By Haileyesus Lemita

First edition
2021
2021
Table of contents
Table of contents............................................................................................................2
CHAPTER ONE-GENERAL SURGERY.........................................................................1
Wound Healing............................................................................................................... 1
Perioperative Care......................................................................................................... 6
Post-operative Complications.......................................................................................9
Fluid and Electrolyte Management............................................................................ 14
Shock............................................................................................................................. 23
Varicose Veins..............................................................................................................31
CHAPTER TWO-TRAUMA.............................................................................................37
Systemic Response to Injury...................................................................................... 37
Advanced Trauma Life Support (ATLS)....................................................................41
Burn Injuries..................................................................................................................47
CHAPTER THREE-THE BREAST................................................................................ 53
Surgical Anatomy and Physiology............................................................................. 53
Benign Breast Conditions........................................................................................... 58
Breast Cancer...............................................................................................................62
Rare Cases of Breast Cancer.................................................................................... 75
CHAPTER FOUR -THE THYROID................................................................................78
Surgical Anatomy and Physiology............................................................................. 78
Diagnostic Modalities...................................................................................................82
Antithyroid medications............................................................................................... 84
Thyroidectomies...........................................................................................................86
Disorders of Thyroid Gland.........................................................................................88
Malignant Thyroid Disease....................................................................................... 101
CHAPTER FIVE-THE STOMACH...............................................................................109
Surgical Anatomy and Physiology...........................................................................109
Diagnosis of Gastric Disease................................................................................... 114
Gastritis....................................................................................................................... 117
Peptic Ulcer Disease................................................................................................. 119
 Gastric Carcinoma..................................................................................................... 128
Postgastrectomy Complications.............................................................................. 132
Gastric Lymphoma.....................................................................................................135
Gastrointestinal Stromal Tumors (GISTs).............................................................. 136
CHAPTER SIX-THE PANCREAS............................................................................... 137
Surgical Anatomy and Physiology...........................................................................137
Diagnostic Modalities................................................................................................ 140
Congenital Anomalies............................................................................................... 140
Acute Pancreatitis......................................................................................................142
Chronic Pancreatitis.................................................................................................. 146
Pancreatic Neoplasms.............................................................................................. 148
CHAPTER SEVEN-THE BILIARY SYSTEM..............................................................150
Surgical Anatomy and Physiology...........................................................................150
Diagnostic Modalities................................................................................................ 153
Gallstone Disease (Cholelithiasis)...........................................................................156
Other Benign Diseases and Lesions.......................................................................166
Tumors of the Biliary Tract....................................................................................... 171
CHAPTER EIGHT-THE INTESTINES........................................................................ 176
Intestinal obstruction................................................................................................. 176
Colorectal Cancer...................................................................................................... 187
Osteomies...................................................................................................................204
CHAPTER NINE-THE URINARY SYSTEM...............................................................206
Surgical Anatomy and Physiology...........................................................................206
Benign Prostatic Hyperplasia................................................................................... 208
Renal Stones (Nephrolithiasis)................................................................................ 214
CHAPTER TEN-ORTHOPEDIC SURGERY..............................................................216
Musculoskeletal Fractures........................................................................................216
Fracture Healing.........................................................................................................220
General Principles of Fracture Management......................................................... 222
Treatment of Open Fractures...................................................................................227
 Complications of Fractures.......................................................................................227
Amputations................................................................................................................232
Bone Tumors.............................................................................................................. 236
CHAPTER ELEVEN-NEUROSURGERY................................................................... 244
Traumatic Brain Injury (TBI)..................................................................................... 244
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CHAPTER ONE-GENERAL SURGERY

Wound Healing
Understanding the process of wound healing is of paramount importance in
surgery because surgery is a trauma by definition and it causes wound. This
wound has to heal somehow; otherwise it will cause damage to the body. Studying
about wound healing will guide us how to manage post-operative patients. “… the
injury alone has in all cases a tendency to produce the disposition and means of a
cure.” John Hunter (1728-1793).

A wound can heal in one of the following ways

 Wound repair: the effort of injured tissues to restore their structure and
function after injury. Accuracy of healing is sacrificed for the speed of
repair. This is the common way wounds heal
 Regeneration: perfect restoration of the preexisting tissue architecture in
the absence of scar formation. This is found in;
o Embryonic development
o Lower animals
o Some tissues such as bone and liver.
Wound closure types;
 First intention/primary closure: wounds are sealed immediately with
simple suturing, skin graft, or flap; as in surgical wounds.
 Second intention/spontaneous closure: involves no active intent to seal
the wound. Associated with highly contaminated wound and will close by
re-epithelialization, which results in contraction of the wound.
 Tertiary intention/delayed primary closure: combination of the first two.
Consists of placement of sutures, allowing the wound to stay open for a
few days, and then closure of the wounds.

Phases of wound healing

Wound healing is a complex cellular and biochemical cascade that leads to
restitution of integrity and function. Although individual tissues may have unique
healing characteristics, all tissues heal by similar mechanisms.
There are three overlapping phases of wound healing;
 Hemostasis and inflammation
 Proliferation and matrix synthesis
 Maturation and remodeling

Hemostasis and inflammation (reactive phase)

 This stage can extend up to the 6th day.
 Wounding by definition disrupts tissue integrity and results in division of
blood vessels and direct exposure of ECM to platelets. This results in
platelet aggregation, degranulation, and activation of the coagulation
cascade.

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 After the hemostasis, inflammation sets in with cellular infiltration. Based

on the sequence of infiltration the cells include PMNs, macrophages, and
T-lymphocytes.
o PMNs: phagocytosis of bacteria and debris. They are also a
major source of cytokines.
o Macrophages: activation and recruitment of other cells via
mediators. Phagocytosis, regulating angiogenesis, matrix
deposition and remodeling are also functions of macrophages.
o T-lymphocytes: they truly bridge the transition from inflammatory
to proliferative phase. The mechanism is not fully understood.
Depletion of CD8+ T-lymphocytes enhances healing though.

Proliferation (regenerative or reparative phase)

 Roughly spans days 4 through 12. This stage involves;
o Matrix synthesis by fibroblasts,
o Neovascularization by endothelial cells, and
o Re-epithelialization by adjacent basal epithelial cells.
 This stage is characterized by the formation of granulation tissue, which
consists of a capillary bed, fibroblasts, macrophages, and a loose
arrangement of collagen, fibronectin, and hyaluronic acid.
 Tissue continuity is re-established at this stage.
 Fibroblasts, up on release of cytokines and growth factors (especially
PDGF) from macrophages, enter the wound environment and proliferate,
and then become activated. Then they synthesize the matrix (ECM).
o Fibrous proteins: collagen (type I & III), elastin, fibronectin, and
laminin.
o Proteoglycan synthesis: glycosaminoglycans (dermatan and
chondrotin sulfate*, hyaluronan, heparin sulfate, keratin sulfate)
plus proteins. Glycosaminoglycans are rarely found free.
 The deposition of matrix at the wound site follows a characteristic pattern
o Early matrix scaffolding: fibronectin and collagen type III.
o Then glycosaminoglycans and proteoglycans.
o Final matrix: collagen type I.
 Endothelial cells also proliferate and participate in the formation of new
capillaries (angiogenesis). They migrate from intact venules close to the
wound.
 Re-epithelialization
o While tissue integrity and strength are being re-established, the
external barrier must also be restored.
o Characterized by proliferation and migration of basal epithelial
cells adjacent to the wound.
o It is seen as thickening of the epidermis at the wound edge.
o Complete with in <48 hours in approximated incised wound, but
may take longer in large wound with significant defect.

Maturation and remodeling

 It begins during the fibroplastic phase.

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 Characterized by reorganization of previously synthesized collagen.

Collagen is brocken down by matrix metalloproteinases (MMPs), and the
net wound collagen is the result of the balance between collagenolysis
and collagen synthesis.
 Wound strength and integrity are determined by both the quantity and
quality of the newly deposited collagen.
 Fibrillin, a glycoprotein found in elastin, secreted by fibroblasts, is
essential for the formation of elastic fibers found in connective tissue.
 After several weeks, the amount of collagen reaches a plateau, but the
tensile strength continues to increase for several more months.
 Wound contraction
o All wounds undergo some degree of contraction.
o For wounds that do not have surgically approximated edges, the
area of the wound will be decreased by this action (healing by
secondary intention).
o The myofibroblasts are primarily responsible for wound
contraction.

Classification of wounds
Wounds are classified as either acute or chronic. Acute wounds heal in a
predictable manner and time frame; either by first, second or tertiary intention.
Chronic wounds
 Wounds that have failed to progress through the phases of wound healing
or that have proceeded through the repair process without producing
adequate anatomic and functional result.
 Wounds that have not healed in 3 months.
 Malignant transformation can occur in these wounds (Marjolin’s ulcer).
 Risk factors: steroids, immunosuppressants, chemotherapy, radiotherapy,
malnutrition, morbid obesity, wound dehiscence, and HIV/AIDS.

Excess healing
 Skin (hypertrophic scars, keloids, mutilating or debilitating scars, burn
contractions), tendons (frozen repairs), GI (strictures, stenoses), solid
organs (cirrhosis, pulmonary fibrosis), or the peritoneal cavity (adhesive
disease).

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Fig: The cellular, mechanical and biochemical phases of wound healing

Factors affecting wound healing

Systemic factors Local factors
 Age  Mechanical injury
 Nutrition (calorie, arginine, Zn,  Infection
iron, Vitamin C & A)  Edema
 Trauma  Ischemia/necrotic tissue
 Metabolic disease (DM,  Topical agents
uremia, obesity)  Ionizing radiation
 Immunosuppression  Low oxygen tension, anemia
 Connective tissue disorders  Foreign bodies
 Smoking
Healing in specific tissues
Tissues Peculiar features of healing
GI tract Mesothelial (serosal) and mucosal healing can occur without scarring.
Must be tension free, have adequate blood supply, receive adequate
nutrition, and be sepsis free.
Bone Hematoma formation, soft callus stage, hard callus stage, and remodeling.
The integrity and strength is fully re-established (100%).

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Liver Liver has a perfect restoration of preexisting tissue, like bones.

Cartilage Superficial injury: no inflammation, slow to heal, incomplete regeneration
Deep injury: structural and functional integrity is restored due to exposure
of vascular channels of surrounding damaged tissue. N.B. cartilage is
avascular.
Nerve Survival of axonal cell bodies, regeneration of axons that grow across the
transected nerve to reach the distal stump, and migration and connection
of regenerating nerve ends

Classification of wounds
Based on type of wound Based on wound thickness Based on time elapsed
 Incision  Superficial  Acute; up to 8 hrs
 Laceration  Partial thickness  Chronic; after 8 hrs
 Bruising Surgical wounds
 Full thickness
 Contusion  Clean
 Deep wounds
 Hematoma  Clean contaminated
 Complicated wounds
 Puncture  Contaminated
 Penetrating wounds
 Abrasion  Dirty
Based on involvement of
 Crush structures
 Bone fracture  Simple
 Combined
Treatment of wounds
Wounds can be managed by one or more of the following methods.
 Local care
 Antibiotics
 Dressing
 Skin replacement

Fig: Algorithm for management of acute wounds

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Heritable diseases of connective tissue: Five major types

 Ehlers-Danlos syndrome
 Marfan’s syndrome
 Osteogenesis imperfect
 Epidermolysis bullosa
 Acrodermatitis enteropathica

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Perioperative Care
The preoperative care
 Take a detailed history and do a full physical examination.
 Send appropriate investigations.
 Confirm the diagnosis and the need for surgery.
 Specific medical problems should be corrected to the best possible level.
These conditions include hypertension, cardiac diseases, anemia,
bleeding diatheses, diabetes, asthma, renal disease, and all others.
o Antihypertensive drugs
o Iron or vitamin supplementation or blood transfusion
o Thromboprophylaxis
o Glycemic control
 Risk stratification. The American Society of Anesthesiologists (ASA)
scoring system is the most widely used (see the table below).
 Take a voluntary and informed consent.
 Arrange theatre list.
Grade Description 30 day MR
I Healthy 0.1%
II Mild systemic disease, no functional limitation 0.7%
III Severe systemic disease, definite functional limitation 3.5%
IV Severe systemic disease, constant threat to life 18.3%
V Moribund patient unlikely to survive 24 hrs with or 93.3%
without surgery
E Emergency operation -

Intraoperative care
 The surgeon and the anesthetist are the most important personnel in the
operating theatre.
 Anesthesia;
o General anesthesia causes unconsciousness (and amnesia),
analgesia, and muscle relaxation. Commonly used IV anesthetics
include propofol, thiopentane, etomidate, and ketamin. Isoflurane,
sevoflurane, desflurane, and nitrous oxide are inhaled
anesthetics.
o Local anesthesia: lignocaine, bupivacaine, prilocaine, ropivacaine,
levobupivacaine.
o Commonly used muscle relaxants include suxamethonium,
vencuronium, atacurium, and rocuronium.
Local anesthetic agents
Ester group Amide group
Ester of benzoic acid Ester of paramino-
benzoic acid
Cocaine Procaine Bupivacaine
Butacaine Chloroprocaine Lidocaine
Tetracaine Propoxycaine Prilocaine
Benzocaine Articaine

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Mepivacaine
o Airway management is the role of anesthetist; intubation.
o Mallampati score is used to predict the ease of intubation.
o Class I: soft palate, fauces, uvula, pillars
o Class II: soft palate, fauses, portion of uvula
o Class III: soft palate base of uvula
o Class IV: hard palate only.

Fig: The Mallampati classification

 Common local anesthesia techniques;
o Topical: skin of venepucture in children, nasal surgery for
anesthesia and vasoconstriction, awake fibroptic intubation.
o Nerve block: shoulder surgery, upper limb surgery, lower limb
surgery, dental surgery.
o Transverses abdominis plane block: abdominal surgery (new)
o IV regional anesthesia (Bier’s block): short surgery particularly for
upper limb (e.g., carpal tunnel release)
o Spinal anesthesia alone and in combination with GA or sedation
is used extensively for lower limb, obstetric and pelvic surgery.
o Epidural anesthesia: excellent anesthesia for upper abdominal
and thoracicsurgeries.

Potoperative care
 Nutrition and fluid therapy.
 Wound care.
 Postoperative complications (see below)
 Ambulation
 Following with vital signs.
 The patient could be handed over to the ward when they fulfill the
following criteria;
o Patient is fully conscious
o Respiration and oxygenation are satisfactory
o Patient is normothermic, not in pain, not nauseous
o Cardiovascular parameters are stable
o Oxygen, fluids, and analgesics have been prescribed
o There is no concern related to the surgical procedure

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Post-operative Complications
There are three common approaches to post-operative complications;
1. Based on time after surgery:
a. Immediate: within 24 hours of operation
b. Early: within the first week of operation.
c. Late: after one week to one month.
2. General and surgery specific:
a. General post-op complications
 Bleeding
 Deep vein thrombosis
 Pulmonary embolus
 Fever
 Wound infection
 Wound dehiscence
 Pressure sores/bed sores
 Atelectasis and pneumonia
b. Surgery specific complications
 Abdominal: paralytic ileus, bowel obstruction, abdominal
compartment syndrome, GI bleeding, stomal complications,
anastomotic leak, C. deficile colitis, intestinal fistula,
pancreatic fistula.
 Hepatobiliary: bile duct injury, leak
 Orthopedic: compartment syndrome
 Neck: respiratory obstruction, RLN injury
 Thoracic: fluid overload, bronchopleural fistula, hemothorax,
pleural effusion.
 Cardiac: hypertension, ischemia and infarction, cardiogenic
shock, arrhythmia, heart failure
 Neurosurgery: raised ICP, seizures, weakness, delirium,
cognitive disorders, psychosis, strokes, and TIAs.
 Vascular: loss of patency
 Plastic: non-viability of flaps
 Urology: urinary retention, acute renal failure,
3. Clavian-Dindo: objective measurement of the impact of the surgical
complication on the outcome of the procedure.
Post-operative complications
Organ Complications
system Immediate Early and late
Respiratory Upper airway obstruction, Fever (due to microatelectasis), cough
reduced or impaired ventilation, dyspnea, bronchospasm, hypercapnea,
hypoxemia, vocal cord palsy, atelectasis, pneumonia, pleural effusion,
neck hematomas, bleeding pneumothorax, and respiratory failure
Cardio- Hypotension, hypertension, Myocardial infarction, heart failure,
vascular myocardial ischemia, arrhythmias, stroke
arrhythmias, stoke
Renal and Acute kidney injury, urinary retention, UTIs
urinary

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CNS Post-op delirium, strokes, seizure

Post-operative hemorrhage
 It is most common in the immediate post-op period.
 Management
o Stop the bleeding
o Supportive: oxygen and fluid resuscitation. It may require
correction of coagulopathy.
o Blood transfusion carries risks (acute hemolytic transfusion
reaction, sensitization, fluid overload, hyperkalaemia, transfusion-
related lung injury and transmission of blood-borne infection).

Post-operative fever
 In 40% of patients after major surgery; Post-op fever by post-op day
in most cases the cause is not found. Immediate: drug reaction
 The inflammatory response to surgical Day 1: Atelectasis
trauma may manifest itself as fever, Day 2: Pneumonia
Day 3: UTI
and so pyrexia does not necessarily Day 5: DVT
imply sepsis. Day 7: Wound infection
 There are two major classifications of Day 10: Abscess
etiologies;
o Infectious causes: pneumonia, abscess, bacteremia, empyema,
oteomyelitis, foreign body retention, IV-line associated sepsis.
o Non-infectious causes: atelectasis, dehydration, pulmonary
emboli, drug reaction, allergic reaction, adrenal insufficiency,
pheochromocytoma.

Wound dehiscence
 Disruption of any or all of the Risk factors for wound dehiscence
layers in a wound. It may occur General Local
up to 3% of wounds. Malnourishment Inadequate or poor
Dehiscence, most commonly, Diabetes wound closure
occurs from 5-8th post-op day Obesity Poor local wound
when the strength of the wound Renal failure healing e.g. due to
Jaundice infection, hematoma,
is at its weakest.
Sepsis or seroma.
 The risk factors for dehiscence Cancer Increased intra-
are listed in the table. Steroids abdominal pressure,
 Treatment e.g. COPD, cough
o Most patients require
reoperation
o In some patients it is apt to leave the wound open and treat the
wound with vacuum assisted closure (VAC) pumps or controlling
infection. Infection makes wound healing to stay at the phase of
inflammation and not progress.

Pressure/Bed sores

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 Prolonged surgery or bed rest Grades of bed sores

after surgery predisposes to Grade Description
the development of bed sores. I Intact skin with non-bleachable
Careful positioning and redness. Difficult to detect in dark
padding of the patient skin.
intraoperatively, reduces the II Partial thickness loss of dermis;
risk. ulcer or blister.
 The pressure points include III Full thickness tissue loss, without
visible bone, tendon or muscle.
sacrum, greater trochanter,
IV Full thickness tissue loss with
heels, and scapula. exposed bone, tendon, or muscle.
 Risk factors: poor nutrition,
dehydration, immobility, and nerve block anesthesias.
 Early mobilization prevents bed sores.

Wound infection
 Accounts for 40% of hospital acquired infections in surgical patients.
Occurs in 5-10% of surgical patients.
 Most commonly occur 5-6 days post-operatively. 80-90% occurs within 30
days after operation.
 Surgical wound is considered infected if it meets the following criteria;
1. Gross pus draining from the wound
2. Spontaneously opens and drains pus
3. Fluid that is culture positive or Gram stain positive for bacteria
4. Diagnosis by surgeon.
 Wounds are generally classified in to three based on their depth;
1. Superficial: including skin and subcutaneous tissue.
2. Deep: including fascia and muscle.
3. Organ space: including internal organs.
 Criteria to diagnose wound infection (CDC);
CDC criteria for diagnosis of wound infection
Superficial Deep Organ space
Infection <30 days <30 day after surgery with <30 days after surgery with
after surgery; & no implant or soft tissue no implant; or
Involves skin and involvement; or < 1 year after surgery with
ST only, plus one of < 1year after surgery with implant and infection;
the following implant; involves soft deep involves any part of
1. Purulent tissues (fascia and operation site, plus one of
discharge muscles); plus one of the the following
2. Diagnosis by following 1.Purulent discharge
surgeon 1. Purulent discharge 2.Culture of aspirate
3. Erythema, pain, 2. Abscess on radiology 3.Abscess on radiology
and edema 3. Diagnosis by surgeon 4.Diagnosis by surgeon
4. Fever, pain, tender,
dehiscence.
 Etiologies (bacteria)
o S. aureus and CoNS are the most common.
o GI: Enterobacter spp and E. coli. In most studies, group D
Enterococcus continues to be a common pathogen.
 Surgical wound classification based on infection rate;

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o Clean: 1-3%
o Clean contaminated: 5-8%
o Contaminated: 20-25%
o Dirty: 30-40%
 Risk factors for wound infection
Patient factors Local factors Microbial factors
Older age Open surgery (vs. lap) Prolonged
Immunosuppression Poor skin prep hospitalization
Obesity Contaminated Toxin secretion
Diabetes instruments Resistance
Chronic inflammation Inadequate prophylaxis
Malnutrition Prolonged procedure
Smoking Local tissue necrosis
Renal failure Blood transfusion
Anemia Hypoxia, hypothermia
Peripheral vascular disease

 Management of surgical wound infections

o Preventive measures
 Control patient factors
 Prophylactic antibiotics
 Surgeon’s personal hygiene
o Treatment of wound infection
 Debridement and irrigation with NS.
 IV antibiotics
 Some may require reoperation
Criteria for surgical wound classification
Clean Clean cont. Contaminated Dirty
No hollow viscus Hollow viscus entered Uncontrolled Untreated,
entered but controlled spillage from uncontrolled
Primary wound No inflammation viscus spillage from viscus
closure Primary wound closure Inflammation Pus in operative
No inflammation Minor break in aseptic Open, traumatic wound
No brakes in aseptic technique wound Open suppurative
technique Mechanical drains Major break in wound
Elective procedure used aseptic technique Severe
Bowel-prep inflammation
Hollow viscus: respiratory, alimentary, genital, and urinary tract

Examples of the types of surgical wounds;

 Clean: herniorrhaphy, excisional surgery, and brain, heart, joint, thyroid,
and transplant surgeries, incisions of blunt trauma.
 Clean contaminated: appendicectomy, bowel surgeries, gallbladder,
biliary, vaginal, oropharyngeal and pancreatic surgeries.
 Contaminated: acute abdominal conditions and open fresh accidental
wounds.
 Dirty: abscess drainage, pyocele, empyema gallbladder, old traumatic
wounds, and fecal peritonitis. The organisms causing postoperative
infection were present in the operative field before the operation.

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Causes of post-op paralytic ileus Causes of post-op GI bleeeding

Pancreatitis Peptic ulceration
Intra-abdominal infection Stress erosion
Retroperitoneal hemorrhage and Mallory-Weiss tear
inflammation Gastric varices
Electrolyte inbalance AV malformations
Lengthy surgical procedure From anastomosis
Medications (narcotics, psychotropic agents) Diverticulosis
Pneumonia
Inflamed viscera
Stomal complications Risk factors for anastomotic leak
Stoma: poor location, retraction, ischemic Technical: blood supply, tension, bowel
necrosis, detachment, abscess formation, prep, drains,
opening wrong end;; prolapse, stenosis, Location: pancreaticoenteric, colorectal,
parastomal hernia, fistula formation, gas. emergency
Peristomal skin: excoriation, dermatitis;; Local: septic environment, fluid collection,
parastomal varices, dermatoses, cancer. smoking, steroid
Systemic: high output, bowel obstruction, Bowel related: radiotherapy, compromised
non-closure distal lumen, Crohn’s disease, Vit C, iron,
cyteine, and zinc deficiency.

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Fluid and Electrolyte Management

Fluid and electrolyte management is paramount to the care of the surgical patient.
Changes in both fluid and electrolyte composition occur preoperatively,
intraoperatively, and postoperatively, as well as in response to trauma and sepsis.

Body fluids
Total body water (TBW)
 50-60% of total body weight.
 Total body weight and TBW is constant for an individual.
 Lean tissues such as muscle and solid organs have higher water content
than fat and bone. Obese individuals have lower total body water
percentage than malnourished individuals.
 Total body water in specific populations;
o Average young adult male = 60%
o Average young adult female = 50%
o Newborns = 80%
o At one year = 65%
 Total body water is divided in to three functional fluid compartments;
o Extracellular fluid (one-third of TBW); 20% of total body weight
 Plasma (intravascular fluid); 5% of total body weight
 Interstitial (extravascular) fluid; 15% of total body weight
o Intracellular fluid (two-thirds of TBW); 40% of total body weight
Composition of fluid compartments
 Extracellular fluid;
o Sodium is the principal cation
o Chloride and bicarbonate are the principal anions
o The plasma has slightly higher protein content than interstitial
fluid, which results in higher plasma cation composition.
 Intracellular fluid;
o Potassium and magnesium are principal catioins
o Phosphate, sulfate, and proteins are principal anions
 Water is evenly distributed throughout all compartments, so that a given
volume of water increases the volume of any one compartment a little.
 Sodium, however, is confined to ECF, and because of its osmotic and
electrical properties, it remains associated with water.
 Therefore, sodium-containing fluids are distributed throughout ECF. But
these fluids expand the interstitial space by approximately three times as
much as the plasma. (the ICF:plasma/IVF ratio is 3:1)
Osmotic pressure
 The physiologic activity of electrolytes in solution depends on;
o Number of particles per unit volume (mmol/L),

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o Number of electric charges per unit volume (mEq/L), &

o Number of osmotically active ions per unit voume (mOsm/L).
Equivalent = atomic weight (g)/valence

 The movement of water across a cell membrane primarily depends on

osmosis.
 The principal determinants of osmolality are the concentrations of sodium,
glucose, and urea (BUN).
Calculated serum osmolality = 2 sodium + (glucose/18) + (BUN/2.8)
 The osmolality of intra- and extra-cellular fluids is maintained between
290 and 310 mOsm in each compartment.
 Any change in osmotic pressure in one compartment is accompanied by a
redistribution of water until the effective osmotic pressure between
compartments is equal.
 An isotonic change in volume in either one of the compartments is not
accompanied by the net movement of water as long as the ionic
concentration remains the same.
 For practical clinical purposes, most significant gains and losses of body
fluid are directly from the extracellular compartment.

Body fluid changes

Normal exchange of fluids
 Average daily intake = 2000mL
o 75% = oral intake
o 25% = derived from solid foods
 Daily water losses;
o Sensible losses
 Urine = 800-1200mL
 Stool = 250mL
 Sweat = 0
o Insensible losses = 600mL
 Skin = 75%
 Lungs = 25%
 To clear the products of metabolism, the kidneys must excrete a minimum
of 500-800mL of urine per day, regardless of the amount of oral intake.

Composition of body fluids

Secretion Electrolyte (mEq/L)
Na+ K+ Cl- … H+ Rate (mL/day)
Salivary 50 20 40 30 - 100-1000
Basal gastric 100 10 140 - 30 1000
Stimulated gastric 30 10 140 - 100 4200

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Bile 140 5 100 - - 500-1000

Pancreatic 140 5 75 - - 1000
Duodenum 140 5 80 - - 100-2000
Ileum 140 5 70 - - 100-2000
Colon 60 70 15 - - -

Normal exchange of compositions

 The typical individual consumes 3-5 g of dietary salt per day, with the
balance maintained by the kidney.
 With hyponatremia, sodum excretion can be reduced to as little as
1mEq/d and with hypovolemia, sodium excretion can be maximized as
much as 5000mEq/d.
 Sweat is hypotonic; results in only small sodium loss.
 GI losses are isotonic to slightly hypotonic and are appropriately replaced
by isotonic fluids.
Classification of body fluid changes
 Disturbances in volume
 Disturbances in concentration
 Disturbances in composition

Unlike with sodium, the concentration of most other ions in the ECF can be altered
without significant change in the total number of osmotically active particles,
producing only a compositional change. For instance, doubling the serum
potassium concentration will profoundly alter myocardial function without
significantly altering volume or concentration of the fluid spaces.

Most important serum electrolytes

Serum concentration Daily intake Excretion
Na+ 135-145mmol/dL 3-5g of NaCl Urine, stool, sweat
K+ 3.5-5mmol/L 50-100mmol Urine (90%), stool
Ca+ 8.5-10.5mg/dL 500-1000mg Urine, stool
P 2.5-4.5mg/dL 800-1000mg Urine
Mg++ 1.3-2.2mg/dL Urine

Disturbance in fluid volume

 Extracellular volume deficit
o The most common fluid disorder in surgical patients and can be
acute or chronic.
o Acute: associated with CVS & CNS signs.
o Chronic: display tissue signs such as decrease in skin turgor, and
sunken eyes, in addition to CVS & CNS signs.
o Laboratory examinations;
 Elevated BUN

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 Urine osmolality is higher than serum

 Low urine sodium, typically <20mEq/L, serum sodium
does not necessarily reflect volume status and therefore
not used as a measurement of fluid deficit.
o Causes of volume deficit [in surgical patients]
 GI losses are the most common; from NGT suction,
vomiting, diarrhea, or enterocutaneous fistula.
 Secondary sequestration can also lead to massive
volume deficits: soft tissue injuries, burns, intra-
abdominal processes such as peritonitis, obstruction, or
prolonged surgery.
 Extracellular volume excess
o May be iatrogenic or secondary to renal dysfunction, congestive
heart failure, or cirrhosis.
o Both plasma and interstitial volumes usually are increased.
o Symptoms are primarily pulmonary and cardiovascular.
Signs and symptoms of volume disturbances
System Volume deficit Volume excess
Generalized Weight loss Weight gain
Decreased skin turgor Peripheral edema
Cardiac Tachycardia Increased cardiac output
Orthostasis/hypotension Increased central venous pressure
Collapsed neck veins Distended neck veins
Murmur
Renal Oliguria -
Azotemia
GI Ileus Bowel edema
Pulmonary - Pulmonary edema

 Volume control
o Osmoreceptors
 Detect changes in fluid osmolality and drive changes in
thirst and dieresis.
 Hypothalamus is also stimulated to secrete vasopressin,
which increases water reabsorption in the kidneys.
o Baroreceptors
 Modulate volume in response to changes in pressure
and circulating volume through specialized sensors
located in the aortic arch and carotid sinuses.
 Baroreceptor responses are:
 Neuronal: sympathetic and parasympathetic
 Hormonal: rennin-angiotensin, aldosterone,
ANP, and renal prostaglandins.

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Disturbance in concentration
 Changes in serum sodium concentration are inversely proportional to
TBW. Therefore, abnormalities in TBW are reflected by abnormalities in
serum sodium levels.
 Hyponatremia
o Extracellular volume can be low, normal, or high. In most cases
hyponatremia is due to sodium depletion or dilution.
o Dilutional (hypervolemic) hyponatremia results from excessive
ECF;
 Excess oral water intake
 Excess IV water administration (iatrogenic)
 Increased ADH secretion in post-op patients
 Drug induced: antipsychotics, TCAs, and ACEIs.
 Physical signs of volume overload are absent.
 Laboratory evaluation reveals hemodilution
o Depletional hyponatremia
 Decreased intake of sodium
 Low sodium diets
 Entral feeds, which are typically low in sodium
 Increased loss of sodium containing fluids
 GI losses
 Renal losses
 A concomitant ECF fluid deficit is common.
o Hyperosmolar causes
 Hyperglycemia
 Mannitol administration
 For every 100-mg/dL increment in plasma glucose above
normal, the plasma sodium should decrease by 1.6
mEq/L.
o Pseudohyponatremia
 Extreme elevation in plasma lipids and proteins can
cause pseudohyponatremia, because there is no true
decrease in extracellular sodium relative to water.
o Normovolemic hyponatremia: SIADH
 Hypernatremia
o Results either from loss of free water or gain of sodium in excess
of water.
o Hypervolemic hypernatremia
 Iatrogenic administration of sodium containing fluids
 Mineralocorticoid excess: hyperaldosteronism,
Cushing’s syndrome, congenital adrenal hyperplasia.
 Urine sodium >20mEq/L and osmolarity >300mOsm/L

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o Normovolemic hypernatremia
 Renal causes: diabetes insupidus, diuretics, renal
diseases.
 Non-renal causes: GI loss, skin loss.
o Hypovolemic hypernatremia
 The same conditions that cause normovolemic
hypernatremia can cause hypovolemic hypernatremia.
 Urine sodim is <20mEq/L and urine osmolarity is <300
o Symptomatic hypernatremia usually occurs only in patients with
impaired thirst or restricted access to fluid.
o Symptoms are rare until the serum sodium concentration
exceeds 160mEq/L but, once present, are associated with
significant morbidity and mortality.
Clinical manifestations of abnormalities in serum sodium
Body system Hyponatremia Hypernatremia
CNS Headache, confusion, Restlessness, lethargy, ataxia,
hyperactive or hypoactive deep irritability, tonic spasms, delirium,
tendon reflexes, seizures, coma, seizures, coma
increased ICP.
Musculoskeletal Weakness, fatigue, muscle Weakness
cramps/twitching
GI Anorexia, nausea, vomiting, -
watery diarrhea
CVS Hypertension and bradycardia if Tachycardia, hypotension, syncope
ICP increases significantly
Tissue Lacrimation, salivation Dry sticky mucus membranes, red
swollen tongue, decreased saliva
and tears
Renal Oliguria Oliguria
Metabolic - Fever

Disturbances in composition
 Hyperkalemia
 Hypokalemia
 Hypercalcemia
 Hypocalcemia
 Hyper and hypo- magnesemia
 Hyper and hypo phosphatemia

Fluid therapy
There are two components to fluid therapy
1. Maintenance therapy
2. Replacement therapy
a. Deficit replacement
b. Ongoing fluid loss replacement

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Fluid therapy can be administered via parentral or entral routes.

Types of IV fluids
 There are two types of IV fluids; crystalloids and colloids.
 Crystalloids;
o Solutions of electrolytes and water.
o Decreases colloid osmotic pressure.
o Increases both intravascular and interstitial ECF volumes.
o The most widely used fluids, with low cost and outstanding safety
profiles.
 Colloids
o High molecular weight molecules.
o They preserve high colloid osmotic pressure in the blood.
o Preferentially increase the intravascular volume.
o Its use is limited due to their price, doubtful effectiveness, and
potential complications.
Types of IV fluids
Isotonic Hypotonic Hypertonic
Crystalloids Normal saline (0.9% 0.45% NaCl 3.5% NaCl
NaCl) Distilled water 5% NaCl
Ringered lactate D5W (5% 7.5% NaCl
Hartmann’s solution glucose/dextrose)
Colloids Dextrans
Albumin
Hetastarch
Gelatins
Blood products

Maintenance fluid therapy

Maintenance fluid therapy is usually undertaken when the patient is not expected
to be able to eat or drink for a prolonged period of time (e.g. perioperatively, on
ventilation). Maintenance therapy replaces the ongoing losses of water and
electrolytes under normal physiologic conditions via urine, sweat, respiration, and
stool.
Serum sodium concentration provides the best estimate of water balance in
relation to solute;
 A normal serum sodium concentration implies that the patient is in water
balance in relation to sodium but does not provide any information on
volume status.
Increased water intake is required if the patient has fever, sweating, burns,
tachypnea, surgical drains, polyuria, or ongoing significant gastrointestinal losses.
Decreased water intake is required in a number of clinical settings, including
oliguric renal failure, the use of humidified air, edematous states, and
hypothyroidism.

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Maintenance fluid needs

 Maintenance needs on hourly basis;
o 4mL/kg/hr for the first 10kg
o 2mL/kg/hr for the next 10kg and
o 1mL/kg/hr for the rest of the body weight
 Maintenance needs on daily basis;
o 100mL/kg for the first 10kg
o 50mL/kg for the next 10kg and
o 20mL/kg for the rest of the body weight
 At body weights >65 kg, water requirements do not show the same
incremental increase as with lower weights. As a result, for individuals
with a body weight >65 kg, total maintenance water needs are generally
capped at 2.5 liters daily.
Factors affecting maintenance water needs
Source Increased needs Decreased needs
Skin Burns Enclosed incubator
Fever Mist tent
Phototherapy
Prematurity
Radiant heater
Sweat
Lungs Tachypnea Humidified air
Tracheostomy
GIT Diarrhea
Emesis
Ileostomy
NGT
Renal Polyuria Oliguria/anuria
Miscellaneous Surgical drain Hypothyroidism
Increased activity

Replacement fluid therapy (Resuscitation)

The goal of replacement therapy is to correct existing abnormalities in volume
status and/or serum electrolytes. Replacement returns the patient to a normal
volume and electrolyte status.

There is no formula that can be used to accurately estimate the total fluid deficit. If
pre- and post-deficit body weight is known, then weight loss provides a reasonable
estimate of fluid losses.

Rate of replacement;
 Severe volume depletion or hypovolemic shock: at least 1 to 2 liters of
isotonic saline are generally given as rapidly as possible in an attempt to

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restore tissue perfusion, Fluid replacement is continued at a rapid rate

until the clinical signs of hypovolemia improve.
 Mild to moderate hypovolemia: rapid fluid resuscitation is not necessary
in these patients. To avoid worsening of the volume deficit, the rate of
fluid administration must be greater than the rate of continued fluid losses
which equals urine output & insensible & other fluid losses.
Choice of replacement fluid;
 Largely dependent on:
o The type of fluid lost
o Concurrent electrolyte disorders
 For most patients: isotonic or one-half isotonic saline.
 For patients with hypovolumic shock;
o Crystalloids, usually saline solutions, are preferred over colloid-
containing solutions for the management of patients with severe
volume depletion not due to bleeding.
o Blood products or substitutes for bleeding patients.
 For patients with hypernatremia;
o Should generally be corrected slowly for patients with chronic
hypernatremia (>48hrs).
 D5W IV at 70mL/hr in a 50kg patient and 100mL/hour in
a 70kg patient.
 The goal is to lower the serum sodium by a maximum of
10mEq/L in a 24-hour period.
o Acute hypernatremia (within 48 hrs) can and should be corrected
rapidly. Note that nearly all patients with hypernatremia have the
chronic form; acute hypernatremia is uncommon.
 D5W IV at 3-6mL/kg/hr. Once the serum sodium
concentration has reached 145 mEq/L, the rate of
infusion is reduced to 1 mL/kg/hr and continued until
normonatremia (140 mEq/L) is restored.
 The goal of this regimen is to lower the serum sodium by
1-2 mEq/L/hr and to restore normonatremia in less than
24 hours.
Body responses to hypernatremia
The initial response to hypernatremia is osmotic water movement out of
brain cells and other cells.

Within two to three days, brain volume is largely restored due both to salt
and water movement from the cerebrospinal fluid into the brain. At this
time, neurologic symptoms are less likely and improvement is seen if
there were symptoms due to the acute hypernatremia.

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Rapid lowering of the plasma sodium concentration once the cerebral

adaptation has occurred causes additional osmotic water movement into
brain cells, resulting in cerebral edema that can lead to an
encephalopathy characterized by seizures and rarely permanent damage
or death.

 For patients with hyponatremia;

o Overly rapid correction is also potentially harmful if there has
been adaptation to the electrolyte disturbance (> 48hrs).
o Isotonic or hypertonic saline should be used in hyponatremia.

Replacement of ongoing fluid losses

 Once volume deficits have been replaced and maintenance fluids have
been calculated and given, the overall fluid balance of the patient can be
maintained by replacement of fluid losses beyond those considered to be
maintenance.
 Ongoing losses from nasogastric tubes, stomas, fistulas, and other
measurable sources are recorded during the course of care and can be
replaced in fairly straightforward fashion.

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Shock
Introduction
What is shock?
 Shock is a life-threatening condition of circulatory failure manifested as
hypotension.
 Shock is a state of cellular and tissue hyoxia due to reduced oxygen
delivery and/or increased oxygen consumption or inadequate utilization.
 Shock is the most common and therefore the most important cause of
death in surgical patients.
Classification of shock
 Distributive shock
o Septic shock
o Neurogenic shock: TBI, spinal cord injury
o Anaphylactic shock: IgE mediated, non-IgE mediated, non-
immunologic, idiopsthic
o Inflammatory shock (SIRS): burn, trauma, pancreatitis, fat
embolism, viscus perforation
 Non-distributive shock
o Hypovolemic shock
 Hemorrhagic: traumatic, surgical or non-traumatic
 Non-hemorrhagic:
 GI losses (vomiting, diarrhea, external drains)
 Skin losses (heat stroke, burns, dermatologic
conditions- Stevens-Johnson syndrome)
 Renal losses (drug induced or osmotic dieresis,
salt wasting nephropathies, hypoaldosteronism)
 Third space losses (postop, trauma, intestinal
obstruction, crush injury, pancreatits, cirrhosis)
o Cardiogenic shock: cardiomyopathic, arrhytmogenic, mechanical
(valvular diseases)
o Obstructive shock: pulmonary embolism, pulmonary hypertension,
tension pneumothorax, pericardial tamponade, constrictive
pericarditis, restrictive cardiomyopathy

Pathogenesis of shock
The following events occur sequentially
 Reduced tissue oxygenation/perfusion or increased utilization
 Cellular hypoxia
 Cell membrane ion pump failure

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 Intracellular edema, leakage of intracellular contents in to the extracellular

space, and inadequate regulation of intracellular pH.
 Acidosis and endothelial dysfunction
 Serum lactate levels are elevated >1.5mmol/L
Common to most forms of shock is diminished CO and/or SVR.
The core pathophysiologies of the two types of shock are;
 Non-distributive: decreased blood volume and/or cardiac output
 Distributive: decreased peripheral vascular resistance (TRP)

Pathophysiology of shock
Cellular Switch to anaerobic metabolism – lactic acidosis
Microvascular Injury to capillary endothelium due to activation of immune and
coagulation systems
Cardiovascular Decrease in preload and after load results in reflex tachycardia
and systemic vasoconstriction (except distributive shock)
Respiratory Metabolic acidosis causes increased RR
Renal Reduced GFR and urine output
Endocrine Activation of RAAS, release of cortisol

Comparison
Hypovolemic Cardiogenic Obstructive Distributive
Cardiac output Decreased Decreased Decreased Increased
TPR Increased Increased Increased Decreased
Venous Decreased Increased Increased Decreased
pressure
Mixed venous Decreased Decreased Decreased Increased
saturation
Base deficit Increased Increased Increased Increased

Stages of shock
 Non-progressive (compensated) stage – cryptic shock or pre-shock
o Compensatory responses maintain tissue perfusion
 Compensatory tachycardia and tachypnea
 Peripheral vasoconstriction
 Progressive (decompensated) stage – shock
o Compensatory mechanisms become overwhelmed, and signs
and symptoms of shock appear;
 Symptomatic tachycardia, dyspnea, diaphoresis,
metabolic acidosis, hypotension, oliguria, delayed
capillary refill and cool dry skin.
o Reverted to normal by resuscitation
 Irreversible stage – end-organ dysfunction
o Anuria and acute renal failure develop
o Acidemia further depresses CO

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o Hypotension becomes severe and recalcitrant to therapy

o Hyperlactatemia often worsens
o Restlessness evolves into obtundation and coma
o Death is common in this phase of shock.
 Exceptions: in distributive shock;
o Warm and moist skin
o Pink skin
o Pounding pulse?
Compensatory mechanisms
Neuronal: baroreceptors, Increased heart rate
chemoreceptors, nociceptors Increased serum glucose
Tachypnea
Hormonal: RAAS, cortisol, Aldosterone: increases sodium and
ADH water reabsorption
ADH: vasoconstriction and water
reabsorption
Circulatory Increased heart rate
Vasoconstriction
Regional arteriolar vasodilation

Signs and symptoms of advancing stages of hemorrhagic shock

Class I Class II Class III Class IV
Loss (mL) Up to 750 750-1500 1500-2000 >2000
Loss (%) Up to 15% 15-30% 30-40% >40%
PR <100 >100 >120 >140
BP Normal Normal Decreased Decreased
Pulse pressure Normal/increased Decreased Decreased Decreased
RR 14-20 >20-30 30-40 >35
UOP (mL/h) >30 >20-30 5-15 Negligible
Mental status Slightly anxious Mildly Anxious, Confused,
anxious confused lethargic
Stage one hypovolemic shock can be exemplified by voluntary blood
donation.

Clinical manifestations
 Hypotension
o Absolute: SBP <90mmHg, MAP <65mmHg
o Relative: drop in SBP >40mmHg
o Orthostatic: >20mmHg fall in SBP or >10mmHg fall in DBP with
standing.
o Profound: e.g. vasopressor dependent
 Tachycardia
 Tachypnea
 Oliguria: this may be due to;

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o Shunting of renal blood flow to other vital organs

o Direct trauma to the kidneys (e.g. aminoglycosides)
o Intravascular volume depletion
 Mental status change
o Poor perfusion or
o Metabolic abnormality
 Cool, clammy skin
o Compensatory peripheral vasoconstriction
o Ischemia from underlying PAD
 Warm hyperemic skin
o Early distributive shock (prior to compensatory vasoconstriction) or
o Terminal shock (failure of compensatory vasoconstriction)
 Metabolic acidosis
 Hyperlactatemia
 Specific types of shock
o Distributive: hypotension without clinical signs of reduced preload
(normal skin turgor, moist mucous membranes, normal IVC on
imaging) or fluid overload (no peripheral edema, or distended neck
veins, normal CVP-8-12mmHg and mixed venous oxyhemoglobulin
saturation->70%).
o Cardiogenic: hypotension in association with the clinical and
radiologic manifestations of;
 Pulmonary edema: diffuse lung crackles, distended neck
veins.
 Raised CVP: >12mmHg
 Low SvO2 (<70%)
 Large dilated ventricle(s) and poor left ventricle function,
valular or septal abnormalities on Echo.
o Hypovolemic: presence of reduced preload in the context of known or
suspected cause. Reduced skin turgor, dry mucous membranes, a
collapsible IVC, and low CVP-<8mmHg.
o Obstructive: hypotension associated with distended neck veins but
usually without the clinical signs of fluid overload or reduced preload.
The exceptions are patients with subacute cardiac tamponade who
often have evidence of fluid overload on examination.

Diagnosis of shock
 History and examination
 Laboratory tests
o Serum lactate
o Renal and liver function tests
o Cardiac enzymes and natriuretic peptides

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o Complete blood count and differential

o Coagulation studies and D-dimer level
o Blood gas analysis
 Imaging studies
o Chest radiography
 To detect common causes (e.g. pneumonia)
 Detect complications of shock (e.g. ARDS)
 Findings on CXR
 Hypovolemic shock: clear
 Obstructive shock: pneumothorax (clear if caused by
pulmonary embolism)
 Septic shock: pneumonia (heterogeneous opacities
with air bronchogram)
 Cardiogenic shock: pulmonary edema
 Aortic dissection: widened mediatinum
 Viscus perforation: air under right hemi-diaphragm.
o Abdominal radiography: intestinal obstruction, perforation
o CT scan of;
 Head (TBI, stroke),
 Spine (spinal injury),
 Chest (pneumonia, pneumothorax, ruptured aneurysm,
dissection),
 Abdomen & pelvis (intestinal obstruction, perforation,
abscess), and
 Pulmonary artery (pulmonary embolism)
o Ultrasound (FAST)
o Pulmonary arterial catheterization (PAC): cardiac output, systemic
vascular resistance, pulmonary artery occlusion pressure, right atrial
pressure, and mixed venous oxyhemoglobin saturation (SvO2)

Treatment of shock

Principles of treatment of shock

 Hemodynamic support and ABC’s
 Intervention for life-threatening conditions
 Reverse the etiology

Hemodynamic support
 IV fluids
o The amount of fluid depends on the type of shock

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 Obstructive shock from PE or cardiogenic shock from LV

infarction need 500-1000mL; while those with RV
infarction and sepsis nessd 3-5L of fluid.
 Those with hemorrhagic shock often need >3-5L (often
inclusive of blood products)
o
 If the initial IV fluid fails to restore physiology,
o Add more fluids in hypovolemic shock or
o Vassopressors in other types of shock
 Adrenergic agents: norepinephrine (initial dosing 8-
12mcg/min IV) is the most commonly used agent. Others
include phenylephrine 100-200mcg/min IV,
 Inotropic agents: dobutamine initial (dose 0.5-1mcg/min
IV) is the most commonly used inotropic agent.

Fig: Initial fluid therapy for hemorrhagic shock.

Damage control surgery;
 The minimum surgery required to allow safe transfer to a definitive facility.
 Secure the airway
 Control bleeding
 Prevent pressure build ups

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 Prevent infection
Common conditions needing lifesaving interventions
 Anaphylactic shock
o Hypotension, inspiratory stridor, oral and facial edema, hives,
history of recent exposure to common allergens.
o Interventions: IV adrenaline
 Tension pneumothorax
o Tachypnea, unilateral pleuritic chest pain and diminished breath
sounds, distended neck veins, tracheal deviation away from the
affected side, and risk factors for tension pneumothorax (eg,
trauma, recent procedure, mechanical ventilation, underlying
cystic lung disease).
o Interventions: needle decompression or emergent tube
thoracostomy.
 Pericardial tamponade
o Dyspnea, tachycardia, hypotension, elevated JVP, distant heart
sounds, pulsus paradoxus, and known risk factors (eg, trauma,
bleeding diathesis, known pericardial effusion, recent thoracic or
pericardial procedure).
o Interventions: pericardiocentesis and rarely emergency
thoracotomy.
 Hemodynamically significant hemorrhage
o Traumatic: FAST, drainage (peritoneal lavage, chest tube for
hemothorax), or surgical intervention (splenic rupture)
o Non-traumatic
 Ruptured abdominal aortic aneurysm: surgery
 Upper or lower GI hemorrhage: endoscopic intervention,
embolization, or surgery.
 Life threatening arrhythmias: cardioversion, atropine, vasoactive agents,
or pace-maker placement.
 Septic shock
o Fever, hypotention, and suspected source of infection
o Interventions: IV antibiotics and IV fluid resuscitation
 Myocardial infarction
o Hypotension associated with anterior crushing chest pain,
respiratory distress, and the ECG changes consistent with ST
elevation myocardial infarction (STEMI).
o Elevated troponin or creatine phosphokinase levels and
pulmonary edema on chest radiography.
o Interventions: antiplatelet agents, balloon angioplasty.
Reverse the etiology

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 Early attempt should be made to treat the underlying cause of shock.

 In some cases the etiology is clear: e.g. hemorrhagic shock from gunshot
 In other cases the etiology is less obvious: e.g. obstructive shock from
pulmonary embolism
 Once the diagnosis is known, specific therapy should be refined.
 Response to therapy should be monitored;
o Blood pressure
o Urine output
o Mental status
o Serum lactate level

Varicose Veins
Varicose veins are normal veins that have dilated under the influence of increased
venous pressure. They are chronic venous disorders. Varicosity is a penalty for
verticality against gravity! The different types of chronic venous diseases include;
 Varicose veins: subcutaneous dilated veins three millimeters or greater in
diameter.
 Telangiectasias: dilated intradermal venules less than one millimeter in
diameter. Synonyms: spider veins, hypen webs and thread veins.
 Reticular veins: dilated bluish subdermal veins, one to three millimeters in
diameter.

Common locations of varicose veins

 Lower limb: the most common
 Esophagus (esophageal varices)
 Rectum (hemorrhoids)
 Pampiniform plexus
 Perineum, vulva
Classification of chronic venous ulcers (CEAP)
Clinical classification C0: no signs of venous disease
C1: telangiectasia or reticular veins
C2: varicose veins
C3: edema
C4a: pigmentation or eczema
C4b: lipodermatosclerosis or atrophie blanche
C5: healed venous ulcer
C6: active venous ulcer
Etiologic classification Ec: congenital
Ep: primary
Es: secondary
En: no venous cause identified
Anatomical classification As: superficial veins
Ap: perforator veins
Ad: deep veins

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An: no venous location identified

Pathophysiological classification Pr: reflux
Po: obstruction
Pr,o: reflux and obstruction
Pn: no venous pathophysiology identified

Anatomy of the venous system of the lower limb

 Superficial system: long and short saphenous veins and their tributaries
 Perforators;
o Thigh perforators: Dodd’s perforator
o Knee perforators: Bodd’s perforator
o Leg perforators: Cockett’s perforators; 3 in number
 Lower perforator: below and behind medial malleolus
 Middle perforator: 10cm above the medial malleolus
 Upper perforator: 15cm above the medial malleolus
 Deep system: femoral and poplietal veins, branches of poplietal vein
(anterior tibial, posterior tibial, and peroneal veins), and valveless veins
draining the calf muscles (soleal veins)

Tributaries of the long saphenous vein

At the termination In the thigh In the leg
 Superficial circumflex  Lateral superficial  Anterior vein of the leg
iliac vein femoral vein  Posterior arch vein
 Superficial epigastric  Medial superficial They connect long and
vein femoral vein short saphenous veins and
 Superficial external  Transverse are called communicators.
pudendal vein suprapatellar vein
 Transverse
infrapatellar vein

Epidemiology
Approximately 23% of adults in US have varicose veins. The prevalence is higher
in westernized and industrialized countries, most likely due to alteration in life
styles and activity.

Risk factors
 Gender: more common in females because of hormonal factors
 Age: prevalence increases with age. With advancing age, the elastic
lamina of the vein becomes atrophic and the smooth muscle layer begins
to degenerate.
 Increased body mass index and height
 Family history (hereditary)

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 Occupation and lifestyle: smokers, occupations involving prolonged

standing.
 Immobility
 Increased intra-abdominal pressure: chronic constipation, pregnancy, tight
clothes, sports, pelvic tumors

Pathophysiology
Perfectly normal veins dilate and become tortuous under in response to continued
high pressure. In a subset of patients with hereditary vein wall weakness, even
normal venous pressures produce varicose changes.

Elevated venous pressure is due to;

 Mostly, venous insufficiency due to valve incompetence
o Excessive dilation of veins so that their delicate valve leaflets no
longer meet.
o Direct trauma to the valve
o Thrombotic valve injury
 Outflow obstruction
o Intravascular thrombosis or
o Extrinsic compression

Clinical features
Symptoms of varicose veins
 Leg heaviness, exercise intolerance, pain, pruritus, burning sensation,
restless legs, hight cramps, edema, skin changes, paresthesias.
Symptoms of telangiectasias
 Burning, swelling, throbbing, cramping, leg fatigue.
Aspects of symptoms
 Subjective symptoms are more severe early in the progression of disease,
less severe in the middle phases, & worse with advancing age.
 They do not correlate with the size or extent of visible varices or with
volume of reflux.
 Not all symptomatic patients are aware of their symptoms.
 Pain is improved by walking or raising the leg; unlike that of arterial
insufficiency which is worse with ambulation and even elevation.
 Pain may be associated to hormaonal changes in females (menstrual
cycle, pregnancy, exogenous hormonal therapy and sexual intercourse).
Physical examination
 Inspection
o The site, extent, and anatomical relation of the varicose veins,
blow outs, saphenavarix, and dilated veins over abdomen.
Collapsibility and Morrisey’s test.

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o Ankle flare, hyperpigmentation, edema, dermatitis, ulcer, and

talipes equines deformity.
o Uncomplicated varicose veins will always collapse on raising the
leg. But, varicose veins secondary to pelvic vein thrombosis or
arterio-venous fistula will not collapse.
o Venous ulcers are typically superficial, painless, with rugged
irregular borders, unhealed granulation, and hyper-pigmentation
around the ulcer around the medial aspect of the ankle.
 Palpation
o A firm, thickened, thrombosed superficial vein in an area of leg
pain or tenderness.
o Fascial defects in the calf along the course of the abnormal vein
o Deep boggy or spongy pockets in the calf muscle.
 Clinical tests
o Morrissey’s (cough impulse) test: SF incompetence
 Standing position
 Keep a finger at the SF junction and ask the patient to
cough. Fluid thrill is indicative of SF incompetence.
 Or on suine position, raise the leg and empty the vein.
Ask the patient to cough and look for an impulse.
o Trendlenberg I test: SF incompetence
 Supine position.
 Empty the varicose vein and occlude at SF junction with
thumb or tourniquet. Ask the patient to stand and
immediately release the occlusion. Rapid gush of blood
from above downwards indicates SF incompetence.
o Trendlenberg II test: perforator incompetence
 Supine position.
 Empty the varicose vein and occlude at SF junction with
thumb or tourniquet. Ask the patient to stand without
releasing the occlusion. Slow filling of the long
saphenous is seen in perforator incompetence.
o Multiple tourniquet test: site of perforator incompetence
 Supine position.
 Empty the varicose vein and apply four (3-5) tourniquets.
First at SF junction, second at mid thigh, third just below
the knee and the last at the lower third of the leg.
 Appearance of veins;
 Between 1st and 2nd tourniquets: incompetence
of thigh perforators.
 Between 2nd and 3rd tourniquets: incompetence
of ankle perforators.

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 Between 3rd and 4th tourniquets: incompetence

of leg perforators.
 On releasing the tourniquets one by one from below
upwards, sudden retrograde filling of the veins occur.
o Modified Perthe’s test: to rule out deep vein thrombosis
 Standing position
 Apply tourniquet at SF junction and ask the patient to
have a brisk walk.
 Severe pain in the calf or more prominence of superficial
veins indicat DVT.
 Elastic bandage was used in original Perthe’s test.
 Other tests
 Homan’s test: ankle dorsiflexion induces pain
 Mosse’s sign: palpation of calf induces pain
o Fegan’s test: to locate the perforator in the deep fascia
 Standing position
 Mark the varicosities and ask the patient to lie down
 Elevate the limb to empty the vein and palpate the vein
throughout its course. The defects in deep fascia have a
circular, buttonhole consistency.
o Schwartz test:
 Standing position
 Place the fingers of the left hand over a dilated segment
of the vein and with the right index finger tap the vein
below.
 A palpable impulse suggests a superficial column of
blood in the vein and it also suggests incompetence of
the valves in between the segment of the vein

Diagnosis
Laboratory tests are not useful for patients with varicose veins.
Venous imaging
 Hand-held Doppler: biphasic flow
 Duplex ultrasound: the standard imaging modality
 Contrast venography
 Magnetic resonance venography (MRV)
Physiologic measurements
 Venous refilling time: to detect venous insufficiency
o Normal: at least 2 minutes
o Mild and asymptomatic venous insufficiency: 40-120 seconds
o Significant venous insufficiency: 20-40 seconds
 Maximum venous outflow: to detect venous obstruction

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o The measure of the speed with which blood can flow out of a
maximally congested lower leg when a tourniquet is suddenly
removed.
 Calf muscle pump ejection fraction: used to detect failure of the calf
muscle pump to expel blood from the lower leg.

Treatment
Correcting the venous disorder
 Elastic compression stockings
 Medical therapies
o Sclerotherapy (chemical sclerosis or endovenous chemoablation)
o Laser ablation
 Surgery
o Ligation of sahenofemoral junction with vein stripping
o Phlebectomy
o Endovenous radiofrequency thermal ablation
o Endovenous laser thermal ablation
o Perforator ligation
Local treatment of the superficial manifestations after treating the venous
insufficiency or other underlying causes

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CHAPTER TWO-TRAUMA

Systemic Response to Injury

Minor insults result in localized inflammation that is transient and most often
beneficial, while major host insults lead to systemic inflammatory effect. Systemic
inflammation is a central feature of both sepsis and severe trauma. The degree of
the systemic response is proportional to the severity of injury, and is an
independent predictor of subsequent organ dysfunction and mortality. Response to
trauma results in a ‘sterile inflammation’. The clinical features of trauma are similar
to those observed in infection (see the table below).
Clinical spectrum of infection
Term Definition
Infection Identifiable source of microbial insult
SIRS Two of the following criteria are met
(systemic Temperature: ≥380C (100.40F) or ≤360C
inflammatory (96.80F)
response Heart rate: ≥90bpm
syndrome) Respiratory rate: ≥20bpm
PaCO2: ≤32mmHg or mechanical ventilation
WBC count: ≥12,000/μL or ≤4000/μL or ≥10%
band forms
Sepsis Identifiable source of infection + SIRS
Severe sepsis Sepsis + organ dysfunction
Septic shock Sepsis + cardiovascular collapse (requiring
vasopressor support)

The detection of injury is mediated by;

 Damage-associated molecular patterns (DAMPs); for trauma
 Pathogen-associated molecular patterns (PAMPs); for infection
The best characterized DAMP is high-motility group protein B1 (HMGB1). Others
include heat shock proteins, S100 protein, mitochondrial DNA, and etc. DAMPs
(and PAMPs) are ligands for pattern recognition receptors (PRR). There are four
distinct classes of innate immunity PRRs;
 Toll-like receptors (TLRs),
 Calcium-dependent (C-type) lectin receptors (CLRs),
 Retinoic acid-inducible gene (RIG)-I-like receptors (RLRs), and
 Nucleotide binding domain, leucine-rich repeat containing (NBD-LRR)
proteins.
Responses to injury include:
 Innate immune system activation; two general responses:
o Acute pro-inflammatory response
o Anti-inflammatory response
 Suppression of adaptive immunity.

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Neuroendocrine response to injury

There are two neuroendocrine pathways that orchestrate the host response;
 Hypothalamic-pituitary-adrenal (HPA) axis, which results in the release of
glucocrticoid hormones, and
 Sympathetic nervous system, which results in the release of the
catecholamines; epinephrine and norepinephrine.
There are multiple stimuli for the neuroendocrine response;
 Trauma (pain, hypovolemia, hypoxemia)
 Infection
 Fear and anxiety
The following hormones are those with a generally increased secretion in trauma.
 Cortisol
 Rennin
 Aldosterone
 Catecholamines
 Vasopressin (ADH)
 Glucagon (and insulin)
 Growth hormone

The cellular stress response

 Reactive oxygen species and oxidative stress response
 The heat shock response
 The unfolded protein response

The metabolic stress response

The essence of the response is to allow the body to reprioritize limited resources
away from peripheral tissues and towards vital organs and injured tissue. The
natural response to injury includes immobility, anorexia, and catabolism. The
metabolic response to injury is divided in to two phases; “ebb” and “flow” phases.
Injury

Ebb phase Flow phase

Hours Days Weeks

Shock Catabolism Anabolism

Fig: Phases of the physiologic response to injury
The ebb phase
 Lasts for about 24-48 hours after injury.
 It may be attenuated by proper resuscitation, but not completely abolished.

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 Characterized by hypovolemia, decreased BMR, reduced cardiac output,

hypothermia, lactic acidosis and decreased urinary nitrogen excretion.
 Predominant hormones: catecholamines, cortisol, and aldosterone
(RAAS).
 The main role is to conserve both circulating volume and energy stores for
recovery and repair.
The flow phase
 It is a hypermetabolic phase which corresponds to SIRS.
 Involves metabolization of body energy stores for recovery and repair, and
subsequent replacement of the lost or damaged tissue.
 Characterized by tissue edema, increased BMR, increased cardiac output,
raised body temperature, leukocytosis, increased oxygen consumption
and gluconeogenesis.
 It may be subdivided in to two;
o Catabolic phase
 Lasts for 3-10 days.
 Release of counter-regulatory hormones and
inflammatory cytokines results in significant fat and
protein metabolism.
 This results in weight loss, and increased urinary
excretion of nitrogen.
o Anabolic phase: may last for weeks depending on the extent of
injury and the subsequent need for repair and recovery.
 Key catabolic elements of the flow phase
o Hypermetabolism
 Increase in muscle protein degradation with decrease in
the muscle protein synthesis.
 Acute phase protein response: hepatic protein
metabolism
 Positive reactants (e.g. CRP, fibrinogen); plsma
concentration increases.
 Negative reactants (e.g. albumin); plasma
concentration decreases.
o Insulin resistance: following surgery or trauma, hyperglycemia
develops as a result of increased glucose production, and
decreased peripheral uptake. The degree of insulin resistance is
proportional to the magnitude of the injurious process.

Changes in body composition following trauma

Normal body composition
 An average male has 20% fat and 80% fat-free/lean mass.

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 The fat free mass is composed of protein (17%), water (60%), and minerals
(4%).
 The protein mass can be;
o Skeletal muscle protein: 6%
o Non-skeletal muscle protein: 11%
 Protein turnover is in order of 150-200g per day.
Metabolism during [unstressed] fasting
 A normal adult requires 22-25kcal/Kg/day to maintain basal metabolic needs
(i.e., at rest and fasting).
 The principal sources of fuel during short-term fasting (<5 days) are muscle
protein and fat, with fat being the most abundant source.
 180g of glucose will be used to support obligate glycolytic cells such as
neurons, leukocytes, RBCs, and renal medullae.
 Sources of plasma glucose during fasting
o Glycogenolysis (NE, glucagon, vasopressin)
o Gluconeogenesis: sources
 Lactate from glycolysis in muscles, RBCs & WBCs.
 Glycerol from lipolysis.
 Aminoacids from proteolysis (skeletal muscles* & solid
organs)
 During prolonged starvation systemic proteolysis is reduced which reflects
adaptation by vital organs to use ketones.
Metabolism after injury
 The magnitude of metabolic expenditure is proportional to the severity of the
insult. Thermal injuries and severe infections have the highest energy
demands.The main labile energy reserve is fat, and the main labile protein
reserve is skeletal muscle.
 Metabolism of lipids
o Lipids are the primary energy source during stressed states (50-80%).
o Lipolysis occurs mainly in response to catecholamine stimulation of
hormone-sensitive triglyceride lipase.
o Oxidation of 1g of fat yields 9kcal of energy.
o Major sources: dietary and exogenous sources.
o Minor source: hepatic synthesis from carbohydrate and amino acids.
o Increased lipolysis and reduced systemic carbohydrate availability
during starvation diverts excess acetyl-CoA towards hepatic
ketogenesis.
 Metabolism of carbohydrates
o Oxidation of 1g of carbohydrate yields 4kcal of energy.

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o Glucose production occurs at expense of protein stores (i.e., skeletal

muscles), hence, the primary goal of administration of maintenance
glucose in surgical patients is to prevent muscle wasting.
o Glucose transportation family;
 GLUT 1: placenta, brain, kidney, colon
 GLUT2: liver, pancreatic β-cells, kidney, small intestine
 GLUT3: brain, testis
 GLUT4: skeletal muscle, heart muscle, brown and white fat
 GLUT5: small intestine, sperm
 Metabolism of proteins
o The average protein intake in healthy young adult is 80-120g/d and
every 6g of protein yields 1g of nitrogen.
o Degradation of 1g of protein yields 4kcal of energy.
o After an injury a patient can lose 1.5% of lean body mass due to
proteolysis.
o Protein catabolism after injury provides substrates for
gluconeogenesis and synthesis of acute phase reactants.
o Skeletal muscles are preferentially depleted while visceral protein is
relatively preserved.

Advanced Trauma Life Support (ATLS)

 Trauma, or injury, is defined as cellular disruption caused by an exchange
with environmental energy that is beyond the body’s resilience which is
compounded by cell death due to ischemia/reperfusion.
 Trauma remains the most common cause of death for all individuals
between the ages of 1 and 44 years and is the third most common cause
of death regardless of age.
The ATLS is developed in the late 1970’s by the American College of Surgeons
Committee on Trauma (ACSCT).
The initial management of a seriously injured patient consists of:
1. Primary survey
2. Secondary survey
3. Definitive care and
4. Tertiary survey
ATLS refers to the primary survey as assessment of the “ABCDE’s”. The concepts
in the primary survey are pursued simultaneously in coordinated team
resuscitation.
A. Airway with cervical spine protection
B. Breathing
C. Circulation
D. Disability
E. Exposure

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Airway with cervical spine protection

 This is a priority issue because restoring cardiovascular integrity without
adequate oxygen in the blood will be futile.
 Patients with abnormal voice, abnormal breathing sounds, tachypnea, or
altered mentation require airway evaluation.
 Blood, vomitus, mucus secretions, tongue, foreign bodies, and soft tissue
swelling can cause airway obstruction.
 Management
o Suctioning for blood, mucus, or vomitus
o Chin lift or jaw thrust for tongue fall (comatose patients)
o An oral airway or nasal trumpet
o Intubation (endotracehal*, nasotracheal);
 Inability to protect the airway due to altered mental status
(the most common indication);
 Apnea;
 Impending airway compromise due to inhalation injury,
hematoma, facial bleeding, soft tissue swelling, or aspiration;
and
 Inability to maintain oxygenation.
o Cricothyroidotomy and insertion of 6.0 endotracheal tube. It is
relatively contraindicate in patients under the age of 11, due to the
risk of subglottic stenosis.
o Thracheostomy;
 Laryngotrachel separation or laryngeal fractures
 When cricothyroidotomy is contraindicated
 It is best performed in OR.
 Cervical spine protection
o All patients with blunt trauma require cervical spine immobilization
until injury is excluded. This is accomplished by;
 Applying hard collar
 Placing sandbags on both sides of the patient’s head.
o For penetrating neck wounds, however, cervical collars are not
believed useful.

Breathing and ventilation

 All injured patients should receive supplemental oxygen and should be
monitored by pulse oximetry.
 The following conditions pose immediate threat to life due to inadequate
ventilation, and should be recognized during the primary survey;
o Tension pneumothorax
o Open pneumothorax
o Flail chest

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o Massive air leak

Tension pneumothorax
o Presumed in any patient with respiratory distress and hypotension in
combination of one of the following signs;
o Tracheal deviation away from affected side
o Lack of or decreased sound on affected side
o Subcutaneous emphysema on affected side
o May have distended neck veins
o Hypotension;
o Differentiates tension pneumothorax from simple pneumothorax
o Is due to compression of major vessels as a result of increased
intra-thoracic pressure.
o Management
o Needle decompression: with 14-gauge angiocatheter in the 2nd
ICS in the MCL; performed in the field.
o Definitive management is insertion of chest tube;
 In the safe triangle: between 6th rib below, lateral border
of pectoralis major anteriorly, and MAL laterally).
 Usually in the 5th ICS in the anterior axillary line.
Open pneumothorax (sucking chest wound)
 Full thickness loss of chest wall with free communication of air between
the pleural space and the atmosphere.
 This compromises ventilation due to equilibration of atmospheric and
pleural pressures.
 Complete obstruction of the defect without chest tube insertion may
convert open to a tension pneumothorax.
 Management
o Temporary: three-way dressing which acts as a flutter valve.
o Definitive: closure of the defect and tube thoracostomy remote
from the wound.
Flail chest
 Occurs when three or more contiguous ribs are fractured in at least two
locations.
 Paradoxical movement of this free floating segment of chest wall is
evident due to the negative intra-thoracic pressure.
 It is the decreased compliance & increased shunt fraction caused by the
associated pulmonary contusion that causes acute respiratory failure.
 Pulmonary contusion often progress for the first 12 hours.
 Resultant hypoventilation and hypoxemia may require intubation and
mechanical ventilation.
Massive air-leak

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 Occurs from major tracheobronchial injuries.

 There are two types;
o Type I injuries occur within 2cm of the carina. Often not
associated with pneumothorax due to envelopment of mediastinal
pleura.
o Type II injuries occur in the distally within the tracheobronchial
tree and manifest with pneumothorax.
 Bronchoscopy confirms the diagnosis and directs management.

Circulation with hemorrhage control

 It can be initially approximated by palpating peripheral pulses. SBP must be
60 for carotid artery to be palpable, 70 for femoral pulse, and 80 for radial
pulse.
 Any episode of hypotension (SBP<90mmHg) is assumed to be due to
hemorrhage until proven otherwise.
 Patients may have paradoxical bradycardia.
 BP & PR should be measured every 5 minutes in patients with significant
blood loss until normal vital signs are restored.
 Massive concealed hemorrhage may occur in one or more of the body cavities
and potential spaces;
o Chest cavity: insert chest tube
o Peritoneal cavity: exploratory laparotomy
o Pelvic cavity: stabilize pelvic bones with a tight band around pelvis
o Long bone fractures: reduce and stabilize the fracture
 Management
o IV access for fluid resuscitation with two peripheral catheters, 16-
gauge or larger in adults. Intraosseous needles can be placed in
patients in whom peripheral angiocatheter access is difficult.
 Initial access is best secured in the groin or ankle.
Saphenous vein cutdowns at the ankle provide excellent
access.
 Secondary access is best secured in femoral vein for chest
traumas, and jugular or subclavian for abdominal traumas.
o External control of any visible hemorrhage;
 Manual compression (applying pressure) with gauze and
gloved hands.
 Cauterization
 Fracture reduction
 Applying a tourniquet is controversial; it may exacerbate
ischemic events specially in extremities.
 Four life-threatening injuries must be identified during the circulation section;
1. Massive hemothorax

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2. Cardiac tamponade
3. Massive hemoperitonem
4. Mechanically unstable hip fractures
 Three critical tools are used to differentiate these in a polytrauma patient;
o Chest radiograph
o Pelvic radiograph
o FAST (focused abdominal sonography for trauma)
Massive hemothorax
 Defined as >1500mL of blood or, in pediatrics, 25% of the patient’s blood
volume in the pleural space.
 Causes of massive hemothorax;
o Blunt trauma: multiple rib fracture
o Penetrating trauma: great vessel or pulmonary hilar injury
 It is an indication for operative intervention, but chest tube is critical to facilitate
lung re-expansion.
Cardiac tamponade
 Most common after penetrating thoracic wounds. Occasionally, blunt rupture
of hear (sp. atrial appendages) is seen.
 Acutely, <100mL of pericardial blood may cause tamponade.
 Classic presentation: Beck’s triad;
o Distended neck veins
o Muffled heart tones
o Hypotension
 Diagnosis is achieved by ultrasound of pericardium
 Management
o Fluids, (or pericardial drain in patients with unstable
hemodynamics)
o Pericardiocentesis: effectitve in 80% of patients.
o Resuscitative (emergency department) thoracotomy-RT
 Indications for resuscitative thoracotomy;
o Salvageable post-injury cardiac arrest:
 Patients sustaining witnessed penetrating trauma to the torso
with <15 min of prehospital CPR.
 Patients sustaining witnessed blunt trauma with <10 min of
prehospital CPR.
 Patients sustaining witnessed penetrating trauma to the neck or
extremities with <5 min of prehospital CPR.
o Persistent severe post-injury hypotension (SBP≤60 mmHg) due to:
 Cardiac tamponade
 Hemorrhage – intra-thoracic, intra-abdominal, extremity, cervical
 Air embolism

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Hemorrhagic shock and fluid resuscitation

 Classic signs and symptoms of shock are; tachycardia, hypotension,
tachypnea, altered mental status, diaphoresis, and pallor.
 The quantity of blood loss correlates with physiologic abnormalities.
o Tachycardia is the earliest sign of ongoing blood loss.
o Blood pressure does not change until over 1500mL of blood loss.
Signs and symptoms of advancing stages of hemorrhagic shock
Class I Class II Class III Class IV
Loss (mL) Up to 750 750-1500 1500-2000 >2000
Loss (%) Up to 15% 15-30% 30-40% >40%
PR <100 >100 >120 >140
BP Normal Normal Decreased Decreased
Pulse pressure Normal/increased Decreased Decreased Decreased
RR 14-20 >20-30 30-40 >35
UOP (mL/h) >30 >20-30 5-15 Negligible
Mental status Slightly anxious Mildly Anxious, Confused,
anxious confused lethargic
 Fluid resuscitation begins with 2L (adult) or 20mL/Kg (child) IV bolus of
isotonic crystalloids, typically Ringer’s lactate
 Patients who have good response to fluid infusion and evidence of good
peripheral perfusion are presumed to have adequate perfusion.
 Urine output;
o Adult: 0.5mL/Kg/hr
o Child: 1mL/Kg/hr
o Infant: 2mL/Kg/hr
 Based on response to initial fluid therapy, patients can be classified as;
o Responders,
o Transient responders, and
o Non-responders.
 Responders
o Evidenced by normalization of vital signs, mental status, and
urine output. They are unlikely to have ongoing blood loss.
 Transient responders and non-responders
o Evidenced by persistent hypotension (SBP<90mmHg) and
tachycardia.
o Transient responders respond initially to volume loading, but then
deteriorate hemodynamically again. They are difficult to triage
and treat.
o Both have ongoing hemodynamic instability.
o Differential diagnoses:
 Cardiogenic or hemorrhagic shock
 Overwhelming multisystem injury
 Tension pneumothorax

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 Pericardial tamponade
 Blunt cardiac injury
 Myocardial infarction
 Bronchovenous air embolism
 Persistent hypotension due to hemorrhage is associated with high
mortality. A rapid search for the source/s of bleeding includes;
o Visual inspection
o FAST
o Chest and pelvic radiographs.
 For persistent hypotension, the current trend is to activate a massive
transfusion protocol (MTP) in which red blood cells (RBC), fresh frozen
plasma (FFP), packed platelets and cryoprecipitate are administered early.
 MTP is needed when a patient needs >10U RBCs in 24 hrs. It is given in a
ratio of 1:1:1.
 Response to resuscitation is assessed by the following parameters;
o Mean arterial pressure (MAP = 1/3SBP + 2/3DBP) should be >
60mmHg (60-100mmHg)
o Urine output = 0.5 for adults and 1 for children ml/kg/hr
o Lactate (most important) should be <2.5mmol/L
o Vital signs; especially pulse rate
o Base deficit
o PaO2 >100mmHg

Disability and exposure

 GCS should be determined.
o 13-15: mild head injury
o 9-12: moderate head injury
o ≤8: severe injury
 Neurologic evaluation is critical before administration of neuromuscular
blockade for intubation.
 Neurogenic shock
o First recognized due to paralysis, decreased rectal tone or
priapism.
o Typified by hypotension with relative bradycardia.
 Seriously injured patients must have all their clothing removed to avoid
overlooking limb- or life-threatening injuries.

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Burn Injuries
Initial evaluation
 Primary survey
 Secondary survey; evaluation of other injuries
 Estimation of burn size: see the following figure.
o In children under 3 years old, the head accounts for a larger
relative surface area
o Diagrams such as the Lund and Browder chart give a more
accurate accounting of the true burn size in children.
 Diagnosis of CO and cyanide poisoning

Fig: The rule of nines: estimation of total body surface area (TBSA)

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Fig: The Lund and Browder chart

Classification of burn injuries

 Thermal burns: temperatures less than 440C do not cause thermal burn
due to high temperature.
o Flame burn: most common and have highest mortality due to
their association with structural fires and accompanying
inhalational injury and/or CO poisoning.
o Contact burn
o Scald burn
o Cold injury (acute and frostbite)
 Electrical burns: have special concerns including the potential for cardiac
dysarythmias and compartment syndromes with concurrent

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rhabdomyolysis. They have entry and exit points. There are two types of
electrical burns;
o Low voltage (home appliances-<1500v): cause small, localized,
deep burn.
o High voltage (>1500v): damage by flash (external burn) and
conduction (internal burn).
 Chemical burns: the most important components of initial therapy are
careful removal of the toxic substance from the patient and irrigation of the
affected area with water for a minimum of 30 minutes, except in cases of
concrete powder or powdered forms of lye, which should be wept from the
patient to avoid activating the aluminum hydroxide with water. There are
two major types of chemical burns;
o Alkali burns: often deep dermal and full-thickness
o Acid burns;
 Weak concentrations: superficial
 Strong concentrations: deep dermal

Burn depth
Dupuyteren’s classification
 Superficial (first degree)
o Involves the epidermis
o Painful erythematous but do not blister
 Partial-thickness (second degree)
o Dermal involvement, extremely painful, with weeping & blisters.
o Two classes: superficial and deep
 Full-thickness (third degree): leathery, painless (due to damage to the
sensory nerves), and non-blanching
 Fourth degree: involvement of underlying tissues
Jackson’s classification
 Zone of coagulation: the most severely burned portion and is typically at
the center of the wound with coagulative necrosis; much like third or fourth
degree burns.
 Zone of stasis: variable degrees of vasoconstriction and resultant
ischemia; much like second degree burn. Appropriate resuscitation and
wound care may help prevent conversion to deeper wound.
 Zone of hyperemia: the least area of a burn which will heal with minimal or
no scarring and is most likely a superficial or first degree burn.

Prognostic factors of burn injury

 Age of the patient*
 Percentage of TBSA*

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 Presence of inhalational injury

 Depth of the burn
 Type and density of the burn
 Comorbidities: HIV, cancer, kidney or liver disease
 Co-existent trauma
 Pneumonia

Management
 ATLS (ABC’s of life)
 Resuscitation
o In children with burns over 10% TBSA and adults with burns over
15% TBSA, consider the need for intravenous fluid resuscitation.
o Most commonly used formula: Perkland or Baxter formula
 4ml/kg/%TBSA of lactated Ringer’s solution of which half
is given during the first 8 hours after burn and the
remaining half is given over the subsequent 16 hours.
o If the TBASA is not known, use the 4:2:1 or 100:50:20 rule of
maintenance fluid therapy.
 Indications for admission;
o Suspected airway or inhalational injury
o Burn likely to require resuscitation
o Burn likely to require surgery
o Burn to the hands, feet, face, and perineum
o Patients with comorbidities
o Patients at extremes of age
o TBSA >20% for adults and >10% for children
o At least third degree burn
o Burn with associated potentially serious sequelea including high
tension electric burn and concentrated acid burn (e.g. HCl)
 Burn wound care
o Clean by saline water
o Aspirate blisters
o Topical antibiotics
o Escharotomy
o Dressing
 Tetanus prophylaxis
 Skin grafting

Complications of burn injuries

 Airway obstruction
 Aspiration pneumonia

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 Atelectasis
 Acute renal failure (hypovolemia, sepsis, tissue toxins-myoglobulin)
 Broncoalveolar infection, pulmonary edema
 Compartment syndrome
 Dehydration
 Hyperkalemia
 Infection by streptococcus

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CHAPTER THREE-THE BREAST

Surgical Anatomy and Physiology

The anatomy of the breasts
Embryology
 At 5th or 6th week of fetal development, two ventral bands of thickened
ectoderm are evident (mammary ridges, milk lines).
 These ridges disappear after short time except for small portions that
persist in the pectoral region.
 Accessory breasts (polymastia) or accessory nipples (polythelia) may
occur when normal regression fails.
 A primary bud develops from an ingrowth of ectoderm. The primary buds
then initiate development of 15-20 secondary buds.
 Epithelial cords develop from the secondary buds into surrounding
mesenchyme.
 Major (lactiferous) ducts develop, which open in to shallow mammary pit.
During infancy, a proliferation of mesenchyme transforms the pit into a
nipple.
 If there is the failure of a pit to elevate above skin level, an inverted nipple
results; found in 4% of infants.
 The breasts remain undeveloped in the female until puberty, when it
enlarges in response to ovarian estrogen and progesterone; which initiate
epithelial proliferation and connective tissue elements.
 However, the breasts remain incompletely developed until pregnancy
occurs.

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Fig: The mammary milk line

Functional anatomy
 The breast has a protuberant conical shape, with the base of the cone
measuring 10-12cm in diameter.
 The breast is composed of 15-20 lobes, which are each composed of
several lobules; the structural unit of breast.
 Cooper’s suspensory ligaments are fibrous bands of connective tissue
that travel through the breast. They insert perpendicularly into the dermis
and provide mechanical support.
 Mature female breast extends from;
o 2nd or 3rd rib to 6th or 7th rib; the mammary fold
o Lateral border of the sternum to the anterior axillary line.
 The deeper or posterior surface rests on the fascia of the pectoralis major,
serratus anterior, and external oblique abdominal muscles.
 The axillary tail of Spence extends laterally across the anterior axillary fold.
The upper outer quadrant contains greater volume of breast tissue than
do other quadrants.
 Considerable variations in the size, contour, and density of the breast ar
evident among individuals.
 The epidermis of the nipple-areola complex is pigmented and is variably
corrugated.
 With pregnancy, the breast undergoes proliferative and developmental
maturation.
 A mature breast is composed of three principal tissue types;
o Glandular epithelium
o Fibrous stroma and supporting structures
o Fat

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 The duct system;

o Different portions of the duct system are associated with different
disease processes
 Larger ducts: duct papilloma and ectasia
 Distal smaller;
 Fibroadenoma during development of breast.
 Cysts and sclerosing adenosis during involution.
 Blood supply; branches of axillary artery
o Perforating branches of internal mammary
o Lateral branches of posterior intercostals
o Branches from axillary artery, including highest thoracic, lateral
thoracic and pectoral branches of the thoracoacromial artery.
 Veins follow the course of arteries;
o Perforating branches of internal thoracic veins
o Perforating branches of the posterior intercostals veins
o Tributaries of the axillary vein
 Lymphatic vessels parallel the blood vessels;
o Axillary lymph nodes
o Internal mammary/parasternal nodes
o Supraclavicular
o Others
 Innervations:
o Lateral cutaneous branches of 3rd through 6th intercostals nerves
o Cutaneous branches from the cervical plexus; specifically the
anterior branches of the supraclavicular nerve.
o Intercostobrachial nerve; a lateral cutaneous branch of 2nd
intercostals nerve is seen during surgical dissection. Resection of
the nerve causes loss of sensation over the medial aspect of
upper arm.

Axillary lymph node groups

Level Lymph node group Drainage
I (below or lateral Lateral/axillary vein Most of upper limb
to pectoralis Anterior/pectoral/external Most of lateral breast
minor) mammary
Scapular/posterior/subsc Lower posterior neck, posterior
apular trunk, posterior shoulder
II (superficial or Central From anterior, lateral, and
deep to pectoralis posterior groups
minor) Interpectoral/Rotter’s LNs From breast
III (medial to Subclavicular/apical From all other groups
pectoralis minor)

Physiology of the breast

 Estrogen, progesterone, and prolactin are the major hormonal stimuli for the
development and function of breasts;
o Estrogen: ductal proliferation

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o Progesterone: glandular/lobular proliferation

o Prolactin: lactogenesis
 Other hormonal stimuli: oxytocin (milk-letdown), thyroid hormone, cortisol, and
growth hormone.
 At puberty, there is a decrease in the sensitivity of the HPA axis to negative
feedback and an increase in sensitivity to positive feedback from estrogen.
 This results in increased GnRH, FSH, and LH and ultimately estrogen and
progesterone.
 During pregnancy;
o Breast enlarges due to ductal and lobular epithelial proliferation,
o The areolar skin darkens, and
o The accessory areolar (Montgomery’s) glands become prominent.
 After delivery of placenta, circulating levels of progesterone and estrogen
decrease, permitting full expression of the lactogenic action of prolactin.
 Oxytocin release results from auditory, visual, and olfactory stimuli associated
with nursing and initiates contraction of myoepithelial cells which results in
compression of alveoli and expulsion of milk in to lactiferous ducts.
 Senescence: after menopause;
o Decreased secretion of estrogen and progesterone
o Involution of ducts and alveoli of the breast
o Increased density of fibrous connective tissue
o Breast tissues are replaced by adipose tissue

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Fig: The breast at different physiologic states: A. adolescence B. pregnancy C.

lactation D. senescence
A list of disorders of the breast
Congenital Breast cancer (Foote-Stewart classification)
Amastia Invasive ductal carcinoma- adenocarcinoma
Polymastia (scirrhous/simplex/non-special type; NST);
Polythelia 80%
Mastitis of infants Special-type cancers; 10% total
Diffuse hypertrophy Medullary carcinoma; 4%
Gynecomastia Mucinou/colloid carcinoma; 2%
Inflammatory Papillary carcinoma; 2%
Bacterial mastitis Tubular carcinoma; 2%
Breast abscess Invasive lobular carcinoma; 10%
Tuberculosis of breast Paget’s disease of nipple
Duct ectasia/periductal mastitis Rare: adenoid cystic, aquamous, apocrine
Hidradenitis suppurativa
Mondor’s disease
Benign tumors To qualify as special type cancer, at least 90%
Fibroadenoma of the cancer must contain the defining
ANDI histologic features.
Carcinoma in-situ (ductal and lobular) NST: non-special type
Phyllsoides tumor

ANDI classification of benign breast disorders

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Age group Normal Disorder Disease

Early Lobular development Fibroadenoma Giant fibroadenoma
reproductive Stromal development Adolescent hypertrophy Gigantomastia
(15-25 y) Nipple eversion Nipple inversion Suareolar abscess
Mammary duct fistula
Late Cyclical menstruation Cyclical mastalgia Incapacitating
reproductive mastalgia
(25-40 y) Nodularity
Epithelial hyperplasia Bloody nipple discharge
of pregnancy
Involution Lobular involution Macrocysts -
(35-55 y) Sclerosing lesions
Ductal involution
Dilatation Duct ectasia Periductal mastitis
Sclerosis Nipple retraction -
Epithelial turnover Epithelial hyperplasia Epithelial hyperplasia
with atypia
ANDI: aberrations of normal development and involution
The horizontal component defines ANDI along a spectrum from normal to disorder to disease.
The vertical component indicates the period during which the condition develops.

Page’s classification of benign breast disorders (pathologic)

Non-proliferative Proliferative without atypia Proliferative with atypia
Cysts & apocrine metaplasia Sclerosing adenosis Atypical lobular
Duct ectasia Radial and complex hyperplasia
Mild ductal epithelial hyperplasia sclerosing lesions Atypical ductal
Calcifications Ductal epithelial hyperplasia hyperplasia
Fibroadenoma & related lesions Intraductal papillomas
[Fibrocystic disease]

Common clinical presentations of breast diseases

Lump Smooth, well defined Hard: cyst
Nodular, irregular Rubbery: fibroadenoma
Hard: breast cancer
Pain With lump Fibroadenosis, cysts, periductal mastitis, breast
abscess, and sometimes cancer
Without lump Cyclical mastalgia, non-cyclical mastalgia,
trauma, and very rarely carcinoma breast
Nipple Blood Duct papilloma, carcinoma breast
discharge Pus Breast abscess
Milk Lactation, galactocele, mammary fistula
Serous/green Fibrocyctic diseases, duct ectasia,
fibroadenosis, carcinoma breast
Nipple Slit-like Duct ectasia, chronic periductal mastitis
retraction Circumferential Carcinoma breast

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Benign Breast Conditions

Bacterial infections
Postpartum period is the most common time for breast infections to occur. And
they are most commonly related to lactation. Those unrelated to lactation are less
common and can be of two classes;
 Intrinsic/primary
 Extrinsic/secondary to infection in adjacent structures
The most common intrinsic and extrinsic infections are periductal mastitis and
infected sebaceous cyst, respectively.
S. aureus and Streptococcus species are the most frequent pathogens.
Breast abscess
 Typically seen in staphylococcal infections.
 Present with point tenderness, erythema, and hyperthermia.
 Those associated with lactation present within few weeks of breastfeeding.
 Breast abscesses have two clinical stages;
o Cellulitic stage: severe pain, swelling, tense, tender, warm
o Breast abscess: high grade fever, chills, rigors, fluctuation
 May result in subcutaneous, subareolar, interlobular (periductal), and
retromammary abscesses.
 S. aureus infections tend to be deep and localized, whereas streptococcal
infections present with diffuse superficial involvement.
 Breast infections can be chronic, with recurrent abscess formation.
 Treatment (currently);
o Antibiotics and repeated US guided aspiration
o Operative incision & drainage is now reserved for;
 Resistance to antibiotics and repeated aspiration
 Other indications (thinning or necrosis of overlying skin)
o Streptococcal infections are treated with local wound care and
administrations of IV antibiotics.
Puerperal infections
 Epidemic puerperal mastitis;
o Initiated by highly virulent strains of MRSA.
o Transmitted via suckling neonate,
o Stop breast feeding, start antibiotics, and initiate surgical therapy.
 Non-epidemic (sporadic) puerperal mastitis;
o Infection of interlobular connective tissue of the breast.
o Nipple fissuring and milk stasis.
o Empty the breasts and start antibiotic therapy.
Recurrent periductal mastitis (Zuska’s disease)

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 Recurrent retroareolar infections and abscesses.

 Smoking is a risk factor.
 Antibiotics + incision and drainage as necessary.

Hidradenitis suppurativa
 A chronic inflammatory condition of the nipple-areola complex or axilla.
 Origin;
o Nipple-areola complex: accessory glands of Montgomery
o Axilla: sebaceous glands
 Women with chronic acne are predisposed.
 Nipple-areolar disease may be confused with Paget’s disease of nipple or
invasive breast canrcinoma.
 Axillary disease is often multifocal and contigious.
 Treatment;
o Antibiotics and incision & drainage
o Excision may be required with flaps or grafts.

Mondor’s disease
 A variant of thrombophlebitis that involves superficial veins of anterior
chest wall and breast; most commonly lateral thoracic vein,
thoracoepigastric vein, and less commonly superficial epigastric vein.
 Typically present with pain in the lateral breast or anterior chest wall.
 A tender firm cord is found to follow the distribution of the vein.
 Rarely bilateral, no evidence of thrombophlebitis in other areas, self-
limiting, and not indicative of cancer.
 Treatment;
o Anti-inflammatory medications
o Application of warm compresses along the vein.
o Usually resolves within4-6 weeks.

Fibroadenomas/breast mouse
 Predominant in younger women aged 15-25 years.
 Usually grow to 1 or 2 cm and then are stable, but may grow larger.
o Normal: ≤1cm
o Disorders: 1-3cm (large fibroadenomas)
o Disease: >3cm or multiple (more than five in single breast)
 Smooth, round, rubbery, mobile, painless breast lump.
 The precise etiology is unknown. They are hormone dependent.
 They have histologically normal cellular elements with abundant stroma;
unlike adenomas which have sparse stroma. They are surrounded by a
well marked capsule.

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 Diagnosis: ultrasound and sometimes core-needle biopsy.

 Treatment;
o Most are self-limiting and many go undiagnosed.
o Cryoablation and US-guided vacuum assisted biopsy for smaller
lesions <3cm.
o Surgical excision for larger lesions.

Breast cysts (Macrocysts)

 Are involutional disorders, have high frequency of occurrence.
 Common in women from 35-55 years.
 When the stroma involutes too quickly, alveoli remain and form microcysts,
which are precursors of macrocysts.
 They present with painful or painless lump with or without excessive
secretion of thin fluid.
 Often multiple and bilateral.
 They are common, often subclinical, and do not require specific therapy.
 They are typically 5-10mL, but may grow larger; >75mL.
 Diagnosis: needle biopsy.
 Treatment;
o Aspiration; usually under US guidance.
o Surgical excision;
 Recurrence after 2 aspirations
 Blood stained aspirate
 Residual lump after aspiration

Duct ectasia/periductal mastitis/plasma cell mastitis

 A clinical syndrome characterized by dilated subareolar ducts.
 Pathogenesis: two theories;
o A primary event leads to stagnation of secretions, epithelial
ulceration and leakage of duct secretions. This produces local
inflammation with periductal fibrosis and subsequent nipple
retraction.
o A primary event that leads to weakening of the ducts and
secondary dilation.
 The disease is more common in smokers.
 Presents with a wide spectrum of problems including nipple discharge,
slit-like nipple retraction, painful and tender inflammatory masses,
abscesses (subareolar) and fistulas.
 Unlike puerperal abscess, subareolar abscess is usually unilocular and
often from single duct.
 Treatment;

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o Aspiration and culture of the aspirate

o Antibiotics (combination of metronidazole and dicloxacillin or co-
amoxiclav) while awaiting culture results.
o Antibiotics are then continued based on sensitivity tests.
o Treatment for fistula = fistulectomy with primary closure and
antibiotic coverage.
o Surgery; total duct excision.
 Large abscess >50% of areolar surface
 Recurrence involving different ducts
 Marked nipple inversion
 Older patient
 Purulent discharge from other ducts
 Recurrence after fistulectomy.

Traumatic fat necrosis

 May be acute or chronic and occur in fat middle aged women (40-50 years
of age).
 Following trauma, a lump, often painless, appears.
 This may mimic carcinoma and biopsy is required.
 It is due to saponification of the adipose tissue due to release of fatty
acids and glycerol.
 Treatment = biopsy/excision.
Change in surface appearance of the breast
Eczema Paget’s disease
Bilateral Unilateral
Commonly occurs at lactation Occurs at menopause
Itches Does not itch
Vesicles No vesicles
Nipple intact Nipple may be destroyed
No lumps There may be an underlying lump

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Breast Cancer
Epidemiology
 Breast cancer is the most Epidemiologic types of breast cancer
common site-specific cancer in Type Prevalence
women (29% of newly Sporadic 65-75%
Familial 20-30%
diagnosed cancer) and the
Hereditary (BRCA, p53, 5-10%
leading cause of death (14%) PTEN, ATM,
from cancer for women aged STK11/LKB1,
20-59 years. MSH2/MLH1, Unknown)
 More common in less industrialized nations, although Japan is an
exception.
 20% of women above 90 years develop breast cancer in Ethiopia.

Risk factors of breast cancer;

 Hormonal risk factors
o Increased exposure to estrogen
 Early menarche
 Late menopause
 Nulliparity
 Hormone replacement therapy
 Oral contraceptive pills (OCP)
 Obesity is associated with long-term increase in
estrogen exposure because the major source of
estrogen in postmenopausal women is the conversion of
androstenedione to estrone by adipose tissue.
 Alcohol consumption increases serum level of estradiol.
 High fatty meals increase serum estrogen levels.
o Latter age at first pregnancy (>30 years); the terminal
differentiation of breast epithelium associated with full-term
pregnancy is protective.
o Shorter/no breast feeding
 Non-hormonal risk factors
o Gender
o Breast irradiation during adolescence, a period of active breast
development, magnifies deleterious effect.
o Genetic: BRCA1/2 mutation, previous history of breast cancer,
family history of breast cancer
o Age
o Lobular carcinoma in-situ (and not DCIS)

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o History of benign breast diseases; florid ductal epithelial

hyperplasia, and atypical ductal or lobular hyperplasia.
High risk female population
 Family history
 BRCA mutation carriers
 Family member with BRCA mutation
 Radiation exposure to the chest between ages 10-30
 Self or family history of the following syndromes;
o Li-Fraumeni syndrome
o Cowden syndrome
o Bannayan-Riley-Ruvalcaba syndrome.
 Cancer prevention for high-risk populations
o Chemoprevention
 Tamoxifen*, raloxifen
 Aromatase inhibitors: exemestane, anastrozole
o Risk-reduction surgery
 Mastectomy and reconstruction
 Salpingo-ophrectomy
o Intensive screening for breast cancers;
 Mammography
 MRI
 Clinical breast examination (CBE)
 Breast self awareness (BSA)
BRCA mutation
 Inherited in an autosomal dominant fashion with high penetrance.
 Distinguishing clinical features;
o Early age at onset,
o Higher prevalence of bilateral cancer,
o Presence of associated cancers: ovarian, colon, prostate,
pancreatic, gallbladder, stomach, and melanoma.
BRCA1 mutation BRCA2 mutation
 Predisposing factor for 45% of hereditary breast  Life-time risk of developing
cancer and ≥80% of hereditary ovarian cancer. cancer is 85% for breast
 Life-time risk for developing cancer is 85% for cancer and 20% for ovarian
breast cancer and 40% for ovarian cancer. cancer.
 Invasive ductal carcinomas  Invasive ductal carcinomas
 Poorly differentiated  Well differentiated
 Hormone receptor negative (tripple)  Hormone receptor positive

Natural history
 Skin retraction is produced when desmoplastic response entraps
Cooper’s ligaments due to invasion of the surrounding breast tissue.

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 Peaud’ orange appearance: localized edema that occurs when lymphatic

drainage from the skin is disrupted.
 With continued growth, cancer cells invade the skin, and eventually
ulceration develops.
 The size of the primary tumor correlates with disease-free and overall
survival, but there is a close relation between cancer size and axillary
lymph node metastasis.
 Tumor size and nodal status remain the powerful predictors of late
recurrence.
 Recurrences;
o 20% are local-regional
o >60% are distant
o 20% are both.
 Lymph node metastasis;
o Metastatic nodes at first are ill-defined and soft but become firm
and hard with continued growth.
o Axillary nodes are sequentially involved in levels.
o Nodal metastasis is the most important prognostic correlate.
o 95% of women who die of breast cancer have distant metastasis.
o Women with node-negative disease had <30% recurrence, which
is up to 75% for node-positive disease.
 Distant metastasis;
o Successful implantation of metastatic foci occurs after a primary
cancer exceeds 0.5cm, which corresponds to 27th cell doubling.
o It may seed pulmonary circulation via;
 Axillary veins, and
 Intercostals veins, or
 Baston’s plexus which courses the length of vertebral
column.
o Common sites in order of frequency:
 Bone; 70% (lumbar vertebra, pelvic bones, long bones)
 Lung and pleura; 20-30%
 Soft tissues; 5-15%
 Liver; 10-12%
 Brain and adrenals
o Brain metastases are more likely to be seen with triple receptor
negative cancer (ER, PR, & HER2 receptor negative).
o For 10 years after initial treatment, distant metastases are the
most common cause of death.
o Estrogen receptor-negative cancers are more likely to recur in the
first 3-5 years.

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o Estrogen receptor-positive cancers have recurrence which drops

off more slowly.

Carcinoma in-situ
It is when the tumor did not yet invade the basement membrane. There are two
types of breast carcinoma in-situ;
 Ductal carcinoma in-situ (DCIS), and
 Lobular carcinoma in-situ (LCIS)
DCIS is more commonly diagnosed than LCIS by a ratio of >2:1. The clinical and
pathologic characteristics of the two are listed in the table below.
DCIS follows four sequential growth patterns;
 Papillary growth pattern,
 Cribriform growth pattern,
 Solid growth pattern, and then
 Comedo growth pattern
Characteristics LCIS DCIS
Age 44-47 (45) 54-58
Sex Only in female (12X more 5% of male breast ca
common in whites than
blacks)
Incidence 2-5% 5-10%
Clinical signs None Mass, pain, nipple discharge
Origin TDLU Epithelium lining minor ducts
Mammographic signs None Microcalcifications
Premenopausal 2/3 1/3
Multicentricity 60-90% 40-80%
Bilaterality 50-70% 10-20%
Histology Distortion of TDLU Comedo (worst),
Normal nuclear to Intermediate (mixture of noncomedo
cytoplasm ratio patterns)
Cytoplasmic mucoid Noncomedo (solid, cribriform, or
globules papillary)
Microcalcifications
Axillary metastasis 1% 1-2%
Incidence of 5% 2-46%
synchroneous
invasive carcinoma
Risk of invasive 25-35%; a risk rather 5-fold; anatomical precursor of
cancer than anatomic precursor; invasive ductal carcinoma
65% will progress to
invasive ductal
carcinoma.
Multicentricity: occurrence of a second breast cancer outside the breast quadrant of primary cancer or
at least 4cm away. Multifocality: occurrence of a second cancer within the same breast quadrant as
primary cancer or within 4cm of it. TDLU: terminal duct lobular unit.

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Invasive breast carcinoma

Paget’s disease of the nipple
 Present as a chronic, exematous eruption of the nipple.
 Associated with DCIS (and sometimes invasive cancer).
 Biopsy: cells identical to the underlying DCIS (pagetoid feature/change).
 Pathogmonic: large, pale, vacuolated cells (Paget cells) in rete ridges.
 Confused with superficial spreading melanoma. Differentiation is based
on the presence of S100 in melanoma and CEA in Paget’s disease.
 Treatment: lumpectomy or mastectomy based on the extent of
involvement, presence of DCIS or invasive cancer underneath.
Sirrhous carcinoma (non-special type)
 80% of invasive breast cancers.
 Axillary metastasis = 25% in screening and 60% in symptomatic cases.
 Most common in peri- and postmenopausal women in 5th to 6th decade.
 Presents as a solitary, firm mass with poorly defined margins.
 75% are hormone receptor positive.
 Poorer prognosis than special types.
Medullary carcinoma
 4% of invasive breast cancers.
 A frequent phenotype of BRCA1 hereditary disease.
 Soft and hemorrhagic, may have rapid increase in size due to necrosis &
hemorrhage.
 Bulky and positioned deep within the breast.
 Microscopic characterstics;
o Dense lymphoreticular infiltrate
o Large poorly differentiated pleomorphic nuclei with active mitosis.
o Sheet like growth pattern with minimal/no ductal or alveolar
differentiation.
 Bilaterality = 20%.
 50% associated with DCIS.
 <10% demonstrate hormone receptors.
 Better prognosis than NST and invasive lobular carcinoma.
Mucinous/colloid carcinoma
 2% of invasive breast cancers.
 Present in the elderly as bulky tumor.
 Defined by extracellular pools of mucin around cancer cells.
 Over 90% display hormone receptors.
 Lymph node metastasis = 33%.

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 5- and 10-year survival rates are 73% and 59% respectively.

Papillary carcinoma
 2% of invasive breast cancers.
 Presents in the 7th decade.
 Small; rarely attain a size of 3cm in diameter.
 Defined by papillae with fibrovascular stalks and multilayered epithelim.
 87% express hormone receptors.
 5- and 10-year survival rates are similar to mucinous and tubular
carcinoma.
Tubular carcinoma
 2% of invasive breast cancers.
 Usually diagnosed in perimenopause and early menopause.
 Histology: haphazard array of small, randomly arranged tubular elements.
 94% express hormone receptors.
 10% will develop axillary metastasis.
 Distant metastasis is rare.
 Long-term survival approaches 100%
Invasive lobular carcinoma
 10% of invasive breast cancers.
 Histology: small cells with round nuclei, inconspicuous nucleoli, and scant
cytoplasm. Special stains may show intracytoplasmic mucin which may
displace the nucleus (signet-ring cell carcinoma).
 Presentation: from inapparent to involvement of entire breast.
 Frequently multifocal, multicentric, and bilateral.
 Insidious growth pattern and subtle mammographic features.
 Over 90% express estrogen receptor.

Diagnosis of breast cancer

Fig: Triple assessment of breast symptoms

Clinical features
 Lump in the breast; 30%.
 Other less common features:

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o Breast enlargement or asymmetry,

o Nipple changes, retraction or discharge,
o Ulceration or erythema of breast skin,
o Axillary mass.
 Breast pain is usually associated with benign breast disease.
 Examination;
o Symmetry, size, and shape
o Evidence of edema; peaud’ orange, nipple retraction, erythema,
or skin retraction.
o Lymphadenopathy

Fig: Benign and malignant nipple discharges

Discharges from the nipple (principal causes are in bold)
Discharge from the surface Discharge from more than one duct
Paget’s disease Blood-stained:
Skin diseases (eczema, Carcinoma
psoriasis) Ectasia
Rare causes (e.g. chancre) Fibrocystic disease
Discharge from a single duct Black or green:
Blood-stained: Duct ectasia
Intraduct papilloma Purulent:
Intraduct carcinoma Infection
Duct ectasia Serous:
Serous (any colour): Fibrocystic disease
Fibrocystic disease Duct ectasia
Duct ectasia Carcinoma
Carcinoma Milk:
Lactation
Rare causes (hypothyroidism, pituitary tumour)

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Fig: The relationship of carcinoma of the breast to breast quadrants; the most
common being the upper outer quadrant
Imaging techneques
 Mammography; suggestive diagnosis
o Solid mass with or without stellate features,
o Asymmetric thickening of breast tissue
o Clustered microcalcifications
 Ductography: the primary indication is bloody nipple discharge.
o Small filling defects: intraductal papillomas
o Irregular masses or multiple intraluminal filling defects: cancers.
 Ultrasonography
o Second only to mammography for;
 Resolving equivocal mammographic findings.
 Defining cystic masses and
 Demonstrating echogenic qualities of specific solid
lesions
o Cysts: smooth surfaces with echo-free center
o Benign: smooth contours, round or oval shapes, weak internal
echoes, and well-defined anterior and posterior margins.
o Breast cancer: irregular border.
o Also used to guide FNAC, and examination for nodal status.
o Ultrasound is not used for screening.
 MRI for high risk women and those with newly diagnoses breast cancer.
Breast biopsy
 Fine needle aspiration cytology
 Core biopsy: allows distinguishing CIS from invasive cancer.
 Open/excisional biopsy.
TNM staging of breast cancer
Primary tumor (T)

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 TX: Primary tumor cannot be assessed

 T0: No evidence of primary tumor
 Tis: Carcinoma in situ
 T1: Tumor ≤2 cm in greatest dimension
 T2: Tumor >2 cm but ≤5 cm in greatest dimension
 T3: Tumor >5 cm in greatest dimension
 T4: Tumor of any size with direct extension to the chest wall and/or to the
skin (ulceration or skin nodules)
Regional lymph nodes (N)
 NX: Regional lymph nodes cannot be assessed
 N0: No regional lymph node metastases
 N1: Metastases to movable ipsilateral level I, II axillary lymph node(s)
 N2: Metastases in;
o Ipsilateral level I, II axillary lymph nodes that are clinically fixed or
matted; or
o Clinically detected* ipsilateral internal mammary nodes in the
absence of clinically evident axillary lymph node metastases.
 N3: Metastasis in;
o Ipsilateral infraclavicular (level III axillary) lymph node(s) with or
without level I, II axillarylymph node involvement; or
o Clinically detected ipsilateral internal mammary lymph node(s)
with clinically evident level I, II axillary lymph node metastases; or
o Ipsilateral supraclavicular lymph node(s) with or without axillary
or internal mammary lymph node involvement
Distant metastasis (M)
 M0: No clinical or radiographic evidence of distant metastases
 M1: Distant detectable metastases as determined by classic clinical and
radiographic means and/or histologically proven larger than 0.2 mm
TNM stage groupings 5-year survival (%)
Stage0 TIS N0 M0 100
Stage IA T1 N0 M0 100
Stage IB T0 N1 M0 100
T1 N1 M0
Stage IIA T0 N1 M0 92
T1 N1 M0
T2 N0 M0
Stage IIB T2 N1 M0 81
T3 N0 M0
Stage IIIA T0 N2 M0 67
T1 N2 M0
T2 N2 M0
T3 N1 M0
T3 N2 M0

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Stage IIIB T4 N0 M0 54
T4 N1 M0
T4 N2 M0
Stage IIIC Any T N3 M0 Not available, this stage
was defined recently
Stage IV Any T Any N M1 20

Breast cancer therapy

In-situ breast cancer (stage 0)
Lobular carcinoma in-situ
 Observation
 Chemoprevention
 Risk-reduction surgery (bilateral total mastectomy)
Ductal carcinoma in-situ
 Gold standard = mastectomy + SLND
 Limited disease = breast conserving therapy (BCT)
 Non-palpable DCIS = excisional biopsy with image guided needle
localization.
 Adjuvant tamoxifen for ER-positive disease
Breast conserving therapy (BCT)
 Resection of primary tumor
o Segmental mastectomy
o Lumpectomy
o Partial mastectomy
o Wide local excision
o Tylectomy
 Adjuvant radiation; reduces recurrences
 Assessment of regional nodal status
Early invasive breast cancer (stage I & II)
 Breast conserving therapy (BCT)
o Equivalent survival rate to total mastectomy
o Better quality of life, and psychological and esthetic outcomes
o Standard surgery for early invasive breast cancer
o Contraindications;
 BRCA mutation carriers (absolute contraindication)
 Multicentric disease
 Prior radiation to breast or chest wall
 Persistently positive surgical margins after re-excision
 Scleroderma or SLE
 Total mastectomy is done when BCT is contraindicated.
 Sentinel lymph node dissection (SLND) for clinically negative nodes
 Axillary lymph node dissection (ALND) for clinically positive nodes
 Chemotherapy;
o Doxorubicin, cyclophosphamide, and paclitaxel

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o Add trastuzumab for HER-2/neu positive, node positive cancer

o Tamoxifen for ER-positive diseases.
Advanced local-regional breast cancer (stage III)
 Neoadjuvant (preoperative) therapy reduces local-regional cancer burden
enough to permit subsequent surgery to control local-regional disease.
o Chemotherapy; especially for estrogen receptor negative tumors
o Radiotherapy; especially for estrogen receptor positive tumors
 Surgical options;
o Modified radical mastectomy: standard surgery.
o BCT; only for selected patients with stage IIIA disease in whom
neoadjuvant chemotherapy has reduced tumor size to permit
BCT.
 Surgery is followed by adjuvant radiation.
 Chemotherapy is used to maximize distant disease-free survival, whereas
radiation therapy is used to maximize local-regional control and disease-
free survival.
Distant metastasis (stage IV)
 Accounts for 25% of newly diagnosed breast cancers in our setup
(Hawassa University Comprehensive Specialized Hospital).
 Treatment is not curative, but it can prolong survival and enhance quality
of life.
 Endocrine therapy associated with minimal toxicity; candidates:
o Hormone receptor positive cancers
o No visceral crisis (immediately life threatening disease)
 Cytotoxic chemotherapy; candidates:
o Hormone receptor negative cancers
o Visceral crisis
o Endocrine-resistant disease
 Palliative treatment of metastatic disease
o Surgical or radiation treatment for patients with anatomically
localized metastatic problems;
 Brain metastasis, pleural effusion, pericardial effusion,
biliary obstruction, ureteral obstruction, impending oe
existing pathologic fracture of long bones, spinal cord
compression, and painful bone metastasis.
o Bisphosphonates for patients with bone metastasis
 Surgical resection of primary tumor may result in better prognosis and
palliation of symptoms; but it is a matter of debate.

Surgical therapies-Mastectomies
Simple/total mastectomy

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 Removal of the entire breast; sometimes with SLND, but axillary contents
are undisturbed.
 Indications;
o Prophylactic mastectomies
o Large DCIS
Modified radical (Patey) mastectomy (MRM)
 Removes all breast tissue, the nipple-areola complex, skin, the levels I, II
and III axillary lymph nodes, and the pectoralis minor.
 The pectoralis minor which was divided and removed by Patey may be
simply divided, giving improved access to level III nodes, and then left in-
situ or occasionally the axillary clearance can be performed without
dividing pectoralis minor.
 Anatomic boundaries;
o Lateral: anterior margin of latissmus dorsi
o Medial: midline of sternum
o Superior: subclavius muscle
o Inferior: caudal extension of breast, 2-3cm inferior to
inframammary fold
 This procedure preserves;
o Pectoralis major
o Lateral pectoral nerve
o Medial pectoral nerve
 It is a standard surgery for advanced local-regional invasive breast cancer
(stage III).
Radical mastectomy (Halsted radical mastectomy)
 Removes all breast tissue and skin, the nipple-areola complex, the
pectoralis major and pectoralis minor muscles, and the level I, II, and III
axillary lymph nodes.
Others
 Skin sparing mastectomy
 Nipple-areolar sparing/subcutaneous mastectomy
o Tumor located more than 2–3 cm from the border of the areola,
o Smaller breast size,
o Minimal ptosis,
o No prior breast surgeries with periareolar incisions,
o Body mass index less than 40 kg/m2,
o No active tobacco use,
o No prior breast irradiation, and
o No evidence of collagen vascular disease.
 Prophylactic mastectomy

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 Extended radical mastectomy: is radical mastectomy + intrapleural en

bloc resection of internal mammary lymph nodes by sterna splitting.

Non-surgical therapies
Radiation therapy
 Used for all stages of breast cancer depending on whether the patient is
undergoing BCT or mastectomy.
 It is also given as an adjuvant therapy for stage III breast cncer.
Chemotherapy
 Women with positive nodes and cancers ≥0.5cm in size.
 Women with negative nodes and cancers 0.6-1.0cm in size with
unfavourable prognostic features like;
o Vascular invasion
o Higher nuclear grade
o High histopathologic grade
o HER-2/neu overexpression
o Negative hormone receptor status
 Women hormone receptor negative and cancers >1cm in size.
 Preoperative chemotherapy for stage III breast cancer.
 Special-type cancer that is >3cm.
Hormonal/endocrine therapy
 Antiestrogen therapy (tamoxifen)
 Aromatase inhibitors (anastrozole and letrostrozole)
 Ablative endocrine therapy (oophrectomy, adrenalectomy and/or
hypophysectomy)
 Anti-HER2/neu therapy (trastuzumab

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Rare Cases of Breast Cancer

Male breast cancer
 Fewer than 1% of all breast cancers occur in men.
 Jewish and blacks have the highest incidence.
 Preceeded by gynecomastia in 20% of men.
 Associated with radiation exposure, estrogen therapy, testicular
feminizing syndromes, and Klinefelter’s syndrome.
 Types of cancers;
o DCIS: <15%
o Infiltrating ductal carcinoma: >85%
o Special-type cancers are rare.
 Men do worse because of the more advanced stage at diagnosis.
 Treatment is surgical; the most common being MRM.

Phylloides tumors
 Usually occur in women >40 years of age.
 Classified as benign, borderline, and malignant.
 Mammographic differentiation of the three types is difficult.
 Sharply demarcated from the breast tissue.
 Connective tissue composes the bulk of these tumors.
 Cystic areas represent sites of infarction and necrosis. These gross
alterations give the gross cut tumor surface its classical leaf like
(phylloides) appearance.
 Have greater cellular activity than fibroadenomas.
 Always monoclonal; fibroadenomas can be either mono- or polyclonal.
 Treatment;
o Surgical resection
o Large phylloides tumors may require mastectomy.

Inflammatory breast cancer

 An ominous clinical category of breast cancer associated with diffuse
tumor involvement of the lymphatic channels within the breast and
overlying skin.
 Accounts for <3% of breast cancers.
 Stage IIIB by definition.
 Characterized by skin changes; brawny induration, erythema with raised
edges, and edema (peaud’ orange).
 Present as a painful, swollen breast, which is warm with edema.

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 Clinical differentiation is difficult: especially from bacterial infection and

advanced scirrhous carcinoma.
 The pathologic hallmark of inflammatory cancer is the presence of tumor
cells within dermal lymphatics.
 More than 75% present with palpable axillary lymphadenopathy and
distant metastasis in 25% at diagnosis.
 Treatment;
o Neodjuvant chemotherapy with anthracyclin containing regimen
and then surgery: MRM.
o Adjuvant chemotherapy may be indicated.
o Adjuvant radiation to supraclavicular, internal mammary and
axillary lymph nodes.
o 5-year survival after treatment approaches 30%
Others
 Squamous cell (epidemoid) carcinoma
 Adenoid cystic carcinoma
 Apocrine carcinomas
 Sarcomas
 Lymphomas
Relative risk of invasive breast cancer in benign breast conditions
No increased risk Adenosis, sclerosing or florid
Apocrine metaplasia
Cysts
Duct ectasia
Fibroadenoma
Fibrosis
Hyperplasia
Mastitis
Periductal mastitis
Squamous metaplasia
Slightly increased risk (1.5-2 times) Hyperplasia, moderate or florid, solid or papillary
Papilloma with a fibrovascular core
Moderately increased risk (5 times) Atypical hyperplasia; ductal or lobular
Insufficient data to assign a risk

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CHAPTER FOUR -THE THYROID

Surgical Anatomy and Physiology

Anatomy of the thyroid
Embryology
 The thyroid gland develops from a median down growth of a column of
cells from the pharyngeal floor between the first and second pharyngeal
pouch around the third week of gestation, subsequently marked by the
foramen caecum of the tongue. The calcitonin producing parafollicular or
C cells are derived from ultmobranchial bodies (neuroectoderm) from the
fourth pharyngeal pouch.
 The parathyroid glands develop from third and fourth pharyngeal pouches.
The thymus also develops from third pouch.
Gross anatomy of the thyroid
 Butterfly shaped, brown in color, firm in consistency, and located posterior to
strap muscles.
 Normal weight is approximately 20 grams.
 It has two lobes connected in the midline by an isthmus.
 A pyramidal lobe is present in about 50% of patients.
 It has a true capsule which sends septa on to the gland forming pseudolobules
and condenses posteriorly to form posterior suspensory or Berry’s ligament.
 Arterial supply
o The superior thyroid artery arises from ipsilateral external carotid
artery and divides in to anterior and posterior branches at the apices
of the gland.
o The inferior thyroid artery arises from thyrocervical trunk. It crosses
RLN, necessitating identification of RLN before ligation.
o Thyroida ima artery arises from aorta or innominate in 1-4% of
individuals.
 Venous drainage
o Superior thyroid vein: drains in to IJV.
o Middle thyroid vein/s: least consistent, drains in to IJV.
o Inferior thyroid vein: forms plexus and drains into brachiocephalic
veins.
o Kocher’s vein may be present which drains lower or middle thyroid.
 Innervations
o Vagus nerve
 Recurrent laryngeal nerve
 Superior laryngeal nerve
 Parasympathetic: via branches of laryngeal nerves.
o Sympathetic innervation is provided by fibers from the superior and
middle cervical sympathetic ganglia.
 Lymphatic system
o The thyroid gland is endowed with an extensive network of lymphatics.

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o There are two compartments

 Central: medial to carotid sheath
 Lateral: lateral to carotid sheath

Fig: Levels of lymphatic system of the t hyroid

The lymphatic system of the thyroid: levels

Level I IA: submental
IB: submandibular
Level II Upper jugular group
Level III Middle jugular group
Level IV Lower jugular group
Level V Posterior triangle group including supraclavicular nodes
Level VI Central neck nodes (pretracheal or Delphic nodes)
Level VII Anterior mediastinal nodes (prelaryngeal nodes)

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Fig: Anatomy of the thyroid

Physiology of the thyroid

 Iodine metabolism
o Daily requirement is 0.1mg which can be derived from the foods such
as fish, milk, and eggs or additives in bread or salt.
o In the stomach and jejunum, iodine is rapidly converted in to iodide
and absorbed in to blood stream.
o Iodine is actively transported in to the thyroid follicular cells.
o The thyroid stores >90% of the body’s iodine.
 Thyroid hormone synthesis
o Step 1; Iodide trapping (ATP dependent), through Na+/I- symporter.
Note that this symporter is also found in the placenta, the only other
site.
o Step 2; Oxidation of iodide in to iodine and iodination of thyrosine
residues on Tg to form iodothyrosines; catalyzed by thyroid
peroxidase (TPO)
o Step 3; Coupling reaction
o Step 4; Thyroglobulin (Tg) is hydrolysed to release free
iodothyrosines (T3 & T4), and mono- and diiodothyrosines.
o Step 5; Deiodination of mono- and di-iodothyrosines to yield iodine
which is reused.
o T4 is entirely produced by the thyroid gland; whereas only 20% of T3
is produced by the gland. Most of the T3 is produced by peripheral
deiodination of T4 in the liver, muscles, kidney, and anterior pituitary.

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o Thyroid hormones are transported in the serum bound to carrier

proteins; globulin, prealbumin, and albumin. Only about 0.02% of
thyroid hormone is free.
o T3 versus T4; T3:
 Is more potent
 Has much lower plasma level
 Is less tightly bound to serum proteins; enters tissues easily
 Three to four times more active
 Has shorter half life (1 day versus 1 week)
 Regulation
o HPT axis (TRH and TSH)
o Autoregulation: Wolff-Chaikoff effect.
o Epinephrine and HCG stimulate thyroid hormone synthesis.
o Inhibition of thyroid hormone synthesis;
 Antithyroid drugs
 Wolff-Chaikoff effect:excessively large doses of iodide may
lead to initial increased organification, followed by
suppression. This stunning effect is transient.
 Corticosteroids: suppress HPT axis, inhibit peripheral
conversion, and lower serum TSH. Act rapidly!
 Beta blockers; they do not directly inhibit thyroid hormone
synthesis, but they are valuable in controlling peripheral
sensitivity to catecholamines.
 Thyroid hormone function
o Thyroid hormone receptors are in the nucleus; and similar to nuclear
receptors for glucocrticoids, mineralocorticoids, vitamin –D, estrogens,
and retinoic acid.
o Thyroid affects almost every system in the body and the effect is
usually catabolic.
 Brain development and skeletal maturation
 It increases BMR (the minimum possible energy required to
sustain life without any activity), oxygen consumption, and
heat production.
 Positive inotropic and chronotropic effects on heart.
 Maintain respiratory centers in the brain.
 Increase GI motility.
 Increase protein and bone turnover and speed of muscle
contraction and relaxation.
 Increase glycogenolysis, hepatic gluconeogenesis, intestinal
glucose absorption, and cholesterol synthesis and
degradation.
 Calcitonin
o Secreted by parafollicular cells of the thyroid.
o It lowers serum calcium in mammals.
o Its effects in human are minimal.

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Diagnostic Modalities
Tests of thyroid function
A multitude of different tests are vailable. No single test is sufficient to assess
thyroid functions in all conditions. TSH is the only test necessary in most patients
with thyroid nodules that clinically appear to be euthyroid.
Tests Normal values and interpretations
Serum TSH 0.5-5μU/mL
T4 hormone
Total 55-150nmol/L
Free 12-28pmol/L
T3 hormone
Total 1.5-3.5nmol/L
Free 3-9pmol/L
Serum TRH TSH should increase by 6μIU/mL from base line after 30-60’ of
administration of 500μg TRH IV.
Thyroid Include anti-Tg, anti-TPO or antimicrosomal, and TSI
antibodies Anti-Tg and anti-TPO do not determine thyroid function.
Elevated in autoimmune thyroid disorders such as Hashimoto’s
thyroiditis (95%) and Grave’s disease (75% and 90% respectively)
Serum Increases dramatically in thyroiditis, Grave’s disease, and TMNG. It
thyroglobulin is most important in monitoring patients with differentiated thyroid
cancers for recurrence, particularly after total thyroidectomy and RAI
ablation.
Serum calcitonin 0.4pg/mL
A sensitive marker for MTC

Thyroid imaging
Radionuclide imaging
 I123 is used for diagnostic purposes and have a half life of 12-14 hours. We
use gamma rays.
 I131 is used for therapeutic purposes and have a half life of 8-10 days. We
use beta rays and sometimes gamma rays.
 Gives information about the size, shape and functional activity.
 Based on functional activity;
o Hot nodules (5%); <5% risk of malignancy
o Warm nodules (10%); 10% risk of malignancy
o Cold nodules (80%); 20% risk of malignancy

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Ultrasonography
 Non-invasive, portable, no radiation.
 Distinguish solid from cystic lesions. Solid lesions have higher risk for
being malignant.
 Size and multicentricity of swelling
 Malignancy risk stratification based on echotexture, shape, borders,
presence of calcifications, and vascularity
 Guides FNAB.
 Assessing cervical lymphadenoahty
CT/MRI
 Evaluating the extent of large, fixed, or substantial goiters, and their
relationship to the airway and vascular structures.
Neck and thoracic inlet x-ray
 To rule out retrosternal extension

Fine needle aspiration biopsy (FNAB)

It is the investigation of choice in discrete thyroid swellings. It has excellent patient
compliance, readily repeatable, simple and rapid. It can be performed with or
without ultrasound guidance. Stained with Papanicolaou’s or Wright stain
Ultrasound guidance is required for
 Nodules that are difficult to palpate
 Cystic or solid nodules that recur after initial aspiration
 Multinodular goiters
69% are benign, 4% are malignant, 17% are non-diagnostic, and 10% are the
rest – indeterminate (AUS/FLUS, FN or suspicious for FN, and suspicious for
malignancy.)

Bethesda FNAB report;(risk of malignancy is based on Uptodate-Bethesda 2017)

1. Thy1: Non-diagnostic (2-20% - 17%)
 Aspiration of <10 follicles or acellular specimen, cystic fluid, or blood
or clotting artifact.
 To be deemed diagnostic, 10-15 follicles should be aspirated.
 The risk of malignancy is 5-10%.

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 Treatment: repeat FNAB with ultrasound guidance.

2. Thy1c: Benign (cystic or colloid/follicular nodule) (60-70%)
 Most common: follicular nodule (adenomatoid, colloid, and follicular
nodule.). Others include Hashimoto’s thyroiditis, and granulomatous
thyroidtis.
 False negative: 3%
 Risk of malignancy: 0-3%
 Treatment: aspirate cystic lesions three times before moving to
surgery. Observe colloid nodules and if there is continued growth or
compressive symptoms, do surgery with or without prior repeat FNAB.
3. Thy2: AUS/FLUS (3-6%)
 Risk of malignancy is 10-30%.
 Repeat FNAB. Clinical evaluation or surgery may be apt because of
worrisome clinical and ultrasound features.
4. Thy3: Follicular neoplasia or suspicious for follicular neoplasm
 They might be follicular carcinomas.
 Suspicion for follicular neoplasm is preferred by some laboratories
because 35% turn out not to be follicular neoplasm.
 Risk of malignancy = 25-40%
 Treatment: lobectomy
5. Thy4: Suspicious for malignancy
 Carcinomas with only subtle features of malignancy. Also includes
lesions suspicious for medularu carcinoma and lymphoma
 Risk of malignancy = 60% (50-75%)
 Treatment: lobectomy or near total thyroidectomy
6. Thy5: Malignant (4%)
 Risk of malignancy = 97-99%
 Treatment: near total or total thyroidectomy

Antithyroid medications
Antithyroid medicatios
Thioamides Iodine
Propylthiouracil (PTU) Lugol’s solution
Methimazole SSKI
Carbimazole KI
Anion inhibitors Radioactive iodine (I131)
Thiocyanate Other drugs: propranolol, steroids,
Percholate amiodarone

Thionamide class (PTU, methimazole and carbimazole)

 They inhibit oxidation, organification, and coupling. PTU has an added effect
of inhibiting peripheral conversion, and because of this, PTU is the popular
choice for rapid treatment of hyperthyroid conditions like thyroid storm.
 They do not inhibit release of preformed hormones and so they have slow
onset of action; 3-4 weeks.

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 Methimazole is generally preferred because it is administered once per day.

Carbimazole is converted to the active metabolite methimazole.
 PTU is preferred in pregnancy and lactation because it has lower risk of
transplacental transfer.
 Dosages
o PTU = 100-300mg TID
o Methimazole = 10-30mg TID then QD.
o Carbimazole = 10mg TID.
 Side effects
o Common minor: pruritus, rash, urticaria, arthralgia, arthritis, fever,
nausea, vomiting.
o Teratogenicity: more severe with methimazole and carbimazole
compared with PTU.
o Rare but serious effects
 Agranulocytosis
 Hepatotoxicity
 ANCA-positive vasculitis
 Pancreatitis
o Management of the side-effects
 Stop the medication & seek medical care.
 Agranulocytosis: admit the patient, stop the medication, and
put them on broad spectrum antibiotics. Surgery should be
withheld till granulocyte count reaches 1000/mm3.
 When the drugs are discontinued, 40-80% of patients develop recurrence after
1-2 years.
 Indications for antithyroid medications;
o Preparation for RAI ablation
o Preparation for surgery
o Curative treatment
 Small, non-toxic goiters <40g
 Mildly elevated T3 and T4 levels
 Negative/low titers of TSI
 Rapid decrease in size with antithyroid medications.
Iodine in the treatment of hyperthyroidism
 Mechanisms of action
o Acute inhibition of thyroid hormone release
o Inhibition of organification (Wolff-Chaikoff effect)
o Decrease the size and vascularity of the thyroid
 N.B. Since they inhibit both release and synthesis, their onset of action is very
rapid (2-7 days).
 Patients with Grave’s disease are more sensitive to its inhibitory effects.
 Primarily used with short term (often 1-2 weeks, but may be up to 4-6 weeks)
for
o Pre-op for thyroidectomy in Grave’s disease
o As adjunctive in Grave’s disease
o Thyroid storm
 Formulations

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o Lugol’s solution; 5% iodine and 10% KI: 6.25mg iodide/iodine per

drop (10*-30 drops)
o Saturated solution of KI (SSKI): 50mg iodide/drop
o KI tablets: 130mg
Radioactive iodine (RAI) therapy
 8-12 mCi PO.
 It ablates the gland within 6-18 weeks.
 Avoids surgery and concomitant risks, reduce cost, and is easy.
 Indications
o Older patients with small or moderate sized goiters
o Those who have relapsed after medical or surgical therapy
o Those in whom antithyroid drugs and surgery are contraindicated.
 Absolute contraindications
o Pregnant women (planning pregnancy within 6 months of treatment)
o Breast feeding women
 Relative contraindications
o Young patients (children and adolescents)
o Multinodular goiters with toxicity.
o Those with ophthalmopathy
 Complications of RAI therapy are depicted in the following table.
Complications of RAI (I131) therapy
Acute Chronic
Neck pain, swelling, Bone marrow suppression Increasd risk of cancer
tenderness Leukemia Anaplastic thyroid
Thyroiditis Ovarian/testicular damage, cancer
Sialadenitis infertility Gastric cancer
Hemorrhage Increased spontaneous Hepatocellular cancer
Cerebral edema abortion rate Lung cancer
Vocal cord paralysis Pulmonary fibrosis Breast cancer
Nausea and vomiting Chronic sialadenitis, Bladder cancer
Bone marrow suppression nodules, taste dysfunction hypoparathyroidism

Anion inhibitors: thiocyanate, percholate

 Block the uptake of iodine through competitive inhibition of the iodine
transporter.
 Cause aplastic anemia, so are rarely used clinically.
Beta blockers (propranolol 20-40mg QID/TID)
 For all patients with symptomatic thyrotoxicosis, all elderly patients, patients
with coexistent cardiac disease and patients with resting HR>90bpm.
 They reduce peripheral manifestations of hyperthyroidism and decrease
peripheral conversion of T4 to T3.

Thyroidectomies
“Thyroidectomy is a bloody surgery”
Preoperative preparations
 Antithyroid drugs till operation day

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 Lugol’s solution or SSKI 7-10 days preoperatively (3 drops twice daily)

 In urgent surgery and in patients with reaction to antithyroid drugs in
which it is not possible to render the patient euthyroid before surgery, the
patient can be prepared with beta blockade and KI alone. Steroids can be
a useful adjunct in this situation.
The extent of thyroidectomy to be performed used to be determined by the desired
outcome (risk of recurrence vs. euthyroidism) and surgeon experience.
Indications
 When RAI is contraindicated
o Confirmed cancer or suspicious thyroid nodules
o Young
o Desire to conceive soon
o Severe reaction to antithyroid medications
o Large goiters >80g causing pressure symptoms
o Reluctant to undergo RAI therapy
 Smokers with moderate to severe Grave’s disease
 Desiring rapid control of hyperthyroidism
 Poor compliance to antithyroid medications.
Types of thyroidectomies;
 Total thyroidectomy = 2 X total lobectomy + isthmusectomy
o Leaves <1g of thyroid tissue behind.
 Near total thyroidectomy = 2 X subtotal lobectomy + isthmusectomy
o Leaves 1-4g of thyroid tissue behind
 Subtotal thyroidectomy
o Leaves 4-7g of thyroid tissue behind
o Two types
1. Bilateral subtotal thyroidectomy (remenant tissue left on
both sides)
2. Hartley-Dunhill procedure (total lobectomy +
isthmusectomy + subtotal lobecctomy)
o Indicated for the rest of the patients.
 Lobectomy = total lobectomy + isthmusectomy
Complications of thyroidectomies
 Hemorrhage
o Intraoperative: Lugol’s solution
o Hematoma: immediately release the stitch and then OR.
 Upper airway obstruction
 RLN injury
 Superior laryngeal nerve injury
 Thyroid insufficiency
 Parathyroid insufficiency
o Present 2-5 days after surgery with hypocalcemia
o The most frequent complication of total or near-total
thyroidectomy. It is rare following lobectomy.
o Transient hypoparathyroidism occurs in up to 20% of patirnts,
while permamnent one occurs in 0.8-3 %.

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o The hallmark of acute hypocalcemia is tetany: both muscular

(peripheral neuromuscular irritability) and sensory dysfunction;
 Mild: peri-oral numbness, paresthesias of hands and feet,
muscle cramps.
 Severe: carpopedal spasm, laryngospasm, and focal or
generalized seizures.
o Trouseau and Chevostek sign is a late feature.
o Rx. Slow calcium gluconate infusion.
 Thyrotoxic crisis (thyroid storm)
 Wound infection
 Hypertrophic scar or kelloid scar
 Stitch granuloma
Indications for operation in thyroid swellings
Neoplasia FNAC positive Thy 3-5
Clinical presentation Age
Male sex
Hard texture
Fixity
RLN injury
Lymphadenopathy
Recurrent cyst
Toxic adenoma
Pressure symptoms
Cosmesis
Patient interest

Neck dissection for nodal metastases

 Central neck dissection
o Dissection of dissection of lymph nodes medial to the carotid sheath.
o They are frequently involved in patients with PTC, MTC, and hurthle
cell carcinoma.
o Preserve RLN and parathyroids.
 Lateral neck dissection
o To remove the lateral compartment nodes.
o Along the posterior border of sternocleidomastoid muscle.

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Disorders of Thyroid Gland

Disorders of The Thyroid Gland
Benign Non-toxic Simple
goiter Nodular
Developmental anomalies Thyroglossal duct cyst and sinus
Lingual thyroid
Ectopic thyroid
Pyramidal lobe
Hyper- Increased Grave’s*, TMNG*, toxic adenoma*, drugs
thyroidism hormone (amiodarone, iodine), struma ovarii, hydatiform
synthesis mole, TSH-secreting pituitary adenoma,
[thyroid cancer]
Releases of Thyroiditis (acute phase of Hashimoto’s and
preformed subacute thyroiditis), factitious (iatrogenic),
hormone hamburger thyrotoxicosis
Hypo- Primary Iodine deficiency*, Hashimoto’s thyroiditis*, RAI
thyroidism therapy*, postthyroidectomy*, excessive iodine
intake, subacute thyroiditis, medications
(antithyroid, lithium), dyshormonogenesis
Secondary Pituitary tumor, pituitary resection or ablation
Tertiary Hypothalamic insufficiency, resistance to
thyroid hormone.
Solitary Almost all thyroid swellings present with solitary nodule except puberty
nodule goiters, colloid goiters, diffuse toxic goiter (Grave’s), & multi-nodular goiter.
Bethesda classification for thyroid FNAB;
 Non-diagnostic: (2-20%) 1-4% risk of malignancy
 Benign: 60-70%. The most common lesion is follicular nodule.
o Cyst
o Colloid nodule
 AUS/FLUS: (3-6%) the risk of malignancy is 15-35% for FLUS and
60-75% for AUS.
 FN/suspicious for FN: nodules that might be follicular carcinomas.
Up to 35% risk of malignancy
 Suspicious for malignancy: risk of malignancy is >60%
 Malignant
Malignant  Follicular epithelium
 Papillary carcinoma: differentiated (80%)
 Follicular carcinoma: differentiated (10%)
 Anaplastic carcinoma: poorly differentiated (1%)
 Parafollicular ‘C’cells: medullary carcinoma (5%)
 Lymphoid cells: lymphoms (<1%)
 Metastatic and local infiltration

Developmental abnormalities
Thyroglossal duct cyst and sinus
 The most common congenital cervical anomaly.
 80% are found in juxtaposition to the hyoid bone.
 Usually asymptomatic but become symptomatic when infected.

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 1-2cm, smooth, well defined, middline neck mass which moves up with
protrusion of tongue.
 1% of thyroglossal duct cysts are found to contain cancer;
o 85% are papillary
o Squamous, hurthle cell, and anaplastic cancers are rare
o MTCs are not found.
 Treatment: Sistrunk operation
o En bloc cystectomy and excision of central hyoid bone.
Lingual thyroid
 Represents failure of median thyroid anlage to descend and may be the
only thyroid tissue present.
 Many of these patients develop hypothyroidism.
 Interventions are necessary for pressure symptoms or hemorrhage.
 Treatment
o Exogenous thyroid hormone
o RAI ablation with thyroid hormone replacement.
o Surgical excision is rarely needed.
Ectopic thyroid
 Normal thyroid tissue can be found anywhere in the central neck
compartment.
 Thyroid tissue has been observed adjacent to aortic arch, upper
pericardium, or interventricular septum.
 Thyroid tissue lateral to carotid sheath and jugular vein, previously termed
lateral aberrant thyroid, almost always reprent metastatic thyroid cancer in
lymph nodes. The ipsilateral thyroid usually contains PTC.
Pyramidal lobe
 In 50% of individuals.
 It is a remnant of duct thyroglossal duct that contains thyroid tissue and
projects up from the isthmus.
 It is normally not palpable, but is enlarged and palpable in Grave’s
disease, diffuse nodular goiter, or lymphocytic thyroiditis.

Fig: Classification of goiters

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Simple/non-toxic goiter
 Epidemiology of goiters in general
o Worldwide, the most common cause of goiter is iodine deficiency.
o No racial predilection exists.
o Male to female ratio = 1:4
o Most goiters are benign, causing only cosmetic disfigurement.
o Morbidity and mortality may result from compression of surrounding
structures, thyroid cancer, hyperthyroidism, or hypothyroidism.
o It can be diffuse, uninodular, or multinodular.
 Etiologies of goiters in general
o Elevated TSH secondary to thyroid hormone deficiency
 Inborn errors of thyroid hormone synthesis
 Iodine deficiency
 Goiterogens: cassava, cabbage
o TSH receptor antibodies: e.g. TSI
o Pituitary resistance to thyroid hormone
o Adenomas of the hypothalamus or pituitary gland
o Tumors producing HCG
o Thyroid tumors
o Inflammatory goiter

Etiologies of non-toxic goiter

Classification Specific etiology
Endemic Iodine deficiency, dietary goitrogens (cabbage, cassava, kelp)
Medications Iodine, amiodarone, lithium
Thyroiditis Subacute, chronic (Hashimoto’s)
Familial Dyshormonogenesis
Neoplasm Adenoma, carcinoma
Resistance -
to thyroid
hormone

 Goiterogens
o Vegetables of brassica family (cabbage, cassava, kale, rape)
 They contain thiocyanate, drugs such as PAS, and
antithyroid drugs
 Thiocyanates and percholates interfere with iodine trapping;
carbimazole and thiouracil interfere with oxidation &
organification.
o Iodides in large quantities are goiterogenic because they inhibit
organification.
 Pathophysiology of multinodular goiter
o Stage I: diffuse hyperplasia and hypertrophy of thyroid due to TSH
stmulation as a result of reduced thyroid hormones.
o Stage II: fluctuation of TSH levels cause some areas of the thyroid to
be overstimulated and are converted to active follicles.

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o Stage III: the follicles become necrotized due to inadequacy of blood

supply and many such necrotized follicles join to form multinodular
goiter. The nodules contain inactive tissue but the internodular tissue
is active.
 Clinical features
o Most are asymptomatic.
o As the goiter becomes large, compressive symptoms ensue.
o Positive Pemberton’s sign in substernal goiter.
o Sudden enlargement from hemorrhage may cause acute pain.
o Soft, diffusely enlarged gland (simple goiter) or nodule/s of various
size and consistency (nodular).
 Diagnostic tests
o Euthyroid
o FNAB in patients who have dominant nodule or one that is painful or
enlarging as carcinomas have been reported in 5-10% of multinodular
goiters.
 Treatment
o Most do not need treatment. Small benign euthyroid goiters do not
need treatment.
o TSH suppression (T4)
o Iodine administration for endemic goiters
o Surgery (near-total or total): indications
 Enlarging despite TSH suppression
 Obstructive symptoms
 Substernal extension
 Malignancy suspected or proven by FNAB
 Cosmetically unacceptable
 Patient wishes
o Patients require lifelong T4 after surgery.
Retrosternal goiter
 A goiter is considered intrathoracic if at least 50% of the thyroid tissue is
located intrathracically.
 Mediastinal goiters can be;
o Primary (1%): arise from ectopic mediastinal thyroid tissue.
o Secondary (99%): from downward extension of cervical thyroid
tissue.
 Virtually all intrathoracic goiters can be removed through cervical incision,
but median sternotomy may be required for patients who have;
o Invasive thyroid cancers
o Previous thyroid operation
o Primary mediastinal goiters without cervical thyroid tissue.

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Fig: Approach to a patient with goiter

Grave’s disease (Diffuse toxic goiter)

Introduction and epidemiology
 It is an autoimmune disease.
 The most common cause of hyperthyroidism in North America (60-80%)
 Has strong familiar predisposition.
 Female preponderance (7-8:1).
 The typical age range is 20-40 years. Most affected women are aged 30-
60 years.
Etiology

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 Postpartum state
 Iodine excess, lithium therapy
 Bacterial and viral infections.
 Genetic factors
Pathogenesis
 Once initiated, the process causes T-helper lymphocytes to stimulate B
lymphocytes to synthesize antibodies directed against thyroid hormone
receptor.
 These antibodies are
o TSI; thyroid stimulating immunoglobulins
o TSH-binding inhibiting immunoglobulins
 TSI stimulate thyrocytes to grow and synthesize excess thyroid hormone
which is the hallmark of Grave’s disease.
Pathology
 Macroscopically, the gland is diffusely enlarged with increase in
vascularity.
 Microscopically, the gland is hyperplastic with minimal colloid present.
Clinical features (three groups)
 Thyrotoxicosis (those related to hyperthyroidism)
o Heat intolerance
o Increased sweating and thirst
o Weight loss despite adequate appetite probably due to the
profuse sweating, diarrhea and restlessness.
o Symptoms of increased adrenergic stimulation; palpitation (and
high output heart failure), nervousness, fatigue, emotional liability,
hyperkinesis, & tremor.
o Increased bowel movements and diarrhea are the most common
GI symptoms.
o Amenorrhea, decreased fertility, and increased miscarriage.
o Children experience rapid growth with early bone maturation.
o Older patients may present with cardiovascular complications
such as AF and CHF.
o Physical examination
 Weight loss
 Facial flushing
 Warm and moist skin
 Tachycardia or AF
 Fine tremor, muscle wasting, and proximal muscle group
weakness with hyperactive tendon reflexes.
 Extrathyroidal manifestations (those specific to Grave’s disease)
o Ophthalmopathy: 50%
 Due to inflammation caused by cytokine release from
killer T lymphocytes and cytotoxic antibodies.
 Periorbital edema, conjunctival swelling, and congestion
(chemosis), proptosis, limitation of gaze.
o Dermopathy (pretibial myxedema: the name is a misnomer as it is
seen in thyrotoxicosis, not myxedema/hypothyroidism): due to

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deposition of glycosaminoglycans in the pretibial region and

dorsum of foot.
o Thyroid acropachy: subperosteal bone formation and swelling in
the metacarpals.
 Goiter
o Diffuse and symmetrical enlargement.
o Overlying bruit or thrill and loud venous hum.
Diagnosis
 Thyroid function test: suppressed TSH with or without elevated free T4 or
T3 level. If free T4 levels are normal, free T3 levels should be determined
(T3 toxicosis).
 If eye signs are absent radionuclide scan should be performed.
o Elevated uptake with diffusely enlarged gland is confirmative.
 Thyroid antibodies
o TPO and anti-Tg are elevated in up to 75%, but not specific
o TSI (THR-Ab) is diagnostic and is elevated in 90% of patients.
 MRI of orbits in evaluating Grave’s ophthalmopathy.
Treatment
There are three treatment modalities:
 Antithyroid drugs
 Thyroid ablation with radioiodine I131
o The mainstay of treatment in North America.
o Most patients become euthyroid after 2 months; 50% after 6
months.
o May lead to progression of Grave’s ophthalmopathy.
 Thyroidecctomy
o Goal: complete and permanent control with minimal morbidity.
o Pregnancy is a relative contraindication. Surgery (subtotal) is
best performed in the second trimester.
o Continue antithyroid medications for 7 days after operation. Why?
Half-life.
o Indications for total or near-total thyroidectomy (procedure of
choice)
 Coexistent thyroid cancer
 Refused RAI therapy
 Severe ophthalmopathy
 Life threatening reactions to antithyroid medications
o Subtotal thyroidectomy for the remaining patients.
 Ophthalmopathy stabilize or improve in most patients after total
thyroidectomy.

Toxic mutinodular goiter

 Occur in older individuals, who often have a prior history of a non-toxic
multinodular goiter.
 The presentation is often insidious.
 Hyperthyroidism may be precipitated by iodine-containing agents: Job-
Basedow hyperthyroidism.

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 Signs and symptoms are similar to Grave’s disease, except that

o Signs and symptoms come after long standing swelling
o Extrathyroidal manifestations are absent
o The goiter is multinodular; not diffuse
 Diagnostic tests
o TSH is suppressed and T4 & T3 are elevated.
o Increased RAI uptake, showing multiple nodules with increased
uptake and suppression of the remaining gland.
 Treatment
o Control hyperthyroidism
o Surgery; near-total or total thyroidectomy
o RAI: Unlike Graves' disease, in which the goal of radioiodine
therapy is destruction of the gland with eventual hypothyroidism,
most patients are euthyroid after radioiodine therapy (for TMNG
and toxic adenoma) because the radioiodine preferentially
accumulates in the hyperfunctioning nodules.

Toxic adenoma (Plummer’s disease)

 A single hyperfunctioning nodule.
 Typically in young patients who note recent growth of a long standing
nodule along with symptoms of thyrotoxicosis.
 Characterized by somatic mutations in the TSH-R gene.
 Already attain a size >3cm before hyperthyroidism occurs.
 Physical examination reveals a solitary thyroid nodule without palpable
tissue on the contralateral side.
 Rarely malignant.
 RAI shows a “hot” nodule with suppression of the rest of the gland. This
means unlike TMNG, the nodule is active but the surrounding tissue is
inactive.
 Treatment
o Smaller nodules: antithyroid medications or RAI
o Larger nodules
 Higher doses
 Surgery for young patients and those with larger nodules.

Thyroid storm (Hyperthyroid crisis)

 Hyperthyroidism accompanied by
o Fever (hyperthermia)
o CNS agitation, or depression,
o Cardiovascular dysfunction: CHF or AF
o GI dysfunction-diarrhea, including hepatic failure
 Precipitating factors
o Abrupt cessation of antithyroid medications
o Infection
o Thyroid or non-thyroid surgery
o Trauma in patients with thyrotoxicosis

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o Occasionally: amiodarone, iodinated contrast agents, and RAI

therapy.
 Management
o Oxygen supplementation
o Hemodynamic support: IV fluid – dehydration.
o Non-aspirin compounds to treat pyrexia; e.g. paracetamol.
Aspirin should be avoided to prevent decreased protein binding
and subsequent increase in free T3 &T4 levels.
o Hormone suppression
 Beta-blockers to reduce peripheral conversion and
decrease hyperthyroid symptoms
 Lugol’s solution or sodium ipodate (IV) to decrease
iodine uptake and thyroid hormone release.
 PTU to block thyroid hormone synthesis and peripheral
conversion.
o Corticosteroids to prevent adrenal exhaustion and block hepatic
thyroid hormone conversion.
o CHF: diuretics
o Hyperexcitability: diazepam

Hypothyroidism
 Deficiency in circulating levels of thyroid hormone leads to;
o Hypothyroidism or
o In neonates, cretinism
 Clinical features
o Cretinism
 Down facies
 Dwarfism
 Failure to thrive and mental retardation
o In children or adolescents, it results in delayed development and
abnormal distention, umbilical hernia, and rectal prolapse.
o Symptoms in adults
 Tiredness
 Weight gain
 Cold intolerance
 Constipation
 Menorrhagia
 Facial and periorbital myxedema due to deposition of
glycosaminoglycans in the subcutaneous tissue.
 Rough and dry skin with a yellowish hue from reduced
conversion of carotene to vitamin A.
 Loss of outer two thirds of eyebrows.
 Enlarged tongue
 Libido and fertility are impaired in both sexes.
 Bradycardia, cardiomegally, pericardial effusion, reduced
CO, and pleural effusion.
o Features of secondary hypothyroidism
 Pale, waxy skin; loss of body hair; and atrophic genitalia.

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 Laboratory findings
o Low circulating T3 & T4
o Raised TSH in primary thyroid failure
o Low TSH levels that do not increase following TRH stimulation in
secondary hypothyroidism.
o Thyroid antibodies are elevated in autoimmune disease and
sometimes in nodular goiter and thyroid neoplasms.
 Treatment
o Thyroid hormone replacement
 T4 50-200μg per day
 Starting dose of 100μg per day is safe, but lower doses
(25-50μg daily) are required for elderly patients and
those with coexisting heart disease.
 Baseline ECG
 T4 dosage is titrated against clinical response.and TSH
levels.
 Myxedema coma
o It is rare life-threatening clinical condition that represents severe
hypothyroidism with hysiologic decompensation.
o It is a medical emergency.
o Precipitating factors; infection, cold exposure, trauma, burns,
stroke, MI, CHF, respiratory acidosis, GI hemorrhage,
hypoglycemia, hyponatremia, acidosis, hypercarbia, drugs (beta
blockers, tranquilizers, lithium, phenytoin, anesthetics, narcotics,
sedatives, rifampin).
o Clinical features
 Symptoms of hypothyroidism
 Symptoms of precipitating events
 Mental state change: lethargy, delirium, or coma
o Treatment
 Maintain adequate airway
 Initial emergency treatment with large doses of IV T4
(300-600μg) with careful monitoring in the ICU and then
maintenance with 50-100μg IV daily till patient is able to
take orally.
 Treat precipitating factors

Thyroiditis (Inflammatory goiter)

Types of thyroiditis
Acute (suppurative) thyroiditis
Subacute thyroiditis
 Painful thyroiditis
 Painless thyroiditis
Chronic thyroiditis
 Lymphocytic (Hashimoto’s) thyroiditis
 Riedel’s thyroiditis

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Acute suppurative thyroiditis

 Thyroid gland is inherently resistant to infection due to extensive blood
supply and lymphatics, high iodine content and fibrous capsule.
 Streptococcus and anaerobs account for about 75% of cases.
 More common in children and often proceeded by URTI or otitis media.
 Severe neck pain radiating to the jaw or ear, fever, chills, odynophagia,
and dysphonia.
 Pyriform sinus fistula should always be suspected in recurrent cases.
 Complications
o Systemic sepsis
o Tracheal or esophageal rupture
o Jugular vein thrombosis
o Laryngeal chondritis and perichondritis
o Sympathetic trunk paralysis
 Diagnosis is established by;
o Leukocytosis on blood tests and FNAB for Gram’s stain, culture
and cytology.
o CT scan
 Treatment
o Parentral antibiotics and drainage of abscess.
o Thyroidectomy for persistent cases.
Painful subacute thyroiditis (De Quervian’s thyroiditis?)
 Viral in origin.
 30-40 years old women.
 Neck pain which may radiate to the angle of mandible or ear.
 History of upper respiratory tract infection.
 The gland is enlarged, exquisitely tender and firm.
 Progress through four stages;
o Hyperthyroid phase: all
o Euthyroid phase: all
o Hypothyroidism: 20-30%
o Euthyroid phase/resolution: >90%
 ESR is typically >100mm/hr and RAIU is decreased.
 Treatment
o Self limited, so treatment is symptomatic. Aspirin and other
NSAIDs and steroids in more severe cases.
o Thyroidectomy only if chronically non-responsive and recurrent.
Painless subacute thyroiditis
 Considered autoimmune.
 May occur sporadically or in the post-partum period.
 More common in women between 30-60 years of age.
 The gland is normal sized or minimally enlarged, slightly firm, non-tender
gland.
 Laboratory tests and RAIU is the same as painful one except that ESR is
normal.
 The clinical course also parallels painful thyroiditis.

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 Treatment
o Beta blockers and thyroid hormone replacement.
o Thyroidectomy or RAI therapy only when recurrent and disabiling.
Hashimoto’s thyroiditis (struma lymphatosa)
 An autoimmune process marked by the transformation of thyroid tissue in
to lymphoid tissue.
 The most common inflammatory disorder of thyroid.
 The leading cause of hypothyroidism in the developed world (iodine
deficiency is the most common cause of hypothyroidism in the developing
world).
 Antibodies are targeted against
o Thyroid peroxidase: 95%
o Thyroglobulin: 60%
o TSH-R: 60% and
o Sodium-iodine symporter: 25%
 There is a support for inherited predisposition.
 Clinical features
o More common in women (1:10-20) between ages of 30-50 years
old.
o Minimally or moderately enlarged firm granular and painless
anterior neck mass.
o Hypothyroidism (20%), hyperthyroidism/Hashitoxicosis (5%).
o 80X higher risk for development of thyroid lymphoma.
 Diagnostic tests
o Elevated TSH and presence of thyroid antibodies usually confirm
the diagnosis.
o FNAB if suspicious or rapidly growing.
 Treatment
o Thyroid hormone replacement
o Surgery may occasionally be indicated if there is suspicion of
malignancy or for goiters causing compressive symptoms or
cosmetic deformity.
Riedel’s thyroiditis/Riedel’s strauma or invasive fibrous throiditis
 A rare variant of thyroiditis.
 Characterized by replacement of all or part of the thyroid parenchyma by
fibrous tissue and invasion in to adjacent tissues.
 There is a suggestion that it is a primary autoimmune disease.
 Associated with other focal sclerosing syndromes including retroperitoneal,
periorbital, and retro-orbital fibrosis, and slerosing cholangitis.
 Occur predominantly in women between ages 30-50 years.
 Typically, a painless, hard anterior neck mass, which progress over weeks
to years to produce symptoms of
o Compression: dysphagia, dyspnea, choking, and hoarseness.
o Hypothyroidism and hypoparathyroidism
 Physical examination reveals a hard “woody” thyroid with fixation to
surrounding tissues.

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 Diagnosis should be confirmed by open biopsy because the hardness of

the gland renders FNAB inadequate.
 Treatment
o Surgery is the mainstay of treatment.
o Thyroid hormone replacement

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Malignant Thyroid Disease

It accounts for less than 1% of malignancies. It is more common in women (2%
and 0.5%). It is the most rapidly increasing cancer in women.
Molecular genetics
 RET proto-oncogene mutation
o Germline: MEN2 and familial MTCs.
o Somatic: MTCs (30%) and pheochromocytoma.
 RET/PTC rearrangement: due to radiation exposure in children below 5
years of age.
 p53 mutation: rare in PTCs but common in undifferentiated thyroid
cancers and thyroid cancer cell lines.
Types of malignant thyroid disease
 Differentiated AGE AT PRESENTATION
o Papillary carcinoma (80%) Papillary: 30-40
o Follicular carcinoma (10%) Follicular: 40-50
 Undifferentiated Medullary:50-60
o Medullary carcinoma (5%) Anaplastic: 60-80
o Anaplastic carcinoma (<1%)
 Thyroid lymphoma (<1%)
 Metastatic disease: from breast colon, rectum or local spread.

Types of malignant thyroid disease

Origin Differentiated Undifferentiated
Follicular cells Papillary carcinoma Anaplastic carcinoma
Follicular carcinoma
Parafollicular cells Medullary carcinoma
Lymphoid cells Lymphoma
Secondary Local invasion Local invasion
Metastasis Metastasis

Papillary thyroid carcinoma (PTC)

 The most common thyroid malignancy in iodine sufficient areas.
 Predominant thyroid cancer in children and individuals exposed to radiation.
 2:1 female to male ratio.
 Mean age at presentation is 30-40.
 Clinical features
o Most patients are euhtyroid and present with a slow growing painless
mass in the neck.
o Pressure symptoms in advanced cases.
o Lymph node metastases are common, especially in children and
young adults, and may be the presenting symptom.
o Distant metastasis is late presentation but ultimately develop in up to
20% of patients. Most common sites are lungs, followed by bone, liver,
and brain.

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 Pathology
o Grooving and crowding of nuclei.
o Orphan Annie nuclei (intranuclear cytoplasmic inclusions)
o Psammoma bodies; microscopic calcifications
o Multifocality (85%).
o Variants of papillary carcinoma
 Tall cell, insular, columnar, diffuse sclerosing, clear cell,
trabecular, and poorly differentiated.
 Represent <1% of papillary carcinoma
 Generally associated with worse prognosis
o Minimal or occult microadenomas: ≤1cm.
 Diagnosis
o FNAB of thyroid mass or lymph nodes establishes the diagnosis
o Neck ultrasound
 Prognostic indicators
o Generally excellent prognosis (>95% 10 year survival).
o Prognosting scores: AGES, MACIS, AMES, DeGroot.
o Incorporates age, metastasis, local invasion, size of the tumor,
histologic grade and the like.
o DeGroot and colleagues;
 Class I: intrathyroidal
 Class II: cervical nodal metastasis
 Class III: extrathyroidal invasion
 Class IV: distant metastasis
 Treatment
o Near-total or total thyroidectomy for primary cancers >1cm unless
there are contraindications for the surgery.
o Thyroid lobectomy for small (<1cm), incidentally discovered, low risk,
unifocal, intrathyroidal papillary carcinomas in the absence of prior
head and neck irradiation or clinically involved cervical node.
o Biopsy-proven lymph node metastases are managed with modified
radical or functional neck dissection.
o Prophylactic lateral neck dissection is not necessary, because
cancers do not appear to metastasize from lymph nodes.

Follicular thyroid carcinoma (FTC)

 Common in iodine-deficient areas.
 Women have higher incidence (3:1).
 Mean age of presentation is 50 years.
 Present as solitary nodules, occasionally with rapid size increase, and
longstanding multinodular goiter.
 Cervical lymphadenopathy is uncommon at presentation (5%), although
distant metastasis may be present.
 <1% are hyperfunctioning and cause thyrotoxicosis.
 FNAB is unable to distinguish between follicular adenoma and carcinoma.
Large follicular neoplasias (>4cm) in an older patient are more likely to be
malignant.

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 Multiple tumor markers are used to support diagnosis.

 Pathology
o Solitary lesions surrounded by capsule.
o Malignancy is defined by the presence of capsular and vascular
invasion.
 Treatment
o Lobectomy; because 80% of patients diagnosed by FNAB as having
follicular neoplasia will have benign adenomas.
o Total thyroidectomy;
 In older patients with follicular lesion >4cm (50% risk of being
malignant in this setting).
 Atypia on FNAB
 Family history of thyroid cancers
 History of radiation exposure
 Thyroid cancer; by intraoperative frozen section.
o Prophylactic neck dissection is not needed, because nodal
involvement is infrequent. It is considered in large tumor.
o Mortality rate is 15% at 10 years and 30% at 20 years.
o Poor prognostic signs;
 Age >50 at presentation
 Tumor size >4cm
 Higher grade
 Marked vascular invasion
 Extrathyroidal invasion
 Distant metastasis
Hurthle cell carcinoma
 A variant of FTC that accounts for 3% of all thyroid malignancies.
 Histology: sheets of eosinophilic cells packed with mitochondria.
 They are in all rights similar to FTC except that they;
o Derived from oxyphil cells of thyroid
o Are more often multifocal and bilateral (30%)
o Usually do not take up RAI (50%)
o Are more likely to metastasize to nodes (25%) and distant sites
o Are associated with higher mortality rate (20% at 10 years)
 Management is similar to that of FTC. Routine central node removal.
Post-op management of differentiated thyroid cancer
 RAI therapy is indicated for patients with
o Unifocal cancers >1cm or
o Multifocal cancers; at least one being >1cm.
 External beam radiotherapy
o Unresectable, totally invasive or recurrent disease and
o Metastasis in support bones to prevent fracture
 Chemotherapy (doxorubicin and paclitaxel); but there is no role for routine
chemotherapy.
 Thyroid hormone (T4 0.1mg tablets)
o Supplementation: 0.1mg (1 tab)
o Replacement therapy: 0.2mg (2 tab)

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o TSH suppression: 0.3mg (3 tab)

Follow-up of patients with differentiated thyroid cancers
 Serum TSH should be kept below 0.1mU/mL
 Imaging
 Thyroglobulin measurement at 6 or 12 month intervals. Tg>2ng/mL
following rTSH stimulation is highly sensitive identifying patients with
recurrent disease.

Medullary thyroid carcinoma (MTC)

Arises from parafollicular or C cells of the thyroid which are derived from
ultimobranchial bodies. Most cases occur sporadically, but up to 25% occur in a
spectrum of several inherited syndromes caused due to RET proto-oncogen
mutation. These syndromes include
 MEN2A (Sipple’s syndrome): MTC, pheochromocytoma, primary
hyperparathyroidism, lichen planus amyloidosis.
 MEN2B: MTC, pheochromocytoma, Marfanoid habitus, mucocutaneous
ganglioneuromatosis
 Familial MTC
 [MEN1-Wermer’s syndrome: hyperparathyroidism, islet cell canrcinoma,
and pituitary adenoma]. It is not a familial MTC. I wrote it just in case!
Clinical features
 A neck mass that may be associated with palpable cervical
lymphadenopathy (15-20%).
 Pain or aching is more common in these patients.
 Pressure symptoms.
 Distant metastasis to liver, bone (often osteoblastic), and lung occur late
in the disease course.
 1.5:1 female to male ratio.
 Most patients present between 50-60 years; patients with familial disease
present earlier.
 MTCs secrete calcitonin, CEA, ACTH, calcitonin gene-related peptide,
histaminadases, prostaglandin E2 and F2α, and serotonin.
o Diarrhea, Cushing’s syndrome.
Pathology
 Typically unilateral (80%) in patients with sporadic disease.
 Bilateral tumors occur in up to 90% of familial patients.
 Generally >50% bilateral.
 The presence of amyloid is a diagnostic finding, but
immunohistochemistry of calcitonin is more commonly used as a
diagnostic tumor marker.
 Stain positive for CEA and calcitonin gene-related peptide.
Diagnosis
 Raised serum calcitonin or CEA levels; low serum calcium.
 FNAB cytology
 Screen for RET mutation, pheochromocytoma, and HPT: all patients.

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 Calcitonin is more sensitive marker, but CEA is a better predictor of

prognosis.
 Neck ultrasound
Treatment
 Treat pheochromocytoma first if present.
 Total thyroidectomy is the treatment of choice because of the high
incidence of multicentricity, more aggressive course, and the fact that RAI
therapy is not effective.
 Prophylactic bilateral neck dissection is required because central
compartment nodes are involved early in the disease process.
 Tumor debulking in locally recurrent or widely metastatic disease.
Post-op follow-up and prognosis
 Annual measurements of calcitonin and CEA.
 USG, CT, and MRI to locate recurrent disease.
 The prognosis is related to stage, and 10 year survival rate is;
o 80% without nodal involvement
o Decreases to 45% in patients with lymph node involvement.
 According to prognosis: from best to worst;
o Non-MEN familial MTC
o Those with MEN2A
o Sporadic disease
o Those with MEN2B (35% survival at 10 years).

Anaplastic thyroid carcinoma

Women are more commonly affected and majority of tumors present in the 7th and
8th decades. The patient typically presents with a long standing neck mass, which
rapidly enlarges and may be painful. Compression symptoms are common. The
tumor is large and may be fixed or ulcerated. Lymph nodes usually are palpable at
presentation. Evidence of metastasis may also be present.
Diagnosis is confirmed by FNAB
 Reveals giant multinucleated cells
 DDx; lymphoma, MTC, direct extension from laryngeal carcinoma, or
other metastatic carcinoma or melanoma.
 Spindle cells: consider sarcomas.
There are three main histologic growth patterns; which may show predominance of
one or a mixture of various patterns:
1. Spindle cell,
2. Squamoid, and
3. Pleomorphic giant cells
Treatment
 All forms of treatment have been disappointing.
 Intrathyroid: total or near-total thyroidectomy with therapeutic lymph node
dissection.
 Extrathyroid: en bloc resection.

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 Avoid tracheostomy as long as possible, unless there is an impending

airway obstruction.
 Adjuvant radiation and cytotoxic chemotherapy are administered typically
in combination.
Prognosis
 It is one of the most aggressive thyroid malignancies.
 Few patients survive beyond 6 months.

Thyroid lymphoma
 Most are non-Hodgkin B-cell type.
 Most develop in patients with chronic lymphocytic thyroiditis.
 Similar presentation with anaplastic carcinoma. May present with acute
respiratory distress.
 The diagnosis is suggested by FNAB, but core needle biopsy may be
necessary for definitive diagnosis.
 Treatment
o Total surgery is recommended for cancers without local infiltration or
for palliative reasons.
o Respond rapidly to chemotherapy (CHOOP – cyclophosphamide,
doxorubicin, vincristine, and prednisolone).
o Combined therapy with radiation is often recommended. They are
highly sensitive to radiation.
o Thyroidectomy and lymph node dissection are used to alleviate
symptoms.
 Prognosis
o Depends on histologic grade of the tumor and whether the tumor is
disseminated.
o The 5 year survival rate is 50% (lower in patients with extrathyroidal
disease).

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Fig: The risk of malignancy in solitary thyroid swellings (rule of twelve)

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CHAPTER FIVE-THE STOMACH

Surgical Anatomy and Physiology

The anatomy of the stomach
Stomach is the asymmetrical, pear shaped, most proximal abdominal organ of the
digestive tract. It has four main parts; fundus, body, antrum, and pylorus.
The stomach is attached to the liver, colon, spleen, pancreas, and kidney; and this
explains why volvulus of the stomach is rare.
 Gastro-hepatic ligament/lesser omentum/pars flaccid attaches the
stomach with the liver.
 Gastrosplenic ligament tethers the stomach with the spleen. It contains
the short gastric artery.
 Gastroduodenal ligament; it contains the portal triad.
 Gastrocolic omentum/ligament abuts the stomach with the transverse
colon.
 Hepatoduodenal ligament.

Fig: Gross anatomy of the stomach

Arterial and venous supply of the stomach
 The stomach is the most richly vascularized portion of the GIT.
 It has four major arteries that arise from celiac trunk: from largest to the
smallest;
o Left gastric artery
o Right gastroepiploic artery
o Right gastric artery
o Left gastroepiploic artery
o Others;
 Short gastric arteries from splenic artery
 Small branches from phrenic and splenic circulations
 Veins generally parallel arteries;
o Right and left gastric (coronary) veins drain in to portal vein,
though occasionally the left gastric vein drains in to splenic vein.
o The right gastroepiploic vein drains in to SMV.
o The left gastroepiploic vein drains in to the splenic vein.

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Fig: Blood supply of the stomach

Lymphatic drainage
 The gastric lymphatics parallel the blood vessels.
 Gastric cancers may metastasize to any nodal groups regardless of the
cancer location.
 There are three levels of gastric lymph nodes;
o D1: perigastric lymph nodes (stations 1-6).
o D2: lymph nodes along the celiac trunk and its branches and
along proximal SMA (stations 7-12).
o D3: distant/para-aortic nodes.

Fig: Lymph node stations of the stomach.

Innervation of the stomach
 Parasympathetic innervation: vagus
o

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o Left/anterior gastric nerve continues along the lesser curvature as

the nerve of Latarjet and ends at the incisura terminalis as ‘crow’s
foot’, sending branches to the antropyloric region. It also sends
branches to the body of stomach.
o Right/posterior vagus nerve sends a branch named criminal
nerve of Grassi to the posterior fundus.
 Sympathetic innervation
o Originates at spinal levels T5-T10 and travels through the
spalanchnic nerves to celiac ganglion. Postganglionic fibers from
celiac ganglion travel along with blood vessels.
 Intrinsic nervous system
o Auerbach’s myenteric nervous system and
o Meissner’s submucosal nervous system.
Histology
 Four distinct layers
o Mucosa:
 Columnar glandular epithelia, submucosa, and
muscularis mucosae.
 Types of epithelial cells
 Chief cells: 44%
 Mucus cells: 40%
 Parietal cells: 13%
 Endocrine cells: 3%
o Submucosa: branching blood vessels, lymphatics, inflammatory
cells, nerve fibers, and collagen. The mucosa and submucosae
are folded in to the grossly visible gastric rugae
o Muscularis externa/propria;
 Incomplete inner oblique layer
 Complete middle circular layer
 Complete outer longitudinal layer
o Serosa/visceral peritoneum

Gastric glandular organization

Cells Location Function
Parietal/oxyntic Body Secretion of acid and intrinsic factor
Mucus Body, antrum Mucus
Chief/zymogen Body Pepsin
Surface epithelia Diffuse Mucus, bicarbonate,
prostaglandins?
ECL Body Histamine
G Antrum Gastrin
D Body, antrum Somatostatin
Gastric mucosal Body, antrum Gastrin-releasing peptide
interneurons
Enteric neurons Diffuse Calcitonin gene-related peptide
Endocrine Body Gherlin

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Fig: Mammalian gastric gland

The physiology of the stomach

The stomach has two general functions;
 Secretory: production of acid, pepsin, intrinsic factor, mucus, and variety
of GI hormones.
 Motor functions;
o Storage: receptive relaxation and accommodation
o Grinding and mixing
o Controlled gastric emptying
o Periodic interprandial housekeeping
Acid secretion
 Functions of gastric acid
o Physical and (with pepsin) chemical breakdown of food.
o Inhibits proliferation of ingested pathogens
 Gastrin, acetylcholine, and histamine stimulate parietal cells to secret
hydrochloric acid. D-cells inhibit acid secretion by secreting somatostatin.
H. pylori inhibit the function of D-cells.
 Physiologic acid secretion occurs in response to ingestion of food, and
there are three phases;

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o Cephalic phase: 30%

o Gastric phase: 60%
o Intestinal phase: 10%
 Interprandial basal acid output is 2-5mEq/hr; about 10% of the maximal
acid output (MAO).

Fig: Physiologic control of acid secretion.

Pepsinogen secretion
 Most potent stimulus: food ingestion.
 Most important mediator: acetylcholine.
 Somatostatin inhibits pepsinogen secretion.
 Pepsinogen I is produced by chief cells, and pepsinogen II is produced by
surface epithelial cells.
 Pepsinogen is cleaved in to pepsin in the acidic environment.
 Pepsin catalyzes the hydrolysis of proteins.
Intrinsic factor
 Secreted by parietal cells.
 Stimulants are the same as acid secretion.
 Intrinsic factor binds luminal vitamin B-12, and the complex is absorbed in
the terminal ileum via mucosal receptors.
Gastric mucosal barrier
 Components

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o Mucus barrier
o Bicarbonate secretion
o Epithelial barrier: hydrophobic phospholipids, tight junctions, and
restitution.
o Microcirculation (reactive hyperemia)
o Afferent sensory neurons.
 Mediators: PGs, NO, EGF, histamine, etc.
Gastric motility
 Excitatory neurotransmitters: acetylcholine, tachykinins, substance-P,
neurokinin, motilin, gastrin, and serotonin.
 Inhibitor neurotransmitters: NO, VIP, somatostatin, dopamine
 Serotonin modulates both contraction and relaxation.
 Interstitial cells of Cajal (ICC), also modulates GI motility.
 The proximal stomach serves short term food storage and regulates basal
intragastric tone.
 The distal stomach mixes and grinds food, and is the major determinant of
gastric emptying of solids.
 The pylorus is an effective regulator of gastric emptying and effective
barrier to duodenogastric reflux.
Gastric emptying
 Liquid emptying is faster than solid emptying.
 Osmolarity, acidity, caloric content, nutritional composition, and particle
size are important modulators of gastric emptying.
 CCK inhibits gastric emptying.
 Liquid emptying is delayed in the supine position. Liquids have a half
emptying time of 12 minutes. They have an initial rapid phase followed by
a slower linear phase of emptying.
 Solids have a half time emptying less than 2hrs. They have initial lag
phase during which much of the grinding and mixing occurs, followed by a
linear emptying phase.

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Diagnosis of Gastric Disease

Signs and symptoms
 The most common symptoms are pain, weight loss, early satiety, and
anorexia.
 Nausea, vomiting, and anemia are also frequent complaints.
 Dyspepsia is a name given to a combination of symptoms; pain, bloating,
nausea, and early satiety; which is synonymous with the non-medical term
indigestion.
 Common causes of indigestion are GERD, and disorders of stomach,
gallbladder, and pancreas.

Diagnostic tests
Esophagogastroduodenoscopy (EGD)
 Alarming symptoms that indicate immediate need for upper endoscopy;
o Weight loss, recurrent vomiting, dysphagia, bleeding, & anemia.
 Performed under conscious sedation.
 Inserted transnasally after 8 hrs of fast, under direct vision.
 All patients with gastric ulcer should have biopsy specimen to rule out
gastric cancer.
 Gastric lavage should be done before sending a patient for EGD.
Benign gastric ulcer Malignant gastric ulcer
Convergence of mucosal folds towards Loss of convergence
the ulcer
Punched out due to acid digestion Everted edge
Peristalsis around the ulcer >2cm size
Slough will be seen in floor
Local aperistalsis

 Endoscopy cannot diagnose the following due to normal gastric mucosa;

o Linitis plastic
o GIST
o Lymphoma
o Carcinoids
Barium meal
 To study the esophagus and stomach.
 Highly useful in;
o Linitis plastic
o Hour glass contraction
o Hiatus hernia
o Volvulus of stomach

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o Stenosing lesions
o To know stomach dilatation
o Lesions near fundus
o Gastrojejunal fistula
X-rays
 Plain abdominal x-rays: for diagnosis of gastric perforation
(pneumoperitoneum) and delayed emptying (large air-fluid level).
 Double-contrast GI series is better than EGD in diagnosing gastric
diverticula, fistula, tortuosity, stricture location, and size of hiatal hernia.
CT/MRI
 MRI for quantitative test for gastric emptying.
 Screening and staging of gastric disease.
 Arteriography in gastric hemorrhage.
Endoscopic ultrasound (EUS)
 Best way to stage gastric adenocarcinoma loco-regionally.
 Submucosal masses.
 Reassurance in differentiating benign from malignant disease.
 Assess response to chemotherapy.
Gastric secretory analysis
 Basal acid output = >5mEq/h
 Maximal acid output (average of the two final stimulated 15 min periods) is
usually 10-15 mEq/h
 Peak acid output (the highest of the four stimulated periods)
Tests for H. pylori
 It has high positive predictive value but unreliable negative predicting
value.
 Types of tests
o Serologic test
o Stool antigen test
o Urea breath test
o Biopsy of gastric mucosa (invasive tests)
 Histology: gold standard
 Rapid urease test: strong presumptive evidence
Diagnostic tests for gastric diseases
Esophagogastroduodenoscopy (EGD) or upper GI endoscopy
X-rays
CT/MRI
Endoscopic ultrasound (EUS)
Scintigraphy
Tests for H. pylori
Antroduodenal motility testing and electrogastrography

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List of disorders of the stomach

Inflammatory lesions Isolated gastric varices
 Gastritis Gastric volvulus
 Peptic ulcer disease (PUD) Mallory-Weiss syndrome
Polyps Gastric diverticula
 Neoplastic: adenomas*, fundic Bezoars (phytobezoars* or trichobezoars)
gland polyps Foreign bodies
 Non-neoplastic: hyperplastic*, Watermelon stomach (gastric antral
inflammatory, and vascular ectasia)
hamartromatous. Hypertrophic gastropathy (Ménétrier’s
Leiomyomas disease)
Lipoma Malignancies
Heterotopic pancreas  Carcinoma
Gastric motility disorders  Lymphoma
 Gastroparesis  Gastrointestinal stromal tumor
 Rapid gastric emptying (GIST)
 Sensory and motor (functional  Leiomyosarcoma
dyspepsia)  Carcinoid
 Dumping, stasis, & Roux  Zollinger-Ellison syndrome
syndrome
Upper GI hemorrhage

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Gastritis
Gastritis is gastric mucosal inflammation. The most common cause of gastritis is H,
pylori. Other causes include alcohol, NSAIDs, Crohn’s disease, tuberculosis and
bile reflux.
H. pylori gastritis (previously type B gastritis)
 Affects antrum. These patients are prone to PUD.
 Pangastritis is also a very common manifestation, but gastritis of the
corpus alone is uncommon. These patients are prone to gastric cancer.
 Intestinal metaplasia is associated with chronic pangastritis with atrophy.
Autoimmune gastritis
 Circulating antibodies against parietal cells are present.
 This results in atrophy of parietal cell mass, hypochlorrhydria and
ultimately achlorrhydria.
 Malabsorption of VB12 may result in pernicious anemia.
 These patients are prone to develop gastric carcinoma.

Fig: Pathophysiology of autoimmune gastritis

Erosive gastritis
 Caused by agents that disrupt gastric mucosal barrier; NSAIDs and
alcohol are common causes.
 NSAID-induced gastric lesion is associated with inhibition of the cyclo-
oxygenase type 1 (COX-1) receptor enzyme, hence reducing
prostaglandin secretion.
Reflux gastritis
 Caused by enterogastric reflux and common after gastric surgery.
 It may also occur in patients who had cholecystectomy.
 Its histologic feature is different from other forms of gastritis.
 Treatment;
o Bile chelating or prokinetic agents

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o Surgery is considered for most severe cases.

Stress gastritis
 A common sequelea of serious illness, trauma, shock or respiratory failure.
 Characterized by a reduction in blood supply to superficial mucosa of the
stomach.
 There are multiple superficial (non-ulcerating) erosions which begin from
the proximal stomach and progress distally.
 They present within 1-2 days after traumatic event.
 They may also occur in;
o CNS disuse: Cushing’s ulcer
o Burn injury involving >30% of TBSA: Curling’s ulcer
Other forms of gastritis;
 Lymphocytic gastritis
 Eosinophilic gastritis
 Granulomatous gastritis
 AIDS gastritis
 Phlegmatous gastritis

Peptic Ulcer Disease

Peptic ulcers are focal defects in the gastric or duodenal mucosa that extend into
the submucosa or deeper. They may be acute or chronic, and are caused by
imbalance between mucosal defense and acid/peptic injury. PUD is one of the
most common GI disorders with prevalence of about 2% and a life time prevalence
of about 10%, peaking around 70 years.

Aggression Defense Repair

Acid Bicarbonate Restitution

Pepsin Blood flow Mucoid cap
NSAIDs Mucus Proliferation
H. pylori Cell junctions Growth factors
Apical resistance

Fig: Balance of aggressive and defensive factors

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Cytoprotective mechanisms of prostaglandin

 Stimulation of glycoprotein (mucin) secretion by epithelial cells
 Stimulation of bicarbonate secretion by epithelial cells
 Stimulation of phospholipid secretion by epithelial cells
 Enhancement of mucosal blood flow and oxygen delivery to epithelial
cells via local vasodilation
 Increased epithelial cell migration towards the luminal surface (restitution)
 Enhanced epithelial cell proliferation
Pathophysiology and etiology
 The final common pathway to ulcer formation is acid-peptic injury of
gastroduodenal mucosal barriers; “no acid, no ulcer”.
 Acid/pepsin secretion with H. pylori or NSAIDs is the absolute requirements
for duodenal ulcer formation.
 Acid secretion in gastric ulcers is variable. There is no hyperacidity in majority
of cases.
 The large majority of peptic ulcers are caused by H. pylori infection and NSAID
use.
 Other causes: smoking, ZES, antral G cell hyperfunction and/or hyperplasia,
systemic mastocytosis, trauma, burns, and major physiologic stress, and
drugs (aspirin, cocaine).
 H. pylori predisposes to ulceration both by acid hypersecretion and
compromise of mucosal defenses.
o They inhibit antral D cells.
o The ammonia produced by the bacteria is damaging to the SEC.
o Alkalinization of the antrum which causes hypergastrinemia (antral
acidification is a potent antagonist to gastrin secretion).
 How do H. pylori survive in the stomach?
o They have the enzyme urease which buffers the acid by converting
urea in to ammonia and bicarbonate.
o Flagella help the bacteria to navigate through the mucus layer and
attach to superficial epithelial cells.
 NSAID use causes ulcers predominantly by compromising mucosal defenses.
Complications of PUD are much more common in patients taking NSAIDs.
 Smoking causes ulceration by;
o Increasing gastric acid secretion
o Increasing duodenogastric reflux
o Decreasing gastroduodenal prostaglandin production
o Decreasing pancreaticoduodenal bicarbonate production
 Common sites for peptic ulcers;
o First part of the duodenum**
o Lesser curvature of the stomach*

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o Stoma following gastric surgery

o The esophagus
o Meckel’s diverticulum
Modified Johnson’s classification of gastric ulcer disease
Type Description
I The most common type. Located near angularis incisura. Normal or decreased
acid secretion.
II Associated with active or quiescent duodenal ulcer disease. Normal or increased
acid secretion.
III Prepyloric ulcer disease. Associated with normal or increased acid secretion.
IV Located near gastro-esophageal junction. Normal or decreased acid secretion.
V NSAID-induced ulcer disease. May occur anywhere in the stomach.

Fig: Modified Johnson’s classification of gastric ulcer

Comparison between duodenal and gastric ulcers
Parameters Duodenal ulcer Gastric ulcer
Prevalence More common Less common
Sex incidence M>F (2:1) M=F
Age Younger age Older age
Socio-economy Higher Lower
Ulcers Similar but smaller Similar but larger
The pain Relived by meal. Awakens Exacerbated by meal. Unlikely to awaken
from sleep at night. the patient from sleep.
Risk of Not associated Considered malignant unless proved
malignancy otherwise by biopsy.

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Clinical manifestations
 The pain.
o Burning, epigastric pain with no radiation.
o 2-3 hours after meal in duodenal ulcer.
o Occurs with eating in gastric ulcers.
 Periodicity is a classical feature.
 Bloating, nausea and vomiting.
 Alteration in weight; weight loss or sometimes weight gain (in duodenal ulcer).
 Bleeding and/or anemia; stool positive for occult blood.
 Bleeding from the posterior duodenal ulcers due to the presence of
gastroduodenal artery. Anterior duodenal ulcers complicate with perforation.
 A history of OTC drug use or PUD.
 On examination, the patient may reveal epigastric tenderness, there is unlikely
to be much else to find, except there is complication such as gastric outlet
obstruction.
Diagnosis
 Upper GI endoscopy; the investigation of choice.
o For all patients above 45 years and with the above symptoms.
o For all patients with alarming symptoms.
 Double contrast erect abdominal X-ray
o Perforation: air under the diaphragm (80%)
o Duodenal atresia: double bubble appearance
o Jejuna atresia: triple bubble appearance
 All gastric ulcers should be appropriately biopsied to rule out H. pylori and
malignancy.
 Barium meal: gastric ulcers
o Direct: ulcer crater or niche
o Indirect signs
 Notch or incisura at greater curvature
 Constant deformity
 Rugal convergence
 Coarseness and irregularity
o Suspect malignancy:
 >1 inch on lesser curvature
 Ulcers on greater curvature
 Tests for H. pylori may be indicated.
 Serum gastrin level to rule out gastrinoma.
Complications
 The three most common complications of PUD, in decreasing order of
frequency, are;

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o Bleeding,
o Perforation, and
o Obstruction.

Bleeding peptic ulcer

 The most common cause of upper GI bleeding and the most common cause of
ulcer related death.
 Tend to occur in older and/or medically complicated patients.
 Present with melena and/or hematemesis. Abdominal pain is quite uncommon,
shock may be present.
 NGT aspiration is confirmatory of upper GI bleeding.
 Early endoscopy is important to diagnose the cause of bleeding and assess
the need for haemostatic therapy.
 Treatment
o Acid suppression
o Endoscopic haemostatic modalities
 Injection with epinephrine
 Electrocautery
 Mechanical clip
o Operation for persistent bleeding or re-bleeding and for elderly
patients who do not tolerate repeated episodes of bleeding. Only 25%
of patients will need operation. Essentially all the deaths from
bleeding occur in this group.

Perforated peptic ulcers

 More common indication for operation than bleeding.
 Two times more common in male.
 Present as acute abdomen due to peritonitis. The patient often can give the
exact time of onset of the excruciating abdominal pain.
 Sequence of events after perforation;
o Chemical peritonitis due to gastric and duodenal secretions; mainly
hydrochloric acid.
o Stage of delusion/illusion as a result of dilution of the secretions by
reactive secretion of fluid.
o Bacterial peritonitis supervenes within hours.
 Marked involuntary guarding and tenderness are evoked by gentle
examination. The patients prefer to stay still.
 Upper chest X-ray shows free air under the diaphragm in about 80% of
patients.
 Treatment
o Analgesia and antibiotics

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o Resuscitation with isotonic fluid.

o Operation
o Non-operative management
 If there is objective evidence that the leak has sealed (i.e.,
radiologic contrast study).
 In the absence of clinical peritonitis.

Gastric outlet obstruction (GOO)

 Occurs in no more than 5% of patients with PUD.
 Usually due to duodenal or prepyloric ulcer disease.
 It may be;
o Acute: from inflammation and peristaltic dysfunction
o Chronic: from cicatrix
 The two most common causes of GOO are;
o Gastric cancer and
o Peptic ulcer disease.
 Other causes include: gastric lymphoma, GIST, gastric polyps, and etc.
 Clinical features
o Typically present with non-bilious vomiting.
o Pain or discomfort is common.
o Profound hypokalemic hypochloremic hyponatremic metabolic
acidosis with paradoxical aciduria.
o Weight loss.
o Salient features of GOO;
 A succession splash may be audible.
 After 2 hours of taking meal
 Hold the pelvis and hear the splash with ear or if not
audible, use stethoscope. Most of the times if the
splash is present it will be heard by ears.
 Visible gastric peristalsis (VGP)
 Distended abdomen on auscultoscrapping
 Diagnosis
o Confirmed by endoscopy.
o Barium meal;
 Dilation of stomach
 Deformed duodenal cap
 Stasis ulcer
 Distal duodenal normality
 Delayed emptying time
 Normal stomach empties in 3-4 hours
 >6 hours: hypotonia, pylorospasm

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 >24 hours: organic pyloric stenosis (e.g. GOO)

Differential diagnoses of gastric outlet obstruction
 Gastric cancer  Annular pancrease
 Peptic ulcer disease  Pancreatic cancer
 Crohn’s disease  Hypertrophic pyloric stenosis
 Caustic injury  Chronic pancreatitis
 Large gastric polyps  Superior mesenteric artery
 Gastric tuberculosis syndrome
 Gastric bezoars  Lymphadenopathy
 Gastric volvulus  Cholangiocarcinoma

 Treatment
o Decompression with NGT, IV hydration and electrolyte repletion and
acid suppression.
o Balloon dilation and operation
 Acute ulcers with obstruction are treated conservatively
(above), but most patients with significant obstruction from
chronic ulceration will require substantial intervention; either
ballooning or operation.

Medical treatment of peptic ulcer disease

 PPIs are the mainstay of medical treatment for PUD, but high dose H2RAs and
sucralfate are also quite effective.
 PUD patients should stop smoking.
 H. pylori eradication: PPI + 2 antibiotics
o PPI + clarithromycin 500mg bid + amoxicillin 1000mg bid for 10-14d
o PPI + clarithromycin + metronidazole 500mg bid for 10-14d
o PPI + amoxicillin for 5d, the PPI + clarithromycin + tinidazole 500mg
bid for 5d
Indications for diagnosis and treatment of H. pylori
 Active PUD
 Confirmed history of PUD (previously untreated H. pylori)
 Gastric MALT lymphoma (low grade)
 After endoscopic resection of early gastric cancer
 Uninvestigated dyspepsia (depending on H. pylori prevalence)

Surgical treatment of peptic ulcer disease

The indications for surgery are;
 Bleeding
 Perforation
 Obstruction
 Intractability or non-healing
o Multiple recurrences
o Large ulcers (>2cm)

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o Complications
o Suspected malignancy
Differentials for intractable or non-healing PUD
 Cancer: gastric, pancreatic, or duodenal
 Persistent H. pylori infection
o Tests may be negative
o Consider empiric treatment
 Non-compliant patient: failure to take medications
or still using NSAIDs or smoking
 Motility disorder
 Zollinger-Ellison syndrome

Surgical options in the treatment of PUD

Indication Duodenal Gastric
Bleeding 1. Oversewa 1. Distal gastrectomyb
2. V + A 2. Oversew, biopsy, V + D
3. Oversew, V +D 3. Oversew and biopsya
Perforation 1. Patcha 1. Biopsy and patcha
2. Patch, HSV 2. Wedge excision, V + D
3. Patch, V + D 3. Distal gastrectomyb
Obstruction 1. HSV + GJ 1. Biopsy; HSV + GJ
2. V + A 2. Distal gastrectomyb
Intractability/non- 1. HSVb 1. HSV and wedge excision
healing 2. V + D 2. Distal gastrectomy
3. V + A
a
Unless the patient is in shock or moribund, a definitive procedure should be considered.
b
Operation of choice in low-risk patient (read Blatchford and Rockall risk stratification).
GJ = gastrojejunostomy; HSV = highly selective vagotomy; V +A = vagotomy and antrectomy;
V + D = vagotomy and drainage
Most patients undergoing operation for bleeding and perforated PUD have these procedures.

Highly selective vagotomy (HSV)

 Also called parietal cell vagotomy or proximal gastric vagotomy
 Severs the vagal nerve supply to the proximal two-thirds of the stomach.
 Reduces acid secretion by 75%, and GI side-effects are rare.
 HSV may be substituted for truncal vagotomy.
 Taylor procedure: posterior truncal vagotomy and anterior seromyotomy. It is
an attractive and simple alternative to HSV with similar results.
Vagotomy and drainage (V + D) procedures
 Safe and quick
 10% have dumping and/or diarrhea
 Unlike HSV, it is widely accepted as an operation for complicated PUD.
 Also used for type II and III gastric ulcers.
 The two paradigmatic V + D procedures are;
o Truncal vagotomy and gastrojejunostomy (GJ)
 Truncal vagotomy denervates the antropyloric mechanism.

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 GJ is a good choice for patients with GOO or severely

diseased duodenum. The anastomosis is done between
proximal jejunum and the most dependent part of greater
curvature.
 Antecolic GJ: for malignant cases
 Retrocolic GJ: for benign cases.
o Truncal vagotomy and pyloroplasty
 Pyloroplasty is useful in;
 Pyloroduodenostomy
 Focal pyloric scarring
 When GJ is technically difficult
 There are three types of pyloroplasty;
 Heineke-Mickulicz: most common
 Finney pyloroplasty
 Jaboulay pyloroplasty
Vagotomy and distal gastrectomy
 Distal gastrectomy leaves 50% of gastric remenant.
 Addition of vagotomy should be considered for type II and III gastric ulcers.
 Vagotomy + antrectomy (V + A)
o Antrectomy leaves 60-70% of gastric remnant.
o Low recurrence
o Applicable for many patients with complicated PUD.
o High operative mortality and is irreversible.
o GI continuity after antrectomy;
 Billroth I gastroduodenostomy
 Billroth II loop gastrojejunostomy
o Avoid in unstable patients, and in patients with extensive
inflammation and/or scarring of proximal duodenum, because secure
anastomosis may be difficult.
 Subtotal gastrectomy (leaves 25% of gastric remnant) without vagotomy is
used to treat to treat PUD today.
 Pylorus preserving gastrectomy was first reported as a surgical option for
gastric ulcer which could minimize both dumping and duodenogastric reflux.

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Gastric Carcinoma
Gastric cancer is a major cause of cancer Frequencies of gastric cancer
death worldwide. It is actually a curable Adenocarcinoma: 94%
disease provided that it is detected at early Lymphoma: 4%
Malignant GIST: 1%
stage and treated adequately. Early Others: angiosarcoma, carcinoid,
diagnosis is therefore, key to success with squamous cell carcinoma, and
this disease. Unfortunately, the late carcinosarcoma
Secondaries
presentation of many cases is the cause
Direct invasion: colon, pancreas
for the poor overall survival figures. The Peritoneal seeding: ovary
only treatment modality able to cure the Hematogeneous: melanoma or breast
disease is resectional surgery.
Epidemiology
 Gastric cancer is the fourth most common cancer type and the second
leading cause of cancer death worldwide.
 The estimated 5-year survival is 27%
 A disease of the elderly.
 Twice as common in blacks.
 Higher incidence in lower socioeconomic status.
Etiology/risk factors
 H.pylori infection: 3-fold increased risk. H. pylori infected patients have
decreased risk for development of carcinoma of distal esophagus and
cardia region.
 Smoking
 Pernicious anemia
 Premalignant conditions
o Atrophic gastritis Decreased risk
o Hyperplastic polyp Aspirin
o Adenoma Diets high in fresh fruits and
vegetables
o Benign gastric ulcer Vitamin C and E
o Stomach remnant
o Ménétrier’s disease
o Intestinal metaplasia
 Blood group A
 Diet; starchy diet high in pickled, salted, or smoked foods. Dietary nitrates
are possible causes of gastric cancer. Gastric bacteria convert nitrate in to
nitrite; a proven carcinogen.
 Family history
 Previous gastrectomy or GJ >10 years ago
 Familial adenomatous polyposis
 Hereditary non-polyposis colon cancer (HNPCC)
Pathology

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 Gastric dysplasia is a universal precursor to gastric adenocarcinoma.

 There are four gross forms of gastric cancer;
o Polypoid
o Fungating
o Ulcerative
o Scirrhous
 Early gastric carcinoma
o Adenocarcinoma limited to mucosa and submucosa regardless of
LN status. 10% have LN metastasis.
o 70% are well differentiated, and 30% are poorly differentiated.
o 95% cure rate with adequate gastric resection and
lymphadenectomy.
o Location of primary tumor: 40% proximal, 30% middle, and 30%
distal.
o Types of early gastric adenocarcinoma (Japanese classification)
 Type I (protruding): polypoid tumors
 Type II (superficial): with or without minimal elevation or
depression;
 IIA: superficial elevated
 IIB: superficial flat
 IIC: superficial depressed
 Type III (excavated): deep depression
 Advanced gastric carcinoma
o Involves muscularis externa and, sometimes, the serosa with or
without lymph node involvement.
o Classified in to four (Bormann classification);
 Type I: polypoid
 Type II: ulcerated with elevated borders
 Type III: ulcerated and infiltrates the gastric wall
 Type IV: diffuse (linitis plastica)
 Histologic classifications
o Lauren classification
 Intestinal; 53%
 Diffuse; 33%
 Unclassified; 14%
o WHO (Japanese) classification. The Japanese classification is
similar to, but more detailed than WHO classification.
 Adenocarcinoma
 Papillary
 Tubular
 Mucinous

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 Signet-ring cell
 Adenosquamous carcinoma
 Small cell carcinoma
 Undifferentiated carcinoma
 Others
o Ming classification
 Expanding; 67%
 Infiltrative; 33%
Lauren classification of gastric cancer
Features Intestinal Diffuse
Etiology Environmental Familial, blood group A, pernicious
anemia, genetic predisposition
Location Atrophic gastritis, intestinal Normal gastric mucosa
metaplasia, and dysplasia Proximal stomach
Distal stomach
Sex M>F F>M
Age Older Younger
Histology Gland formation Poorly differentiated signet-ring cells
Spread Hematogenous spread Transmural/lymphatic spread
Localized infiltration Diffuse infiltration
Nodular hepatic metastases Diffuse hepatic metastases
Infrequent peritoneal dissemination Frequent peritoneal dissemination
Mutation Microsatellite instability, APC, p53, Decreased E-cadherin, p53, p16
p16
Prognosis Good Bad
H. pylori Associated Associated

Clinical features
 Most common symptoms are weight loss and decreased food intake due
to anorexia and early satiety.
 Abdominal pain is also common.
 Other symptoms: nausea, vomiting, and bloating.
 Acute GI bleeding is unusual (5%), but chronic blood loss is common and
manifests as iron deficiency anemia and heme-positive stool.
 Dysphagia is common if it involves the cardia.
 Paraneoplastic syndromes: Trousseau’s syndrome (thrombophlebitis),
acanthosis nigricans (skin hyperpigmentation), or peripheral neuropathy.
 Physical examination
o Typically normal.
o Other than signs of weight loss, specific findings indicate
incurability.
o Lymph node involvement;
 Cervical lymphadenopathy

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 Supraclavicular LAP (on the left referred to as Virchow’s

nodes/Troiser’s sign)
 Axillary (on the left referred to as Irish nodes)
o Distant metastasis;
 Liver mass, malignant ascites
 Pleural effusion
 Rectovesical deposits (Bloomer’s shelf-drop metastasis)
 Periumblical nodules (Sister Mary Joseph’s nodules)
 Ovary (Krukenberg’s tumor)
 Modes of spread
o Direct; stomach, pancreas, colon, liver, & diaphragm.
o Lymphatic; cervical, supraclavicular, and axillary.
o Hematogeneous: first to liver. Uncommon before LAP
o Transperitoneal: ascites, Bloomer’s shelf, Sister Joseph’s
nodules, Krukenberg’s tumor.
Diagnostic evaluation
 Upper GI endoscopy and biopsy (gold-standard)
o All patients above age 45
o All patients with alarming symptoms
o Patients with family history of gastric cancer
 Upper GI series
 Abdominal/pelvic CT/MRI for preoperative staging of the cancer.
 EUS for local staging of tumor. 80% accurate.
 PET scanning
 Staging laparoscopy and peritoneal cytology.
Treatment
 Surgical resection is the only curative treatment.
 Obvious exceptions include;
o Patients unable to tolerate abdominal operation
o Patients with highly metastasized disease
 The goal of curative treatment is resection of all tumor (R0 resection), and
adequate lymphadenectomy.
 Extent of resection
o Standard: radical subtotal gastrectomy
 Removal of 75% of distal stomach, including pylorus and
2 cm of duodenum, greater and lesser omentum, and all
associated lymphatic tissue.
o Unless required for R0 resection, total gastrectomy confers no
additional survival benefit and has adverse nutritional or quality-
of-life consequences, and higher morbidity and mortality.

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o Proximal subtotal gastric resection: is an alternative to total

gastrectomy for proximal tumors. It requires an
esophagogastrostomy.
o Reconstruction after resection;
 Billroth I after distal gastrectomy
 Billroth II gastrojejunostomy after radical subtotal
gastrectomy
 Roux-en-Y: if small gastric remnant is left
 Roux-en-Y esophagojejunostomy after total gastrectomy.
The construction of jejuna pouch can be beneficial
nutritionally.
 Extent of lymphadenectomy;
o D1 lymphadenectomy: dissection of stations 1 through 7
o D2 lymphadenectomy: dissection of D1 & D2 nodes.
o The standard radical subtotal gastrectomy is called D1 resection
o Total gastrectomy is a D2 resection.
 Chemotherapy and radiation;
o For highly metastatic disease.
o Chemotherapy is important when D1 or less than adequate D1
gastrectomy is done.
o After D2 lymphadenectomy chemotherapy has no such a
significant survival benefit.

Postgastrectomy Complications
Complications of gastric surgery
Complications of vagotomy Complications of gastrojejunostomy
Gastric stasis Stomal obstruction
Gallstones Retrograde intussusceptions
Diarrhea Gastrojejunocolic fistula
Hypoacidity; bacterial overgrowth Stump carcinoma
Complications of gastrectomy Osteoporosis
Anemia Roux syndrome
Weight loss
Dumping syndrome
Roux syndrome
Bile reflux

Dumping syndrome
 A phenomenon caused by destruction or bypass of the pyloric sphincter.
 Occurs in 5-10% of patients after pyloroplasty, pyloromyotomy, or distal
gastrectomy.
 Consists of constellation of post-prandial symptoms ranging in severity from
annoying to disabling.
 There are two types of dumping syndrome;

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o Early dumping syndrome, and

o Late dumping syndrome
 Treatment
o Dietary management
 Small dry foods
 Avoid liquids during meals
 Adding dietary fibers at meal time
o Octreoid 100 μg (can be increased up to 500 μg) bid if dietary
management fails.
o Only a very small percentage of patients ultimately require surgery.
Features Early dumping Late dumping
Onset 15-30 minutes after meal 2-3 hours following meal
Cause Abrupt delivery of hyperosmolar Post-prandial reactive
load in to small bowel causing hypoglycemia due to rise of
hypovolemia insulin level.
Relief Lying down or saline infusion Administration of sugar
Exacerbation Taking meal Exercise
Symptoms Diaphoresis, weakness, light- Tremor, fainting, weakness,
headedness, tachycardia, nausea, sweating, dizziness.
vomiting, bloating.
Treatment Small dry foods, octreoid Dietary management and
octreoid.

Diarrhea
 Diarrhea may be the result of;
o Truncal vagotomy,
o Dumping, or
o Malabsorption.
 It occurs soon after surgery and is not associated with other symptoms; a fact
that distinguishes it from dumping.
 Treatment
o Cholestyramine, codein or loperamide
o Octreoid should be tried
o Rarely operation is considered in debilitating post-vagotomy diarrhea
unresponsive to medical management.

Gastric stasis
 Gastric stasis after gastric surgery can be due to;
o Motility disorder: preexisting, or secondary to deliberate or
unintentional vagotomy or resection of dominant pacemaker.
o Obstruction: mechanical or functional
 Present with vomiting (undigested food), bloating, epigastric pain, and weight
loss.

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 Evaluation: EGD, upper GI and small bowel series, gastric emptying scan, and
gastric motor testing.
 After ruling out obstruction, medical treatment is successful in most cases of
motor dysfunction.
o Dietary modification
o Promotility agents
o Intermittent oral antibiotics
 Gastroparesis following V + D may be treated with subtotal gastrectomy.

Bile reflux
 Most patients are asymptomatic, but a small subset of patients have bile reflux
gastritis and present with nausea, bilious vomiting, and epigastric pain, and
quantitative evidence of excess enterogastric reflux.
 Enterogastric reflux is greatest after Billroth II and least after vagotomy and
pyloroplasty, with Billroth I giving intermediate values.
 Symptoms often occur months or years after index operation.
 Ddx: afferent or efferent loop obstruction, gastric stasis, and small bowel
obstruction.
 Evaluation: plain abdominal x-rays, upper GI endoscopy, upper GI series,
abdominal CT, and gastric emptying scan.
 Treatment is usually operative. There are many options (read).

Roux syndrome
 In a subset of patients who had distal gastesctomy and Roux-en-Y GJ.
 Difficulty with gastric emptying.
 Present with vomiting, epigastric pain, and weight loss.
 Endoscopy, upper GI series.
 Treatment
o Medical: promotility agents
o Surgical: paring down the gastric remnant

Gallstones
 Secondary to vagal denervation of gallbladder with attendant gallbladder
dysmotility and stasis.
 Cholecystectomy if gallbladder appears abnormal.

Weight loss
 Weight loss is common after gastric resection and/or vagotomy.
 The degree of weight loss tends to parallel the magnitude of the operation.
 Causes of weight loss after gastric surgery;

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o Altered dietary intake (most common): due to small stomach

syndrome, postoperative gastroparesis, anorexia, or self imposed
dietary modification due to dumping and/or diarrhea.
o Malabsorption
 Consultation with dietitian may prove invaluable.

Anemia
 The most common metabolic side-effect after gastric surgery.
 Iron absorption takes place primarily in the proximal GIT, and is facilitated by
acidic environment. Intrinsic factor is made by parietal cells. Vitamin B12
bioavailability is affected by an acidic environment.
 Types of anemia
o Iron deficiency anemia
o Vitamin B12 deficiency anemia
 Nutrient status should be corrected with oral and/or parentral supplementation.

Bone disease
 Calcium absorption occurs primarily in the duodenum, which is bypassed with
GJ.
 Fat malabsorption may occur because of blind loop syndrome and bacterial
overgrowth or inefficient mixing of food and digestive enzymes. This can affect
absorption of vitamin D, a fat soluble vitamin.
 Manifest as pain and/or fractures years after the index operation.
 Dietary supplementation of calcium and vitamin D may be preventive.

Gastric Lymphoma
The stomach is the most common site of primary GI lymphoma, and over 95% are
non-Hodgkin’s type. Most are B-cell type, thought to arise from MALT. About half
are high grade and half are low grade.
They are associated with H. pylori infection. Low grade MALT lymphoma arises
from a background of chronic gastritis associated with H. pylori.
They may present similarly with gastric carcinoma. The tumors may bleed and/or
obstruct. Systemic symptoms such as fever, weight loss, and night sweats
Diagnosis is by endoscopy and biopsy. Diffuse infiltration is more suggestive of
secondary gastric involvement.
Low grade lymphomas are treated with H. pylori eradication. Radiation and
chemotherapy should be considered for resistant disease.
High grade lymphomas are mostly treated with radiation and chemotherapy. For
disease limited to stomach and regional lymph nodes, radical subtotal D2
gastrectomy may be performed.

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Gastrointestinal Stromal Tumors (GISTs)

GISTs arise from interstitial cells of Cajal (ICC). Stomach is the most common site
for GISTs; two-thirds occur in the stomach. They are submucosal tumors that grow
slowly. Most common route of metastasis is hematogeneous often to liver and/or
lung. Any lesion >1cm can behave in a malignant fashion and recur. Thus all
GISTs are best resected along with normal margin of tissue. Commonly present
with bleeding due to ulceration. Other symptoms include weight loss, abdominal
pain, fullness, early satiety. Diagnosis is by endoscopy and biopsy. Most GISTs
occur in the body of the stomach. They are almost always solitary. Wedge
resection with clear margins is adequate surgical treatment. Five year survival
flowing resection is 50%. GISTs are usually positive for the proto-oncogen c-kit.
Imantinib administration is recommended.

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CHAPTER SIX-THE PANCREAS

Surgical Anatomy and Physiology

Anatomy of the pancreas
 Pancreas [Greek ‘pan’ (all) and ‘kreas’ (flesh)].
 A retroperitoneal organ crossing L1 & L2 (the level of transpyloric plane).
 Lies obliquely from C-loop of duodenum to splenic hilum.
 Weight = 75-100g.
 Length = 15-20cm.
 Pancreatic pathologies usually present with poorly localized and ill-defined
nature due to the fact that it is situated deep in the abdomen and sealed in the
retroperitoneum.
 The transverse mesocolon attaches to its anterior margin.
 Regions of the pancreas
o Head, neck, body, and tail.
o The head lies anterior to vena cava, right renal artery, & renal veins.
o The neck lies anterior to portal vein.
o The superior mesenteric vein joins splenic vein to form portal vein
behind the neck of the pancreas.
o The superior mesenteric artery lies parallel to and just to the left of the
superior mesenteric vein.
o The uncinate process and the head of the pancreas wrap around the
right side of the portal vein and end posteriorly near the space
between the SMV & SMA.
o The common bile duct runs in the deep groove on the posterior
aspect of the head of pancreas.
o The body and tail lie just anterior to the splenic artery and vein.
o The splenic vein runs in a groove on the back of the pancreas. The
splenic artery, often tortuous, runs parallel and just superior to splenic
vein.

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Fig: Anatomy of the pancreas

 Pancreatic duct anatomy
o Main pancreatic duct (duct of Wirsung)
 The duct from the smaller ventral bud which joins CBD and
drains in to the duodenum thru the major papillae.
o Accessory pancreatic duct (duct of Santorini)
 The duct from the larger dorsal bud, which arises from the
duodenum, directly drains in to the duodenum thru the lesser
papillae.
o The ducts from each anlage usually fuse in the pancreas.
o The anatomy of the pancreatic ductal system highly varies.

Fig: Anatomy and embryology of pancreatic ductal system

 Vascular anatomy
o Arterial supply
 Celiac trunk
 Splenic artery
 Superior pancreaticoduodenal artery (anterior and
posterior) a branch of gastroduodenal artery.
 Superior mesenteric artery
 Inferior pancreaticoduodenal artery (anterior and
posterior)
o Venous drainage from the pancreas occurs via corresponding
pancreatic veins, tributaries of the splenic and SMV.
o Pancreatic lymph vessels follow the blood vessels.
 Most vessels end in pancreaticosplenic nodes
 Some end in pyloric nodes.
 Efferent vessels from these nodes drain to superior
mesenteric nodes or celiac nodes via hepatic nodes.
 Neuroanatomy
o The pancreas is innervated by sympathetic and parasympathetic
nerves.
o The parasympathetic system stimulates endocrine and exocrine
secretions and sympathetic system inhibits secretion.
o The pancreas also has rich supply of afferent sensory fibers, which
are responsible for the intense pain associated with panceatitis.

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Histology and physiology

 The pancreatic mass
o Exocrine pancreas: 85%
o Extracellular matrix: 10%
o Blood vessels and major ducts: 4%
o Endocrine pancreas: 2%
 Exocrine pancreas
o Pancreas secrets approximately 500-800mL per day of colorless,
odorless, alkaline (pH 8.4), isosmotic pancreatic juice (a combination
of acinar and ductal secretions).
o All pancreatic enzymes are produced as inactive zymogens except
pancreatic amylase. Pancreatic lipase is also secreted in an active
form, but colipase, secreted by the pancreas, binds to it and
increases its activity.

Pancreatic enzymes
Enzyme Substrate Product
Carbohydrate
Amylase (active) Starch, glycogen Glucose, maltose,
maltoriose,
dextrins
Protein
Endopeptidases Cleave bonds Amino acids,
Trypsinogen (activated by enterokinase) between dipeptidases
Chymotrypsinogen (activated by aminoacids
enterokinase and trypsin)
Proelastase (activated by enterokinase -
and trypsin) Cleave
Exopeptidases aminoacids from
Procarboxy peptidase A & B (activated by end of peptide
entrokinase and trypsin) chain
Fat
Pancreatic lipase (acitve) Triglycerides 2-Monoglycerides,
fatty acids
Phospholipase A2 (activated by trypsin) Phospholipases -
Cholesterol esterase Neutral lipids -
N.B. Enterokinase is produced by duodenal mucosa.

 Endocrine pancreas (Islets of Langerhans)

o Clusters of endocrine cells
 β cells (75%): produce insulin, amylin (islet
amyloidpolypeptide - IAPP), and pancreastatin
 α cells (20%): produce glucagon
 δ cells: produce somatostatin
 ε cells: produce gherlin
 PP cells: produce PP (pancreatic polypeptides)
o B cells form an inner core in the islets.
o Islets in the head and uncinate process (ventral anlage) have a higher
percentage of PP cells and fewer α-cells, whereas islets in the body

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and tail (dorsal anlage) contain the majority ofα-cells and few PP
cells.
o In contrast to acinar cells which secrete all types of enzymes, islet
cells specialize in secreting only one hormone.

Diagnostic Modalities
Investigations of the pancreas
 Serum enzyme levels
 Pancreatic function tests
 Morphology
o Ultrasound scan
o Computed tomography
o Magnetic resonance imaging
o Endoscopic retrograde cholangiopancreatography
o Endoscopic ultrasound
o Plain radiography

Congenital Anomalies
Congenital anomalies of pancreas
More frequent Less frequent
Cystic fibrosis Aplasia
Annular pancreas Hypoplasia
Pancreas divisum Hyperplasia
Rotational anomalies Hypertrophy
Polycystic disease Dysplasia
Ectopic pancreas, accessory pancreas Pancreatic gallbladder
Choledochal cysts VHL syndrome
Vascular anomalies
Horseshoe pancreas

Cystic fibrosis
 Cystic fibrosis is generally thought of as a pulmonary as most its of the
morbidity and mortality is related to pulmonary complications.
 A multisystem disorder of the exocrine glands that affects the lungs, intestines,
pancreas, and liver.
 Characterized by elevated sodium and chloride ion concentration in sweat.
“the child is salty when kissed”
 Autosomal recessive inheritance.
 It occurs most frequently in Caucasians.
 CFTR (cystic fibrosis transmembrane conductance regulator) mutation.
 This gene creates a cell membrane protein that helps control the movement of
chloride ion across cell membrane.
 Most of the organ damage is due to blockage of narrow passages by
thickened secretions.

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 Pancreatic insufficiency leads to fat malabsorption.

 Steatorrhea is present from birth.
 DM in older patients; islets appear normal though.
 The liver may become cirrhotic.
 Infertility
o Absence of vas deferens in men and
o Thick cervical mucus in women
 Outside newborn period
o Poor growth
o Poor appetite
o Rancid greasy stools
o Abdominal distention
o Chronic respiratory disease
o Finger clubbing
o Delayed secondary sexual characteristics
 Diagnosis
o Genetic testing
o Sweat test
 Levels of sodium and chloride ions in the sweat above
90mmol/L confirm the diagnosis.
o Treatment
 Treatment is aimed at control of secondary consequences of
the disease.
 Preserve pulmonary function by physiotherapy and
antibiotics
 Malabsorption: oral pancreatic enzyme preparations.
 Diet should be low in fat but contain added salt.
 End stage: lung transplantation
Clinical manifestations of cystic fibrosis
Pulmonary Gastrointestinal
Bronchiectasis GERD
COPD Meconium ileus
Airway hyperreactivity Intussusceptions
Obstructive sleep apnea Rectal prolapse
Hemoptysis Fibrosing colonopathy
Constipation
GI cancers
Pancreatic disease Hepatobiliary disease
Pancreatic insufficiency Cystic fibrosis-related liver disease (CFLD)
Pancreatitis Micro-gallbladder
Cystic fibrosis-related diabetes Chilelithiasis
(CFRD) Chilecystitis

Pancreas divisum
 Occurs when the embryological ventral and dorsal pancreas fail to fuse.
 Incidence:
o 5% in autopsy series
o 10% in ERCP and MRCP series

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o 25-50% in patients with recurrent acute pancreatitis, chronic

pancreatits, and pancreatic pain.
 A large volume of secretions flowing throught the narrow papilla often leads to
incomplete drainage, which may then cause obstructive pain or pancratitis.
 Exclude pancreas divisum in patients with idiopathic recurrent pancreatitis.
 Diagnosis: MRCP, EUS, or ERCP, augmented by injection of secretin.
 Treatment
o Endoscopic sphincterotomy and stenting of minor papillae (ERCP)
o Surgical interventions;
 Sphincteroplasty
 Pancreatojejunostomy
 Resection of pancreatic head

Annular pancreas
 A result of failure of complete rotation of ventral pancreatic bud.
 A ring of pancreatic tissue surrounds the third part of duodenum.
 Most often associated with congenital duodenal stenosis or atresia and is
therefore more common in children with Down syndrome.
 Duodenal obstruction typically causes vomiting in the neonate.
 The usual treatment is bypass (duodenoduodenostomy).
 The disease may occur later in life in which case resection of the head of
pancreas is preferable.

Ectopic pancreas
 Stomach
 Duodenum or small intestine (including Meckel’s diverticulum)
 Gallbladder
 Adjoining the pancreas
 In the hilum of the spleen
 Within the liver

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Acute Pancreatitis
Definition and epidemiology
 Acute pancreatic inflammation associated with little or no fibrosis.
 It is the most common GI diagnosis in USA.
 Mortality rate = 1/100,000; the 14th most fatal and 9th most common non-
cancer GI death.
 Incidence = 5-80/100,000.
Etiology
 The two most common causes of acute pancreatitis, which account for more
than 80% of the cases, are;
1. Gallstones
2. Alcohol
 Others are listed in the following table.
Etiologies of acute pancreatitis
Alcohol Ischemia
Biliary tract disease Hypoperfusion
Hyperlipidemia Atheroembolism
Hereditary Vasculitis
Hypercalcemia~ Pancreatic duct obstruction
Trauma Neoplasms
External Pancreas divisum
Surgical Ampullary and duodenal
ERCP (1-3%) lesions
Drugs Infections
Thiazide diuretics, furosemide, estrogens, azathiprin, Venoms (scorpion)
6-mercaptourine, 1-asparaginase, methyldopa, Idiopathic
sulfonamides, tetracycline, pentamidine,
procainamide, nitrofurantonin, valproate, ACEIs,
dideoxyinosine.

Pathophysiology
 Activation of zymogens inside acinar cells, which cause acinar cell injury.
 Then the subsequent events include;
o Inflammatory cell recruitment and activation, and
o Generation and release of cytokines and other mediators.
Clinical features
 Pain is the cardinal symptom;
o Sudden, reach maximum within minutes, and persists for hours or
even days.
o Severe, constant, and refractory to usual doses of analgesics.
o First in the epigastrium, but may be localized to either upper quadrant
or felt diffusely.
o Radiation to the back in 50% of patients.
o Relieved by sitting or leaning forward.
o Mimics most causes of acute abdomen.
 Nausea, repeated vomiting, and retching.
 Examination

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o From well to gravely ill general appearance.

o SIRS; presence of two of the following;
 Heart rate >90/min,
 Temperature <36 or >380C,
 Respiratory rate >20/min or pCO2 <32mmHg, and
 WBC count <4000 or >12000/mm3
o Bluish discoloration of skin due to bleeding in to fascial planes;
 Grey Turner’s sign: bleeding in to flanks.
 Cullen’s sign: bleeding in to umbilicus.
o Abdominal examination;
 Distension due to ileus or ascites
 Mass in the epigastrium
 Guarding in the upper abdomen
o Pleural effusion 10-20%
o Pulmonary edema and pneumonitis
Local complications of acute pancreatitis
Acute (<4wks, no defined wall) Chronic (>4wks, defined wall)
Content No infection Infection No infection Infection
Fluid Acute pancreatic Infected Pseudocyst Infected
fluid collection APFC pseudocyst
(APFC)
Solid ± fluid Acute necrotic Infected Walled off Infected
collection (ANC) ANC necrosis (WON) WON

Systemic complications of acute pancreatitis

Pulmonary Hematologic
Pneumonia, atelectasis Hemoconcentration
ARDS DIC
Pleural effusion GI hemorrhage
Cardiovascular Peptic ulcer
Hypotension Erosive gastritis
Hypovolemia Portal/splenic vein thrombosis with
Sudden death varices
Non-specific ST-T wave changes Metabolic
Pericardial effusion Hyperglycemia
Renal Hypocalcemia
Oliguria Hypertriglyceridemia
Azotemia Encephalopathy
Renal artery/vein thrombosis Sudden blindness (Purtscher’s
CNS retinopathy)
Psychosis Fat necrosis
Fat emboli Intra-abdominal saponification
Alcohol withdrawal syndrome Subcutaneous tissue necrosis

Diagnosis
 Abdominal pain consistent with acute pancreatitis.
 Elevation of serum amylase or lipase >3X upper normal limit.
o Normal serum amylase level does not exclude acute pancreatitis,
especially if the patient presented few days later.
o Serum lipase is more sensitive and specific than amylase.

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 CECT only if the diagnostic criteria are not met.

 Gallstones should be investigated by ultrasonography.
 Assessment of severity: many scoring systems are available.
o Ranson and Glascow scoring is specific for acute pancreatitis.
o Others: APACHE, SOFA, MODS, SAPS, and modified Marshall.
o Regardless of the system, persisting organ failure indicates a severe
attack.
Determinants No local Sterile local Infected local
complication complication complication
No organ failure Mild Moderate Severe
Transient organ Moderate Moderate Severe
failure
Persistent organ Severe Severe Critical
failure

o The risk of mortality reflects the severity;

 Mild: <1%
 Moderate: 10%
 Severe: 20-40%
 Critical: >50%
o Multiple organ failure is defined as two or more organs registering 2
or more points on these scoring systems.
Ranson’s prognostic signs of acute pancreatitis
Criteria for acute pancreatitis not due to gallstones
At admission During the initial 48 hrs
Age >55yrs Hct fall >10 points
WBC >16,000/mm3 BUN elevation >5mg/dL
Blood glucose >200mg/dL Serum calcium <8mg/dL
Serum LDH >350IU/L Arterial PO2 <60mmHg
Serum AST >250U/dL Base deficit >4mEq/L
Estimated fluid sequestration >6L
Criteria for acute gallstone pancreatitis
At admission During the initial 48 hrs
Age >70 yrs Hct fall >10 points
WBC >18,000/mm3 BUN elevation >2mg/dL
Blood glucose >220mg/dL Serum calcium <8mg/dL
Serum LDH >400IU/L Base deficit >5mEq/L
Serum AST >250U/dL Estimated fluid sequestration >4L
Definition
 <3 criteria: mild, uncomplicated
 3-6 criteria: moderate
 >6 criteria: severe`or critical disease

Management
1. Pain management
o NSAIDS
o Opioids for more severe disease
2. Fluid resuscitation

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o Normal saline, crystalloids

o Ringered lactate: superior
3. Nutritional support
o Entral route is preferred; parentral route is offered only if the calculated
nutritional requirements cannot be achieved by entral route.
o Commenced after initial fluid resuscitation and within 24 hrs of admission.
o Introduced through NGT and increased in stepwise fashion.
4. Early (within 24-48hrs) ERCP reduces complications, and not mortality, in
calculous pancreatitis.
5. Antibiotics
o Broad spectrum antibiotics is usually used in established infections,
o Evidences do not support prophylactic use.
6. Managing local complications
7. Managing organ failure
8. Cholecystectomy to prevent recurrent gallstone pancreatitis.

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Chronic Pancreatitis
Chronic pancreatitis is a progressive inflammatory disease in which there is
irreversible destruction of pancreatic tissue. It has multifactorial etiology, highly
variable presentation, and challenging to treat successfully. The prevalence
ranges from 5-40 per 100,000. The disease occurs most frequently in males (4:1),
and the mean age of onset is about 40 years.

Etiology
 High alcohol consumption;
o The most common cause accounting for 60-70% of cases.
o But only 5-10% of people with alcoholism develop the disease.
 Other causes
o Duct obstruction due to trauma, acute pancreatitis, gallstones,
and tumors
o Metabolic diseases such as hyperlipidemia and
hyperparathyroidism
o Autoimmune disease
o Hereditary pancreatitis, CF, infantile malnutrition, ingestion of
cyanogenic glycosides in cassava
o Idiopathic
Pathology
 At the onset of disease when symptoms have developed, the pancreas
may appear normal. Later, the pancreas enlarges and becomes hard as a
result of fibrosis.
 Singer and Chari classification of chronic pancreatitis based on
histopathology and etiology;
o Calcific/lithogenic (largest subgroup): alcohol, hereditary, tropical,
hyperlipidemia, hyperclacemia, drug-induced, idiopathic
o Obstructive: pancreatic tumors, ductal stricture, gallstone,
trauma-induced, pancreas divisum
o Inflammatory: unknown cause
o Autoimmune: PSC, sjogren’s syndrome, primary biliary cirrhosis
o Asymptomatic pancreatic fibrosis: chronic alcoholic, tropical
climates
Clinical features
 Pancreatic symptoms
o Upper abdominal or diffuse pain is the outstanding symptom. The
pain is often dull and gnawing with radiation to the shoulder.
o Nausea and vomiting.
 Malabsorption, steatorrhea, and weight loss.
 Pancreatogenic diabetes
 Complications usually bring the patient to the attention of the surgeon.
Any of the complications of acute pancreatitis can occur in chronic
pancreatitis.
Diagnosis
 Laboratory studies

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o Pancreatic products in the blood: enzymes, PP.

o Pancreatic exocrine secretions:
 Direct: enzymes, bicarbonate
 Indirect: bentiromide test, schilling test, fecal fat,
chymotrypsin and elastase,
 Imaging techniques
o Plain radiography
o Ultrasonography
o Computed tomography
o ERCP
o MRCP
o EUS
Endoscopic ultrasound features of chronic pancreatitis
Ductal changes Parenchymal changes
Duct size >3mm = dilation Inhomogeneous echo = edema
Tortuous pancreatic duct = ductal Reduced echogenic foci (1-3mm) =
irregularity edema
Intraductal echogenic foci = stones or Enhanced echogenic foci =
calcification calcifications
Echogenic duct wall = ductal fibrosis Prominent interlobular septae = fibrosis
Side-branch ectasia = periductal Lobular outer gland margin = fibrosis,
fibrosis glandular atrophy
Large, echo-poor cavities (>5mm) =
pseudocyst

Treatment
 Medical therapy
o Treat the addiction
o Alleviate abdominal pain
o Nutritional and pharmacologic measures
o Treat the diabetes
o Enzyme therapy
o Antisecretory therapy: somatostatin
 Neurolytic therapy of celiac plexus
 Endoscopic management
 Surgical therapy
o When medical therapy has failed.

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Pancreatic Neoplasms
Pancreatic neoplasms
Exocrine pancreatic neoplasms Endocrine pancreatic neoplasms
Carcinoma of pancreas Insulinomas (most common)
Gastrinoma (Zollinger Ellison
syndrome)
VIP-secreting tumor
Glucagonoma
Somatostatinoma
Non-functioning tumors

Pancreatic cancer


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CHAPTER SEVEN-THE BILIARY SYSTEM

Surgical Anatomy and Physiology

The gall bladder
 The gallbladder is a pear shaped structure, 7.5-12cm long, with an average
capacity of 30-50mL.
 It is found on the underside of the liver at the junction of the right and left lobes.
 When obstructed, the gallbladder can distend up to 300 mL.
 Anatomical divisions; fundus, body, infundibulum, and a neck.
 The fundus contains most of the smooth muscles of the organ, in contrast to
the body, which is the main storage area and contains most of the elastic
tissue.
 Mucus membranes have mucosal indentations that sink in to the muscle coat:
these are the crypts of Luschka.
 The same peritoneal lining that covers the liver covers the fundus and the
inferior surface of the gallbladder.
 Anatomic variations:
o The gallbladder may have a complete peritoneal covering and is
suspended in a mesentery off the inferior surface of the liver,
o It may be embedded deep inside the liver parenchyma (an
intrahepatic gallbladder).
 Layers of the gallbladder (histology)
o Mucosa
 Single, highly folded, tall columnar epithelium that contains
fat globules and cholesterol.
 Tuboalveolar glands in the infundibulum and the neck
(absent in body and fundus) secret mucus.
 Supported by a lamina propria.
o Muscle layer
 Has circular, longitudinal and oblique fibers which are not
well developed.
 The perimuscular subserosa contains connective tissue,
nerves, vessels, lymphatics and adipocytes.
o Serosa
 It is covered by serosa except where the gallbladder is
embedded in the liver.
 The gallbladder differs histologically from the rest of the GIT in that it lacks a
muscularis mucosae and submucosae.
 Neurovascular supply:
o The cystic artery which is usually a branch of the right hepatic artery
(90% of the time) supplies the gallbladder. It is nearly always found in
the triangle of calot (hepatocystic triangle); an area bounded by;
 Cyctic duct laterally,
 Common hepatic duct medially, and
 The liver margin superiorly.

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o Contents of the triangle of Calot;

 Right hepatic artery and its branches.
 Cystic artery
 Nodes of Lund
o Venous drainage;
 Small veins that enter directly in to the liver, or
 Cystic vein that carries blood back to portal vein.
o Lymphatic drainage;
 Cystic lymph nodes of Lund (sentinel node) found in the
junction between cystic and common hepatic ducts receive
lymph from subserosal and submucosal lymphatic vessels.
Efferent vessels from here go to hilum of the liver and celiac
lymph nodes.
 The subserosal lymphatic vessels also connect with the
subcapsular lymph channels of the liver, and this accounts
for the frequent spread of carcinoma of the gall bladder to the
liver.
o Nerve supply;
 Vagus nerve: the hepatic branch, and
 Sympathetic fibers from celiac plexus (C8 & C9).

Bile ducts
 The extrahepatic bile ducts consist of the right and left hepatic ducts, the
common hepatic duct, the cystic duct, and the common bile duct or
choledochus. This is a classical finding in one-third of the population; two-
thirds of the population has the variants (not abnormalities).
 The common bile duct enters the second portion of the duodenum through a
muscular structure, the sphincter of Oddi.
 The left hepatic duct is longer than the right and has greater propensity for
dilation as a consequence of distal obstruction.
 The common hepatic duct is 1-4cm in length and diameter of about 4mm.
 The cystic duct is about 3cm in length, but the length is quite variable. The
lumen is usually 1-3mm in diameter. The segment of it adjacent to GB neck
bears mucosal folds called the spiral valves of Heister, and the wall is
surrounded by a sphincteric structure called the sphincter of Lϋtken.
 The common bile duct;
o 7-11cm in length and 5-10mm in diameter.
o Four parts:
 Supraduodenal; 2.5cm, in free edge of lesser omentum.
 Retroduodenal
 Infraduodenal
 Intraduodenal; surrounded by the sphincter of Oddi, and
terminates by opening on the summit of the ampulla of
Vater.There, the pancreatic duct frequently joins it.
 The union of the common bile duct and the main pancreatic duct:
o In 70% of people, these ducts unite outside the duodenal wall and
traverse the duodenal wall as a single duct.

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o In about 20%, they join within the duodenal wall and have a short or
no common duct, but open through the same opening into the
duodenum.
o In about 10%, they exit via separate openings into the duodenum.
 The extrahepatic bile ducts are lined by a columnar mucosa with numerous
mucous glands in the common bile duct.
 A fibroareolar tissue containing scant smooth muscle cells surrounds the
mucosa. A distinct muscle layer is not present in the human common bile duct.
 Neurovasculatures;
o The arterial supply is derived from gastroduodenal and the right
hepatic arteries.
o The nerve supply is the same as for the gallbladder.

Functions of the gallbladder

 Reservoir for bile.
 Absorptive function: concentration of bile 5-10 times.
o The gall bladder stores approximately 80% of the bile
secreted by the liver during fasting.
o This storage capacity is possible because of the remarkable
absorptive capacity of the gallbladder; as the gallbladder
mucosa has the greatest absorptive power per unit area of
any structure in the body.
o Active absorption of water, sodium chloride and bicarbonate
by the mucous membrane of the gall bladder.
o The proportion of bile salts, bile pigments, cholesterol and
calcium increases.
 Secretory function;
o Mucus glycoprotein secretion (20mL/day) which protects the
mucosa from lytic action of bile and facilitate smooth
passage of bile.
o Hydrogen ion secretion: acidification facilitates calcium
solubility and prevents precipitation as calcium salts.
 Motor activity;
o Gallbladder filling is regulated by the sphincter of Oddi which
creates pressure gradient between the gall bladder and bile
ducts.
o Gallbladder emptying is facilitated by its gallbladder
contraction and sphincter of Oddi relaxation.
o One of the main stimuli to gallbladder emptying is the
hormone cholecytokinin (CCK) released from duodenal
mucosa in response to a meal.
 Neurohormonal regulatioin;
o Vagus stimulates contraction.
o Sympathetic stimulation is inhibitory.
o VIP, somatostatin and its analogs are inhibitors.
o CCK is stimulatory.

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Sphincter of Oddi
 4-6mm in length.
 It is a complex of four parts;
o Superior choledochal sphincter
o Inferior choledochal sphincter
o Ampullary sphincter
o Pancreatic sphincter
 Functions;
o Regulates flow of bile and pancreatic juice in to duodenum.
o Prevents regurgitation of duodenal contents in to biliary tree.
o Diverts bile in to gallbladder.

Fig: Anatomy of the gallbladder and bile ducts

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Diagnostic Modalities
Blood tests: CBC and LFT
 Elevated WBC count may indicate or raise suspicion of acute cholecystitis.
 Elevated WBC count and raised bilirubin, ALP, and ALT may indicate
cholangitis.
 Cholestasis is characterized by elevated conjugated bilirubin and ALP. Serum
aminotransferases may be normal or mildly elevated.
 In patients with biliary colic or chronic cholecystitis, blood tests will typically be
normal.

Ultrasonography
 Initial investigation of choice. The standard diagnostic test.
 Non-invasive, painless, no radiation.
 Depends on skills and experience of the operator.
 Not satisfactory in patients with obesity, ascites and distended bowel.
 It will show stones in the gallbladder with sensitivity and specificity of >90%.
o Stones are acoustically dense.
o They block passage of sound waves and produce post acoustic
shadow.
o Move with change in position unlike calcified polyps.
 It can demonstrate the size, thickness of gallbladder and presence of
inflammation around the gallbladder.
 Cholecystitis
o Thickening and local tenderness.
o Acute: edema in the wall or between wall and liver.
o Chronic: contracted, thick-walled gallbladder.
o When stone obstructs the neck, the gallbladder may become very
large but thin-walled.
 Extrahepatic bile ducts
o Are visualized except for retroduodenal portion.
o Dilation.
o Stones in the CBD.
o Periampulary tumors

Plain x-rays
 They show radio-opaque gallstones in 10% of patients.
o Rarely the center of stone may contain radiolucent gas in a triradiate
or tetraradiate fissure giving rise to a characteristic Mercedes Benz or
seagull sign.
 Calcification of gallbladder: porcelain gallbladder.

Computed tomography
 Inferior to USG in diagnosing gallstones.
 It is less affected by body habitus and is not operator dependent.
 It allows visualization of the liver, bile ducts, gallbladder and pancrease.

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 Particularly useful in detecting hepatic and pancreatic lesions.

 The major application of CT scan is to define the course and status of the
extrahepatic biliary tree and adjacent structures.
 The modality of choice in staging of cancers of liver, gallbladder, bile ducts
and pancrease.

Magnetic resonance cholangiopancreatography (MRCP)

 It is non-invasive and can provide either cross-sectional or projection images.
 Demonstrates ductal obstruction, strictures, or other intraductal abnormalities.
 It offers a single non-invasive test for diagnosis of biliary tract and pancreatic
diseases.

Endoscopic retrograde cholangiopancreatography (ERCP)

 It is both a diagnostic and therapeutic modality.
 The ampulla of Vatter can be visualized and cannulated.
 It provides ductal anatomy and can identify cause of obstruction such as
calculi and malignant strictures. It is particularly important in determining the
cause and level of obstruction.
 Bile aspirates can be sent for cytology and microbilogical examination and
endoluminal brushings can be taken from stricture for cytological studies.
 Therapeutic applications;
o Stone removal; especially distal CBD stones.
o Stent placement
 ERCP has evolved in to a mainly therapeutic rather than a diagnostic
technique.

Percutaneous transhepatic cholangiography (PTC)

 An invasive procedure done only when bleeding tendencies have been
excluded and patient’s prothrombin time is normal.
 Antibiotics should be given prior to procedure.
 Demonstrates areas of stricture and obstruction.
 Particularly useful in patients with bile duct strictures and tumors.
 Bile can be sent for cytology.
 Therapeutic interventions;
o Catheter can be placed for external biliary drainage.
o Biliary stent placement.
o Sphincterotomy.
 Potential risks: bleeding, cholangitis, bile break, & catheter related problems.

Biliary radionuclide scanning (HIDA Scan)

 Provides a non-invasive evaluation of the liver, gallbladder, bile ducts, and
duodenum with both anatomic and functional information.
 Primary use of HIDA scan is for diagnosis of acute cholecystitis.
 The sensitivity and specificity are 95% each.
 The gallbladder will be visualized within 30 minutes in 90% of individuals and
100% within 1 hour.
 Non-visualization of gallbladder is suggestive of acute cholecystitis.

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 Reduced or delayed visualization: chronic cholecystitis (contracted GB).

Summary: Diagnostic modalities
 Blood tests: CBC & LFT
 Plain x-ray
 Ultrasonography
 Radioisotope scan
 Computed tomography
 Magnetic resonance cholangiopancreatography (MRCP)
 Endoscopic retrograde cholangiopancreatography (ERCP)
 Percutaneous transhepatic cholangiography (PTC)
 Oral and IV cholangiography

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Gallstone Disease (Cholelithiasis)

Epidemiology
 The most common biliary pathology.
 Affects 11-36% of the general population.
 Risk factors;
o Age above 40 years.
o Female gender: 3X more prevalent.
o Body habitus: obesity, pregnancy, crohn’s disease.
o Previous surgeries:
 Terminal ileal resection
 Vagotomy involving the hepatic branch (first and largest
branch of left vagus nerve) - truncal vagotomy
 Gastric resection
o Dietary factors: high [animal] fatty meal.
o Hemolytic disorders: hereditary spherocytosis, sickle cell disease,
and thalassemia.
o Medications: OCP, somatostatin analogs,
o Family history: first degree relatives of patients have a twofold
greater prevalence.
o Prolonged NPO with parentral nutrition.
Natural history
 Gallstones are asymptomatic in more than 80% of cases. Asymptomatic
gallstones are usually diagnosed incidentally.
 For unknown reasons, approximately 3% of asymptomatic patients
become symptomatic per year. Once symptomatic, patients tend to have
recurrent bouts of biliary colic.
 About two-thirds of asymptomatic individuals remain symptom free after
20 years. All of these indicate that it is a very mild disease.
 Symptomatic gallstone disease progresses to complications in 3-5% of
symptomatic patients per year.
 Complications of gallstone disease;
o Acute cholecystitis,
o Chronic cholecystitis,
o Choledocholithiasis,
o Ascending cholangitis,
o Gallstone pancreatitis,
o Cholecystocholedochal fistula,
o Gallstone ileus,
o Mucocele
o Empyema and perforation of gallbladder, and
o Gallbladder carcinoma.
o Mirizzi syndrome.
Gallstone formation
 The major organic solutes in bile are bilirubin, bile salts, phospholipids, and
cholesterol.

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 Gallstones are classified by their cholesterol content as;

o Cholesterol stones;
 Accounts for 80% of gallstones.
 >70% cholesterol by weight. Pure cholesterol stones account
for only 10% of gallstones and they are usually single stones
with smooth surface.
 Others are usually multiple, variable in size, and irregular or
mulberry-shaped and soft.
 <10% are radio-opaque.
o Pigment stones; <20% cholesterol and are dark due to presence of
calcium bilirubinate. They can be black or brown.
o Black stones;
 Calcium bilirubinate, carbonate, and phosphate.
 Most often secondary to hemolytic disorders and in cirrhosis.
o Brown stones
 Major part: calcium bilirubinate and bacterial cell bodies.
 <1cm in diameter, brownish-yellow, soft, and often mushy.
 They may form either in the bile ducts mainly or gallbaldder.
 Usually secondary to bacterial infection (e.g. E. coli) caused by
stasis.
 Associated with parasitic infection: Clonorchis sinensis and
Ascaris lumbricoides.
o Mixed stones: 20-70% cholesterol by weight.
 Formation of gallstones is a complex process. It is mainly caused due to
cholesterol supersaturation.
 Main mechanisms;
o Hypersecretion of cholesterol
o Abnormal gallbladder emptying
o Decreased enterohepatic circulation
o Deconjugation of bilirubin.
Clinical manifestations: symptomatic cholelithiasis
 Biliary colic (the first attack): in10-25% of patients.
o Severe RUQ pain which radiates to the back or right shoulder.
May last for minutes or even several hours. Frequently starts
during the night and wakes the patient from sleep.
 Dyspepsia, flatulence, food intolerance, particularly to fats, and alteration
in bowel frequency.
 When patients start to have recurrent bouts of biliary colic, it is called
symptomatic cholelithiasis.
 Blood tests are normal.
 The only pertinent finding is detection of stones on ultrasound.
Now we are going to discuss some of the complications of gallstone disease.

Acute cholecystitis
 Pathogenesis;
o Gallstones (calculous): 90-95%
o Acalculous: 5-10%. In <1% of the cases, the cause is a tumor.

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 More frequently, the stone dislodges and the inflammation resolves.

 When it remains obstructed and secondary bacterial infection supervenes,
acute gangrenous cholecystitis occurs.
 Rarely perforation of ischemic areas occurs.
 When gas forming bacteria are the part of secondary bacterial infection, gas
may be seen in the gallbladder, an entity called emphysematous gallbladder. It
is common in elderly diabetics.
 Clinical manifestations
o Severe RUQ or epigastric pain (more severe than pain associated
with uncomplicated biliary colic) radiating to the right upper back or
interscapular area, aggravated by taking fatty meals.
o Fever, anorexia, nausea, and vomiting.
o Reluctant to move.
o Focal tenderness and guarding in the RUQ.
o A mass, gallbladder and adherent omentum, is usually palpated.
o Murphy’s sign: inspiratory arrest with deep palpation in right subcostal
area.
o Mild to moderate leukocytosis (12,000-15,000c/mm3).
o High WBC above 2000 is suggestive of complicated cholecystitis:
gangreneous cholecystitis, perforation, or cholangitis.
o Serum liver chemistries are normal, but mild elevation of serum
bilirubin may be present along with ALP, ALT, and amylase.
o Severe jaundice is suggestive of CBD stone or Mirizzi syndrome.
o Mirizzi syndrome: obstruction of the bile ducts by severe
pericholecystic inflammation secondary to impaction of a stone in the
infundibulum of the gallbladder that mechanically obstructs the bile
duct. There are four types.
 Type I: Compression of CBD without lumen narrowing.
 Type II: Compression of CBD with lumen narrowing.
 Type III: Compression causing CBD wall necrosis.
 Type IV: Stone ulcerating into CBD resulting in
cholecystocholedochal fistula.
 Ultrasonography is the most useful radiologic test for diagnosis of acute
cholecystitis;
o Demonstrates the stone,
o Thickness of the gallbladder,
o Presence of pericholecystic fluid, and
o Sonographic Murphy’s sign.
 Treatment
o Conservative/non-operative management
 Nil per mouth (NPO): bowel rest
 IV fluid: maintenance (2.5-3L/d NS or RL)
 Administration of analgesics; tramadol 50mg PRN.
 Administration of antibiotics.
 Broad-spectrum, single, effective, and fast acting.
 3rd generation cephalosporins or 2nd generation
cephalosporin with metronidazole are usually used.

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 Aminoglycosides with metronidazole for allergic

patients.
 In Hawassa University-CSH
o Ceftriaxone 1g IV and metronidazole 500mg
BID.
 Subsequent management.
 If the symptoms are subsiding, oral fluids can be
reinstated followed by regular diet. Do USG to
confirm diagnosis; MRCP, if there is jaundice to
exclude choledocholithiasis; and CT if there is any
concern about diagnosis or presence of
complications.
 Cholecystectomy can be done on the next available
list, or the patient is allowed home to return when the
inflammation has completely resolved – after
approximately 6 weeks.
 If the condition of the patient becomes worse
(increased pain and temperature), abandon
conservative treatment;
o Cholecystectomy, or
o Percutaneous cholecystostomy if the
patient has co-morbid conditions.
o Prophylactic cholecystectomy: Indications;
 Elderly patients with diabetes (fear of emphysematous
cholecystitis),
 Patients who will be isolated from medical care for long
period,
 Population with increased risk of gallbladder cancer,
 Porcelain gallbladder,
 Large stones; >3cm,
 Patients with congenital hemolytic anemia, and
 Those undergoing bariatric surgery for morbid obesity.
o Cholecystectomy
 Preparation for operation;
 Full blood count
 Renal profile and liver function tests
 Prothrombin time
 Chest x-ray and electrocardiogram (if over 45 years
or medically indicated)
 Antibiotic prophylaxis
 Deep vein thrombosis prophylaxis
 Informed consent
 Emptying bladder before operation
 Cholecystectomy is the most common major abdominal
procedure.
 Absolute contraindications are uncontrolled coagulopathy
and end-stage liver disease.

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 Serious complications are rare.

 The mortality rate for laparoscopic cholecystectomy is 0.1%.
 Wound infection and cardiopulmonary complications are rare
in laparoscopic cholecystectomy. However, laparoscopic
cholecystectomy is associated with higher rate of injury to
bile ducts.

Cholecystectomy Open Laparoscopic

Complications More Less
CBD injury Less (0.1-0.2%) More (>1%)
Mortality rate Higher Lower (<1%)
Hospital stay 4-5 days As short as one day
Return to work One month One week

o Medical treatments;
 Oral dissolution treatment: inhibits HMG-CoA, a rate limiting
step in cholesterol synthesis.
 CDCA: chenodeoxycholic acid
 UDCA: ursodeoxycholic acid
 Direct contact dissolution
 MTBE: methyl terbutyl ether
Tokyo Consensus Guidelines for severity grading of acute cholecystitis.
Grade III (severe) acute cholecystitis
Associated with dysfunction of any one of the following organs/systems:
1. Cardiovascular Hypertension requiring treatment with dopamine ≤5
dysfunction μg/kg/min, or any dose of norepinephrine (noradrenaline)
2. Neurological dysfunction Decreased level of consciousness
3. Respiratory dysfunction PaO2/FiO2 ratio <300
4. Renal dysfunction Oliguria; creatinine >2.0 mg/dL
5. Hepatic dysfunction Prothrombin time (PT-INR) >1.5
6. Haematological Platelet count <100 000/mm3
dysfunction
Grade II (moderate) acute cholecystitis
Associated with any one of the following conditions:
1. Elevated white cell count (>18 000/mm3)
2. Palpable tender mass in the right upper abdominal quadrant
3. Duration of complaints >72 hours
4. Marked local inflammation (gangrenous cholecystitis, pericholecystic abscess,
hepatic abscess, biliary peritonitis, emphysematous cholecystitis)
Grade I (mild) acute cholecystitis
Does not meet the criteria of grade II or grade III acute cholecystitis. Grade I can also be
defined as acute cholecystitis in a healthy person with no organ dysfunction and mild
inflammatory changes in the gallbladder, making cholecystectomy a safe and low-risk
operative procedure

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Chronic cholecystitis (Biliary colic)

 About two-thirds of patients with gallstone disease present with chronic
cholecystitis characterized by recurrent attacks of pain often inaccurately
labeled as biliary colic.
 Pathologic changes vary from normal gallbladder with minor inflammation
to a shrunken, non-functioning gallbladder with gross transmural fibrosis
and adhesion to nearby structures.
 The mucosa is initially normal or hypertrophied, but later becomes
atrophied, with epithelium protruding into the muscle coat, leading to the
formation of the so-called Aschoff-Rokitansky sinuses.
 Clinical features
o Constant and increasingly severe RUQ or epigastric pain which
radiates to the right upper back or between scapula, and lasts for
1-5hrs.
o Mild RUQ tenderness during episodes of pain.
o WBC counts and liver function tests are normal in uncomplicated
gallstones.
o Atypical presentations are not uncommon;
 Only 50% of patients relate it to meals.
 Atypical pain site, duration or radiation.
 Bloating, belching.
 When pain lasts >24hrs, impacted cystic duct stone or
acye cholecystitis should be suspected.
 An impacted stone with cholecystitis will result in what is
called hydrops of the gallbladder.
 Abdominal ultrasound is the standard diagnostic test for gallstones.
o Sludge and stones
o Cholesterolosis: accumulation of cholesterol in macrophages in
gallbladder mucosa, producing the classic macroscopic
appearance of a “strawberry gallbladder”.
o Adenomyomatosis (cholecystitis glandularis proliferans):
hypertrophic muscle bundles and ingrowths of mucosal glands in
to muscle layer. There are three types of cholecystitis glandularis
proliferans;
 Polypus
 Intramural or diverticular stones
 Fistula
 Treatment
o Avoid dietary fats and large meals.
o Cholecystectomy.

Choledocholithiasis (CBD stones)

 May be small or large and single or multiple and are found in 6-12% of
patients with gallstones.
 The incidence increases with age.
 Types of CBD stones;

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o Primary: usually brown stones and are associated to biliary stasis

due to biliary stricture, papillary stenosis, tumors, or other
secondary stones. Rare!
o Secondary: are usually cholesterol stones. More common.
 Clinical features
o Usually silent and discovered incidentally.
o They may cause obstruction, cholangitis, or gallstone pancreatitis.
o Pain similar to biliary colic. It is clinically indistinguishable from
symptomatic cholelithiasis, but blood tests and USG.
o Nausea and vomiting.
o Mild RUQ tenderness and mild icterus.
o Elevation of serum bilirubin, ALP, and ALT.
 Ultrasonography
o Documenting stones in the gallbladder.
o Dilated CBD (>8mm in diameter is dilated) in a patient with
gallstones, jaundice and biliary pain is highly suggestive.
 Endoscopic cholangiography is the gold standard for diagnosing CBD
stones. Cannulation of the ampula of Vater and diagnostic
cholangiography are achieved in 90% of cases.
 PTC is rarely needed for secondary CBD stones, but frequently done for
therapeutic and diagnostic purposes in primary stones.
 Treatment
o Sphincterotomy and ductal clearance of the stone (ERCP) for
more distal stones.
o CBD exploration (open or laparoscopic); for proximal stones.
There are many options:
 Irrigation: flushing the stone in to duodenum with saline
after relaxation of sphincter of Oddi with glucagon.
 Ballon catheter
 Wire basket
 Choledochotomy with T-tube. The T-tube is removed
after doing T-tube cholangiography after 7-10 days and if
the CBD is patent.
o If the CBD is dilated >1.5cm, then we do cholecystectomy + side
to side choledocoduodenostomy.

Cholangitis
 It is one of the two main complications of choledochal stones, the other
being gallstone pancreatitis.
 It is an ascending bacterial infection due to obstruction of bile ducts.
 Both significant bacterial contamination and biliary obstruction are
required for the development of clinical cholangitis.
Biliary obstruction Bacterial contamination
 Gallstones (most common)  E. coli
 Strictures (benign or malignant)  Klebsiella pneumonia
 Parasites  Salmonella
 Instrumentation  Proteus
 Indwelling stents  Streptococcus faecalis

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 Partially obstructed biliary-  Enterobacter

enteric anastomoses.  Bacteroides fragilis

 Clinical presentations
o Typically older, and female
o Most commonly present with fever, epigastric or RUQ pain, and
jaundice (Charcot’s triad) in two-thirds of patients.
o It may progress to Reynold’s pentad (fever, RUQ pain, jaundice,
septic shock, and mental status change).
o Atypical: little if any fever, pain, or jaundice.
o Mortality rate is 5%.
o On abdominal exam. Findings are indistinguishable from acute
cholecystitis.
o Laboratory investigations;
 Leukocytosis
 Hyperbilirubinemia
 Elevation of ALP, AST, and ALT.
 Imaging modalities;
o USG: stones, dilated ducts, site of obstruction.
o The definitive diagnostic test is ERCP, if not then PTC: level of
obstruction, bile culture, removal of stone.
o CT/MRI: ductal dilation, and pancreatic and periampulary masses.
 Treatment
o IV antibiotics and fluid resuscitation.
o 15% of patients do not respond to the above measures, so do
emergency biliary decompression.
 ERCP: sphincterotomy and stone retrieval or placement
of stent (for diastal pathologies).
 Choledocholithiasis
 Periampullary malignancies
 Percutaneous transhepatic drainage:
 More proximal or perihilar
 Stricture in a biliary-enteric anastomosis
 Failure of endoscopic rout
 Emergent operation, if neither ERCP nor PTC is
available.
o Definitive operative therapy should be deferred until cholangitis
has been treated.

Biliary pancreatitis
 Gallstones in the CBD are associated with acute pancreaitis.
 Ultrasonogram of biliary tree is essential.
 Treatment
o ERCP with sphincterotomy and stone removal for patients with
gallstones and severe pancreatitis. During the same admission,
remove the gallbladder once pancreatitis has subsided.

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o Cholecystectomy and intraoperative cholangiogram or

preoperative ERCP for patients with gallstones and mild and self-
limited pancreatitis. [the stone has already passed]

Cholangiohepatitis (Recurrent pyogenic cholangitis)

 Common in east and south-east Asia.
 Affects both sexes equally.
 Occurs most frequently in 3rd and 4th decades.
 Caused by bacterial contamination;
o E. coli
o Klebsiella species
o Bacteroides species
o Enterococcus faecalis
 Often associated with parasites; C. sinensis, A. lumbricoides,
Opisthorchis viverrini.
 Pathogenesis: see the figure below.
 Clinical features
o Usually present with Charcot’s triad.
o Recurrence is one of the most characteristic feature.
o The episodes may vary in severity but eventually lead to
malnutrition and hepatic failure.
 Imaging
o USG: stone in the biliary tree, pneumobilia, liver abscess,
stricture. Gallbladder may be thickened but inflamed in 20% of
patients and rarely contain stones.
o MRCP and PTC are the mainstay of biliary imaging. They can
detect obstructions, define strictures and stones, and allow
emergent decompression.

Fig: Pathogenesis of cholangiohepatitis

 Treatment
o Emergent decompression in septic patients
o Percutaneous hepatic abscess drainage

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o The long term goal of therapy is to extract stones and debris and
relieve strictures.
Summary: Operative interventions for gallstone diseases
 Cholecystostomy (PTC)
 Choledochotomy
 Cholecystectomy
o Open
o Laparoscopic
 Bile duct exploration
 CBD drainage procedures
o Choledochoduodenostomy (Kocher maneuver)
o Choledochojejunostomy
o Hepaticojejunostomy
 Transduodenal sphincterotomy
o Endoscopic (ERCP)
o Open

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Other Benign Diseases and Lesions

Acalculous cholecystitis
 Acute inflammation of the gallbladder can occur without gallstones.
 Typically develops in critically ill patients in the ICU;
o Extensive burns
o Sepsis
o Major operations
o Multiple trauma
o Prolonged illness with MODS
 The cause is unknown, but gallbladder distention with bile stasis and
ischemia are usually incriminated.
 Signs and symptoms in the alert patient are similar to acute calculous
cholecystitis. In the sedated or unconscious patient, fever, elevated WBC
and liver enzymes indicate further investigation.
 Ultrasonography is the diagnostic test of choice.
o Distended gallbladder with thickened wall
o Biliary sludge
o Pericholecystic fluid
o Presence or absence of abscess
 Abdominal CT: to rule out other sources of infection.
 Acalculous cholecystitis requires urgent intervention;
o Percutaneous cholecysteostomy
o Open cholecystostomy
o Cholecystectomy

Choledochal cysts
 Congenital cystic dilations of the extrahepatic and/or intrahepatic biliary
tree.
 They are rare; more common in eastern world.
 Eight times more common in females.
 Frequently diagnosed in infancy or childhood, but as many as half of the
patients are diagnosed when they reach adulthood.
 The cause is unknown.
 Requirements for biliary cyst formation;
o Weakness of the bile duct wall and
o Increased pressure secondary to partial obstruction
 In >90% of cases, long common channel is present.
 They are classified in to five types (I-V).
 The cysts can vary in size from 2cm in diameter to giant cysts.
Types of choledochal cysts
Type I Fusiform or cystic dilations of extrahepatic biliary tree; the most
common (>50%).
Type II Saccular diverticulum of an extrahepatic bile duct. <5%.
Type III Bile duct dilation within the duodenal wall (choledochoceles). 5%.
Type IV Multiple cysts. 5-10%.

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 Type IVa: affects both extra and intrahepatic ducts

 Type IVb: affects extrahepatic ducts only.
Type V Intrahepatic biliary cysts. 1%

 Clinical features
o Adults commonly present with jaundice or cholangitis.
o Less than one half of patients present with the classical triad of
abdominal pain, jaundice, and a mass.
o The risk of cholangiocarcinoma is as high as 15% in adults
 Ultrasonography or CT will confirm the diagnosis.
 Treatment
o Type I, II, & IV: excision of extrahepatic biliary tree, including
cholecystectomy, with a Roux-en-Y hepaticojejunostomy.
o Type IV: additional segmental resection of the liver.
o For type III: sphincterotomy is recommended.

[Primary] sclerosing cholangitis

 It is an uncommon disease.
 Characterized by inflammatory strictures involving both extrajepatic and
intrahepatic biliary tree.
 It is a progressive disease which eventually results in secondary biliary
cirrhosis.
 Two types;
o Primary: no known cause.
o Secondary: bile duct stones, cholangitis, previous biliary surgery,
or toxic agents.
 Disease associations;
o Ulcerative colitis; two-third of patients*
o Riedel’s thyroiditis
o Retroperitoneal fibrosis
 Autoimmune reactions, chronic low-grade bacterial or viral infections,
toxic reactions, and genetic factors are suggested to play a role in the
pathogenesis of PSC.
 10-20% of the patients develop cholangiocarcinoma, an aggressive one,
at any time during the course of the disease.
 Clinical features
o Mean age = 30-45 years.
o Male to female ratio = 2:1.
o Approximately half are asymptomatic at the time of diagnosis.
o Usually present with intermittent jaundice, fatigue, weight loss,
pruritus, and abdominal pain.
o Cyclic remissions and exacerbations are typical, but the clinical
course is highly variable.
o The clinical course of ulcerative colitis and PSC seems
independent of one another.
o Median survival year = 10-12 years, and most die from hepatic
failure

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o PSC recur in 10-20% of patients and may require

retransplantation.
 Diagnosis
o Elevation of ALP and bilirubin (cholestatic pattern) is suggestive.
o ERC revealing multiple dilations and beadings or strictures in
both intrahepatic and extrahepatic bile ducts is confirmatory.
o Site of involvement;
 Both intra and extrahepatic ducts = 87%
 Intrahepatic ducts only = 11%
 Extrahepatic ducts only = 2%
 The hepatic duct bifurcation is the most severely affected
segment.
o Liver biopsy: determines the degree of hepatic fibrosis & cirrhosis,
but not diagnostic.
o Evaluate the patient for IBD.
Complications of primary sclerosing cholangitis
 Fat-soluble vitamin deficiencies (A, D, E, and K)
 Metabolic bone disease
 Dominant biliary strictures
 Cholangitis and cholelithiasis
 Cholangiocarcinoma
 Gallbladder cancer
 Hepatocellular carcinoma (in patients with cirrhosis)
 Colon cancer

 Treatment
o There is no known effective medical therapy and no known
curative treatment for PSC.
o Endoscopic or percutaneous biliary duct dilation and stenting.
o Resection of extrahepatic biliary tree with hepaticojejunostomy
for patients with extrahepatic or bifurcation strictures but without
cirrhosis or significant hepatic fibrosis.
o Liver transplantation in advanced liver disease.
o Proctocolectomy for UC doesn’t result in improvement.
Benign causes of biliary duct strictures
 Operative injury: vast majority
 Congenital biliary atresia
 Inflammatory: stones, cholangitis, parasitic, pancreatitis, sclerosing
cholangitis, radiotherapy, Mirizzi syndrome
 Other traumas
 Idiopathic

Bile duct injuries

 Majority are iatrogenic.
 More than half of the patients present within the first post-op month.

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 The remainder will present months or years later, with recurrent

cholangitis or cirrhosis.
 The management of bile duct injuries depends on the type, extent, and
level of injury, and the time of its diagnosis.
Strasberg and Bismuth classification of bile duct injuries
Strasburg classification
Type A Injury to the cystic duct or from minor hepatic ducts draining the
liver bed.
Type B Occlusion of biliary tree, commonly aberrant right hepatic duct(s)
Type C Transection without ligation of aberrant right hepatic duct(s)
Type D Lateral injury to a major bile duct.

Type E (1-5) Injury to the main hepatic duct; classified according to level of
injury.
Bismuth classification of type E (1-5)
E1 (Bismuth type 1) Injury more than 2 cm from confluence
E2 (Bismuth type 2) Injury less than 2 cm from confluence
E3 (Bismuth type 3) Injury at the confluence; confluence intact
E4 (Bismuth type 4) Destruction of the biliary confluence
E5 (Bismuth type 5) Injury to aberrant right hepatic duct

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Fig: Strasberg and Bismuth classification of bile duct injuries

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Tumors of the Biliary Tract

Benign tumors
 Papilloma and adenoma* (most common)
 Multiple biliary papillomatosis
 Granular cell myoblastoma
 Neural tumours
 Leiomyoma
 Endocrine tumours
Malignant tumors
 Gallbladder carcinoma (60-70%)
 Bile duct carcinoma (30-40%)

Carcinoma of the gallbladder

 A rare malignancy.
 Very aggressive tumor with poor prognosis.
 Median survival is 6 months and 5-year survival rate is about 5%.
 Incidence
o 5th most common GI malignancy in western.
o Accounts for only 2-4% of all malignant GI tumors.
o Two to three times more common in females.
o Peak incidence is the 7th decade.
o Incidence increases in native USA, Mexico and Chile.
 Etiology
o Cholelithiasis is the most important risk factor.
 Up to 90% of patients have gallstones.
 But 20-year risk is <0.5% (1.5% for high-risk).
 Larger stones (>3cm) have 10-fold increased risk.
 Symptomatic > asymptomatic.
 Pathogenesis is chronic inflammation.
o Gallbladder polyps; specialy in polyps > 10mm
o Porcelain gallbladder (>20%)
o Choledochal cysts
o Sclerosing cholangitis
o Anomalous pancreatico-biliary junction
o Carcinogens: azotoluene, nitrosamines
 Pathology
o Adenocarcinomas: 80-90%
 Papillary (<10%): better prognosis
 Nodular
 Tubular
o Others: squamous cell, adenosquamous, oat cell, and others
o Spread of the tumor
 Lymphatic
 Venous
 Direct invasion into the liver

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 At the time of diagnosis;

 Only 25% are localized to the gallbladder.
 35% has regional nodal involvement and/or
extension to adjacent liver.
 40% have distant metastasis.
 Clinical manifestations and diagnosis
o Signs and symptoms are indistinguishable from cholelithiasis and
cholecystitis. These include RUQ pain, nausea, and vomiting.
Jaundice, weight loss, anorexia, ascites, and abdominal mass
are less common presenting symptoms.
o More than half are not diagnosed before surgery.
o Laboratory findings are not diagnostic, but if abnormal, arre most
often consistent with biliary obstruction.
o USG: tumor, liver invasion, LAP, bile duct dilation. 70-100%
sensitivity.
o CT/MRI
o MRCP
 Treatment
o Surgery remains the only curative option for gallbladder cancer
as well as for cholangiocarcinoma.
o Unfortunately, majority of the patients have advanced disease at
presentation, and are not candidates for surgery.
o Palliative procedures for unresectable cancer and jaundice or
duodenal obstruction remain the most common procedure for
gallbladder cancer.
o There are no proven effective options for adjuvant radiation or
chemotherapy for patients with gallbladder cancer.
o Recurrence after resection occurs most commonly in the liver, or
the celiac or retropancreatic nodes.

Bile duct cancer (Cholangiocarcinoma)

 Incidence
o A rare tumor (0.3%).
o Male to female ratio is 1.5:1.
o Average age of presentation is between 50 and 70.
 Etiology
o Minority of patients have known risk factors.
o PSC is a major risk factor; 20 fold. It occurs at an earlier age in
patients with PSC (30-50 years). Disease is multifocal and
advanced with resultant poor prognosis.
o Other risk factors
 Cholangiohepatitis, hepatitis C infection, chronic typhoid
carriers
 Parasites: Opistorchis viverrini, Clonorchis sinensis
 Congenital: choledochal cysts, Caroli’s disease
 Carcinogens: thorium dioxide, vinyl chloride,dioxin,
asbestos
 Post-op biliary-enteric anstomosis

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 Pathology
o Adenocarcinomas: >95%
 Nodular: the most common
 Scirrhous
 Diffusely infiltrating
 Papillary
o Anatomic location;
 Biliary confluence: 60%. Also called hilar
cholangiocarcinoma or Klatskin tumor. Further divided in
to four by Bismuth-Corlette classification.
 Distal CBD: 20-30%
 Intrahepatic: 10-20%
Bismuth-Corlette classification
Type I Confined to common hepatic duct
Type II Common hepatic duct and the bifurcation without involvement of
the secondary intrahepatic ducts (right and left hepatic ducts).
Type III
IIIa Common hepatic duct and right hepatic duct
IIIb Common hepatic duct and left hepatic duct
Type IV Common hepatic duct and both hepatic ducts

Fig: Bismuth-Corlette classification of bile duct cancer

 Clinical manifestations and diagnosis
o Painless jaundice is the most common presentation.
o Pruritus, mild RUQ pain, anorexia, fatigue, weight loss.
o Cholangitis is the presenting symptom in 10% of patients.
o Except for jaundice, physical examination is usually normal.
o Laboratory
 Elevated ALP and GGT
 Tumor markers
 CA-19-9 is most commonly used, it has a
sensitivity of 79% and specificity of 98% at
serum value >129U/mL.

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 Others are non-specific; e.g. CA 125

o The initial tests are usually ultrasound or CT scan.
 Perihilar: dilation of intrahepatic bile ducts but normal or
collapsed gallbladder and extrahepatic bile ducts.
 Distal: dilation of the whole biliary tract including
gallbladder and intrahepatic ducts.
o PTC defines the proximal extent of the tumor, which is the most
important factor in determining respectability.
o ERCP is used particularly in distal bile duct tumors.
 Treatment
o Surgical excision is the only potentially curative treatment. Owing
to the advanced stage at presentation, complete surgical excision
is possible in <10% of patients only.
o For most patients treatment is palliative, aimed to provide biliary
drainage to prevent liver failure and cholangitis.
o Most patients with unresectable disease die within 1 year of
diagnosis from liver failure or biliary sepsis.

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CHAPTER EIGHT-THE INTESTINES

Intestinal obstruction
Introduction
Intestinal obstruction is among the most commonly encountered causes of acute
abdomen. Small bowel obstruction accounts for 85% with the rest being large
bowel obstruction. Intestinal obstruction may be classified in to two types;
 Dynamic/mechanical: in which peristalsis is working against a mechanical
obstruction.
 Adynamic: in which there is no mechanical obstruction; peristalsis is
absent or inadequate.

Causes of intestinal obstruction

Intraluminal Intramural Extramural
Fecal impaction Strictures Bands/adhesions
Foreign bodies Tuberculous Hernia
Bezoars Crohn’s disease Peritoneal carcinomatosis
Gallstones Malignant
Worms Radiation-induced Adynamic
Meconium ileus Malignancy Paralytic ileus
Polyps Intussusception Pseudo-obstruction
Food bolus Volvulus
Diverticuli
Congenital
The most common causes of intestinal obstruction in descending order of
frequency (in our set-up – Ethiopia)
 Volvulus
 Adhesions
 Hernia
 Malignancies
The diagnostic work-up should focus on distinguishing:
1. Dynamic from adynamic obstruction
2. The etiology of the obstruction
3. Small from large bowel obstruction
4. Partial from complete obstruction
5. Simple from strangulated obstruction

Pathophysiology-mechanical obstruction
Bowel proximal to the obstruction dilates and the bowel below the obstruction
exhibits normal peristalsis until it becomes empty and collapses.

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Initially, proximal peristalsis increases in attempt to relieve the obstruction. If the

obstruction is not relieved, the bowel continues to dilate; ultimately there is a
reduction in peristaltic strength, resulting in flaccidity and paralysis.

The distention proximal to the obstruction is caused by two factors;

 Intestinal gas produced due to significant overgrowth of bacteria. The
majority of the gas is made of nitrogen (90%) and hydrogen sulphide.
 Fluid made up of various digestive juices.

Dehydration and electrolyte loss are due to;

o Reduced oral intake
o Defective intestinal absorption
o Losses as a result of vomiting
o Sequestration in bowel lumen
o Transudation of fluid in to peritoneal cavity.
Strangulation
 Compromise of blood supply to a bowel which ultimately renders it
ischemic. Venous return is compromised before arterial supply. Once the
arterial supply is impaired, hemorrhagic infarction occurs.
 Causes of strangulation;
o Direct pressure on the bowel wall
 Hernia
 Adhesion/bands
o Interrupted mesenteric blood flow
 Volvulus
 Intussusception
o Increased intra-luminal pressure
 Closed-loop obstruction
Closed-loop obstruction
 Occurs when a bowel is obstructed at both proximal and distal points.
 The distention is principally confined to the closed loop; distention
proximal to the obstructed segment is not typically marked.
 Common examples;
o Classically seen in malignant stricture of the colon with a
copetent ileocaecal valve.
o External or internal hernias
o Volvulus
Gallstone ileus
 Occur in the elderly secondary to erosion of a large gallstone directly
through the gallbladder in to the small intestine.
 Classically about 60cm proximal to ileocaecal valve.

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 The Rigler’s triad; are radiologic features of gallstone ileus the presence
of two of which is pathogmonic for gallstone ileus;
o Small bowel obstruction
o Pneumobilia
o Atypical mineral shadow
Adhesions [and bands]
 Any source of peritoneal irritation results in local fibrin production, which
produces adhesions between apposed surfaces.
 Early fibrinous adhesions may disappear when the cause is removed or
they may become vascularised and replaced by mature fibrous tissue.
 The common causes include;
o Acute inflamma: sites of anastomosis, retroperitonealization of
raw areas, trauma, ischemia
o Foreign materials: talc, starch, gauze, silk
o Infection: peritonitis, tuberculosis
o Chronic inflammatory conditions: Crohn’s disease
o Radiation enteritis
 There are several factors that may limit adhesion formation;
o Good surgical technique
o Washing of the peritoneal cavity with saline to remove clots
o Minimising contact with gauze
o Covering anastomosis and raw peritoneal surfaces
Intussusception
 Invagination or telescoping of a portion of a bowel in to immediately
adjacent segment; almost invariably proximal in to the distal.
 Most common in children 5-10 months; and 90% of them are idiopathic
but an upper respiratory tract infection or gastroenteritis may precede it.
Most are treated non-operatively by radiologic reduction.
 Children with pathologic lead point (diverticuli, polyp, duplication, HSP)
are generally older than those with idiopathic disease.
 Hyperplasia of Peyer’s patches in the terminal ileum may be an initiating
event.
 Weaning, loss of passively acquired maternal immunity and common viral
pathogens have all been implicated.
 Adult intussusceptions are far less common and usually have a distinct
pathologic lead point, which can be malignant in up to one half of cases.
 CT is the investigation of choice, where a pathogmonic “target sign” may
be seen.
 Types of intussusception;
o Ileocolic: 77%
o Ileoileocolic: 12%

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o Ileoileal: 5%
o Others: >5%
 An intussusception is composed of three parts;
o Intussusceptum: the entering or the inner tube;
o The returning or middle tube; and
o Intussusceipiens: the sheath or outer tube
 The part that advances is the apex, the mass is the intussusception and
the neck is the junction of the entering layer with the mass.

Fig: Mechanism and nomenclature of intussusception

What is a lead point?
 A lesion or variation in the intestine that is trapped by peristalsis and
dragged into a distal segment of the intestine, causing intussusception.
 It can be;
o An underlying disorder (25% of cases): Meckel diverticulum (the
most common), polyps, small bowel lymphoma, duplication cysts,
vascular malformations, inverted appendiceal stumps, parasites
(eg, Ascaris lumbricoides), immunoglobulin A vasculitis (IgAV;
Henoch-Schönlein purpura [HSP]), cystic fibrosis, and hemolytic-
uremic syndrome.
o Postoperative: most commonly after abdominal surgery.
Volvulus
 Twisting or axial rotation of a portion of bowel about its mesentery.
 It causes obstruction (>1800 torsion) and ischemia (>3600 torsion).
 Colonic volvulus ranks after cancer and diverticulitis as a cause of LBO in
USA. It is responsible for 5% of all cases of intestinal obstruction and 10-
15% of LBO.
 In the developing world (volvulus belt), volvulus accounts for more than
50% of the cases of LBO.

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 Common sites of volvulus in the large bowel;

o Sigmoid: 80%
o Caecum: 15%
o The transverse colon: 3%
o Splenic flexure: 2%
 Primary or secondary;
o Primary forms are secondary to congenital malrotation, abnormal
mesenteric attachements, or congenital bands. Examples include
volvulus neonatorum, caecal volvulus, and sigmoid volvulus.
o Secondary volvulus, the more common variety, is due to rotation
of a segment of bowel around an acquired adhesion or stoma.
 Factors predisposing to [sigmoid] volvulus;
o Band of adhesion
o Overloaded pelvic colon
 Chronic constipation: developed world.
 High fiber diet: developing world (our setup)
o Long pelvic mesocolon
o Narrow attachment of pelvic mesocolon.
 Presentation can be classified as;
o Fulminant: sudden onset, severe pain, early vomiting, rapidly
deteriorating course.
o Indolent: insidious onset, slow progressive course, less pain, late
vomiting.
 Compound volvulus (ileosigmoid knotting)
o Rare condition.
o The long pelvic mesocolon allows the ileum to twist around the
sigmoid colon, resulting in gangrene of either or both segments of
bowel.
o The patient presents with acute intestinal obstruction, but
distension is comparatively mild.
o Plain radiography reveals distended ileal loops in a distended
sigmoid colon.
o At operation, decompression, resection and anastomosis are
required.

Clinical presentations
Cardinal symptoms; (the classical quartet)
 Pain
o The first symptom encountered
o Sudden onset of severe colicky central (small bowel) or lower
abdominal (large bowel) pain.
o Coincides with peristaltic activity.

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o The colicky pain is replaced with mild and more constant diffuse
pain with increasing distention.
o Doesn’t usually occur in paralytic ileus.
 Vomiting
o The more distal the obstruction, the longer the interval between
the onset of symptoms and appearance of vomiting.
o With time, the vomitus changes from digested food to feculent
material due to bacterial overgrowth.
 Distention
o The degree of distention depends on the site of obstruction in
SBO, and is greater the more distal the lesion.
o Distention is early and marked in large bowel obstruction.
 Constipation
o Can be absolute (neither feces nor flatus passed) or relative (only
flatus passed).
o Absolute constipation is the cardinal feature of complete
obstruction.
o Some patients may pass flatus or feces obstruction as a result of
evacuation of the distal bowel contents.
o Absolute constipation is absent in;
 Richter’s hernia
 Gallstone ileus
 Mesenteric vascular occlusion
 Functional obstruction associated with pelvic abscess
 All causes of partial obstruction.
Other late manifestations
 Dehydration; most common in SBO because of repeated vomiting and
fluid sequestration.
 Hypokalemia; present in strangulation.
 Pyrexia is rare and may indicate;
o Onset of ischemia
o Intestinal perforation
o Inflammation or abscess
o Hypothermia indicates septicemic shock or neglected cases of
long duration.
 Abdominal tenderness
o Localized tenderness indicates impending or established
ischemia (strangulation)
o Peritonism or peritonitis indicates overt infarction and/or
perforation.
 Bowel sounds

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o High-pitched at the onset

o Scanty or absent if the obstruction is longstanding and the small
bowel has become inactive.
o Normal bowel sounds are of negative predictive value.
Strangulation
 Constant and severe pain
 Tenderness with rigidity and peritonism
 Shock
Intussusceptions
 An infant or toddler with intermittent crying and drawing up of the legs in a
previously well male patient is the classical presentation. The episodes
usually occur at 15- to 20-minute intervals. They become more frequent
and more severe over time.
 Redcurrant jelly stool: blood and mucus (later).
 Vomiting is often a prominent symptom, often starting shortly after the first
episodes of abdominal pain. Initially, emesis may be nonbilious, but it
often becomes bilious as the obstruction progresses.
 Sausage shaped lump that hardens on palpation: 60% of cases
 Emptiness in the right iliac fossa (sign of Dance)
Volvulus of small intestine
 Primary or secondary and usually occurs in the lower ileum.
Caecal volvulus
 Common in females in the 4th and 5th decades
 Present acutely with features of obstruction
 Usually a clockwise twist
 Diagnoses is not usually made preoperatively
Sigmoid volvulus
 Presents with symptoms of large bowel obstruction
 Classically in anti-clockwise direction.
 Younger patients develop more acute form.
 More chronic form may be seen in the elderly.
 Emptiness in the left iliac fossa.

Summary of clinical features of intestinal obstruction

 In high small bowel obstruction, vomiting occurs early, is profuse and causes
rapid dehydration. Distension is minimal with little evidence of dilated small bowel
loops on abdominal radiography
 In low small bowel obstruction, pain is predominant with central distension.
Vomiting is delayed. Multiple dilated small bowel loops are seen on radiography
 In large bowel obstruction, distension is early and pronounced. Pain is less
severe and vomiting and dehydration are later features. The colon proximal to the
obstruction is distended on abdominal radiography. The small bowel will be

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dilated if the ileocaecal valve is incompetent.

Imaging: plain abdominal X-ray (erect)

Small bowel obstruction
 Dilated bowel loops >3cm in diameter
 Multiple, central air-fluid levels; the number of air-fluid levels is
proportional to the degree of obstruction and its site. They are more
numerous in distal obstruction.
 Paucity of air in the rectum
 The jejunum is characterized by its valvulae conniventes, which
completely pass across the width of the bowel and are regularly spaced,
giving a ‘concertina’ or ladder effect.
 Ileum – the distal ileum has been described as featureless.
Large bowel obstruction
 Dilated bowel loops >6cm in diameter (>9cm in the caecum)
 Peripherally located few air-fluid levels.
 Caecum – a distended caecum is shown by a rounded gas shadow in the
right iliac fossa
 Large bowel, except for the caecum, shows haustral folds, which, unlike
valvulae conniventes, are spaced irregularly, do not cross the whole
diameter of the bowel and do not have indentations placed opposite one
another.

Intussusceptions
 Plain abdominal x-ray: small or large bowel obstruction with the absence
of caecal air shadow in ileocolic cases.
 Barium enema: claw sign.
 CT scan: target sign or sausage shaped soft tissue mass. CT is currently
the most sensitiveinvestigation (58-100% accuracy).
Imaging in volvulus
 Caecal volvulus: caecal dilation, single air-fluid level, small bowel dilation,
and absence of air in the colon. Abdominopelvic CT if the diagnosis is
doubtful.
 Sigmoid volvulus
o Plain abdominal radiography
 Massive colonic distention,
 Omega sign or U sign or the Frimann Dhal’s sign,
 Two air-fluid levels
o Barium enema

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 Bird’s beak appearance at the termination point of

sigmoid volvulus.

Treatment
Supportive management
 Commonly recommended in the initial recommendation for:
o Partial small bowel obstruction
o Obstruction occurring in the early postoperative period
o Intestinal obstruction due to Crohn’s disease
o Carcinomatosis
 Conservative treatment includes;
o NGT decompression
o Fluid replacement (NS or RL)
o For uncomplicated small bowel obstruction, antibiotics should not
be administered. Although administering broad-spectrum
antibiotics is practiced because of concerns for bacterial
translocation.
Surgical treatment
 Principles of surgical intervention include management of;
o The bowel segment at the site of obstruction
o The dilated bowel
o The underlying cause
 Adhesions are lysed and divided
 Tumors are resected
 Hernias are reduced and repaired
 Non-viable bowel segments are resected and
anastomosed.
 Volvuluses are manually decompressed if suitable.
 Intussusceptions are reduced if possible

Differentiation between viable and non-viable intestine

Viable Non-viable
Circulation Dark color becomes lighter Dark color remains
Visible pulsations in mesenteric No detectable pulsation
arteries
Appearance Shinny Dull and lusterless
Intestinal Firm Flabby, thin, and friable
musculature
Peristalsis May be observed No peristalsis

 If there is complete obstruction, but there is no evidence of bowel

ischemia or closed loop obstruction, surgery can be reasonably deferred
until the patient is adequately resuscitated.

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 Indications for early surgical intervention;

o Obstructed external hernia
o Features suspicious of intestinal strangulation
o Obstruction in a ‘virgin’ abdomen
 Where the obstruction is likely to be secondary to adhesions, conservative
management may be continued until 72 hours, in hope of spontaneous
resolution.
 Intussusceptions;
o Radiologic reduction with air or barium enema for patients with
normal vital signs, and no evidence of bowel perforation.
o Surgery: indications;
 Failed radiologic reduction
 Peritonitis and/or perforation
 Suspicion of strangulation
 Pathologic leading point
 Presence of shock (hemodynamic instability)
 Persistent focal filling defect (not all), showing a mass
lesion.
o Surgical options;
 Manual reduction: 1% risk of recurrence
 Resection and anastomosis: recurrence is nonexistent.
 If manual reduction is not possible or
 If pathologic lead point is seen.
 Caecal volvulus
o Radiologic diagnosis of cecal volvulus is generally considered
indication for surgical intervention because the obstruction in this
condition cannot be reliably reduced with colonoscopy.
 Sigmoid volvulus
o In patients with no evidence of peritonitis or ischemic bowel;
 Start with resuscitation and detorsion with
sigmoidoscopy, rectal tube or colonoscopy.
 Then do elective surgery during the same hospital
admission after 2 weeks.
o In patients with evidence of pepritonitis or ischemic bowel or in
patients in which detorsion has failed, emergency surgery is
indicated.
o Surgical options;
 Resection with primary anastomosis
 Viable bowel ends,
 No evidence of peritoneal contamination, and
 Hemodynamically stable patient.

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 Hartmann’s procedure: resection with end colostomy.

The colostomy is reversed after 3-6 months.
 Evidence of ischemic bowel,
 Peritoneal contamination, or
 Unstable patient.

Chronic large bowel obstruction

Organic causes
 Intraluminal (rare): fecal impaction
 Intrinsic intramural: strictures (Crohn’s disease, ischemia, diverticular),
anastomotic stenosis
 Extrinsic intramiural (rare): metastatic depositis (ovarian), endometriosis,
stomal stenosis
Functional causes
 Hirschprung’s disease
 Idiopathic megacolon
 Pseudo-obstruction
Clinical features
 Constipation appears first; associated with distention
 Vomiting is a late feature
 Plain abdominal radiography confirms large bowel obstruction.
Organic diseases require decompression with either laparotomy or stent.
Functional diseases require colonoscopic decompression in the first instance and
conservative management.

Adynamic obstruction-Paralytic ileus

A state in which there is failure of transmission of peristaltic waves secondary to
neuromuscular failure. The following varieties are recognized;
 Postoperative; when after 72 hour after surgery there has been;
o No return of bowel sounds
o No passage of faltus
 Infective
 Reflex ileus; following fractures of spine or ribs, retroperitoneal
hemorrhage or even application of plaster jacket
 Metabolic: uremia and hypokalemia are the most common factors.
Abdominal distention becomes more marked. Colicky pain is not a feature.
Distention increases pain from the abdominal wound. Effortless vomiting.
Radiology is consistent with intestinal obstruction.
Management
 NGT suction and restriction of oral intakes until bowel sounds and
passage of flatus return.

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 Electrolyte management.
 Specific treatment is directed towards the cause.

Adynamic obstruction-Pseudo-obstruction
An obstruction, usually of the colon, that occurs in the absence of a mechanical
cause or acute intra-abdominal disease.
It can be;
 Neuropathic;
 Myopathic; and/or
 Interstitial cells of Cajal (ICC) abnormalities
Patients may have diarrhea due to bacterial overgrowth.

Small intestine pseudo-obstruction may be primary or secondary and consists of

recurrent subacute obstruction. The diagnosis is made by exclusion of mechanical
cause. Treatment consists of correction of underlying disorder. Metoclopramide
and erythromycin may be of use.

Colonic pseudo-obstruction may occur in an acute or a chronic form. The former

known as Ogilvie’s syndrome, presents as acute large bowel obstruction. Once
identified, pseudo-obstruction requires treatment of any identifiable cause.

Factors associated with pseudo-obstruction

Metabolic Postoperative (for example fractured neck
Diabetes of femur)
Hypokalaemia Retroperitoneal irritation
Uraemia Blood
Myxodoema Urine
Intermittent porphyria Enzymes (pancreatitis)
Severe trauma (especially to the lumbar Tumour
spine and pelvis) Drugs
Shock Tricyclic antidepressants
Burns Phenothiazines
Myocardial infarction Laxatives
Stroke Secondary gastrointestinal involvement
Idiopathic Scleroderma
Septicaemia Chagas’ disease

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Colorectal Cancer
Epidemiology
Colorectal cancer is the most common malignancy of the GIT. It is the third most
common cancer and cancer related deaths. The incidence is similar in men and
women. Rectal cancer is more common in men, whereas colon cancer is more
common in women. Approximately 80% of colorectal cancers occur sporadically,
while 15-20% are familial, and 5% are inherited.
Risk factors
 Age is the dominant risk factor. More than 90% of cases are diagnosed in
people older than 50 years old.
 Hereditary risk factors;
o Familial adenomatous polyposis (FAP)
o Hereditary non-polyposis colon cancer (HNPCC) or Lynch
syndrome
o Attenuated familial adenomatous polyposis (AFAP)
 Environmental and dietary factors;
o Low socio-economic status
o Diets high in animal fat and low in fiber; and red meat.
o Alcohol intake
o Obesity and sedentary lifestyle
 Polyps
 Inflammatory bowel diseases
o Ulcerative colitis*, Crohn’s disease, and indeterminate colitis.
o The association between UC and CRC depends on;
 The extent of colitis; pancolitis has the highest risk.
 The duration of the disease; duration of 5 years is
associated with 1-2% risk, the risk increases to 8% by
10years, and 18% after 30 years.
 The activity of the disease; more risk in patients with
active inflammation.
 Cigarette smoking; especially after more than 35 years of use.
 Patients with ureterosigmoidostomy (urinary diversion) are at an
increased risk for both adenoma and carcinoma formation; on average 20-
30 years after the operation.
 Acromegally
 Pelvic irradiation
 After cholecystectomy and ileal resection there is increased bile salts and
so more prone for carcinoma colon.
Protective factors of colorectal cancer

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Physical activity Drugs

Diet (vegetables and fruits) Aspirin and NSAIDs
Fiber Hormone therapy in women
Resistant starch Statins
Folic acid and folate Antioxidants
Vitamin B6 Bisphosphonates
Calcium and dairy products Angiotensin II inhibition
Vitamin D
Magnesium
Garlic
Fish consumption
Coffee intake

Colorectal polyps
 Majority of colorectal cancer evolve from adenomatous polyps; adenoma-
carcinoma sequence within approximately 10 years. Although most
neoplastic polyps do not evolve in to cancer.
 Polyps can be pedunculated or sessile.
 Classification of colorectal polyps;
o Neoplastic/adenomatous (tubular, villous, tubulovillous, serrated):
they are dysplastic.
o Non-neoplastic (no dysplasia)
 Hyperplastic
 Hamartromatous (juvenile, Puertz-Jeghers, Cronkite-
Canada, Cowden syndrome, Bannayan-Riley-Ruvalcaba
syndrome)
 Inflammatory (pseudopolyp, benign lymphoid polyp)
 Neoplastic polyps
o Risk of malignancy in neoplastic polyps;
 Tubular = 5%
 Villous = 40%
 Tubulovillous = 22%
o Invasive carcinomas are rare in polyps smaller than 1 cm; the
incidence increases with size. The risk of carcinoma in polyps
larger than 2 cm is 35-50%.
o Treatment; surgical
 Pedunculated = colonoscopic snare excision
 Sessile = special colonoscopic techniques (saline lift,
piecemeal snare excision, and endoscopic mucosal
resection).
 Rectal sessile = transanal operative excision.
o Complications: perforation, and bleeding.

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 Hyperplastic polyps are not considered premalignant, but cannot be

distinguished from adenomatous polyps and are therefore removed.
Larger polyps; >2cm may have slight risk of malignancy.
 Hamartromatous (juvenile) polyps
o Are not premalignant.
o Characteristic polyps of childhood.
o They have to be removed because they are grossly identical to
adenomatous polyps.
o Bleeding is a common symptom. Intussusceptions and/or
obstruction may occur.
 Puertz-Jeghers syndrome: polyposis of small intestine and to a lesser
extent colon and rectum, with characteristic melanin spots on the buccal
mucosa and lips.
 Cronkite-Canada syndrome
o GI polyposis with alopecia, cutaneous pigmentation, and atrophy
of the fingernails and toenails.
o Diarrhea is the prominent symptom, and vomiting, malabsorption,
and protein-losing enteropathy may occur.
 Cowden’s syndrome is an autosomal dominant disorder with hamartomas
of all three embryonal cell layers. Facial trichilemmomas, breast cancer,
thyroid disease, and gastrointestinal polyps are typical of the syndrome.
 Inflammatory polyps (pseudopolyps)
o Occur most commonly in the context of inflammatory bowel
diseases, but may also occur after amoebic colitis, ischemic
colitis, and schistosomal colitis.
o Not premalignant, but should be removed since they are grossly
indistinguishable from adenomatous polyps.
Familial adenomatous polyposis (FAP)
 Autosomal dominant condition
 Accounts for 1% of colorectal adenocarcinomas
 Genetic abnormality = APC mutation (75% of cases)
 Hundreds to thousands of adenomatous polyps after puberty.
 Lifetime risk = 100% at the age of 50 years.
 They also have increased risk for developing adenomas anywhere in the
GIT. Periampulary carcinoma is a particular concern.
 Treatment is surgical; depends on the age of the patient, presence and
severity of symptoms, extent of rectal polyposis, and presence and
location of cancer or desmoids tumors.
 Surgical options;
o Total poctocolectomy with an end (Brooke) ileostomy
o Total abdominal colectomy with ileorectal anastomosis

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o Restorative proctocolectomy with ileal pouch-anal anastomosis ±

temporary ileostomy
 Screening
o Flexible sigmoidoscopy of first degree relatives beginning at age
10-15 years.
o APC gene testing
 Positive: start at 10-15 years
 Negative: start at age 50 years
 Refused or unavailable: begin at age 10-15 till age 24
years. Then it is done every 2 years till age 34, every 3
years till age 44, and then every 3-5 years.
 Extraintestinal manifestations;
o Endodermal derivatives
 Adenomas and carcinomas of the duodenum, stomach,
small intestine, thyroid and biliary tree
 Fundic gland polyps
 Hepatoblastoma
o Ectodermal derivatives
 Epidermoid cysts
 Pilomatrixoma
 Congenital hypertrophy of the retinal pigment epithelium
 (CHRPE)
 Brain tumours (Turcot’s syndrome)
o Mesodermal derivatives
 Desmoid tumours
 Osteomas (mandibular/Gardener’s syndrome)
 Dental problems
Hereditary non-polyposis colon cancer (HNPCC)
 Autosomal dominant condition
 More common than FAP (1-3% of all colon cancers)
 Genetic defect = errors in mismatch repair
 Associated with development of colon cancer at an early age (40-50
years).
 70% of affected individuals will develop colorectal cancer.
 The risk of synchronous or metachronous colorectal cancer is 40%.
 More often in the proximal colon than sporadic cases and have better
prognosis regardless of age.
 Extracolonic malignancies;
o Endometrial carcinoma; most common
o Others: ovarian, pancreas, stomach, small bowel, biliary, and
urinary tract carcinomas.

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 The Amsterdam criteria (I and II) to diagnose HNPCC;

o Three affected relatives with histologically verified
adenocarcinoma of the large bowel (one must be a first-degree
relative of one of the others) in two successive generations of a
family with one patient diagnosed before age 50 years.
 Classification of HNPCC
o Lynch syndrome I (familial colon cancer)
o Lynch syndrome II (HNPCC associated with other GI or
reproductive system cancers)
 Screening
o Colonoscopy annually starting at age 20-25 years
o Transvaginal ultrasound or endometrial aspiration biopsy
o Annual proctoscopy
 Treatment is surgical
o Total colectomy with ileorectal anastomosis
o Prophylactic hysterectomy and bilateral salphingo-ophrectomy

Histopathology
 There are four gross morphological forms of CRC;
o Ulcerative; more common on the right side.
o Fungating/cauliflower; more common on the right side
o Annular/stenosing; more common on the left side
o Tubular/infiltrating; more common on the left side
 Histology;
o Tubular columnar adenocarcinomas: 90%
o Mucinous adenocarcinoma: 5-10%.
o Signet ring cell carcinoma
o Small cell/oat cell carcinoma: rare – extremely poor prognosis.
o Squamous cell carcinoma.
o Undifferentiated carcinoma.

Prevention: Screening and Surveillance

 Why screening?
o Majority of colorectal cancers are sporadic. Most of the times no
one knows who is going to get colorectal cancer.
o Most colorectal cancers arise from adenomatous polyps.
Preventive measures focus on early identification and removal of
these premalignant lesions.
o Many cancers are asymptomatic; and screening may detect
these at an earlier and curable stage.
 Screening is meant for asymptomatic patients; a patient with GI complaint
requires a complete evaluation, usually by colonoscopy.

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 Screening does not decrease the incidence but improves the prognosis
and outcome of a disease through early detection and intervention of
premalignant lesions or early stage cancer.
 Screening modalities;
o Fecal occult blood testing (FOBT)
 Sensitivity = 50%
 Specificity = 90%
 Reduces colorectal cancer by 33%, and metastatic
disease by 50%
 A positive FOBT should be followed by colonoscopy.
o Flexible sigmoidoscopy
 60-70% reduction in mortality from colorectal cancer.
 Cannot identify lesions in the proximal colon.
o Colonoscopy
 The most accurate and most complete method for
examining the large bowel; the gold-standard.
o Double contrast barium enema
 For detecting proximal colon lesions.
o CT colonography (virtual colonoscopy)
 Screening guidelines for sporadic cases;
o Begin at 50 years for average-risk population;
 Asymptomatic
 No family history of colorectal carcinoma
 No personal history of polyps or colorectal carcinoma
 No familial syndrome
o Recommended procedures
 Serial yearly FOBT,
 Flexible sigmoidoscopy every 5 years, or
 Colonoscopy every 10 years.
 Screening guidelines for familial and hereditary cases;
o Screening is started at an earlier age;
 FAP; begin at 10-15 years
 HNPCC; begin at 20-25 years
 Non-syndromic familial colon cancer; at 40 years.
o Screen more frequently
o Colonoscopy is almost always required
o Other modalities like CT colonography and double contrast
barium enema are sometimes also needed.

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Fig: Screening for colorectal cancer in average risk population

Advantages and disadvantages of screening modalities

Advantages Disadvantages
FOBT Easy and non-invasive May not detect most polyps
Low cost Low specificity
Good sensitivity with repeat Colonoscopy required for positive result
testing Poor compliance with serial testing
Sigmoidoscopy Examines colon most at risk Invasive
Very sensitive for polyp Uncomfortable
detection in left colon Slight risk of perforation and bleeding
Does not require full bowel May miss proximal lesions
prep (enemas only) Colonoscopy required if polyp identified
Colonoscopy Examines the entire colon Most invasive
Highly sensitive and specific Uncomfortable and requires sedation
Therapeutic Requires bowel prep
Risk of perforation and bleeding
Costly
Double Examines entire colon Requires bowel prep
contrast Good sensitivity for polyps Less sensitive for polyps <1cm
barium enema <1cm May miss lesions in the sigmoid colon
Colonoscopy required for positive result
Virtual Non-invasive Requires bowel prep
colonoscopy Sensitivity may be as good Insensitive for small polyps
as colonoscopy Minimal experience and data
Colonoscopy enquired for positive result

Clinical Presentations
Symptoms of colorectal cancer are nonspecific and generally develop when the
cancer is locally advanced.
 Change in bowel habit and rectal bleeding: classic first symptoms

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 Abdominal pain, bloating, and other signs of obstruction typically occur

with large tumors and suggest more advanced disease.
 Left sided tumors are more likely to cause obstruction due to;
o Annular and tubular types of carcinoma are more common
o Relatively small caliber of the bowel
o More solid stool consistency
 Bleeding and iron deficiency anemia is more common in right sided
cancers than left sided tumors.
 Obstruction and perforation are emergency presentations.
 Rectal tumors may cause bleeding, tenesmus, and pain.
 Patients may be asymptomatic and/or present with unexplained anemia,
weight loss, or loss of appetite.
 Colorectal cancer should be suspected in an older patient with
unexplained anemia.
 Metastatic symptoms;
o Liver metastasis: 15% at presentation; jaundice
o Lung metastasis: cough, chest pain
Differential diagnoses of right lower quadrant mass (consider age, sex, duration, etc.)
 Colon cancer (caecal)  Bone tumors arising from iliac crest
 Appendicial mass; secondary to;  Leiyomyosarcoma
o Infection  Crohn’s disease
o Lymphoma  Lipomas
o Mucocele  Volvulus
o GIST  Psoas abscess
o Kaposi sarcoma  Typhylitis
o Adenocarcinoma
 Ovarian tumors
o Cysts
 Tubo-ovarian abscess
o Dermoid tumors
 Myoma
 Ileocolic tuberculosis
 Aneurysm
 Appendicial abscess
 Undescended testis
 Abdominal wall tumors
 Unascended kidney
 Mesenteric lymphadenopathy
Retroperitoneal masses do not move with respiration nor do they fall forward up on
stooping. Ovarian cysts, psoas abscesses, and pelvic abscesses cross the
inguinal ligament.

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Fig: Distribution of colorectal cancer by site; more than 65% occur on the right

Comparison between right side and left side tumors

Right side tumors Left side tumors
Anemia* Obstruction*
RIF mass Perforation (caecal)
Perforation is less common Tenesmus
Ulcerative and fungatng Annular and tubular

Routes of spread;
 Regional lymph node metastasis is the most common form of spread.
o Colon cancers follow the major venous outflows
o Upper rectal tumors: along superior rectal vessels to inferior
mesenteric lymph nodes.
o Lower rectal tumors: along middle rectal vessels
o Spread along inferior rectal vessels is rare, except ii:
 Involvement of anal canal
 Blockage of proximal lymphatics
o T-stage is the single most important predictor of lymph node
spread;
 Tis = no risk
 T1 and T2 (small tumors confined to the bowel wall) = 5-
20%
 T3 and T4 (larger tumors invading through the bowel
wall or adjacent organs) >50%
 Local spread;
o Invasion of bowel wall and perforation

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o Involvement of adjacent tissues and other viscera

o Colon obstruction
o Ureteric obstruction (rectal cancer)
 Distant metastasis
o The most common site is the liver. Tumor size and grade is also
correlated with risk of metastasis.
o Lung: rarely occur in isolation
o Peritoneal seeding: carcinomatosis

Fig: Diagrammatic representation of clinical manifestations of colorectal cancer

TNM staging of colorectal carcinoma
Tumor stage (T) Nodal stage (N)
TX: cannot be assessed NX: cannot be assessed
T0: no evidence of cancer N0: no lymph node metastasis
Tis: carcinoma insitu N1: metastasis to 1-3 pericolic or perirectal
T1: submucosal invasion nodes
T2: invasion of muscularis propria N2: metastasis to ≥4 pericolic or perirectal
T3: invasion through muscularis nodes
propria into subserosa or into non- N3: metastasis to any lymph node along a
peritonealized pericolic or perirectal major named vascular trunk
tissues Distant metastasis (M)
T4: invasion of other organs or MX: cannot be assessed

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tissues or perforates the visceral M0: no distant metastasis

peritoneum of specimen M1: distant metastasis present

TNM staging of colorectal cancer and 5-year survival

Stage TNM 5-year survival (%)
I T1-2, N0 93.2
IIa T3, N0 84.7
IIb T4, N0 72.2
IIIa T1-2. N1 83.4
IIIb T3, N1 64.1
IIIc T3, N2 or T4, N1-2 44.3
IV Tany, Nany, M1 8.1
General staging principles
 Early stage (I &II): tumors without nodal or distant metastasis
 Locally advanced disease (III): tumors with only nodal metastasis
 Advanced disease (II): distant metastatic disease

Investigations
 Baseline investigations (CBC, blood group and RH, organ function tests)
 Fecal occult blood test (FOBT)
 Flexible sigmoidoscopy
 Colonoscopy: gold-standard
 Double contrast barium enema
 CT-colonography
 Abdominal ultrasound: to see a mass and secondaries
 CEA values ≥8 are associated with poor prognosis
 Abdomino-pelvic CT for staging

Preoperative evaluation
 Staging
 Examine the colon for synchronous cancer (5%). Synchronous cancers
refer to a second primary colon cancer diagnosed at the same time or
within one year from when the index cancer is diagnosed
 Antiembolism stockings should be fitted and the patient started on
prophylactic subcutaneous low molecular weight heparin.
 Bowel preparation
o Mechanical cleansing;
 3 day regimen of low-residue or liquid diet combined with
laxatives and enemas.
 Currently: isotonic lavage solution containing polyethylene
glycol (PEG) or castor oil.
 Other alternative = mono- and di-basic sodium phosphate.
 Postoperative infection rate is 30-60%

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o Antibiotic administration
 Cephalosporin and metronidazole or ampicillin, gentamycin,
and metronidazole.
 Postoperative infection rate can reduce below 10%
o NPO 6 hours prior to surgery
Treatment of colorectal cancer;
 Depends on the stage of disease
 Is multidisciplinary (surgeon, radiologist, and internist).
 Is individualized.
Surgical excision of the tumor is the conventional management option;
 Carcinoma of caecum or right colon: right hemicolectomy. Right
hemicolectomy removes a portion of the distal ileum, the cecum,
ascending colon, and the transverse colon to the right of the middle colic
artery.
 Carcinoma of right transverse colon and hepatic flexure: extended right
hemicolectomy. Extended right hemicolectomy expands right
hemicolectomy to include the transverse colon over to the splenic flexure.
 Carcinoma of left transverse colon and splenic flexure: extended left
hemicolectomy.
 Carcinoma of left descending and sigmoid colon: left hemicolectomy. Left
hemicolectomy removes the transverse colon to the left of the middle colic
artery, left colon and sigmoid colon to the level of the upper rectum.
 Rectal carcinoma
o Local excision
 Transanal excision: low rectal cancers
 Transanal endoscopic surgery
 Posterior excisions: mid- or upper rectum cancers
o Sphincter sparing procedures (low anterior resection-LAR).
 Intersphincteric resection for lower rectal cancer
 Total mesorectal resection
o Anterior resection is the general term used to describe resection
of the rectum from an abdominal approach to the pelvis with no
need for a perineal, sacral, or other incision. Three types of
anterior resection have been described.
 High anterior resection: distal sigmoid and rectum
 Low anterior resection: lesions in upper and mid-rectum
 Extended low anterior resection: for lesions in distal
rectum but several centimeters above the sphincter.
o Abdominal perineal resection: resection of the sigmoid colon,
rectum, and anus, and the construction of a permanent end
colostomy. (Hartmann’s procedure)

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o Multivisceral resection
 Other palliative approaches include a bypass or proximal stoma for
obstructing lesions.
 Complications;
o Ureter, bladder, and seminal vesicle injury
o Urinary retention/bladder dysfunction: most common after APR
o Impotence
o Perineal hernia
o Necrosis
Chemotherapy
Radiotherapy has limited role in colonic cancer (metastasis to liver, peritoneum),
but is more important in the treatment of rectal cancers.

Treatment options for colon cancer based on stages

Stage Treatment option
0 Polypectomy
I: malignant polyp Segmental colectomy
(T1, N0, M0) Polypectomy
Early stage (I & II) Stage I: surgery
Stage II: surgery ± adjuvant chemotherapy.
Adjuvant chemotherapy is added for;
 Younger patients and
 Patients with high histologic grade tumors
Locally invasive Surgery + adjuvant chemotherapy
(III) Patients with MSI-high stage II disease do not benefit from
chemotherapy and do well without it.
Neoadjuvant chemotherapy is rarely needed in bulky tumors.
Advanced (IV) Palliation is the focus of the therapy
 Chemotherapy for all patients
 Diverting stomas
 Bypass surgery
 Colonic stenting for obstructing lesions
 Angiographic embolization for bleeding tumors
 External beam radiotherapy
Unlike other malignancies, highly selected patients with isolated
resectable metastasis may benefit from resection (metastasectomy).
 20% of metastases limited to the liver are resectable
 Very few of lung metastases are resectable
 Other sites are potentially difficult to resect

Treatment options for rectal cancer based on stage

Stage Treatment option
0 Local excision (transanal excision)
Radical resection if transanal excision is not technically possible
Localized (I) Radical excision ± chemoradiation
Local excision + adjuvant or neoadjuvant therapy
Locally advanced (II & Stage II: surgery + adjuvant chemoradiation

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III) Stage III: neoadjuvant chemotherapy + surgery + adjuvant

chemoradiation
Metastatic disease (IV) The same as colon cancer

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Fig: Extent of resection for carcinoma of the colon. A. Cecal cancer. B. Hepatic
flexure cancer. C. Transverse colon cancer. D. Splenic flexure cancer. E.
Descending colon cancer. F. Sigmoid colon cancer.

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Emergency operations
 Obstruction;
o Common in the right or transverse colon
o Treated by resection and primary anastomosis
o Diversion and ileostomy is rarely needed.
 Perforation;
o Caecum is at highest risk for perforation
o Primary resection with anastomosis and proximal protective
colostomy or ileostomy.
o Primary resection without anastomosis.
Follow-up and surveillance
 Colonoscopy within 12 months after initial diagnosis. If that study is
normal, colonoscopy should be repeated every 3-5 years thereafter.
 CEA every 3-6 months for 2 years.
o If post-op levels doesn’t fall: incomplete resection or occult
metastasis
o If post-op levels increase: recurrence or secondaries
 Slow rise indicates loco-regional disease
 Rapid rise indicates metastasis
o Not used as a follow-up investigation in poorly differentiated
tumors as they will not produce CEA.
 Patients who have undergone local resection of rectal tumors probably
also should be followed with frequent endoscopic examinations (every 3–6
months for 3 years, then every 6 months for 2 years).
 CT scans annually for 5 years.
Recurrent colorectal cancer (Metachronous colon cancer)
 Incidence = 20-40%
 Most occur within the first 2 years after initial diagnosis
 Adjuvant chemotherapy any delay recurrences.

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Fig: Terminology of types of colorectal resections:

 AC: Ileocecectomy;
 A BD: Ascending colectomy;
 A  BF: Right hemicolectomy;
 A BG: Extended right hemicolectomy;
 E FG H: Transverse colectomy;
 GI: Left hemicolectomy;
 FI: Extended left hemicolectomy;
 J K: Sigmoid colectomy;
 A BJ: Subtotal colectomy;
 A BK: Total colectomy;
 A BL: Total proctocolectomy.

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Osteomies

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CHAPTER NINE-THE URINARY SYSTEM

Surgical Anatomy and Physiology

The anatomy of urinary system
The kidneys
 Paired retroperitoneal organs invested in a fibro-fatty layer;
o Fascia of Zuckerkandl posteriorly and
o Gerota’s fascia anteriorly
 Posterior relations;
o Posteromedially: psoas mucle
o Posterolatereally: quadratus lumborum
 Anterior relations;
o They are confined by the posterior layer of peritoneum.
o Left: spleen lies superlaterally; separated from the kidney and
Gerota’s fascia by the peritoneum.
o Right: liver is situated superiorly and anteriorly; and also
separated by the peritoneum.
 Renal vasculature;
o Renal arteries are branches of abdominal aorta. The right renal
artery passes posterior to the vena cava and is significantly
longer than the left renal artery.
o Within the kidney, there is no anastomotic arterial flow.
o Renal veins are tributaries of inferior vena cava. The left renal
vein passes anterior to the aorta and is much longer than the
right renal vein. The left renal vein, unlike the right one, has
collateral venous drainage from;
 Left gonadal vein,
 Left inferior adrenal vein, and
 A lumbar vein.
 The collecting system of the kidney;
o Composed of several major and minor calices that converge into
the renal pelvis.
o The renal pelvis can have a predominantly intrarenal or
extrarenal position.
o The renal pelvis tapers in to the ureteropelvic junction (UPJ)
where it joins with the ureter.
The ureters
 Small muscular structures that course anterior to psoas muscle from renal
pelvis to the bladder.

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 Blood supply;
o Proximal: from aorta and renal artery and comes mainly from the
medial direction.
o Distal: from branches of the iliac arteries and comes laterally.
 They course along the pelvic sidewall and pass under the uterine arteries
in women.
 They enter the bladder at the lateral aspect of the base.
 They course through the bladder at an oblique angle and open in to the
bladder at the ureteral orifices that are close to bladder outlet; forming the
trigon in between.
The bladder
 Situated in the retropubic space in extraperitoneally.
 A portion of the bladder dome is adjacent to the peritoneum.
 Physiologic volume = 200-400mL.
 The rectum lies posterior to the bladder in males; whereas the vagina and
uterus are posterior in females.
 It is lined by transitional epithelium. It has a special smooth muscles called
detrusor muscle.
 Around the male bladder neck is the smooth muscle internal sphincter
innervated by adrenergic fibers, which prevent retrograde ejaculation.
 Fascial and ligamentous supports;
o Condensations of fascia pass forward and laterally to the ureter
to join with prostatic fascia.
o Median and lateral umbilical ligaments.
o Condensations of fascia around superior and inferior vascular
pedicles.
 Arteries:
o Superior vesical artery from anterior trunk of internal iliac artery
o Inferior vesical artery from anterior trunk of internal iliac artery
o Branches from obturator and inferior gluteal arteries
 Veins:
o Vesical plexus on lateral and inferior surfaces.
o In males the prostatic plexus is continuous with vesical plexus.
o In females, similar large veins are continuous with vaginal plexus.
 Innervation:
o Parasympathetic input: S2, S3, & S4
o Sympathetic input: T11-L2
o Somatic innervation: pudendal nerve and inferior hypogastric
plexus.

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Fig: The nervous control of the bladder

The prostate
 Three zones (McNeal);
o Peripheral zone: site for prostatic cancer
o Central zone
o Transitional zone; site of BPH
 Capsules;
o True: condensation of peripheral part of the gland.
o False: from pelvic fascia. Prostatic plexus are embedded in it.
 Lobes = 5; anterior, posterior, 2 lateral, and middle/median lobe.
 Smooth muscles in the upper part of the prostate and bladder neck form a
separate sphincter, closing during ejaculation. Resection of this tissue
during prostatectomy is responsible for retrograde ejaculation.
 Between the prostate and the rectum lies Denonvilliers’ fascia, this is the
main anatomic barrier that prevents prostate cancer from regularly
penetrating into the rectum.
The urethra
 It has four components;
o Prostatic: compressed in between the lateral lobes of prostate.
o Membranous: located where urethra the urethra penetrates the
pelvic floor; and is the usual site for urethral rupture at the time of
pelvic fracture.
o Bulbar
o Penile: within the corpus spongiosum
 The urethral lining changes from transitional epithelium proximally to
stratified squamous cell epithelium distally.

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Benign Prostatic Hyperplasia

Epidemiology
Occurs in men over 50 years of age; by the age of 60 years, 50% of men have
histological evidence of BPH.

It is s a common cause of significant lower urinary tract symptoms in men and is

the most common cause of bladder outflow obstruction in men >70 years of age.
The prevalence of histologically diagnosed BPH increases from 8% in men aged
31 to 40, to 40-50% in men aged 51 to 60, to >80% in men older than age 80 and
100% in men aged more than 100 years.

Risk factors;
 Age >50
 Race; black = white, but black men <65 years may need treatment more
often than white men.
 Family history?
 Alcohol consumption
 Prostatitis
 Obesity and metabolic syndrome

Pathophysiology
The pathogenesis of BPH remains incompletely understood. Serum testosterone
levels slowly but significantly decrease with advancing age; however, levels of
oestrogenic steroids are not decreased equally. According to this theory, the
prostate enlarges because of increased oestrogenic effects.

BPH develops primarily in the periurethral or transitional zone of the prostate. It

affects both glandular epithelium and connective tissue stroma to variable degrees.
The hyperplastic nodules are composed primarily of stromal components and to
lesser extent epithelial cells.

Effects of BPH (BPH, BOO, & LUTS)

 No symptoms, no bladder outflow obstruction (BOO)
 No symptoms, but urodynamic evidence of BOO
 Lower urinary tract symptoms, no evidence of BOO
 Lower urinary tract symptoms and BOO
 Others (acute/chronic retention, haematuria, urinary infection and stone
formation)
 Anatomical effects;

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o Prostatic urethral lengthening, narrowing, and compression

o Trabecuation and diverticuli formation in the bladder
o Hydroureter and hydronephrosis: end results

Clinical features
Lowe urinary tract systems (LUTS)
 Voiding or obstructive symptoms (WISHED)
o Weak-stream (poor flow)
o Intermittency
o Straining
o Hesitancy
o Sensation of incomplete Emptying (voiding)
o Dribbling
 Storage or irritative symptoms (FU2N2D)
o Frequency
o Urgency
o Urge incontinence
o Nocturia
o Nocturnal incontinence (enuresis)
o Dysuria
 Note that voiding symptoms are more pertinent to BOO because irritative
symptoms can also be caused by other entities like UTI and bladder
tumors.
Bladder outlet obstruction (BOO) – a urodynamic diagnosis
 Urine flow rate <10ml/sec (normal = >15ml/sec)
 Voiding pressure >80mmmH2O (normal = <60mmH2O)
Complications
 Acute urinary retention
 Chronic urinary retention
 Recurrent infection (UTI)
 Bladder stone
 Hematuria
 Hydroureter and/or hydronephrosis
 Renal failure
 Pyelonephritis and pyonephrosis
 Inguinal herinia (due to straining)
 Bladder diverticuli
 Bladder cancer
Physical examination
 Suprapubic abdominal distention: urinary retention. Acute retentions are
painful unlike chronic retentions.

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 Signs of renal failure

 Digital rectal examination
o The prostate has smooth surface, regular border, firm
consistency, not fixed to rectal mucosa & palpable medial sulcus
but the upper border isn’t reachable.

Investigations
 Serum prostate-specific antigen (PSA) to exclude prostatic cancer
 Urine flow rate measurement
 Pressure flow uridynamic studies
 Blood tests: serum creatinine, electrolytes, CBC, blood group, and RH.
 Urinalysis
 Cystourethroscopy
 Upper urinary tract imaging (IVU or USG): hematuria or infection
 Transrectal ultrasound

Treatment
Treating BPH is all about relieving symptoms and improving the quality of life, if
not necessarily taking the prostate out. Management of BPH depends on the
severity of the symptoms. The severity of the symptoms is graded by the
international prostate scoring system (IPSS).

International prostate scoring system (IPSS)

Not at all <1 in 5 < half of About > half of Almost
the time half of the the time always
time
Frequency 0 1 2 3 4 5
Urgency 0 1 2 3 4 5
Nocturia 0 1 2 3 4 5
Weak stream 0 1 2 3 4 5
Intermittency 0 1 2 3 4 5
Straining 0 1 2 3 4 5
Incomplete 0 1 2 3 4 5
emptying
Interpretation
 ≤7: mild – conservative management
 8-19: moderate – medical management
 20-35: severe – surgery management

Conservative management
 Watchful waiting
 Avoiding fluids at the evening
 Reducing coffee and alcohol intake

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 Why watchful waiting in mild BOO? Because the risk may outweigh the
benefits of surgery due to;
o Postoperative complications like incontinence, or
o General surgical complications or
o Anesthetic complications.
 One-third of the patients will spontaneously improve; one-third will not
progress; while the last third of patients will progress and will need
medical or surgical interventions.
Medical management
 Alpha-1 blockers
o They act on alpha receptors in the smooth muscles of the
prostate and decrease its tone. For this reason they are usually
used for small sized prostates; causing BOO due to smooth
muscle contraction.
o Prazosin, terazosin, doxazocin, and tamsulosin
 5-alpha reductase inhibitors
o They block the conversion of testosterone to the more potent
DHT, depriving the prostate of its stimulatory signal; hence
decreasing its size. They are used for larger sized prostates.
o Fenasteride
Surgical management
 Indications for surgical management
o Acute urinary retention
o Chronic retention
o Hydroureter and hydronephrosis
o Complications: stone, infection, diverticuli (especially those with
neck >2cm)
o Hemorrhage (hematuria): recalcitrant to medical treatment.
o Elective prostatectomy for severe symptoms
 Operational options
o Endoscopic: transurethral resection of prostate (TURP). This is
preferred for prostates <80ml.
o Open surgery; better for larger prostate sizes.
 Trans vesical prostatectomy (TVP)
 Has additional benefit of treating bladder
complications of BOO; so it is indicated, even
for small sized prostates, in these cases.
 Retropubic prostatectomy (RPP) – Millini procedure
 Perineal approach: now obsolete
o Counseling men undergoing prostate surgery;
 Retrograde ejaculation
 Rectile impotence: family planning

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 Success rate: family planning

 Risk of reoperation
 Morbidity rate
Complications of prostatectomy
 Hemorrhage
 Perforation of bladder, prostatic capsule, or rectal mucosa
 Sepsis
o Routine use of prophylactic antibiotics is recommended based on
local antimicrobial sensitivity profiles.
o A blood culture should be taken and antibiotics given parenterally
(e.g. amoxicillin plus cefuroxime, or gentamicin).
 Urethral stricture
o This may be secondary to
 Prolonged catheterization
 Use of an unnecessarily large catheter
 Clumsy instrumentation or
 Presence of the resectoscope in the urethra for too long
a period.
o Treatment: cutting the densely fibrotic stricture.
 Bladder neck contracture
 Urinary incontinence
o It is usually urge incontinence.
o Mostly due to bladder over-activity; so reassure the patient and
treat conservatively.
o If they develop infection (UTI) appropriate intervention should be
made.
 Retrograde ejaculation and impotence.
o Retrograde ejaculation occurs commonly (>50%) because of
disruption to the bladder neck mechanism.
o Impotence in men with good sexual function before surgery is
uncommon.
 Water intoxification (TURP syndrome)
o Caused due to absorption of water used for irrigation in to the
circulation at the time of transurethral resection.
o Can give rise to congestive heart failure (CHF), hyponatremia,
and hemolysis.
o Confusion, and other cerebral events mimicking stroke.
o Treatment involves fluid restriction and diuretics; specially loop
diuretics which selectively promote excretion of water.
o The incidence of this condition has been reduced since the
introduction of isotonic glycine for irrigating during resection

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 General complications: Pulmonary atelectasis, pneumonia, myocardial

infarction, congestive cardiac failure and deep venous thrombosis.
 Death rate = 0.2-0.3%
 Reoperation
o After TURP = 15-18 after 8 years
o After open surgery = 5% after 8 year

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Renal Stones (Nephrolithiasis)

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CHAPTER TEN-ORTHOPEDIC SURGERY

Orthopedic surgery is a specialty with which every physician should be familiar.
Anyone who cares for patients in an outpatient or emergency room setting will find
that the majority of presenting complaints involve the musculoskeletal system. A
basic understanding of musculoskeletal anatomy is assumed, and understanding
the principles of care for musculoskeletal trauma is essential.

Musculoskeletal Fractures
Accidents continue to be a prominent cause of death and disability throughout the
world. In the first 5 decades of life, trauma accounts for more deaths than any
other cause. Communication among collaborating specialists is central to patient
care; and the trauma and emergency department findings need to be relayed
precisely to consulting specialists. The most practical and universally understood
characterizations of injuries are those that adhere to basic anatomic and
mechanical principles. A fracture is a disruption of the normal architecture or
continuity of bone.

Types of fractures
Acute fractures: have sharp, well defined edges of the fragments. They are most
often caused by trauma; and might be called traumatic fracture and they result
from high-energy accidents.
Chronic fractures: have rounded and sclerotic appearances after resorption of
bone has occurred at the fracture ends.
Incomplete fractures: they are more common in children and are termed greenstick
fractures. In adults, they are called infractions.
Stress fractures: due to chronic repetitive trauma that cause microscopic
disruptions when the bone is stressed beyond its failure point. They are
considered overuse injuries.
Pathologic fractures: when a bone fails through an area weakened by preexisting
diseases such as primary bone tumors, metastatic lesions, infections, metabolic
disease, and injury to an old fracture site.
Insufficiency or fragility fracture: fractures in osteoporotic bone. They are
technically pathologic fractures. They are usually due to accidents with much lower
energy than acute fractures; such as fall from a standing height. Examples include
hip fractures, vertebral compression, and distal radius fractures.
Open fractures: when an overlying wound produces communication between the
fracture site and the outside environment. Closed injuries are when there is no
such communication. The severity of the injury is graded based on;
1. Wound size
2. Energy of fracture
3. Degree of contamination and

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4. Soft tissue injury

Gustillo Anderson classification of open fractures
Grade Wound size Soft tissue injury Contamination Energy
I <1cm Minimal Clean (0-2%) Low
II 1-10cm Moderate Very little (2- High
5%)
III >10cm Extensive Contaminated High
IIIA >10cm Extensive, but with adequate tissue (10-50%) High
to cover the fractured bone.
IIIB >10cm Extensive, the bone is exposed and High
requires a flap or graft to be covered
IIIC Any size Any degree, associated with major High
arterial injury that needs repair. (25-50%)
The following fractures are grade three without any other requirement;
 Segmental fractures
 Comminuted fractures
 Farmyard fractures
 Close-range high velocity bullet injuries
 Fractures that have been open for at least 8 hours before treatmenet

Intra-articular fracture: a fracture that extends to a joint. They are normally caused
by a compressive, or axial, load across the joint. Condylar fractures of humerus
and radius are intra-articular fractures.
Long bone fractures: characterized by anatomic location;
 Epiphysis: area between the growth plate (physis) or physical scar
 Metaphysis: between epiphysis and shaft; includes the growth plate
 Diaphysis: the shaft of the bone between the proximal and distal
metaphyses.
 So, fractures can be described according to these three sections as
proximal, middle, or distal.
Supracondylar fracture: fractures involving the epicondyles of humerus and femur.
The articular surfaces are called condyles, and condylar fractures are intra-
articular fractures.
Based on pattern of cortical disruption;
 Simple fractures;
o Transverse: occur when bending moment is applied
o Oblique: occur when bending moment is applied
o Spiral: result from rotational force about the long axis of bone
 Complex fractures;
o Segmental: simple fracture at two separate sites.
o Comminuted: presence of multiple fragments in a fracture.
o Butterfly fragment: area of comminution in one of the simple
fracture patterns.

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Displacement: loss of alignment of the fracture fragments.

 Angulation: the angle created by the displaced fracture fragments. It is
described by the direction of the apex that fracture fragments form (e.g.,
200 apex lateral). Vollar angulation.
 Translation: is the relationship of the proximal fracture to the distal one. It
is described by the percent overlap. A fracture with 100% translation in
any plane is completely displaced.
 Distraction: a fracture in which the distal fragment is separated from the
proximal fragment by a gap. (not shown in the figure below)
 Shortening/bayoneted fracture
 Rotation: full-length film of the limb is required.

Fig: Types of fracture displacement

Soft tissue injuries
There are four broad classifications
 Strains
 Sprains
 Ruptures
 Contusions

Ligamentous injuries
 When a ligament is injured but still in continuity, it is termed sprain. The
severity of ligamentous injuries is graded.
 Grade I: stretching of a ligament or ligament complex; they do not result
in instability.
 Grade II: partial ruptures of ligaments; results in minor instability.
 Grade III: complete rupture; lead to significant instability. Avulsion
fractures fall in to this category.
Strain: injury to a muscle or tendon. These injuries are most commonly of an
overuse nature.
 First degree: blunt injury due to direct low energy trauma that causes mild
contusion. Fascia is intact and bleeding is minimal.

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 Second degree: more serious trauma. Fascia is still intact, and there is
more bleeding.
 Third degree: trauma of greater magnitude. The fascia is partially torn,
and there is widespread bleeding.
 Fourth degree: severe trauma that causes complete tear of a muscle, tear
of fascia, and diffuse bleeding.
Systematic description of a fracture;
1. Whether the fracture is open and its grade;
2. Intra-articular fracture, if present;
3. The side of the body and the injured bone;
4. Pattern followed by its location; and
5. Displacement
e.g. an open GAIIIB left humeral oblique distal fracture with 50% translation; a
closed GAI condylar right femoral transverse distal fracture with 100 apex medial
angulation.

Growth plate injury

Growth plate injuries in children and adolescents can lead to abnormal growth or
growth arrest, either complete or partial.
 Complete growth arrest results in length abnormalities
 Partial growth arrest results in angular deformities
The severity of injury to the physis is classified in the Salter-Harris classification.
Salter-Harris classification of physical fractures (type VI six is added by Mecer Rang)
Type Definition
I Simple fracture line just involving the physis
II Fracture line through the physis exiting through the metaphysic
III Fracture line through the physis exiting through the epiphysis (intra-articular)
IV Fracture line across the epiphysis, cross physis and across metaphysic
V A crush injury of the physis
VI Injury to perichondral structures by direct trauma

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Fig: Salter-Harris classification; with mnemonics

Fracture Healing
Bone is a composite structure with mineral and organic components.
 The mineral component is made up of a compound called
hydroxyapatite (Ca5(PO4)3(OH)); which provides the strength, stiffness,
and rigidity characteristic of bone.
 The organic or protein component consists primarily of type I collagen,
which lends tensile strength and resiliency.
The outer covering of bone, the periosteum, provides the vascular supply that
plays an essential role in fracture healing. The periosteum in children is
substantially thicker and more robust than in adults, accounting in part for the
more rapid healing of pediatric fractures.
Bone is unique in healing itself completely with a tissue that is indistinguishable
from the original tissue hence there is no scar left. The term bone regeneration and
not fracture healing is more appropriate.
Following a fracture, a bone can heal in two different ways;
1. Direct/ primary bone healing
2. Indirect/secondary bone healing
Direct bone healing
 Heals directly with bone without callus formation.
 Happens when fragments are anatomically reduced and rigidly fixed.
 It has two stages;
 Osteoclastic remodeling of the bone across fracture interface
 Osteoblastic laying down of lamellar bone across the interface
 It occurs in;
 Rigidly fixed fractures (absolute stability), and

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 Intrra-articular fractures: hyaluronic acid found in the joint

synovial fluid inhibits hematoma formation.
Indirect bone healing
 This is the common method of bone healing where both external and
internal callus are formed.
 Bone healing is divided in to three slightly overlapping stages;
o Inflammatory
o Reparative
o Remodeling
 Inflammatory phase is dominated by vascular events;
o Hematoma is formed.
o Resorption of fracture edges (radiographically distinct)
o Osteoprogenitor cells begin to form new bone
 Reparative phase
o New blood vessels develop. Nearly complete immobilization is
required during inflammatory and early reparative phase not to
disrupt these vessels.
o Once neovascularization is complete, progressive loading and
stress across thr fracture site are desirable to augument callus
formation.
o Callus formation;
 Soft callus
 Hard callus
o If immobilization is complete, membranous bone healing takes
place. If incomplete bone heals by endochondral ossification.
o Clinical union marks the end of the reparative phase.
 Remodeling phase
o Callus becomes completely ossified.
o The bone undergoes structural remodeling.
o Remodeling occurs quickly in young children.
 Problems with indirect bone healing;
o Less anatomic union
o Chances of mal-union significant
o Delayed joint mobilization
o Possibility of fracture
Factors affecting fracture healing
Those in favor of union Those detrimental to union
 Adequate circulation  Poor circulation  Medications: NSAIDs,
 Hormones like growth  Infection steroids, ciprofloxacin
hormone, parathormone,  Diabetes  Distraction
thyroxine, etc.  Anemia  Segmental fractures
 Good nutrition and  Hypothyroidism  Comminution
mineral supplements

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help passively  Malnutrition  Osteoporosis

 Bioelectric fixation  Chronic alcohol use  Soft tissue interposition
 Smoking  Inadequate and improper
immobilisation

General Principles of Fracture Management

Generally there are two stages of fracture management;
 Acute management;
o ATLS (ABCDs)
o Secondary survey
o Radiologic assessment
o Immobilization
o Pain management
o Patient education
 Definitive management
o Reduction
o Immobilization
o Rehabilitation
Two existential problems have to be overcome.
 How to hold fracture: hold versus move
 Avoiding unnecessary risks: speed versus safety
These four factors dominate fracture management and are termed fracture
quartets.

Reduction of fractures
Reduction means re-establishing limb continuity provisionally. After resuscitation,
there should not be undue delay in attending the fracture; swelling of the soft
tissue during the first 12 hours makes reduction increasingly difficult. However,
there are some situations in which reduction is unnecessary;
 Little or no displacement
 Displacement does not matter initially; e.g. fractures of clavicle
 Reduction is unlikely to succeed; e.g. compression fractures of vertebra.
Reduction should aim for adequate apposition and normal alignment of the bone
fragments. There are two general priorities in reducing fractures;
 Anatomical reduction: for intra-articular fracture, and
 Mechanical alignment: for extra-articular fractures
Reduction techniques include;
 Closed reduction
 Open reduction
Closed reduction
 Done under appropriate anesthesia and muscle relaxation.
 A three-fold maneuver;

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o Traction of distal fragment in the line of bone

o Disimpaction and repositioning
o Reduction and adjusting alignment in each plane
 This is most effective when the periosteum and muscles on one side of
the fracture remain intact; the soft tissue strap prevents over-reduction
and stabilized the fracture after it has been reduced.
 Some fractures are difficult to reduce by manipulation because of powerful
muscle pull and may need prolonged traction.
 Indications;
o All minimally displaced fractures
o Most fractures in children
o Fractures that are not unstable after reduction
Open/operative reduction
 Indications;
o When closed reduction fails
o Large articular fragment that needs accurate positioning
o Avulsion fractures
 As a rule, however, open reduction is merely the first step to internal
fixation.

Immobilization of fractures
The word immobilization should be obsolete because the objective here is seldom
complete immobility but prevention of displacement. But the word immobilization
will still be used in this book because it is the word in common use in our setup
(Hawassa University-CMHS).
What are the options for immobilizing a fracture?
 Continuous traction
 Cast splintage
 Functional bracing
 Internal fixation
 External fixation
Closed methods are most suitable for fractures with intact soft tissues.
Contraindications to non-operative methods;
 Severe soft tissue damage
 Inherently unstable fractures
 Multiple fractures
 Fractures in confused or unconscious patients.
Continuous traction
 Applied to a limb distal to the fracture to exert a continuous pull in long
axis of the bone, with counter-force in opposite direction.

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 Useful for oblique or spiral shaft fractures that are easily displaced by
muscle contraction.
 Traction cannot hold a fracture still.
 Speed is the weakest member of the quartet. That means a patient will
stay long in hospital. So, as soon as the fracture is sticky (deformable but
not displaceable), traction should be replaced by functional bracing.
 Types of traction;
o Traction by gravity: for upper limb injuries
o Skin traction: for children; a pull of up to 4 or 5 kg.
o Skeletal traction: a pull of one-fifth to one-seventh of the body
weight. A stiff wire or pin is inserted;
 Behind the tibial tubercle for hip, thigh and knee injuries
 Throught he calcaneum for tibial fractures
 Then a cord is tied to then to apply traction.
o The fracture is reduced and held in one of three ways;
 Fixed traction
 Balanced traction
 Combined traction
 Complications of traction
o Circulatory compromise
o Nerve injury
o Pin site infection
Cast splintage
 We usually use plaster of Paris (POP).
 Move is the weakest member of the qurtet; that means joints encased in
the plaster are prone to stiffness – termed fracture disease.
 Stiffness can be minimized by;
o Delayed splintage; using traction until movement has been
regained
o Replacing by functional braces after few weeks
 Technique;
o Apply stockinet
o Protect bony prominences by wool
o Apply the plaster
o Mold the plaster
 Functional positions;
o Knee is slightly flexed, the ankle at right angle, and the tarsus
and forefoot neutral.
o In the upper limb, the position of the splinted joints varies with the
fracture.
 Complications;

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o Tight cast
o Pressure sores
o Skin abrasion or laceration
o Loose cast
Functional bracing
 Uses either POP or other lighter thermoplastic materials.
 Prevents joint stiffness and still permitting fracture splintage.
 Segments of casts are applied to shafts of the bones, leaving joints free;
the cast segments are then connected by metal or plastic hinges.
 Most widely used for fractures of femur or tibia.
 Usually applied only when the fracture is beginning to unite; after 3-6
weeks of traction or plaster.
 It comes well on all the four quartets.
Internal fixation
 Hold a fracture securely so that movement can begin at once.
 With early movement, the fracture disease (stiffness and edema) is
avoided.
 Safety is the weakest member of the quartet; the greatest danger is sepsis
which may lead to loss of all the other members of the quartet.
 The risk of infection depends up on;
o The patient: devitalized tissue, dirty wound, unfit patient
o The surgeon: experience, training, and assistance
o The facility
 Indications for internal fixation;
o Fractures that cannot be reduced except by operation
o Fractures that are inherently unstable
o Fractures prone to re-displacement
o Fractures liable to be pulled apart by muscle action
o Fractures that unite poorly or slowly; e.g. femoral neck
o Pathologic fractures in which bone disease may prevent healing
o Multiple fractures
o Fractures in patient who present nursing difficulties (paraplegics,
the elderly, multiple injuries)
 Types of internal fixation;
o Intrafragmentary screws
o Wires (transfixing, cerclage, and tension banding)
o Plates and screws
o Intramedullary nails or rods
o Circumferential bands
 Complications;
o Infection

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o Non-union
o Implant failure
o Re-fracture
External fixation
 Components of external fixators; the pins, clamps, and external rods.
 Holds a fracture by pins, transfixing screws or tensioned wires that pass
through the bone above and below the fracture and are attached to
external frame.
 Especially applicable to tibia, and pelvis but also femur, humerus, lower
radius and even hands.
 Indications for external fixation;
o Severe soft tissue damage
o Contaminated soft tissue
o Fractures around joints in which soft tissues are too swollen to
allow safe surgery (internal fixation).
o Severe multiple injuries (sp. bilateral femoral fractures)
o Ununited fractures
o Infected fractures
 Ways of enhancing external fixation stability;
o Pin factors
 Increasing the diameter of pins (most important)
 Increasing the number of pins
 First pin closer to the fracture
 Decreasing the distance between pins.
o Bar factors
 Increasing the diameter of bars
 Increasing the number of bars
 Bar closer to the bone
o Increasing planes
o Pre-drilling with smaller sized drillers
o Periodic tightening of clamps
 Technical types of external fixation;
o Unilateral uniplanar
o Unilateral biplanar
o Bilateral uniplanar (through-through)
o Bilateral biplanar
 Complications;
o Soft tissue injury
o Overdistraction
o Pin-track infection

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Rehabilitation of function
The objectives are to reduce edema, preserve joint movement, restore muscle
power, and guide the patient back to normal function through;
 Elevation of limb, never dangle, never force
 Active exercise
 Assisted movement
 Functional activity

Treatment of Open Fractures

The four essential principles of open fracture management
 Antibiotic prophylaxis
 Urgent wound and fracture debridement
o Wound excision
o Wound extension
o Delivery of the fracture
o Removal of devitalized tissue
o Wound cleansing
o Leave nerves and tendons alone
 Stabilization of the fracture
 Early definitive wound closure
o GA I & II: can be immediately closed
o Severe grades: skin graft or flaps are needed

Complications of Fractures
General complications of fractures;
 Shock
 Multi-organ dysfunction syndrome (MODS)
 Tetanus
 Fat embolism
 Crush syndrome
Local complications (early and late);
 Early (urgent): local visceral injury, vascular injury, nerve injury,
compartment syndrome, haemarthrosis, infection, gas gangrene.
 Early (less urgent): fracture blisters, plaster sores, pressure sores, nerve
entrapment, myositis ossificans, ligament injury, tendon lesions, joint
stiffness, algodystrophy.
 Late: delayed union, non-union, mal-union, avascular necrosis, muscle
contracture, joint instability, and osteoarthritis.
Common vascular injuries
Injury Vessel

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First rib fracture Subclavian

Shoulder dislocation Axillary
Humeral supracondylar fracture Brachial
Elbow dislocation Brachial
Pelvic fracture Presacral and internal iliac
Femoral supracondylar fracture Femoral
Knee dislocation Poplietal
Proximal tibia Poplietal and its branches

Common nerve injuries

Injury Nerve
Shoulder dislocation Axillary
Humeral shaft fracture Radial
Humeral supracondylar fracture Radial or median
Elbow medial condyle Ulnar
Monteggia fracture-dislocation Posterior interosseous
Hip dislocation Sciatic
Knee dislocation Peroneal

Causes of delayed union

 Biological: inadequate blood supply, severe STI, perosteal stripping
 Biocmechanical: imperfect splintage, over-rigid fixation, infection
 Patient related: immense, immoderate, immovable, impossible patients

Causes of non-union (CASS)

 Contact
 Alignment
 Stability
 Stimulation

Compartment syndrome
 Fractures of the arm or leg can give rise to severe ischemia, even if there
is no damage to major vessels. It results in a vicious cycle of nerve and
muscle ischemia and necrosis.
 Nerves may regenerate but muscle, once infracted, can never recover
and is replaced by inelastic fibrous tissue (Volkmann’s contracture).
 A similar cascade of events may be caused by swelling of a limb inside a
tight plaster cast.
 High risk injuries: fracture of elbow, forearm bones, proximal tibia, and
also multiple fractures of hand or foot, crush injuries, and circumferential
burns.
 Clinical features;
o The classic features of ischemia are the five P’s;
 Pain

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 Paraesthesia
 Pallor
 Paralysis (weakness in active muscle contraction)
 Pulselessness
o The earliest features are pain (bursting sensation), altered
sensibility and paresis.
o There is no pathogmonic feature; what you need is strong
suspicion.
o Do stretch test; ischemic muscles are highly sensitive to stretch.
o The diagnosis is confirmed by intracompartmental pressure
measurements;
 Normal pressure is 0-8mmHg at rest.
 Differential pressure (∆P) – the difference between
diastolic pressure and compartment pressure – of less
than 30mmHg is an indication for immediate
decompression.

Fig: The vicious cycle of compartment syndrome

 Treatment
o Remove casts, bandages, and dressings
o Elevate the limb to the level of heart (not higher, not lower)
o Give analgesics
o If the clinical signs are sift, examine at 30-minute intervals for a
maximum of 2 hours.

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o Fasciotomy;
 ∆P < 30mmHg
 Three or more signs present
 No improvement after 2 hours of observation
o Muscle will be dead after 4-6 hours of total ischemia – there is no
time to lose!

Gas gangrene
 A life threatening infection caused by clostridium (sp. C.welchii).
 They multiply on tissues with low oxygen tension.
 Toxins produced by the organisms destroy the cell wall and rapidly lead to
tissue necrosis.
 Clinical features appear within 24 hours of injury;
o Intense pain and swelling with brownish discharge .
o Gas formation is not marked.
o Little or no pyrexia but pulse rate is increased.
o A characteristic smell becomes evident (once experienced this is
never forgotten).
o Rapidly the patient becomes toxic and may lapse into coma or
death.
o Anaerobic cellulitis is different from gas gangrene;
 Superficial gas formation is abundant
 Toxemia is slight
 Prevention;
o Deep penetrating wounds in muscular tissue should be explored,
all dead tissue excised, and left open if there is any doubt about
tissue vability.
o There is no effective antitoxin against C.welchii.
 Treatment;
o Early diagnosis is the key to life saving.
o General measures: fluid replacement and IV antibiotics
o Hyperbaric oxygen; to limit spread
o Decompression of wound and removal of dead tissue is the
mainstay of treatment.
o Amputation may be essential in advanced cases.

Avascular necrosis
 Common sites prone to avascular necrosis;
o Head of femur: femoral neck fracture
o Proximal scaphoid; fracture of its waist
o The lunate; dislocation
o The body of talus; fracture of its neck

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 Ischemia develops during the first few hours but clinical and radiologic
effects are not seen until weeks or even months later.
 Clinical features;
o No symptoms but pain if the fracture fails to unite or if the bone
collapses.
o Characteristic increase in x-ray density;
 Disuse osteoporosis
 Collapse of trabeculae
 Treatment;
o Treatment is necessary when joint function is threatened.
o Femoral neck fractures;
 Arthroplastyfor old people
 Realignment osteotomy for younger people
o Avascular necrosis in the talus or scaphoid may need no more
than symptomatic treatment. Arthrodesis of wrist is seldom
needed.

Myositis ossificans
 Heterotopic ossification in the muscles;
 Causes;
o Dislocation of an elbow
o Blow to the brachialis, deltoid, or quadriceps
o Without local injury in unconscious or paraplegic patients
 Clinical features;
o Soon after injury the patient complains of pain, local swelling, and
soft tissue tenderness.
o X-ray is normal but bone scan may show increased activity.
o Over the next 2-3 weeks the pain subsides, but the joint
movement is limited; x-ray may show fluffy calcification in the soft
tissue.
o By 8 weeks, the bony mass is easily palpable and is clearly
defined on x-ray.
 Treatment;
o No vigorous muscle stretching exercises
o Rest the joint in functional position until pain subsides
o Then begin gentle active movements
o Excise the mass when the condition has stabilized months later
o Indomethacin or radiotherapy to prevent recurrence.

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Muscle contracture
 Following arterial injury or compartment syndrome, the patient may
develop ischemic contractures of the affected muscles – a phenomenon
called Volkmann’s ischemic contracture.
 Most common sites: forearm and hand or leg and foot.
 Wasting and clawing of fingers or toes in severe cases.

Amputations
Indications (in their order of frequency)
 Peripheral vascular diseases (PVD)
 Trauma (the leading cause in the young); unsalvageable:
o Mangled limbs
o Crush injury
o Un-repairable vascular injury
 Tumors; especially osteosarcoma and Ewing’s sarcoma (second most
common in our set-up)
 Severe infection not responding to repeated debridement and culture
guided antibiotics (diabetic foot ulcer, gangrene, necrotizing fasciitis, etc.)
 Severe electrical burns
 Congenital anomalies, incompatible with life (proximal focal femoral
deformity, focomelias, hemimelias)
 Frostbite (alcoholics, psychos, soldiers).
Wagner’s classification of diabetic foot ulcer
Grade 1 Skin and subcutaneous tissue
Grade 2 To bone
Grade 3 Abscess or osteitis
Grade 4 Partial foot gangrene
Grade 5 Whole foot gangrene

University of Texas classification of diabetic foot ulcers

Grade 0 Pre- or post-ulcerative (A-D)

Grade 1 Full thickness ulcer not involving tendon,

capsule, or bone (A-D)

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Grade 2 Tendon or capsular involvement without bone

palpable (A-D)

Grade 3 Probes to bone (A-D)

A: non-infected
B: infected
C: ischemic
D: infected and ischemic

Types of lower extremity amputation;

 Hip disarticulation
 Above-knee-amputation
 Transcondylar-Gritti-Stokes amputation
 Knee disarticulation
 Peg-leg amputation: below-knee amputation done close to knee joint (5cm
stump).
 Below-knee-amputation (Burgess amputation)
 Foot amputations
o Ankle disarticulation
o Midfoot and hindfoot amputations
 Lisfranc/tarsometatarsal disarticulation
 Chopart: talonavicular and calcaneocuboid joints are
disarticulated.
 Syme: removal of the whole foot with cutting of tibia and
fibula just above the ankle joint.
 Boyd: Syme’s amputation in which anterior part of the
calcaneum is excised just distal to the peroneal
tuberosity with retaining heel flap.
 Pirogoff: it is like Syme’s amputation except posterior
part of the calcaneum is retained along with heel flap.
o Transmetatarsal/Gillie’s amputation

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o Toe amputation
 Simple amputation: partial or complete amputation of
any toe.
 Ray amputation: amputation of the toe along with all or
part of the corresponding metatarsal bone.
Types of upper extremity amputations
 Shoulder disarticulation
 Short above elbow
 Standard above elbow
 Elbow disarticulation
 Very short below elbow
 Medium below elbow
 Long below elbow
 Wrist disarticulation
 Transmetacarpal
Types of flaps;
 Long posterior flap in below-knee amputation
 Equal flaps in above-knee amputation
Post-operative care;
 Pain relief
 Physiotherapy
 Regular dressing
 Crutch is used initially, after 3months, prosthesis is placed.
 Rehabilitation.

Fig: Different levels of amputation in upper and lower limbs

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Fig: Different levels of lower limb amputations

Complications of amputation
 Early: hemorrhage, hematoma, infection, breakdown of skin flaps, gas
gangrene
 Late complications
o Pain
o Ulceration of stump
o Ring sequestrum formation
o Flap necrosis
o Painful scar
o Phantom limb
o Joint contracture
o Stamp neuroma
o Bone overgrowth in pediatric age group
 Pain in the amputated limb can be due to;
o Amputation
o Neuroma
o Phantom pain
o Physiologic
Prostheses
It is the substitution to a part of the body to achieve its optimum function.
(Orthroses are supplement for limb function.)

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Type of amputation Prostheses used

Syme’s amputation Elephant boot, Canadian Syme’s prosthesis.
Below-knee amputation Patellar tendon bearing (PTB) prosthesis and solid ankle
cushion heel (SACH).
Above-knee amputation Suction type prosthesis. It is placed above the stump. It is
better and well-tolerated.
Non-suction type prosthesis. It is placed at the ends. It
requires additional support
Hind-quarter amputation Tilting table prosthesis (TTP) or Canadian prosthesis is
used here.

Bone Tumors
The most common bone malignancies
 Myeloma
 Osteosarcoma
 Chondrosarcoma (20-27%)
Most common bone malignancies in order of their frequency
Below 30 years Above 30 years
Osteosarcoma Myeloma (common above 70 years)
Ewing’s sarcoma Chondrosarcoma
Chondrosarcoma Fibrosarcoma

Principles of treatment of bone tumors

Tumor excision
 Intracapsular (intralesional) excision and curettage
o Benign lesions with very low risk of recurrence
o Debulking for incurable tumors
 Marginal excision: for benign lesions
 Wide excision (2.5cm away from the tumor)
o For grade IA
o For grade IIA in conjunction with chemotherapy
 Radical excision: for high grade tumors (IIA or IIB)
Limb salvage (for grade II sarcomas)
 Wide excision of the tumor
 Dealing with the resulting defect
o Vascularized or non-vascularized bone grafts for short diaphysial
segments
o Custom made implants for longer gaps
o Large allografts, endoprostheses, or allograft-endoprosthetic
composite for osteo-articular segments.
Amputation
Multi-agent chemotherapy (methotrexate, doxorubicin (adriamycin),
cyclophosphamide, vincristine, and cisplatin)
Radiotherapy

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Fig: Surgical options of bone tumors management

Classification of bone tumors (modified WHO)
Origin Benign Malignant
Bone forming Osteoma Osteosarcoma
Osteoid osteoma
Osteoblastoma
Cartilage forming Chondroma Chondrosarcoma
Osteochondroma
Chondroblastoma
?Chondromyxoid fibroma
Enchondroma
Fibrous tissue Fibroma (ossifying, non- Fibrosarcoma
ossifying)
Fobromatosis
Mixed ?chondromyxoid fibroma
Giant-cell tumors Benign osteoclastoma Malignant osteoclastoma
Marrow tumors Ewing’s sarcoma
Myeloma
Vascular tissue Hemangioma Angiosarcoma
Hemangiopericytoma Malignant
Hemangioendothelioma hemangiopericytoma
Other connective tissue Fibroma Fibrosarcoma
Fibrous histiocytoma Malignant fibrous

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Lipoma histiocytoma
Liposarcoma
Other tumors Neurofibroma Adamantinoma
Neurilemmoma Chordoma

Classification of bone tumors based on X-ray features

Type of Benign Well defined borders with narrow zone of transition
lesion No or solid periosteal reaction
Malignant Poorly delineated with wide zone of transition
Periosteal reactions;
 Onion-skin appearance/lamellatd
 Sunburst appearance
 Codman’s triangle
Bone Geographic Non-ossifying fibroma
destruction Chondromyxoid fibroma
Ewing’s sarcoma
Moth-eaten Multiple myeloma, metastases, lymphoma, Ewing’s
sarcoma
Permeative MM, lymphoma, lleukemia, Ewing’s sarcoma
Anatomic Epiphysis Chondroblastoma, giant cell tumor
location Metaphysis Osteosarcoma, chondrosarcoma, osteochondroma,
enchondroma, giant cell tumor, simple bone cyst,
osteoblastoma
Diaphysis Osteoid osteoma, chondromyxoid fibroma, round cell
tumors (ES, MM,), NOF, adamantinoma, fibrous dysplasia

Osteosarcoma
Osteosarcomas are primary malignant tumors of bone that are characterized by
the production of osteoid or immature bone by the malignant cells.
Epidemiology
 They are uncommon tumors; accounts for only 1% of all cancers.
 The most common primary malignancy of bone in children and
adolescents younger than 20 years of age (10-20 years).
 As the age approaches 20 years, osteosarcoma is more common;
whereas Ewing’s sarcoma is more in common in children around 10 years
old.
 The fifth most common malignancy among adolescents and young adults
aged 15-19.
 Bimodal age distribution;
o Early adolescence
 Peaks at 13-16 years of age
 More common in boys than girls.
 More common in blacks than whites.
 Most common sites are metaphysis of long bones.
 Majority are sporadic.

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o Adults over 65 years

 Are considered secondary neoplasms.
 More common sites are metaphysis of long bones.
 More commonly occur in axial skeleton than in children.
 Males are affected more commonly than females.
 More common in whites than blacks.
 One-third arise from a setting of Paget’s disease of bone
or as a second or later tumor.
 Prevalence of bone cancers
o Osteosarcoma = 56%
o Ewing’s sarcoma = 34-36%
o Chondrosarcomas = <10%
Risk factors;
 Prior radiation
 Prior exposure to chemotherapy; particularly alkylating agents
 Paget’s disease
 Benign bone lesions;
o Chronic osteomyelitis
o Fibrous dysplasia
o Sites of bone infarcts
o Benign bone tumors
 Inherited conditions
o Hereditary retinoblastoma (RB1 mutation)
o Li-Fraumeni syndrome (TP53 mutation)
o Rothmund-Thomson syndrome (poikloderma congenitale)
Molecular pathogenesis
 The etiology is unknown but the relationship between rapid bone growth
and the development os osteosarcoma is suggested by the following;
o Peak incidence during the adolescent growth spurt
o Mostly appear at sites where the greatest increase in bone length
occurs (distal femur, proximal tibia, & proximal humerus)
o Occur at earlier age in girls, corresponding to their more
advanced skeletal age and earlier growth spurt
 These data suggest that bone tumors arise from an aberration of the
normal process of bone growth and remodeling at a time when rapidly
proliferating cells are particularly susceptible to oncogenic agents, mitotic
errors, or other events leading to neoplastic transformation.
 In contrast to Ewing’s sarcoma and many soft tissue sarcomas,
osteosarcomas are not associated with any characteristic chromosomal
translocations.
Clinical presentation;

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 Localized pain, typically of several months duration. Pain frequently

begins after injury, and may wax and wane over time.
o Rapid expansion with stretching of surrounding tissues,
o Central haemorrhage
o Degeneration in the tumour
o Incipient pathological fracture
 Systemic symptoms are generally absent.
 The most important finding is a soft tissue mass, which is frequently firm
and tender to palpation.
 Most common sites in descending order of frequency;
o Distal femur
o Proximal tibia
o Proximal humerus
o Middle and proximal femur
o Other bones
 Laboratory abnormalities;
o Elevated ALP, LDH, & ESR.
o They donor correlate with disease extent, although a very high
LDH level is associated with poor outcome.
 10-20% have demonstrable metastasis at presentation.
 Distant metastasis most commonly involves lungs, but also involves
bones.
 Prognosis is worse for adults, especially those over 65 years.
Diagnosis;
 Plain radiograph (no finding is pathogmonic)
o Destruction of trabecular bone pattern, indistinct margins, and no
endosteal bone response.
o Mixture of radiodense and radioluscent areas, estruction of cortex,
and periosteal new bone formation.
o Codman’s triangle: incomplete response of host periosteal bone.
It is formed between the cortex of bone, the elevated periosteum,
and an imaginary line joining theses two.
o Soft tissue mass in a radial or sunburst pattern. This occurs
because of the tumor cells following capillaries.
 CT/MRI
 Biopsy for definitive diagnosis
Staging systems
 The musculoskeletal tumor society (MSTS) staging system*
 American joint committee on cancer – TNM staging; not widely used.
MSTS staging of bone tumors; generally
Stage Characteristics Metastasis

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Benign
1 (latent) Well-defined margin. Grows slowly and then No
stops
Remains static/heals spontaneously
E.g. Osteoid osteoma
2 (active) Progressive growth limited by natural barriers No
Not self-limiting. Tendency to recur
E.g. Aneurysmal bone cyst
3 Growth not limited by natural barriers (e.g. giant No
(aggressive) cell tumour)
Malignant
IA Low grade; intracompartmental No
IB Low grade; extracompartmental No
IIA High grade; intracompartmental No
IIB High grade; extracompartmental No
III Low or high grade; intra- or extra-compartmental Yes

 Histologic classification;
o Malignant sarcomatous stroma, associated with the production of
tumor osteoid and woven bone.
o Histologic types of osteosarcoma;
 Conventional osteosarcomas (intramedullary highgrade):
90%
 Osteoblastic: 50%
 Chondroblaastic: 25%
 Fibroblastic: 25%
 Histologic variants: worse prognosis
 Small cell
 Telangiectatic
 Multifocal
 Undifferentiated high grade pleomorphic
sarcoma of bone
 Surface (juxtacortical)
o Parosteal; low grade; most common
o Periosteal; moderate-grade
o High grade
Treatment;
 Neoadjuvant chemotherapy for 8-12 weeks
 Wide excision; provided the tumor is resectable and there are no skip
lesions, with replacement with graft or implant.
 In some cases amputation may be more appropriate.

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Chondrosarcomas
Chondrosarcomas are a heterogeneous group of malignant bone tumors that
share in common the production of chondroid (cartilaginous) matrix.
Epidemiology
 Third most common primary malignancy of bone after myeloma and
osteosarcoma.
 Accounts for 20-27% of primary malignant osseous neoplasms.
 Highest incidence is in the 4th and 5th decades.
 Men are affected more often than women.
Histologic grading
 Grade 1: low grade/atypical cartilaginous tumor (ACT/CS1)
 Grade 2: intermediate grade
 Grade 3: high grade
 Most conventional chondrosarcomas are grade 1 or 2.
Precursor lesions
 Osteochondroma
 Enchondroma
Histologic classification of chondrosarcomas;
 Conventional chondrosarcoomas
o Central chondrosarcoma
 Arises from enchondroma
 From metaphysis of femur or pelvis.

o Peripheral chondrosarcoma
 Arises a t cartilage cap of osteochondroma
 Very large tumor and very fluffy and poorly outlined
calcification.
 More common in pelvis and scapula
 Less common subtypes
o Periosteal/juxtacortical chondrosarcoma
 Features of both chondrosarcoma and periosteal
osteosarcoma.
 Usually in femur
o Mesenchymal chondrosarcoma
 Younger age
 More aggressive
o Clear cell chondrosarcoma
 Very slowly growing
 Resembles aggressive chondroblastoma
 Common in the head of femur rather than metaphysis.
o Myxoid chondrosarcoma

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o Differentiated chondrosarcoma
Molecular pathogenesis
 Nearly always found in bones that arise from endochondral ossification.
 Germline mutation in the exostosin (EXT1 or EXT2) genes.
Clinical features;
 Slowly growing tumors
 Dull aching pain
 Gradually enlarging lump
 Medullary lesions may present with pathological fracture.
 Common sites;
o Metaphysic of long bones
o Pelvis
o The ribs
Treatment
 Wide excision with prosthetic replacement
 The tumor does not respond to either radiotherapy or chemotherapy
 Prognosis is determined largely by the histologic grade
 They have tendency to recur; recurrent cases present with the same or
higher grade of differentiation.

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CHAPTER ELEVEN-NEUROSURGERY

Traumatic Brain Injury (TBI)

Introduction
 Normal cerebral blood flow = 55mL/min/100g; ischemia develops when
the rate drops below 20mL/min/100g.
 The brain utilizes;
o 20% of body’s oxygen supply
o 15% of cardiac output
 Flow depends on cerebral perfusion pressure (CPP);
CPP = MAP – ICP
CPP = (90-110mmHg) – (5-15mmHg)
CPP = (75-105 mmHg)
 The Monro Kellie principle;
o Cranium is a rigid box, containing a nearly incompressible brain.
o Contents of the cranium (volume = 1600mL);
 Brain; 80%, <1300mL
 Blood; 10%, <150mL
 CSF; 10%, <150mL
o Any expansion in its contents will first result in expulsion of fluid
components (CSF and blood).
o Further expansion is associated to exponential rise in ICP and
brain herniation.
 Clinical signs and symptoms of raised ICP;
o Pupillary dilatation (unilateral or bilateral)
o Asymmetric pupillary reaction to light
o Decerebrate or decorticate posturing (usually contralateral to
blown pupil)
o Papilledema
o Progressive deterioration of the neurologic exam not attributable
to extracranial factors
o Headache, projectile vomiting, and sizures
o Cushing’s triad is a late feature;
 Arterial hypertension
 Bradycardia
 Abnormal respiratory pattern
o [The first three are signs of uncal herniation]

Epidemiology
 TBI is the leading cause of death [in US].

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 Rates are highest in two age groups;

o Adolescents and young adults (15-24 years)
o Elderly (>65 years)
 Incidence is higher in males; as with most traumatic injuries.
 Risk factors for TBI;
o Male gender
o Alcohol and drug use
o Lower socioeconomic status
o Psychiatric and cognitive disorders
 Common causes of TBI;
o Motor-vehicle accidents
o Fall down injuries
o Sport-related accidents
o Violence and/or fight
o Military combat related-trauma
Risk stratification for intracranial injury
Low risk Moderate risk High risk
Asymptomatic History of change or loss of Depressed level of
Headache consciousness on or after injury consciousness not
Dizziness Progressive headache clearly due to EtOH,
Scalp hematoma, Drug intoxication drugs, metabolic
laceration, contusion, Posttraumatic seizure abnormalities, postictal,
or abrasion Unreliable or inadequate history etc.
No moderate nor high Age < 2 yr (unless trivial injury) Focal neurological
risk criteria Vomiting findings
No history of loss of Posttraumatic amnesia Decreasing level of
consciousness Signs of basilar skull fracture consciousness
Multiple trauma Penetrating skull injury
Serious facial injury or depressed fracture
Possible skull penetration or
depressed fracture
Suspected child abuse
Significant subgaleal swelling

Classification of TBI
 Based on clinical grounds;
o Minimal: GCS = 15 without loss of consciousness (LOC) or
amnesia.
o Mild: GCS = 14 or, GCS = 15 with LOC<5mins or impaired
alertness or memory
o Moderate: GCS 9-13 or LOC ≥5mins or focal deficits
o Severe: GCS = 3-8
 Based on neuroimaging findings;
o [Scalp injury]
o Skull fracture (vault or base fractures)

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o Closed head injuries (CHI)

 Cerebral concussion
 Cerebral contusion
 Diffuse axonal injury
 Traumatic intracranial hematomas
 Epidural hematoma
 Subdural hematoma (acute and chronic)
 Subarachinoid hemorrhage
 Intraparenchymal hemorrhage
 Intraventricular hemorrhage

Pathophysiology
 The Pathophysiology of TBI is divided in to two separate but related
categories; primary brain injury and secondary brain injury.
 Primary brain injury;
o Occurs at the time of trauma.
o Common mechanisms;
 Direct impact
 Rapid acceleration/deceleration
 Penetrating injury
 Blast waves
o Results in concussion, contusions, lacerations, hematomas or
diffuse axonal injuries along with cerebral edema and swelling.
o Coagulopathy may be caused by the systemic release of tissue
factor and brain phospholipids.
 Secondary brain injury; occur sometime after the injury.
o Systemic insults
 Hypoxia (PO2 <60mmHg)
 Electrolyte imbalance
 Hyperthermia
 Hypotension (SBP<90mmHg)
 Anemia secondary to blood loss
 Infection
 Seizures
 Coagulopathy
o Intracranial insults
 Ischemia
 Raised ICP
 Cerebral edema
 Extra-axial lesions
Indications for CT in TBI patients
Within 1 hour Within 8 hours

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GCS <13 at any point Age >65 years

GCS <15 at 2 hours Coagulopathy (e.g. aspirin, warfarin or
Focal neurological deficit rivaroxaban use)
Suspected open, depressed or basal skull Dangerous mechanism of injury (e.g. fall
fracture from a height, road traffic accident)
More than one episode of vomiting Retrograde amnesia >30 minutes
Post-traumatic seizure

Approach to a patient with traumatic brain injury

ABCDs of life
Secondary survey
Imaging and other investigations
Medical management
 Maintenance of BP (SBP > 90mmHg), and ventilation (PaO2 >60mmHg or oxygen
saturation >90%)
 Intubation: indications;
o Depressed level of consciousness; GCS ≤8
o Need for hyperventilation
o Severe maxillofacial trauma
o Pharmacologic administration of sedatives
 Antiepileptic drugs (seizure prophylaxis): phenytoin for 7 days.
o Loading dose = 15mg/kg IV
o Maintenance dose = 300-400mg/day PO; an increase up to 600 may be
necessary.
o Associated with lower rates of early post-traumatic seizures, but do not
decrease the risk of late seizures or post-traumatic epilepsy.
o Indications;
 Open and depressed skull fracture, or penetrating injury
 Suspected intra-cranial hemorrhage
 Seizure at the site of accident (with in 24 hours)
 GCS <10
 History of significant alcohol use
 Contusion on head CT
 Temperature management
 Glucose management
 DVT prophylaxis
o Pneumatic compression stockings
o Antithrombotic therapy should be weighed against the potential risk of
hemorrhage expansion
 Ulcer prophylaxis (Cushing’s ulcer)
 Fluid and electrolyte management
 Nutritional support
 Management of raised ICP
o Initial treatment
 Elevation of head to 300
 Optimization of venous drainage; loosen collars
 Monitor central venous pressure
 Avoid excessive hypervolumia
 Monitor ICP; if
 GCS <9 and there is abnormal CT finding
 GCS < 9 and normal CT + two of the following
o Age >40

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o Motor posturing
o SBP < 90mmHg
o Secondary interventions
 Osmotic therapy: mannitol (0.25-1gm/kg over 20 minutes),
hypertonic saline
 Hyperventilation? It may increase ischemic damage to
penumbra. Hyperventilate to Pco2 30-35mmHg. Carbondioxide
is the most potent cerebrovascular vasodialator.
Hyperventilation lowers ICP by reducing Pco2 which causes
cerebral vasoconstriction; thus reducing intracranial blood
volume.
 Sedation (codein or lorazepam): to decrease metabolic demand
 For resistant cases, barbiturate coma, indused hypothermia,
and decompression may be indicated.
Definitive and/or surgical management
(Note that management focuses at limiting the extent of secondary brain injury.)

Scalp injury
 It is a densely vascularized tissue, so significant blood loss can result.
 Treatment;
o Direct pressure initially
o Simple laceration = irrigation and primary closure
o Short laceration: single-layer percutaneous suture closure
o Long or multi-armed laceration: debridement and closure.

Cranial vault fractures

 Skull fractures, whether from penetrating or blunt trauma, imply a high
degree of force.
 Compared with simple or comminuted skull fractures, a depressed skull
fracture (DSF) requires higher degree of force.
 Occipital bone or basilar skull fractures require an even higher degree of
force owing to the strength and thickness of the bone.
 Can be open or closed; and the fracture line may be linear, multiple,
stellate, or comminuted.
 Treatment;
o Closed fractures don’t require specific treatment.
o Open fractures require repair of the scalp and debridement.
o Indications for craniotomy;
 Depressed greater than the cranial thickness
 Dural tear (indirect signs on CT);
 CSF leak through the fracture
 Pneumocranium in the absence of basal skull
fracture
 Contusion of brain under the fracture site

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 Bone fragment inside brain parenchyma

 Intracranial hematoma
 Frontal sinus involvement
 Cosmetic difficulty
o Craniotomy is required to elevate the fracture, repair dural
disruption, and obtain hemostasis.

Skull base fractures

 Indicate significant impact.
 Assymptomatic ones require no treatment; those requiring interventions
include those with cranial nerve deficits or CSF leak (otorrhea, rhinorrhea)
 Temporal bone fractures;
o CN – VI & VII damage (vertigo, deafness, facial palsy)
o Otorrhea: CSF drainage in to the pharynx via Eustachian tube or
from the ear.
o Battle’s sign: echymosis behind the ear due to extravasation of
blood.
 Anterior skull base fractures;
o Damage to olfactory nerve (anosmia)
o Rhinorrhea: CSF drainage from the nose
o Raccoon’s eyes: periorbital echymosis
 How to differentiate CSF leakage;
o CSF is a clear fluid
o CSF may be tingled with blood in a trauma patient so do the halo
test. Allow a drop of the fluid to fall on a paper, if blood is mixed
with CSF, the drop will form a double ring, the darker central spot
containing blood surrounded by a light halo of CSF.
 Managememnt;
o Many CSF leaks will heal with elevation of the head of the bed for
several days. Few require lumbar drain.
o Cranial neuropathies are managed conservatively;
 Documentation of extent of impairment and recovery
 Steroids may benefit them
 Patients with abrupt onset of facial nerve palsy who do
not respond to steroids within 48-72 hours may be
considered for surgical decompression of petrous portion
of facial nerve.

Concussion
 Temporary neuronal dysfunction following non-penetrating head trauma;
they may occur without head trauma.

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 Definitions vary: some require transient loss of consciousness, while

others include any alteration in mentation.
 Largely reflect functional disturbance rather than structural injury.
 Memory difficulties, especially amnesia of the event, are very common.
 The head CT is normal and deficits spontaneously resolve over minutes to
hours.
 Colorado grading system;
o Grade 1: only confusion
o Grade 2: amnesia
o Grade 3: loss of consciousness
 Second-impact syndrome:
o The brain remains in hypermetabolic state for weeks after injury.
o The brain is also susceptible to even minor traumas in the first 1-
2 weeks after concussion.

Contusion
 Bruise of the brain.
 Breakdown of small vessels and extravasation of blood in to brain.
 Appear bright on CT scan.
 The frontal, occipital, and temporal lobes are most often involved.
 Mechanisms;
o Coup: when a moving object hits a stationary head. The brain is
contused on the side of impact.
o Counter-coup: when a moving head hits a stationary object. The
brain is contused opposite the site of impaction. These results
from deceleration of the moving brain against the skull.

Diffuse axonal injury (DAI)

 It is caused by damage to axons throughout the brain, due to rotational
acceleration and then deceleration.
 Loss of consciousness for greater than six hours in the absence of a
specific focal lesion and the presence of cerebral edema on CT imaging.
 Grading of diffuse axonal injuries;
o Mild: coma >6-24hrs, followed by milt to moderate memory
impairment, mild to moderate disabilities
o Moderate: coma >24hrs, followed by confusion and long-standing
amnesia. Mild to severe memory impairment, behavioral and
cognitive deficits.
o Severe: coma lasting months with flexor and extensor posturing.
Cognitive, memory, speech, sensorimotor, and personality
deficits. Dysautonomia may occur.

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 Axons may be completely disrupted and then retract forming axon balls.
 In severe cases small hemorrhages can be seen, especially on MRI.
Hemorrhage is classically seen in corpus callosum and dorsolateral
midbrain.
 It is usually a pathologic diagnosis made at postmortem.
 CT often appears normal, but the hemorrhagic foci can be seen.

Penetrating injury
 Two main subtypes:
o Missile; e.g. bullet
o Non-missile; e.g. knives
 Important investigations;
o X-ray and CT
o Cerebral angiography (CAG) if object passes near major artery or
dural venous sinus.
 Management;
o Operative exploration
 To remove any protruding object
 Debridement, irrigation, hemostasis, and definitive
closure.
o Small objects buried in the parenchyma are left in place to
prevent iatrogenic brain injury.
o Antibiotics are given to decrease chances of meningitis and
abscess formation.

Epidural hematoma (EDH)

 Accumulation of blood between the skull and the dura.
 Results from arterial disruption; especially the middle meningeal artery
(36%). Other sources of bleeding include: middle meningeal vein, diploic
veins, or venous sinuses.
 Associated with low energy trauma.
 It has a classic three-stage clinical presentation that is seen in only 20%
of the cases;
o Loss of consciousness from the concussive aspect of trauma
o Lucid interval while the hematoma expands subclinically; during
which the patient wakes and is fine except some headache but
there is no neurologic deficit.
o Deterioration as the hematoma grows; due to raised ICP and
herniation. Uncal herniation from EDH classically results in:
 Ipsilateral third cranial nerve palsy = ipsilateral pupillary
dilation

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 Contalateral hemiparesis: due to compression of

cerebral peduncle. But this is not uniformly seen. Shift of
the brain stem away from the mass may produce
compression of the opposite cerebral peduncle on
tentorial notch which can produce ipsilateral hemiparesis
(so called Kernohan’s phenomenon or Kernohan’s notch
phenomenon), a false localizing sign.
 On head CT, the blood clot is
o Bright (hyperdense),
o Biconvex (lentiform),
o Crosses midline
o Has defined border that usually respects cranial suture lines, &
o Typically found over convexities (especially the temporal region)
 Treatment;
o Open craniotomy and evacuation for patients who meet one of
the following criteria (those who do not meet any of the following
criteria are managed conseratively);
 Clot volume ≥30cm3
 Maximum thickness ≥1.5cm
 GCS score ≤8
 Midline shift >5mm
o Prognosis for open evacuation is better for EDH than SDH.

Acute subdural hematoma

 Accumulation of blood between arachnoid membrane and the dura.
 Bleeding is typically from bridging vein running from the cerebral cortex to
the dural sinuses.
 This results in expanding hematoma with rapid deterioration and signs of
raised ICP without lucid interval.
 Due to high energy trauma.
 Elderly and alcoholics are at higher risk after head trauma.
 On head CT, the clot is
o Bright (hyperdense) or mixed-density,
o Cresent shaped (lunate),
o Has less distinct border, and
o Does not cross midline due to the presence of falx.
o Mostly over the cerebral hemispheres
 Treatment;
o Open craniotomy; indications
 Thickness >1cm
 Midline shift >5mm
 GCS drop by ≥2 from time of injury to hospitalization

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 ICP >20 or fixed dilated pupils

o Non-operatively managed hematomas may stabilize and
reabsorb, or evolve in to chronic SDH.
o The prognosis is worse for acute SDH than EDH because it is
associated with greater parenchymal injury.

Chronic subdural hematoma

 A collection of blood breakdown products that is at least 2-3 weeks old.
 Usually occur in alcoholics, the elderly, and patients on anticoagulation
without clear history of trauma.
 May present with headache, seizure, confusion, contralateral hemiparesis,
or coma.
 On head CT;
o Acute hematomas are hyper dense (bright) for 3 days
o After this they fade in to isodensity with the brain
o After 2-3 weeks it becomes hypodense (dark); traces of white are
seen due to recurrent hemorrhages in to the collection. These
hemorrhages may expand the collection to make it symptomatic –
acute-on-chronic SDH.
 Treatment;
o A chronic SDH >1cm or any symptomatic SDH should be
surgically drained.
 Bur hole can effectively drain most SDH because unlike
acute SDH, which consists of thick clot, chronic SDH
consists of a vicious fluid with texture and dark-brown
color.
 Bur hole locations;
 First: temporal
 Second: frontal
 Third: parietal
 Fourth: posterior fossa
 The procedure is converted to open craniotomy if the clot
is too congealed, membranes prevent drainage, or if
there is persistent hemorrhage.
 Subdural or subgaleal drains may be left in plae for 1-2
days.
 Mild hydration and bed rest.

Subarachnoid hemorrhage
 Trauma is the most common cause.

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 Unlike aneurysmal SAH where blood is thickest near the circle of Willis,
traumatic SAH (tSAH) usually appears as high density spread thinly over
convexity and filling sulci or basal cisterns.
 Presentation is often a thunder clap headache (worst headache)
 CT is the investigation of choice.

Intraparenchymal hemorrhage
 Most often associated with Causes of delayed deterioration (talk and
hypertensive hemorrhage or deteriorate/die syndrome”)
Delayed intracranial hematoma (70%)
arteriovenous malformations Post-traumatic brain edema
(`AVMs). Hydrocephalus
 Bleeding may occur in Seizures
Metabolic abnormalities (hyponatremia,
contused part of the brain
hypoxia, hypoglycemia)
within 24 hours and present Meningitis
with delayed neurologic deficit. Hypertensive shock
So patients with contusion on Vascular events (CVST, SAH, carotid
dissection, cerebral embolism)
head CT should be reimaged
after 24 hours.
 Indications for craniotomy;
o Clot volume >50cm3
o Clot volume >20cm3 with;
 Referable neurologic deterioration (GCS 6-8) and
associated midline shift >5mm, or
 Basal cistern compression

Sequelea of head injuries

Second impact syndrome
 Patients who sustained a mild concussion are more likely to develop rapid
diffuse cerebral edema (within 2min), increased, ICP, and eventual
herniation, coma, and death if they subsequently suffer a second head
injury.
Post-concussive syndrome
 Constellation of symptoms that develop within 4 weeks of the injury and
may persist for months.
 Headache, dizziness, impaired concentration, easy fatigability, emotional
disinhibition, and depression.
 Treated with analgesia, anti-depressants, and anti-emetics.
Post-traumatic epilepsy
 Seizure activity >7 days from traumatic injury.
 Incidence is highest in patients with compound skull fracture, intracranial
hemorrhage or presence of early acute symptomatic seizure.
 Cannot be prevented by prophylactic use of antiepileptics

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Persistent vegetative state (PVS)

 Disruption of cerebral cognitive function with sparing of brainstem function.
 Recovery is rare if it persists for >3 months; no recovery documented after
12 months of symptoms.

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