea. (If hydrocephalus is left untreated – the
increased intracranial pressure will press on the brain stem –where the
respiratory centers are located- which will lead to this)
 Irritability, drowsiness, vomiting
1.7.2 JUVENILE & ADULT:
Night (sleep) →
 Headaches (Most common symptom) (Usually in the early morning. Why? hypoventilation→
Because during sleep, the patient will hypo ventilate, which will lead to ↑ increased Co2 retention
CO2 → ↑ vasodilation → blood stasis & ↑ intracranial pressure) → vasodilatation →
symptoms are worse
 Projectile Vomiting. (The symptoms are usually relived after vomiting. Why?
Vomiting (on waking up)
Because vomiting leads to hyperventilation which will reverse the CO2 → hyperventilation→
retention and cause vasoconstriction of the blood vessels → ↓ Intracranial washing out of Co2 →
pressure) vasoconstriction and less
 Seizures. (Acute manifestation) dilations → symptoms
improve
 Decreased level of consciousness.
 Focal neurological deficit. (Depending on the cause of the hydrocephalus)
 Collection of CSF around previous shunt site X-ray is not a
 Progressive visual disturbances diagnostic procedure for
 Papilledema (When the hydrocephalus has been there for days, not in the hydrocephalus now
acute onset) You will see widening of
the suture of skull
1.8 INVESTIGATIONS secondary to increased
intracranial pressure
 CT scan: easy, available and you can do it in minutes (Method of choice)
o The pattern of ventricular enlargement can help delineate the
cause:
o Allows you to see any lesions
o Suitable for acute hydrocephalus
 Lateral & 3rd ventricle dilatation
 normal 4th ventricle: suggests aqueduct stenosis
 deviated or absent 4th ventricle: suggests posterior  Classical
fossa tumor “obstructive hydrocephalus” Radiological Sign:
 Generalized dilatation: suggests a communicating -Separation of sutures
hydrocephalus. -Pressure of the gyri on
the bone

334
6 Common Congenital Neurosurgical Diseases

 MRI:
o Shows more anatomical details
o Allows better visualization  Example: Aqueductal stenosis
o Not available in the ER, takes longer time than a CT

CT Scan

Lateral ventricles dilated but 3rd Posterior fossa tumor

ventricle not very dilated > lesion in
3rd ventricle that prevents CSF
from entering the 3rd ventricle at
level of foramen of Monro

Communicating hydrocephalus

1.9 TREATMENT There’s no medical

treatment, you can use
1.9.1 SURGICAL TREATMENT some medication to
reduce the volume of
 Endoscopic choroid plexectomy was tried but found unsuccessful. Not done CSF and reduce
now because all children die during the operation ICP, but CSF is actively
 Replaced now by Choroid plexus coagulation We use endoscope, produced by the choroid
introduce telescope in the ventricle, and it helps in reduction of CSF plexus so it’s difficult to
formation get rid of the problem

1.9.2 INTRACRANIAL SHUNTS

 In obstructive hydrocephalus where the subarachnoid spaces are still
patent

335
 Hydrocephalus 7

1.9.2.1 ENDOSCOPIC THIRD VENTRICULOSTOMY

 The endoscope is passed through a burr hole to the third ventricle where  Endoscopic third
the floor is fenestrated just anterior to mamillary bodies. (So we bypass the ventriculostomy: 1st line
treatment now
obstruction in the aqueduct or posterior fossa).The hole is enlarged by
introducing the endoscope or an inflatable balloon.
1.9.2.2 VENTRICULOCISTERNOSTOMY:
 Shunt between lateral ventricle and the cisterna magna.
 It has high morbidity and mortality. (Not done any more)
1.9.3 EXTRACRANIAL SHUNT:
Extra-cranial Shunt: if
 From the ventricular system, usually the you have communicating
lateral into another body cavity; the hydrocephalus or if you
don’t have the facility or
peritoneal cavity (VP Shunt), right atrium capability to do
(VA Shunt) and occasionally pleural endoscopic third
cavity. ventriculostomy
 Aim is to normalize the intracranial
pressure
 Specially designed shunt valve with the
appropriate rate of flow and pressure.
Regulate the CSF flow in a unidirectional
way.
 Shunts are made of silicon which is well tolerated by the body. It causes
minimal or no tissue reaction or intravascular thrombosis
1.9.4 COMPLICATIONS OF VP SHUNTS
1.9.4.1 MECHANICAL FAILURE
 Under drainage or over drainage
 Blockage (Obstruction) (Most common complication)
 Improper placement
 Migration of the shunt system
 25 to 40% in the first few months after surgery, later on 4 to 5 %.
1.9.4.2 SHUNT BLOCKAGE (OBSTRUCTION)
 50% of mechanical failure, highest in the immediate post operative period.
 Proximal occlusion (In brain)
o By brain debris or choroid plexus
o Ideally the catheter should lie away from the choroid plexus
 Shunt valve blockage
o By brain debris or blood clots or due to failure of the valve system
 Distal obstruction (In abdomen)
o Less frequently than the proximal obstruction
o Accumulation of particles
o Catheter encysted or isolated in one area of the peritoneal cavity
Following infection or adhesion
 Catheter migration, disconnection , or fracture Sometimes catheter pass
through stool or coming out through the anus
1.9.4.3 SHUNT INFECTION
 Most dreadful complication

336
8 Common Congenital Neurosurgical Diseases

 About 5%, and may result in further risk of intellectual impairment.

 Organisms If you press valve and
there is no fluid passing
o Staphylococcus epidermidis about 40% Commonest cause. It’s through shunt > distal
normally found in the skin and it easily reaches the shunt, causing obstruction
CSF infection “meaning meningitis leading to disability ”
o Staph aureus about 20% by. If you press shunt &
o Streptococci and gram negative organisms are less frequent. valve collapse and
doesn't refill again >
 Clinical features infection leads to increase CSF volume so patient suffer proximal obstruction
from hydrocephalus symptoms again
o Early, within 8-10 weeks.
o Fever, malaise, headache & irritability, neck stiffness.
o Peritonitis is less common.
o Patients with Staph epidermis may look remarkably well with only
intermittent fever or irritability.
o Diagnosed by blood culture, routine blood examination and CSF
examination. (CSF sample should be taken from the shunt)
 Treatment of shunt infection:
o Removal of shunt and the external ventricular drainage plus
antibiotics.
 Take the shunt out → put temporally external drainage →
treat the infection by antibiotics till the CSF cleared of
infection → then replace the external drainage by internal
shunt
 External drainage very useful b/c we can drain the CSF, take
sample of CSF for culture and to inject antibiotics intra
ventricular to treat infection or speed up the clearance of
infection
 Treatment with antibiotics alone. For patients who have very low grade of
infection & Clear CSF
o Antibiotic prophylaxis is controversial however it was found that
intra-operative antibiotics or antibiotics for the first 24 hours give the
best results.
1.9.5 LESS COMMON COMPLICATIONS:
 Subdural collection from over drainage
 Slit ventricle syndrome, (over drainage) > cause collapse of ventricles
 Disconnection or fracture of shunt tubing
 Seizures THE NERVOUS SYSTEM
2 DEVELOPMENTAL SEQUENCE
Types:
2.1 DEVELOPMENTAL SEQUENCE Open  occurs when
the brain and/or spinal
cord are exposed at birth
 Neural plate invaginates as neural folds push up through a defect in the
 Neural folds eventually form neural groove skull or vertebrae.
 Cells of neural fold eventually meet
Closed  occurs when
 Form the neural tube the spinal defect is
 Neural tube runs anterior – posterior along embryo covered by skin.
 Surrounding ectoderm eventually encloses neural tube

337
 Neural tube defect 9

 When neural tube closes off brain and spinal cord are formed and this
process is completed on day 28 of pregnancy begin > so if the spina bifida
formed at 28 day it’s formed!
 Spinal cord covered posteriorly by spinal process and laminae
3 NEURAL TUBE DEFECT

3.1.1 SPINAL DYSRAPHISM

 Spina Bifida
 Failure of closure of posterior neural arch
 Open or Closed
 80% in lumbosacral region (Occasionally in the head)

CNS:
 Neuroectoderm in origin > neural plate >
neural groove > neural fold > more
folding > ends try to proximate and touch
each other > forming neural tube >
migrate rostral forming brain & caudally
> spinal cord
 Then it’ll be covered by mesoderm >
forms the bones “bodies vertebra” &
lamina & spinal process (posteriorly) >
failure of that is called spina bifida
 Myelomeningocele: herniation of S.C > if
S.C outside the canal & will affect the
lower limb of baby b/c it’s not functioning
 Meningocele: only contains CSF
covered by meninges Commonly in
lumber area  If there’s
associated coetaneous
lesions that alert us to
a bigger problem
Hair tuft, Dimples. Sinus,
3.2 TYPES OF MYELODYSPLASIA Pigmintation, Lypoma,
Focal abnormalities
 Spina bifida occulta Example: Intraspinal
 Lipomeningocele “lump of fat in spinal canal” tumors
 Meningocele
 Myelomeningocele = Spina Bifida One of the causes or
recurrent meningitis in
3.2.1 SPINA BIFIDA OCCULTA children (You’ll find signs
 Found incidentally when the patient does x-ray of an underlying problem
for any reasons. like a tuft of hair or
dimpling)
 5-10% of population so it’s common.
 Not clinically significant “asymptomatic” Split cord syndrome
 Tuft of hair, dimple sinus or port wine stain Early life 
 High incidence of underlying defect Asymptomatic As they
 No treatment required, U/S or MR get older they might
Spina Bifida Occulta: The two have sphincter control
laminae try to reach each other problems, weakness in
but are not touching each other the lower limbs
and do not form

338
10 Common Congenital Neurosurgical Diseases

3.2.2 MENINGOCELE
(Sac filled with CSF but no spinal cord)
 Cystic CSF-filled cavity lined by meninges so no neural abnormalities
“motor or sensory deficit in lower limbs” but some have some autonomic
deficits like sphincters; Incontinent or nocturnal enuresis.
 No neural tissue
 Communicates with spinal canal
 Look for other cong. Anomalies
 Seldom any neurological deficit
 Usually discovered incidentally
 Dx: U/S or MRI
 Urgent excision if CSF leak (If ruptures), otherwise deferred
 Perhaps indefinitely if small

 Examination
-Locally  Size, content
-Assess skin quality (for
surgery)
-If there’s CSF leak  it
is a surgical emergency
 Risk of Infection
-Translumination test to
know the content
-Neurological
examination
-Examine the sphincter
to see if there’s any
problem with the anus
3.2.3 MENINGOMYELOCELE (incontinence)
-Check for other
 Most common
associated anomalies
 Risk increases with each pregnancy 5% (E.g.: Kyphosis), size of
 Female predominance the head.
 High association with other anomalies -Get the family
 Spinal cord and roots protrude through the bony defect, lie within cystic collaborations from other
cavity, if ruptured, CSF will leak trans-illumination (emergency case). specialties depending on
 Because the S.C outside >> the pt will have autonomic, sensory and motor the child’s problem
deficit in the lower limbs and they are born with paraplegia.
 Observe limb movements (degree & level of neurological damage)
 Note dilated bladder & patulous annual sphincter
 Dx: U/S or MRI (MRI is more accurate)
 If ruptured; immediate closure & replacement of neural tissues into spinal
canal
 Gross hydrocephalus, multiple serious cong. anomalies; many adopt
thoughtful conservative treatment
 Look for other cong. Anomalies : gross hydrocephalus , Chiari malformation
and other multiple serious cong. Anomalies
 Many adopt thoughtful conservative treatment.

339
 Neural tube defect 11

 Ruptured meningiocele/ meningiomyocele is a surgical ER

3.3 ANTENATAL DIAGNOSIS

 Maternal U/S,
 MRI
 Serum/amniotic fluid for alpha-fetoprotein
& acetylcholinesterase
 Contrast enhancing amniography
 Possibility of therapeutic abortion
3.4 PREVENTION

 Give folic acid supply during pregnancy

3.5 TREATMENT

3.5.1 SHORT TERM TREATMENT

 If the defect has normal skin covering>>> Treatment in elective basis (no
needs to emergency surgery)
 Thin or no skin covering at all, ruptured sac >>>early surgery as possible to
prevent meningitis.
3.5.2 LONG TERM TREATMENT
 Early treatment of hydrocephalus
 Regular follow up in spina bifida clinic
 Urological, orthopedic, paediatrics, and physical therapy
 Uological; urinary incontinence, vesicoureteric reflux, repeated UTI, renal
impairment, hypertension and stunted growth
 Orthopedic; feet deformity, and tendon transfer, pelvic and spine
deformities
 Neurosurgical; tethered cord, chiari II malformation, shunted hydrocephalus
 You have to see them at least once or twice a year
3.6 ANENCEPHALY

(No brain)
 Defective closure of the rostral neural tube
 results in anencephaly or encephalocele
 Neonates with anencephaly have a rudimentary brainstem , or midrain , no
cortex or cranium
 Rapidly fatal condition if born alive

3.7 CLINICAL MANIFESTATIONS  Myeloschisis or
rachischisis: where there
According to the level of spinal bifida (Meningomyelocele) is defect in the bone and
 Lower Lumbar (L5,S1)  Distal weakness in the feet and sphincters the spinal cord exposed
incontinent outside no skin covering
> type of
 Upper lumbar (L1)  Complete paraplegia of the lower limbs. Meningomyelocele
Sever neurological deficit
in the lower limbs.

340
12 Common Congenital Neurosurgical Diseases

3.8 INCIDENCE
 2/1000 birth .2-.3/1000 in Scandinavia b/c they put folic acid in flour and
they do therapeutic abortion once baby diagnosed with spina bifida.
 Risk increase to 5% if a sibling is affected
 Teratogens; Sodium Valporate
 Associated with Hydrocephalus, Chiari II and aqueduct forking
3.9 CAUSES

 The main cause is Folic acid deficiency; since the development of the
nervous system end in day of 28 of pregnancy. The woman should take
folic acid when they plan to get pregnant.
 Teratogens; Sodium Valporate (antiepileptic drug , if you start giving this
medication, once she becomes pregnant she may develop baby with spina
bifida > so you need to change it before pregnancy )
3.10 OTHER CONGENITAL ANOMALIES

 Tethered spinal cord

 Diastematomyelia
 Lipomeningocele Definition: fat in the meningocele.
 Congenital dermal sinus: The baby is born with back dermal sinus with tuft
of hair, check for spina bifida in this baby.
3.10.1 DIASTEMAMYELIA
 A bone or fibrous band divides spinal cord in two longitudinal sections 
 Associated lipoma may be present, which tethers cord to vertebra
 Signs &Symptoms include weakness, numbness in feet, urinary
incontinence, decreased or absent reflexes in feet
 Dx: CT
 Rx - surgery to free cord
3.10.2 ENCEPHALOCELE
Large cyst in the skull contains CSF or brain
 Usually occipital
 May contain occipital lobe, or cerebellum
 Often associated with hydrocephalus
 Immediate treatment if ruptured
 Outcome depends upon contents
3.10.3 CHIARI I MALFORMATION
 Cerebellum herniation through foramen magnum >> crowding of the area
>> affect the
 CSF circulation >> dilation of the CSF within the S.C; this is called
syringomyelia
 Two types:
o Type A no spinal bifida (Meningomyelocele)
o Type B with spinal bifida

341
 Neural tube defect 13

3.10.4 CLINICAL MANIFESTATION OF CHIARI MALFORMATION

 Babies have clinical manifestation called foramen magnum syndrome,
which include symptoms like:
o Pressure of the S.C in that area.
o Stretching of lower cranial nerves, associated syringomyelia
o Leads to neck pain, Headache, upper limbs symptoms, weakness of
hands, loss of fine touch,loss in temperature sensation in the tip of
the fingers ,upper motor neurons manifestations of the lower limb.

Chiari I malformation Arachnoid cyst

Downward herniation of
cerebellar tonsil through
foramen magnum into cervical
spinal canal

342
14 Common Congenital Neurosurgical Diseases

3.10.5 ARACHNOID CYSTS

 Developmental anomaly  Intra-arachnoid cavity filled with CSF  Benign
 Treatable  Good prognosis
 Majority in the sylvian fissure
 Space occupying lesion symptoms  Convulsions, raised ICP
 In supracellar space  Can produce endocrine dysfunction
 Diagnosis
o CT scan (Not the best) Can be confused with a tumor
o MRI is more precise
 Treatment  Shunting

3.10.6 CRANIAL SYNOSTOSIS

 Early fusion of sutures  Scull deformity
 Coronal  Normally allows the head to enlarge in the anterior-posterior
direction  Early closure leads to Brachycephaly
 Sagittal  Normally allows the head to enlarge in the lateral direction Early
closure leads to Scaphocephaly
 Metopic  Early closure leads to Trigonocephaly (Triangular shape to the
head)
 Cosmetic problems  Must be fixed
 Global  All sutures involved  Must be fixed because the brain doesn’t have
room to grow

Brachycephaly Scaphonocephaly Trigonocephaly

4 MCQS

1. Which statement is true:

a. Spina bifida occulta is a neurosurgical emergency.
b. Meningocele contains spinal cord.
c. Spina dysraphism occurs most commonly in lumbosacral region.
d. None of the above
2. In arachnoid cyst, what is false?
a. Occurs commonly in the temporal area.
b. All cases should be treated urgently to avoid complications
c. May present with seizures
d. May be asymptomatic

343
 MCQs 15

3. The most common type of cerebral herniation is:

a. Central
b. Cingulate
c. Transtentorial
d. Tonsillar
4. The investigation of choice in increased ICP is:
a. Skull x-ray
b. MRI
c. Lumbar puncture
d. CT scan
5. Hydrocephalus is defined as:
a. Accumulation of CSF with ICP
b. Soft tissue contusion
c. Intracranial hemorrhage
d. Enlargement of the head
6. Obstructive hydrocephalus is best treated by:
a. Surgery
b. Drainage
c. Craniotomy
d. Endoscopic third ventriculostomy
7. In Spina Bifida, the following is correct except:
a. It is a failure of closure of posterior neural arch
b. Contains spinal cord in menengeocele
c. There are two types, Open and Closed
d. 80% in lumbosacral region

 Answers: 1:C, 2:B, 3:C, 4:D, 5:A, 6:D, 7:B

344
 Parathyroid Gland 1

COMMON NECK SWELLINGS

1 PARATHYROID GLAND

 General characteristics
o We have four parathyroid glands in the posterior aspect of the thy
thyroid gland
o Both the superior and the inferior parathyroid glands receive blood
supply from the inferior thyroid artery
 Embryology of The parathyroid glands:
o The upper parathyroid glands originate from the 4th pharyngeal
pouch
o The lower parathyroid glands originate from the 3rd pharyngeal
pouch
 Physiology of the Parathyroid:
o Ca2+ homeostasis: release of Parathormone/Parathyroid hormone
(PTH) to raise Ca2+ levels in the blood
o Vitamin D regulation: PTH induces Vit.D hydroxylation in the kidney,
and this process is necessary for Vit.D activation.
o Calcitonin: is released from the c-cells of the thyroid gland decrease
Ca2+ levels. These are not of physiological significance.
1.1 HYPERPARATHYROIDISM:

 Definition: Is an increase secretion of PTH from the parathyroid glands that

leads to increase serum calcium, decreased serum phosphate.
Hyperparathyroidism can be either primary or secondary.
1.1.1 PRIMARY AND SECONDARY HYPERPARATHYROIDISM
 Primary is more common and is due to increase secretion from the any of
the glands due to hyperplasia, adenoma or carcinoma.
 Secondary hyperparathyroidism is due disordered metabolism (chronic
kidney disease or Vit.D metabolism disorders) that causes hypocalcaemia
for prolonged times and secondary enlargement of the parathyroid glands.
 Serum levels of PTH are increased along with Ca2+ (because PTH
increases Ca2+ levels)
 Hyperparathyroidism is the most common cause of hypercalcaemia in
society 
 The most common cause of hypercalcaemia in the hospital is
malignancy 
1.1.2 EPIDEMIOLOGY:
 Statistics from Western countries indicate a 0.1-0.5% prevalence rate for
PHP.
 No evidence for geographical variation
 1200- 6000 cases were expected in Aseer area alone, but when
Prof.Shehri investigated the prevalence of cases, they only found 30!
 Uncommon in children
 2-3 times in females

345
2 Common Neck Swellings

1.1.3 CAUSES:  If a patient presents

1. Adenoma: most common cause of 1ry hyperparathyroidism is: (84% of with hypercalcemia,
elevated serum PTH a
cases) neck lump, it is either
a. Usually NONE is palpable one of two things:
b. Affects one gland  carcinoma of the
2. Hyperplasia: 15% of cases parathyroid gland
a. Usually NONE palpable
b. Usually affects all four glands 
3. Carcinoma: 1% of cases
a. Presents with palpable swelling (unlike adenoma and
hyperplasia) 
1.1.4 SIGNS AND SYMPTOMS:
Mnemonic for
Signs and symptoms are related to increased serum Ca2+ which affects multiple symptoms: “Painful
organs and systems: bones, renal stones,
abdominal groans, and
1. Bone: high levels of PTH activate bone resorption B psychic moans”
and cause bone matrix depletion. Bone involvement
on x-rays can be seen as:
a. Osteopenia is most common sign of
hyperparathyroidism, can be generalized or
local. This bone loss that may lead to
fractures, bone & joint pain.
b. Subperiosteal erosion (picture): is an early and
virtually pathognomonic sign of
hyperparathyroidism.Most commonly in the
middle phalanges of the index and middle fingers,
primarily on the radial aspect   A brown tumor is a
C rare manifestation of
c. Brown tumor (picture): which is only a radiological
hyperparathyroidism.
description and not an actual tumor. Reparative granulation
d. Cyst formation tissue and active,
2. Kidney: stones and glomerular calcification vascular, proliferating
3. Abdomen: abdominal pains where some patients may fibrous tissue may
replace the normal
develop peptic ulcer disease, pancreatitis. marrow contents,
4. Neuropsychiatric symptoms: depression, mood changes resulting in a brown
5. General symptoms: Fatigue tumor. Hemosiderin
6. The symptoms range from: No symptoms  mild, general imparts the brown color
symptoms like fatigue and depression renal symptoms  (hence the name of the
lesions)
bone symptoms
1.1.5 PRESENTATION:
 In the west:
o 60 - 70% detected by routine screening.
o Many are asymptomatic
 In KSA:
o Age 30 – 77 (median 40)
o Majority are Females
o Almost all patients in KSA present with bone symptoms
o 54% have also renal manifestations.

346
 Parathyroid Gland 3

1.1.6 CASES FROM THE DOCTOR:

 Case 1:
40 year old lady that presented with left humerus fracture, past medical history is significant of
bilateral ureteric stones that have been removed and a non-functional left kidney. Serum Ca2+
was 11.2 mg/dl and PO4 2.2mg/dl. Bone symptoms, kidney symptoms (failure and colic), high
calcium and low phosphorus.

 Case 2:
30 year old lady that presented with long history of generalized bone ache, heart burn,easy
fatigability and right humeral fracture, past medical history is significant of left ureteric stone.
Serum Ca2+ was 14.3 mg/dl and po4 2.4 mg/dl. Bone, GI and renal symptoms present, and high
calcium and low phosphorus.

 Case 3:
45 y old lady ESRF, Advanced bone disease (usually pt with renal failure has secondary
hyperparathyroidism b/c of low calcium and phosphate and can transform to tertiary
hyperparathyroidism) , But in this patient with Hx it turns that she has primary hyperthyroidism b/c
of adenoma and for many years she had recurrent renal stones until she reached ESRF!

1.1.7 INVESTIGATIONS:
 ↑ Serum Ca2+
 ↑ PTH
 ↓ Phosphorus
 ↑ Chloride, PTH effects on kidney leads to Ca retention
 Imaging X-Ray: Hand X-Ray  you may see brown tumors.
 Other imaging: U/S can show you Adenoma , CT can sometimes
showadenoma but not always , Last thing is nuclear scan" Sestamibi Scan"
1.1.8 MANAGEMENT:
 All symptomatic patients should be treated: A) Adenoma: surgical removal
or B) Hyperplasia: remove 3 and a half parathyroid glands (subtotal
parathyroidectomy)
 Asymptomatic patients: There is debate on wither asymptomatic patients
should be treated or only followed up
 Postoperative management: Be careful of bone hunger syndrome which
might cause tetany.
1.1.9 CONCLUSION:
 PHP is a very under diagnosed disease in Saudi Arabia.
 Patients are not diagnosed early
 Complications could be serious and these are avoidable.
1.1.10 RECOMMENDATIONS
 The medical community needs to be more aware of the disease.
 The diagnosis should be especially considered in the following cases:

347
4 Common Neck Swellings

 Patients with bilateral or recurrent renal stones 

 Patients with suggestive radiological bone changes
 Patients with high serum calcium level
2 THYROID DISEASES

2.1.1 GENERAL CONSIDERATIONS

 Q: Thyrotoxicosis vs. Hyperthyroidism?
o A: Thyrotoxicosis is the clinical condition of presence of high levels
of thyroid hormones in the Blood.
o Hyperthyroidism is over activity of the thyroid gland, thus it causes
thyrotoxicosis
o Thyroid disease can present as:
 Lump “goiter”
 Change in function (hypo or hyper)
 Q: If we see a lump, how can we tell if it is a thyroid lump?
o A: Ask the patient to swallow. If it doesn’t move with swallowing then
it is not thyroid disease (could be dermoid cyst, lipoma, lymph
Node). If it moves then it is one of two:
 Thyroid lump “goiter”
 Thryroglossal cysts
 Then you ask the patient to stick his tongue out and if the lump moves then
it is a thyroglossal cyst. Because Thryroglossal cysts extend to the tongue.
2.1.2 EXAMINATION:
 A suspected thyroid nodule should be treated as a lump anywhere in the
body, but the fluctuation test can not be done due to the presence of
pretracheal fascia which fixes the thyroid in position.
 Ultrasound and FNA (Fine Needle Aspiration) are used to differentiate
between different conditions. In the thyroid gland, usually what feels like
cyst turns out to be solid and what feels solid turnsout to be a cyst.
 Other Important examination points for the thyroid gland:
 A-Neurological Examination:Reflexes are brisk and exaggerated in
hyperthyroidism, Reflexes are delayed in hypothyroidism
 Eye Examination : There are three
1) Exophthalmos: the eye ball is pushed forwards by the increase in
retro-orbital fat, edema, and cellular infiltration. 
2) Lid lag (ask the patient to look down andfollow your finger or a pen
and you will seehis eye lid moving slower than his cornea)
3) Lid retraction
 Hand: Moist, sweaty, pulse is high in hyperthyroidism
2.1.3 CAUSES OF THYROID SW ELLING:
1. Thyroid cyst:
a. Benign
b. Diagnosed by U/S and FNA
c. Treated by aspirating the cyst
d. If it reoccurs up to two times aspirate it again but in the 3rd time
surgery should be done

348
 Thyroid Diseases 5

2. Multinodular goiter:
a. Can present as:
i. Incidentally
ii. With or without symptoms of hyper or hypothyroidism

Toxic Goiter:
A goiter that is associated with hyperthyroidism is described as a toxic
goiter. Examples of toxic goiters include diffuse toxic goiter (Graves’s
disease), toxic multinodular goiter, and toxic adenoma (Plummer
disease).Nontoxic goiter: A goiter without hyperthyroidism or
hypothyroidism is described as a nontoxic goiter. It may be diffuse or
multinodular.

iii. Local compression causing dysphagia, dyspnea, stridor,

plethora or hoarseness
iv. Solid
b. Diagnosed by US, FNA and then nuclear scan
i. Warm scan is normal like the lobe on the rightside of the
picture
ii. Hot: abnormal
iii. Cold (circled area): abnormal. And it means that area is not
up taking iodine hence it is no longer thyroid tissue,
indicative of malignancies in 15% of patients.
3. Inflammatory (thyroiditis)
a. Acute, very rare
b. Sub-acute, very rare
c. Hashimoto "chronic": most common and usually presents with
hypothyroidism> dx by serological markers, on biopsy lymphocytes,
monocytes, etc
4. Benign tumor: Follicular adenoma
5. Malignant tumor
2.2 THYROTOXICOSIS

 Thyrotoxicosis can be a manifestation of a number of thyroid conditions, but

the most common are:
1) Grave’s disease (usually affects the young)
2) Toxic multinodular goiter
3) Toxic nodule
2.2.1 SIGNS AND SYMPTOMS
1. Nervousness
2. Weight loss with Increased appetite
3. Warm moist skin
4. Heat intolerance
5. Sweating
6. Muscular weakness
7. Menstrual irregularities
8. Tachycardia +/- Arrhythmias ( especially in elderly where they may
present with atrial fibrillation)
9. Goiter

349
6 Common Neck Swellings

10. Systolic Bruit & thrill (a bruit maybe heard when applying the
stethoscope of the swelling) 
11. Eye signs (mentioned earlier)
2.2.2 LAB TESTS
 Increases T4, T3
 Decreased TSH (due to inhibition by high levels of T4 and T3)
2.2.3 MANAGEMENT
1. Medical
2. Radio-nuclear iodine
3. Surgery

Case:
Aisha is a 55-year old lady that presented to your clinic. Her main complaint is related to
some recent difficulty in hearing. The family noticed that she started to have difficulty in
understanding that she gained weight, and her voice started to be coarse.

Q: How to diagnose?
A: Decreases T4, T3, Increased TSH

2.3 THYROID CANCER

2.3.1 GENERAL CONSIDERATIONS:

 Thyroid cancers are usually non-functional, meaning they do not produce
symptoms
 Cancers can appear as solitary nodules or diffusely enlarged glands.
 A young patient " younger than 20" with a single thyroid nodule
should be considered as a case of thyroid cancer (papillary
carcinoma is the most common) until proven otherwise 
 Lymphatic spread of the cancer does not affect the prognosis
2.3.2 TYPES OF THYROID CANCER:  MEN IIa: medullary
1. Papillary carcinoma: carcinoma,
hyperparathyroidisim,
a. Accounts for 85% pheochormocytoma
b. Overall most common endocrine cancer
c. Appears in early adult life  MEN IIb: Medullary
carcinoma, mucosal
d. Lymphatic spread neuromas,
e. Good prognosis, 5 year survival is >95% pheochromocytoma and
2. Follicular carcinoma: marfanoid shape
a. Accounts for about 10%
b. Differentiation between benign and malignant is not easy
c. Blood spread
d. Doesn’t spread to lymph but spreads to bone and blood 
e. Prognosis not as good
3. Medullary carcinoma:
a. Accounts for about 7%
b. Arises from C-Cells
c. C-cells secrete calcitonin

350
 MCQs: 7

d. Familial medullary carcinoma accounts for 25% of medullary

carcinomas the other 75% are sporadic
e. Associated with MEN IIa/IIb syndrome (multiple endocrine
neoplasia)
f. Prognosis is not good, especially if it's part of MEN that's why we
screen family and we remove thyroid before age of 6 years.
g. Produces amyloid
4. Undifferentiated (anaplastic):
a. Usually in Old patients
b. Accounts for about 1%
c. Rapidly growing
d. Locally invasive
e. Rarely curable
5. Lymphoma
a. More common in our part of the world
b. Usually diagnosed post op
c. Treated by Chemo/radiotherapy.
3 MCQS:

1. The third postoperative day following thyroidectomy a patient c/o

tingling of her finger tips and is found to have serum calcium of
1mmol/l/. The next step in treatment should be:
a. Careful observation until the Calcium level increases
b. Administration of Vit. D
c. Administration of dihydrotachysterol
d. Administration of 1,25(OH) 2D (Calcitriol)
e. Administration of calcium gluconate by slow intravenous drip
2. Medullary Thyroid Carcinoma:
a. Is a tumor of Para follicular C cells
b. Produces thyroxin as the principle hormone
c. Are TSH dependent
d. Can be treated by radio-iodine ablation
e. T3 act as a tumor marker
3. What is the least likely cause of Hypercalcemia?
a. Metastatic tumor
b. Sarcoidosis
c. Acute pancreatitis
d. Hyperparathyroidism
e. Vit. D deficiency
4. The approach to patient with thyroid nodule includes the following
except:
a. Thyroid scan.
b. Fine needle aspiration.
c. Ultrasonography.
d. TSH T4 T3.
e. Calcitonin level.

Answer key: 1:E 2:A 3:E 4:E

351
 Introduction 1

BREAST DISEASES
1 INTRODUCTION

Overview of the structure and function of the breast.

1.1 ANATOMY OF THE BREAST

 Breasts (mammary glands) are modified sebaceous glands.

 The breast extends from the 2nd to the 6th ribs and transversely from the
lateral border of the sternum to the mid-axillary line.
1.1.1 BREAST BORDERS:
 Upper border: collar bone.
 Lower border: 6th or 7th rib.
 Inner border: edge of sternum.
 Outer border: mid-axillary line.
1.1.2 BREAST DIVISIONS:
Each breast is divided into 5 segments.
 Four quadrants:
By horizontal and vertical lines intersecting at the nipple (upper outer
quadrant, upper inner quadrant, lower outer quadrant, and lower inner
quadrant). Majority of benign or malignant tumors lie in the upper outer
quadrant 
 Tail of Spence (the axillary tail): an additional lateral extension of the breast
tissue toward the axilla.
1.1.3 EXTERNAL ANATOMY OF THE BREAST:  Glands of
 th
Nipple: pigmented and cylindrical, at the 4 intercostal space (at age 18) Montgomery can get
obstructed (blocked)
 Areola: pigmented area surrounding the nipple. and inflamed which
 Glands of Montgomery (Montgomery‟s Tubercles): sebaceous glands within could raise concerns to
the areola, which act to lubricate the nipple during lactation the female of a serious
pathology, even though
1.1.4 MUSCULATURE RELATED TO THE BREAST: it‟s a simple occlusion.

 The breast lies over the muscles that encases the chest wall. The muscles
involved include the pectoralis major (60%), pectoralis minor, serratus
anterior (30%), external oblique, latissimus dorsi, subscapularis, and rectus
abdominis fascia (10%).
1.1.5 INTERNAL ANATOMY OF THE BREAST:
The breast is composed of 3 different types of tissue:

352
2 BREAST DISEASES

1. Glandular tissue: It is the milk-producing tissue.

Each mammary gland consists of 15-20 lobes.
Each lobe is further divided into 20-40 lobules
composed of clusters of milk-secreting glands
(alveoli/acini) and is drained by a lactiferous
duct that opens onto the nipple.
2. Fibrous (supporting) tissue: Strands of
connective tissue called the suspensory
ligaments of the breast (Cooper‟s ligaments)
extend through the breast to the underlying
muscle separating the breast‟s lobes
3. Fatty tissue: Subcutaneous and retro-
mammary fat. It gives the bulk of breast. No fat
beneath areola and nipple.

1.1.6 LYMPHATIC DRAINAGE OF THE BREAST:

Internal mammary
 Superficial lymphatic nodes drain the skin and deep lymphatic nodes drain nodes most of the time
the mammary lobules. they can‟t be felt on
palpitation, they‟re only
o Axillary, infraclavicular, supraclavicular, parasternal (internal mammary) seen on imaging.
 Lymphatic drainage of the breast:
o The medial portion of the breast  to the internal mammary nodes
o The central and lateral portions 75-80%  drain to the axillary lymph
nodes
o Axillary lymph nodes:
Axillary lymph nodes can be classified anatomically into 5 groups and
clinically into 3 levels.
 Anatomical classification of axillary lymph nodes:
1. Anterior (pectoral) group: deep to pectoralis major.
2. Posterior (subscapular) group: along subscapular vessels.
3. Lateral group: along the axillary vein.
4. Central group: within the axillary pad of fat.
5. Apical group: which drains all of the other groups, lies behind the clavicle
at the apex of axilla.
 Clinical/surgical classification of axillary lymph nodes:
o This surgical classification is used in axillary dissection. It is based on
the relationship of the lymph nodes to pectoralis minor. There are 3
levels of axillary lymph nodes and options for dissection: 
1. Level 1: any lymph node below pectoralis minor (first group involved
in malignancy), account for 80% of lymph nodes.
2. Level 2: any lymph node behind pectoralis minor.
3. Level 3: any lymph node above pectoralis minor.
1.2 PHYSIOLOGY OF THE BREAST

Normal physiological breast changes in females.

 Puberty: need estrogen and progesterone.
o Estrogen: growth and appearance, milk-producing system.
o Progesterone: lobes & alveoli, alveolar cells become secretory.

353
 Clinical Approach 3

o Asymmetry is common 
 Menses:
o Progesterone: 3-7 days prior to menses, engorgement.  Asymmetry is a
common concern
o Physiologic nodularity: retained fluid. among female
o Mastalgia. adolescents. Typically,
 Pregnancy and lactation: the asymmetry is more
noticeable during
o Glandular tissue displaces connective tissue.
puberty and eventually
o Increases in size. breast size evens out
o Nipples prominent and darker. during development. If it
o Mammary vascularization increases. was a major and
o Colostrum present. persistent asymmetry a
breast augmentation or
o Attain Tanner stage V with birth. reduction surgical
 Aging: procedure may be
o Perimenopause: decrease in glandular tissue, loss of lobular and considered AFTER
alveolar tissue. breast
development/puberty is
o Fatten, elongate, pendulous. complete (NEVER
o Infra-mammary ridge thickens. interfere surgically
o Suspensory ligaments relax. during puberty).
o Nipples flatten.
o Tissue feels “grainy”.
Milk lines
1.3 NORMAL VARIATIONS OF THE BREAST

 Accessory breast tissue and supernumerary nipples, which develop along

the milk lines (sites of accessory breast tissue and nipples).
 Hair.
 Lifelong asymmetry.

Supernumerary
nipple

2 CLINICAL APPROACH  Management of a

patient with a breast
 History lump:
 Clinical examination - History and
 Imaging examination
 Cytology and tissue diagnosis. - Ultrasound and
mammogram if above
2.1 SPECTRUM OF COMPLAINTS 35 years old.
- FNAC or core biopsy
or excision biopsy
 Women come to see a breast surgeons for the following reasons: - Definitive treatment
1. Breast lump (painful/painless) - 60%  which is either:
2. Anxiety – 20% o Observation
3. Breast pain without a lump – 10% o Excision
o If malignant, along
4. Nipple discharge – 5% the lines of cancer
5. Change in breast contour – 2% cases

354
4 BREAST DISEASES

6. Nipple-areolar complex disorder – 1%

7. Axillary mass – 1%
8. Screen detected lesion – 1%
 Triple assessment of a patient with a lump:
 History and examination
 Mammogram (99%) if above 35 years old
 F.N.A
2.2 HISTORY   Breast presentation:
Full and complete history should be taken, particular attention should be paid to: -Skin dimpling:
carcinoma, aging, breast
 Age of the patient (e.g. 45 y/o lady has a higher risk than 16 y/o) infection, previous
 Breast development stating from childhood to present. breast surgery
 Endocrine status of patient mainly menstruation and OCP use. -Changes in
 Size of lump in relation to menses. nipple/areola: Duct
ectasia, carcinoma,
 Pattern of pain in relation to menses. paget‟s disease,
 How regular the cycle is and quantity of blood. eczema
 Changes in breast during previous pregnancies e.g. abscess, nipple -Painless lump:
discharge, retraction of nipple. carcinoma, cyst,
 Number of pregnancies. fibroadenoma,
 Breast feeding fibroadenosis
 Abnormalities which took place during previous lactation period e.g. -Painful lump: cyst,
abscesses, nipple retraction, milk retention. periductal mastitis,
abscess, sometimes
 Family history of breast diseases especially cancer and particularly in near carcinoma
relatives.
-Pain and tenderness
 Nipple discharge. (no lump): cyclical, non-
 Age at menarche. cyclical, very rarely a
 Age at 1st birth. carcinoma
 L.M.P. -The cardinal signs of a
 For post-menopausal women: H.R.T (hormonal replacement therapy) and late cancer of the
date of menopause. breast: hard, non-
tender, irregular lump,
tethering or fixation,
2.3 CLINICAL EXAMINAITON  palpable axillary lymph
nodes.
 Exposure: from the waist and above.
 Position: sitting, supine and 45o
 Inspection
o Inspect both breasts by having the patient perform the following
maneuvers while sitting:
o Patient‟s arms by her side.
o Patient‟s arms above her head.
o Patient‟s arms on her hips with valsalva (pectoral contraction maneuver).
o Leaning forward while sitting.
o Note for size, symmetry, skin changes (dimpling or tethering), nipple
complex (inversion or retraction), color, contour, and scars.
o Inspect axillae with the patient‟s arms over her head.
 Palpation:
o Patient should be lying supine.
o Place pad under shoulder to flatten breast.

355
 Clinical Approach 5

o Raise arm over her head.  Breast self-

o Abnormal finding? Check the other breast. examination and
o Palpate both breasts mammography:
 Palpate Sitting -BSE should be done
 Rest arm in your hand and palpate axilla. Her arm should be relaxed. once a month, preferably
 Palpate supra-clavicular and infra-clavicular nodes just after period. If the
women is post-
o Using preferred pattern menopausal, she should
o Palpate with pads of three fingers choose a day that she
o Note for any nipple discharge will remember each
o Palpate all lymph nodes (must examine ALL) month
 From distal arm to under arm with deep palpation -Mammogram should be
 Axillary (pectoral, medial, lateral, posterior, central) done annually or every 2
 Supraclavicular years if >50 years old
 Infra-clavicular
 Nodes deep in the chest or abdomen
 Infra-mammary ridge: shelf in the lower curve of each breast (Usually
missed during clinical examination)
o Examine normal side first.
o Examine abdomen and the back/lumbar spine (for metastasis)

 Imaging features
which can be associated
with ductal carcinoma in
situ (DCIS):
- Micro-calcifications
2.4 IMAGING linear (75-90%)
- Circumscribed mass
 When to image? - Ill-defined mass
- Prominent duct or
o Investigation of a palpable lump or nipple discharge. nodule
o Screening in appropriate groups (asymptomatic 40 y/o) - Architectural distortion
o Metastatic adenocarcinoma with an unknown primary. - Asymmetry
- Sub-areolar mass
2.4.1 MAMMOGRAPHY Benign Vs. Malignant
calc.:
2.4.1.1 DIAGNOSTIC VS. SCREENING MAMMOGRAPHY:
Based on size 
 Diagnostic mammography  performed in order to evaluate a breast Macrocalc. are always
complaint or abnormality detected by clinical examination. benign. Microcalc.
 Screening mammography  performed for asymptomatic „well‟ women to mostly benign but can be
malignant.
detect unsuspected lesions. E.g. routine screening for women who are 40 Based on shape 
years or older. Benign: punctate, linear,
spherical, popcorn,
2.4.1.2 CARDINAL MAMMOGRAPHIC FEATURES OF MALIGNANCY vascular, smoothly
dense.
 Speculated mass (stellate lesions)  check for the presence of a surgical Malignant: mostly ductal,
scar. All other stellates are presumed invasive carcinoma that requires work segmental and
up and biopsy. If unexplained, don‟t be seduced by stability. clustered.
Based on distribution 
 Architectural distortion without mass should be treated as stellate lesion. widespread bilateral
 MICRO-calcifications with casting or irregularity 60% of localization distribution is suggestive
biopsies are for calcifications, but only 25% of these yield malignancy. of a benign process

356
6 BREAST DISEASES

 Distribution (casting, linear, segmental, clustered)  segmental and

clustered indicate malignancy.
 Morphology (pleomorphism).
 Relationship to parenchyma.
 Circumscribed density with distinct margins.
 Asymmetric density

Speculated margins Segmental calcifications

2.4.2 BENIGN VS. MALIGNANT IMAGING CHARACTERISTICS IN

BREAST CANCER:

2.4.3 ULTRASONOGRAPHY
2.4.3.1 ROLE OF ULTRASOUND:
 Characterize a mammographic abnormality.
 Characterize a mammographically occult clinical abnormality.
 Initial examination in the younger women.
 Imaging guided biopsies.
 Some utility in distinguishing benign from malignant lesions.
 Still no role in screening even in the mammographically dense breast
 Developing role in monitoring neo-adjuvant therapy?
 What does ultrasound look for?
o Location of a lesion.
o Solid Vs. Cystic.
o Margins.
o Surrounding structures.
2.4.3.2 ADVANTAGES AND DISAVDVANTAGES OF ULTRASOUND

357
 Clinical Approach 7

 Advantages:
o Painless
o Does not use ionizing radiation
o Very good at detecting cysts
o Can “see through” mammographically dense breasts (done at any age)  Cysts can present as
a palpable mass or a
 Disadvantages: focal tender area within
o Not good for screening the breast the breast. A majority of
o Cannot always characterize lesions precisely cysts are found in
o More operator-dependent than mammography asymptomatic women
on their screening
2.4.3.3 ULTRASONOGRAPHIC FEATURES mammogram.
-On mammography:
 Cysts: they appear as a mass
and may have
o Contain no or few echoes
associated benign
o Have smooth margins rim/eggshell
o Often compressible with ID calcifications.
o Have posterior enhancement -On ultrasound: it is the
(increased echoes=whiter) confirmatory diagnostic
test, demonstrates a
 Benign masses: U/S Fibroadenoma well-defined mass
o Have smooth margins devoid of internal
o Have relatively uniform internal appearance echotexture (if any
o Don‟t disturb surrounding tissues internal echoes are
present, U/S guided
o Are usually wider than tall FNA is recommended to
 Malignant masses: fully exclude
o Have irregular or indistinct margins malignancy)
o Have heterogeneous internal
appearance
o Often cut across surrounding tissue
Speculated margins (suggestive
planes of malignancy)
o Are often taller than wide or rounded
(special types)
o The normal breast tissue appear as symmetrical waves under U/S.
Malignant lesions disturb that pattern but benign lesions follow that Benign mass: a simple
pattern. cyst

2.4.3.4 ULTRASOUND CORRELATION

Ultrasound/clinical correlation is as important as ultrasound/mammographic
correlation! Ultrasound can be considered as an extension of palpation.
 Challenges for ultrasound correlation:
o Small lesions in larger breasts.
o Small lesions deep within echogenic parenchyma.
o Dense parenchyma interspersed with fatty lobules.
o Surgically scarred breasts.
o Multiple mammographic lesions.
o Complicated cysts.
o Cellular malignancies.
 Fundamentals of mammographic/ultrasound correlation:
o Correlate lesion location
o Correlate lesion size
o Correlate lesion margin

358
8 BREAST DISEASES

o Don‟t assume that previous imaging assessment was correct (pull out all
the films if necessary).
o Take account of both mammographic & ultrasonography appearances.
o Most probably benign lesions are benign. Out of 543 probably benign
lesions in 5514 screening mammograms, only 1 was malignant (0.2%),
and 21% regressed or disappeared.
 Key points:
o Meticulous imaging technique.
o Careful correlation of mammogram with ultrasound, and imaging with
clinical findings.
o Clear communication reduces errors.
2.5 CYTOLOGY AND BIOPSY

 Fine-needle aspiration cytology

o Procedure description: a thin needle is inserted into the mass for sampling
of cells that are later on examined under a microscope.
o Clinical, U/S guided, mammotomes.
o Sensitivity 80-98%
o False negative 2-10%
o Scoring of result code 9  code 5
 Core biopsy
o Tissue diagnosis
o Painful
o Costly
o Receptor status
 Open biopsy
2.6 NIPPLE DISCHARGE

• 5% of women coming to the clinic complain of nipple discharge.

• 95% of these complaints are benign.  For further
evaluation of
spontaneous nipple
2.6.1 CAUSES OF NIPPLE DISCHARGE
discharge a ductography
Commonest causes in non-pregnant women: can be performed.
Ductography is useful in
 Carcinoma detecting the location of
 Intra-ductal papilloma (most common cause)  the lesion within the duct
 Fibrocystic changes and the extent of
 Duct ectasia involvement. This
information can be
 Hypothyroid extremely helpful in pre-
 Pituitary adenoma (prolactin secreting adenoma, can present with surgical planning.
galactorrhea)
2.6.2 CLINICAL CHARACTERISTICS:
 Physiologic discharge (e.g. lactation)  usually bilateral, multiple ducts,
non-spontaneous, screen for phenothiazine use (antipsychotic)
 Pathologic discharge  Unilateral, spontaneous (without squeezing the
nipple), single duct, discolored discharge

2.6.3 CLINICAL EVALUATION

359
 Common Benign Breast Disorders 9

 Most important points in history of nipple discharge are 

o Is it spontaneous or on pressure? Is it coming from single or multiple? Galactocele:
o Colors: Serous, serosanguinous, bloody, clear, milky, green, blue-black. Def.: Cyst containing
 R/O mass by clinical examination and mammogram. milk.
 Identify source of discharge and test for presence of blood in discharge CP: dull aching pain with
 Consider ductography a well formed lump
 Lab tests: thyroid, prolactin. Diagnosis: clinically or
U/S
Management: aspiration
both therapeutic and
diagnostic under full
aseptic technique to
prevent infection. If it
appeared small on U/S
there‟s no need to
aspirate just reassure
the patient. If it
accumulates again then
aspirate again while
reassuring the patient
that it‟ll resolve after
lactation period.

2.6.4 MANAGEMENT:
 Physiologic
o Treat cause if present
o Follow-up 6 months (observation)
 Pathologic
o Biopsy and excise (single duct excision or total duct excision)
3 COMMON BENIGN BREAST DISORDERS  Additional notes:
 Big cyst >2 cm must
 Fibrocystic changes aspirate
 Fibroadenoma  Atypia or hyperplasia
 Intraductal papilloma  if atypia / hyperplasia
 Mammary duct ectasia / dysplasia changes
were present must
 Mastitis EXCISE, if simple then
 Fat necrosis just reassure the patient
 Phylloides tumor & conservative
 Male gynecomastia management.
 Galactocele  Complicated cyst (i.e.
both solid and cystic
3.1 FIBROCYSTIC CHANGES components) 
Biopsy is needed from
3.1.1 CHARACTERISTICS solid component to
exclude malignancy.
 Most common breast pathology
 Constant cyst (i.e.
 Lumpy, bumpy breasts doesn‟t change with
 50-80% of all menstruating women multiple imaging in
 Commonest incidence among age 30-50 different times)  must
- 10% in women less than 21 biopsy
 Caused by hormonal changes prior to menses

360
10 BREAST DISEASES

 Relationship to breast cancer doubtful

3.1.2 SIGNS AND SYMPTOMS
 Mobile cysts with well-defined margins
 Singular or multiple
 May be symmetrical
 Upper outer quadrant or lower breast border
 Pain, discomfort and tenderness
 Cysts may appear quickly and decrease in size
 Lasts half of a menstrual cycle
 Subside after menopause, if no HRT.
3.1.3 INVESTIGATIONS  Fibroadenoma:
To leave alone or to
 Aspirate cyst fluid 
excise?
o If bloody  go for surgical biopsy.
o If non-bloody and disappear completely  observe.  EXCISE if 
o If non-bloody and doesn‟t resolve  surgical biopsy. - >3-4 cm or giant
fibroadenoma
 Imaging for questionable cysts
o In young patients only U/S is performed show multiple cysts -localized
o In 40 and above patients both U/S and mammogram are performed to -painful
exclude any underlying malignant pathologies. -rapidly growing
-a family history of
3.1.4 MANAGEMENT malignancy (does NOT
mean that fibroadenoma
 Treatment based on symptoms is pre-malignant but
 Reassure patient done only to relieve the
 „‟Atypical Hyperplasia‟‟ on pathology report indicates increased risk of breast patient‟s worries)
cancer must excise -patient‟s preference
 Comfort measures: -indeterminate diagnosis
o Eliminate Methylxantines (coffee, chocolate): may take 6 months for -if 35 y/o and older
relief. recommended
o Local heat/cold If left alone  it‟ll either
o Wear a good supporting bra remain the same or
o Low-Sodium diet regress (some patients
during pregnancy it
o Vitamin E: Antioxidant but do not take more than 1200/day
regresses) or increase in
 Medications for mastalgia: size or calcify
o NSAIDS (simple analgesia)
o Monophasic oral contraceptive pills (to stabilize hormonal levels)
o Spironolactone
o Dopamine Agonists: Bromocriptine
o Rare or former use: Danazol (for severe cases, side effects include
acne and hirsutism, only 50% respond to it, mostly not used), Tamoxifen,
GnRH agonist (Luprolide)
3.2 FIBROADENOMA

3.2.1 CHARACTERISTICS
 Second most common breast condition (most common lump)
 Most common in black women
 Late teens to early adulthood (15-30 years old of age)
U/S Fibroadenoma

361
 Common Benign Breast Disorders 11

 Rare after menopause

 Totally benign, and NO malignancy potential
3.2.2 SIGNS AND SYMPTOMS
 Firm, rubbery, round, mobile mass
 Painless, non-tender
 Solitary, 15-20% are multiple
 Well circumscribed
 Mostly located in upper-outer quadrant of the breast Mammogram showing multiple
calcified fibroadenomas
 1-5 cm or larger (if more than 5 cm it is called a giant fibroadenoma)
3.2.3 INVESTIGATIONS AND TREATMENT

 Triple assessment
 Imaging: U/S mostly used because its more common in young and
mammogram
 Biopsy
 Excision and close follow-up
3.3 INTRADUCTAL PAPILLOMA
 Papilloma: To leave
or to excise?
3.3.1 CHARACTERISTICS
 If single papilloma 
 Slow-growing can observe and see if it
 Overgrowth of ductal epithelial tissue disappears
 Usually not palpable  If it doesn‟t resolve 
 Cauliflower-like lesion excise
 Length of involved duct  If presented with
 Most common cause of persistent bloody nipple discharge (IMPT) intraductal
PAPILLAMATOSIS
 40-50 years of age (appears as multiple
filling defects on
3.3.2 SIGNS AND SYMPTOMS ductogram) considered a
 Watery, serous, serosanguinous, or bloody discharge pre-malignant condition
 must excise
 Spontaneous discharge
 Usually unilateral Exclude malignancy in
young by US or
 Often from single duct  pressure elicits discharge from single duct ductogram (filling
 50% no mass palpated defect), if 40 and above
by U/S, ductogram and
3.3.3 INVESTIGATIONS AND TREATMENT mammogram

 Test for occult blood

 Ductogram
 Biopsy
 Excision of involved duct
3.4 MAMMARY DUCT ECTASIA

3.4.1 CHARACTERISTICS
 Inflammation and dilation of sub-areolar ducts behind nipples, completely
benign

362
12 BREAST DISEASES

 May result in palpable mass because of ductal rupture

 Greatest incidence after menopause
 Etiology Unclear  Ducts become distended with cellular debris causing
obstruction
3.4.2 SIGNS AND SYMPTOMS
The problems behind
 Multi-colored discharge this condition:
o Thick, pasty (like toothpaste)  Infection:
o White, green, greenish-brown or serosanguinous
Duct
 Intermittent, no pattern ectasiastasisrisk of
 Bilaterally from multiple ducts infectionhigher chance
 Nipple itching with drawing or pulling (burning) sensation of abscess (periductal
mastitis) caused by
3.4.3 INVESTIGATIONS AND TREATMENT mixed organismsbroad
spectrum antibiotics and
 Test for occult blood abscess drainage.
 Imaging  Mammogram and sonogram Similar presentation to
 Biopsy  Excision of ducts if mass present malignancy:
 Antibiotics Inflammationcan
 Close follow-up retract nipple patient is
worried about
malignancy U/S and
mammogram according
3.5 MASTITIS to agereassure the
patient, if 40 and above
3.5.1 CHARACTERISTICS take aspiration for
cytology
 Breast infection when bacteria enter the breast via the nipple
-left picture: slit-like
 Ducts infected nipple characteristic of
 Fluid stagnates in lobules duct ectasia
 Usually during lactation -right picture: nipple
 Penicillin resistant staphylococcus common cause retraction from
carcinoma
3.5.2 SIGNS AND SYMPTOMS
 Pain and tenderness
 Nipple discharge: -Pus -Serum -Blood
 Localized induration
 Fever and rigor  Lactating women
 Abscess: localized tenderness, severe fever and rigor presented with fever,
painful and tender
3.5.3 TREATMENT breasts  most likely
mastitis broad-
 Antibiotics spectrum antibiotics
o „‟Oxacillins‟‟ for PP mastitis (PP=postpartum=after childbirth) (cephalosporin 1
st

o Cephalosporin for other abscesses  cephalexin, Keflex generation IV), warm

sponges, if abscess
 Empty breast if PP must drain it.
 Incision and drainage of abscess
3.6 FAT NECROSIS

3.6.1 CHARACTERISTICS
 Cause

363
 Common Benign Breast Disorders 13

o Trauma to breast (e.g. seat belt trauma in car accidents)

o Surgery
 Necrosis of adipose tissue
3.6.2 SIGNS AND SYMPTOMS
 Pain or mass  usually non-mobile mass
 Inflammatory
3.6.3 TREATMENT carcinoma vs. mastitis:
 Resolves over time without treatment but may be excised -may have similar
appearance, but
3.7 PHYLLOIDES TUMOR (CYSTOSARCOMA) completely different
history

3.7.1 CHARACTERISTICS -inflammatory carcinoma

non-lactating elderly,
 Giant fibroadenoma (a variant of fibroadenoma) with rapid growth (patient peau d‟orange, must
presents with a history of a rapidly growing mass) perform U/S,
mammogram and
 Malignant potential, lesions > 3 cm are more likely to be malignant biopsy.
 Most are benign, 25% recur locally if incompletely excised
 The malignant form of this lesion mostly locally malignant (about 10%) can  Can a lactating
female with abscess still
metastasize hematogenously to the lungs and not to the axillary lymph breast feed her
nodes newborn? YES, except if
 Often occurs in women aged 40+ her baby appeared to be
sensitive to antibiotic
3.7.2 INVESTIGATIONS AND TREATMENT administered

 Imaging: both mammography and ultrasound, they present as well-defined

masses that are very similar to a benign fibroadenoma. The malignant forms
are more likely to have cystic spaces on U/S  Carcinoma vs. fat
necrosis:
-fat necrosis is important
because both clinically
and radiologically can
appear very similar to
malignancy. In order to
exclude cancer a biopsy
should be performed.

 Treatment  excision is the only treatment! Chemotherapy and

radiotherapy are not effective.
3.8 MALE GYNECOMASTIA

3.8.1 CHARACTERISTICS
 Diffuse hypertrophy of breast
 30-40% of male population
 Adolescence and older men
 Caused by imbalance of estrogen/testosterone
 Medical conditions (hepatitis, COPD, hyperthyroidism, TB)
 May be associated with genetic cancer families

364
14 BREAST DISEASES

 Must exclude testicular and adrenal malignancies (hormone producing

tumors)
 Medications associated with gynecomastia:
o Marijuana
o Narcotics
o Phenothiazines
o Diazepams
o Anything that affects the CNS
3.8.2 TREATMENT
 If pre-puberty  wait to see if it resolves
 Change medication
 Treat underlying illness
 Occurs in families with genetic mutation
o Colon, prostate cancer
4 BREAST CANCER

4.1 FAST FACTS

 Killer of women:
o USA 1:8
o KSA? 1:15
o 187000 cases of cancer breast in one year (USA)
o 45000 deaths due to it in one year (USA)
 Breast cancer is the most common cause of death from cancer in western
women
 Every day in Australia, over 30 women discover they have breast cancer
 In Australia 11,400 people (11,314 women and 86 men) were diagnosed with
breast cancer in 2000.
 9 out of 10 women who get breast cancer do not have a family history of the
disease
 Age is the biggest risk factor in developing breast cancer – over 70% of cases
occur in women over 50 years
 Women aged 50–69 who have a breast screen every two years can reduce their
chance of dying from breast cancer by at least 30%
 Breast cancer is the most common cancer in women aged over 35 years - 25%
of all cancers diagnosed
 The average age of diagnosis of breast cancer in women is 45 - 55 years
 During the period 1994 to 1998, the five year survival rate for women diagnosed
with breast cancer was 85 %
 Although we know of many factors that contribute to the risk of women getting
breast cancer, the cause remains unknown
 Most common type of breast cancer is ductal carcinoma.
 Five year survival rates

365
 Breast Cancer 15

Stage at diagnosis Survival rates (%)

Localized 96.8
Regional 75.9
Distant 20.6
*based on U.S. statistics from 1986 to 1993, reprinted with permission from American Cancer Society.

 Established risk factors for breast cancer in women:

Relative - Age (older age group higher risk)
risk - Country of birth (North America, Northern Europe)
- Mother and sister with history of breast cancer, especially at an early age
>4 - Biopsy confirmed atypical hyperplasia and a history of breast cancer in a
first degree relative

- Nodular densities on mammogram occupying >75% of breast volume

- History of cancer in one breast
Relative - Radiation to chest
risk - Mother or sister with history of breast cancer, diagnosed at an early age
- Biopsy-confirmed atypical hyperplasia without a family history of breast
2.1 cancer

- Socioeconomic status (high)

- Place of residence (Urban
- Race/ethnicity (White >45 and Black <45)
- Religion (Jewish)
- Nulliparity, breast cancer >40 years of age
Relative - Age at first full-term pregnancy, age at menarche, age at menopause
risk - History of primary cancer in endometrium, ovary
1.1 - Obesity (Obese breast cancer > 50 years, Thin breast cancer <50 years)

4.2 STAGING CLASSIFICATION OF BREAST TUMORS

Stage 0 Stage 1 Stage 2 Stage 3 Stage 4

Neither Tumor less Tumor more than 2 Tumor more than 5 Tumor of any size with 50 y/o female with a
palpable than 2 cm, no cm but less than 5 cm, with skin distant metastases such 2 cm tumor and liver
tumor nor lymph node cm, 1 ipsilateral involvement or as bone, liver, lungs, metastasis  stage 4
axillary involvement axillary lymph node fixation, and brain and including
lymph involvement involvement of supraclavicular node
nodes. (movable) fixed lymph node involvement

366
16 BREAST DISEASES

4.3 HISTOPATHOLOGICAL TYPES OF BREAST CANCER

 Surgical treatment of
breast cancer depending
 Infiltrating (or invasive) Ductal Carcinoma (IDC) on stage:
o Starting in a milk passage, or duct, of the breast, this cancer breaks
Stage 1 and 2  WLE or
through the wall of the duct and invades the breast‟s fatty tissue. It mastectomy, axillary
can spread to other parts of the body through the lymphatic system nodes then radiotherapy
and through the bloodstream. Infiltrating or invasive ductal carcinoma and chemotherapy
accounts for about 80 percent of all breast cancers. Most common Stage 3  neo-adjuvant
type. chemotherapy then
 Infiltrating (or invasive) Lobular Carcinoma (ILC) surgery
o This type of cancer starts in the milk-producing glands. About 10 to 15 Stage 4  no role of
percent of invasive breast cancers are invasive lobular carcinomas. surgery
These are multicenteric, and they can appear in the other breast as
well (bilateral).
 Medullary Carcinoma
o This type of invasive breast cancer has a relatively well-defined
distinct boundary between tumor tissue and normal breast tissue. It
accounts for about 5 percent of all breast cancers. The prognosis for
medullary carcinoma is better than that for invasive lobular or invasive
ductal cancer
 Colloid Carcinoma
o This rare type of invasive disease, also called mucinous carcinoma, is
formed by mucus-producing cancer cells. Prognosis for colloid
carcinoma is better than for invasive lobular or invasive ductal cancer.
 Tubular Carcinoma
o Accounting for about two percent of all breast cancers, tubular
carcinomas are a special type of invasive breast carcinoma. They
have a better prognosis than invasive ductal or lobular carcinomas
and are often detected through breast screening.  Mammogram of
 Adenoid Cystic Carcinoma DCIS with malignant
o This type of cancer rarely develops in the breast; it is more usually microcalcifications. Note
the fine, linear,
found in the salivary glands. Adenoid cystic carcinomas of the breast heterogeneous clustered
have a better prognosis than invasive lobular or ductal carcinoma. calcifications associated
with an ill-defined mass
4.4 PROGNOSTIC FACTORS lesion. Although the
hallmark imaging feature
 Size of tumor for DCIS is the presence
of microcalcifications,
 Grade of tumor DCS can also present
 Lymph nodes involvement less frequently without
them.
5 BREAST CANCER: Treatment

5.1 DUCTAL CARCINOMA IN SITU TREATMENT

367
 Breast Cancer: Treatment 17

 Depending on the degree of DCIS the options of treatment are

o Total mastectomy
o Lumpectomy
o Lumpectomy and radiation therapy
 DCIS does not spread to the axillary lymph nodes so these are usually not
removed.
5.2 LINES OF TREATMENT

 Surgery:
o For Stage I and II WLE or mastectomy + axillary nodes.
o Surgical Intervention: 1. Mastectomy 2. W.L.E (wide local excision)
 Radiotherapy.
 Chemotherapy.
 Hormonal therapy.
 Ovarian ablation.
 Reconstruction
5.2.1 CHEMOTHERAPY
 Chemotherapy for breast cancer is usually given in cycles every 3 or 4 weeks.
 The common schedules include:
o CMF (Cyclophosphamide, Methotrexate and 5-Flurouracil)
o AC (Adriamycin, Cyclophosphamide)
o Taxol or Taxotere
 Chemotherapy side effects:
o Fatigue
o Anorexia
o Nausea and vomiting
o Hair loss
o Effects on the blood.
o Mouth problems
o Skin problems
o Fertility
o Bowel problems
5.2.2 RADIOTHERAPY
 Side effects
Common reactions Uncommon reactions
During the course of  skin reddening and  skin blistering
treatment irritation  nausea
 Fatigue  rib fractures (less than 1
 loss of hair in every 100)
 sore throat
After the course of  Discomfort and  Pneumonitis and
treatment sensitivity in the treated scarring (about 1 or 2
area. women in every 100
 increased firmness women between 6
 swelling of the treated weeks and 6 months
breast after therapy

368
18 BREAST DISEASES

5.2.3 TAMOXIFEN
 Tamoxifen is a drug that has been used for the treatment of breast cancer. It
can increase survival for some women with breast cancer and reduce their
risk of developing cancer in the opposite breast. Tamoxifen is sometimes
used whose breast cancer recurs.
 It is also being tested to see if it can prevent the development of breast
cancer in unaffected women who are at an increased risk because of a
strong family history of the disease.
 Tamoxifen is taken by mouth. Tablets are either 10 mg or 20 mg.
 It is usually started after surgery or after the completion of radiation Rx
 Tamoxifen should take it at the same time each day.
 Currently the recommended length of Tamoxifen therapy is five years.
Common side effects Uncommon side effects
 Hot flushes or sweats  Light-headedness, dizziness,
 Irregular menstrual periods (in headache or tiredness
women who have not gone through  Rash
the menopause)  Nausea
 Vaginal irritation, including vaginal
dryness or discharge
 Fluid retention and weight gain

5.3 LYMPHOEDEMA

 Definition: Lymphedema is long-term swelling of the arm after axillary

surgery or radiotherapy to the axilla.
 Symptoms: include a general heaviness of the arm, a swelling of the fingers
or sometimes difficulty putting on a long sleeve.
 The earlier treatment is started the easier it is to achieve good results.
 Less than 1 in 10 women who have had either lymph glands removed or
radiation to the armpit will develop noticeable lymphedema. This risk
increases to 1 in 3 if the pt. had both of these treatments.
 It can occur any time after the operation, even up to 10 years.
5.4 POST-OPERATIVE BREAST RECONSTRUCTIONS

 The aim of breast reconstruction is to rebuild the breast shape and, if

desired, the nipple and the areola.
 Benefits:
o Reconstruction usually doesn‟t restrict any later treatments, nor does it
usually interfere with radiotherapy, chemotherapy or hormone therapy.
o The patient will not need to wear an external prosthesis.
o Follow-up after the operation is no more difficult and any recurrence of
cancer in the area can still be detected.
o Some women feel more self-confident and feminine after reconstruction
 There are two main types of breast reconstruction:
o tissue or skin expander with breast implants
o flap reconstruction

369
 MCQs 19

6 MCQS

1. Ductal carcinoma in situ (breast):

a. In the great majority of cases presents as a palpable mass
b. Usually present as mammographic finding of micro-calcification
c. Mastectomy is the treatment of choice in all cases
d. Axillary dissection is an integral part of its surgical treatment
2. It is advisable to remove a fibroadenoma if:
a. It is painful
b. It is more than 3 cm in size
c. There is a positive family history of breast cancer
d. All of the above
3. All the following are mammographic features of breast carcinoma except?
a. Skin and nipple discharge
b. Diagnostic for women below 20
c. Speculated mass
d. Micro-calcification
4. All true for fibroadenma except:
a. Microscopically have both epithelial and stromal components
b. During pregnancy and lactation may undergo partial/total infarction
c. Affect old females
d. Are pseudocapsulated

5. Regarding intraductal papilloma. All true except?

a. Characterized by papillary configuration
b. Solitary intraductal papilloma‟s are lesion of large duct
c. May present with bloody nipple discharge
d. Does not require surgical excision
6. Which of the following factors increases the risk of breast cancer among
women?
a. Obesity and nulliparity
b. Age at menarche
c. Multiple pregnancies
d. Low-fiber diet

 Answer Key: 1;B , 2;D , 3;B , 4;C , 5;D , 6;A

370
 Adrenal diseaes 1

ADRENAL GLAND DISEASE

1 INTRODUCTION

1.1 HISTORY

 1563: Anatomy
 1855: Addison described clinical features of the syndrome named after him
(primary adrenal insufficiency)
 1912: Cushing described hyper-cortisolism [Cushing’s disease vs. syndrome:
Disease, problem in pituitary but syndrome is anything else apart from
pituitary]
 1934: The role of adrenal tumors in hypercortisolism understood
 1955: Pheochromocytoma was first described by Frankel (before that all
patients with this disease died b/c of crisis and there was no treatment)
 2003: First robotic adrenalectomy was performed.
1.2 EMBRYOLOGY  The adrenals start
producing hormones
 Paired gland (almost as big as dates) during childhood but in
o Cortex (coelomic epithelium) very low levels > not
 Outermost layer: Zona glomerulosa  Mineralocorticoids enough to differentiate
b/w male and female,
 Intermediate layer: Zona fasciculata  Glucocorticoids but between the ages of
 Innermost layer: Zona reticularis (3rd year)  Sex hormones 10-12 it starts
o Medulla (ectoderm: neural crest) functioning, finally at the
 Medulla: secrete 20% nor epinephrine, and 80% epinephrine age of 13 differences
 Ectopic tissues: spread in the neck & torso (chest, abdomen & pelvis). That’s appear.
why pheochromocytoma maybe thoracic in origin.
1.3 ANATOMY

 The adrenals cannot be palpated normally; if it was palpable it's most likely  The adrenals are
cancer. located deeply
 What is clipped in surgeries (adrenalectomy) is the veins! Any tear may (retroperitoneal organs),
which makes it difficult to
cause severe hemorrhage..
remove them.
 The adrenal vein returns the blood from the medullary venous plexus and One approach: from the
receives branch from the cortex. It emerges from the hilum and on the right back below 12th rib,
side and opens into the inferior vena cava, and on the left side into the renal enter fascia surrounding
vein. adrenal gland > not
applicable to all adrenals
 That’s why the right side is shorter (more prone to bleed), while the left side is e.g. big adrenals
longer.
 When sampling the right adrenal we take from Right adrenal vein and for left
adrenal we take from Left renal vein.
 Each gland has 3 arteries and one vein. Arteries comes from:
o Inferior phrenic > superior suprarenal artery
o Abdominal aorta > middle suprarenal artery
o Renal artery > inferior suprarenal artery
1.4 PHYSIOLOGY

371
2 Adrenal Gland Disease

The adrenal glands secrete different hormones base on the layer that is  The precursor for all
secreting. these hormones is
cholesterol and
 Adrenal cortex in each layer there is an
o Aldosterone enzyme converting it to
o Cortisol the appropriate hormone
o Sex steroids & there is a limiting step
 Adrenal medulla: > once a disease affects
it, it leads to over-
o Noradrenaline (20%) secretion in one way and
o Adrenaline (80%) problem in the other
way.
1.5 ADRENAL IMAGING

 CT scan: to differentiate between benign and malignant

o Benign
 Intensity, texture similar to liver  CT scan is the gold
 Low attenuation standard
 Homogeneous (one color, there is no hypo & hyper density at the
same time)
 Smooth border
 Smooth contour  Tissue biopsy will
 < 4 cm in greatest dimension (the first criteria to be checked and give you a definite
diagnosis (if it's a benign
then the others, size should be less than 4) or malignant mass) - but
o Malignant lesions: CT can give you an
 High attenuation (>30 HU) [hyper-vascular – more white] indication
 Heterogeneous
 Irregular borders
 Local/ vascular invasion
 Lymphadenopathy
 Metastases.
 Large size (>6cm) ) (black size 6cm-12cm malignant .. remove it
black size 2cm - 4cm  cyst)
 MRI. (CT still gold standard but if MRI is available, it’ll give a better picture)
 Nuclear scan. (If you suspect pheochromocytoma - to look at the function of
the mass > see uptake of gland)
 PET scan. (If you are looking for cancer > hot spots)
2 ADRENAL DISEAES

2.1 INCIDENTALOMA ( MOST COMMON )

 Found in 1-4 % of CT scans

 Incidence increases with age
 Causes:
o Small nonfunctioning adrenal tumors: MOST COMMON (>80%)
o Some with subclinical secretions of hormones (usually missed by the
patient and physician)
o Subclinical Cushing 5%
o Pheochromocytoma>if functioning  interfere regardless of size 5%
o Adrenocortical cancer 5%
o Metastatic carcinoma 2%
o Conn’s

372
 Adrenal diseaes 3

2.1.1 CLINICAL PATHWAY

PAC: Plasma aldosterone concentration

PRA: Plasma renin activity
PAC: PRA for Conn’s. Metanephrine: look for pheochromocytoma. Single dose dexamethasone:
for Cushing’s.
----------------------------------------------------------------------------------------------------------------------------------
 If functioning mass  Surgery.
 If non-functioning mass  CT scan
 CT may show:
 Benign appearance (< 4 cm) you repeat the scan after 3-12 months.
 If it secretes or has a malignant appearance we perform surgery.
 Handled based on the Size and function.

2.2 HYPERALDOSTIRONISM (CONN'S)

2.2.1 CAUSES:
1. Primary hypertension + metabolic alkalosis + with or without hypokalemia
 primary hyperaldosteronism
a. Adenoma (Most common)
b. Idiopathic bilateral adrenal hyperplasia.
c. Unilateral adrenal hyperplasia.
d. Adrenocortical carcinoma.
e. Familial (rare)
2. Secondary to any decrease in renal perfusion  Causes secondary
hyperaldosteronism
a. Renal artery stenosis
b. CHF (congestive heart failure)

373
4 Adrenal Gland Disease

c. Liver cirrhosis
d. Pregnancy
e. Primary hyperaldosteronism

High aldosterone
 Na and water retention + K+ loss → ECF volume expansion & HTN
 Hypokalemia → myopathy; muscle weakness
 Acid excretion (H+ secretion from tubules) → metabolic alkalosis
 Renin angiotensin system controls aldosterone secretion:
o Renal stenosis → ↓ blood flow to kidney → juxtaglomerular apparatus senses decreased flow
(decreased volume) → retain Na+ and water → ECF expansion
∴ Anything that causes a decrease in renal perfusion can cause secondary hyperaldosteronism

2.2.1.1 PRIMARY HYPERALDOSTERONISM

 Excessive production of aldosterone by the adrenal glands independent of
any regulation by the renin-angiotensin system
 Age 30-50 years (middle age group)
 Female > male, 2:1 (females usually more prone to endocrine diseases and
cancers)
 Prevalence 5-13%
 Clinical features: “patients will mostly present with fatigue (weakness b/c of
↓K+) & persistent HTN (uncontrolled, even w/3-4 medications)”
o HTN (hypertension) with or without hypokalemia 
o Weakness, polyuria, parasthesias, tetany, cramps
o Metabolic alkalosis, relative hypernatremia
o Elevated aldosterone secretion and suppressed plasma renin activity
(b\c of aldosterone hypersecretion)
 Diagnosis of 1ry hyperaldosteronism
a. Screening tests:
i. PAC (ng/dl) / PRA (ng /ml) >20 (ordered by the
endocrinologist not the surgeon)
ii. Plasma aldosterone > 15 ng/dl (could mean it’s Conn’s)
b. Confirmatory tests:
i. Sodium suppression test (to differentiate b\w primary &
secondary)
1. In primary secretion is not affected ≠ in secondary
secretion is suppressed
ii. Urinary aldosterone excretion >14 ug/ 24hr
2.2.2 TREATMENT AND MANAGEMENT
1. Pre-operative preparation:
a. Spironolactone: competitive aldosterone antagonist (corrects
pathology caused by aldosterone by binding to its receptors)
i. Promotes K retention (K+ sparing diuretic)
ii. Reduces extracellular volume
iii. Reactivates the renin-angiotensin-aldosterone system
b. Amiloride: not as common as spironolactone
c. Other K+ sparing diuretics
2. Surgery:

374
 Adrenal diseaes 5

a. Laparoscopic adrenalectomy
b. Open surgery
3. Medical treatment (if surgery is not possible) due to:
a. Unfit patients.
b. Bilateral gland pathology. (Bilateral adenoma or hyperplasia)
4. Prognosis
a. 1/3 persistent hypertension: patients should know that 1/3 of patient
won’t be cured from hypertension
b. K levels will be restored (Normal daily activity is restored).
i. Usually after treatment they get back to their normal lives
with no complaints of HTN
2.2.3 CLINICAL PATHWAY

375
6 Adrenal Gland Disease

 Some medication induce aldosteronism → stop them and then start screening and confirmatory
tests
 If you confirm hyperaldosteronism → do CT
 Venous sampling: catheters all the way to IVC from right & left side → see the
 gradient
 Lateralization (hormones higher in right than left) → this is the diseased gland → right
adrenalectomy
 If no gradient → give medical treatment b\c you can't take out both adrenals, otherwise you
have to replace adrenal hormones i.e. glucocorticoids and mineralocorticoids

2.3 PHEOCHROMOCYTOMA

“When there is a patient with pheochromocytoma in the ward everyone is ready; the
physician, surgeon, anesthetist and ICU physician- to arrange an ICU bed, administer
α- & β-blockers, and prepare the OR. Why? B/c they might lose him if BP shoots up
>bleeding > death.”

2.3.1 EPIDEMIOLOGY  If you suspect

 Less than < 0.1% of patients with hypertension pheochromocytoma, DO
NOT treat it as
 Not common in our community outpatient. The patient
 5% of tumors discovered incidentally on CT scan (less than 4-5 cm but could die in crisis.
functioning)
 Most occur sporadically (no genetic predisposition)
 Associated with familial syndromes, such as:
o Multiple endocrine neoplasia type2 (MEN2A) 40%
o MEN 2B
o Reckling hausen disease (Neurofibromatosis type I)
o VonHippel-Lindau disease
 90% of patients with pheochromocytoma are hypertensive (Once you
diagnose the patient for the first time with HTN you HAVE to perform an US
to the abdomen)
o Hypertension is less common in children
 In children, 50% of patients have multiple (bilateral) or extra-adrenal tumors
2.3.2 SIGNS & SYMPTOMS
Clinical findings are variable
 Episodic or sustained hypertension
 Triad of palpitation, headache, and diaphoresis
 Anxiety, tremors and weight loss
 Dizziness, nausea, and vomiting
 Abdominal discomfort, constipation, diarrhea
 Visual blurring
 Tachycardia, postural hypotension
 Hypertensive retinopathy (in short period of HTN history, few years only!)
2.3.3 ESSENTIAL FEATURES
 Episodic HEADACHE (due to HTN), excessive SWEATING, PALPITATIONS, and
VISUAL BLURRING
 HYPERTENSION, frequently sustained, with or without paroxysms 

376
 Adrenal diseaes 7

 Postural tachycardia and hypotension

 Elevated urinary catecholamines or their metabolites, hyper-metabolism,
hyperglycemia
 Rule of 10s: 
o 10% malignant
o 10% familial
o 10% bilateral
o 10% multiple tumors
o 10% extra-adrenal (“all places including head and neck“ but the
commonest is the abdomen, that's why we have to U/S the abdomen)
2.3.4 EXTRA ADRENAL PHEOCHROMOCYTOMA
Very RARE
 Abdomen (75%) [Closest to normal site so it is the most common]
 Bladder (10%)
 Chest (10%)
 Pelvis (2%)
 Head and neck (3%)
2.3.5 WORK UP
 History and physical exam
 Suspect pheochromocytoma based on symptoms
 CT, MRI, or other scans
 Plasma and urine studies (metanephrines, catecholamines, VMA)
 Begin treatment with a-blockers
 Possible MIBG scan
 Operative excision of tumor
2.3.5.1 LAB FINDINGS
 Hyperglycemia “and they cannot maintain fasting; they become hypoglycemic
– we can differentiate it from Cushing”
 Elevated plasma metanephrines
 Elevated 24-hour urine metanephrines and free catecholamines
 Elevated urinary vanillylmandelic acid (VMA) 
 Elevated plasma catecholamines
2.3.5.2 IMAGING
 Adrenal mass seen on CT or MRI
 Characteristic bright appearance on T2-weighted MRI
 Asymmetric uptake on MIBG nuclear scan
o Particularly useful for extra-adrenal, multiple, or malignant
pheochromocytoma
o Not useful for sporadic biochemical syndrome with unilateral mass

377
8 Adrenal Gland Disease

Clinical presentation
Biochemical Dx

Positive Equivocal Negative

Suppression test

Negative Positive

CT scan

Unilateral Bilateral Bilateral Unilateral nodules <1

adenoma normal nodules cm or >2 cm

Selective venous sampling

Unilateral Bilateral Normal

Laparoscopic Medical
adrenalectomy treatment

2.3.6 CONSIDERATIONS
 Avoid arteriography or fine-needle aspiration as they can precipitate a
hypertensive crisis
 Early recognition during pregnancy is important because if left untreated,
half of fetuses and nearly half of the mothers will die.
 Patients with pheochromocytoma usually die of high blood pressure, as the
adrenal gland itself is very sensitive if it were to be touched in surgery there
will be a surge of secretions, which leads to a severe increase in blood
pressure leading to a BP of 250 leading to intracranial hemorrhage!
RULE OUT:
 Other causes of hypertension
 Hyperthyroidism
 Anxiety disorder
 Carcinoid syndrome
2.3.7 TREATMENT
 All patients with suspected Pheochromocytoma should be ADMITTED
and treated as an in-patient.
 HYPERTENSIVE CRISIS (can develop multisystem organ failure, mimicking
severe sepsis)
 Some patients can present w/septic shock, if you can’t explain it → suspect
pheochromocytoma

378
 Adrenal diseaes 9

 Medical:
o α-Adrenergic blocking agents should be started (ATLEAST 2 weeks
before the surgery) as soon as the biochemical diagnosis is established
to restore blood volume, to prevent a severe crisis, and to allow
recovery from the cardiomyopathy.
o Good alpha and beta-blocker control → smooth anesthesia, smooth
surgery, and smooth recovery after.
 Surgical:
o Indications: ALL pheochromocytoma should be excised
o Contraindications to surgery:
 Metastatic disease (because we cannot control it)
 Inadequate medical preparation (α-blockage) without proper α-
blockade surgery is contraindicated.
2.4 CUSHING'S

 Disease vs. Syndrome?

o Cushing's disease: secondary to pituitary adenoma
o Cushing's syndrome: secondary to anything else
2.4.1 CLINICAL PATHWAY

379
10 Adrenal Gland Disease

 If we suspect Cushing first we do simple low dose (screening test) → suppression = normal
patient
 If “+ve” (there is no suppression) = Cushing’s
 Next step: ACTH dependent or not?
 In high dose test: if not suppressed it’s either ectopic e.g. pulmonary carcinoma OR adrenal
tumor (difference is in ACTH level: undetectable in adrenal & very high in ectopic), if pituitary it
will be suppressed by high but not low dose dexamethasone
“All will be suppressed by high dose but there is a difference in the reading – so we do CT chest
(for ectopic) & MRI for brain (Cushing’s disease) to confirm the diagnosis”

2.5 ADRENOCORTICAL CARCINOMA

 Essential features:
o Variety of clinical symptoms through excess production of adrenal
hormones
o Complete surgical removal of the primary lesion and any respectable
metastatic sites has been the mainstay of treatment.
 Epidemiology:
o These tumors are rare; 1—2 cases per million persons in the US
o Less than 0.05% of newly diagnosed cancers per year
o Bimodal occurrence "in the very young and the very old", with tumors
developing in children< 5 years of age and in adults in their fifth through
seventh decade of life
o Male to female ratio is 2:1, with functional tumors being more common
in women
o Left adrenal involved slightly more often than the right (53% vs. 47%);
bilateral tumors are rare (2%)
o 50—60% of patients have symptoms related to hypersecretion of
hormones (most commonly Cushing’s syndrome and virilization)
o Feminizing and purely aldosterone-secreting carcinomas are rare
o 50% of patients have metastases at the time of diagnosis
o It is very difficult to diagnose, because the symptoms appear when it is
too late (just like pancreatic cancer)
 Signs & symptoms:
o Symptoms of specific hormone excess (cortisol excess, virilization,
feminization)
o Palpable abdominal mass “b\c the mass very big”
o Abdominal pain
o Fatigue, weight loss, fever, hematuria
 Lab findings:
o All laboratory abnormalities depend on hormonal status of tumor
o Elevated urinary free cortisol or steroid precursors
o Loss of normal circadian rhythm for serum cortisol
o Low serum adrenocorticotropic hormone (ACTH)
o Abnormal dexamethasone suppression test
o Elevated serum testosterone, estradiol, or aldosterone levels
 Imaging:
o Evaluation of adrenal glands with CT or MRI (adrenocortical carcinomas
are typically iso-dense to liver on T1-weighted MRI, and hyper-dense
relative to liver on T2-weighted MRI images)

380
 Summary 11

o MRI more accurately gauges the extent of any intracaval tumor

thrombus.  Right sided surgeries
are always more difficult
 Considerations than left sided ones.
o Mean diameter of adrenal carcinoma at diagnosis is 12 cm (black size Right tumors go to the
6cm to 12cm  malignant .. remove it , black size 2cm to 4cm  cyst) IVC creating big thrombi
o Radiographic evaluation of suspected metastatic sites for purposes of and that makes the
staging should be undertaken prior to thought of any surgery. surgery more difficult.
(restrict part of IVC
o We should rule out: Pheochromocytoma remove the thrombus 
anastomose it again)
3 SUMMARY
All tissues involved
Remember: should be removed,
such as part of kidney or
 Any functioning tumor or disease should be removed unless the patient is part of liver or maybe
unfit or it is bilateral go with medical treatment. lymph nodes.
 Any nonfunctional, small in size we follow up.
 The gold standard for adrenalectomy is laparoscopy. 
4 OPERATIVE APPROACHES  Adenomas are
usually brown in color:
 In surgeries they clip “ligate” the adrenal vein not the artery, they are usually We open the splenorenal
ligament then push the
very small branches and very fragile liver, pancreas, or
 We remove splenorenal ligament then push kidney away to remove adenoma stomach to the right side
alone. and isolate left kidney
with the adrenal and clip
5 MCQS “ligate” the adrenal vein -
we do not bother with
the artery; usually very
1. A 30-year-old primigravida complains of headaches, restlessness, sweating, small branches.
and tachycardia. She is 18 wk pregnant and her blood pressure is 200/120
mm Hg. Appropriate workup might include:
a) Exploratory laparotomy
b) Mesenteric angiography In laparoscopy we
c) Head CT scan use 5 ports:
d) Abdominal CT scan 5 ports .5-1 cm
2 for the surgeon
e) Abdominal ultrasonogram One for camera
2. The most likely diagnosis in a patient with hypertension, hypokalemia, and a 2 for assistance
7-cm suprarenal mass is:
a) Hypernephroma
b) Cushing’s disease
c) Adrenocortical carcinoma
d) Pheochromocytoma
e) Carcinoid

 Answer Key: 1;E , 2;C

381
 Introduction 1

VENOUS DISEASE
1 INTRODUCTION

1.1 ANATOMY

 Venous blood flow of the Lower Limb is divided into 3 components: the
superficial, communicating, and deep veins. (Figure 3,4)
 The superficial system comprises both the greater and lesser Saphenous veins
and their tributaries. (Figure1,2)
 The superficial venous system is connected to the deep venous system
through smaller communicating or perforator veins. (Figure 3)
 Veins have valves (varying in number). Their job is to prevent
blood from refluxing. (figure 5,6)

Figure 1 Figure 2

Figure 3 Figure 4

382
2 Venous Disease

Figure 5 Figure 6

1.2 PHYSIOLOGY

1.2.1 THE FLOW OF THE VENOUS

Depends on many factors:
 Hydrostatic pressure (figure 9)
o The hydrostatic pressure is (+)ve in LL and (–)ve in UL compared to the
heart.
o total pressure of the LL is higher That's why problems mainly will be in
lower limb
 Alternating pressures of the chest and abdomen during breathing: (figure 8)
o Chest is always negative in pressure.
o But abdomen:
 In expiration diaphragm will go up creating a (–) ve pressure, which
will lead to blood sucking to heart, and subsequent blood sucking
from the legs.
 On inspiration diaphragm will go down, creating a (+)ve pressure
which will lead to closure of veins.
 That cycle will continue and form a valve like function.
 Calf muscle pump: (figure 7)
o When calf muscles are at rest, deep veins expand and blood is drawn in
from the superficial veins.
o With calf-muscle contraction, blood is forced up the deep veins (opening
the valves) towards the heart.
o Movement of blood (Normal):
 From superficial to deep.
 From down to up.

383
 Introduction 3

Figure 7 Figure 8

Figure 9

1.2.2 AMBULATORY VENOUS PRESSURE:

 NORMALLY: (figure 10)
o When lying supine: pressure in lower limbs is low (10 mmHg)
o When rising: deep veins start pulling blood from superficial veins slowly→
so pressure starts to increase gradually.
o When standing: deep veins continue to pull blood and pressure
increases reaching (90 mmHg)
o When walking: calf muscle pump starts working and pushes blood up the
vein through the valves→ so pressure drops to (25 mmHg). Valves then
close, to prevent the pressure from increasing again by preventing the
blood from refluxing.
o If you stop and stand still, calf pump stops and the deep veins start to pull
blood from the superficial veins again, so pressure builds up again.
 IF VALVES DEFECTED;
o When rising and standing: blood will reflux from the valve, so the pressure
will increase rapidly.
o When walking: blood will reflux through the valve and the pressure
remains high.
 Values:
o Supine and walking positions are not a problem (low pressure) standing is
the problem (high pressure)

384
4 Venous Disease

 Supine = 10 mmHg
 Standing= 90 mmHg
 Walking= 25 mmHg
 Methods of measurement: see below in investigations

Figure 10

2 CHRONIC VENOUS INSUFFICIENCY  In secondary

incompetence the
 The presence of (irreversible) skin damage in the lower leg as a result of problem is away from
sustained venous HYPERTENSION the valve, for example:
*Obstruction in the pelvis
2.1 PATHOPHYSIOLOGY (tumor) or a collateral
vein bypassing the valve
 Primary valve incompetence (figures 11-13)
*DVT
o Defect in the valve itself “floppy valve” (fig. 11-13)
o Congenital causes *Pregnancy
 Secondary valve incompetence:
o Reflux (90%)
o Obstruction (10%)

Figure 11 Figure 12 Figure 13

385
 Chronic Venous Insufficiency 5

Figure 14: Note: the (down-to-up) and (out-to-in) mechanism is disturbed because of obstruction.

2.2 CLINICAL EVALUATION

2.2.1 HISTORY
 Take a good history
 Ask about risk factors that can cause secondary causes (pregnancy, DVT,
tumors, previous surgeries)
 Ask about skin changes in details

2.2.2 PHYSICAL EXAMINATION

 Make sure you thoroughly examine the Gaiter’s Area for clinical classification!!
 Clinical manifestations (classification; C1-C6) of chronic venous insufficiency:
Figures 15-20

Gaiter’s Area:
Area around medial and
lateral malleolus is
common site for venous
ulceration because this
area is skin on bone (no
tissue and fat between
them) so the blood and
inflammatory stuff will go
C1: Telangectasia/ Spider directly from the veins to
C2: Varicose veins C3: Edema but no skin changes skin leading to certain
viens
manifestation.

386
6 Venous Disease

C4: Lipodermatosclerosis/
C5: Healed ulcer C6: Active ulcer
Pigmentation/ eczema

2.2.3 INVESTIGATIONS
2.2.3.1 NON-INVASIVE
 Doppler (figure 21, 23)
o Machine used to HEAR blood flow in the veins
o You can detect which valve isn’t working, or an obstruction, by listening for
abnormalities in the sound of the flow.
 Duplex: (figure 22, 24-26)
o This is a form of ultrasound machine that allows visualization of a portion of
the venous system. It can determine the direction and speed of blood flow
within the veins.
 So duplex has the same principle of Doppler but you can use it to visualize also
 Check the slides for more pictures
Figure 21-26

387
 Chronic Venous Insufficiency 7

2.2.3.2 INVASIVE TESTING:

 AVP (ambulatory venous pressure) 
o It is a test to measure the venous pressure in supine, standing, and
walking positions. To compare it with normal changes.
o Method:
 It is performed by placing a small needle into one of the veins on
the back of the foot and connecting the needle to a blood
pressure measurement machine.
 20-21gauge Butterfly Needle
 Superficial Dorsal Vein (Foot) or Ankle Vein
o Normally:
 when walking
 A decrease in pressure from Pressure 80 - 90mm Hg to
20-30 mm Hg
 Or a: > 50% drop
 Then after standing still Venous Refilling Time: 20 seconds
o Abnormal results if: 

388
8 Venous Disease

 Lack of sufficient drop in pressure with ambulation

 Pressure doesn’t decrease enough on walking and the
difference between the standing and walking pressure is
<50%
 This means that the pressure remains high in the veins
although it is supposed to drop because of walking
 Short venous refill time
 It takes less than 20 seconds
 This means the blood is filling veins quickly and the valves
aren’t working efficiently to stop the blood from refluxing

Normal

Figure 27

Deep Venous Incompetence

Figure 28

 Venography (phlebography): (figure 29, 30)

o Contrast injected to visualize veins.
o Not used much nowadays, due to its complications. But still has
specific indications

389
 Treatment 9

Figure 29 Figure 30

3 TREATMENT

3.1 PRINCIPLES OF TREATMENT:

1. Always exclude secondary causes by doing a thorough physical
exam and history and investigations
2. Restoration of blood pumping towards the heart
3. Remove the problematic vein (provided that there is another functioning
vein draining the same area)

3.2 SOME METHODS OF TREATMENT:

1. Stocking: (figure 31)
 Physical principle applies pressure, is higher pressure down and lowers
pressure up to make blood go up.
 Problem is low compliance, although it usually solves the problem.
2. Ablate vein: (figure 33)
 Chemically or thermally or laser
o Denaturation of vein wall collagen → contraction → fibrous
obliteration of the vein
 Provided that there is another functioning vein draining the same area.
3. Sclerotherapy (figure 32)
 Sclerotherapy is the injection of a sclerosing agent into a vein, causing an
inflammatory reaction in the endothelium of the vein wall. The vein walls
adhere together under compression and form a scar (fibrotic tissue) that is
absorbed by the body. Remember this works only to the small veins not
big ones.
4. Conventional surgery: problematic vein tied above and below, then taken out.
Not used anymore

3.3 SPECIFIC MEASURES:

1. Telangiectasias and reticular veins: Stocking or Sclerotherapy
2. Varicose veins

390
10 Venous Disease

 Stocking
 Sclerotherapy
 Endovenous laser therapy (EVLT)/ Surgery
3. C3 to C6:
 Stocking/ Sclerotherapy/ EVLT/Surgery

Figure 31

Figure 32: Sclerotherapy

Figure 33: Endovenous Laser Therapy (ELT)

391
 Introduction 1

ATHEROSCLEROSIS
1 INTRODUCTION

 It is an inflammatory process that causes clogging, narrowing and hardening of

the large and medium sized arteries.
1.1 RISK FACTORS

 Non modifiable
o Male
o Advanced age
o Family history
 Modifiable
o Major
 Smoking
 Hypertension
 Diabetes
 Hyperlipidemia
o Minor
 Homocystenemia
 Obesity
 Hypercoaguble states
 Physical inactivity
1.2 PATHOGENESIS

 The key word in Atherosclerosis is inflammation

o Fat deposits accumulate and will cause endothelial injury that will initiate
the inflammatory process
o Formation of fibrous plaque by platelets
o Calcification of the arterial wall (this is the cause of atherosclerosis)
o Fat by itself is NOT harmful but it is the rupture of the plaque
o Rupture of the wall will cause clotting (atherothrombosis)
1.3 CLINICAL SPECTRUM OF ATHEROSCLEROSIS

 The message you should take is that

Atherosclerosis is a systematic disease
that affects the entire body not only
specific areas. The spectrum includes:
o Cerebrovascular accidents
o Coronary artery disease
o Renal artery disease
o Visceral artery disease (mesenteric)
o Peripheral artery disease (Aorto-iliac
& upper and lower limb is a marker
for atherosclerosis)
 Intermittent claudications
 Limb ischemia

392
2 Atherosclerosis

1.4 BURDEN OF ATHEROSCLEROSIS

We always concentrate
on the symptoms related
 It is the number one killer worldwide and here in Saudi Arabia and it predicted to the organ itself and
to increase forget to think about the
bigger picture. When we
2 PERIPHERAL ARTERY DISEASE (PAD) think about the
peripheral artery disease
we think only about the
2.1 IMPORTANCE OF PAD peripheral complication
like claudications,
 PAD is a marker of systemic atherosclerosis amputation
 Patients with either symptomatic or asymptomatic PAD generally have In reality we have to
widespread arterial disease think about the mortality
 Patients with PAD have the following: about 7% per year
o Coexisting disease:
 35-92% have coexisting Coronary artery disease (CAD)
 25-50% have coexisting Cerebrovascular disease (CVD)
o Cause of death in PAD patients:
 40-60% die from CAD
 10-20% die from CVD

 Patients with PAD have a 6 fold (imp!) increased risk of cardiovascular disease
mortality compared to patients without PAD even the patient with or without
symptoms
 Natural history 
o Annual mortality rate is 6.8%
o Annual risk of Myocardial infarction is 2%
o Annual risk of intervention is 1%
o Amputation 0.4%
2.2 PRESENTATION
The concept you
should keep in your
 Symptomatic
mind that
o Intermittent claudications atherosclerosis is one
 Pain at a lower limb group of muscles at exertion that is relieved by disease, one group of
rest (Think of it like Angina) symptoms and one
o Critical limb ischemia treatment. But different
arterial trees are
 This is a limb threatening condition affected so patients will
 Pain at rest present with different
 Tissue loss (Ulcer) symptoms.
 Gangrene
 Asymptomatic 

393
 Peripheral artery disease (PAD) 3

2.3 DIAGNOSIS

2.3.1 SYMPTOMATIC:
 History
 Physical examination
 Investigations
o They are primarily used for:
 Confirming the diagnosis after a history and examination and exclude
other diseases
 Assess severity
o ABI measurements
o Non invasive tests:
 Arterial duplex: Doppler + US. Good for anatomical involvment
 CTA: CT + contrast
 MRA
o Invasive tests: the conventional angiogram (GOLD standard) 
 Very accurate in mapping out the arteries but the Duplex is better in
assessing dynamic views
2.3.2 ASYMPTOMATIC: 
 SCREENING with ABI measurement
 Around 90% of patients with PAD are asymptomatic but they also carry the
same risk!!!!
 We have to screen high risk groups even if they don’t carry symptoms, for
example:
o Old age (>50), family history, male
 If you notice in the natural history part we mentioned that the mortality is 7%
but the intervention level is 1%. And that is because 90% are asymptomatic!
 That is why we need screening to see past the tip of the iceberg and decrease
the mortality and the cardiovascular mortality and morbidity associated with
those pts.

Symptomatic 10%

Asymptomatic 90%

2.3.3 ABI (ANKLE-BRAHCIAL INDEX)

 It is the index between the systolic pressure of the Ankle and the brachial
systolic pressure
 ABI = (Highest ankle systolic pressure (PT or DP) / Highest brachial systolic
pressure
o PT= Posterior Tibial artery
o DP= Dorsalis Pedis artery

394
4 Atherosclerosis

 Results:
o Normally it is >0.9
o Abnormal if <0.9 (Abnormal results indicate PAD)
 Mild 0.8 – 0.9
 Moderate 0.5 – 0.8
 Severe <0.5
 Very severe <0.25
 The ABI has limited use in evaluation calcified vessels that are not
compressible in Diabetics
2.4 TREATMENT OF PAD

2.4.1 GOALS OF TREATING PAD:

1. Relief of symptoms
2. Improving the quality of life
3. Limb salvage
4. Prolonging survival
2.4.2 STRATEGIES IN TREATING PATIENTS WITH PAD:
 Risk factor modification (modifiable)
o Diet and weight control
o Exercise
o Antiplatelets: to prevent thrombus
o Hypertension control: <140/90 (130/80 for
diabetics)
o Diabetes control: HbA1c <6
o Lipid control
o Smoking cessation
 Improve limb circulation
o Conservative:
 exercise program that promotes
angiogenesis and growth of collaterals
around the ischemic area
o Intervention: Revascularization
 Angioplasty (+/- Stenting the artery)
 Surgical bypass
 Last strategy in treating PAD:
o Major amputation
 Affects function: Whole leg amputation
 Primary amputation (we start with amputation)
 Secondary (we start with angioplasty or bypass but the patient does
not respond)
o Minor amputation: Doesn’t affect function
 BKA=Below knee amputation
 AKA=Above knee amputation

395
 Carotid artery disease 5

3 CAROTID ARTERY DISEASE

 Stroke is the third leading cause of death and a principal cause of long term
disability
 Prevention of stroke is MORE IMPORTANT than treatment
3.1 PRESENTATION

 Symptomatic:
o Transient Ischemic Attacks (TIA): Loss of motor or sensory function for
less than 24 hours
o Amurosis Fugax: transient visual loss for less than 24 hours
o Stroke
 Asymptomatic
3.2 DIAGNOSIS

 Symptomatic
o History
o Examination
o Investigations
 Asymptomatic
o It is detected by hearing a carotid bruit. It is very important that you screen
for a carotid bruit in all patients with risk factors or over 50.
o Arterial duplex:
 Note that stenosis is measured by velocity and not anatomical
diameter
3.3 TREATMENT OF CAD

 Goals of treatment:
o Prevention of strokes
o Prolong survival
 Strategies in treating patients with CAD Endartectomy
o Risk factor modification
 Diet and weight control
 Antiplatlets double
 Exercise
 Hypertension control
 Diabetes control
 Lipid control
 Smoking Cessation
o Improving brain circulation:
 Revascularization with Carotid Endarterectomy (best method) and
standard of care 
 Angioplasty with or without Stenting
 This intervention is currently under investigation Stenting still needs
 Indication: more evidence but it is
o Hostile neck reserved for certain
groups of patients
o Hostile carotid disease
o Part of a RCT

396
6 Atherosclerosis

 Indications to intervene:
o Symptomatic
 >70% stenosis: NACET study shows decrease stroke at 2 years from Hostile neck/carotid
26% to 9% disease means a
 50-69% stenosis: Marginal benefit but greater for male patients who already has
 Recovered ischemic stroke patients undergone a
endartectomy and
o Asymptomatic surgery is difficult
 >60% stenosis: ACAS study shows decrease stroke at 4 years from
11% to 5%
4 ACUTE LIMB ISCHEMIA

 Sudden decrease or worsening in the limb perfusion causing a potential threat

to the limb viability resulting from a sudden obstruction of the arterial system
4.1 CAUSES:

 Embolus (Most common cause) 

 Thrombosis
 Trauma
 Iatrogenic
 Arterial dissection
4.2 POSSIBLE SOURCES FOR AN
EMBOLUS:

 Spontaneous 80%:
o Cardiac source: most common cause
 Arrhythmias, MI, prosthetic valve,
endocarditis
o Non-Cardiac
 Proximal plaque, aneurysm,
paradoxical emboli
 Iatrogenic 20%
o Angiographic manipulation
o Surgical manipulation
 Common sites of embolus lodgement in the
arterial tree:
o Femoral is the most common
4.3 PRESENTATION OF ACUTE LIMB ISCHEMIA

 Sudden onset of diffuse and poorly localized leg pain

 6 Ps
o Paresthesias
o Pain
o Poikilothermia
o Pallor
o Pulselessnes
o Paralysis
 Investigations
o Acute limb ischemia is a clinical diagnosis 

397
 MCQs 7

o If time allows especially if atherosclerotic thrombus is suggested,

preoperative angiography is often wise
4.4 TREATMENT OF ACUTE LIMB ISCHEMIA 

 Goal of management: Rapid restoration of adequate arterial perfusion without

the development of morbid local or systemic complications
 Preserving the limb but not on the expense of life
 EMERGENCY
o Golden time is 6 hours from the appearance of symptoms
o ABC (most important step)
o IV Heparin
o Rapid surgical thromboembolectomy
 +/- Surgical bypass
 +/- Thrombolytic therapy
 +/- Primary amputation
4.5 REPERFUSION INJURY

 It is a worrisome complication of revascularization

 Effects can be, local:
o Compartment syndrome
 It is a condition where the pressure inside the compartment rises due
to edema after the ischemic injury.
 The raise in pressure will stop the blood flow to the area and cause
more ischemia
 Needs emergency fasciotomy 
 Systemic: 
o Hyperkalemia:
 Due to muscle ischemia and breakdown
 Leads to cardiac arrest
 Treated or prevented with Calcium Gluconate
o Acidosis: Bicarbonates should be given
o Myoglobinuria
 Leads to acute renal injury
 Patient should be given a lot of fluids
5 MCQS

1. All of the following are signs of critical limb ischemia except:

A. Intermittent claudications
B. Pulselessness
C. Poikilothermia
D. Paresthesiasis
2. All of the following can happen in reperfusion injury except:
A. Acidosis
B. Compartment syndrome
C. Hyperkalemia
D. Hyperglycemia

 Answers: 1;A , 2;D

398
 Introduction 1

VASCULAR INVESTIGATIONS
1 INTRODUCTION

 Blood vessels are a series of tubes that are used to pump blood
throughout the body.
 There are 3 types of blood vessels: arteries, veins and lymphatics.
 Arteries carry oxygen rich blood away from the heart to every part of the
body, including the brain, kidneys, intestine, arms, legs and heart itself.
When a disease occurs in the arteries, it's called arterial disease.
 Blood flows back to the heart from all parts of the body through veins.
When disease occurs in the veins, it's called venous disease.
 Fluids return from the skin and other tissues to the veins through
lymphatics.
1.1 VASCULAR DISEASES:

 Arterial diseases: such as aortic dissection which is caused by a tear in

the inner layer of the aortic wall and then blood will flow between the layers
and separate them or arterial occlusion. A lot of patients come with arterial
occlusive diseases.
 Acute: ischemia
 Chronic: intermittent claudication or dilatation (arterial aneurysmal
disease)...Etc.
 Venous diseases: deep vein thrombosis commonly referred to as “DVT”,  More Frequency >
occurs when a blood clot, or thrombus, develops in the large veins of the less penetration of the
tissue e.g. for superficial
legs or pelvic area, or chronic venous insufficiency which is an all-‐
structures.
inclusive term for vascular malformations, vascular tumors, and other
congenital vascular defects. The more commonly used term, Chronic -More frequency >better
Venous Insufficiency (CVI), implies abnormally formed blood vessels that resolution.
one is born with... etc. -Less frequency >
 Lymphatic. deeper penetration of the
tissue e.g. abdominal
1.2 TYPES OF INVESTIGATIONS: investigation,
-Less frequency > lesser
 Invasive ( in vascular surgery invasive procedures are the gold standard) resolution.
 Noninvasive.
2 NON INVASIVE VASCULAR TESTS

 Utilizes instrument; Utilizes the sound energy

 Doppler Ultrasound.
 Sound –longitudinal mechanical wave of any frequency.
 Audible Sound range 20-20,000 cycles/sec . 20Hz-20kHz
 Ultrasound-’Ultra’ means ‘Above’ human hearing - >20,000
cycle/sec(20kHz).
 Diagnostic Ultrasound –2MHz-12MHz (2million-12million cycle/sec) 

399
2 Vascular Investigations

2.1.1 DOPPLER ULTRASOUND

 We transmit X
 Based on principle of Doppler effect/shift frequency and receive Y
frequency. These are
 Normally blood vessels contain moving blood if there’s a block it’ll stop utilized to know if blood
moving. is moving properly or no.
 Ultrasound interaction with stationary object:

a. No frequency change.
b. No Doppler Effect or shift.
c. Sound won’t be heard.
 Ultrasound encounters moving object:

a. Doppler Effect or Shift occurs.

b. Change perceived frequency of ultrasound emitted by moving object.
c. Sound will be heard (3 voices)
 In clinical practice: moving targets RBC traveling with in the blood vessel.

 Source & Receiver of sound: ultrasound transducer

2.1.2 ULTRASOUND TRANSDUCER
 Transducer: device converts one
form of energy to another.
 Ultrasound Transducer:
 Use piezoelectric crystals.
 Converts Electro potential energy
(voltage) into Mechanical vibration
(ultrasound) & Mechanical
vibration into Voltage.

400
 Non Invasive Vascular Tests 3

2.1.3 TYPES OF DOPPLER INSTRUMENTS

 Continuous Wave (CW)
 Pulsed Wave (PW)

Continuous Wave (CW) Pulsed Wave (PW)

Doppler transducer Transmits continuously Single piezoelectric crystal – both transmission
 CW: the pocket
Doppler, the one the
ultrasound & Receive simultaneously. & reception. doctor uses.
Alternate pulses On & Off.
-CW: It’s not specific; it
Have two Piezoelectric crystals, one Transmit X Transmit pulse – system waits – pulse travels to
does not give a specific
& other Receive Y. sample volume (specific area) – echo pulse area or a structural
returns picture of the vessels. It
only gives the
Advantages: anatomical location in
Magnitude of detectable velocity – limitless. Specific for depth and range. general. (Gives a rough
No mixture of signals like CW Doppler. idea)
- PW is more advanced

Disadvantages:
Not specific for depth Limited maximum detectable velocity unlimited
Detects any & all vessels in beam path. for CW Doppler.

2.1.4 ANGLE OF INCIDENCE

 Doppler or frequency shift is what we hear & see on graphic display.
 Affected by ‘angle of flow’ or ‘angle of incidence’
 The smaller the Doppler angle, the higher the frequency shift.
 Optimal Doppler signals: transducer angle 45-60 towards direction of
flow.

401
4 Vascular Investigations

2.1.5 ARTERIAL ASSESSMENT – DOPPLER ULTRASOUND  Triphasic: normal.

 Audible interpretation - Monophasic: peripheral

a. Waveform analysis. arterial disease.
b. Hand held Doppler.

 Normal Peripheral Arterial Doppler signal: TRIPHASIC 

 Triphasic arterial signal:
a. 1st sound – phase: large, high velocity, forward flow, systolic
component.
b. 2nd sound – phase: smaller reverse flow early diastole.
c. 3rd sound – phase: smaller forward flow late diastole.
 Audible interpretation & Wave form analysis

 PVR (Pulse Volume Recording): Normal PVR:

1) Brisk systolic upstroke Anacrotic limb.
2) Sharp systolic peak.
3) Gradual down stroke Catacrotic limb.
4) Dicrotic notch-reflective wave-during diastole normal peripheral
resistance.

402
 Non Invasive Vascular Tests 5

2.1.5.1 ARTERIAL PRESSURE MEASUREMENTS:

For Peripheral arterial occlusive disease
 Sequence of pressure measurement tests:
a. Systolic Brachial & Ankle pressure at rest.
b. Calculation of ABI.
c. Toe pressure-non compressible tibial arts.
d. Segmental pressure and waveforms: low ABI.
e. Stress testing: severity of claudication & to R/O pseudo-claudication.
 Contraindication to pressure measurements:
a. Acute DVT; closure of veins makes it worse.
b. Bandages & casts
c. Ulceration
d. Trauma
e. Surgical site
1) Ankle Brachial Index (ABI):
Before the test Consider :
a) Patient supine arms at sides.
b) Basal state (10mnts pretest rest).
c) CW Doppler ultrasound.
d) Appropriate size pressure cuffs.
When testing :
a) Record bilateral systolic brachial pressure &
systolic Ankle pressure (dorslis pedis &
post.tib art)
b) Interpretation-Ratio highest ankle to
brachial pressure.

403
6 Vascular Investigations

ABI & Relation to PAOD:

a) 0.97 -1.25 Normal  Vessels are non-
b) 0.75 – 0.96 Mild PAOD compressible in: DM,
c) 0,50 – 0.74 Moderate elderly, renal failure or
d) <0.5 Severe any condition where
e) <0.3 Critical arteries are calcified.
f) >1.5 Vessels non compressible 

2) Toe Pressure

 This test is done if the ABI showed very high values  like in diabetic patient.

rd
Normal toe pressure – 2/3 systolic ankle pressure
 Plethysmographic device –it records changes in volume (It is used as a sensor)

rd
Inflate cuff above 2/3 of ankle pressure.
 BP cuff (2.5cm) around the base of the toe.
 Gradual deflate until arterial tracing demonstrate return of pulsatile flow – recorded as
systolic toe pressure.

3) Segmental Pressures

 Drop in ABI at rest or post exercise indicates hemodynamically significant disease proximal
to cuff.
 Segmental pressure measurement – localizes the diseased arterial segment.
 Pressure difference between two adjacent segments <20mm of Hg. (1)
 Gradient >30mm of Hg - Hemodynamically significant disease between adjacent levels (2).;
Due to the significant drop between two segments e.g. from 120 to 90 (narrowing pressure
which is caused by occlusion)
(1) (2)

4) Exercise (Stress) Test

 Treadmill stress test.
 Reactive hyperemia stress test.
 Assess functional limitation due to PAOD
 Differentiates PAOD – Pseudoclaudication Ex;
neurogenic claudication.
 Resting ankle & brachial pressures.
 Pressure cuffs secured in place –ankle and
arm.
 Walk at 2mph at 12% gradient-5mnts or point
claudication symptoms.
 Return supine position & measure ankle

404
 Non Invasive Vascular Tests 7

pressure 30 seconds and 1 minute post

exercise.
 Measure till baseline pressure is recovered.
Note:
 Duration of exercise.
 Distance walked.
 Symptoms prevented by exercise.
Interpretation:
 Normal: no drop in ankle pressure.
 Minimal disease pressure returns to baseline
in 2 minutes.
 Single level disease: pressure returns to
 Arterial flow: pulsatile
baseline in 3-5 minutes. triphasic
 Multi-level disease: pressure returns to
baseline >10 minutes. Venous flow: wind-like;
normal response 

2.1.6 DOPPLER ASSESSMENT OF VEINS

 Five qualities of normal venous flow:
a. Spontaneity.
b. Phasicity; with respiration it changes because in inspiration there is no
flow because there’s no venous return. Expiration increases in venous
flow.
c. Augmentation.
d. Valvular competence.
e. Non pulsatility.
 In cases of DVT: Normal five qualities of venous flow are lost; because the
vein is closed there will be no sound.

2.2 ULTRASOUND IMAGING DUPLEX

 Imaging Principles:
a. Amplitude mode (A-mode) method of presenting returning echoes of
US on a display screen.
b. A-mode: displayed as vertical deflections or spikes, projecting from
baseline. Stronger echoes-higher amplitude signals.

405
8 Vascular Investigations

c. B-mode: Brightness mode Returning echoes displayed as series of

dots.
d. Position of each doctor responds to distance from the sound source
rightness corresponds to amplitude of returning echo – Gray scale
intensity.

 Duplex Scan:
a. Combination of B-mode imaging with pulsed Doppler US – gives both
anatomical & physiological information of vascular system →Duplex
Scan.
b. Addition of color frequency mapping →Color Duplex imaging.

 Uses of color duplex imaging:

a. Arterial:
i. Identify obstructive or aneurysmal atherosclerotic disease;
ii. Peripheral arteries
iii. Carotid arteries
iv. Renal & visceral arteries
v. Surveillance of bypass grafts.
b. Venous Duplex
i. Diagnosis of DVT.
ii. Assessing competence of deep vein valves.
iii. Superficial venous reflux & identifying Sapheno Femoral &
Popliteal Jnc refluxes.
iv. Preoperative mapping of saphenous vein.
 Criteria for Duplex examination of venous system
Normal Abnormal (DVT) 
 Easily compressible  Non compressible
 Should be echo free  Echogenic thrombus in vein
 Normal valve motion  Incompetent valves
 Normal Doppler signals  Absent Doppler signals

406
 Invasive Vascular tests 9

3 INVASIVE VASCULAR TESTS

3.1 ARTERIOGRAPHY

 Gold Standard.
 Good resolution.
 Seldinger technique
 Access –commonly femoral artery & brachial artery; easiest accessible
artery, least complications with larger arteries, never access small arteries.
 Inject iodinated contrast into the catheter you inserted in the large artery.
3.1.1 TYPES OF CONTRAST
Ionic or high osmolar Nonionic or low osmolar ; commonly used
 Water soluble  Has same no of iodine ions ,no cations

rd
 Hypertonic, osmolality 5-10 times of Osmolality 1/3 of high osmolar contrast
blood.  Still hypertonic twice that of plasma.
 Causes discomfort at injection site.  Less nephrotoxic
 More nephrotoxic; more  More expensive
complications.

3.1.2 COMPLICATIONS   Pseudo aneurysm; is

a pulsatile swelling
Local General Allergic reaction to contrast
around the artery due to
 Hemorrhage  Renal – nephrotoxicity  Minor – nausea, vomiting, leaking of blood no
 Thrombosis  Cardiac- hypertension, head ache, chills, fever, dilatation of vessel.
 Pseudo aneurysm arrhythmias, CCF. itching.
 AV fistula  Neurological – Carotid  Intermediate - hypotension.
 Intimal dissection angiogram – TIA stroke, urticaria, bronchospasm.
 Embolization convultions.  Major-anaphylaxis, pulmonary
 Pulmonary-bronchospasm, edema, laryngeal edema
pulmonary edema.

407
10 Vascular Investigations

3.2 VENOGRAM

We do it when we are not sure of US results.

3.2.1 ASCENDING VENOGRAPHY
 Relatively invasive study.
 Requires painful venipuncture.
 Injection of iodinated contrast.
 Exposure to radiation.
 Gives information about anatomy and patency of deep veins.
 Locates the incompetent perforator’s veins.
 Inject about 40-60 ml of contrast into superficial foot arch veins and
tourniquet tied above ankle to visualize deep veins.
 Indication: High clinical suspicion of DVT with negative or equivocal
noninvasive vascular tests (Duplex).
 Complications: same as pervious + thrombophlebitis.
3.2.2 DECENDING VENOGRAM
 Indication: to assess the competency of the valves
a. To distinguish primary deep venous valvular incompetence from
thrombotic disease.
b. Identify level of deep venous reflux and morphology of venous valves.
 Venographic categories of Deep vein reflux (not imp)
1) Grade 0 – normal valve function no reflux
2) Grade 1 – minimal reflux confined to upper thigh
3) Grade 2 – extensive reflux reach lower thigh
4) Grade 3 – extensive reflux reach to calf level
5) Grade 4 – no valvular competence immediate reflux distally to calf.
4 LYMPHEDEMA

 Lymphedema: accumulation of lymph in the limbs.

 Minimal invasive investigation to identify edema of lymphatic origin:
a. Lymphoscintigraphy
b. CT & MRI
4.1 LYMPHOSCINTIGRAPHY

 Isotope Lymphography
a. Radiolabelled Colloid or Protein injected first web of foot.
b. Gama Camera monitoring of tracer uptake.
 Measurement of tracer uptake within the lymph nodes after a defined
interval – distinguishes lymph edema from edema of non-lymphatic origin.
 Appearance of tracer outside the main lymph routes – dermal back flow
indicates Lymph reflux & proximal obstruction.
 Poor transit of isotope from injection site – suggest hypoplasia of
lymphatics.
4.2 CT & MRI

408
 Other Modalities of Vascular Investigations 11

 Honeycomb pattern in the subcutaneous compartment, characteristic of

lymphedema.

4.3 DIRECT CONTRAST X RAY LYMPHOGRAPHY

 Lymphangiography.
 Lymph vessels identified by injecting vital dyes and lymph vessel
cannulated.
 Lipiodol contrast directly injected.
 Normal limb shows opacification of 5-15 main lymph vessels as converge to
inguinal lymph nodes.
 Lymphatic obstruction-contrast refluxes into dermal network – dermal
backflow.
5 OTHER MODALITIES OF VASCULAR INVESTIGATIONS

Minimally invasive procedures;

 CT, CT Angiogram.
 MRI, MR Angiogram.
6 IMPORTANT NOTES

 Person with abdominal aortic aneurysm , what’s the best for

diagnostic and surveillance purposes? → noninvasive
ultra sound or duplex.
 For follow up of aneurysm, which is 3 cm →US
 Start treating aneurysm when it’s 5cm because larger has higher
incidence of rupture, less than that don't treat just follow up with US.
 For following up after an open surgery (Endovascular Repair)
EVR →CT
 Person with abdominal aortic aneurysm ,what’s the best for
therapeutic and plan management purposes? →CT
 Local diseases causing Limb swelling →DVT, chronic venous insufficiency,
lymphedema.
 For DVT, chronic venous insufficiency →diagnosed by US or
duplex US.
 To assess or diagnose lymphatic vessels or lymphedema
→lymphoscintigraphy (not lymphangiography) sometimes MRI magnetic
resonant angiogram (minimal invasive )
 MRV →venogram (not used because it needs a special software).

409
12 Vascular Investigations

7 MCQS

1) In non-invasive assessment of peripheral arterial disease, the following is an

appropriate candidate for exercise test:
a. Patient with rest pain in the foot
b. Patient with intermittent claudication and normal resting ABI
c. Patient with venous ulcer
d. Patient with resting ABI of <0.4
e. Patient with acute ischemia

2) 15-year old girl presented with progressive painless unilateral leg swelling:
a. Most likely cause is chronic venous insufficiency
b. Most likely cause is primary lymphedema
c. Patient needs arteriogram to confirm diagnosis
d. Is due to secondary lymphedema
e. Common treatment is lymphatic bypass surgery

3) 50- year old male patient with swelling, pigmentation and ulceration around the
ankle:
a. Most likely cause is chronic lower limb ischemia
b. Needs arteriogram for diagnosis and management
c. Needs non-invasive assessment by Doppler and duplex for obstruction and
valvular incompetence of the venous system
d. Brown skin pigmentation is due to excess of melanocyte activity in the skin
e. Usually managed by amputation of limb

4) 30 year old female , 26 weeks pregnant has painful swollen and pale left lug
and her pedal pulses are well felt:
a. Arteriogram is indicated because of pale left leg
b. Optimal initial diagnostic test is venous duplex examination
c. Appropriate treatment would be warfarin
d. Venography should be the initial diagnostic test
e. Heparin is contraindicated in this patient

5) 50 year old diabetic male smoker present with rest pain and gangrene of the
1st toe, the following statement are correct:
a. ABI in the above patient is the ratio of ankle diastolic pressure to brachial
diastolic pressure
b. ABI in normal person in <0.9
c. The above patient has critical ischemia and usually ABI <0.4
d. Calcification of arteries in this patient can give very give ABI results
e. Always ABI is measured in standing position

6) In vascular investigations:
a. Doppler is used only for arterial investigations
b. Duplex scan can be used to evaluate the lymphatic system

410
 MCQs 13

c. Bleeding is a common cause of death with venogram

d. None of the above is true

7) Venous system of the lower limb:

a. Consists of superficial, middle and deep systems
b. No connection between its parts
c. Superficial femoral and profunda veins join to form the common femoral vein
d. Great saphenous vein starts posterior to the medial malleolus

8) A 32 year old woman presented to the clinic with thickening skin of her medial
aspect of the leg, which was associated with dermatitis and hyperpigmentation.
Which type of presentation is this?
a. Telangictasia
b. Lipodermatosclerosis
c. Healed ulcer
d. Active venous ulcer

9) Evaluation does not include which of the following tools?

a. Doppler
b. Duplex
c. Venogram
d. AVP

10) All of the following can treat the previous case except:
a. Stocking
b. Endovenous laser ablation
c. Endovenous laser therapy
d. Surgical ligation

Answers: 1;B , 2;B , 3;C , 4;B , 5;C , 6;C , 7;C , 8;B , 9;D , 10;A

411
 Types of Injuries 1

PERIPHERAL NERVE INJURIES

1 TYPES OF INJURIES

1.1.1 PERIPHERAL NERVE INJURIES

 Axillary nerve
 Musculocutaneous nerve
 Median nerve
 Ulnar nerve
 Radial nerve

2 BRACHIAL PLEXUS INJURIES

2.1 BASIC ANATOMY

 It is formed from the union of the anterior rami of the 5th,6th,7th,8th cervical
and 1st thoracic nerves (C5, C6, C7,C8,T1)
 The plexus is divided into Roots, Trunks, Divisions, Cords and terminal
Branches
2.2 CLASSIFICATION OF BRACHIAL PLEXUS INJURIES

 Open injuries (stab wounds or gunshot wounds):

o Can be at any level (roots, trunks, divisions, etc.)
o Classified into:
 Supraclavicular (roots, trunks, divisions)
 Infraclavicular (divisions, cords, terminal branches)
 Closed injuries:
o More common than open injuries
o Injury is most commonly at the roots level
o Caused by car accidents, outstretching of the shoulder like when
playing sports or during difficult deliveries where the baby is pulled in
emergency situations

412
2 Peripheral Nerve Injuries

o Examination of closed injuries: Nerves are not examined, Roots

are examined by examining dermatomes (sensation) and
myotomes (movement)
Root Dermatome Myotome
C5 Shoulder tip + lateral arm Shoulder abduction +
external rotation
C6 Lateral forearm + thumb Elbow flexion
and index finger
C7 Middle finger Wrist extension
C8 Ring and little finger + lower Making a fist
aspect of medial forearm
T1 Upper aspect of medial Finger crossing
forearm + medial arm

2.3 TYPES OF CLOSED BRACHIAL PLEXUS INJURIES

2.3.1 UPPER BRACHIAL PLEXUS LESION

 Called Erb’s palsy (Erb-Duchenne Palsy)
 Injury to C5, C6 and C7
 C5: loses the ability to abduct the shoulder and external rotation
 C6: loses the ability to flex elbow
 C7: loses the ability to extend the wrist
o Clinically:
 The patient will have (opposite to the normal function of the
damaged nerves):
 Shoulder adduction
 Internal rotation
 Extension of the elbow
 Wrist flexion
 This is called waiter’s tip posture
 Associated injuries:
o Injury to the phrenic nerve which arises from the 3rd, 4th, and 5th
cervical roots, so half of the diaphragm will be paralyzed
o In adults X-ray will show elevated hemi diaphragm
o In children the intercostals are not strong enough to compensate so the
baby will have breathing problems (obstetric palsy)
2.3.2 LOWER BRACHIAL PLEXUS LESION
 Called Klumpke’s palsy
 Injury to C8 and T1
o C8: loses the ability to make a fist
o T1: loses the ability to cross fingers
 Clinically: The patient will have simian hand and clawing of all fingers
 Associated injuries:
o Sympathetic nerves to the face come from a branch of the first thoracic
nerve T1
o If T1 is injured then sympathetic to the face are lost on one side and
that will result in Horner syndrome, which is:
 Ptosis (dropping of the upper eyelid)

413
 Peripheral Nerve Injuries 3

 Miosis (constricted pupil)

 Anhydrosis (inability to sweat)
2.3.3 TOTAL PALSY
 Injury to all roots C5, C6, C7, C8, T1
 Patient is unable to move entire limb: flail limb
 Quick clinical hints:
o Upper lesion (C5, C6, C7) → Erb’s palsy and phrenic nerve symptoms
o Lower lesion (C8, T1) → Klumpke’s palsy and sympathetic symptoms
o Total lesion (C5, C6, C7, C8, T1) → flail limb and both phrenic and
sympathetic symptoms
3 PERIPHERAL NERVE INJURIES

3.1 AXILLARY NERVE

 Isolated injuries to the Axillary nerve most commonly happens with

shoulder dislocation
 Supplies the Deltoid and Teres minor muscle
 Clinical features:
o Motor:
 To the deltoid muscle so the patient will not be able to abduct his
shoulder
 The patient can still initiate abduction (action of supraspinatus)
 It also supplies teres minor that does external rotation which is the
same action of infraspinatus, so the patient can still externally rotate
his arm
o Sensory:
 Loss of sensation over the skin of the lateral arm on lower half of the
deltoid
 Summary: loss of abduction and sensation over the lateral arm
3.2 MUSCULOCUTANEOUS NERVE

 Isolated injuries usually happen with stab wounds or gunshots

 Supplies corachobrachilis, biceps , brachalis muscles
 Clinical features:
o Motor:
 Corachobrachilis and brachalis are not important clinically
 Biceps:
 Weak supination (because the supinator muscle can
compensate)
 Loss of flexion
o Sensory:
 Loss of sensation over the lateral forearm and the thumb
 Summary: loss of elbow flexion and sensation over the lateral forearm +
weak supination

414
4 Peripheral Nerve Injuries

3.3 RADIAL NERVE

 Runs in the spiral groove so injuries happen in humours bone fractures

 Distribution:
o Upper arm (axilla): supplies the triceps -strong extensor of the elbow
o Lower arm (above the elbow):
 Brachioradialis
 Extensor Carpi radialis longus – wrist extension
o Forearm:
 Sensory branch: sensation over the three and a half fingers laterally
on the dorsal side
 Motor branch called the posterior interossous nerve: thumb and
finger extension
 Clinical features:
o Humours fracture in spiral groove with radial nerve injury:
 Normal elbow (triceps is supplied higher, spared)
 No wrist extension (drop wrist)
 No thumb and finger extension
 Numbness or loss of sensation
o Posterior interossous nerve injury:
 Stab wound in the forearm
 Elbow and wrist are normal
 Thumb and finger extension are lost
 Finger muscles:
 metacarpophalengeal (MP) joints
o Extension is by the radial nerve
o Flexion is by the ulnar nerve by the interossie
and lumbrical
 Intraphalengeal joints (IP)
o Extension is by the ulnar nerve by the
interossie and lumbrical muscles
o Flexion by the long flexors of the forearm
 No sensory symptoms!!! Pure motor nerve
 Saturday night palsy:
o Very high injury of the radial nerve due to compression of the nerve in
the axilla
o Everything is affected (wrist, elbow, fingers, thumb and sensation)
o Called like this because drunk people sleep with an arm behind the
chair that causes the compression
 Summary:
o Remember where the lesion happened
o Injury to the radial nerve in the axilla: all motor and sensory functions
are lost
o Injury to the nerve in the spiral groove: triceps is spared and everything
else is lost
o Injury in the forearm to the posterior interossous nerve: elbow, wrist and
sensation are normal.

415
 Peripheral Nerve Injuries 5

3.4 FOREARM

3.4.1 MUSCLES
 5 superficial muscles:
o Pronator teres → pronation of the forearm
o Flexor carpi radialis → wrist flexion
o Palmaris longus → wrist flexion
o Flexor carpi ulnaris → wrist flexion
o Flexor digitorum superficialis → flexion of the proximal Intraphalengeal
joints (PIP) so flexes the middle phalynx
 3 deep muscles:
o Flexor digitorum profundus
o Flexor pollicis longus
o Pronotor quadrates
3.4.2 NERVE SUPPLY
 All of these muscles are supplied by the median nerve except 1 and a half
are supplied by the ulnar nerve:
o Flexor carpi ulnaris
o Half of flexor digitorum profundus to the little and ring finger
 The median nerve has 2 branches
o Superficial which supplies the superficial group
o Deep (anterior interossous nerve) which supplies the deep 2 and a half
muscles (PURE MOTOR)

3.4.3 HAND MUSCLES

 Hypothenar: opposition of the little finger
 Thenar: opposition of thumb + adduction of the thumb (adductor pollicis)
 Interossie: abduction and adduction of the fingers + MP flexion + IP
extension
 Lumbricals: MP flexion + IP extension
3.4.4 NERVE SUPPLY
 The hand has 20 muscles
o 15 supplied by the ulnar nerve (3 hypothenar + 8 interossei (dorsal and
palmar) + 2 lumbricals + adductor pollicis + Palmaris brevis)
o 5 by the median nerve (3 thenar + 2 lumbricals (1st and 2nd)
 All the actions are from the ulnar nerve except 2 are from the median
nerve:
o Opposition of the thumb
o Index and middle lumbricals

3.5 MEDIAN NERVE

 Motor:
o Superficial flexors except flexor carpi ulnaris
o Deep flexors except half of flexor digitorum profundus to little
and ring finger
o Thenar muscles

416
6 Peripheral Nerve Injuries

o Index and middle lumbricals

 Sensory: lateral 3 and a half fingers on the palmer side
 Clinically:
o Anterior interosseous nerve injury:
 Affects the deep 2 and half muscles:
 Half of Flexor digitorum profundus
 Flexor pollicis longus
 Pronotor quadrates (pronation is not lost because of
pronator teres)
 Sign: the patient “cannot make a perfect O” with the thumb,
index and middle fingers because he can’t flex the tips of the
index and middle finger (DIP joint: this is the action of the flexor
digitorum profundus muscle)
 Median nerve injury at level of wrist:
o Common in patients who attempt suicide
o Loss of opposition
o Loss of sensation 3 and a half lateral
o Lumbricals are lost but interossie do the job
o They still can make an “O”, bend the wrist and flex the PIP
 Carpal tunnel syndrome:
o Loss of sensation first
o If untreated weakness of opposition
 Summary:
o Injury to median nerve at level of the wrist: loss of opposition and
loss of sensation
o Injury to anterior interosseous branch of median nerve: patient
cannot make an O + normal sensation
3.6 ULNAR NERVE

 Motor:
o Flexor carpi ulnaris
o Medial half of flexor digitorum profundus
o Lumbricals + interossie + hypothenar + adductor pollicis
 Sensory: medial 1 and a half fingers front and back of the hand
 Clinically:
o Ulnar nerve injury:
 loss of flexor carpi ulnaris and half of flexor digitorum profundus
 loss of sensation
 all of the hand muscles
 cannot oppose the little finger
 atrophy of hypothenar muscles
 Cannot adduct or abduct the fingers
 Ends up with ulnar claw hand
o Ulnar nerve injury at the wrist:
 Sensation is lost
 All hand muscles:
 Hypothenar atrophy
 No opposition of the little finger
 Cannot adduct or abduct the fingers

417
 MCQs 7

 Loss of thumb adduction resulting in froment’s sign

 Froment’s sign: you ask the patient to hold a pen with his
thumb but he cannot so he contracts the flexor pollicis
longus because the adductor pollicis is lost
 Summary of ulnar nerve injury:
o Ulnar claw
o Loss of sensation
o Hypothenar atrophy
o Positive froment’s sign
o Cannot adduct or abduct the fingers
3.7 MEDIAN AND ULNAR NERVE INJURY AT THE WRIST

 Loss of intrinsic muscles

 Loss of sensation
 Clawing of all the fingers = ape hand (semian hand)
4 MCQS

1. Erb’s palsy:
a. C5 and C6
b. C7 alone
c. C8 and T1
d. Total palsy
e. Lower brachial plexus injury
2. The abductor pollicis longus muscle is supplied by:
a. Median nerve
b. Ulnar nerve
c. Anterior interosseous nerve
d. Radial nerve
e. Axillary nerve
3. The main action of the C6 root of the brachial plexus is:
a. Making a fist
b. Crossing the fingers
c. Elbow flexion
d. Wrist extension
e. Elbow extension
4. The intrinsic muscles of the hand are supplied by:
a. C5
b. C6
c. C7
d. C8
e. T1
5. Klumpke’s palsy has all the following characteristics except:
a. Can result from motor cycle injury
b. Anhidrosis
c. Loss of dermatomes
d. Phrenic nerve palsy
e. Miosis
6. A patient with posterior interosseous nerve palsy:
a. Unable to extend his wrist.

418
8 Peripheral Nerve Injuries

b. Can extend the IPJs of the fingers.

c. Can extend the MPJs of the fingers.
d. The sensation over the radial half of the hand is lost.
e. None of the above.
7. Lateral cutaneous nerve of the forearm is a branch of which nerve:
a. Axillary
b. Radial
c. Musclocutaneous
d. Ulnar
e. None of the above
8. in a patient with anterior interossous nerve palsy, what is false:
a. Can pronate the forearm
b. Can flex the PIP of the index
c. Have positive O sign
d. Can flex the IPJ of the thumb
e. All of the above are true

9. After nerve injury, nerve recovery is at rate of:

a. 1 mm/day
b. 2 mm/day
c. 3 mm/day
d. 4 mm/day
e. 5 mm/day
4.1 ANSWER YES OR NO

1. A patient cut his median nerve at the wrist:

a. Has he lost opposition of the thumb?
b. Has he lost any sensation?
c. Can he flex the tip of the index finger?
2. A patient is known to have "Saturday night palsy" is there Loss of
supination?
3. Can a patient with erb's palsy also have phrenic nerve palsy?
4. A patient has klumpke's palsy:
a. C5, c6, and c7 are completely intact?
b. Only c8 or T1 are injured?
c. Can move his shoulder, the elbow and the wrist?
d. Can't make a fist?
e. Can use his intrinsic muscles of the hand?
f. Will have clewing of all fingers "simian hand"?
g. Can have phrenic nerve palsy?
h. Can have Horner's syndrome?
5. patient has cut his median nerve at the level of his arm:
a. Can he flex his wrist?
b. The patient will flex more in the radial deviation?
c. Is the FDS completely paralyzed?
d. Is the FDP completely paralyzed?
e. Is there sensory loss?
f. Can he still oppose his thumb?

419
 MCQs 9

g. Can he flex the tip of the thumb?

h. Can he flex the tip of the index finger?
i. Can he flex the tip of the little finger?
j. Can he flex the PIP of the little finger?
k. Does he have sensation of the volar aspect of the little finger?
l. Does he have sensation of the volar aspect of the thumb?
m. Can he flex the tip of the ring finger?
n. Can he flex the PIP joint of the ring finger?
o. Can he flex the PIP joint of the index finger?
6. Can a patient with erb's palsy also have horner's syndrome?
7. Patient comes with a stab wound to the axilla which cut his radial
nerve:
a. He's unable to extend his elbow
b. He can extend the wrist
c. He's unable to extend and radially abduct the thumb
d. He's unable to extent the MP joints of the finger
e. He will have wrist drop
f. Can he extend the IP joints of the fingers
8. Patient presents with superficial radial nerve injury (cut in the mid
forearm) will only have sensory loss?
9. Patient presents with posterior interosseous nerve injury:
a. His triceps is paralyzed.
b. He has loss of sensation over the dorsum of the thumb.
c. He is unable to extend the elbow.
d. Can he extend the wrist?
e. Can he extend the thumb?
f. His supinator muscle is paralyzed.
g. Can he supinate the forearm?
h. Will thumb radial abduction be lost?
i. Will MP joint extension be lost?
j. Will IP joint extension be lost?
k. Can he extend the IP joint of the little finger?
l. Is there loss of sensation?
10. Can a patient with erb’s palsy make a good fist?
11. A patient comes to the clinic with isolated axillary nerve injury.
a. Clinical examination is mainly the teres minor.
b. He will not be able to initiate abduction.
c. He will not be able to externally rotate.
12. Patient has paralysis of the extensor digitorum:
a. Can he extend the IP joint of the thumb?
b. Can he extend the IP joint of the index?
13. Clinically, only two things are important when it comes to
musclocutaneous nerve injury: biceps and lateral cutaneous nerve of
the forearm.
14. A patient with injury to roots C5, C6, and C7:
a. Can’t abduct or external rotate, so he will go into adduction and
internal rotation.
b. Can’t flex the elbow, so he will go into elbow extension.
c. Can extend the wrist.
d. Will have complete claw hand.

420
10 Peripheral Nerve Injuries

4.2 TRUE OR FALSE

1. Patient presents with injury to the anterior interosseous nerve:

a. Patient lost sensation at the tip of the thumb
b. Patient lost sensation in the palm of the thumb.
c. Patient’s sensation is normal.
d. Patient’s pronation is normal.
e. Patient cannot flex his wrist.
f. Patient cannot oppose the thumb.
g. Patient can flex the MP joint of the thumb.
h. Patient can flex the IP joint of the thumb
i. Patient can flex the tip of the index.
j. Patient can adduct the thumb.
k. Patient can flex the PIP joint of the index.
l. Patient can flex the tip of the thumb.
m. Patient can pronate the forearm.
n. Patient cannot make a perfect O.
o. Patient has no sensory loss in the hand.
p. Patient cannot flex the little finger.
q. Patient can flex the MP joint of the index finger.
r. Patient cannot flex the PIP joint of the index finger.
s. Patient can flex the tips of the index and middle fingers
2. Patient who has cut his posterior interosseous nerve cannot
supinate?
3. Patient cut his ulnar nerve at the wrist:
a. He can feel the back of his little finger
b. He can flex his wrist
c. He can flex the wrist in ulnar and radial deviation
d. He cannot flex the tip of the index finger.
e. He can flex the tip of the little finger.
f. He can flex the PIP joint of the little finger.
g. He can feel the palmar surface of the little finger.
h. He can feel the dorsal surface of the little finger.
4. Patient cut his median nerve at the level of his elbow:
a. He had lost the ability to oppose the thumb.
b. He has sensory loss.
c. He is still able to flex his wrist.
d. Thumb tip flexion is normal.
e. Pronation is lost.
5. Complete loss of the ulnar nerve:
a. The caused by cutting the ulnar nerve at the wrist
b. Is caused by cutting the ulnar nerve in the arm
c. Loss of wrist flexion.
d. Can’t flex the wrist in ulnar deviation
e. Can flex the tips of the fingers.
f. Inability to flex the tips of the ring and little fingers.
g. Able to flex the IP joints of the fingers
h. There’s no sensory loss.
i. Can feel the back of the hand.
j. Can’t feel the front of the hand.

421
 MCQs 11

k. Able to oppose the thumb and the little finger.

l. Is able to adduct and oppose the little finger.
m. Will have Froment’s sign.
n. Is able to adduct and abduct the fingers.
o. Is able to flex the PIP joints of the little finger
6. A patient cut his ulnar nerve in the mid-forearm:
a. He can feel the back of his hand.
b. He can feel the front of his hand.
c. He can adduct and abduct the fingers.
d. He can adduct the thumb,
e. He has Froment’s sign.
f. He cannot oppose the little finger.
g. He cannot oppose the thumb.

 MCQs: 1=a, 2=d, 3=c, 4=e, 5=d, 6=b, 7=c, 8=d, 9=a
 Yes/No:
1= (a) yes, (b) yes, (c) yes
2= no
3= yes
4= (a) yes, (b) no, (c) yes, (d) yes, (e) no, (f) yes, (g) no, (h) yes
5= (a) yes, (b) no, (c) yes, (d) no, (e) yes, (f) no, (g) no, (h) no, (i) yes, (j) yes, (k) yes, (l) no, (m)
yes, (n) yes, (o) no
6= no
7= (a) yes, (b) no, (c) yes, (d) no, (e) yes, (f) yes
8= yes
9= (a) no, (b) no, (c) no, (d) yes, (e) no, (f) yes, (g) yes, (h) yes, (i) yes, (j) no, (k) yes, (l) no
10= yes
11= (a) no, (b) no, he will be able to initiate abduction, (c) no, he will be able to externally rotate the
arm
12= (a) yes, (b) yes
13= yes
14= (a) yes, (b) yes, (c) no, (d) no
 True/False:
1= (a) F, (b) F, (c) T, (d) T, (e) F, (f) F, (g) T, (h) F, (i) F, (j) T, (k) T, (l) F, (m) T, (n) T, (o) T, (p) F,
(q) T, (r) F, (s) F
2= F
3= (a) T, (b) T, (c) T, (d) F, (e) T, (f) T, (g) F, (h) T
4= (a) T, (b) T, (c) T, (d) F, (e) T
5= (a) F, (b) T, (c) F, (d) T, (e) F, (f) T, (g) F, (h) F, (i) F, (j) T, (k) F, (l) F, (m) T, (n) F, (o) T
6= (a) F, (b) F, (c) F, (d) F, (e) T, (f) T, (g) F

422
 Introduction 1

HAND INJURIES
1 INTRODUCTION The ulnar nerve is
the most important
1.1 HISTORY nerve in the hand
because it controls all
 Hand dominance action except opposition
of the thumb by the
 Occupation median nerve
 Previous hand trauma or injury
Ulnar supplies all
 Smoking muscles except thumb
o Patients who smoke have vasoconstriction of blood vessels and that muscles (Abductor
makes connecting an amputated finger have a high chance of failing so pollicis brevis, flexor
the doctor must know before he goes into the OR pollicis brevis,
Opponens pollicis) and
o No point in wasting time, this procedure takes 6-8 hr so if pt smoker from 2 lumbricals by the
beginning say you can’t median nerve
 Tetanus –BUT Adductor pollicis
o Make sure the patient is vaccinated, if not give him vaccination supplied by ulnar nerve.
o Any open wound there is risk of infection (tetanus)
 Acute vs. Chronic
o Acute e.g. Trauma, burns, laceration, fractures, dislocation, infection
o Chronic e.g. Lumps , Carpal tunnel syndrome and nerve compressions,
arthritis
 Mechanism of injury and complaint
o Trauma, Laceration, Swelling or lump, Arterial or Venous injury,
Dislocation, Infection, Numbness
1.2 EXAMINATION There are no intrinsic
muscles on the dorsum
1. Inspection of the hand all of them
1. Compare both hands (always compare to a normal hand) are on the volar surface
2. Dorsum then volar surface •Radial nerve doesn’t
 Skin ( Ulcers or lesions or color) give any motor supply to
hand only sensation
 Swelling
 Wasting 2 groups of hand
 Position normal position of hand if u put it on table: flexion cascade muscles:
“the flexor tendons are stronger then extensor tendons”. If someone –Extrinsic
can’t do this >injury to flexor tendons. •Originate from the
2. Palpation forearm and insert in the
hand
o Feel Tenderness, sensation, temperature, Capillary refill
3. Check Movement –Intrinsic
o Move Range of Motion •Originate and insert in
 Passive, Active the hand
 Examine FDS, FDP, & extensor tendons
o Test Specific Nerves (Sensory + Motor)
 Median ( sensation to lateral three and a half volar side)
 Ulnar (sensation to medial one and a half on the volar and dorsal
side)
 Radial (lateral three and a half dorsal)

423
1
2 Hand Injuries

2 HAND INFECTIONS

2.1 PARONYCHIAL INFECTION

 Most common hand infection

 Infection of the nail bed or nail plate
 Present with redness around the nail
 Could be just cellulitis and redness or
abscess
 Most common organism is Staph Aureus
 Treatment:
o Antibiotics + warm saline soaking
o If there is no response in 48 hours you Example for incision and drainage
must do Incision and drainage
o If there is an abscess then you must do
incision and drainage
 If someone gets paronychial infection
frequently (6 times a year) think of chronic
infection
o Most common cause of chronic infection
is candida (fungi)
 Treatment:
o Suspect Candida so send swab
o If + give oral antifungal or topical
o If no response then remove the skin and
clean then graft
2.2 FELON

 38% of all surgical infections(very

common)
 Infection of the finger pulp
 This area is very sensitive because it has
many nerve endings
 2 point discrimination is maximal at this area
 So when it develops an abscess between it
and the skin it causes nerve compression
and SEVERE PAIN
 Treatment:
o Antibiotics + warm salt soaks
o If no response incision and drainage
 Incision must be made from the side to not loose sensation
2.3 HERPETIC WHITLOW

 HSV type 1 vesicular eruption of the

fingertip
 Vesicles that contain clear fluid

424
2
 Hand Infections 3

 Happens to children (biting nails) and dentists

 Very painful
 Very contagious (patients need isolation)
 Treatment by acyclovir (antiviral medication)
2.4 COLLAR ABSCESS

 Abscess of the hand web-Space

(Connection point between the volar
and dorsal parts)
 Presents with redness, swelling and
abducted finger
 Treatment:
o Antibiotics if early with observation
as in or out patient
o Incision and drainage in the OR
(complex area)
2.5 FLEXOR TENOSYNOVITIS
Catheter irrigation
 Each finger has 2 flexor tendons; one •You pass a catheter
moves PIP (attached to middle phalanx), between 2 ends of the
flexor sheath and you
the other DIP (attached to distal phalanx).
keep it there until the
 Infection of the flexor tendon sheath due to area is clean
trauma •Until you clean out all
 Can extend to the forearm the pus, if you are not
 4 signs: happy leave this catheter
o Sausage-shaped fingers in, take the patient to the
ward and nurses will
o Flexed position irrigate every 6hr and u
o Pain with passive extension will take it out after 48-72
o Tenderness along the tendon hr,
 Treatment: •if you are still not happy
o Must be IMMEDIATE because of with the wound open the
high risk of sepsis,necrosis and whole finger and clean
then close loosely never
amputation close infected wound
o You have to do incision and completely.
drainage
o Antibiotics
o Catheter irrigation (irrigate the
sheath with saline)
o If the infection is bad, it can cause
thrombosis of artery, ischemia of
nerve and insensate the fingers.

2.6 HAND BITES

 The problem with bites is that the saliva is full of bacteria

 Human: Staph, Strep, Eikenella 
 Dogs:
o Pasteurella Multocida (very dangerous), Staph, Strep

425
3
4 Hand Injuries

o With street dogs, the most likely cause is rabies

o All must get rabies treatment: IgG and rabies vaccine (5 injections in
abdomen at day 1,3,7,14,28)
 Cats:
o More dangerous than dog bites (more concentration of bacteria within
the saliva)
o Pasteurella Multocida
 All of them should be admitted for IV antibiotics
 Most of dog & human bites respond well to Augmentin Tetanus
 If given the antibiotics and there’s no response in 48 hours, we do incision +
drainage

3 NECROTIZING FASCIITIS

 Flesh eating disease of the soft tissue

 Occurs in diabetics with low
socioeconomic status
(immunocompromised)
 Pt presents with infection and is unstable
(hypotension , tachycardia, ALOC and
low urine output )
 Caused by Group A B-hemolytic strep
 Infection of the fascia
 Skip lesions on the skin
 Has high mortality rate
 Treatment:
o Patient needs to be intubated and
admitted to ICU
o Needs extensive debridement and IV
Antibiotics
o So stabilize the pt, take him to the
OR, and open all of the infected area
in whichthe fascia will look gray with a
bad smell. Once you see a healthy
area > skip and open again to make
sure that there’s no extension.
o Some patients don’t respond to the
1st or2nddebridement > amputation!

426
4
 Flexor Tendons 5

4 FLEXOR TENDONS  No muscles in finger

(only tendons) so it will
4.1 ANATOMY survive in case of
ischemia more than 6
hours.
 There are 8 muscles with almost 12 tendons
in the flexor side, (4FDS, 4FDP, FPL, FCU,
FCR, PL)
o FCU,FCR, PL: flex the wrist
o 4FDS: flex PIP joint
o 4FDP: flex DIP joint
o FPL: flex thumb
 Origin
o Medial epicondyle to the forearm then
develops tendons and goes through the
carpal tunnel to insert into the hand and
fingers
 Nerve Supply
o All of them by the median nerve
o Except: FCU and medial ½ of FDP
4.2 MECHANISM OF INJURY

 Closed vs. Open

o Closed:
 Completely flexed and then sudden severe hyperextension
o Open
 Laceration: Knife being the most common tool for it
 Crush injury
 Degloving injury
4.3 VERDAN’S 5 ZONES

 Classified mainly to get an idea of the expected outcome after repair

 Zones 3,4 and 5 have a good chance; as you go distally (zone 2), chances
of full recovery are less because of the small space
 Zone 1: Only affects the FDP
 Zone 2:
o FDP&FDS
o Extends from MCP joint to insertion of FDS
 Zone 3:
o From distal area of carpal tunnel to MCP joint
o Dangerous because it also affects nerves and arteries
 Zone 4: Area under carpal tunnel
 Zone 5: The distal forearm

427
5
6 Hand Injuries

4.4 PULLY SYSTEM AND TENDON BLOOD SUPPLY

 Small ligaments are present in front of the tendons to hold them in place
(A1-A5, C1-C3). Each tendon has its own blood supply.

4.5 CLINICAL EXAMINATION AND FINDING

 Loss of flexion cascade

 Open wound most commonly
 Tendon could be visible in the wound
 Inability to flex the digit at PIP or DIP

Closed injury
If open wound > tendon ends are seen

Normal Cascade

428
6
 Flexor Tendons 7

How to examine FDS and FDP?

FDS FDP

The Flexor Digitorum Superficialis (FDS) The Flexor Digitorum Profundus (FDP)
inserts into the middle phalanx of each finger. inserts into the distal phalanx of each
It is tested by blocking the finger MCP joint finger. It is tested by blocking the finger PIP
and asking the patient to flex the PIP joint. To joint and asking the patient to flex the DIP
block the MCP joint, hold the proximal joint. To block the PIP joint, hold the middle
phalanx in extension just distal to the MCP phalanx in extension just distal to the PIP
joint, so that the MCP joint is unable to bend joint, so that the PIP joint is unable to bend
when the patient tries to flex the finger. when the patient tries to flex the finger.

4.6 FLEXOR TENDON REPAIR

 Explore the wound in zigzag fashion

o In OR; because this area has nerves and blood vessels
o Zigzag not straight cut why? It’ll cause flexion contraction
 Find the 2 ends of the cut tendon and pull it out then insert needle
 Repair : > 25 different technique for the repair
 Non absorbable suture> because of the poor blood supply

Needle to hold it in place

4.7 FLEXOR TENDON SPLINTS

 You can’t let patient use his hand the

repair will be cut! Also to keep it in the
functional position to make sure
adhesions will not damage function

429
7
8 Hand Injuries

 The wires allows pt to move fingers without tension. U don’t want cause
adhesion if u let it 3-4 weeks without movements.

5 REPLANTATION

5.1 INDICATIONS AND CONTRAINDICATIONS

 Indications
o Amputated Thumb: It provides 50% of
hand Function
o Children: The risk of loss is higher than
adults because vessels are very small
& more difficult.
o Multiple digits: You try to fix 2-3 so he
can hold things.
o Partial or whole hand: Because they
have a lot of function problems.
 Contraindications
o Life threatening injury: You want to
save the pt’s life it’s more important.
o Sever chronic illness
o Multilevel injury
o Severely crushed injury
o Single digits: Because the pt will not
have functional defects.
o Severe contamination
o Avulsion injury: Finger gets pulled out;
artery needs to be reattached at wrist
level
 Duration of surgery 6-8 hours
 40% chance of failure
 Can’t work 3-6 months
5.2 GENERAL PRINCIPLES

 Resuscitate the patient

 Preserve amputated part in cold water not directly on ice (frostbites)
 Warm ischemia time > must operate within 6-8 hours. If cold > within 12-24
hours (longer)
 Successful replant after 28 hours: The longer its preserved, the better.
 X-ray the hand and the amputated part
o Make sure no fractures because in that case you can’t replant it
 Consent for vein, nerve, tendon and skin graft
 Prepare the amputated part
 1st Shorten the bone
 Arthrodesis
 2nd Repair flexor and extensor tendon
 Repair (3rd) Digital artery (4th) vein and (5th) nerve
 6thSkin closure +/- skin graft

430
8
 Hand Fractures 9

5.3 COMPLICATIONS

5.3.1 WHITE FINGER

 No blood Flow (Low arterial flow)
 Technical or non- technical
 If patient is a smoker don’t bother to replant
o Ensure pt is warm
o Well-hydrated
o Prevent hypotension
o Loosen dressing
o Remove sutures
o Re-Explore and check arteries if all doesn’t work
5.3.2 BLUE FINGER
 Veins are not draining (High venous flow)
o Elevate limb
o Loosen dressing
o Remove sutures
o Leeches
o Remove nail
o Heparin injections
o Re-Explore
 Leeches, in case of venous congestion,
suck the blood relieving the congestion
6 HAND FRACTURES

6.1 UNSTABLE FRACTURE

 Cannot be reduced closed or cannot be held reduced without fixation

 30% risk of infection in open fracture including open Distal Phalanx fracture
o Reduced to 3% with antibiotics
o The distal phalanx fracture with subungal hematoma (bleeding in nail)
should be considered an open fracture
o Healing 4/52’s for phalangeal fracture whereas 5-6/52’s for metacarpal
fracture
6.1.1 ACCEPTABLE HAND FRACTURES
 Tuft distal phalanx
 AP displaced metapheseal fracture in children
 MC (metacarpal) neck fracture
o <15 in index and middle finger
o <30-40 in ring and little finger
 MC (metacarpal) base fracture
o Adult < 20 angulation
o Children < 40 angulation
Child patient: growth palate in base
of phalanx and head of metacarpals.

431
9
10 Hand Injuries

6.1.2 UNACCEPTABLE PHALANGEAL FRACTURES (NEED FIXATION)

 Rotational angulation
 Sever dorsal angulation
 Lateral angulation
6.2 PEDIATRICS HAND FRACTURES – SOLTER HARRIS
CLASSIFICATIONS

 Type I – A transverse fracture through the growth plate 6%.

 Type II – A fracture through the growth plate and the metaphysis, sparing
the epiphysis 75% incidence, away from joint.
 Type III – A fracture through growth plate and epiphysis, sparing the
metaphysis 8% goes to joint
 Type IV – A fracture through all three elements of the bone, the growth
plate, metaphysis, and epiphysis 10%, above and below joint.
 Type V – A compression fracture of the growth plate (resulting in a decrease
in the perceived space between the epiphysis and diaphysis on x-ray) 1%
 Fracture in child (growth plate) will affect grow, if the fracture in one side
after 6 years pt will come with angulation of finger b/c one side grow and
other didn’t.

6.3 INDICATION FOR FIXATION NON-ARTICULAR

 Angulation
 Rotation
 Shortening

432
10
 Hand Fractures 11

1. Transverse fracture of 2. Spiral fracture 3. Gun shots and bone loss

proximal phalanx.

 Fractures of metacarpal bone:

o Head
o Shaft
o Base
 Ask pt where the area of maximum tenderness is, thenlook at this area on X-
ray

433
11
12 Hand Injuries

6.4 TECHNIQUE OF FIXATION

 1st do x-ray; if it’s reduced, you don’t need to fix it>Close reduction splint
 If it doesn’t stay in place > Close reduction K-Wire fixation
 ORIF (Open Reduction Internal Fixation)
o Lag Screw
o Plate
o Circulage wire

Circulage wire & K-wire

Metacarpal & phalanges fractures fixed with K-

Wire fixation

Two are put to prevent rotation

Lag Screw , usually used in spiral fractures

434
12
 Carpal Tunnel Syndrome 13

7 CARPAL TUNNEL SYNDROME

7.1 INCIDENCE

 The most common nerve compression in the upper limb: 1 – 10% of the
population
 As high as 60% in people with repetitive hand movement: Because of hand
swelling
 Anatomy
o Base (floor) is the bony carpal arch
o Bridge (roof) is the flexor retinaculum
o Borders: scaphoid, trapezium, pisiform, triquetral.
o Has 9 flexor tendons and the median nerve
7.2 AETIOLOGY

 Due to increase in volume of the content or reduction of the tunnel size

o Acromegaly
o Trauma
o OA
o Ganglion, Lipoma
o Inflammation Tenosynovitis, gout
o DM, Thyrotoxicosis, Pregnancy
o Congenital:
 Abnormal muscle, persistent median artery
7.3 SYMPTOMS

 Pain
 Numbness
 Paraesthesia in the median nerve distribution
o Radial 3.5 digits
 Night pain
o When the patient sleeps on his hand, everything swells so he wakes up
with more numbness in the morning.
 Pain radiates proximally to the shoulder
 Weakness
 Clumsiness
7.4 CLINICAL FEATURES

 Weakness & wasting of the hand thenar muscles. When they hold
something, it falls.
 Altered sensation in the median nerve distribution
 Positive Tinels sign
o Tap over the carpal tunnel area of the wrist 5 or 6
times> tingling or paresthesia in the median nerve
distribution
 Positive Phalan test
o This position should be held for about 1 minute>
numbness or tingling along the median nerve

435
13
14 Hand Injuries

distribution
o Reverse Phalan test
 The more severe the compression the faster the numbness
7.5 INVESTIGATIONS

 X-Ray
 CT scan
 MRI
 Nerve conduction studies: Most common test used
7.6 TREATMENT

 Non-Operative (Mild)
o Splints
 Rests the hands but once stopped > symptoms will return
o NSAID’s
o Steroid Injections
 Operative (Persistent)
o All Open technique
 The best approach
o Limited incision Technique
o Endoscopic Techniques
 Lots of reports of injuries to the median nerve

436
14
 MCQs 15

8 MCQS

1. The true statement regarding tendon injuries in the hand is:

a) Flexor digitorum superficialis inserts on the distal phalanx
b) Flexor digitorum profundus inserts on the middle phalanx
c) The tendons of flexor digitorum superficialis arise from a common
muscle belly
d) The best results for repair of a flexor tendon are obtained with injuries in
the fibro-osseous tunnel (zone 2)
e) The process of healing a tendon injury involves formation of a tenoma

2. Which of the following statements regarding carpal tunnel syndrome is

correct?
a) It is rarely secondary to trauma
b) It may be associated with pregnancy
c) It most often causes dysesthesia during waking hours
d) It is often associated with vascular compromise
e) Surgical treatment involves release of the extensor retinaculum

 Answers: 1;E , 2;B

437
15
 Hemangioma 1

SKIN AND SOFT TISSUE

TUMORS
1 HEMANGIOMA

 It is the commonest skin tumor, and the commonest benign tumor of

infancy. 
 It is classified based on the likelihood of proliferation or regression to:
o Involuting; will regress on its own.
o Non-involuting; won't regress on its own.

1.1 INVOLUTING HEMANGIOMA (HEMANGIOMA OF CHILDHOOD)

 It makes up to 95% of all hemangiomas.

 It is a neoplasm of endothelial cell origin, i.e. it is a hamartoma, not a true
neoplasm.
 Presents at birth or during the first 2-3 weeks after birth, and grows rapidly
for 4-6 months.
 Undergoes complete spontaneous slow involution; usually completely
disappears at the age of 5-7 years.

1.1.1 CLASSIFICATION:
 Both benign tumors
A. Superficial (strawberry news): and hamartomas are
 A type of capillary hemangioma (a nevus vasculosum capillary composed of normal
cells in excessive
hemangioma).
quantities, but benign
 Very superficial in the dermis. tumors have a normal
 Appears as a sharp demarcated, red, slightly raised lesion with an irregular arrangement whereas
surface. hamartomas have an
abnormal arrangement
B. Deep (cavernous hemangioma):
of cells.
 Arises from below subcutaneous tissues.
 Appears as a blue tumor covered by normal skin. In involuting
hemangioma, the deeper
C. Combined:
they go the bluer they
 Combined dermis and deep dermis. become, whereas the
 Firm, usually purple to blue depending on the depth. more superficial the
more cherry red they get.
 May extend deeply into subcutaneous tissues.

1.1.2 TREATMENT:
 No need for treatment, just observe, unless it involves a vital organ or
interferes with physiological functions, e.g. eyelid.

1.2 NON-INVOLUTING HEMANGIOMA:

 True benign tumors.

 Usually present at birth.

438
2 Skin and Soft Tissue Tumors

 There is no rapid growth phase; its growth is proportional to the growth of

the child.
 Persists to adulthood.
 Causes severe aesthetic (cosmetic) problems.
 May cause arteriovenous fistulas eventually leading to cardiac failure.
 Treatment is not satisfactory.

1.3 PORT WINE STAIN

 An extensive intradermal hemangioma, just below the epidermis, which is

mostly made up of a collection of dilated venules and capillaries. It has a
deep purple red color.
 May involve any portion of the body, usually as flat patches in the face.
 Usually follows the correlation of sensory branches of the 5th nerve; so if it
involves one branch of the trigeminal, it will spread to half of the face,
whereas if it involves both branches it will spread to the whole face.
 Microscopically, it appears as thin walled capillaries distributed throughout
the dermis, lined by thin mature flat endothelial cells.
 Treatment:
o Unsatisfactory.
o Tattooing.
o Radiotherapy: causes a scar as it destroys both blood vessels and the
skin overlying the lesion.
o Laser has a special wavelength affecting the blood vessels without
affecting the skin, but it is expensive.

2 BASAL CELL CARCINOMA (BCC; RODENT ULCER)

 The most common malignant cancer of all skin tumors.

 Locally invasive malignant tumor, which may lead to massive ulceration.
 Very rare to metastasize. 
 Affects ages over 40, and men are more affected than women.
 Risk is increased in:
o Individuals with high cumulative exposure to UV light through sunlight,
e.g. live in tropical areas.
o Those with fair, white skin, especially when the person has blond or red
hair and blue, green, or gray eyes, e.g. westerners working in KSA.
 Mostly presents in the face and the neck.
 Grows slowly (not aggressively), steadily and painlessly, and several
months or years may pass before the patient finally visits a doctor.
 Death may occur due to secondary complications of invading deeper
tissues or major blood vessels.
 Appearance:
o Small translucent, skin elevated nodule with rolled pearly edges.
o Tetangiectatic vessels may occur on the surface.
o Flat and white or waxy appearance with firm palpation.

439
 Squamous Cell Carcinoma (SCC) 3

o Histologically, it appears as elongated strains of basal cells that infiltrate

the dermis.

2.1 BASED ON APPEARANCE, THERE ARE 4 FORMS:

1. Erythernatous (superficial) basal cell carcinoma:

 Occurs most frequently on the trunk.
 Appears as a reddish plaque with an atrophic center, and smooth,
slightly raised borders.
2. Pigmented basal cell carcinoma (frequent in our country):
 Sometimes mistaken with melanoma, but it is darker.
 Extends deep to the subcutaneous tissue.
3. Nodular basal cell carcinoma.
4. Cystic basal cell carcinoma.

2.2 TREATMENT:

 Curettage and electrodessication (cautery), with excising a safety margin of

2-3 mm.
 Surgical excision (the best treatment): small moderate sized lesions, with
removal of the subcutaneous tissue and do reverse face-lift flab if the lesion
occurs in the face. 
 Radiotherapy: good for treatment of structures that are difficult to
reconstruct but hospitalization is not required. Should not be used in
patients under 40 years, due to mutation, or in patients who failed to
respond to radiation therapy. Treatment usually lasts 4-6 weeks.
 The more well differentiated the tumor the more radioresitant it is. And the
more undifferentiated the tumor the more radiosensitive it is.

3 SQUAMOUS CELL CARCINOMA (SCC)

 The second most common cancer in light skinned people, but the first in
dark skinned ones.
 There is a potential for metastatic spread. 
 The causative agents are the same as basal cell carcinoma, along with:
o Excessive contact with hydrocarbons such as tar, gasoline, and paints.
(i.e. occupational hazard related)
o Exposure to ionizing radiation.
o Chronic ulcers.
o Scars of thermal bums healed repeatedly by fibrosis (especially if it was
over a joint), which may lead to Marjolin's ulcer.
 Most common sites are the face and neck, e.g. ears cheeks, and the lower
lip, and the back of the hand.
 Presents as:
o Locally invading without metastasizing.
o Premalignant tumor, as Bowen's disease or chronic radiation dermatitis.

440
4 Skin and Soft Tissue Tumors

o Rapidly growing, widely invasive with metastasis, especially SCC

arising from normal skin.
o Initially starts as an erythematous plaque or nodules with indistinct
margins.
o Surface may be: flat, verrucose (warty) or ulcerative.
 Histologically, malignant epithelization is seen extending down into the
dermis like horns of pearls, which is not seen in basal cell carcinoma
(BCC). 

3.1 TREATMENT  Sarcomas

metastasize through
 Surgical excision with 4-5 mm margin in all directions. blood, while carcinomas
 Radiotherapy: the more well differentiated the tumor, the more it resembles metastasize through
lymphatics.
normal skin, the less potential to metastasize, and the less radiosensitivity,
and vice versa.

4 MALIGNANT MELANOMA (MM)

 Incidence is over 300,000 of skin tumors every year in USA, 9000 of these
are melanomas, i.e. 4.6%.
 2/3 of all skin tumor deaths are from melanomas. 
 Incidence of and survival also were increased from 41% to 67%.
 Whites have a higher incidence than blacks, but there is NO sexual
predominance.
 Risk factors:
o UV radiation.
o Family history.
o Average person has 15-20 nevi, 1/3 of the melanomas arise from a pre-
existing pigmented nevi.

4.1 TYPES OF NEVI:

1. Junctional nevi: (arise from the junctional layer, which is the dividing layer
of the skin)
 Small, circumscribed, light brown or black colored, flat, slightly raised
and rarely contains hair.
 Mainly lies between epidermis and dermis.
 May be formed in mucous membranes, genitalia, soles and palms.
 More likely to be malignant.
2. Intradermal nevi:
 Small spots, color ranges from blue to bluish black, flat and dome
shaped.
 Compound; found in both epidermis and dermis.
 Less likely to become malignant.
3. Dysplastic nevi:
 Pink base with indistinct irregular edges.

441
 Malignant Melanoma (MM) 5

 Usually have embryonic tissues, i.e. ectoderm, mesoderm, or

endoderm.
 Most dangerous type in newborns.
 Family history is important.
 Most lesions are small, and suspicious lesions must be excised.
o Congenital: excision in 1% of newborns also with dysplastic is
considered to be premalignant.

4.2 HISTOLOGICAL CLASSIFICATION:

 Superficial spreading melanoma (the commonest): arises from a

preexisting mole; common in blacks without sexual predominance.
 Nodular melanoma: becomes large and ulcerated before it is noticed.
 Lentigo maligna (melanoma): most commonly occurs in old patients,
especially from a preexisting mole.
 Acral lentiginous melanoma.

4.3 CRITERIA THAT SUGGEST MELANOMA FROM MOLE, AND

CONSEQUENTLY SUGGESTS ITS EXCISION:

 Color: focal shades with red, blue, white or darkening in color.

 Size: recent rapid diameter enlargement of more than 10 mm.
 Shape: irregular margin, notching and indentation.
 Surface: ulceration, bleeding, crusting, irregular elevation.
 Symptoms: pruritus, inflammation and pain.
 Location: back, lower extremities, location is subjected to BANS area;
Back, posterolateral part of the Arm posteroiateral part of the Neck and
Scalp; they are the anatomical areas that have a higher risk rate and a
lesser survival rate.

4.4 STAGING (CLARK'S CLASSIFICATION):

 Based on the histologic level of invasion of the tumor.

 Performed after excisional biopsy.
Level Feature Mortality and
morbidity rates
I In situ; above basement membrane (confined to the epidermis) 0%
II Invades the papillary layer of the dermis 4%
III Lesions reach the junction of the papillary and reticular layers 33%
IV Lesions invades the reticular dermis 61%
V Lesion invades subcutaneous tissue 78%

4.5 NODE DISSECTION:

 Advised prophylactically as:

o Level I and II: no need of dissection.
o Level III: some will do it and some will not.

442
6 Skin and Soft Tissue Tumors

o Level IV and V: dissection is mandatory.

 Not advisable in:
o Lymphatic drainage of sites involved. (e.g. if there’s a melanoma
involving the breast, you can’t simply excise all of the lymphatics
groups!)
o Patients over 70 years old.
o Serious concurrent disease.
o Unresectable distant metastasis.

4.6 PROGNOSIS:

 Depends on the tumor size and depth of invasion.

 Less than 2 cm in diameter and less than 0.7 mm in depth is curable by
wide local excision.
 Nodular melanoma with ulceration has a poor prognosis.
 Lesions in the extremities have a better prognosis than trunk lesions.
 Women have a better 5 years survival rate than men.

4.7 NONSURGICAL TREATMENT (IMMUNOTHERAPY):

 Small metastatic lesions treated with BCG may be tried on healthy patients.
 Melanoma is radioresistant; so radiotherapy is rarely used in treatment and
may be used in palliation.
 Chemotherapy with phenylalanine and alanine-mustard and other drugs.
 Survival is better in limbs because a limb can be isolated and treated
 Long-term palliative treatment of large lesions, which underwent surgery, is
with radiotherapy and chemotherapy.

5 MCQS

1. According to Clark's classification invasion of papillary layer in malignant

melanoma is:
a. Clark 1
b. Clark 2
c. Clark 3
d. Clark 4
e. Clark 5

2. Basal cell Carcinoma:

a. Metastasis is usually to Lymph nodes before systemic Metastasis
b. Metastasis is usually systemic before lymph nodes Metastasis
c. Metastasis is usually to both lymph nodes and systemic Metastasis
at
 the same time
d. Metastasis is usually to skin as " Satellite " Lisions
e. Does not develop Metastasis

3. Patients with Gorlin Syndrome are known to develop:

a. Basal Cell Carcinoma
b. Melanoma

443
 MCQs 7

c. Squanous Cell Carcinoma

d. Bowen's disease lesions
e. Dysplastic nervi

4. Squanous Cell Carcinoma of the skin:

a. Is Radio Sensitive
b. Is best treated by Chemotherapy
c. Surgery is done with 5cm skin margin
d. Usually seen in children
e. Its Metastasis is usually systemic before lymph node metastasis

5. Melanoma:
a. Nodular melanoma has a better prognosis than all other types
b. Acrol Melanoma is known to have the best prognosis
c. Is Radio sensitive
d. Usually develops metastasis to lymph nodes before
systemic
 metastasis
e. Is more common is black populations

6. A melanoma with Clark level II:

a. Reaches the epidermis
b. Reaches the Basal layer
c. Reaches the Reticular Dermis
d. Reaches Junction of Reticular and papillary dermis
e. Reaches the papillary Dermis

7. Majolin’s ulcer:
a. Is a type of basal cell carcinoma
b. Is a type of squamous cell carcinoma
c. Is a type of Melonama
d. Is a type of ulcer is a blue nervus
e. Is a type of an ulcer in a dysplastic nervus

8. Strawberry hemangioma in a newborn in the cheek:

a. Best treated by surgical excision
b. Best treated by steroid injection
c. Best managed by observation for 4-5 years
d. None of the above
e. All of the above

 Answers: 1:b, 2:e, 3:a, 4:a, 5:d, 6:e, 7:b, 8:c.

444