FANOS’ SURGERY

Preface

Rotary is a global network of 1.2 million neighbors, friends, leaders, and problem-solvers that see a world
where people unite and take action to create lasting change across the globe, in our communities, and in
ourselves. Rotary’s 35,000+ clubs work together to promote peace, fight disease, provide clean water,
sanitation, and hygiene, save mothers and children, support education and grow local economies.
"Rotaract" stands for "Rotary in Action", and is a community service organization for young men and
women between the ages 18 and over.

Rotaract club of Fanos is a volunteer organization sponsored by Rotary club of Addis Ababa West. The
club’s main area of focus are maternal and child health, disease prevention and treatment, education and
literacy in addition to community development. The pass it on project, which aims to stir up the public
through books, happens to be one of the club’s promising projects. This medical guide book was prepared
by volunteers and members of the project who are medical students of Tikur Anbessa Specialized Hospital.

Medical students from all over the world go through rigorous training to be the doctors that have earned
the white coat. We wanted to lessen the loads of our fellow medical students by providing a guide book
with notes compiled from different reference books. Medical students will have gained quick review from
this book and will be inspired to edit and publish better medical books. Fanos’ surgery will allow
undergraduate students to prepare a well-crafted case report and it will equip them for bedsides, rounds,
long and short exams. The guidebook is focused on approach to cases and we have tried to include
frequently encountered surgical cases that will help students revise after a long read.

Nanati Jemal
Pass-it-on Project Manager
Acknowledgement

We would like to extend our deepest gratitude to the senior doctors of Tikur Anbessa Specialized
Hospital whose comments and suggestions have gone towards shaping this book to its present
form. We would also like to sincerely thank our Families who have put up with our late night zoom
meetings and readings in order to complete this book. In addition, our heartfelt appreciation goes
to authors of similar guide books who have inspired and motivated us.

This book wouldn’t come to light without our compilers and editors who have dedicated their time
to help the generation that will follow them. In spite of the constant bickering about the content of
the book, we have achieved something to be proud of. Last but not least, we would like to thank
our fellow classmates who have supported and appreciated the Fanos’ series and it is for this
reason we dedicate the book to 2009 undergraduate batch of Tikur Anbessa Specialized Hospital,
A.A.U, SoM.
Disclaimer

This book is prepared by medical students and is intended for educational purposes only. It is not a
substitute for professional medical advice, diagnosis or treatment. Never ignore professional
medical advice in seeking treatment because of something you have read on this book. The content
of this book are notes compiled from different standard textbooks mentioned on the reference
section at the end of the book.
 Contributors and Reviewers

Content By: Reviewed By:

 Enas Hassen  Dr. Abiy Hailu (Plastic and Reconstructive Surgeon)
 Eyerusalem Nega  Dr. Endale Anberber (Endocrine Surgeon)
 Fitsum Solomon  Dr. Ephraim Teffera (Cardiothoracic Surgeon)
 Matyas Wondwossen  Dr. Abeselom Lemma (Urologist)
 Mikiyas Mesay  Dr. Kibruyisfaw Zewdie (Neurosurgeon)
 Nanati Jemal  Dr. Matiyas Seid (Orthopedic Surgeon)
 Samuel Mesfin
 Thomas Mesfin
 Zemichael Getu

Compiled By:

 Samuel Mesfin

Coordinator:

 Nanati Jemal

Graphic Design By:

 Samuel Mesfin

First Published on December 17th, 2020

Contents

Part 1: Plastic Surgery

1.1. Wound………………………………….……….2 1.3. Burn…………………………………………………………24
1.2. Skin Tumor……………………………………13 1.4. Hand Examination……………………………………38
1.2.1. Basal Cell Carcinoma………..…18 1.5. Cleft Lip and Palate………………………………….43
1.2.2. Squamous Cell Carcinoma…..20 1.6. Soft Tissue Tumor..…………………………….……48
1.2.3. Melanoma……………………….….22 1.7. Video QR Codes.………………………………………55

Part 2: Endocrine Surgery

2.1. Approach to Breast Pathologies…....57 2.2. Approach to Thyroid Disorders………….……71
2.1.1. Periductal Mastitis…………....63 2.2.1. Physiologic Goiter……………….………76
2.1.2. Subareolar Abscess…………...64 2.2.2. Endemic Goiter……………….…………..77
2.1.3. Tuberculous Mastitis………...64 2.2.3. Toxic Goiter………….…….…….…..……78
2.1.4. Fat Necrosis………….…….……..64 2.2.4. Inflammatory Goiter………….….……80
2.1.5. Fibrocystic Disease…………....65 2.2.5. Neoplastic Goiter…………….…….……82
2.1.6. Fibroadenoma…………....…….65 2.3. Thyroid Examination…………….…….…….….…86
2.1.7. Phyllodes Tumor………………..66 2.4. Breast Examination………………..…….…………91
2.1.8. Duct Papilloma…………...…….66 2.5. Video QR Codes…………..…….…….…….….……96
2.1.9. Breast Cancer…………....……..67

Part 3: Cardiothoracic Surgery

3.1. Approach to Dysphagia………………..98 3.2.3. Pulmonary Contusion………...........132
3.1.1. Esophageal Cancer…………..107 3.3. Mediastinal Tumor……….............................134
3.1.2. Achalasia……………………..…..114 3.3.1. Thymoma………...............................141
3.1.3. Gastro-Esophageal Reflex 3.4. Chest Tube………………..….............................145
Disease (GERD)……..………...117 3.5. Needle Thoracostomy………........................158
3.2. Chest Trauma……………………………...121 3.6. Tracheostomy………………............................160
3.2.1. Pneumothorax………………...128 3.7. Video QR Codes……………............................168
3.2.2. Hemothorax…………….……...131
 Part 4: Urology
4.1. Bladder Outlet Obstruction……….…….170 4.4.1. Renal Trauma……………………….…….....219
4.1.1. Benign Prostatic Hyperplasia.171 4.4.2. Ureteral Trauma……………………….......222
4.1.2. Prostatic Cancer…………….…….175 4.4.3. Bladder Trauma………………….…………..224
4.1.3. Bladder Cancer………….….….….179 4.4.4. Urethral Trauma…………………………....227
4.1.4. Urethral Stricture………….…....194 4.5. Urethral Catetherization…………………...……....233
4.1.5. Neurogenic Bladder……….......197 4.6. Suprapubic Cystostomy…………………………......236
4.2. Urolithiasis……………………………...….…..199 4.7. Hypospadias……………………….…………..............238
4.3. Renal Cell Carcinoma…………..….….…..203 4.8. Video QR Codes……………………….……..............247
4.4. Urologic Trauma………………………….…..213

Part 5: Gastrointestinal Surgery

5.1. Liver Abscess……………………….……….....249 5.7.3. Acute Pancreatitis………………………..362

5.1.1. Pyogenic Liver Abscess…..……254 5.8. Perianal Emergency………………………………....369
5.1.2. Amoebic Liver Abscess………..258 5.8.1. Anorectal Abscess…………….………….370
5.2. Obstructive Jaundice (OJ) ……………….262 5.8.2. Fistula In ano………………………………..373
5.2.1. Choledocholithiasis……………..272 5.8.3. Anal Fissure…………………………….…...376
5.2.2. Exocrine Pancreatic Cancer…275 5.8.4. Hemorrhoids…………………………...…..378
5.2.3. Cholangiocarcinoma……………279 5.9. Abdominal Trauma…………………………….……..381
5.3. Colorectal Cancer…………………………….282 5.9.1. Diaphragm Injuries……………….……...385
5.4. Gastric Outlet Obstruction (GOO) …..294 5.9.2. Duodenal Injuries………………….……..385
5.4.1. Peptic Ulcer Disease (PUD)….299 5.9.3. Pancreatic Injuries………………….…….386
5.4.2. Gastric Cancer……………………..307 5.9.4. Hollow Viscus Injuries…………….…….386
5.5. Small Bowel Obstruction (SBO) ………319 5.9.5. Solid Organ Injuries………………….…..386
5.6. Large Bowel Obstruction (LBO) ………328 5.10. Ostomy……………………………………………….…..391
5.6.1. Volvulus……………………………..334 5.10.1. Colostomy…………………………….…...393
5.7. Acute Abdomen………………………………338 5.10.2. Ileostomy…………………………….…....395
5.7.1. Acute Appendicitis……………..346 5.11. T-Tube…………………………………………………….397
5.7.2. Acute Cholecystitis……………..357 5.12. Hernia……………………………………………………..400
 5.12.1. Inguinal Hernia…………………406 5.13. Nasogastric Tube (NGT) ………………………….420
5.12.2. Femoral Hernia…………………415 5.14. Video QR Codes……………………………………….425
5.12.3. Incisional Hernia……………….418

Part 6: Pediatric Surgery

6.1. Approach to Scrotal Swelling………….427 6.2.5. Hydrocele…………………………………......433
6.2.1. Testicular Torsion……………….431 6.2.6. Varicocele……………………………….........435
6.2.2. Torsion of the Appendix 6.2.7. Spermatocele (Epididymal Cyst).……437
Testis…………………………………………….432 2 6.2.8. Testicular Cancer……………………..…....437
6.2.3. Epididymitis…………………..…...432 6.2. Video QR Codes…………………………………….…....438
6.2.4. Scrotal Trauma…………………...433

Part 7: Neurosurgery
7.1. Head Injury………………………………….440 7.5. Neural Tube Defects (NTDs) ……………………485
7.2. Spinal Cord Injury…………………….….460 7.6. Hydrocephalus………………………………………...493
7.3. Peripheral Nerve Injury……………….472 7.7. Video QR Codes……………………………………….499
7.4. Brain Tumor……………………………..….475

Part 8: Orthopedics
8.1. Fracture……………………………………...501 8.2.4. Differential Diagnosis of Primary Lytic
8.2. Bone Tumor………………………………..510 Lesions…………………………………………………….519
8.2.1. Osteosarcoma……………….….518 8.3. Fracture Management…………………………….523
8.2.2. Chondrosarcoma……………….518 8.4. Talipes Equinovarus
8.2.3. Ewing’s Sarcoma……………….519 (Idiopathic Club-Foot) …………………………….529
8.5. Video QR Codes……………………………………….534

Index…………………………………………………………………………………………………………………………………………….…536
Reference…………………………………………………………………………………………………………………………………….….538
This Page Is Intentionally Left Blank
 Part 1: Plastic Surgery

Long Case Discussion

 Content By:
 Eyerusalem Nega
 Nanati Jemal 1.1 . Wound …………………………………………………2
 Edited By:
 Samuel Mesfin 1.2 . Skin Tumor…………………………..……………...15
 Reviewed By: 1.3 . Burn ………………..…………….....................24
 Dr. Abiy Hailu
(Plastic and Reconstructive
Surgeon)

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 1.1. Wound

 History …………………………………………….2
 Wound examination…………………………4
 Discussion of the Case………………………7

History
 Take proper information of the wound
 When and where did the wound occur?
o Acute: surgical/ traumatic wound
o Chronic:
 Leg ulcers  Pressure ulcer
 Pressure sores  Malignancy associated
 Ischemic ulcer  Diabetic foot ulcer
 Pressure sore frequency in descending order include:
o Ischium o Lateral malleolus
o Greater trochanter o Medial malleolus
o Scrum o Occiput
o Heel
 Alcohol and drug consumption
 What caused the wound?
o Mechanical
 Puncture wounds
- X-ray exam to rule out retained foreign bodies
- Treat according to published protocols due to HIV and
hepatitis virus
 Abraded wounds  Cut
 Incised

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  Animal bite
- Was post rabies exposure prophylaxis given
- Ask provocation history
- Ask change in behavior of the dog
- Vaccination history of the dog
 Torn wound  Crush injury
 Shot wound
o Chemical
 Acid  Base
o Thermal
 Burning  Freezing
o Radiation injury
o Special
 Toxins
 Venom
 Skin necrosis

 The circumstances of the injury

 Other diseases:
o Diabetes Mellitus
o Tumor
o Atherosclerosis
o Allergy
 The state of patient’s vaccination against Tetanus
 The applied first-aid

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 Wound Examination

 Is the wound tidy or untidy?

Table 1.1: Tidy Vs Untidy Wound

Tidy Untidy
 Incised  Crushed or avulsed
 Clean  Contaminated
 Healthy  Devitalized
 Seldom tissue loss  Often tissue loss
 <4 hours  >4 hours
 Puncture wound <1cm  >1 cm, animal bite
 Can be closed primarily with the expectation of  Usually heal by secondary intention
primary healing

 Asses the degree of contamination

Table 1.2: Degree of Contamination
Type Characteristics Infection Rate
 No hollow viscous entered 1-3%
 Primary wound closure
Clean

 No inflammation
 No breaks in aseptic technique
 Elective procedure

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  Hollow viscous entered but controlled 5-8%
Clean contaminated

 No inflammation
 Primary wound closure
 Minor break in aseptic technique
 Mechanical drain used
 Bowel preparation preoperatively
 Uncontrollable spillage from viscus 20-25%
Contaminated

 Apparent inflammation
 Open traumatic wound
 Major break in aseptic technique

 Untreated, uncontrollable spillage from viscus 30-40%

 Pus in operative wound
Dirty

 Open suppurative wound

 Severe inflammation

Table 1.3: Rate of infection before and after prophylaxis

Type of surgery Infection rate (%) Rate before prophylaxis
Clean 1-2 Same
Clean-contaminated <10 Gastric surgery upto 30%
Billiard surgery upto 20%
Contaminated 15-20 Viable upto 60%
Dirty <40 Upto 60% or more

o Check integrity of the skin?

 Closed wound: Skin has not been compromised but trauma to the underlying
structure has occurred
1) Contusion or bruise
 Is caused by internal bleeding into the interstitial tissues at different
levels
 Usually initiated by blunt trauma, which causes damage through
physical compression

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 2) Hematoma
 A blood-filled localized collection under the skin or body tissue that
occurs due to internal blood vessel damage

3) Abrasion
 They are made by a scraping injury to the skin surface, typically in an
irregular fashion.
 Most are superficial and will heal by epithelialization.

 Open wound: wounds in which skin has been compromised and underlying tissue
are exposed

1) An incised wound:
 Is defined as a very regular cut made by a sharp object such as a
knife, glass or blade
 Less contaminated

2) Lacerated wound:
 Made when a surface is cut in an irregular fashion down to the
underlying tissue.
 Deeper than abrasions and more irregular than incised wounds.
 They are caused by blunt injuries like fall on a stone and RTA

3) Penetrating injuries

 A wound in which the skin is broken and the agent causing the wound
entering subcutaneous tissue or deeply lying structure or cavity.
 Eg. Stab injuries, bullet injuries
 Internal organs may be involvoved.
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 o Check depth of the wound
 Superficial– epidermis
 Partial thickness– Dermis
 Full thickness – S/C tissue
 Deep wound – Deeper [if the fascia is involved]

Discussion of the Case

 Introduction……………..………..………….7
 Classification…………………..………..……7
 Wound Healing…………………..………….8
 Wound Management…………………….10

Introduction
 Wound is a break in the skin which may result from physical, mechanical or
chemical damage, or develop as a result of the presence of an underlying medical or
physiological disorder.

Classification

 Can be classified according to

o The etiology
 Mechanical  Thermal
 Chemical
o Rank-Wakefield classification system

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  Tidy  Untidy
o Duration of wound healing
 Acute  Chronic
o Integrity of the skin
 Open  Closed
o Degree of bacterial contamination
 Clean  Contaminated
 Clean-contaminated  Dirty
o Wound depth o Severity

Wound Healing
 Phases of Wound healing: normal wound heals by 3 phases
1) The inflammatory phase
2) The proliferative phase
3) The remodeling phase (maturing phase)

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  Types of wound healing
o Primary Intention - Skin edges opposed
o Secondary Intention - Wound left open
o Tertiary Intention – Wound closure or cover
Table 1.4: Primary intention vs Secondary intention
Features Primary intention Secondary intention
 Cleanliness  Clean  Not clean

 Infection  Not infected  Infected

 Margins  Surgically clean  Irregular

 Suture  Used  Not used

 Healing  Small granulation tissue  Large granulation tissue

 Outcome  Linear scar  Irregular wound

 Complication  Not frequent  Frequent

 What are factors that influences wound healing?

Table 1.5: Factors that Influence Wound Healing
Local General
 Mechanical injury  Age
 Infection  Nutrition: low Vitamin C
 Edema  Trauma
 Foreign bodies  Connective tissue disorders
 Low oxygen tension  Metabolic disease: uremia, jaundice
 Ischemia/necrotic tissue  Immunosuppression

 Topical agents

 Ionizing radiation

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 Abnormal wound healing:
o Deficient scar formation
o Excessive repair components
o Contracture
o Atrophic or Hypertrophic scar
o Pigment changes
Table 1.6: Features of Abnormal Wound Healing

Hypertrophic scar Keloid

 No normal tissue  Has normal tissue
 In places with tension  Above sternum everywhere
 Every race  Black/ brown race
 Resolves after a year or so  Continues to grow
 Manage by:  Manage by:
1. Massage and silicon sheet, Inject 1. Give Pre-op steroid then excise with
steroid intra-op steroid – in Ethiopia
2. If above fails- scar release 2. Excise and immediate Radiotherapy
(within 24-48 hour) – best
3. Bleomycin Injection

Wound Management
 The goals
1. Avoid further tissue damage
2. Achieve wound closure as rapidly as possible
3. Restore function to the injured tissue
4. Facilitate the patient’s expedient return to normal daily activities
5. Restore the patient’s quality of life.

 ATLS protocol for acute wound management

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 o Primary survey: rapid assessment and treatment of life-threatening injuries.
 Airway
 Breathing
 Circulation
 Disability
 Exposure and Environment
o Secondary survey
 Thorough history and physical examination
o Definitive care
 Wound debridement
 Foreign bodies removal
 Wound preparation
 Follow reconstructive ladder for wound closure

 Use of antibiotics
 Tetanus prophylaxis
 Wound dressings: no ideal wound
dressing exists.
 Edema control: compression therapy
 Rehabilitation and POD
 Rabies post exposure prophylaxis
 Improve systemic conditions:
o Fluid and hydro-electrolyte
o Nutrition
o Rx of coexisting diseases

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 Management based on type of wound:
1) Abrasion:
 Will heal on its own hence clean and prevent infections
2) Contusion:
 Apply cold compressor for 24 hour then hot compressor to stimulate
vasculature and interstitial bleeding can be absorbed
3) Incised:
 Clean and primary suturing
4) Lacerated:
 Excise and primary suturing
5) Crushed or devitalized:
 Wound debridement then allows for edema to subside for 2-3 days
followed by delayed primary suturing
6) Deep vitalized wound:
 Allow complete granulation following debridement
 If small wound, do secondary suturing
 If large, use split skin graft to cover the defect
7) Wound with tension:
 Fasciotomy to avoid compartment syndrome
8) Amputation:
 Compressive gauze and elevate hand- to stop bleed (don’t ligate artery in
order to avoid nerve damage)
 Wash then apply saline soaked gauze then put in ice bag
 Re- implantation with microvascular surgery
9) Facial injury:
 Worry about facial nerve and parotid duct injury
 Wash aggressively then use tiniest suture
 Remove the suture as soon as possible: eyelid on 3rd Post-op and the rest
of face on 5th post-op day

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 1.2. Skin Tumor
 Case Discussion.…………………………………..13
 History…………………………..…………………….13
 Physical Examination………..………………….14
 Investigation…………………..……………………17
 Management.………………...……………………17
 Discussion of the Case………………………….18

Case Discussion

 A 65-year- old male presents with a progressive skin lesion of 8 years duration. It began
on his forehead and proceeded to involve left half of his face including his outer ear.
Associated with that he complains of difficulty hearing on his left ear and loss of sensation
on the left side of his face. He has no bleeding or pain. He works as farmer for a living. On
physical examination, there is a destructive lesion with ulceration around the ear canal
with extension to the mastoid process of temporal bone. There is surrounding hypo and
hyperpigmentation around the lesion.

History
 Duration
 Progression
 Check for symptoms of infection: fever, discharge
 Is there associated symptom: hearing loss, loss of sensation, pain, ulceration,
bleeding
 Is there any concerns about a particular lesion or if patients have noticed a new
mole or a change in a pre-existing mole?
 Asses risk factors:
o Occupation history: to assess for sun and radiation exposure
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  Patient’s tendency to sunburn and history of blistering sunburns
during childhood or teenage years
 Degree of sun exposure in the past 5 to 10 years
 Occupational exposure
 Phenotypically: fair skin, light colored eyes, red hair, northern
European region
o Previous local (herbal) treatment
o Chemical carcinogen: arsenic
o Immunosuppressed patient: organ transplant patients, HIV patients
o Chronic inflammation: scars, burns, ulcers, sinus tracts Burn history:
Marjolijn’s ulcer is a risk factor for SCC
o Race
o Family history
o Smoking
o Blood type: mainly for BCC
 In a cohort study, the risk of developing BCC was 4% lower among
patients with A, AB, or B blood types compared to those with type
O blood.
o HPV infection
o Inherited disorders
 Xeroderma  Epidermolysis bullosa
pigmentosa  Albinism

Physical Examination
1. Check for lymphadenopathy on all accessible areas
2. Do total body skin examination (TBSE)
 Examine the face and rest of the head and neck while the patient is sitting on
the examination table.
 Examine the scalp.
 Examine all surfaces of the arms and hands.

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  Ask the patient to lie down on his/her back for viewing the chest, abdomen,
anterior thighs, anterior legs, dorsal feet, soles, and toe webs.
 Ask the patient to turn over.
o Examine the calves, posterior thighs, buttocks, and back.
o The upper body could also be examined when the patient is sitting or
standing.
3. Describe the lesion:
 Where is it?
 What does it look like?
 Is there a change in pigmentation? Diversity of colors?
 Border regularity?
FOR Basal cell Carcinoma:
1. Nodular: 60% of the BCC
 Pink or fresh colored papule with translucent quality
 Telangiectasia vessel is seen within the papule
 Ulceration is common
2. Morepheaform: 5-10%
 Smooth, flesh colored papules or plaques that are frequently atrophic
 Firm quality will ill-defined borders
3. superficial: 30%
 On trunk
 Slightly scaly papule that is light in color
 Atrophic in center and rimmed with fine
translucent micro papules
For Squamous Cell Carcinoma:
 SCC can develop on any cutaneous surface, including the head, neck, trunk,
extremities, oral mucosa, periungual skin, and anogenital areas
1. SCC in situ (bowen’s disease):
 Well-demarcated, scaly patch or plaque

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  Lesions are often erythematous, but can also be skin-colored or
pigmented.
 Tends to grow slowly, enlarging over the course of years
2. Erythroplasia of Queyrat
 Describe SCC in situ involving the pens
 Presents as a well-defined, velvety, red plaque
 Patients may experience pain, bleeding, or pruritus
3. Invasive SCC
 Are often asymptomatic, but may be painful or pruritic.
 Local neurologic symptoms (eg, numbness, stinging, burning, paresthesia,
paralysis, or visual changes) occur in approximately one-third of patients.
 Well-differentiated lesions
o Usually appear as indurated or firm, hyperkeratotic papules,
plaques, or nodules.
o Lesions are usually 0.5 to 1.5 cm in diameter, although some are
much larger.
o Ulceration may or may not be present.
 Poorly differentiated lesions
o Are usually fleshy, soft, granulomatous papules or nodules that
lack the hyperkeratosis
o May have ulceration, hemorrhage, or areas of necrosis.
For Melanoma:
 Asymmetry (if a lesion is bisected, one half is not identical to the other half)
 Border irregularities
 Color variegation (brown, red, black or blue/gray, and white)
 Diameter ≥6 mm
 Evolving: a lesion that is changing in size, shape, or color, or a new lesion
 The revised Glasgow seven-point checklist- Another set of criteria for referral or
biopsy was developed from a retrospective review of patients with melanoma, and
subsequently revised.

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 o It includes three major and four minor features:
 Major:  Minor:
- Change in size/ - Diameter ≥7mm
new lesion - Inflammation
- Change in shape - Crusting or bleeding
- Change in color - Sensory change

Differential diagnosis
1. Skin tumour
2. Skin TB
3. Leishmaniosis

Investigation
 FNA of skin  Head CT
 Wedge biopsy with normal skin  FNA of lymph nodes
 Organ function test: LFT, RFT
 Chest x-ray, ultrasound/CT staging, and bone scans may be necessary

Principles of management
1) Surgical excision
2) Destructive therapy – cryosurgery, electrodessication & curettage
3) Topical 5-FU for premalignant lesions
4) Radiotherapy, chemotherapy
5) Block dissection of regional lymph nodes in melanoma is indicated if the nodes
are clearly involved and there are no other secondary

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 Discussion of the Case

 Introduction…………………………………………..18
 Basal Cell Carcinoma………………………………18
 Squamous Cell Carcinoma………………………20
 Melanoma……………………………………………..22

Introduction

 Anatomy of the skin:

o The largest organ of the body
o Divided into Epidermis and Dermis
 Functions:
o Thermoregulation o Metabolic functions
o Protection o Sensation

1.2.1. Basal Cell Carcinoma

• The most common
• Arises from:
o Cells of the basal layer of the epithelium
o The external root sheath of the hair follicle
• Directly related to the sun exposure
• It does not arise from malignant changes occurring in preexisting mature epithelial
structures.
• It requires stromal participation for survival
• It never metastasizes
• Can be low risk or high risk based on the likelihood of recurrence after treatment
1. Low Risk:
o Location and size
P a g e 18 | 548
  Less than 6 mm in diameter in high-risk areas (eg, central face, nose,
lips, eyelids, eyebrows, periorbital skin, chin, mandible, ears,
preauricular and postauricular areas, temples, hands, feet)
 Less than 10 mm in diameter in other areas of the head and neck
 Less than 20 mm in diameter in all other areas (excluding hands and
feet)
o Pathology
 Nodular or superficial histopathologic growth pattern
 Lacks perineural invasion
o Other
 Primary lesion (not recurrent)
 Well-defined clinical borders
 Lacks history of radiation therapy at site
 Immunocompetent patient
2. High Risk:
o Location and size
 Greater than or equal to 6 mm in
diameter in high-risk areas
 Over 10 mm in diameter in other areas of
the head and neck
 Over 20 mm in diameter in all other
areas
o Excluding hands and feet
o Aggressive pathologic features
 Morpheaform, sclerosing, or mixed
infiltrative
The H zone:
 Micronodular
 The dark pink shaded regions of the  Basosquamous (keratinizing)
face o Recurrent lesions
 Is associated with an increased risk
o Lesions in sites of prior radiation therapy (RT)
of recurrence of malignant epithelial
o Lesions with poorly defined borders
tumors
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 o Lesions in immunocompromised patients
o Perineural invasion
 Tumor growth in or around nerves

1.2.2. Squamous Cell Carcinoma

• They arise from the Keratinizing cell layer of the epidermis

• Arise from the malphigian or basal layer of the epidermis
• They may develop in pre-existing
o Bowens disease
o Actinic Keratosis
o Immunosuppressed patients
o Malignant transformation of viral warts
o Chronic sinuses and ulceration (Marjolin’s ulcer)
 Etiology:
o UV radiation
 Direct photochemical damage to cutaneous DNA
 Injury to DNA repair mechanism
 Partial suppression of cell mediated immunity
o Ionizing radiations
o Chemical carcinogens
 Arsenic  Hydrocarbons - tars
o Human papilloma virus
 Epidermodysplasia  Verrucous carcinoma
o Chronic inflammation
 Burns  Varicose ulcers
 Chronic osteomyelitis
o Congenital diseases
 Xeroderma  Albinism
pigmentosa
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  Staging of basal cell and squamous cell carcinoma (see next page)

Table 1.7 TNM Staging of Basal Cell and Squamous Cell Carcinoma
Classification Definition
Primary tumor
TX  Primary tumor cannot be assessed
T0  No evidence of primary tumor
Tis  Carcinoma in situ
T1  Tumor ≤ 2cm in greatest dimension
T2  Tumor > 2cm in greatest dimension but ≤ 5cm in greatest
dimension
T3  Tumor > 5cm in greatest dimension
T4  Tumor invading deep extra dermal structures (e.g. cartilage,
skeletal muscle, or bone)
Regional lymph nodes
NX  Regional lymph nodes cannot be assessed
N0  No regional lymph node metastasis
N1  Regional lymph node metastasis
Distant metastasis
MX  Distant metastasis cannot be assessed
M0  No distant metastasis
M1  Distant metastasis
Histopathologic Grade
GX  Grade cannot be assessed
G1  Well differentiated
G2  Moderately differentiated
G3  Poorly differentiated
G4  Undifferentiated

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 1.2.3. Melanoma

Introduction:
• Is a cancer of melanocytes?
• Usually arises in skin
• Can arise anywhere that melanocytes exist:
o The bowel
o Mucosa
o The retina
Remember
o The leptomeninges
 Tumors on hands, feet and
• Relatively less common
trunk especially the back
• The incidence in the black population is
have a poorer prognosis
much lower being 0.6 per 100,000
than those on the limbs.
• It is more common in young adults 20-39
 Tumors that have
• Malignant Melanoma can occur at any site regressed or ulcerated
on the skin surface with a predilection for have a worse prognosis,
the legs of young women and the trunks of possibly because their true
men thickness is masked
• 90% of malignant melanomas arise from
otherwise normal skin
o Only 10% from an existing nevus

Types of melanoma
• Superficial spreading melanoma:
o The most common
• Nodular melanoma
o This is a raised, polypoid lesion
o It has the worst prognosis
• Lentigomaligna melanoma
o This arises in a background of lentigomaligna
• Amelanotic
o It has no dark color

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 • Acral
o Lentiginous melanoma
o This is the least common occurring on hairless skin
o It is the commonest type in black races and south east Asia
 Staging of Melanoma

Table 1.8. TNM pathologic staging overview

Stage Tumor Node Metastasis
0 Tis N0 M0
IA T1a or T1b N0 M0
IB T2a N0 M0
IIA T2b or T3a N0 M0
IIB T3b or T4a N0 M0
IIC T4b N0 M0
IIIA T1a/b or T2a N1a or N2a M0
IIIB T0 N1b or N1c M0
T1a/b or T2a N1b/c or N2b
T2b or T3a Na/b/c or N2a/b
IIIC T0 N2b/c or N3b/c M0
T1a/b, T2a/b or T3a N2c or Na/b/c
T3b or T4a Any N > N1
T4b N1a/b/c or N2a/b/c
IIID T4b N3a/b/c M0
IV Any T, Tis Any N M1

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 1.3. Burn

 Introduction….………………..……...…….....24
 Classification…………………..………..……….24
 Pathophysiology…………..……..…...………28
 Burn Wound Assessment……….....……..30
 Investigation…………………..……...………..32
 Admission Criteria…………………..…….....32
 Management…………………..……..…….…..32
 Other Etiologies of Burn….…..…….………35
 Complications……………………...…….……..36

Introduction

 Burn injury implies coagulative necrosis to the skin and underlying tissue due to
thermal, electrical, chemical, radiation,cold exposure.
 It generally occurs in temperatures greater than 44° C.

Classification
Based on etiology:
 Thermal (90%):
o Flame - Overheated rusty air
 Majority in Adults, suicidal/Homicidal/Accidental
 Most common cause of hospital admission
 Have the highest mortality
o Scald – hot liquid
o Contact - Too hot or too cold object
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  Too long contact
 Chemical:
o Contact with harmful chemicals.
o It is potentially severe burn.
o Initial therapy:
 Carefull removal of the toxic substance
 Irrigation of the affected are with water for minimum of 30 minutes,
except in cases of concrete powder or powdered lye
o Certain chemicals can be systematically absorbed and cause metabolic
derangements.
 Formic acid  hemolysis and hemoglobinuria
 Hydrofluoric acid -> hypocalcemia.
o The mainstay treatment is calcium based therapies.
o Topical calcium gluconate on the burn wound and IV calcium gluconate for
systemic symptom
o Alkalis burn more than acids
o Burn tends to be deep until the corrosive agent is completely removed
 Electrical
o Special considerations are cardiac arrest and compartment syndrome with
rhabdomyolisis.
o Baseline ECG is recommended
o Can be:
 High voltage
 Low voltage
 Radiation

Based on depth:
 First degree burn
o Superficial and involve just the epidermis.
o Sunburn and inconsequential
o Painful, blanch with pressure, No edema, No blister
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 o Heals with in 4-7 days
o For example – sun burn
 Second degree burn (Partial thickness burn)
o Involves variable amounts of dermis.
o Exremely painful with weeping and blisters
o It is classified as superficial or deep by depth of the involved skin.
i. Superficial partial:
 Goes no deeper than the papillary dermis.
 Clinical features:
o Blistering
o Blanches with pressure
o Pinprick sensation is normal
o It appears as pink and moist
 Superficial partial-thickness burns heal without residual scarring in 2
weeks.
 The treatment is non-surgical.
ii. Deep partial thickness:
 Involve damage to the deeper parts of the reticular dermis.
 Clinically features:
o The epidermis is usually lost
o Abundant fixed capillary staining
o Non blanching
o Reduced sensation.
 Deep dermal burns take 3 or more weeks to heal without surgery
 Usually lead to hypertrophic scarring.
 Third degree burn (Full Thickness Burn):
o Clinical features:
 Leathery –Dry  Non blanching
 Discolored  No blisters
 No pain
 Fourth degree burn:
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 o Involving structures beneath the skin such as underlying fat, muscle, bones or
internal organs
 Classification based on depth is dependent upon:  Along with burn size and
o The burn sources patient age, burn depth is a
o The thickness of the skin primary determinant of
o The duration of contact and mortality.
o The heat dissipating capability of the skin  Itis also a primary determinant
of healing, patient’s long term
Based on severity – which is related to: appearance and functional
 The size (TBSA) outcome.
 The depth
 The age of the patient
 Minor burn
o Partial thickness: <15% body surface area in adults and <10% of TBSA in
children
o <2% of TBSA full thickness burn
o Nothing involving the head, feet, hands or perineum.
o Can be treated as an outpatient
 Moderate burn
o Partial thickness burn area of 15-25% body surface area in adults and 10-20%
of TBSA in children.
o 2-10% TBSA full thickness burn
o Superficial partial-thickness burns of the head, hands, feet or perineum.
o Suspect:
 Child abuse.
 Concomitant trauma
 Significant pre-existing diseases
o Require hospitalization
 Major burn
o Partial thickness burn surface involvement of 25% body surface area in adults
and >20% TBSA in children and elderly
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 o Full-thickness burns 10% body surface area
o Deep burns of the head, hands, feet, joint, and perineum
o Inhalation injury
o Chemical or high-voltage electrical burn
o Comorbidities and associated injuries
o Require specialized care

Pathophysiology

 Although most affected organ in burn injury is the skin, Burn injury has both local
and systemic effects
 Local effect- The local changes that occur consist in the formation of three zones:
o Zone of coagulation:
 Area that is in intimate contact with the causative agent.
 Most severely injured area.
 Typically in the center of the wound.
 Coagulated and with frank necrosis occurs with irreversible tissue
damage
 Need excision and graft
o Zone of stasis:
 Moderate injury, peripheral to zone of coagulation
 Decreased perfusion due to inflammation and impaired vasculature
 Has a potential to recover or progress to coagulative necrosis
depending on the administration of optimum treatment
o Zone of hyperemia
 Viable tissue, not at risk for further necrosis
o Burn wound edema
o Inflammation
o Increased capillary permeability
 Systemic effects:
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 o Significant burns cause release of inflammatory mediators which cause:
 Vasoconstriction and vasodilatation
 Capillary permeability and edema
o Fluid shift
 Vasoactive mediators  Vasoconstriction-dilatation  capillary
permeability  Protein loss tissue edema.
o Hypovolemia/burn shock /results from:
 Fluid shift
 Insensible fluid loss
 Increase in BMR
 May progress to hypovolumic shock
 Cardiovascular effects
o Hypovolemia  Decreased CO
 Burn shock pathophysiology
o Increased capillary permeability
o Decreased plasma oncotic pressure
o Increased capillary hydrostatic pressure
o Reduced clearance of fluid and protein from interstitial space by lymphatic
ducts
o Intracellular fluid accumulation
o Increased evaporative water loss
o Depressed myocardial function and increased peripheral resistance.
 Renal effects
o Hypovolemia
o Hemoconcentration
o Decreased renal blood flow
o Decreased GFR ->Tubular necrosis ->renal failure
 Immune system effects
o Global depression of immune system in burns of >20 % TBSA
o Skin, cellular and humeral immunity
o Mainly cellular immunity is significantly reduced
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  Predispose to infection (pseudomonas, fungal infection)
 Prolonged allograft skin survival
 Electrolyte disturbance
o Caused by changes in cellular permeability and fluid loss
 Hyponatremia due to fluid loss
 Hyperkalemia due to excessive tissue necrosis; serious
 Cardiologic and neurologic consequences
 GI effects
o Hypovolemia  Hypoperfusion
 Bacterial translocation -> as a cause to sepsis
 Curling ulcer
 Paralytic ileus
 Hypermetabolism
o Tachycardia
o Increased CO due to energy expenditure:
o Proteolysis, lipolysis, nitrogen loss
o Weight loss and decreased strength until all the wounds are grafted
 Variables with higher predictive value of mortality are
o Age
o %TBSA
o Inhalational injury
o coexistent injury
o Pneumonia

Burn Wound Assessment

 Burn wound size

 When calculating the burn wound area, erythema should not be included
 Rule of nine (Wallace) – for first approximation
o Used to estimate medium to large burn in adults

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 o In adults, the anterior and posterior trunk each account for 18%, each lower
extremity is 18%, each upper extremity is 9%, and the head is 9
o tends to over/ underestimate burn area
 Rule of seven – is in pediatrics
 Palm rule:
o The palm including the fingers is estimated to be 1% of TBSA.
o It is used in estimating burnt area in relatively small burn(<15%), patchy burn
wounds and unburnt area in very large burns(>85%).
 Lund and Browder chart:
o Is the most accurate method.
o Takes into account different proportional body surface area in children
according to age.
Burn wound depth
 The history is important; temprature, time and burning material.
 Three important elements in assessing burn depth are:
o Apperance
o Sensation
o Bleeding
 Its difficult to assess depth of a burn initially because it’s a dynamic wound and
hence it’s depth will change depending on the success of resuscitation.
 Obtain a medical history in detail:
o About the burning agent,
o Where the injury happened (closed versus open space)
o The possibility of smoke inhalation, exposure to noxious chemicals, and the
possibility of any related trauma
o History of chronic illnesses such as DM, HTN, and cardiac or renal disease
o Use of regular medications, alcohol, or drugs
o Allergies and history of tetanus immunizations

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 Investigation

 Arterial blood gas

 Hematocrit
 Electrolytes
 Glucose
 BUN
 Urinalysis
 Carboxyhemoglobin
 Cyanide
 Chest x-ray and ECG should also be included. Especially electrical burn

Admission criteria

 Any burn that requires fluid resuscitation or surgery

 Partial and full thickness burns involving areas such as the head, face, hands,
feet, genitalia, perineum and major joints
 Electrical or chemical burns
 Inhalation injury
 Concomitant trauma
 Pre-existing underlying medical condition
 Patients with psychiatric or social background make inadvisable to send them
back

Management of Burn Injury

 Classified into two categories
1. Pre-hospital care
2. Hospital care
Pre-hospital care:
 Remove the patient from the scene
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  Stop the burning process – Stop, drop, roll
 Check for other injuries
 Cool the burn wound
 Give 100% oxygen via a non-rebreathable mask
 Elevate:
o Sitting a patient up with a burned airway may prove life-saving in the event
of a delay in transfer to hospital care
 Transport the patient warm and wrapped in a clean sheet.
 Remove clothing and Jewelry.
Hospital care:
 Primary survey
o Airway - With control cervical spine
o Breathing - Expose chest, ventilation, give oxygen
o Circulation - Control bleeding, Pulse (<_110), B/P (>_100 mmHg), two large
bore cannulas
o Disability- Neurological status
o Exposure with environmental control - Remove clothing, look for other
injury, TBSA, Depth
o Need for escharotomy, weigh the patients
o Fluid resuscitation
Other management:
 Analgesia
o Acute:
 Small burns, especially superficial burns
 Respond well to simple oral analgesia, paracetamol and non-
steroidal anti-inflammatory drugs
o Subacute:
 In patients with large burns
 Continuous analgesia is required, beginning with infusions and
continuing with oral tablets
 Nutrition
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  Curreri formula= 25Kcal/kg/day + 40kcalxTBSA%
 Wound care
 Rehabilitation
 Surgery- Escharotomy, skin graft
 The main pillars in the treatment of burns are:
o Adequate fluid therapy (fluid resuscitation)
o Airway management
o Comprehensive surgical treatment of the patient as a final resolution
 Fluid resuscitation:
o To provide sufficient perfusion to vital organs as well as the peripheral
tissues, especially the damaged skin
o IV fluid resuscitation - In children > 10%TBSA and adults >15 %TBSA
o Parkland formula: 4ml/kg/TBSA, used to calculate volume of fluid to be
given in 24 hours
o In pediatric patients:
 Give maintainance fliud in addition to parkland formula 
6ml/kg/TBSA
o The key is to monitor the resuscitation is urine output
o If oral fluids are used, salt must be added
o Hyponatremia and water intoxication can be fatal
o Secure reliable large bore IV cannulas
o Ringer’s lactate is the fluid of choice.
 They are effective in maintaining intravascular blood volume
and are significantly less expensive
o Patients in increased need of fluid are:
 Children  Delayed
 Large burns resuscitation
 Smoke inhalation  Electrical injury
 Wound care: prophylactic systemic antibiotics adminstration is unnecessary.

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 Other Etiologies of Burn Injury

Inhalational Injury

 It is the main cause of death in many burn injuries.

 It is due to exposure of airways and lungs to toxic chemicals and hot gases, steam.
 Increases the risk of bronchopneumonia
 Is suspected:
o Fire in enclosed space
o Loss of consciousness in the fire
 Symptoms - A hoarse or weak voice
o Stridor
o Cough
o Restlessness
 Signs - Soot around the mouth and nose
o Singed facial and nasal hair
o A swollen upper airway
o Hypoxia
o Pulmonary edema
o ARDS
 Treatment
o Early recognition
o Intubation and ventilation with Humidified oxygen

Electrical Burn
 Extensive deep muscle damage
 Fasciotomy instead of escharotomy
 Myoglobinuria because of rhabdomyolysis
o Leading to ATN and ARF
 Fluid requirement increased titrated to UO of 2mL/kg/hr
 Sodium bicarbonate to alkalinize urine
 Forced diuresis with manitol
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 Cataracts, progressive demyelinating neurologic loss

Chemical Burn

 Alkali Burns
o Liquefactive necrosis hence deeper injury
o Oven bleaches, fertilizers, cement
o Lavage area with copious amount of water
 Acid Burns
o Coagulative necrosis
o Irrigate with water and sodium bicarbonate

Burn Complications

Table 1.9: Early Vs. Late Complications of Burn

Early Late
 Hypo \ hyper volemia  Scarring
o Hypertrophic, keloid
 ARF  Contructures
o Limbs, neck
 Hemolobinuria  Hyper \ hypo pigmentation
 Stress ulcer  Disfigurement
 Pulmonary dysfnction  Functional disability
 Post traumatic distress

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 Short Case Discussion

 Content By:
 Eyerusalem Nega 1.4 Hand Examination …...……………..…..…….…...38
 Nanati Jemal
 Edited By:
1.5 Cleft Lip and Palate ……………….…..….....…....43
 Samuel Mesfin 1.6 Soft Tissue Tumor Examination………..…......48
 Reviewed By: 1.7 Video QR Codes ……………………….…..…..……..55
 Dr Abiy Hailu
 (Plastic and Reconstructive
Surgeon)

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 1.4. Hand Examination

 Introduction……………………………..…….…….38
 Prior steps in hand examination…….….…..38
 Examination of the Hand……………..….…….39

Introduction
 The hand is easily injured and the injuries can sometimes be easily missed which can
unfortunately lead to a permanent disability.
 This is one of the reasons we need to know how to properly examine a hand so as
not to miss injuries.

Prior steps in hand examination

 Wash your hands, introduce yourself
 Take History
1) Personal history
o Age o Occupation
o Handedness o Smoking
2) Injury history
o Mechanism of injury: crush, laceration
o Position of hand at injury
o Time of occurrence
o Previous history of similar injuries
 Was there any disability associated with the prior injury?
3) Previous medical history

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 o Ask about: diabetes, cardiac, pulmonary, or renal disease
o Prior surgical history

Examination of the Hand

1) Inspection (Good exposure and Compare)
 Normal fingers cascade
 Index finger is straighter
 Thumb is bent at Metacarpophalangeal joint and straight at
interphalangeal joint
 Deformity  Swelling
 Nails  Wounds or scars
 Muscular atrophy  Trophic changes
 Check the rotational axis of each finger (look from the tips of the fingers) to
assess for any rotational deformity
2) Palpation
 Warmth?
 Using the dorsal surface of your own hand, feel distal to proximal along
the patient’s hand and forearm, and compare with the contralateral side
 Dryness?
 Anhidrosis  Nerve damage
 Thenar Eminence
 Atrophy seen in carpal tunnel syndrome
 Hypothenar Eminence
 Atrophy with ulnar nerve compression
 Palmar Aponeurosis
 Dupuytren’s Contracture
 Finger flexor sheath: use pad of your thumb
 Palpable nodule: Heberdens (DIPJ) or Bouchards (PIPJ) nodes (present in
osteoarthritis)
3) Vascularity Testing
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  Tissue turgor: wrinkly skin if no or little blood is flowing

 Pulse oximetry: you can see the waves to see for blood flow
4) Range of motion

 Active range of motion and against resistance

 Passive range of motion

 Bilateral comparison for stiffness

 Flexion/extension at MCP, PIP, DIP
o Tight fist and open
 Abduction/Adduction at MCP
o Spread fingers apart and then back together
5) Neurological testing

 Sensory (compare with the other hand)

o Light touch
o Sharp and dull discrimination by a popsicle stick
o 2-point discrimination

 Ulnar nerve: check light

touch sensation on the ulnar
side of 5th finger
 Median nerve: check light
touch on the radial side of
index finger
 Radial nerve: check light
touch sensation on 1st dorsal
web space

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  Pulse
 Color
 Capillary refill (2 sec)
 Temperature

 Motor examination: – Median – Ulnar – Radial

1. Median nerve
 Ok sign: flexion of thumb IP joint and index DIP (“A-OK
sign”) – FDP – FDS – FPL
o Flexor policus tendon: hold MP joint of the
thumb and ask the patient to flex
interphalangeal joint. In partial laceration, ask its
painful with resisted flexion.
o Flexor digitorum profundus: Isolate the proximal
and middle phalanges by holding them firmly
and then asking the patient to flex the distal
phalanx of that finger.
o Flexor digitorum superficialis: isolate the 3
fingers that are not being tested (simply hold
them in the natural anatomical position) and ask
the patient to flex the finger being tested (FDS)

 Test opposition by touching the tip of the thumb to the tip of the little finger
 Test thumb abduction by placing the hand palm up and raising the thumb to the
perpendicular while palpating the belly of the abductor pollicis muscle to insure it
is contraction.
 Wrist flexor: Flex and palate tendons of flexor carpi radialis and ulnaris.
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 2. Radial nerve
 Extensor tendons are commonly injured
 Extend the wrist against resistance (extensors)
 Raise the thumb off of the pillow (Extensor policies longus)
 Hold the wrist passively in extension and ask the patient to
extend their fingers (Extensor digitorum communis)
 Flex 3 and 4 digit and ask the patient to extend the remaining finger- extensor
rd th

digit Minimi and indicispropius

3. Ulnar nerve
 Confirm finger abduction & adduction (tests palmar
and dorsal interossei)
 Test the hypothenar muscle, extend the fingers and
then move the fifth finger away from the others
 Froment's test; Technique:
o The patient is asked to make a strong pinch
between the thumb and index finger and grip a flat
object such as a piece of paper between the thumb
and index finger.
o The examiner then attempts to pull the object out
of the subject's hands.
o There is weakness of the adductor pollicus
innervated by the ulnar nerve which would keep
the Interphalangeal joint relatively straight;
instead, the Flexor policies longus muscle which is
innervated by the median nerve is substituted for
the abductor policies and will cause the
Interphalangeal joint to go into a hyper flexed
position.
 Flex the fingers to 90oat the MCP joints and ask the patient
to extend their fingers again (lumbricals)
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  Adduct fingers- interrosi muscle
1) Skeleton assessment
 Swelling  Tenderness
 Deformity
 Abnormal range of movement (decreased or increased)
2) Stability Testing
 Ulnar collateral ligaments  Radial collateral ligaments

1.5. Cleft Lip and Palate

 Introduction……………..……………..43
 Prevalence……………………………….44
 Embryology……………………..……...44
 Risk Factors………………………………45
 Associated Abnormalities………...45
 Clinical Presentations……………….46
 Prenatal Diagnosis……………………46
 Management……………………………46
 Recurrence Risk…………….……......47

Introduction
 The most common craniofacial malformation identified in the new-born is the
orofacial cleft, which consists of cleft lip with or without cleft palate (CL/P) or
isolated cleft palate (CP).

P a g e 43 | 548
  They can occur as part of a syndrome involving multiple other organs or as an
isolated malformation.

Prevalence
 It varies by race/ethnicity: lowest in American blacks, highest in Native Americans
and Asians, and at an intermediate level in Caucasians.
 The sex ratio among affected infants varies by type of defect:
o CL/P occurs more often in males while CP is more common in females.

Embryology

Cleft Lip
 Complete closure of the lip is usually accomplished by 35 days post conception as the
lateral nasal, median nasal, and maxillary mesodermal processes merge.
 Failure of closure of any one of the three normal sites of fusion can produce
unilateral, bilateral, or (rarely) median lip clefting.
o Unilateral CL on the left side is the most common presentation.
 It can be mild, involving only the upper lip, or can extend into the palate or the
midface, thereby affecting the nose, forehead, eyes, and brain.

Cleft Palate
 Isolated CP occurs when there is primary lack of fusion of the palatal shelves.
 Isolated disruption of palate shelves can occur after closure of the lip because palatal
closure is not completed until 56 to 58 days post conception.

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 Risk Factors
 Genes
o Proliferation defects: eg, sonic hedgehog gene
o Extracellular matrix defects: eg, TGF-alpha variant
o Differentiation defects: eg, TGF-beta gene
o Interferon regulatory factors: eg, IRF-6
 Maternal Medication
o Antiseizure agents o Methotrexate
 Maternal Cigarette smoking  Folate deficiency
 Maternal alcohol consumption
 Maternal obesity: small, but statistically significant risk

Associated Abnormalities
 Fetuses found to have orofacial clefts should undergo careful assessment for
additional structural abnormalities as these defects are noted in:
o As many as 50 percent of newborns with isolated CP
o 20 percent of those with CL and CP
o 8 percent for those with isolated CL
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  The anomalies typically involve the central nervous system/skeletal system (33
percent) and cardiovascular system (24 percent), all sites of tissues with neural
ectodermal origin.

Clinical Presentation
 Cleft lip: no functional disability
 Cleft palate
o Can’t suck o Speech impaired
o Middle ear infection: due to abnormally inserted Eustachian tube
o Middle face abnormalities

Prenatal Diagnosis
 CL/P cannot be diagnosed reliably until the soft tissues of the fetal face can be
clearly visualized sonographically, which is at 13 to 14 weeks by transabdominal
ultrasound, but somewhat earlier by transvaginal ultrasound.
 Three-dimensional ultrasound and magnetic resonance imaging can provide a clear
image of the malformation and may enhance detection of isolated cleft palate.

Management
Obstetrical Management:
 Amniocentesis for karyotype should be offered to women with ultrasound findings
of fetal orofacial clefts and associated anomalies (due to high rate of chromosomal
defects)
 Referral to a comprehensive management team
 The neonatology service that will attend the delivery should be notified in advance
o Can counsel the parents about newborn management issues
o Plan surgical repair
Postnatal Management:
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  During feeding
o Use large hole bottle for feeding
o Feed in erect position to avoid aerophagia
o Burp to remove ingested air
o Frequent small feedings
 Surgery
o Cleft lip: at 10 weeks, 10 pounds, hemoglobin of 10 and <10,000 WBC
o Cleft palate: at 10 months, 10kgs, hemoglobin of 10 and <10,000 WBC
 Dentist, ENT and speech therapist: for cleft palate patient.

Recurrence Risk
 The presence of CL/P or CP in a parent, a prior child born to the couple, or in the family
history requires further investigation if appropriate risk assessment is to be provided.
 Such assessment entails three important considerations
 Delineation of CL/P from isolated CP
o Risk of recurrent isolated CP is higher than the risk of recurrent CL/P
 Determination of a possible microform in the family
 Presence of a possible syndrome
Table 1.10: Relative risk of cleft lip and Palate in a Family Pedigree
Relative Cleft lip (%) Cleft lip/Palate (%) Cleft palate (%)
Sibling 3.5 3.9 3.3
Half sibling 1.0 0.5 1.0
Parent 2.5 2.5 2.1
Offspring 3.5 4.1 4.2
Niece/nephew 0.9 0.8 1.1
Aunt /uncle 0.6 1.1 0.6
First cousin 0.3 0.5 0.4

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 1. 6. Soft Tissue Tumor Examination

 Introduction……………………...…...…...…48
 Epidemiology…………………………...…....48
 Clinical Manifestation…..…………...…..49
 Differential Diagnosis……..…...…...…..52
 Investigation………………………..…...……53

Introduction
 Soft tissue is defined as the supportive tissue of various organs and the
nonepithelial, extra skeletal structures exclusive of lymph hematopoietic tissues.
 It includes fibrous connective tissue, adipose tissue, skeletal muscle, blood/lymph
vessels, and the peripheral nervous system

Epidemiology
 Benign soft-tissue tumors occur at least 10 times more frequently than malignant
ones.
 Overall, the age-adjusted annual incidence of soft-tissue sarcomas ranges from 15 to
35 per 1 million populations.
 The incidence increases steadily with age and is slightly higher in men than in women
 Distribution:
o Approximately 45% of sarcomas occur in the lower extremities
o 15% in the upper extremities
o 10% in the head-and-neck region
o 15% in the retroperitoneum
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 o The remaining 15% in the abdominal and chest wall

Clinical Manifestation
History:
 Asses for risk factors
o Genetics/ family history
 The NF1 gene in neurofibromatosis
o Possible generalized conditions
 Neurofibromatosis is the best example of a generalized disease that
may be associated with one or more soft tissue masses
o Radiation
o Chronic lymphedema:
 Predisposes to lymphangiosarcoma
o Carcinogens
 Hepatic angiosarcoma has been linked to arsenic, thorium dioxide, and
vinyl chloride exposure.
o Trauma: probably draws medical attention to a preexisting lesion
o The patient's age
 Infants and children may present with benign lesions that can
demonstrate local growth, disfigurement, overgrowth of the extremity
or loss of function (lipomas, hemangiomas, lymphangiomas,
neurofibromas, hamartomas, congenital or infantile fibromatosis).
 Soft tissue sarcoma is extremely rare in children, but when it occurs, it
is most likely to be rhabdomyosarcoma.
 In adults, rhabdomyosarcoma is rare in the extremities.
o Infections
 Kaposi sarcoma resulting from human herpesvirus type 8 in patients
with human immunodeficiency virus (HIV).

P a g e 49 | 548
  Epstein-Barr virus in an immunocompromised host also increases the
likelihood of soft-tissue tumor development.
 A mass is the most common sign of a soft-tissue tumor.
o Ask for pain
 Usually is painless and does not cause limb dysfunction.
 It may cause pain or neurologic symptoms by compressing or
stretching nerves, by irritating overlying bursae, or by expanding
sensitive structures.
o Ask for progression rate
 A rapid rate of increase in the size of a mass should arouse suspicion
that the lesion is malignant.
 A mass that has been present for years and that begins to grow may be
transforming from a benign to a malignant lesion, or it may simply be
growth of a benign soft tissue tumor.

Physical Examination:
Aims:
 To determine the location and size of a mass and to exclude other, more common
causes of pain.
 To know whether the mass is deep or subcutaneous, transilluminates (cysts), and
adheres to underlying structures
 Regional lymph nodes should be examined as well.
 Neurovascular examination is useful for the detection of either primary or secondary
tumor involvement.
How to examine:
1) Lymphoglandular exam
 Palpate the regional nodes, although soft tissue sarcomas rarely metastasize by
lymphangitic spread.
 Rhabdomyosarcoma and synovial sarcoma are the most likely diagnoses if nodal
metastases are found

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N.B:
2) Integumentary system
 Extremity masses larger than 5-7  Examine the skin should for evidence of:
cm and deeper than subcutaneous o Cafe au lait spots: fibrous dysplasia
tissue favors a diagnosis of a o Dermatofibromas
malignant soft-tissue tumor. o Axillary freckling, which may suggest
 However, as many as 30% of soft- neurofibromatosis
tissue sarcomas occur in
subcutaneous tissue and exhibit 3) Musculoskeletal exam
relatively less aggressive behavior.  Inspection
o Site
o Overlying skin change
N.B: Dermatofibrosarcoma Pro-
o Ulceration and disfigurement
tuberans
 Palpation
 This lesion is elevated above the o Depth of the mass: is the lesion superficial or
dermis, purplish in color, and it deep to fascia?
characteristically develops satellite o Most lesions developing superficial to fascia are
nodules as it grows. benign. Attempt to move the lesion over the
 It behaves like a low-grade soft fascia, both before and after the patient tenses
tissue sarcoma and is generally the underlying muscle. If the lesion moves with
managed in a similar manner. the muscle, it is likely deep to fascia. If the
physical examination indicates that the lesion
arises in fascia, deep to fascia, or is uncertain,
N.B:
obtain imaging of the mass.

 Examine the other extremities o Size of the mass

and trunk for soft tissue masses; o condition of the overlying tissues

lipomas and less commonly

liposarcoma may present in
multiple sites.  Is there evidence of inflammation that suggests either soft
tissue infection or a rapidly growing tumor?
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N.B:
- Tenderness could also indicate a rapidly growing
 Advanced metastatic carcinoma
tumor, a peripheral nerve sheath tumor, or
or lymphoma may spread to the
infection.
non-nodal soft tissues; therefore,
- Warmness
evidence of a primary cancer
- Fluctuation of mass (fluid)
elsewhere must be evaluated on
 Is there evidence of vascular changes that may suggest
both history and physical
multiple vascular malformations?
examination.
- Compressibility of the mass
- Pulsation
 Document evidence of extremity overgrowth, including measurement of
the extremity length and diameter especially in children.
4) Distal neurovascular status:
 Soft tissue tumors rarely cause a neurological deficit. Instead, nerve deficit usually
indicates that the tumor is arising in the peripheral nerve or is invading the nerve.
o Test for a nerve deficit or evidence of venous or arterial obstruction by
evaluating distal neurovascular status

Differential Diagnosis

Table 1.11: Differential Diagnosis of Soft Tissue Tumor

Child (<16 years)
Benign Malignant
 Hemangioma  Synovial sarcoma
 Fibromatosis  Rhabdomyosarcoma
 Fibrous histiocytoma  Fibrosarcoma/MFH
 Granuloma annulare  MPNST
Young adult (16-45 years)
Benign Malignant
 Ganglion  MFH/ Fibrosarcoma
 Fibrous histiocytoma  Liposarcoma
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 Nodular fasciitis  Dermatofibrosarcoma protuberans
 Neurogenic neoplasm  Synovial sarcoma
 Lipoma  MPNST
 Hemangioma 
Older adult (46 and older)
Benign Malignant
 Ganglion  Liposarcoma
 Lipoma  MFH/ Fibrosarcoma
 Neurogenic neoplasm  Leiomyosarcoma
 Fibrous histiocytoma  MPNST
 Nodular fasciitis  DFSP
Myxoma

Investigation
Imaging:
 Useful for defining anatomic location, tumor extent, and involvement of vital
structures.
 Useful to evaluate the relation of the tumor and surrounding normal structures to
the planned biopsy site and the functional status of the involved limb,
 Check for signs of lymph node involvement
 Plain radiography, CT, MRI, and bone scintigraphy is used to stage the disease.
 PET is being used more frequently to assess the metabolic activity and, presumably,
the biologic aggressiveness of a lesion.
 Angiography to evaluate any vascular involvement by soft tissue tumors has
essentially been replaced by MRI.
 CT is useful in checking for the presence and number of pulmonary metastases
 MRI best defines the relation between a tumor and adjacent anatomic structures,
such as compartment boundaries, nerves, vessels, and muscle.
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Biopsy:
 Is indicated for
o Soft-tissue mass arising in a patient without a history of trauma
o For a mass that persists for more than 6 weeks after local trauma.
o All soft-tissue masses larger than 5 cm, as well as any enlarging or
symptomatic lesion.
 Small, subcutaneous lesions that persist unchanged for years may be considered
for observation rather than biopsy.
o A high level of suspicion is necessary to ensure early treatment.
 Several biopsy techniques are available and the choice of biopsy technique is based
on the size and location of the mass and the experience of the surgeon.
o The techniques including the following:
 Fine-needle aspiration biopsy (FNAB)
 Core needle biopsy
 Incisional biopsy
 Excisional biopsy

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1.7. Video QR Codes

Wound Examination

Burn Assessment

Skin Tumors

Hand Examination

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 Part 2: Endocrine Surgery

Long Case Discussion

 Content By:
 Fitsum Solomon
 Nanati Jemal
 Edited By: 2.1. Approach to Breast Pathologies…………………………57
 Samuel Mesfin
 Reviewed By: 2.2. Approach to Thyroid Disorders………………………….71
 Dr. Endale Anberber
(General and Endocrine
Surgeon)

P a g e 56 | 548
 2.1. Approach to Breast Pathologies
 Case Discussion…………………………….…………………….57
 History…………………………………………………….………….57
 Physical Examination………………………………….……….59
 Investigation…………………………………………….…………62
 Differential Diagnosis……………………….………….……..62
 Discussion of the Differential Diagnosis………….……63

Case Discussion

 45 years old multiparous female patient came to regular OPD with right breast lump of 5-
month duration. The swelling increased in size gradually in the following months. It was
associated with intermittent aching pain of the lump. It showed gradual increment and was
associated with aching pain with no discharge. She also complains of easy fatigability,
anorexia, weight loss, global headache, tinnitus, vertigo and abdominal pain. On
examination there is an Upper outer quadrant mass, firm, tender, 6cm by 5cm in size, oval
shaped, irregular surface, well circumscribed, warm, mobile, not pulsatile and doesn’t
fluctuate. The nipples have no discharge or thickening and are elastic.

History
1) Describe the lump
 Size: it can be expressed as a size of bean or lemon
 Location (Right/Left)
 How the patient felt the lump: it’s important to ask the activity the patient had
had before she felt the lump as most patients feel while they were taking shower
 Duration

P a g e 57 | 548
  Pain: if the lump is associated with pain its most likely periductal mastitis if not
malignant causes can be taken into consideration (advanced cancer with
ulceration or chest wall infiltration may cause pain)
2) Ask the risk factors
 Age: 65+ vs. <65 years, although risk increases across all ages until age 80
 Personal history of breast cancer is important for all age groups
 Past history of benign breast disease should also be asked as some benign lesions
(proliferative lesions) increase risk of breast cancer.
 Smoking history: because its predisposing factor for periductal mastitis
 Family history: Two or more first-degree relatives with breast cancer diagnosed at
an early age
 History of trauma to the breast: trauma can result in fat necrosis
 History of radiation to the breast
 Alcohol consumption
 Early menarche (< 12 years)
 Personal history of endometrium, ovary, or colon cancer
 History of oral contraceptive usage
 Recent and long-term use of menopausal hormone therapy containing estrogen
and progestin
 Age at first full term pregnancy; parity affects risk of breast cancer
 History of TB: TB mastitis
 Diet history: vitamin A deficiency results in sloughing of the myoepithelial cells of
the duct. And also, evidence suggests that long-term consumption of foods with a
high fat content contributes to an increased risk of breast cancer by increasing
serum estrogen levels.
 Breast feeding history: it’s important in preventing breast ca.
 Socioeconomic status of the patient; there are a number of factors involved in
socioeconomic status
o Girls with good nutrition will have their menses at earlier age.
o In high socioeconomic status, girls delay age of first delivery

P a g e 58 | 548
 o Delay of first delivery may need use of hormonal contraceptives
o With high socioeconomic status, there is a tendency for low parity.
o With high socioeconomic status, there is a tendency for not feeding breast
3) Associated symptoms
 Discharge: Unilateral or bilateral? Does the discharge appear only after
compression of the nipple, or is it spontaneous?
 Color of the discharge:
o Milky? (lactational, Non-lactational, hyperprolactinemia)
o Bloody? (Ductal papilloma, ductal carcinoma and duct ectasia)
o Watery? (duct ectasia and fibrocystic disease)
o Greenish? (duct ectasia) o Yellowish? (breast abscess)
 Skin changes: local irritation of the nipple could be because of pagets disease,
breast cancer and eczema.
 Cough, chest pain, fever, chills or night sweats (suspect TB Mastitis)
 Yellowish discoloration of the eyes
 Abdominal swelling: metastasizing breast cancer can cause ascites
 Bone pain: some patients may come with joint or bone pain which reflects
metastasizing breast cancer
 Weight loss  Shoulder or back pain
 Easy fatigability

Physical Examination
 General appearance: acute or chronic sick looking
 Vital signs
 HEENT
o Eye: look for jaundice or anemia
 Lympho-glandular system:
o Inspect all the peripherally accessible lymph nodes for the presence of
enlargement and associated pain; special attention should be given to
axillary and supra/infraclavicular lymph nodes
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 o Breast examination
 Inspection:
o Adequate inspection initially requires full exposure of the chest, but later
in the examination, cover one breast while you are palpating the other.
Inspect the breasts and nipples with the patient in the sitting position and
disrobed to the waist.
o In order to adequately inspect the breast, use four principal views which
are explained below
 Arms at the sides:
o Skin color and thickening
o Size and symmetry of the breasts: Some differences in the size of the
breasts and areolae are common and usually normal.
o Breast contour
o Nipple and areola characteristics: inverted nipple can be suggestive of
breast cancer
 Arms over the heads, hands pressing against hips and leaning
forward:
o Ask the patient to raise her arms over her head and press against the hips
which is crucial in inspecting the fixity of the mass.
o Also ask the patient to lean forward against a wall which helps in
inspecting the mobility of the mass.
 Palpation:
o Palpation is best performed when the breast tissue is flattened.
o The patient should be supine.
o Palpate the rectangular area extending from the clavicle to the
inframammary fold and from the midsternal line to the posterior axillary
line and well into the axilla to ensure that you examine the tail of the
breast.
o A thorough examination takes at least 3 minutes for each breast.
 Use the pads of the 2nd, 3rd, and 4th fingers, keeping the fingers
slightly flexed. It is important to be systematic.
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  The vertical strip pattern is currently the best validated technique
for detecting breast masses.
 Palpate in small, concentric circles applying light, medium, and
deep pressure at each examining point.
 Press more firmly to reach the deeper tissues of a large breast.
 Examine the entire breast, including the periphery, tail, and axilla.
 Carefully examine the breast tissues for:
o Tenderness o Consistency
o Characterize the nodule in terms of:
 Location: mention by quadrant or clock with the distance in
centimeters
 Size: in centimeters
 Shape: irregular or round shape with discreteness or matted
 Boarders: well delineated or poorly circumscribed
 Consistency: soft, hard or firm
 Mobility: confirm the above inspected mobility.
 Examine both the left and the right axilla:
o For the left axilla, ask the patient to relax with the left arm down and
warn the patient that the examination may be uncomfortable.
o Support the patient’s left wrist or hand with your left hand.
o Cup together the fingers of your right hand and reach as high as you can
toward the apex of the axilla Place your fingers directly behind the
pectoral muscles, pointing toward the midclavicular.
o Now press your fingers in toward the chest wall and slide them
downward, trying to palpate the central nodes against the chest wall.
o Of the axillary nodes, the central nodes are most likely to be palpable.
o One or more soft, small (<1 cm), nontender nodes are frequently felt.

P a g e 61 | 548
 Investigation

 Not all patients need both mammography and ultrasound of the breast.
o When age is above 35 years (lax breast), mammography is routine to
look for multifocal / multicentric mass and to screen the contralateral
breast.
o Ultrasound is the choice for a dense breast (age < 35 years).
 Core biopsy is the standard for pathological diagnosis of breast mass or
abnormalities detected on imaging. In the absence of core biopsy, FNA is an
alternative with high specificity.
o Generally, core biopsy is superior to FNA.
 MRI is very rarely indicated in special circumstances
 Indications for bone scan should be mentioned as it is not a routine investigation.
 In the absence of metastatic symptoms, our current metastatic work up is chest
x-ray and abdominal ultrasound.
o This can be replaced by chest and abdominal CT scan.
 When patients present with early breast cancer, negative lymph node status,
favorable histology, avoidance of metastatic work up is a possibility.

Differential Diagnosis

Generally the list of differential diagnosis depends on age, history and physical findings,
 Periductal mastitis
 Subareolar abscess
 Tuberculous mastitis
 Fat necrosis
 Fibrocystic disease
 Fibroadenoma
 Phyllodes tumor
 Ductal papilloma
 Breast cancer

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 Discussion of the Differential Diagnosis
2.2.1. Periductal Mastitis/ Duct Ectasia

 This is a dilatation of the breast ducts, which is often

associated with periductal inflammation.
 Occurs most commonly in middle aged women.
 It results from dilatation of the lactiferous ducts leading
to leakage of secretion followed by local irritation of the
tissues and causing inflammation.
 Smoking is presumed to be the risk factor due to its high
propensity to cause increased virulence of the commensal
bacteria.

 Clinically, patients present

with Nipple discharge, a
subareolar mass, abscess,
and mammary duct fistula
and/or nipple retraction.
 Treatment usually involves
antibiotic therapy and
surgical excision of all the
major ducts.

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 2.1.2. Subareolar Abscess

 It is common in non-lactating women.

 It communicates with lactiferous duct resulting in
mammary fistula.
 In chronic cases, retraction of the nipple can occur
which is partial or slit-like.
 It can also be due to an infected sebaceous cyst

2.1.3. Tuberculous Mastitis

 It is usually associated with active pulmonary

tuberculosis or cervical lymphadenitis.
 It usually occurs in parous women and
characterized by multiple chronic abscesses
and affected surrounding skin.
 Treatment is with anti-tuberculous therapy.

2.1.4. Fat Necrosis

 It usually follows trauma to the breast. It may even cause by
inappropriate physical examination of the breast by the
physician.
 Occurs around 40-50 years.
 The clinical manifestations include palpable hard lump and
nipple retraction.
 Treatment is excision of the necrosed lump (surgery is
uncommonly indicated).
 Most of the time, it is self-limited. Patients may need analgesics
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2.1.5. Fibrocystic Disease

 Synonyms include fibrocystic changes, cystic mastopathy,

chronic cystic disease, chronic cystic mastitis,
Schimmelbusch’s disease, mazoplasia, Cooper’s disease,
Reclus ’disease, and fibro adenomatosis.
 Fibrocystic disease refers to a spectrum of histopathologic
changes which involve fibrosis and cystic alterations of the
breast tissues that are best diagnosed and treated
specifically.

2.1.6. Fibroadenoma

 It usually arises in ages between 15 and 25 with peak age of incidence

20.
 Clinically the patient feels lump which moves freely within the breast.
 It is smooth, round bordered, firm to hard in consistency, and freely
mobile within the breast.
 If it occurs in the elderly, it is fixed due to fibrosis.
 The complications depend on the age and complexity of the tumor.
Elderly patients with family history of breast cancer and with complex
fibroadenomas have increased chance (3 to 4 times) of acquiring
breast cancer.
 Treatment involves excision of the lump.
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2.1.7. Phyllodes Tumor

 It is a fibroepithelial tumor consisting of epithelial cells

with cellular stromal component
 Occurs in premenopausal women with ages of 30-40
years.
 Clinically, patients have lump which moves freely with
no associated nipple retraction.
 It is also called sero-cystic disease of brodie as it
becomes necrosed and cystic discharging serous fluid
due to rapidity of its growth.
 Phyllodes tumor can be benign (majority of the
younger patients), boarder line or malignant.
 Treatment ranges from wide excision to simple
mastectomy depending on the size.

2.1.8. Ductal papilloma

• It is a benign lesion of the breast occurring in middle

aged women.
• Patients usually experience lump with bloody discharge
from the nipple.
• On examination there is a mass beneath the areola
which upon palpation blood oozes out.
• It is a premalignant lesion.
• Treatment is usually surgical excision of the tumor
microdiscectomy.

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 2.1.9. Breast Cancer

 It accounts for 29% of all newly diagnosed cancers in females and is responsible for
14% of the cancer-related deaths in women.
 Etiology and Risk factors
o Age: it is very rare before 20 years but its incidence increases as age
increases. It is common in 35 to 75 years of age.
o Sex: women are 100 times to present with breast cancer than men.
o Ethnicity: more common in whites.
o Gene mutations: mutations in BRCA1 and BRCA2 and p53 mutations (li
Fraumeni syndrome) increase the chance of breast cancer.
o Family history: 3 to 4 times likely to develop in women who have first degree
relative with breast cancer.
o Diet: diet containing fatty foods increases the chance of breast cancer due
excess fat being converted to estrogen.
o Radiation exposure: patients who were previously treated with radiation
therapy for Hopkins disease are more likely to have their breast exposed to
the radiation.
 Clinical features:
o Lump: it’s the most common symptom in which 60% involve the upper outer
quadrant.
o Changes in skin appearance: on examination, there will be typical peau de
orange appearance.
o Bleeding per nipple and nipple reaction.
o Lung and abdominal metastasis: history should include pulmonary and
abdominal symptoms.
o Bone pains and behavioral changes
 Types
A. Carcinoma in situ (CIS)
o It consists of proliferating cells the absence of invasion of cells into the
surrounding stroma and their confinement within natural ductal and alveolar
boundaries.

P a g e 67 | 548
 o LCIS originates from the terminal duct lobular units and develops only in the
female breast by which the average age at diagnosis is 45 years.
o It is characterized by distention and distortion of the terminal duct lobular
units by cells which are large but maintain a normal nuclear: cytoplasmic
ratio.
o DCIS is characterized by a proliferation of the epithelium that lines the minor
ducts, resulting in papillary growths within the duct lumina.
o Paget’s disease is associated with DCIS which presents with chronic,
eczematous eruption of the nipple which may ulcerate.

B. Medullary carcinoma
o Seen in around 15% of cases. It tends to occur in the reproductive age
group.
o Clinically the patient feels softer lump than hard lump. In addition to
undifferentiated cells,
o Occasionally well differentiated gland formation is present. Hence, the
name, medullary adenocarcinoma.
o Presence of lymphatic infiltration is thought to represent a good host
response, thus indicating a good prognosis.
C. Inflammatory carcinoma
o Constitutes less than 1% of breast cancer
P a g e 68 | 548
 o More commonly seen in the reproductive age group and in pregnancy and
lactation.
o Clinical features include breast pain and redness which mimics mastitis.
o Usually it is ER positive.
o It has the worst prognosis.
D. Colloid carcinoma
o It is diagnosed because of production of mucin, intracellularly and
extracellularly.
o Prognosis of this variety of carcinoma breast is better than other infiltrating
duct carcinomas.

 Mode of Spread
o It involves local spread, hematogenous spread and lymphatic spread
o Local spread is due to the growth of the tumor invading and obliterating
the adjacent structures such as the skin causing ulceration and retraction.
o Lymphatic spread involves the central, pectoral, supraclavicular and
subscapular nodes.
o Hematogenous it spreads to the flat bones and the brain.

 Staging:

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Table 2.1: Breast carcinoma TNM anatomic stage group AJCC UICC 2017
T N M Stage Group
Tis N0 M0 0
T1 N0 M0 IA
T0 N1mi M0 IB
T1 N1mi M0 IB
T0 N1 M0 IIA
T1 N1 M0 IIA
T2 N0 M0 IIA
T2 N1 M0 IIB
T3 N0 M0 IIB
T0 N2 M0 IIIA
T1 N2 M0 IIIA
T2 N2 M0 IIIA
T3 N1 M0 IIIA
T3 N2 M0 IIIA
T4 N0 M0 IIIB
T4 N1 M0 IIIB
T4 N2 M0 IIIB
Any T N3 M0 IIIC
Any T Any N M1 IV

 Treatment
o Treatment includes surgery depending on the cancer type and
chemotherapy.

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 2.2. Approach to Thyroid Disorders

 Case Discussion…………………………….………….………71
 Clinical Manifestation………………………………….…..71
 Investigation…………………………………………………….75
 Differential Diagnosis………………………………….……76
 Discussion of the Differential Diagnosis……….……76

Case Discussion

 A 40-year-old patient, who was relatively well until 20 year ago, at which time she started
to develop swelling on the anterior neck. The swelling is small initially & not painful, and it
progressively increased in its size, to attain the current size. There is a relatively rapid
growth for four year. The patient also feels easy fatigability and shortness of breath, on
moderate activity like long distance walking for the last 4 years. She has history of
intolerance to cold. On examination she is Conscious and cooperative, over clothing, all
vital signs are stable, a firm 8x6cm anterior neck swelling, prominent on left, nodular and
non-tender, moves with swallowing and it is more prominent on the right side.

Clinical Manifestation

History
1. Describe the swelling
 Onset: acute durations are more likely stem from inflammatory causes
whereas chronic duration results from endemic goiter or malignant conditions.
 Pain: whether it is painful (thyroiditis) or painless (malignant)

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  Duration: Long duration of thyroid swelling indicates benign condition, e.g.
multinodular goiter (MNG), colloid goiter. Short duration with rapid growth
indicates malignancy such as anaplastic carcinoma. Majority of thyroid
swellings do not produce pain.
 Progression: rapid or slow progression
2. Associated symptoms
 Fever  Difficulty of swallowing
 Shortness of breath  Weight loss
 Easy fatigability (better to include the types of activities the patient used to but
fails to perform)
 Hoarseness of voice  Loss of appetite
 Sweating
3. Ask symptoms steaming from hyperthyroidism
 Increased appetite  Restlessness
 Significant weight loss  Palpitation
 Diarrhea  Shortness of breath
 Irritability  Lack of sleep
 Anxiety  Heat intolerance
4. Assess the symptoms of hypothyroidism
 Weight gain despite  Lack of motivation
decreased appetite  Drowsiness
 Constipation  Lack of motor coordination
 Body swelling  Cold intolerance
5. Dig out the risk factors
 Diet habit: this helps to assess the types of foods the patient regularly eats
that are prone to cause the swelling (for example Cabbage is a risk factor for
endemic goiter) the iodine content of the salt used in foods is also important
to ask about
 Area where the patient came from: helps to figure out if there are other
people living in the same area having the illness and symptoms.

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  Family history
 History of neck radiation therapy: it’s one of the risk factors for malignancy.
 History of drug intake
6. Rule out/ rule in the possible differential diagnoses
 Slow growing lesion with shortness of breath and difficulty of swallowing=>
Endemic goiter.
 Anterior neck swelling with increasing size, symptoms of hyperthyroidism with
predominating cardiovascular symptoms (palpitations) and skin manifestations
such as swelling of feet with positive family history=> Diffuse toxic Goiter
(graves’ disease)
 A swelling with associated sleep disturbance and change in behavior  Toxic
adenoma.
 Anterior neck swelling with gradual size increment manifesting in old ages with
thyrotoxic symptoms  Toxic multi nodular goiter.
 Rapidly progressing anterior neck swelling with associated pain, fever and
hyperthyroid symptoms  Inflammatory goiter (reidels thyroidits)
 Slowly growing swelling with hoarseness of voice, positive history of neck
radiation therapy with old age and positive family history=> thyroid ca.
(medullary)
7. Ask if any treatment have been given

Physical Examination
 General appearance: it is useful to assess the general appearance of the patient
as it depicts hyperthyroid symptoms such as restlessness, hypothyroid symptoms
such as drowsiness.
 Vital signs
o Pulse rate: increased pulse rate is indicative of hyperthyroidism steming
from various causes such as Graves’ disease, toxic multinodular goiter etc.
Rhythm is also important.
o Blood pressure: raised blood pressure results from thyrotoxicosis. Wide
pulse pressure is also a feature of thyrotoxicosis.
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 o Respiratory rate: tachypnea occurs in thyrotoxicosis, graves diseases
o Temperature: increased temperature occurs from hyperthyroidism and
inflammatory thyroiditis whereas decreased temperature results from
hypothyroidism
 HEENT
o Eye: look for exophthalmos; also look for anemia and jaundice
 Lymphoglandular: examination of the cervical and supraclavicular lymph nodes
for enlargement
 Examination of the mass
 Inspection
o Location
o Size and shape: mention the size in cm like 3*5cm
o Surface:
 Smooth  Adenoma, puberty goiter, Graves' disease
 Nodular  Multinodular thyroid
o Boarders
o Smooth  adenoma, puberty goiter, Graves' disease
o Irregular  carcinoma of the thyroid
o Nodular  multinodular thyroid
o Swelling moving with deglutition:
 This is because thyroid gland is enclosed to the pretracheal facia
which moves with swallowing.
 It’s also because of the ligaments of berry with are attached
superiorly to the cricoid cartilage by which during swallowing the
thyroid gland moves together with cricoid cartilage.
o Movement of the swelling on protrusion of the tongue which most likely
indicates thyroglossal cyst.
 Palpation
o Confirm the above inspected areas of the swelling such as size shape and
borders
o Consistency
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 o Fixation: confirm the fixity or mobility of the thyroid gland by holding the
thyroid gland.
o Tracheal position
o Palpation of the lymph nodes
o Palpation of the carotid arteries
o Special testes
o Kocher test
o Berry sign
o Darymple sign
 Percussion:
o Percussion over the sternum gives a resonant note in normal cases.
o In retrosternal goitres, it gives a dull note.
 Auscultation:
o It should be done in the upper pole because of following reasons: Superior
thyroid artery is a direct branch of external carotid artery. It is more
superficial than inferior thyroid artery. Presence of thrill and bruit are the
features of toxic goiter.
o Features of hypervascularization (Grave's disease, malignancy)
 Cardiovascular examination: examine the presence of palpitation
 Integumentary: examine the skin for the presence swelling and associated skin
changes (myxedema in graves’ disease)
 Neurologic examination: examine the deep tendon reflexes as they are brisk in
hyperthyroidism and absent in hypothyroidism

Investigation
 CBC  Ultrasonography
 ESR, CRP  FNAC
 Thyroid function test  Chest x-ray
 CT-scan  Core needle biopsy (rarely)
 Radioactive iodine investigation  MRI (rarely indicated)
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 Differential Diagnosis

A) Physiologic Goiter
 Puberty and Pregnancy goiter
B) Endemic Goiter
 Iodine deficiency goiter
C) Toxic goiter
 Diffuse toxic goiter  Toxic adenoma
 Toxic multinodular goiter
D) Inflammatory goiter
 Acute suppurative thyroiditis  Reidels thyroiditis
 Subacute/dequervians thyroiditis  Autoimmune thyroiditis
E) Neoplastic goiter
 Follicular ca.  Anaplastic ca.
 Papillary ca.  lymphoma
 Medullary ca.

Discussion of the Differential Diagnosis

2.2.1. Physiologic Goiter

Puberty and Pregnancy goiter:

 It is seen in girls at puberty or during pregnancy when the metabolic demands are
high and the production of T3, T4 are comparatively normal. Due to feedback
mechanism,
 TSH levels increase, which stimulate thyroid gland and causes diffuse hypertrophy
and hyperplasia. This is also called physiological goiter and can be treated by giving
tablet thyroxine (T4) 0.2 mg/day to suppress TSH.
 The goiter may disappear if treatment is given in the stage of diffuse hypertrophy.

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 2.2.2. Endemic Goiter

Iodine deficiency goiter:

 The daily requirement of iodine is about 0.1–

0.15 mg.
 Simple goitre is endemic in areas where there is
a very low iodide content in the water and
food.
 Endemic goitre is also found in lowland areas
where the soil lacks iodide or the water supply
comes from distant mountain ranges

 Calcium is also goitrogenic and goitre is common in low iodine areas. Although
iodides in food and water may be adequate, failure of intestinal absorption may
produce iodine deficiency.
 Clinically, the patient is euthyroid.
 The nodules are palpable and often visible; they are smooth, usually firm and not
hard, and the goitre is painless and moves freely on swallowing.
 Complications include tracheal obstruction (due to enlargement of the thyroid
gland and compression of the trachea), secondary thyrotoxicosis which occurs in
30% of the patients and evolution to malignancy.
 Iodine deficiency goitere can be prevented by including iodized salt to daily meal
and limiting the intake of goiterogenic foods suchas cabbage
 Treatment involves surgical removal of the thyroid gland (thyroidectomy) which
may be subtotal or total depending on the status of the patient.
o Total thyroidectomy is the total removal of the thyroid gland with immediate
and lifelong replacement of thyroxine.
o Subtotal thyroidectomy involves partial resection of each lobe, removing the
bulk of the gland, leaving up to 8 g of relatively normal tissue in each remnant
lobes.

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 2.2.3. Toxic Goiter

A) Diffuse Toxic Goiter (Grave’s disease)

 It is an autoimmune disease with a

strong familial predisposition,
female preponderance (5:1), and
peak incidence between the ages
of 40 and 60 years.

 Characterized by thyrotoxicosis, diffuse goiter, and extrathyroidal conditions

including ophthalmopathy, dermopathy (pretibial myxedema), thyroid
acropachy, gynecomastia, and other manifestations.
o Conditions such as postpartum sate, bacterial and viral infections,
iodine excess and lithium therapy may precipitate.
o Genetic mutations also play a role such as HLA gene haplotypes.
o The clinical features are those of hyperthyroid symptoms which are
heat intolerance, increased sweating and thirst, and weight loss
despite adequate caloric intake. Palpitations, nervousness, fatigue,
emotional lability, hyperkinesis, and tremors are also included.
 The most common GI symptoms include increased frequency of bowel
 movements and diarrhea. Female patients often develop amenorrhea,
decreased fertility, and an increased incidence of miscarriages.
 Extra thyroid manifestations include ophthalmopathy (Eye symptoms include
lid lag (von Graefe’s sign), spasm of the upper eyelid revealing the sclera above
the corneoscleral limbus (Dalrymple’s sign), oncolysis, clubbing and
dermopathy characterized occurring in 1% to 2% of patients characterized by
deposition of glycosaminoglycans, leading to thickened skin in the pretibial
region and dorsum of the foot.
• On physical examination, the thyroid usually is diffusely and symmetrically
enlarged, as evidenced by an enlarged pyramidal lobe. There may be an

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 overlying bruit or thrill over the thyroid gland and a loud venous hum in the
supraclavicular space.
• Graves’ disease may be treated by any of three treatment modalities:
antithyroid drugs, thyroid ablation with radioactive 131I, and thyroidectomy.

B) Toxic Multinodular Goiter

 Usually occur in older individuals, who often have a

prior history of a nontoxic multinodular goiter.
 Some patients have T3 toxicosis, whereas others
may present only with atrial fibrillation or
congestive heart failure.
 Symptoms and signs of hyperthyroidism are similar
to Graves’ disease, but extrathyroidal
manifestations are absent.

 Both RAI and surgical resection may be used for treatment. When surgery is
performed, near-total or total thyroidectomy is recommended to avoid
recurrence and the consequent increased complication rates with repeat
surgery.
C) Toxic Adenoma
 A
 Arises from a single hyperfunctioning nodule which
typically occurs in younger patients who note recent
growth of a long-standing nodule along with the
symptoms of hyperthyroidism.
 Physical examination usually reveals a solitary thyroid
nodule without palpable thyroid tissue on the
contralateral side.
o Treatment options range from antithyroid
medications to surgery (lobectomy or istmusectomy
depending on the size of the nodule.
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 2.2.4. Inflammatory Goiter

A) Acute Suppurative Thyroidits

 Acute suppurative thyroiditis is generally a rare disease as the thyroid gland is
highly vascularized and has high concentration of iodine.
 It is more common in children and often is preceded by an upper respiratory
tract infection or otitis media.
 It is characterized by severe neck pain radiating to the jaws or ear, fever,
chills, odynophagia, and dysphonia.
 Complications such as systemic sepsis, tracheal or esophageal rupture,
jugular vein thrombosis, laryngeal chondritis, and perichondritis or
sympathetic trunk paralysis may also occur.
 Treatment consists of parenteral antibiotics and drainage of abscesses.
Thyroidectomy may be needed for persistent abscesses or failure of open
drainage.

B) Subacute (granulomatous or dequervians) Thyroidits

 Subacute thyroiditis or de Quervain's disease occurs due to viral infection. It
usually follows sore throat (mumps virus has been incriminated in a few
cases).
 Patients present with fever, body ache and painful enlargement of thyroid
gland. The gland is enlarged, tende1 to touch, soft to firm and a few
symptoms of hyperthyroidism occur initially.
o ESR is usually increased.
o Majority of the patients respond to conservative treatment in the
form of analgesics and a short course of prednisolone.
o There are no permanent sequelae of this condition.

C) Reidels Thyroidits:
 It is a rare disease of the thyroid characterized by a marked dense, invasive
fibrosis that may extend beyond the thyroid capsule and involve surrounding
structures such as blood vessels, trachea and esophagus leading to
hypoparathyroidism.
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  Although the exact etiology is not known, a more generalized condition known
as fibrosclerosis causing fibrosis in other parts of the body including the
retroperitoneum, mediastinum, lacrimal glands and bile ducts (sclerosing
cholangitis).
o The clinical presentations are symptoms of compression such as
stridor, hoarseness and dyspnea by which in more aggressive cases
dysphagia occurs.
o On physical examination, the thyroid gland is “woody” hard, and
nontender. Laboratory investigations are normal.
o Treatment involves istmusectomy to relieve the compressive
symptoms.
o Thyroxine replacement therapy is necessary in patients with
hypothyroidism.

D) Autoimmune (chronic, lumphocitic, Hashimoto’s) Thyroiditis:

 Hashimoto’s thyroiditis is an autoimmune process that is thought to be
initiated by the activation of CD4+ T (helper) lymphocytes with specificity for
thyroid antigens.
 Hashimoto’s thyroiditis is more common:
o In women (male: female ratio 1:10 to 20)
o Between the ages of 30 and 50 years old.
 The clinical presentation involves that of hypothyroidism.
 Physical examination reveals a diffusely enlarged, firm gland, which also is
lobulated. An enlarged pyramidal lobe often is palpable.
 Treatment involves Thyroid hormone replacement therapy is in overtly
hypothyroid patients, with a goal of maintaining normal TSH levels.

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 2.2.5. Neoplastic Goiter

A) Papillary Carcinoma
 Papillary carcinoma accounts for 80% of all thyroid malignancies in iodine-
sufficient areas
 It is the predominant thyroid cancer in children and individuals exposed to
external radiation.
 Occurs more often in women, with a 2:1 female-to-male ratio
 The mean age at presentation is 30 to 40 years.
 Most patients are euthyroid and present with a slow-growing painless mass in
the neck.
 Dysphagia, dyspnea, and dysphonia usually are associated with locally advanced
invasive disease.
 Lymph node metastases are common
o Especially in children and young adults
o May be the presenting complaint.
 The most common sites of metastasis are:
o Lungs
o Bone
o Liver
o Brain
 Treatment involves surgical removal of the tumor which can be total or near total
thyroidectomy depending on the aggressiveness of the tumor.
 It has an excellent prognosis with a >95% 10-year survival rate.

B) Follicular carcinoma
 Accounts for 10% of thyroid cancers and occur more commonly in iodine-
deficient areas.
 Women have a higher incidence of follicular cancer, with a female-to-male ratio
of 3:1, and a mean age at presentation of 50 years old.

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  Longstanding endemic goitere could lead to follicular carcinoma which can be
hyperfunctioning, leading patients to present with signs and symptoms of
thyrotoxicosis.
 Metastasizes by hematogenous spread.
 FNAC is unable to distinguish benign from malignant follicular tumors
 Treatment involves subtotal or total thyroidectomy.
 In general, it has good prognosis with the cumulative mortality approximately
15% at 10 years and 30% at 20 years.
 Poor long-term prognosis is due to:
o Age over 50 years old at presentation
o Tumor size >4 cm
o Higher tumor grade
o Marked vascular invasion
o Extrathyroidal invasion and
o Distant metastases at the time of diagnosis.
 Hurtle cell carcinoma is a variant of follicular Ca which arises from oxyphilic cells
of the thyroid.
 Hurtle cell tumors differ from follicular carcinomas in that they are:
o More often multifocal and bilateral (about 30%)
o Usually do not take up RAI (about 5%)
o More likely to metastasize to local nodes (25%) and distant sites
o Associated with a higher mortality rate (about 20% at 10 years)

C) Medullary carcinoma
 Accounts for about 5% of thyroid malignancies and arises from the parafollicular or
C cells of the thyroid.
 The female-to-male ratio is 1.5:1.
 Present at a younger age; most patients present between 50 and 60 years old,
although patients with familial disease

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  Medullary thyroid tumors secrete calcitonin and carcinoembryonic antigen (CEA)
which can be used as tumor markers.
o Spreads via lymph nodes.
o Total thyroidectomy + central lymph node dissection is the treatment
of choice.
o Prognosis depends on the stage of the disease.
 The 10-year survival rate is approximately 80% but decreases to
45% with lymph node involvement.

D) Anaplastic carcinoma
 Accounts for nearly 1% of thyroid malignancies.
 Women are more commonly affected with age at presentation 70-80 years.
 History of longstanding goiter can be presumed risk factor
 A typical patient has a long-standing neck mass, which rapidly enlarges/may be
painful.
 Associated symptoms such as dysphonia, dysphagia, and dyspnea are common.
 Spreads via lymphatic route.
 The treatment option includes:
o Total or near total thyroidectomy with therapeutic lymph node
dissection
o Radiotherapy and chemotherapy depending on the status of the patient
and tumor stage.
 It has poor prognosis with few patients surviving 6 months after diagnosis.

E) Lymphoma
 Accounts for <1% of thyroid malignancies.
 Non-Hodgkin B-cell type is the most common variant.
 The clinical presentations are similar to anaplastic carcinoma with the exception of
absence of pain.
 Combined therapy of radiotherapy and chemotherapy is recommended.

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 Short Case Discussion

 Content By:
 Fitsum Solomon
 Nanati Jemal 2.3. Thyroid Examination………………..……………..86
 Edited By:
 Samuel Mesfin 2.4. Breast Examination………………..….……….……91
 Reviewed By:
 Dr. Endale Anberber 2.5. Video QR Codes………….…………..………….……96
(General and Endocrine
Surgeon)

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 2.3. Thyroid Examination
 Inspection…………………………….………….………….86
 Palpation………………………………….………….………88
 Percussion………………………………………………..….90
 Auscultation………….………….………….………………91
 Special Tests………….………….………….……………..91

Inspection

General appearance

 Does the patient appear agitated, anxious and Fidgety? – Hyperthyroidism

A) Hands
 Ask to look at the hands-Thyroid Acropachy in Graves’ disease
o Acropachy means thickening of the
extremities
o Digital clubbing, soft tissue swelling
of the hands and feet
o Periosteal new bone formation (X-
ray finding)
 Put paper on their hands- Tremor in
hyperthyroidism
 Ask to see the palm of their hands
o Dry skin- hypothyroidism
o Palmar Erythema- hyperthyroidism
o Touch the hand to check for sweating
o Feel for pulse
 Pulse rate- increase in hyperthyroidism and decreased in
hypothyroidism
 Pulse rhythm – irregular in Atrial Fibrillation
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B) Face
 Look for sweating- hyperthyroidism
 Dry skin
 Loss of outer 3rd eyebrow- hypothyroidism
 Pemberton’s sign: Ask the patient to raise their arms and look for symptoms of
air hunger, face swelling and distended veins.
C) Eyes
 Exophthalmoses
o Specific for Grave's disease
o May be absent in some patients
o Sign of thyrotoxicosis
o Look down at the patient from above and behind,
so that you are looking at their eyebrows and the
nose below.
o Observe the proptosed eye and whether it is displaced forward or to the
side.
 Intraconal lesions tend to push the globe directly forwards,
whereas extraconal lesions push it to one side
 Lid retraction
o Sign of thyrotoxicosis
o Eyelid retraction is considered to be present if,
with the eyes in primary position (at rest), the
sclera is visible above the superior corneal limbus
 Eye muscle movements – Draw imaginary big ‘H’ to test
for cranial nerve 3,4,6
 Lid lag
o Ask the patient to look at your finger and to look up and down following
your finger
o It is positive when the lid lags while the eyeball move downward and the
upper sclera become visible.
o Sign of thyrotoxicosis
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D) Neck
 Skin changes- erythema  Scars- thyroidectomy
 Masses
o Location o Surface
o Size and shape o Borders
o Movement of swelling with swallowing: due to ligament of berry
connecting cricoid cartilage to thyroid gland.
o Movement with tongue protrusion
 Movement - thyroglossal cyst
 No movement- thyroid mass and lymph node

Palpation

 Examination of thyroid gland is usually done behind the patient to check for
similarity and accessible lymph nodes. But begin in front of the patient see comfort
of the patient.
A) The swelling for:
 Size
 Shape
 Surface
o Smooth
 Adenoma
 Puberty Goiter
 Grave’s disease
o Irregular o Nodular
 Carcinoma  Multi-Nodular Goiter
 Border
o Round in thyroid disorders
 Temperature

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  Consistency
o Soft
 Grave’s disease  Colloid Goiter
o Firm
 Adenoma  Multi-nodular Goiter
o Hard
 Thyroid carcinoma  Calcification in multi-
nodular Goiter
 Movement with swallowing
o Hold the thyroid gland and ask the patient to swallow
o To asses asymmetry of thyroid lobe elevation
o Differentials for a neck mass that moves with swallowing:
 Thyroid disorders
 Sub hyoid bursitis
 Pre-tracheal and pre-laryngeal lymph nodes
 Thyroglossal cysts
 laryngocele
o Differentials for a fixed Thyroid mass
 Malignancy
 Retrosternal Goiter
 Large Goiter
 Previous Surgery
 Intrinsic mobility test

o Restricted in malignancy of the thyroid

 Sternocleidomastoid contraction test
o When one lobe is enlarged
o If the swelling becomes less prominent with this test, it indicates it is deep to
sternocleidomastoid muscle
 Chin test
o In Multi-nodular Goiter (both lobes enlarged)
o Ask the patient to bend chin downward against resistance to contract sternomastoid and
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strap muscles allowing the thyroid glad to be less prominent.
B) The trachea
 Deviation
o Trachea deviated in large goiter
o Trachea will not be deviated in multi-nodular Goiter
 Kocher’s test  Test for tracheal compression
o The swelling is pressed slightly on either side of trachea. If trachea is
already compressed patient will have stridor
o Positive in Tracheomalacia and Malignancy
C) Lymph nodes
 If you palpate lymph nodes, suspect papillary cancer
D) Common carotid artery
 If you palpate a pulse in the posterior triangle of the neck- MNG because
common carotid will be pushed laterally
 If there is absent pulse with pulse in superficial temporal artery (Berry sign)-
Thyroid malignancy

Percussion
 Over sternum
o Resonant- normal lobe
o Dull- Retrosternal Goiter

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 Auscultation

 In the upper pole where there is superior

thyroid artery
o Bruit- toxic goiter

Special Tests
 Check for reflexes – hyporeflexia in hypothyroidism
 Check for pre-tibial myxoedema in Graves
 Assess for proximal Myopathy by asking the patient to stand up while crossing his
arms – hyperthyroidism

2.4. Breast Examination

 Inspection…………………………….…………………91
 Palpation…………………………………………………93

Inspection
A) General appearance
 Does the patient have weight loss? Are they in distress?
B) Arm- if there is edema due to lymphatic blockage
C) Breast

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  Ask the patient to stand in 4 different positions while you are inspecting the
breast
o Hands by the side
o Hands on the hips
 If a mass is visible, observe if
it moves when the pectoralis
muscle contracts which
suggests tethering to the
underlying tissue (e.g.
invasive breast malignancy).
 The maneuver may
accentuate puckering
 Hands raised above and behind head
o You can appreciate prominent peau d’orange
 Leaning forward
o If there is malignancy in the chest wall, breast will not fall forward
 While the patient is in “the hands by the side” position, inspect the following
o Asymmetry of the two breasts:
normal feature in most women.
o Incision scars: lumpectomy
(small scar) or mastectomy (large
diagonal scar).
o Lumps- if visible, characterize it
o Skin changes
 Dimpling: due to malignancy
infiltrating to ligament of cooper
 Peau d’orange- tumor in the areola
 Erythema
 Scaling: of the nipple and/or areola associated with erythema and
pruritis are typical features of Paget’s disease of the breast

o Nipple
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  Is there a discharge?
Differential diagnosis for
 Do you see a central retracted nipple?
Nipple retraction
 If yes, is the retraction slit-like or circumferential?
1) Cancer of the breast  Circumferential indicates malignancy
2) Chronic mastitis  Slit-like can be due to duct ectasia or peri-ductal mastitis
3) Congential  Level of the nipple; compare with the contralateral side
4) Chronic disease- TB  To detect early malignancy
 Destructed nipple in Paget disease

Palpation
A) Breast
 How to examine?
o Ask the patient to place the hand on the side
being examined behind their head to fully
expose the breast.
o Start palpating the asymptomatic breast
o Ensure all 4 quadrants are palpated with
systematic palpation technique.
o Use the flats of your middle three fingers to compress the breast tissue
against the chest wall, as you feel for any masses.
o Use superficial, intermediate and deep pressure palpation.
o Complete palpation of entire breast before examining a mass in detail.

 Clock face method: view the breast as a clock face and

examine each ‘hour’ from the outside towards the nipple.
 Spiral method: begin palpation at the nipple and work
outwards in a concentric circular motion.
 Quadrants method: divide the breast into quadrants and
examine each thoroughly.

P a g e 93 | 548
  Check local rise in temperature and tenderness
o In rapidly growing cancer and inflammatory cancer
 Describe the lump if detected
o Location: breast cancer common in upper and outer quadrant of
breast
o Size
o Shape- breast cancer is usually irregular
o Consistency
 Hard- common in breast cancer
 Firm
 Soft- mastitis carcinomatosis due to tumor necrosis
o Mobility
 Does it move freely? - fibroadenoma
 Does it move with the overlying skin?
 Does it move with pectoral contraction?
o Fluctuance
o Overlying skin changes
 Hold the mass by its sides and then apply pressure to the
center of the mass with another finger. If the mass is fluid-filled
(e.g. cyst) then you should feel the sides bulging outwards.

 Examine the nipple

Milky discharge:  Ask the patient to hold their nipple between

 Normal during pregnancy and when their index finger and thumb and try to express
breastfeeding (bilateral). any discharge
 Galactorrhea  Characterize the Discharge
Purulent discharge  Color
 Thick yellow, green or brown discharge  Consistency (e.g. thick, watery)
with an offensive smell.  Volume
 Mastitis and central breast abscess
Watery and bloody: Ductal carcinoma P a g e 94 | 548
B) Lymph node Examination
 How to examine axillary lymph node?
1. Ensure the patient is positioned lying down on the examination couch at 45°.
2. Ask if the patient has any pain in either shoulder before moving the arm.
3. Begin by inspecting each axilla for evidence of scars, masses, or skin changes.
4. When examining the right axilla, hold the patient’s right forearm in your right
hand and instruct them to relax it completely, allowing you to support the
weight.
5. Palpation should then be performed with the left hand. The reverse is applied
when examining the left axilla.
6. Examination of axilla should cover the pectoral (anterior), central (medial),
subscapular (posterior), humoral (lateral), and apical groups of lymph nodes.

o With your palm facing towards you, palpate behind the lateral edge of the
pectoralis major (pectoral/anterior).
o Turn your palm medially and with your fingertips at the apex of the axilla
palpate against the wall of the thorax (central/medial) using the pulps of
your fingers.
o Facing your palm away from you now, feel inside the lateral edge of
latissimus dorsi (subscapular/posterior).
o Palpate the inner aspect of the arm in the axilla (humoral/lateral).
 Reach upwards into the apex of the axilla with fingertips (warn the
patient this may be uncomfortable).

7. Repeat assessment on the contralateral axilla.

 How to describe the palpable lymph nodes?
o Size
o Fixity
o Consistency
 Hard: significant
 Soft
Secondary infection due to fungating growth
 Firm
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 Investigate if indicated
 Examine the Regional lymph node  Ultrasound if age <35
o Cervical, supra-clavicular and  Mammography if age >35
infra-clavicular lymph nodes  Biopsy
 Educate on self-breast exam

2.5. Video QR Codes

Breast Examination

Thyroid Examination

P a g e 96 | 548
 Part 3: Cardiothoracic Surgery

Long Case Discussion

 Content By:
 Samuel Mesfin
 Zemichael Getu
 Edited By: 3.1 . Approach to Dysphagia………………………………….98
 Samuel Mesfin 3.2 . Chest Trauma………………………………………………..121
 Reviewed By:
 Dr. Ephraim Teffera 3.3 . Mediastinal Tumor………………………………………..134
(General and Cardiothoracic
Surgeon)

P a g e 97 | 548
 3.1. Approach to Dysphagia

 Introduction……………………….…………………….98
 History ……………………………..……………………..100
 Physical Examination………………………………..102
 Investigation…………………………………………….103
 Differential Diagnosis…………….…………………106
 Discussion of the differentials…..………………107

Introduction

 Dysphagia, difficulty with swallowing, refers to problems with the transit of food or
liquid from the mouth to the hypopharynx or through the esophagus.
 Severe dysphagia can compromise nutrition, cause aspiration, and reduce quality of
life.
 Solid Food Dysphagia becomes common when the lumen is narrowed to 60-70% but
can also occur with larger diameters in the setting of poorly masticated food or
motor dysfunction.
 Additional terminology pertaining to swallowing dysfunction:
o Aphagia:
 Denotes complete esophageal obstruction
 Most commonly encountered in acute settings
 For example: food bolus or foreign body impaction
o Odynophagia:
 Refers to painful swallowing, typically resulting from mucosal ulceration
within the oropharynx or esophagus.
 It commonly is accompanied by dysphagia, but the converse is not true.
o Globus Pharyngeus:

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  It is a foreign body sensation localized in the neck that does not interfere
with swallowing and sometimes is relieved by swallowing.
o Transfer dysphagia:
 It frequently results in nasal regurgitation and pulmonary aspiration
during swallowing and is characteristic of oropharyngeal dysphagia.
o Phagophobia:
 Fear of swallowing and refusal to swallow may be psychogenic or related
to anticipatory anxiety about food bolus obstruction, odynophagia, or
aspiration.
 Dysphagia can be classified as
i. With respect to location:
 Oral
Oropharyngeal Dysphagia
 Pharyngeal
 Esophageal Dysphagia
ii. By the circumstances in which it occurs.
 Structural Dysphagia: dysphagia caused by an oversized bolus
or a narrow lumen
 Propulsive/Motor/Physiologic Dysphagia: dysphagia due to
abnormalities of peristalsis or impaired sphincter relaxation
after swallowing.

Table 3.1: Dysphasia Scoring System

0  Able to eat normal diet / no dysphagia
1  Able to swallow some solid foods
2  Able to swallow only semi solid foods
3  Able to swallow liquids only
4  Unable to swallow anything / total dysphagia
There is also an out of 6 grading system

P a g e 99 | 548
 History

 Age: helps to differentiate the commonest causes at specific age groups.

o Esophageal Ca is more common in mid to late adulthood.
 Sex: Some causes of dysphagia are more common in one sex.
o Esophageal Ca is more common in male.
o Some hospital based studies may suggest Females seem more affected in
Ethiopia.
 Elaborate the chief complaint:
o Mode of onset:
 Acute: usually suggests impaction of a foreign body in the esophagus
or acute inflammation of pharynx, retropharyngeal area or esophagus.
 Non acute
o Duration:
 Chronic motility disorders like achalasia present with symptoms lasting
months to years.
 Esophageal Ca present with short history of days to weeks.
o Type of dysphagia:
 Prolonged retention of food within the oral cavity that may seep out
of the mouth, drooling and difficulty in initiating swallowing, nasal
regurgitation, aspiration, associated ENT symptoms  Oropharyngeal
Dysphagia
 Dysphagia localized to the chest  Esophageal Dysphagia
o Intermittent or Persistent:
 Intermittent dysphagia that occurs only with solid food implies
Structural Dysphagia
 Constant dysphagia with both liquids and solids strongly suggests a
Motor Abnormality
o Is the dysphagia to solids, fluids or both?
o Food impaction with a prolonged inability to pass an ingested bolus
even with ingestion of liquid is  Structural Dysphagia
o Progressive or Episodic:

P a g e 100 | 548
  Dysphagia that is progressive over the course of weeks to months
raises concern for neoplasia.
 Episodic dysphagia to solids that is unchanged over years indicates a
benign disease process.
 Ask about the risk factors:
o For oropharyngeal dysphagia:
 History of surgery and radiation therapy, often in the setting of head
and neck cancer.
 Neurogenic causes resulting from cerebrovascular accidents,
Parkinson's Disease, and Amyotrophic Lateral Sclerosis
 Myogenic causes: myasthenia gravis, polymyositis
 Structural lesions causing dysphagia including: Zenker's diverticulum,
Cricopharyngeal Bar, and Neoplasia
o For Esophageal Dysphagia
 Diseases that cause absent peristalsis and weakness of the LES like
scleroderma (it is almost always preceded by cutaneous
manifestations)
 DES
 Achalasia Cardia
o Ingestion of caustic agents or pills
o Prolonged nasogastric intubation
o those are associated with each differential diagnosis (mentioned below)
 Ask for the presence of any associated symptoms like:
o Hoarseness:
 Hoarseness preceding dysphagia  Primary lesion is usually laryngeal
 Hoarseness following dysphagia  May result from compromise of
the recurrent laryngeal nerve by a malignancy (Indicates advancement
of malignancy and location of the tumor i.e upper thoracic tumor)
o Heart burn: related to a reflux disease with or without a stricture.
o Chest pain: frequently accompanies dysphagia whether it is related to Motor
Disorders, Structural Disorders, or Reflux Disease
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 o Accompanying odynophagia: usually is indicative of ulceration
 Infectious
 Pill-induced Esophagitis
o Loss of appetite and significant/remarkable weight loss: red flags for
esophageal Ca
o Respiratory symptoms: can occur due to aspiration or compression.
o Regurgitation: common in achalasia.
o History of atopy: eosinophilic esophagitis
o In patients with AIDS or other immunocompromised states:
 Esophagitis due to opportunistic infections such as Candida, Herpes
Simplex Virus, or Cytomegalovirus
 Tumors such as Kaposi's Sarcoma and Lymphoma should be
considered

Physical Examination

 General appearance:
o Emaciated in case of esophageal ca.
 HEENT:
o A careful inspection of the mouth and pharynx could disclose lesions that may
interfere with passage of food
o Signs of Bulbar or Pseudobulbar Palsy, including Dysarthria, Dysphonia,
Ptosis, Tongue Atrophy, and Hyperactive Jaw Jerk should be elicited.
 Lymphoglandular system:
o Palpable Virchow’s nodes
o Look for neck masses
 Respiratory system:
o Look for signs of pneumonia (aspiration)
o Tracheal deviation due to mass effect
 Abdominal:
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 o Look for metastatic sites in case of esophageal ca like the liver.
o Look for ascites
o Palpable epigastric mass for GEJ cancers
 Integumentary system:
o Changes in the skin may suggest a diagnosis of scleroderma
 Neurologic examination:
o Cranial nerve pathologies suggest functional dysphagia.
o Look for generalized neuromuscular diseases.

Signs of Advancement in Esophageal Cancer

1. Hoarseness: precludes surgery
2. Supraclavicular LN (don't preclude surgery but may indicate bad outcome)
3. Ascites: may preclude Surgery if from lymphatic metastasis
4. Look for frequent Aspirations: as sign of TEF and precludes Surgery
5. Look for cervical esophageal cancer: mostly treated with Radiation Globally

Investigation
 Baseline
 Diagnostic:
1. Barium Esophagram:
A. Pre-Endoscopy
 It is performed in patients with the following:
o History/clinical features of proximal esophageal lesion (eg, surgery for
laryngeal or esophageal cancer, Zenker's diverticulum, or radiation therapy).
o Known complex (tortuous) stricture (eg, post-caustic injury or radiation
therapy)
 In these patients, the blind intubation of the proximal esophagus
during upper endoscopy may be associated with the risk of
perforation due to upper esophageal pathology
 It is a three-phase study assessing mucosa, contour, and function of the esophagus
P a g e 103 | 548
 o First phase: the double contrast phase, conducted
with the patient ingesting high density barium and
CO2 tablets in the upright position where the
mucosa is examined for strictures, ulcers or nodules.
 It is not commonly used in Ethiopia; early
mucosal changes are not common in
Ethiopian setting.
o Next, esophageal function is assessed in the right anterior oblique (RAO) position
with the ingestion of low-density barium in single swallows at 20- to 30-second
intervals. For example, patient with diffuse esophageal spasm, corkscrew
esophagus can be appreciated.
o The final phase, the full-column technique, is performed with the patient in a
semi prone RAO position and low-density barium. Multiple quick swallows
produce a column of barium that fully distends the esophagus. This optimizes
imaging of the distal esophagus and can demonstrate small hiatal hernias, subtle
strictures, or distal rings
B. Post-Endoscopy:
 To determine the underlying cause, exclude malignancy, and perform therapy (eg,
dilation of an esophageal ring) if needed.
2. Esophagoscopy: Esophagoscopy is used to
 Visually assess mucosal and structural
esophageal abnormalities.
 Take biopsies of epithelial abnormalities
(flexible fiberoptic esophagoscopy.)
 Perform endoscopic resection, either mucosal
resection (EMR) or submucosal dissection (ESD)
 Remove foreign body
 Dilate stricture
 Place endostents for inoperable carcinoma esophagus
 Inject sclerosants for varices
3. Endoscopic Esophageal Ultrasound (EUS): it is used to
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  Provide definition of the esophageal wall and
periesophageal tissue not possible to obtain with
routine fiberoptic esophagoscopy.
 Evaluate abnormalities of the esophageal wall
and diagnosing non mucosal esophageal tumors.
 For staging of esophageal cancer
 Probes, which can be passed through the biopsy channel of flexible endoscopes,
can evaluate esophageal strictures that prevent passage of standard ultrasound
equipment
 To take EUS-directed fine-needle aspiration (FNA)  provides cytologic and
pathologic assessment of esophageal tumors, periesophageal masses, and
regional lymph nodes
4. 24-Hour Esophageal Manometry: is indicated
 To establish the diagnosis of dysphagia when
obstruction and eosinophilic esophagitis
have been excluded
 For placement of intraluminal devices such
as a pH probe
 Before anti-reflux surgery; it is possibly
indicated for dysphagia after anti-reflux
surgery or therapy for achalasia
5. Chest X-ray
 To look for aspiration pneumonia
 To look for metastasis and pleural effusion
6. U/S abdomen
 To look for liver and lymph nodes status in abdomen
 To look for ascites
7. CT scan (95% accuracy)

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  To look for local extension, nodal status, periesophageal /diaphragmatic/
pericardial (1%)/ vascular infiltration, obliteration of mediastinal fat and status of
tracheobronchial tree in case of upper third growth
8. PET scan (using 18 F-fluorodeoxyglucose (FDG))
 Not commonly used
 It is functional study
 For staging
o It May down stage Tumors from Stage
III to IV in 20 % of Cases
o Better when used in PET CT; for the
anatomic description
 For treatment response
9. Video assisted thoracoscopic approach
 It can be used for staging

Important Findings in Barium Swallow

 Achalasia cardia‘Bird beak’ appearance; in long standing cases ‘sigmoid oesophagus’.

 DES  Corkscrew appearance.
 GORD shows reflux when done in Trendelen burg’s position.
 Esophageal carcinoma irregular stenosing lesion with shouldering (‘Rat tail’ is a fluoroscopic finding)
 External compression indentation of barium column by superior or posterior mediastinal mass, enlarged
left atria as in mitral stenosis

Differential Diagnosis
1. Esophageal Cancer
2. Gastroesophageal Reflex Disease (GERD)
3. Achalasia

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 Discussion of the Differentials

3.1.1 Esophageal Cancer

 Epidemiology………………………………………………..107
 Risk factors……………………………………………………108
 Clinical Manifestation………………………………….109
 Diagnosis……………………………………………………..110
 Staging………………………………………………………..111
 Management………………………………………………112
 Terminal events…………………………………………..113
 Prognosis………………………………………… …………..113

Epidemiology

"Esophageal cancer belt"  It is 6th most common cancer in the world.

 Highest-risk area, stretching  It is less than 1% of all cancers.

from Northern Iran through the  It is 7% of all GI malignancies.

central Asian republics to North-  In high incidence regions, SCC has no gender specificity

Central China but it is more common in men in low incidence regions

 90 % of cases are SCC  It is common in China, South Africa and Asian countries

 Major risk factors are thought to  It is less common in America and European countries.

include poor nutritional status,  Incidence rates for adenocarcinoma of the esophagus
low intake of fruits and have been increasing dramatically; in contrast, rates for
vegetables, and drinking SCC have been steadily decreasing.
beverages at high temperature.

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 Risk Factors

 Hereditary factors:
o Familial aggregation of esophageal cancer has been described in regions with a
high incidence of esophageal squamous cell carcinoma (SCC).
o Hereditary conditions that increase the risk of esophageal cancer:
 Peutz-Jeghers syndrome (PJS)
 Germline mutations in the PTEN tumor suppressor gene
 SCC:
o Geographic location
o Smoking
o Alcohol
o Dietary factors:

Drinking hot tea (60 to 64°C) or very  Pickled vegetables and other food-products consumed

hot tea (≥65°C), and drinking tea within in high-risk endemic areas that are rich in N-nitroso

three minutes of its being poured was compounds

significantly associated with an  High temperature beverages and foods may increase

increased risk of esophageal SCC the risk of esophageal cancer by causing thermal injury
to the esophageal mucosa
o The presence of specific preexisting esophageal diseases (such as achalasia and
caustic strictures)
 10 - 17 % life time risk of developing SCC proximal to Achalasia cardia
site  Follow up UGIE ever 5 years even if Achlasia is treated.
o Atrophic gastritis and other conditions that cause gastric atrophy are associated
with an approximately twofold increased risk of esophageal SCC (but not
adenocarcinoma)
o Prior gastrectomy
o HPV, particularly serotypes 16 and 18
o Use of oral bisphosphonates
o Current or past history of SCC of the head and neck (ie, oral cavity, oropharynx,
hypopharynx, or larynx)
o Poor oral hygiene particularly in areas where tobacco smoking and heavy alcohol
consumption are not major risk factors.
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 Adenocarcinoma:
o Gastroesophageal Reflux disease (GERD)  esophageal adenocarcinomas arise
from a region of Barrett's metaplasia.
o Smoking increases the risk of adenocarcinoma, particularly in patients with
Barrett's esophagus
o Obesity and metabolic syndrome
o Patients with acid hypersecretory states (such as Zollinger-Ellison syndrome) or
other conditions that are associated with gastroesophageal reflux (such as
surgical myotomy or balloon dilation of the lower esophageal sphincter or
scleroderma), may be at increased risk

Clinical Manifestations
 Early symptoms of esophageal cancer may be subtle and nonspecific.
o Transient "sticking" of meat, hard-boiled eggs, or bread, which can be easily
overcome by the patient with careful chewing, may precede frank dysphagia.
o Approximately 20 percent of patients experience odynophagia (painful
swallowing)
o Patients may also notice retrosternal discomfort or a burning sensation.
o The dysphagia gradually progresses from solids to liquids.
 Weight loss:
o Weight loss is mainly due to changes in diet to accommodate the dysphagia
o From tumor-related anorexia
 Less commonly:
o Regurgitation of saliva or food uncontaminated by gastric secretions can occur
 in patients with advanced disease.
o Hoarseness and/or cough  if the recurrent laryngeal nerve is invaded by either
the primary tumor or associated nodal metastasis
o Aspiration pneumonia
o Chronic gastrointestinal blood  may result in iron deficiency anemia (in 10%)

P a g e 109 | 548
  However, patients seldom notice melena, hematemesis, or blood in
regurgitated food.
 Similarly, acute upper gastrointestinal bleeding is rare and is a result of
tumor erosion into the aorta or pulmonary or bronchial arteries.
o Tracheobronchial fistulas  direct invasion of the mainstem bronchus
 Late complication of esophageal cancer.
 Life expectancy is less than four weeks following the development of
this complication.
o Patients may present with signs or symptoms referable to distant metastatic
disease.
 The most common sites of distant metastases in patients with
esophageal cancer are the liver, lungs, bone, and adrenal glands
 Adenocarcinomas most frequently metastasize to intraabdominal sites
(liver, peritoneum), while metastases from SCCs are usually
intrathoracic.

Definitive Diagnosis
The diagnosis of esophageal cancer requires a histologic examination of tumor tissue
 Biopsy:
o Endoscopic: early esophageal cancers appear as superficial plaques, nodules, or
ulcerations while advanced lesions appear as strictures, ulcerated masses,
circumferential masses or large ulcerations
o Endoscopic resection: if the tumor has a diameter of ≤2 cm, if it involves less
than one-third of the circumference of the esophageal wall and if it is limited to
the mucosa of the esophagus

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 Staging

 Accurate clinical staging of both local tumor extent and the presence or absence of
distant metastases is critical for estimating prognosis and selecting the appropriate
treatment strategy.
 Locoregional Staging:
o Endoscopic ultrasound (EUS) is the preferred method for locoregional staging
 Evaluation of distant metastasis:
o Contrast-enhanced computed tomography (CT) of the neck, chest, and abdomen
o Positron emission tomography (PET)/CT
 Then the TNM staging system is used universally.

Table 3.2: Esophagus and esophagogastric junction cancers TNM staging AJCC UICC 2017
Primary Tumor (T)
T category T criteria
TX  Tumor cannot be assessed
T0  No evidence of primary tumor
Tis  High-grade dysplasia, defined as malignant cells confined to the epithelium
by the basement membrane
T1  Tumor invades the lamina propria, muscularis mucosae, or submucosa
T1a  Tumor invades the lamina propria or muscularis mucosae
T1b  Tumor invades the submucosa
T2  Tumor invades the muscularis propria
T3  Tumor invades adventitia
T4  Tumor invades adjacent structures
T4a  Tumor invades the pleura, pericardium, azygos vein, diaphragm, or
peritoneum
T4b  Tumor invades other adjacent structures, such as the aorta, vertebral body,
or airway
Regional lymph nodes (N)
N category N criteria

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NX  Regional lymph nodes cannot be assessed
N0  No regional lymph node metastasis
N1  Metastasis in one or two regional lymph nodes
N2  Metastasis in three to six regional lymph nodes
N3  Metastasis in seven or more regional lymph nodes
Distant metastasis (M)
M category M criteria
M0  No distant metastasis
M1  Distant metastasis
Prognostic stage groups
T N M Stage group
Tis N0 M0 0
T1 N0-1 M0 I
T2 N0-1 M0 II
T3 N0 M0 II
T3 N1 M0 III
T1-3 N2 M0 III
T4 N0-2 M0 IVA
Any T N3 M0 IVA
Any T Any N M1 IVB

Management
 Early presentation: only in 20% of the cases, curative surgery can be done
o Radical esophagectomy (Proximal extent of resection  10 cm above the
macroscopic tumor and distal is 5 cm from macroscopic distal end of tumor.
Proximal stomach has to be removed commonly with sufficient removal of
contiguous structures)
o LN involvement  Curative resection + radiotherapy + chemotherapy

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 Remaining patients (80%)  Palliation is done:
o If patient is not fit for major surgery
o If there is blood spread
o If there is spread to adjacent organ
o If there is peritoneal/liver spread.
o To relieve pain and dysphagia
o To prevent aspiration and bleeding
 Palliation procedures:
o External or intraluminal RT (Brachytherapy)
o Traction tubes through open surgery
o Pulsion tubes through endoscopes
o Endoscopic laser
o Chemotherapy
o Trans hiatal esophagectomy

Terminal Events and Prognosis of Esophageal Cancer

Terminal Events:
 Cancer cachexia  Immunosuppression
 Sepsis  Tracheo-esophageal fistula
 Mediastinitis
 Bleeding  from erosion into major blood vessel

Prognosis:
 Not good (5-year survival rate is only 10%) because of:
o Early spread o Aggressiveness
o Longitudinal lymphatics o Difficult to approach
o Late presentation.
o Nodal involvement carries bad prognosis

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 3.1.2 Achalasia
 Epidemiology………………………………………….................114
 Etiology…………………………………………............ …………..114
 Clinical Manifestation……………………………………………..114
 Diagnosis………………………………………….......................115
 Management………………………………………….................116

Epidemiology

 Uncommon disorder
 It has an annual incidence of approximately 1.6 cases per 100,000 individuals and
prevalence of 10 cases per 100,000 individuals.
 Men and women are affected with equal frequency.
 Is common between the ages of 25 and 60 years, but can occur at any age.

Etiology
 Idiopathic: This occurs due to absence or degeneration of Auerbach's plexus
throughout the body of the esophagus leading to improper integration of the
parasympathetic impulse.
 Acquired variety is seen in South American countries caused by Trypanosoma cruzi
Chaga’s disease. This organism destroys the ganglion cell of Auerbach’s plexus.
 Stress and emotional factors.
 Vitamin deficiencies are also associated with this disease.

Clinical Manifestations
 The classic triad of presenting symptoms consists of dysphagia, regurgitation, and
weight loss.

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 o However, heartburn, postprandial choking, and nocturnal coughing are also
seen commonly.
 The dysphagia that patients experience begins with liquids and progresses to solids.
 The dysphagia progresses slowly over years and patients adapt their lifestyle to
accommodate the inconveniences that accompany this disease.
 Patients often do not seek medical attention until their symptoms are quite
advanced  will present with marked distension of the esophagus.
 Regurgitation is frequent, and there may be overspill into the trachea, especially at
night.
 It is also known to be a premalignant condition of the esophagus.

Diagnosis
 Esophagram
o Shows dilated esophagus
with a distal narrowing
referred to as the classic
“bird's beak” or “rat tail”
appearance of the barium-
filled esophagus.
o The gastric gas bubble is
usually absent.
o It is not a sensitive test for
achalasia, as it may be
interpreted as normal in up
to one-third of patients
 Manometry
o It is the gold standard test; the manometry tracings show five classic findings:
 The LES will be hypertensive with pressures usually above 35 mm Hg.
 The LES fails to relax with deglutition.
 The body of the esophagus will have a pressure above baseline.

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  The body will also have simultaneous mirrored contractions with no
evidence of progressive peristalsis
 Low-amplitude waveforms indicating a lack of muscular tone.
 Endoscopy
o Is performed to evaluate the mucosa for evidence of esophagitis or cancer.
o Little contribution to the diagnosis of achalasia.

Management
 Is directed towards relieving the obstruction caused by the LES, however, all are
palliative treatments and can’t reverse the degeneration of ganglion cells.
 It can be accomplished by:
o Mechanical disruption of the muscle fibers of the LES:
 Pneumatic dilatation:
 Involves stretching the cardia with a balloon
 Over four to six years, nearly one-third of patients have
symptom relapse and require retreatment.
 Perforation is the major complication.
 Modified Heller’s cardiomyotomy:
 Includes only anterior myotomy with laparoscopic approach in
preference.
 Usually a partial fundoplication is added to reduce the risk of
gastro-esophageal reflux.
o Pharmacological reduction in LES pressure:
 Injection of botulinum toxin:
 It acts by interfering with cholinergic excitatory neuronal
activity at LES.
 The effect is not permanent.
 Oral nitrates or calcium channel blockers:
 Are ineffective for long-term use.

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3.1. 3. Gastro-Esophageal Reflex Disease (GERD)

 Risk Factors……………………………………………………….…117
 Clinical Manifestation…………………………………………..118
 Diagnosis……………………………………………………………..118
 Management……………………………………………………….119

Risk Factors
 It is due to varied anatomical and physiological factors.
 Anatomical Factors:
o Obesity
o Altered length of intra-abdominal esophagus.
o Alteration of phreno-esophageal ligament.
o Altered obliquity of E-G junction.
o Reduced pinching action of right crus of diaphragm.
o Alteration in normal mucosal rosette at E-G junction.
o Alteration in sling mechanism of gastric musculature.
 Physiological Factors:
o Reduced LES pressure. Resting pressure is decreased by secretin,
cholecystokinin, glucagon, calcium channel blockers, coffee, fatty meal.
o Altered transient relaxation period in LOS.
o Reduced esophageal clearance mechanism.
o Delayed gastric emptying due to diabetes, neuromuscular block, gastroparesis,
and medications.
o Increased gastric distension and gastric acid hyper secretion.
 Others
o Alcohol, smoking, stress, lifestyle

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 Clinical Manifestation

 Classic symptoms are heartburn (pyrosis) and regurgitation.

o Heartburn is confined to the epigastric and retrosternal areas. It is identified as
a caustic or stinging sensation. It does not radiate to the back and is not
characteristically described as a pressure sensation.
 Other symptoms of GERD include:
o Dysphagia: is common in the setting of longstanding heartburn and is often
attributable to reflux esophagitis but can be indicative of an esophageal
stricture. However, tumor, diverticula, and motor disorders need to be
excluded.
o Odynophagia: is an unusual symptom of GERD but, when present, usually
indicates an esophageal ulcer.
o GERD-related chest pain: can mimic angina pectoris, and is typically described
as squeezing or burning, located substernally and radiating to the back, neck,
jaw, or arms. The pain can last anywhere from minutes to hours, and resolve
either spontaneously or with antacids. It usually occurs after meals, awakens
patients from sleep, and may be exacerbated by emotional stress.
o Water brash or hypersalivation: is a relatively unusual symptom in which
patients can foam at the mouth.
o Globus sensation: is the almost constant perception of a lump in the throat
(irrespective of swallowing).
o Infrequently nausea
o Extraesophageal symptoms: like chronic cough, hoarseness, and wheezing

Diagnosis
 Diagnosis can be based on symptoms alone in patients with the classic symptoms.
 Patients may require additional evaluation if they have alarm features (like: new
onset of dyspepsia in a patient older than 60, anorexia, unexplained weight loss,
dysphagia, evidence of GI bleeding), risk factors for Barrette’s esophagus or
abnormal gastrointestinal imaging performed for evaluation of their symptoms.
 In patients without the classic symptoms other disorders must be excluded.

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 o Barium swallow in trendelenburg’s position can demonstrate the reverse flow
of barium in to the lower end of the esophagus.
o Endoscopy to exclude other diseases and to assess any mucosal injury.
o Mucosal biopsy to confirm metaplastic transformation.
o Esophageal manometry is used to assess the function of LES.
o 24 hours esophageal pH monitoring is the gold standard. PPI should be
stopped for 3 weeks prior to pH monitoring.

Management
 Life style changes
o Stop smoking and excessive consumption of alcohol.
o Avoid tea, coffee and chocolate.
o A modest degree of head-up tilt of the bed.
o Small frequent meals and avoidance of constricting clothing.
 Medical management
o In a patient whose history and examination are consistent with GERD. It would
be prudent to check for chronic anemia and to prescribe a 6-week course of
acid suppression therapy.
o Double dose of a proton pump inhibitor is the initial approach to medical
management. If the symptoms persist after a trial of medical therapy, a more
extensive evaluation would be indicated.
o The medications available to treat acid reflux include antacids, motility agents,
histamine-2 (H2) blockers, and proton pump inhibitors.
 Surgical treatment indications:
o Failed medical management and noncompliance with medical therapy
o Severe esophagitis and benign stricture
o Barrett's columnar-lined epithelium (without severe dysplasia or carcinoma)
o Upper respiratory symptoms including hoarseness, laryngitis, wheezing,
nocturnal asthma, cough, aspiration, or dental erosion
 Preoperative evaluation

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  Upper endoscopy, esophageal manometry, and assessment of esophageal
length and degree of hiatal herniation are the most useful tests in making
surgical decisions
Procedures
o Hill’s posterior gastropexy
 Intra-abdominal fixation of OG junction (cardia) into median arcuate
ligament to augment the effect of LOS, to enable the effective esophageal
peristalsis.
 Modified Hill’s uses the preaortic fascia and the condensation of the crus as
the anchor for the repair.
 Fewer side effects than fundoplication.
o Fundoplication
 Mobilize the lower esophagus and wrap the fundus of the stomach around it
either totally or partially.
 Most of the antireflux operations are now done a laparascopic approach.
 Total Fundoplication
 360° fundal wrap around the distal esophagus with division of the
short gastric vessels (“floppy”).
 Tends to be associated with slightly more short-term dysphagia but is
the most durable repair in terms of long-term reflux control.
 It also creates an over competent cardia, resulting in the gas bloat
syndrome where the stomach feels with air and the patient feels very
full after small meals and pass excessive flatus. It has been overcome
with the floppy Nissen technique in which the fundoplication is loose
around the esophagus and is kept short in length.
 Partial Fundopliction
 Whether performed posteriorly (Toupet) or anteriorly (Dor, Watson),
has fewer short-term side effects, although this is sometimes at the
expense of a slightly higher long-term failure rate. (does not cause gas
bloat syndrome)

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 3.2 Chest Trauma

 Case Discussion……………………………….121
 Introduction……………………………………121
 History …………………………………………..122
 Physical Examination………………………124
 Investigation…………………………………..125
 Differential Diagnosis……………….…….127
 Discussion of the differentials…………128

Case Discussion

 A 24-year-old male patient presents to the emergency after he sustained a stab injury to
the back. Prior to his admission, he had profuse bleeding and lost consciousness as a
result. Upon arrival, he was unresponsive and tachycardic. After he gained consciousness
he noticed shortness of breath that is worsened by sleeping on the right side and relieved
when intranasal oxygen was supplied; and a severe type of stabbing chest pain. Physical
examination revealed pale conjunctivae, signs of fluid collection in the lower 2/3rd of his
left lung field, pressure bandages covering the stab wound posteriorly and chest tube
inserted in the left anterio-lateral chest

Introduction

 Thoracic injury is common in poly-trauma patients and can be life-threatening,

especially if not promptly identified and treated during the primary survey.
 It can be any type of trauma but mechanical is the commonest and hence discussed
here.

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 Mechanisms that provide the amount of energy needed to produce significant blunt
thoracic trauma are associated with head, abdominal, or extremity injuries  should
be ruled out in the history.
 Types: blunt/penetrating
o Blunt trauma: includes high-speed deceleration injury, crush injuries, falling
down accidents, assaults, sports mishaps, and blast injuries
o Penetrating:
 High velocity: Bullet injuries
 Low velocity: Stab injuries

History
 Elaborate the symptoms that follow the injury: the commonest symptoms patients
experience after chest injury are
o Shortness of breath
o Chest pain: pleuritic (aggravated by taking deep breath or coughing)
o Loss of consciousness following a profuse bleeding: check the table below
 Ask about the mechanism of injury, elaborate the type of the trauma the patient
sustains:
o For bullet injury: ask if the patient remembers the type of gun used, if they
can estimate the distance from the shooter, precisely where they were shot
and the number of times they were shot.
o For stab injury: ask if the patient remembers they type of material, where
they stabbed precisely (to anticipate the type of organ damage), and how
many times they were stabbed.
 Ask for any associated symptoms
o Tachypnea, tachycardia, hypotension, tracheal deviation away from the side
of the injury, neck vein distention  tension pneumothorax
o Fever
o Palpitations, lightheadedness and easy fatigue

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 o Swelling of the face of the upper torso and extremity  subcutaneous
emphysema
o Coughing up of blood or change in voice (hoarseness)
o Pain during swallowing, inability to swallow or vomiting up of blood
o Bluish discoloration of the lips or fingers or cold extremities
o Extremity weakness, pain/numbness/tingling sensation, urinary or bowel
incontinence  Spinal cord injury
 Assess any risk factors
o Ask history of alcohol consumption
o Known Seizure disorders
 Care before referral
o Blood transfusion
o Wound care
o The type of medications given and if chest tube was inserted

Table 3.3: Classification/Stages of Hypovolemic Shock

Stage 1 Stage 2 Stage 3 Stage 4
Blood
loss

<15% 15-30% 30-40% >40%

pressure

Normal (Maintained
Blood

Increased diastolic BP Systolic BP < 100 Systolic BP < 70

by vasoconstriction)

Extreme tachycardia
Heart rate

Slight tachycardia (> Tachycardia

Normal (>140bpm) with weak
100bpm) (> 120bpm)
pulse
Respiratory rate

Normal Increased (> 20) Tachypneic (> 30) Extreme tachypnea

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Mental

Slight anxiety, Decreased LOC,

status

Normal Altered, confused

restless lethargy, coma
Extreme diaphoresis;
Skin

Pallor Pale, cool, clammy Increased diaphoresis

mottling possible
Capillary
Refill

Normal Delayed (>2 sec) Delayed (>2 sec) Absent

Output
Urine

Normal 20–30mL/hr 20ml/hr Negligible

Physical Examination

 General appearance:
o Check if the patient is acutely sick looking: in respiratory distress (check for
oxygen line) or well looking
 Vital sign:
o Temperature: febrile if infected
o Respiratory rate: tachypneic  if the patient develops tension pneumothorax
o Pulse rate: tachycardic  if the patient develops tension pneumothorax
o Blood pressure: hypotensive  if the patient is in shock
o Oxygen Saturation:
 HEENT:
o Head: check if there is an associated head trauma (particularly in a poly
trauma patient)
o Eyes: look for conjunctival pallor
o Mouth and lips: look for cyanosis and dry buccal mucosa
 Respiratory system:
o Inspection: check if there is a reduced chest movement in one side,
intercostals or sub costal retractions or use of accessory muscles of
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 respiration, a chest tube inserted (refer to the short case discussion section
on how to report)
o Palpation: feel if the trachea is central, if tactile fremitus is normal and
comparable and if there is any tenderness
o Percussion: look for dullness or hyper resonance
o Auscultation: check if the breath sounds are vesicular or not and if well heard,
reduced or absent; if there are added sounds or vocal resonances; if bowel
sounds were heard in the lower chest area (diaphragmatic injury).
 Cardiovascular system:
o Veins: reduced venous pressure in the jugular veins
o Hypotension and distended veins at the same time is a near confirmatory
sign of Obstructive Shock
 Abdominal:
o Look for associated abdominal trauma (particularly in a poly trauma patient)
 Integumentary system:
o There might be reduced skin turgor if the patient is in shock
o Check if there are pressure bandages covering the injury site if so focus on the
wound care and describe the lesion underneath the bandages.
 Neurologic examination:
o Detailed examination  particularly if spinal cord injury is suspected due to
trauma to the back
o Check for the tone, power, sensation and sphincter tone.

Investigation
 Do not send unstable patients for investigation.
 If there is a need two doctors and a nurse should accompany the patient with
necessary resource at hand and get prepared to do CPR any time

1. Chest Radiography
 First line diagnostic modality

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  A systematic review of the film should reveal suspected and unsuspected injures.
 It is helpful to:
o Rule out the presence of any foreign bodies.
o Rule out fractures of the bony thorax, including the ribs, clavicles, spine,
and scapulae because fractures of the thoracic cage indicate significant
energy transfer to the patient;
 Those of the upper ribs  trauma to the great vessels
 Those of the clavicle  pulmonary or cardiac contusions.
o Examine the lung fields for:
 Pneumothorax  Pulmonary
 Hemothorax contusion
o Check for mediastinal widening, pneumomediastinum, or shifting:
 Highly suggestive of aortic transection, tracheobronchial or
esophageal injuries, or tension pneumothorax or hemothorax.
o To examine the soft tissues for subtle subcutaneous air or foreign bodies.
o To check for the width of the cardiac silhouette
 Raised suggests tamponade.
2. Chest CT:
 It is not essential for every patient with chest trauma and should not be
performed in the severely hemodynamically unstable patient or in the presence
of obvious life-threatening injuries.
 However, it may reveal injuries not seen clearly on plain radiographs such as:
o Diaphragmatic injuries o Pneumothorax
o Pulmonary contusions o Pneumomediastinum
o Aortic disruption o Hemothorax
 It can also be used to exclude diagnoses made by the less sensitive chest
radiograph

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 3. Ultrasonography:
 E-FAST: extended focused assessment for the sonographic evaluation of the
trauma patient
 Uses an extension of the right and left upper quadrant views to include the right
and left hemithoraces
o Aid in the diagnosis of hemothorax or pneumothorax
4. 12 lead ECG
5. Echocardiography
 Diagnostic tool for detecting injuries, wall motion abnormalities, effusions,
valvular or septal defects, and particularly chamber rupture.
 This should be performed in all patients with an abnormal ECG or who are
hemodynamically unstable
6. CT Angiography
 More sensitive than echocardiography in the diagnosis of aortic and great vessel
injuries: gold standard

Differential Diagnosis

Table 3.4: Differentials for Chest trauma

Blunt Trauma: Penetrating trauma
1. Chest Wall Trauma: 1. Chest wall injury
 Rib Fracture 2. Tracheal/bronchial injuries
 Flail Chest 3. Pulmonary injuries
 Sternal Fracture  Hemothorax
 Clavicular Fracture  Pneumothorax
 Scapular Fracture  Hemopneumothorax
2. Traumatic Asphyxia 4. Cardiac injuries
3. Pulmonary Contusion 5. Air embolism
4. Laryngeal injuries 6. Diaphragmatic injury
5. Tracheobronchial injuries 7. Esophageal injury
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6. Great vessel injuries
7. Blunt Cardiac injuries
8. Diaphragmatic injury
9. Esophageal injury

 Indicators of significant energy transfer; and hence, increased mortality and

morbidity risk are
o First and or second rib fracture
o Scapular fracture
o 11th and 12th rib fracture
o Multiple rib Fracture
o Flail Chest
o Concomitant Head and Abdominal Injury
o Age > 60

Discussion of the Differentials

3.2.1 Pneumothorax

 Introduction…………………………….129
 Clinical Manifestation………………129
 Investigation……………………………129
 Management…………………………..129

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 Introduction

 It is a collection of air in the pleural space.

 It is a common complication of blunt trauma  often sustained from a fractured rib
 It can be: simple, open or tension

Clinical Manifestation

 Patients may present with

o Tachypnea
o Chest pain
o Diminished or absent breath sounds
o Hyper-resonance to percussion

Investigation
 The supine chest radiograph has high specificity for diagnosing a pneumothorax but
its sensitivity is variable.
 Ultrasound may be a more sensitive initial screening tool
 For patients with a risk for pneumothorax (has a history of pleuritic pain, dyspnea
and rib fracture revealed on examination) whose initial radiograph does not reveal
a pneumothorax, repeat the radiograph in six hours.

Management
 Simple Pneumothorax: refer to the chest tube section under short case discussion
 Tension Pneumothorax: refer to the needle thoracostomy section under short case
discussion
 Open Pneumothorax:

o For initial management of an open

pneumothorax, promptly close the
defect with a sterile dressing large
enough to overlap the wound’s edges. P a g e 129 | 548
 o Any occlusive dressing (e.g. plastic wrap or petrolatum gauze) may be used
as temporary measure to enable rapid assessment to continue.
 One can use surgical gloves splint in half
o Tape it securely on only three sides to provide a flutter-valve effect
o As the patient breathes in, the dressing occludes the wound, preventing air
from entering.
o During exhalation, the open end of the dressing allows air to escape from the
pleural space
o Place a chest tube remote from the wound as soon as possible

3.2.2 Hemothorax

 Introduction………………………………………..130
 Clinical Manifestation………………………….131
 Investigation………………………………………..131
 Management……………………………………….132

Introduction

 It is a collection of blood in the pleural

space
 It is said to be massive if accumulation
of blood in one side is >1500ml.
 Commonest source of bleeding is from:
o Intercostal arteries

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 o Internal mammary arteries
o Lacerated lung
 Injuries leading to massive hemothorax include:
o Aortic rupture o Injury to hilar structures
o Myocardial rupture

Clinical Manifestation
 Typical signs and symptoms include:
o Shortness of breath o Reduced tactile fremitus
o Pleuritic type of chest pain o Dull to percussion
o Bulged chest wall o Absent breath sounds
o Reduced chest expansion
o Signs and symptoms of shock might also occur depending on the degree of
hemorrhage (refer Table 3.3).

Table 3.5: Differentiating Massive Hemothorax from Tension Pneumothorax

Physical Signs Tension Pneumothorax Massive Hemothorax
 Neck Veins  Distended  Collapsed
 Chest Movement  Expanded Immobile  Reduced
 Tracheal Position  Deviated away  Usually midline
 Breath sounds  Mostly absent  Reduced
 Percussion Note  Hyper resonant  Dull

Investigation

 A volume of 300 mL (may be as low as 200 ml in Current Digital X-ray) is needed

for hemothorax to manifest on an upright CXR.
 Ultrasound can detect effusion as low us 50ml.

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 Management

 Hemothorax is treated with tube thoracostomy using a large (minimum 36 French)

chest tube.
 Indication for surgical thoracotomy
o Immediate bloody drainage of ≥20 mL/kg (approximately 1500 mL) is
generally considered an.
 Drainage of 1500 ml of blood after 24 hours of the incident is not an
indication for surgery  This is most likely accumulated over time
and in particular in patients appearing stable and with Stable V/S
o Shock and persistent, substantial bleeding  Refer to the short case
(generally >3 mL/kg/hour for consecutive 3- 4 discussion section
hours) are additional indications.

3.2.3. Pulmonary Contusion

 Introduction……………………………………………….132
 Clinical Manifestation………………………………...133
 Investigation………………………………………………133
 Management……………………………………………..134

Introduction

 Pulmonary contusion is defined as pulmonary parenchymal damage with

edema and hemorrhage, in the absence of an associated laceration of a
large pulmonary vessel
 It is another common consequence of blunt chest trauma.
P a g e 132 | 548
 It is a major contributor of mortality after thoracic injury
 It generally develops over the first 24 hours and resolve in about one
week.
 Generally associated with concomitant thoracic cage damage and other
visceral injuries, but can occur isolated without evidence of rib fracture.

Clinical Manifestation
 Classic symptoms include:
o Dyspnea o Cyanosis
o Tachypnea o Hypotension
o Hemoptysis
 Physical examination can demonstrate
o Inspiratory rales
o Decreased breath sounds on the affected side

Investigation
 Chest radiograph:
o Irregular, non-lobular opacification of the pulmonary parenchyma on chest
radiograph is the diagnostic hallmark.
o About one-third of the time the contusion is not evident on initial
radiographs
 Do chest CT
 Chest CT:
o CT scan is the study of choice; it is more sensitive than radiography in
detecting a pulmonary contusion
o Contusions evident on CT but not plain CXR have better outcomes

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 Management

 All patients with a pulmonary contusion should be observed on supplementary

oxygen in a hospital setting
o Because of a tendency of their ventilatory status to deteriorate rapidly.
 Pain control and pulmonary toilet are the mainstays of treatment.
 Prophylactic endotracheal intubation is unnecessary
o But patients with hypoxia or difficulty ventilating require airway
management.
o By standard ATLS protocol, patients with significant hypoxia with PaO2 less
than 65 mm Hg and SaO2 less than 90% despite oxygen supplementation
should be intubated and undergo ventilation within 1 hour after injury
 While opinions vary, fluid resuscitation with crystalloid to euvolemia appears
appropriate (don’t pump too much fluid)
 Common complications are:
o Pneumonia
o Acute respiratory distress syndrome (ARDS)

3.3. Mediastinal Tumors

 Case Discussion………………………………..135
 Introduction…………………………………….135
 History ……………………………………………136
 Physical Examination……………………….137
 Investigation……………………………………138
 Differential Diagnosis………………………140
 Discussion of the Differentials………….141

P a g e 134 | 548
 Case Discussion

 A 20-year-old man with no significant past medical history presented to his primary care
physician for chest discomfort and cough. Two months prior to presentation, he reported
having an unremarkable viral syndrome which resolved with no medical intervention. His
primary care physician prescribed a short course of antibiotics for empiric treatment of
pneumonia with some initial improvement in symptoms. His chest discomfort returned
and he developed progressive dyspnea on exertion. Physical examination was
unremarkable. Imaging studies reveal left-sided mediastinal mass on chest x-ray and a
rounded, well-demarcated mass in the superoanterior mediastinal compartment on CT.

Introduction
 A mediastinal mass can be an incidental finding in patients who undergo plain chest
radiography or advanced imaging studies, such as CT or MRI.
 Symptoms, if present, may be due to direct mass effect of the mediastinal anomaly
or to systemic effects of the illness.
 In general, malignant lesions are more likely to be symptomatic

Table 3.6: The three compartments of the mediastinum

Anterior Compartment Middle Compartment Posterior Compartment:
 It is found anterior to pericardium  It is bounded by:  It extends from the posterior
 It includes:  The pericardium anteriorly pericardial reflection to the
 Extra pericardial aorta and  The posterior pericardial posterior border of the
its branches reflection vertebral bodies and from the
 The great veins  The diaphragm first rib to the diaphragm
 The thoracic inlet  Accoring to the current
 Remember the 4 Ts
 It includes: classification by Shields from
 Thymic Origin
 Trachea and esophagus 1970s onwards just the Spine
 Terrible Lymphoma
 The Pericardium and heart and para spinal space are
 Teratoma
 Intrapericardial great considered posterior
 Thyroid (retrosternal goiter)
vessels mediastinum

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 History

 Identification: Age
o In infants and children: neurogenic tumors and enterogenous cysts are the
most common mediastinal masses
o In adults: neurogenic tumors, thymomas, and thymic cysts are most
frequently encountered lesions
 Commonest complaints: because of the mass effect are:
o Cough o Hemoptysis
o Stridor o Shortness of breath
o In children: respiratory difficulty and recurrent pulmonary infection 
mostly symptomatic
o Pain
 Dull aching pain: commonly
 Severe pain is typically a sign of advanced invasive disease
o Dysphagia  esophageal compression
o Hoarseness  Recurrent laryngeal nerve involvement
o Vascular compression: Superior vena cava
 Facial, neck and upper extremity swelling
 Dyspnea
 Chest pain, upper extremity pain
 Mental status changes
o Hypotension  Tamponade physiology or cardiac compression
o Horner syndrome (Ptosis, miosis, anhidrosis)  Sympathetic ganglion
involvement
o Weakness or paralysis  involvement of the spinal cord
 Elaborate the chief compliant
o Ask the progression of the symptom: slow growth over the course of years
(eg, thymoma in some patients) or rapid expansion (eg, lymphoma)
 Ask if there are any systemic effects:
o Fever, night sweats, and weight loss can be present in the case of
lymphoma

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 o Could also be due to a variety of paraneoplastic syndromes, such as
myasthenia gravis with thymoma.
o Symptoms of thyrotoxicosis
o Symptoms of hyperparathyroidism
 Ask associated symptoms
o Abnormalities in other parts of the body (eg, testicular masses with germ
cell tumors)
o Others are mentioned in the discussion of the differential diagnosis
section below

Physical Examination
 Look for the signs of paraneoplastic syndromes like
o Myasthenia gravis o Hyperparathyroidism.
o Thyrotoxicosis
 Assess metastatic sites in case of thymic cancer (mentioned in the discussion of the
differentials section)
 Besides check:
o General appearance: chronically sick looking in cases of carcinomas
o Vital sign: patients can be febrile or tachycardic
o Lympho glandular system: Check for lymphadenopathy, look for neck masses,
do scrotal examination in males
o Respiratory system: tracheal deviation due to mass effect, signs of pleural
effusion (metastasis)
o SVC obstruction Syndrome:
o Engorged neck veins and Puffy face
o These patients need early intervention either by chemo,
radiation or surgery

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 Investigation

a. Lab studies:
 If there are systemic symptoms:
o Thyroid function test
o Calcium, phosphate and PTH
 For thymic tumors:
o Anti-acetylcholine receptor antibodies  may be positive in some
patients and indicate presence of myasthenia gravis.
 If paraganglionic tumor suspected:
o Fractionated 24-hour urinary metanephrines and catecholamines
 If non-seminomatous germ cell tumor is suspected:
o Alpha-fetoprotein (AFP)  elevated levels of AFP (malignant)
 Specifically, 60 to 80 % of dysembryomas are serum AFP positive.
o Beta-human chorionic gonadotropin (beta-hCG) is associated with
seminoma (10 percent) and non-seminomatous (30 to 50 percent) germ
cell tumors.
 Lactate dehydrogenase (LDH):
o May be elevated in patients with non-seminomatous dysembryoma
o Generally, not as specific as AFP or beta-hCG
o May also be elevated in patients with lymphoma.
b. Imaging studies:
 Chest X-ray
 Chest CT:
o CT with contrast is typically used to evaluate abnormalities seen on plain
radiographs and to:
 Confirm the presence of a mediastinal mass
 Provide detailed information regarding the mediastinal
abnormality including its location, size or relationship to other
structures
 Check tissue characteristics, including presence of fat, fluid, or
calcifications (eg, teratoma)

P a g e 138 | 548
 o Careful on giving Iodinated contrast for Thyroid Origin tumors as it may
convert Subclinical thyrotoxicosis to overt.
 Chest and/or cardiac gated magnetic resonance (MR) imaging:
o Useful in distinguishing compression versus invasion where this distinction
can be difficult on CT
o For example: particularly in cases of large anterior mediastinal masses
 Positron emission tomography (PET):
o For a mediastinal mass that is suspected to be a lymphoma
o To identify a preferred biopsy site
o To monitor response to treatment
o There can be false positive results for nonmalignant conditions such as
teratoma and thymic cysts
 Spine MRI:
o To provide a detailed evaluation of posterior mediastinal masses adjacent
to the spine.
o MR is better than CT for determining whether a mass extends into the
neural foramina or spinal canal, which is important for surgical planning
 Tissue Diagnosis: biopsy
o Percutaneous  Both anterior and posterior mediastinal masses can often
be biopsied under CT guidance
o Endobronchial — Endobronchial biopsy (EBUS) is reasonable to consider
when the mediastinal mass is located immediately adjacent to an airway.
o Surgical
 When percutaneous or endobronchial biopsy is not possible or
cannot provide adequate tissue to definitively establish a
diagnosis, surgical biopsy may be necessary.
 It is known as Chamberlain's Incision

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 Differential Diagnosis

1. Thymoma
2. Bronchogenic cyst
3. Neurogenic tumors

 Other differentials for each compartment are mentioned in the table below

Table 3.7: Differential Diagnosis for Mediastinal Masses

Anterior Compartment Middle Compartment Posterior Compartment
 Thymus:  Bronchogenic cyst  Neurogenic tumors:
o Thymoma o Neurofibroma
o Thymic cyst o Neurosarcoma
o Thymic hyperplasia o Ganglioneuroma
o Thymic carcinoma o Ganglioneuroblastoma
o Neuroblastoma
o Pheochromocytoma
 Lymphoma  Pericardial cyst  Meningoceles
Germ cell tumor: Lymphadenopathy: Thoracic spine lesions
 Teratoma/dermoid cyst  Lymphoma  Pott's disease)
 Seminoma  Sarcoid
 Non-seminoma  Metastatic lung cancer
o Yolk sac tumor
o Embryonal carcinoma
o Choriocarcinoma
 Intrathoracic thyroid  Enteric cys
o Substernal goiter
o Ectopic thyroid tissue
 Parathyroid adenoma  Esophageal tumors

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 Discussion of the Differentials

3.3.1 Thymoma

 Introduction……………………………………..…………….141
 Epidemiology…………………………………..……………..141
 Clinical Manifestation………………………………….....142
 Diagnosis………………………………………..………………142
 Management………………………………………………....142

Introduction
 Clinically present as one of the three:
o An incidental finding identified on imaging in an asymptomatic patient
o Because of local (thoracic) symptoms  mass effect
o Due to symptoms from a paraneoplastic syndrome
 Metastasis of thymic carcinoma is commonly to:
o Kidney o Adrenals
o Extrathoracic LNs o Thyroid
o Liver o Bone
o Brain

Epidemiology
 Thymic tumors are rare neoplasms that arise in the anterior mediastinum
 In adults, thymomas and thymic carcinomas are the most common neoplasms
arising in the thymus.
 Thymomas account for about 20 percent of mediastinal neoplasm
 Most thymoma patients are between 40 and 60 years of age, and there is a similar
incidence in men and women

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 Clinical Manifestation

 Thoracic symptoms:
o Chest pain
o Shortness of breath
o Cough
o Phrenic nerve palsy
o Superior vena cava syndrome
o Pleural or pericardial effusions are the most common manifestation of more
disseminated disease
 Paraneoplastic syndrome:
o The most common paraneoplastic syndrome is myasthenia gravis
o Rarely:
 Addison's disease, Cushing syndrome, panhypopituitarism, thyroiditis
 Agranulocytosis and hemolytic anemia
 Alopecia areata, pemphigus or scleroderma

Diagnosis

 Imaging studies
 Definitive diagnosis of a thymoma or thymic carcinoma requires a tissue diagnosis

Management

 Resectable disease:
o Those with completely encapsulated tumors
o Those with tumors invading readily resectable structures:
 Mediastinal pleura
 Pericardium
 Adjacent lung
o Surgery is indicated as the initial treatment for such patients.
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 o Patients should be evaluated for evidence of myasthenia gravis
 If signs or symptoms are present  Should be treated medically prior
to surgery
 Potentially resectable disease
o For patients in whom a complete resection is not considered feasible as the
initial treatment, those with tumor invasion into:
 The innominate vein
 Phrenic nerve(s)
 Heart/great vessels
o Multimodality therapy incorporating preoperative chemotherapy and
postoperative RT is indicated
 Such disease is considered potentially resectable if neoadjuvant
therapy allows for a partial or complete response.
 Unresectable disease
o Patients who present with:
 Extensive pleural
 Pericardial metastases
 Unreconstructable great vessel or heart involvement
 Tracheal involvement
 Technically unresectable disease
 Distant metastases.
o Systemic therapy, radiotherapy, or chemoradiotherapy may be indicated for
such patients
 Additionally, such treatments are offered to those who are medically
unfit for surgery due to age or comorbidity.
 Treatments are individualized according to the patient’s extent of
disease, symptoms, and performance status.

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 Short Case Discussion

 Content By:
 Samuel Mesfin
 Edited By:
3.4. Chest Tube……..……..……..……..……..……..……145
 Samuel Mesfin 3.5. Needle Thoracostomy……..……..……..……..….158
 Reviewed By: 3.6. Tracheostomy…….…….……..……..……..……..…160
 Dr. Ephraim Teffera
(General and Cardiothoracic 3.7. Video QR Codes……..……..……..……..……..……168
Surgeon)

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 3.4. Chest Tube
 Describe what you see.…………………………...145
 Introduction……………………..………………………145
 Indications……………………..…………………………146
 Contraindications……………………..………………147
 Equipment………………………………………………..147
 Chest tube size and selection……………..…….148
 Preparation ……………………………………..………150
 Insertion techniques………………………..……….151
 Complications…………………………………………..155
 Chest tube Management…………………………..155
 Chest Tube removal………………………..………..157

Describe what you see

 In the left anterio-lateral chest, there is a tube inserted at the 5th intercostal space anterior
to the mid axillary line. There were visible oscillations and the connecting tube drains a
reddish fluid into a bottle which was half filled.

Introduction

 A chest tube (thoracic catheter, thoracostomy tube) is a sterile flexible plastic tube
with a number of drainage holes that is inserted through the chest wall and into the
pleural space or mediastinum.
 A patient may require a chest drainage system anytime the negative pressure in the
pleural cavity is disrupted, resulting in respiratory distress.

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 o Negative pressure is disrupted when air or fluid enters the pleural space.
o A small amount of fluid or air can be absorbed by the body without a chest
tube. A large amount of fluid or air will require drainage.
 Tube thoracostomy is a common procedure in which a tube is placed through the
chest wall into the pleural cavity:
o Primarily to drain air or fluid
o To instill agents to induce pleurodesis or to treat empyema.

Indications
 Insertion of a chest tube is indicated in either emergency or nonemergency
situations
Table 3.8: Indications of Tube Thoracostomy
Emergency Non-emergency
 Pneumothorax  Pleural Effusion:
 In all patients on mechanical ventilation   Malignant pleural effusion
Bronchopleural fistula  Recurrent pleural effusion
 When pneumothorax is large  Sterile effusion
 In a clinically unstable patient  Infected or inflammatory effusion
 For tension pneumothorax after needle o Empyema
decompression o Parapneumonic effusion
 When pneumothorax is recurrent or  Chylothorax
persistent  Hemothorax following chest trauma
 When pneumothorax is secondary to chest  Biliary-pleural or bronchobiliary fistula
trauma o Following combined injury of the
 When pneumothorax is iatrogenic, if large liver, diaphragm, and lung
and clinically significant  most commonly
due to central line placement
 Massive hemothorax (>1.5L)  Treatment with sclerosing agents or pleurodesis
for the treatment of refractory effusion

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 Esophageal rupture with gastric leak into pleural  Postoperative care after:
space o Coronary bypass
o Thoracotomy
o Lobectomy

Contraindication

 There are no absolute contraindications for drainage by means of a chest tube

except when a lung is completely adherent to the chest wall throughout the
hemithorax.
 Relative contraindications include:
o Patients taking anticoagulant medication
o Patients with a coagulopathy
o Skin infection over the chest tube insertion site
o Transudative pleural effusion… secondary to liver failure or CHF
Because it can resolve with diuretics only

Equipment

 Conventional chest tubes feature

multiple drainage fenestrations in the
section of the tube which resides inside
the patient, as well as distance markers
along the length of the tube, and a
radiopaque stripe which outlines the
first drainage hole.

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  1 or 2 % lidocaine
 Needles (size 25 and size 18-21) and syringes
for anesthetizing the skin
 Scalpel, with No. 10 or 11 blade
 Three Kelly clamps
 Straight scissors
 Chest tube
 Silk suture (1 to 0)
 Petroleum gauze
 Drain sponges
 Elastic tape
 Sterile drapes, gown and gloves
 Mask, protective eyewear
 2 % chlorhexidine/povidone iodine
 Drainage system

Chest tube size and Tube Selection

 Tube size is determined by the planned drainage material:
o For air: smaller drains up 12- 16 Fr will be enough and less painful
 Consider NGT if you can’t find proper tubes
o For blood, chlye or pus: 32- 38 Fr are needed

Table 3.9: Chest Tube Size for Age

 Chest tubes are available in a range
Adult/teen male 28-40 Fr
of French (Fr) sizes from 14 to 40
Adult/teen female 26-36 Fr
 Diameter in French = 3 X diameter
Children 18-22 Fr
in millimeter
Newborn 12-14 Fr

Tube Selection:
 Chest tubes of silicone (Silastic) are preferred over older latex rubber tubes because the
later:

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 o Had fewer drainage holes
o Are not well visualized on chest radiographs
o Produced more pleural inflammation
o Have been associated with latex allergy

Table 3.10: Chest tube selection

Pneumothorax
1. Spontaneous pneumothorax  Small-bore catheter (8 to 14 Fr)
2. Large air leak due to bronchial-  Larger-bore tube (24 Fr)
pleural fistulas
3. Traumatic pneumothorax, the  If there is an effusion, then we use a 28-Fr chest tube
size of the chest tube will
depend on what is seen on  if no effusion is seen, then a small-bore
chest radiograph.

4. Tension pneumothorax  Standard thoracostomy tube (24 or 28 Fr) after needle

decompression
Effusion
1. Hemothorax  Large-bore tubes (greater than 28 Fr)
2. Malignant effusion  Smaller-diameter tubes are assumed to be more comfortable
 Optimal-diameter of chest
tube for drainage is not  Larger-diameter tubes may provide better drainage
known.
3. Parapneumonic Effusions  If amenable to drainage with a single catheter, we prefer initial
image-guided placement of a small catheter (10 to 14 Fr)
 If the fluid appears viscous or loculated on chest CT, a larger tube
(16 to 24 Fr) should be used
Empyema
 It depends on the clinical stage  For a stage 1 empyema, a 28-Fr or larger tube
of the empyema  For a stage 2 empyema, a chest tube is still warranted but may fail

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 Preparation

 Explain the procedure to the patient and get

consent
 Put hand of the patient behind the neck: this gives
good exposure and expands ICS making it easier
to put the drain
 Position the patient in either a supine or a semi
recumbent position.
 Maximally abduct the ipsilateral arm or place it
behind the patient’s head.
 Isolate the “triangle of safety”
 Once the fourth to fifth intercostal space is felt,
move your hand laterally toward the anterior
Safe triangle boundary: axillary line  This is the area for incision

 Anterior border of the latissimus dorsi,  The actual insertion site should be one intercostal
 Posterior border of the pectoralis major space above the chest-tube incision site in order
to deal with possible pleuro-cutaneous fistula
 Superior border of the fifth rib4th to 5th
which is a rare occurrence.
ICS at midaxillary line.

 Use full barrier precautions:

o Wash your hands and wear a sterile gown and gloves, protective
eyewear, and a face mask
 Create a large, sterile field on the patient’s skin
o Using sterile gauze and 2% chlorhexidine solution
 Drape the patient, exposing only the marked area.
 Create a wheal of anesthetic in the cutaneous tissue at the marked spot.

o Using a 1% or 2% lidocaine solution and a 25-gauge needle

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 o Draw up more lidocaine solution in a 20-ml syringe. Using a 21-gauge
needle, anesthetize the deeper subcutaneous tissues and intercostal
muscles.
 Locate the rib lying below the intercostal space where the tube will be inserted,
and continue to anesthetize the periosteal surface.
o Use 3ml/kg to calculate the amount of lidocaine solution that may be
used to ensure optimal analgesia (based on %).
 Ex: 2% Lidocaine for a 50Kg person:
 2% = 2gm in 100ml  2000mg in 100ml  20 mg/ml
 3ml/kg x 50kg  150ml  7.5 ml of 2% Lidocaine
o While anesthetizing the rib, find the superior aspect of the rib and use
this to bevel or “march” the needle on top of it.
 Using continued negative suction as the needle advances, with the needle
beveled on top of the rib, confirm entry into the pleural space when a flash of
pleural fluid enters the chamber of the syringe.
 If a pneumothorax is being evacuated:
o The syringe may only fill with air.
o Stop advancing the needle and inject any remaining lidocaine to fully
anesthetize the parietal pleura.
o You may feel the decrement in pressure when you breach the pleura
even if nothing is coming out.
 Withdraw the needle and syringe completely

Insertion Techniques

 Blind insertion of a chest tube is dangerous in a patient with pleural adhesions from
infection, previous pleurodesis, or prior pulmonary surgery  guidance by ultrasound or
CT scan without contrast is preferred.

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 Prophylactic antibiotics are warranted for chest tubes placed in the setting of trauma,
particularly in patients with penetrating injury.
Incision and Dissection
 An incision 1.5 to 2.0 cm in length should be made parallel to the rib.
o Use the Kelly clamp or artery forceps to cut through the subcutaneous layers
and intercostal muscles
o The path should traverse diagonally up toward the next superior intercostal
space.
 Once you have dissected through the subcutaneous tissues, find the surface of the rib
lying below this space with the dissecting instrument.
 Then slide the instrument straight up, until you find the top edge of the rib.
 Use this to bevel or balance the dissecting instrument as you dissect the intercostal
muscles
 Once you reach the parietal pleura, gently push the dissecting instrument through it.
o You may also digitally penetrate the pleura to avoid puncturing
adjacent lung tissue, using your index finger to explore the tract.
 Once your finger enters the pleura, withdraw the Kelly clamp. Use your finger to palpate
within the pleural layer and ensure that the lung falls away from the pleura.
o If it does not, this may indicate the presence of an adhesion, so tube insertion
may be difficult.

Tube Insertion
 Once the distal tip of the tube has passed
through the incision, unclamp the Kelly
clamps or forceps and advance the tube
manually.
 Aim the tube:
o Apically for evacuation of a
pneumothorax
o Basally for evacuation of any fluid.

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 Securing the Tube
 Mattress or interrupted sutures should be used on both sides of the incision
to close the ends.
 Tape the tube to the side of the patient and wrap a petroleum-based gauze
dressing around the tube.
 Cover this gauze with several pieces of regular sterile gauze, and secure the
site with multiple pressure dressings.
 Connect the distal end of the chest tube to a sterile pleural drainage system.
 Once the tube is connected, unclamp the distal end:
o If there is a pneumothorax, bubbling may be seen
o If there is a large pleural effusion, it will begin collecting.
 Do not reclamp the chest tube, once released, unless the pleural drainage
system is being changed.
Radio-opaque marking o Reclamping the tube may lead to the redevelopment of a
on thoracostomy tube
pneumothorax and may create a tension pneumothorax.

Chest Radiograph Confirmation

 Once you have secured the chest tube, obtain an anterior-posterior chest
radiograph to confirm placement, which can be done by identifying the radio-
opaque line along the tube.
 If the proximal drainage hole is outside the pleural space, drainage may be
ineffective and an air leak may result.
o In this circumstance, the tube should be removed and a new chest tube
inserted

Seldinger technique
 Chest tubes can also be placed using a trocar, which is a pointed metallic bar used
to guide the tube through the chest wall.
 This method is less popular due to an increased risk of iatrogenic lung injury.
Placement using the Seldinger technique, in which a blunt guidewire is passed
through a needle (over which the chest tube is then inserted), has been described.
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Functionality of chest tube
 Continuous bubbling in the bottle
 Look for oscillations
o Oscillation is the proof of functionality not bubbling  It may not be present
in most patients

Differentials for non-functional tube /non-oscillation

 Malposition
 The drainage system can hold up
 Misplaced tube
to 2L and can be connected to
 Clogged tube
suction or can be used with
 Kinked tube gravity. It needs to stay below the
 Full bottle level of the patient’s chest.

The 3 compartments of the drainage system

 Collection chamber
 Water seal chamber
 Suction control chamber

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 Complications

 Technical
o Incorrect positioning of the tube, which causes ineffective drainage.
o Intermittent tube blockage from clotted blood, pus, or debris
 Insertion related
o Pain
o Solid organ Puncture
 Lung (commonest), heart, spleen, liver, stomach, colon, and diaphragm
o Bleeding and hemothorax
 Commonly from intercostal artery perforation but can also be from
perforation of major vascular structures such as the aorta or
subclavian vessels
o Intercostal Neuralgia
 From trauma to the neurovascular bundles
o Subcutaneous emphysema
 Position related
o Mal-position
o Re-expansion pulmonary edema (RPE)
 Usually arises after rapid reexpansion of a lung that has been collapsed
for at least three days
 Patients developing RPE typically present soon after chest tube
placement with cough, dyspnea, and hypoxemia, but the clinical
presentation can be delayed for up to 24 to 48 hours.
 Infection
o Drainage site infection
o Pneumonia
o Empyema

Chest Tube Management

 Assessing air leak
o Daily to determine whether the tube can be removed

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 Managing initial drainage: amount should be assessed on a regular basis (hourly, in
the setting of trauma).
o An immediate drainage of 20 mL/kg or the accumulation of >3 mL/kg per
hour of blood  an indication for thoracotomy to identify and manage
thoracic vascular injury
o To minimize the likelihood of developing RPE, limit initial fluid drainage to 1.5
liters by clamping the chest tube and waiting at least one hour before
draining additional fluid.
 Tube:
o If a closed-suction system becomes disconnected:
 The tube should be cleaned with an antiseptic and the tubing
reconnected.
 If a new closed-suction apparatus is immediately available, the new
one should be connected
 The chest tube should not be clamped to avoid tension
pneumothorax.
o If the chest tube is no longer draining and there is a suspicion that it is full of
clot or debris, the tube cleared of obstruction by other maneuvers
 Hold the chest tube near its insertion site with the non-dominant hand
 Compress the tube between the first and second fingers of the
dominant hand  Gently pull toward the drainage system
 If stripping the tube once or twice does not clear the tube
 Twisting the tube 360 degrees
 Pulling the tube out 1 to 2 cm
 Passing a sterile endotracheal tube suction catheter
 Injecting a small volume of sterile saline with a few drops of
povidone-iodine

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 Chest Tube Removal

 To minimize the risk of infectious complications, the tube should be removed as

soon as it is safe to do so.
 Make sure the chest tube is functional first  not draining doesn't mean it has
finished draining.

Table 3.11: Criteria of Chest tube removal

Pneumothorax Effusion
 The lung is fully expanded  The lung is fully expanded.
 No visible air leak is present, and air  Daily fluid output is less than about 100
does not accumulate when suction is to 300 mL/day
removed

 Technique:
o Two people may need to participate so that one can instruct the patient and pull
the tube while the other can quickly occlude the insertion site.
o Cut the skin sutures, using sterile technique.
o Have additional strong nylon or silk sutures ready in case additional sutures are
required to seal the hole.
o Instruct the spontaneously breathing patient to perform a forced Valsalva
maneuver or to inhale to total lung capacity after a full exhalation.
 If the patient is being fully mechanically ventilated, removal should be
timed to end-expiration.
o One operator can pull the tube out while the other quickly occludes the site with
gauze, adds additional sutures to close the opening, and secures the site with a
pressure dressing.
o A chest radiograph 12 to 24 hours after removal is recommended; this
should be done sooner if there is clinical suspicion of a residual air leak or a new
pneumothorax.
o It will take about 3 to 4 weeks for your incision to heal completely

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 3. 5. Needle Thoracostomy

 Introduction……………………..……………………..158
 Equipment………………………………..……………..158
 Indications and Contraindications…………….159
 Techniques……………………………………………….159
 Complications………………………..…………………159
 Aftercare………………..………………..………………160

Introduction

 Needle thoracostomy is insertion of a needle into the pleural space to

decompress a tension pneumothorax.
 Needle thoracostomy is an emergency, potentially life-saving procedure that can
be done if tube thoracostomy cannot be done quickly enough.
 This can be either with a standard chest tube, pigtail catheter, or angiocatheter.

Equipment
 A 14- or 16-gauge needle (an over-the-needle catheter is best)
o 8-cm needles are more successful than 5-cm
needles but increase the risk of injury to
underlying structures
 Transfusion or LP set needle could also work
 Sterile gown, mask, gloves
 Cleansing solution such as 2% chlorhexidine solution

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 Indication and Contraindication

 Indication: a tension pneumothorax that must be decompressed before tube

thoracostomy can be done.
 There are no contraindications because this procedure is only done because of an
immediate threat to life which supersedes other considerations.

Technique
 We perform this on the affected side in the midclavicular
line through the second intercostal space with one of any
readily available kits.
o The angiocatheter from the kit is placed first, which
allows for immediate decompression.

o Then, an 8.3-Fr or 14-Fr pigtail catheter can be placed

immediately over a wire into the pleural space

 A standard-length 14- or 16-gauge angiocatheter is nearly

always successful.
 The 14- to 16-gauge IV needle/ catheter is attached to a 5- or
10-mL syringe and is inserted along the superior margin of the
third rib in the midclavicular line.

Complications
 Because these catheters are small-bore thin-walled catheters
o They are prone to kinking
o They may not completely relieve a tension pneumothorax
 They can also be dislodged
o Leading to reaccumulation of air and recurrent tension pneumothorax.
o Immediately following needle decompression, a standard thoracostomy tube
should be placed
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 Others:
o Lung laceration, bleeding, infection, air embolism
o Intercostal neuralgia due to injury of the neurovascular bundle

Aftercare
 Chest x-ray should be done to confirm expansion of the lung and proper placement of
the chest tube and insert a chest tube as soon as possible

3.6. Tracheostomy

 Introduction………………………………….………….161
 Types of Tracheostomy…………………...……….162
 Functions of Tracheostomy……………………….162
 Indications……………………..…………………………163
 Contraindications………………………….………….163
 Equipment………………………………………………..164
 Techniques………………………………….…………..165
 Post- Op Care…………………………………………..165
 Decannulation………………………………………….166
 Complications…………………………………………..167

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 Introduction

 Airway access for mechanical ventilation

can be provided either by endotracheal
or tracheostomy tube
 Tracheotomy is a surgical procedure
which consists of making an incision on
the anterior aspect of the neck and
opening a direct airway through an
incision in the trachea (windpipe)
 It is either temporary or permanent.
 The resulting stoma (hole) or tracheostomy can serve independently as an airway or
as a site for a tracheostomy tube to be inserted
 This tube allows a person to breathe without the use of his or her nose or mouth.
 Either surgical or percutaneous techniques are widely used in current surgical
practice
Table 3.12: Tracheostomy Vs. Intubation
Tracheostomy Intubation
 Ease of replacement (once tract has formed)  Rapid insertion by skilled consultant in most
Advantages

 Speech, mobility, and swallowing enhanced settings

 Patient can be nursed outside of ICU  Lack of need for surgical procedure (risk,
 Ease of suctioning expense)
 Patient comfort  Lack of stomal complications
 Complications at cuff site  Complications at cuff site
 Stomal complications  Laryngeal complications
 Possible contribution to ultimate laryngeal injury  Replacement requires skill at all times
Disadvantages

 Tracheo-innominate artery fistula formation  Generally, requires ICU level supervision

 Possible increase in pulmonary infections  Injuries at nose or mouth
 Access to mediastinum by infectious agents after
local surgery
 High mortality for inadvertent decannulation
before tract formation

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 Types of Tracheostomy

 Emergency tracheostomy
 Elective or tranquil tracheostomy
 Permanent tracheostomy
 Percutaneous dilatational tracheostomy
 Mini tracheostomy (cricothyroidotomy)
Based on level:  Thyroid isthmus lies against II, III
 High and IV tracheal rings
o Above the level of thyroid isthmus
o Only indication - carcinoma of larynx
 Mid
o Preferred one; through the II or III tracheal rings
o Entail division of the thyroid isthmus or its retraction upwards or downwards
to expose this part of trachea.
 Low
o Below the level of isthmus.
o Trachea is deep at this level and close to several large vessels; also, there are
difficulties with tracheostomy tube which impinges on suprasternal notch

Functions of Tracheostomy
 Alternative pathway for breathing
 Improves alveolar ventilation in cases of respiratory insufficiency
 Protects the airways by using cuffed tube, tracheobronchial tree is protected against
aspiration of:
o Pharyngeal secretions
o Blood, as in hemorrhage from pharynx, larynx or maxillofacial injuries
 Permits removal of tracheobronchial secretions
 Intermittent positive pressure respiration (IPPR)
o If IPPR is required beyond 72 hours, tracheostomy is superior to intubation.
 To administer anesthesia

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 Indications

There are three main indications

1. Respiratory obstruction.
 Infection
 Trauma
 Neoplasms of larynx, pharynx, upper trachea, tongue and thyroid
 Foreign body
 Laryngeal edema
 Congenital anomalies such as Laryngeal web, cysts, tracheoesophageal fistula
Bilateral choanal atresia
2. Retained secretions.
 Inability to cough from coma of any cause or spasm or paralysis of respiratory
muscles
 Painful cough from chest trauma, pneumonia or multiple rib fractures
 Aspiration of pharyngeal secretions due to bulbar polio, polyneuritis, bilateral
laryngeal paralysis
3. Respiratory insufficiency: Chronic lung conditions

Contraindications
 Emphysema
 Chronic bronchitis
 Bronchiectasis
 Atelectasis

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 Relative contraindications to percutaneous tracheostomy include:
 Age under 15 years of age
 Uncorrectable bleeding diathesis
 Gross distortion of the neck from hematoma
 Tumor
 Thyromegaly
 Scarring from previous neck surgery
 Documented or clinically suspected tracheomalacia
 Evidence of infection in the soft tissues of the neck
 Obese and/or short neck which obscures landmarks
 Inability to extend the neck because of cervical fusion
 Rheumatoid arthritis, or other causes of cervical spine instability

Equipment

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 Technique

 Position: Supine with a pillow under the shoulders so that neck is extended
 Inject anesthesia
 A vertical incision in the midline of neck, extending from cricoid cartilage to just above
the sternal notch
o This is the most favored incision and can be used in emergency and elective
procedures.
o It gives rapid access with minimum of bleeding and tissue dissection
 After incision, tissues are dissected in the midline. Dilated veins are either displaced or
ligated
 Strap muscles are separated in the midline and retracted laterally.
 Thyroid isthmus is displaced upwards or divided between the clamps, and suture-ligated
 Trachea is fixed with a hook and opened with a vertical incision in the region of 3rd and
4th or 3rd and 2nd rings
 Confirmation of trachea:
o 5 ml syringe containing 4 % Lignocaine taken, its needle inserted into trachea &
aspirated  Air bubbles confirm presence of needle in trachea.

Post Operatives Care

 Tracheostomy tube of appropriate size is
inserted and secured by tapes
 Skin incision should not be sutured or packed
tightly as it may lead to development of
subcutaneous emphysema.
 Gauze dressing is placed between the skin and
flange of the tube around the stoma
 Tapes of tracheostomy tube tied around the
neck keeping a space for 1 finger. Neck kept
flexed

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 Decannulation

 Constant Supervision for bleeding, displacement, blocking of tubes, removing secretions

 Suctioning (frequently every 15 min the first 24 - 48 hours)
 Tracheostomy tube care
o Inner tube is removed & cleaned when blocked
o Outer tube never removed before 72 hours to allow formation of tracheo-
cutaneous tract
 Prevention of crusting and tracheitis
o Proper humidification using humidifier, nebulizer or keeping boiling kettle in
room.
o Using a few drops of ringer lactate or normal saline or hypotonic saline; Every 2-3
hours
 Adult:
o Plug or seal tube opening and if tolerated for 24 hours, remove tube.
 Child:
o Sequentially reduce size of tube.
o After tube removal  close wound.
o Healing occurs within 1 week.
 Infant or a young child
o Decannulate in operation theatre

Table 3.13: Decannulation difficulty

Organic causes Non-organic causes
 Persistence of cause requiring tracheostomy  Emotional dependence in children
 Obstructing tracheal granulations  Inability to tolerate upper airway
 Tracheal oedema resistance

 Subglottic stenosis  In-coordination of laryngeal opening

 Collapse of tracheal wall reflex

 Long-standing tube leads to impaired
laryngeal development

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 Complications

Acute/Immediate:
 Postoperative hemorrhage
 Aspiration of blood
 Injury to recurrent laryngeal nerve
 Injury to apical pleura (Pneumothorax)
 Injury to oesophagus (May cause tracheoesophageal fistula)
 Obstruction:
o Percutaneous tracheostomy tubes can become partially obstructed by the
posterior membranous trachea following initial placement
Intermediate Complications
 Haemorrhage
 Displacement of tube
o Due to use of improper size tube
 Blocking of tube
o Due to excessive crusting/poor humidification
 Subcutaneous emphysema and pneumothorax
o Due to imperfect positioning of fenestrated cannula and posterior wall
perforation
 Tracheitis/Tracheobronchitis with crusting in trachea
 Pulmonary infections
o Due to compromised airway defense mechanism
 Wound infection & granulation
Chronic:
 Haemorrhage
o Due to erosion of major vessels especially innominate or bracheocephalic
artery
 Tracheal stenosis
o Due to tracheal ulceration and infection
 Tracheoarterial fistula

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 o Due to erosion of trachea by tip of the tube
 Reduced phonation and Laryngeal stenosis
o Due to perichondritis of cricoids cartilage
 Tracheoesophageal fistula  Difficult decannulation
 Keloid/Unsightly scar at tracheostomy site

3.7. Video QR Codes

Chest Tube

Needle Thoracostomy

Tracheostomy

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 Part 4: Urology

Long Case Discussion

 Content By:
 Enas Hassen
4.1. Bladder Outlet Obstruction………………………………..170
 Samuel Mesfin
 Nanati Jemal 4.2. Urolithiasis………………………………………………………..199
 Edited By:
 Samuel Mesfin 4.3. Renal Cell Carcinoma………………………………………….203
 Reviewed By: 4.4. Urologic Trauma…………………………………………………213
 Dr. Abeselom Lemma
(Urologist)

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 4.1. Bladder Outlet Obstruction
 Case Discussion……………………………………………170
 History…………………………………………………….....170
 Differential Diagnosis…………………………………..171
 Discussion of the Differential Diagnosis……….171
 Complication……………………………………………….198

Case Discussion

 62 years old male man present with frequency urgency nocturia hesitancy and dribbling of
2-year duration. He has no associated hematuria, fever or flank pain. On physical
examination he is well nourished and has stable vital sign and DRE of the prostate reveals
enlarged firm, smooth, well circumscribed prostate which is mobile on the underlying
rectal mucosa.

History

 Presentation: lower urinary tract symptoms

o Can be described as
o Voiding (obstructive) symptoms:
 Hesitancy (worsened if the bladder is very full)
 Poor flow (unimproved by straining)
 Intermittent stream – stops and starts
 Dribbling (including after micturition)
 Sensation of poor bladder emptying
 Episodes of near retention
o Storage (irritative) symptoms
 Frequency  Nocturia
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  Urgency  Urge incontinence
 Nocturnal incontinence
o Often occur as mixed symptoms

Differential Diagnosis
1. BPH 5. Bladder stone
2. Prostatic ca 6. Bladder neck stenosis
3. Bladder ca 7. Bladder neck hypertrophy
4. Urethral stricture 8. Neurogenic-bladder

Discussion of the Differential Diagnosis

4.1. 1. Benign Prostatic Hyperplasia

 Introduction………………………………………..171
 Epidemiology………………………………………172
 Risk factors ………………………………………..172
 Clinical Manifestation………………………….172
 Investigation……………………………………….173
 Management………………………………………173

Introduction
 Benign enlargement of prostate which occurs after 50 years, usually between 60 and
70 years.

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  Involves median and lateral lobe (transitional zone)
 It involves adenomatous zone of prostate, i.e. submucosal glands

Epidemiology
 BPH is one of the most common disease in ageing men
 Prevalence increase with age being 50% in 6th decade of life and raising to 80% in
9th decade of life

Risk Factors
 Increased Age
 Family history
 Presence of circulating androgen
 Diet: conception of soya rich food decrease risk of BPH

Clinical Manifestation
History
 Ask if there are lower urinary tract symptoms
 Often mixed obstructive and irritative symptoms
 Intensity of symptoms doesn’t relate to size of the prostate
 Focus on
o Onset, duration and frequency of symptoms
o Precipitating factors
o Sexual history
o Medication intake:
 Anti-histamines
 Anti-hypertensives
 Anti-cholinergic

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  Tricyclic antidepressants
o Previously attempted Rx
 Assess severity of symptoms using International prostate symptom score
Physical examination:
 Focus on
o Suprapubic palpation for distension or tenderness
o Palpation of kidney for possible hydro nephrotic kidney
o Sign of anemia
o DRE: assesses the prostate for
 Size Measure (by finger) & approximate it if reachable
 Contour  Medial sulcus
 Consistency  Nodules
 Fixity
 Possible findings
 Enlarged smooth firm and well-defined prostate – BPH
 Enlarged nodular hard irregular prostate which may be fixed to
rectal mucosal – Prostatic ca

Investigation
 Urine analysis  Acid phosphatase
 Urine culture  Prostate specific antigen (PSA)
 Abdominopelvic US  Renal function test
 Transrectal US (most sensitive)  Serum electrolyte
 Cystoscopy  Urodynamics(Optional)

Management
 Urethral catheterisation for Patient with acute retention
 Medical management.
o Alpha blockers such as terazosin, doxazosin, tamsulosin, and alfluzasin
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  Inhibit smooth muscle contraction of prostate  reduce the
bladder neck resistance so as to improve the urine flow.
o 5-Alpha reductase inhibitors such as finasteride and dutasteride.
 Inhibits conversion of testosterone to dihydro-testosterone.
 Effective in bigger prostates (above 50gms).
 Surgical management
o Indications for Surgery
 Moderate and severe LUTS according to IPSS
 Failed medical treatment
 Acute retention of urine.
 Chronic retention of urine with residual urine more than 200 ml.
 Complications like hydroureter, hydronephrosis, stone
formation, recurrent infection, bladder changes.
 Haematuria.
o TURP: Possible complications include:
 Significant hematuria (temporary), urethral stricture, retrograde
ejaculation and subsequent infertility, sexual dysfunction
(occasionally), or even urinary incontinence after the procedure
 Transurethral resection syndrome, caused by absorption of the
hypotonic irrigating solution that is infused into the prostatic
venous system during the procedure. This can cause
hypervolemia and hyponatremia, which leads to confusion, visual
disturbances, and cardiac arrhythmias.
o Open prostatectomy is used when the prostate is too large (over 100
grams) to remove transurethrally.

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 4.1. 2. Prostatic Cancer
 Introduction………………………………………….175
 Epidemiology………………………………………..175
 Risk factors…………………………………………..176
 Clinical Manifestations………………………….176
 Investigation…………………………………………176
 Staging………………………………………………….177
 Management………………………………………..179

Introduction
 The most common malignant tumour in men over 65 years.
 Occurs in peripheral zone in prostatic gland proper, i.e. commonly in posterior
lobe.
o So, prostatectomy for BPH does not confer protection against
development of carcinoma prostate
 Incidence of prostate cancer in men over 80 years is 70%.
 Histology is an adenocarcinoma

Epidemiology
 Grading of carcinoma is based on dedifferentiation as proposed by Gleason.
 Prostate cancer is the second most common cancer diagnosed in men and fifth
leading cause of cancer death worldwide.
 Incidence of prostate cancer in men over 80 years is 70%.
 African Americans men have higher incidence rate and more aggressive type of
prostate cancer

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 Risk Factors

 Age
 Family history
 Life style: high fat food
 Obesity

Clinical Manifestations
History:
 Commonly asymptomatic
 Bladder outlet obstruction with possible obstructive and irritative symptoms
 Haematuria
 Pelvic pain, back pain, arthritic pain in sacroiliac joint— features of secondaries
 Features of renal failure
 Features of anemia
Physical examination:
 On per rectal examination, prostate feels hard, nodular, irregular often with loss of
median groove
 Patients with advanced diseases may have
o Weight loss
o Bony tenderness
o Lower extremity lymph edema
o Adenopathy
o Over distended bladder

Investigations
 PSA level  Plain X-ray, KUB
 Acid phosphatase  Trans rectal ultrasound (TRUS)
 Hg% and peripheral smear  Trans rectal prostatic biopsy
 Liver function test  CT and MRI for staging
 Rena function test

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 Staging

Table 4.1: Bladder Cancer TNM staging AJCC UICC 2017

Primary Tumor (T)/ Clinical

T category T criteria
TX  Primary tumor cannot be assessed
T0  No evidence of primary tumor
T1  Clinically inapparent tumor that is not palpable
T1a  Tumor incidental histologic finding in 5% or less of tissue
resected
T1b  Tumor incidental histologic finding in more than 5% of tissue
resected
T1c  Tumor identified by needle biopsy found in one or both
sides, but not palpable
T2  Tumor is palpable and confined within prostate
T2a  Tumor involves one-half of one side or less
T2b  Tumor involves more than one-half of one side but not both
sides
T2c  Tumor involves both sides
T3  Extraprostatic tumor that is not fixed or does not invade
adjacent structures
T3a  Extraprostatic extension (unilateral or bilateral)
T3b  Tumor invades seminal vesicle(s)
T4  Tumor is fixed or invades adjacent structures other than
seminal vesicles such as external sphincter, rectum, bladder,
levator muscles, and/or pelvic wall
Regional lymph nodes (N)
N category N criteria
NX Lymph nodes cannot be assessed
N0 No positive regional nodes
N1 Metastases in regional node(s)
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 Distant metastasis (M)
M category M criteria
M0 No distant metastasis
M1 Distant metastasis
M1a Nonregional lymph node(s)
M1b Bone(s)
M1c Other site(s) with or without bone disease
Prostatic Surface Antigen (PSA)
Value
<10
≥10 <20
PSA

<20
≥20
Any value
Prognostic stage groups
T N M PSA Grade Group Stage
group
cT1a-c, cT2a N0 M0 <10 1 I
pT2 N0 M0 <10 1 I
cT1a-c, cT2a, pT2 N0 M0 ≥10 <20 1 IIA
cT2b-c N0 M0 <20 1 IIA
T1-2 N0 M0 <20 2 IIB
T1-2 N0 M0 <20 3 IIC
T1-2 N0 M0 <20 4 IIC
T1-2 N0 M0 ≥20 1-4 IIIA
T3-4 N0 M0 Any 1-4 IIIB
Any T N0 M0 Any 5 IIIC
Any T N1 M0 Any Any IVA
Any T Any N M1 Any Any IVB

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 Management

 Management depends on the tumour grade, stage and the life expectancy of the
patient according to age and comorbidities
 Options include
1. Watchful waiting 4. Radiotherapy
2. Active surveillance 5. Androgen deprivation
3. Radical prostatectomy therapy
 Local disease
o Radical prostatectomy o Androgen deprivation
o Radical radiotherapy therapy
 Advanced diseases
o Palliation therapy
o hormonal ablation
 Surgical  Bilateral surgical orchiectomy
 Pharmacological  luteinizing hormone-releasing hormone
agonist, antiandrogens, such as flutamide and cyproterone.

4.1. 3. Bladder Cancer

 Introduction…………………………………………..180
 Epidemiology…………………………………………180
 Risk factors…………………………………………….181
 Clinical Manifestation…………………………….184
 Investigation…………………………………………..186
 Staging……………………………………………………189
 Management………………………………………….192

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 Introduction

 Many bladder cancer patients survive but they experience multiple recurrences.
o As a consequence, there are a relatively large number of people alive
with a history of bladder cancer.
o In middle-aged and older adult men, bladder cancer is the second
most prevalent malignancy after prostate cancer
 Types
 Primary:
a. Transitional cell carcinoma (90%);
b. Squamous carcinoma arising in an area of metaplasia (7%);
c. Adenocarcinoma (uncommon, but may occur in urachal remnants)
(2%);
d. Sarcomas (rare).
 Secondary: direct invasion from adjacent tumours, i.e. colonic, renal,
ovarian, uterine, prostatic tumours.

Epidemiology
 Bladder cancer is the most common malignancy involving the urinary system
 The ninth most common malignancy worldwide
 United States and Western Europe:
o Urothelial (previously known as transitional cell) carcinoma is the
predominant histologic type (90%)
 Other areas of the world, such as the Middle East:
o Non-urothelial histologies are more frequent  Schistosomiasis
 Typically diagnosed in older individuals
o Median age at diagnosis of 69 years in men and 71 in women
o The age of onset is younger in current smokers than in never-smokers
o Rarely, in children and young adults, where it usually presents with low-
grade, non-invasive disease
 Environmental exposures account for most cases of bladder cancer.
o "Field cancerization"

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  The surface epithelium (urothelium) that lines the mucosal surfaces of
the entire urinary tract is exposed to potential carcinogens that are
either excreted in the urine or activated from precursors in the urine
by hydrolyzing enzymes.
 This effect is one hypothesis to explain the multifocal occurrence that
is a characteristic feature of urothelial carcinomas of both the urinary
bladder and the upper urinary tract.
o Monoclonality hypothesis
 In the majority of cases, multifocal urothelial carcinomas are
monoclonal.
 This supports their presumed origin from a single genetically altered
cell, which then spreads through the urothelium via intraluminal
seeding or intraepithelial migration

Risk Factors
Established:
 Cigarette smoking:
o The extent of smoking appears to be related to the aggressiveness of bladder
cancer:
 Heavy smokers (≥30 pack years) are more likely to have a high-grade
tumor and to have muscle invasive disease at their original
presentation compared with non-smokers
o Smoking cessation  Smoking cessation decreases but does not eliminate
the increased risk of bladder cancer
o Secondhand smoke  Exposure to secondhand smoke in women appears to
be a risk factor for the development of bladder cancer
 Occupational carcinogen exposure:
o Metal workers o Leather workers
o Painters o Textile and electrical
o Rubber industry workers workers

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 o Miners o Excavating-machine
o Cement workers operators
o Transport operators o Paints, plastics or hair dyes
 Drinking water:
o Trihalomethanes (THMs) are formed as a by-product when chlorine or
bromine is used to disinfect water for drinking and may have adverse health
effects at high concentrations.
o High concentrations of arsenic in drinking water and the subsequent
development of bladder cancer
Miscellaneous:
 Chronic Cystitis:
o Recurrent or chronic bladder infections and those who have an ongoing
source of bladder inflammation like prolonged indwelling catheters in the
setting of
 Spinal cord injury
Have a higher risk of bladder cancer
 Bladder calculi
compared with the general population
 Neurogenic bladder
o In this setting, there is a substantially higher incidence of non-urothelial
cancers, especially squamous cell carcinoma
o Leads to Cancer by:
 Repeated chronic irritation
 Obstructive uropathy  Bacterial superinfection  Production of
nitrosamines in the acidic urine  Induction of bladder cancer
 Inflammatory cells  ROS
 HPV:
o High risk serotypes of HPV, especially HPV 16
 Upper urinary tract cancer
o Urothelial cancers of the renal pelvis and ureter are thought to be due to the
same etiologic factors as urothelial cancer of the bladder

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 o Patients with urothelial cancer of the upper urinary tract are at high risk for
the subsequent development of urothelial cancer of the urinary bladder as
well as contralateral upper urinary tract malignancy
 Bladder augmentation
o Augmentation cystoplasty is occasionally used to treat neurogenic bladder,
and may also be undertaken if the bladder does not develop to a sufficient
size to allow for continence
o Patients who undergo a bladder augmentation procedure (including both
ileocystoplasty and gastrocystoplasty) appear to be at increased risk for the
subsequent development of urothelial cancer.
o The cumulative risk is estimated to be approximately 1 percent, with a latent
period of less than 20 years
o These cancers may arise in the residual bladder urothelium or in the intestinal
mucosa of the augmented bladder.
o Tumors have included urothelial carcinomas, adenocarcinomas, and at least
one case of signet cell carcinoma
o Screening: annual cystoscopy beginning 10 years after the bladder
augmentation
Iatrogenic:
 Radiation therapy
 Cyclophosphamide:
o Acrolein, a urinary metabolite of cyclophosphamide, is thought to be
responsible for both hemorrhagic cystitis as well as bladder cancer
o The uroprotectant mesna inactivates urinary acrolein
 Analgesics:
o has been linked to an increased risk of urothelial carcinoma, particularly of
the renal pelvis
Genetics:
 High risk: affected relatives were diagnosed before age 60 years and never-smokers
 P53 and RB mutations
Protective:
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 Clinical Manifestations

 An increase in total fluid intake may dilute excreted urinary carcinogens and reduce
contact time with the urothelium.
 Delayed Diagnosis due to:
o Similarity of the symptoms to those of benign disorders (urinary tract
infection, cystitis, prostatitis, passage of renal calculi)
o Symptoms are often intermittent
History:
 Hematuria: intermittent, gross, painless, and present throughout micturition.
 The point at which gross hematuria is noted during urination can be helpful in localizing its source:
o Hematuria occurring primarily at the beginning of urination  urethral source.
o Blood that is only noticed as a discharge between voiding or as a stain on
undergarments, while the voided urine itself appears clear  the urethral meatus or the
anterior urethra.
o Terminal hematuria, with blood appearing towards the end of voiding  the bladder neck or
prostatic urethra.
o Hematuria occurring throughout voiding  anywhere in the urinary tract, including the bladder,
ureters, or kidneys.

Initial symptoms:
 Painless hematuria: Commonest
 Irritative voiding symptoms (frequency, urgency, dysuria)
 Metastasis
 Autopsy is rare: most become symptomatic eventually
 Pain:
o Usually the result of locally advanced or metastatic tumors.
o Its distribution is related to the size and location of the primary tumor or its
metastases
 Flank pain may result when a tumor obstructs the ureter at any level (bladder, ureter, or renal pelvis).
o Usually is associated with muscle invasive disease or large noninvasive tumors at the
ureteral orifice
 Suprapubic pain is usually a sign of a locally advanced tumor that is either directly invading the
perivesical soft tissues and nerves or obstructing the bladder outlet  urinary retention.
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 Hypogastric, rectal, and perineal pain can be signs of disease invading the obturator fossa, perirectal
fat, presacral nerves, or the urogenital diaphragm.
 Abdominal or right upper quadrant pain may signal the presence of abdominal lymph node or liver
metastases.
 Bone pain may indicate the presence of bone metastases.
 Significant and persistent headache or disordered cognitive function may suggest the presence of
intracranial or leptomeningeal metastases

Voiding symptoms
 Storage symptoms are most common in patients with carcinoma in situ (CIS) of the
bladder
 May also result from:
o Functional decrease in the bladder capacity
o Detrusor overactivity
o Invasion of the trigone
o Obstruction of the bladder neck or urethra
 Irritative voiding symptoms:
o Eg: daytime and/or nocturnal frequency, urgency, dysuria, or urge
incontinence
o Occur in approximately one-third of patients.
o The complex of dysuria, frequency, and urgency in particular is highly
suggestive of bladder CIS.
 Obstructive voiding symptoms:
o Less common and may be due to tumor location at the bladder neck or
prostatic urethra.
o Symptoms include straining, an intermittent stream, nocturia, decreased
force of stream, and a feeling of incomplete voiding.
o On occasion, gross hematuria may result in "clot retention”.
Constitutional symptoms:
 Symptoms such as fatigue, weight loss, anorexia, and failure to thrive are usually
signs of advanced or metastatic disease and denote a poor prognosis.

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  In rare cases, patients may have constitutional symptoms due to renal failure caused
by bilateral ureteral obstruction

Physical Examination:

 Must include digital rectal examination in men and a bimanual examination of the vagina and rectum
in women.
 Although the physical examination is unremarkable in most patients, abnormal findings that can be
seen include the following:
o A solid pelvic mass may be felt in advanced cases.
o Induration of the prostate gland can sometimes be felt on digital rectal examination if the
bladder cancer involves the bladder neck and Invades the prostate.
o An attempt to palpate the base and lateral walls of the bladder should be made, looking for
induration or fixation.
o Inguinal adenopathy can be present, although the inguinal region is not a common site of node
metastases
o Nodularity in the periumbilical region can be seen in advanced lesions involving the dome of the
bladder. This is often seen with urachal cancers, which typically are adenocarcinomas rather than
urothelial tumors
 Abdominal examination may reveal the presence of substantially enlarged paraaortic lymph nodes or
hepatic metastases

Investigation
Urinalysis:
 Include a microscopic and gross examination as well as a dipstick chemical test.
 Nonrefrigerated urine should be examined within 30 minutes of collection.
 The average individual excretes approximately 30,000 red blood cells (RBCs) per
hour:
o Equates to approximately 1 RBC per high-power field (HPF) on microscopic
examination

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 o Hematuria is usually not considered significant unless there are more than 3
RBCs per HPF.
 Color: Urinary pigments that can mimic hematuria include:
o Betalain contained in beets (beeturia)
o Phenazopyridine, a urinary analgesic
o Vegetable dyes
o Urates
o Free myoglobin or hemoglobin
o Serratia marcescens
o Phenolphthalein, which used to be a common component of many over-
thecounter laxative
 Specific gravity
o Affects the stability of white blood cells or RBCs
o When the urinary flow rate is high and the urine is very dilute  RBCs are
lysed and therefore will not be present on microscopic examination, even in
the presence of pathology.
Cystoscopy:
 The gold standard for the initial diagnosis and staging of bladder cancer.
 Any visible tumor or suspicious lesion seen at the initial (diagnostic) cystoscopy:
o Do biopsy or resect transurethrally to determine the histology and depth of
invasion into the submucosa and muscle layers of the bladder
 In patients who presented with a positive urine cytology and whose initial
cystoscopy showed no visible tumor (or suspicious lesion) within the bladder:
o Biopsy of apparently normal appearing urothelium, prostatic urethra, and
selective catheterization of the ureters/renal pelvis with urine specimens for
cytology from the upper tract is required.
 For patients with documented high-risk disease confirmed on a diagnostic
transurethral resection of bladder tumor (TURBT);
o Repeat resection may be indicated to eliminate the risk of understaging
 Procedure:
o Bimanual exam under ansthesia
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 o Insert cystoscope and take urine sample for cytology
o Irrigate the bladder with sterile saline  Visualize
Cytology:
 Specificity >98 but poor sensitivity for low grade tumors
Urine biomarkers
Abdomino-pelvic CT with and without contrast:
 Should include delayed images to identify defects in the collecting system
 CT may demonstrate:
o Extravesical extension
o Nodal involvement in the pelvis or retroperitoneum, visceral, pulmonary, or
osseous metastasis
o Tumor involvement or obstruction of the upper urinary tract
 Disadvantages:
o It may miss tumors <1 cm in size, particularly those in the bladder trigone or
dome
o It cannot differentiate depth of bladder-wall invasion (ie, mucosal versus
lamina propria or muscularis propria)
o Difficult to distinguish inflammatory or iatrogenic edematous
changes from true extravesical tumor extension
o Identification of nodal involvement is relatively low
MRI:
 Gadolinium-enhanced MRI may be superior to CT to detect superficial and multiple
tumors, extravesical tumor extension, and surrounding organ invasion
 It is difficult to tolerate by claustrophobic patients and cannot be used in patients
with pacemakers or other metallic foreign bodies.
Ultrasonography:
 US can
o Confirm the presence of a soft tissue mass
o Evaluate the upper tracts for renal parenchymal disease
o Detect hydronephrosis

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 o To differentiate a non-radiopaque stone from a soft tissue mass by difference
in echogenicity
 But usually cannot determine depth of invasion, extravesical extension, or nodal
status.
Metastatic:
 Commonly to lung, liver and bone
 Imaging of the chest for all patients with muscle-invasive bladder cancer
o CXR: insensitive for lesions <1 cm
o Metastatic lesions are typically non-calcified soft tissue densities
 Bone scan and imaging of the brain are reserved for symptomatic patients

Staging
 Clinical:
o From bimanual exam and imaging studies as well as pathology results from
the cystoscopic biopsy or TURBT
o Jewett, strong and marshall system
o Broadly classified in to
1. Non-muscle invasive bladder cancer
2. Muscle invasive bladder cancer
3. Carcinoma in situ

 Pathologic:
o TNM system, which is based upon pathologic studies of cystectomy
specimens
o This staging system is applied to urothelial carcinoma, squamous cell
carcinoma, undifferentiated carcinoma, and adenocarcinoma arising in the
bladder.

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 Table 4.2: Bladder Cancer TNM staging AJCC UICC 2017
Primary Tumor (T)
T category T criteria
TX  Primary tumor cannot be assessed
T0  No evidence of primary tumor
Ta  Noninvasive papillary carcinoma
Tis  Urothelial carcinoma in situ: "Flat tumor"
T1  Tumor invades lamina propria (subepithelial connective
tissue)
T2  Tumor invades muscularis propria
pT2a  Tumor invades superficial muscularis propria (inner half)
pT2b  Tumor invades deep muscularis propria (outer half)
T3  Tumor invades perivesical soft tissue
pT3a  Microscopically
pT3b  Macroscopically (extravesical mass)
T4  Extravesical tumor directly invades any of the following:
Prostatic stroma, seminal vesicles, uterus, vagina, pelvic wall,
abdominal wall
T4a  Extravesical tumor invades directly into prostatic stroma,
uterus, vagina
T4b  Extravesical tumor invades pelvic wall, abdominal wall
Regional lymph nodes (N)
N category N criteria

NX  Lymph nodes cannot be assessed

N0  No lymph node metastasis
N1  Single regional lymph node metastasis in the true pelvis
(perivesical, obturator, internal and external iliac, or sacral
lymph node)

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N2  Multiple regional lymph node metastasis in the true pelvis
(perivesical, obturator, internal and external iliac, or sacral
lymph node metastasis)
N3  Lymph node metastasis to the common iliac lymph nodes
Distant metastasis (M)
M category M criteria
M0  No distant metastasis
M1  Distant metastasis
M1a  Distant metastasis limited to lymph nodes beyond the
common iliacs
M1b  Non-lymph-node distant metastases
Prognostic stage groups
T N M Stage group
Ta N0 M0 0a
Tis N0 M0 0is
T1 N0 M0 I
T2a N0 M0 II
T2b N0 M0 II
T3a, T3b, T4a N0 M0 IIIA
T1-T4a N1 M0 IIIA
T1-T4a N2, N3 M0 IIIB
T4b Any N M0 IVA
Any T Any N M1a IVA
Any T Any N M1b IVB

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 Management

 Non-invasive tumour
o For patients with non-muscle invasive bladder cancer, conservative
management may allow the preservation of a functional bladder based upon
transurethral resection of bladder tumor (TURBT), potentially combined with
adjuvant intravesical therapy.
o However, this approach must be balanced against the risk of recurrence or
progression
o Intravesical chemotherapy including doxorubicin, mitomycin and adriamycin
can be used
o BCG  Immunotherapy
 Invasive bladder tumour
o Surgery
 Radical cystectomy
 Partial cystectomy
o The only potentially curative treatment for MIBC is radical cystectomy with
regional lymphadenectomy
o Radiotherapy
 Indications for cystectomy:
o Any of the following represents a strong indication to proceed to cystectomy:
 Muscle invasive bladder cancer
 T1 tumors with lymphovascular invasion
 Variant histologies, including micropapillary transitional cell
carcinoma, sarcoma, squamous cell carcinoma, or adeno-
carcinomas
 T1, grade 3 tumors that were incompletely resected
 Prostatic duct/acinar CIS
 Women with bladder neck and/or urethra CIS
o Any of the following represents a relative indication to proceed. However,
decisions regarding cystectomy should be individualized based on the surgical
risks of the patient:

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  Ta or T1 high-grade plus CIS; T1b tumors (ie, deep involvement of
lamina propria)
 Persistent T1, grade 3 tumors identified on reresection
 Recurrent or persistent disease within 6 to 12 months of initiating
treatment with BCG
 Large-volume Ta, low-grade disease
o Cystectomy is also indicated for bladder cancer patients crippled by
symptoms related to bladder pathology (eg, intolerable urinary frequency,
pain, incontinence, and hemorrhage) that cannot be adequately managed
medically.
 Radical cystectomy:
o Entails removal of the bladder, adjacent organs, and regional lymph nodes.
o In men, radical cystectomy generally includes removal of the prostate and
seminal vesicles as well as the urinary bladder.
o In women, removal of the uterus, cervix, ovaries, and anterior vagina is
usually performed en bloc with the bladder.
o Patients who have undergone radical cystectomy for urothelial bladder cancer
are at risk for the development of distant metastases as well as second
primary urothelial tumors in the renal pelvis, ureters, or urethra
 Urinary diversion:
o Removal of the bladder requires that the urinary flow be redirected, which
may take one of several forms:
o A non-continent cutaneous diversion, in which the urine flows from the
ureters through a segment of bowel (usually ileum, termed an ileal conduit)
to the skin surface as a stoma
 Then it is collected in an external appliance.
o A cutaneous continent reservoir may be constructed to avoid the need for
an external appliance.
 The patient self-catheterizes at regular intervals to empty the
reservoir.

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 o An orthotopic neobladder may be formed from a segment of bowel and
attached to the urethra, enabling the patient to void through the urethra.
 Continent diversions may facilitate maintenance of patient
perceptions of quality of life and self-image and increase their
acceptance of radical cystectomy.
 Metastatic Disease:
o Advances in the management of advanced urothelial (transitional cell)
carcinoma using cisplatin-based combination chemotherapy led to
improved survival
o But there was only limited further progress until the development of
checkpoint inhibition immunotherapy
 Pharmacological  luteinizing hormone-releasing hormone
agonist, antiandrogens, such as flutamide and cyproterone.

4.1. 4. Urethral Stricture

 Introduction………………………………………..195
 Etiology……………………………………………….195
 Clinical Manifestation………………………….196
 Investigation………………………………………..196
 Management……………………………………….197

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 Introduction

 Urethral stricture involves scarring that narrows the urethra.

 It restricts flow of urine from the bladder causing BOO.
 It can be ischemic, inflammatory or traumatic.
 Types:
1. Proximal:
o Common in bulbous urethra (70%).
2. Distal:
o Congenital (in the external meatus)
o Often traumatic in children
o Can be on the floor or roof
o It can be single or multiple
o Can be permeable or impermeable to urine.

Etiology
 Congenital
 Inflammatory
a. Post-gonococcal:
 It is most common  70%
 Gonococcal stricture occurs one year after infection
 Retention develops only 10-15 years later
 Common in the bulb of urethra especially in the roof
o Here multiple strictures are common
o Proximal stricture is the narrowest
b. Tuberculous
c. Other infection (urethritis
 Traumatic:
 Bulbous (due to a straddle type of trauma)
 Membranous (due to pelvic fractures)
 Post instrumentation:
 Catheter  Dilator
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  Cystoscope
 Postoperative:
 Prostate surgery (4%)

Clinical Manifestations
History
 Voiding symptoms especially poor urinary stream
 Irritative symptoms such as dysuria and frequency
 retention and often with overflow

Physical examination
 Perineal hematoma
 High riding prostate Sign indicating urethral
injury after trauma
 Blood at the meatus

Investigation

 Urine analysis
 Urine culture
 Urethroscopy
 Urethrography
o Retrograde retrogram must be done before attempting to catheterize the
patient
 Urodynamic studies
 Renal function test
 IVP

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 Management

 Intermittent urethral dilation

 Urethrotomy
o Visual internal cystoscopic urethrotomy or stricturotomy
o External urethrotomy o Anastomotic urethroplasty
o Urethroplasty o Substitution urethroplasty
o Suprapubic line in case of acute retention

4.1. 5. Neurogenic Bladder

 Introduction…………………………………………..197
 Clinical Manifestation…………………………….197
 Investigation…………………………………………..198
 Management………………………………………….198

Introduction
 Neurogenic bladder is the loss of normal function of the bladder secondary to
damage to part of the nervous system
 Causes include:
o Traumatic spinal cord injury o Multiple sclerosis,
o Spinal cord neoplasm o Cerebral palsy
o Spina bifida o Parkinson disease
o Stroke

Clinical Manifestations
History:
 Urinary incontinence  Frequent UTI
 Urinary retention  Urinary urgency

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  Urinary frequency.
Physical examination:
 Neurologic examination including:
o Anal tone
o Bulbocavernous muscle reflex

Investigation
 Tests to locate the neuroanatomic lesion (CT and MRI of brain, spine)
 Urine analysis and urine culture
 Cystoscopy To rule out other
 Post void residual urine volume (PVR) causes of BOO
 Ultrasound

Management
 Behavioural therapy
 Medical management
o Anticholinergic therapy o Prophylactic antibiotics
 Surgical management
o Bladder augmentation o Botulinum toxin Injection

Complications of Bladder Outlet Obstruction

 Acute urinary retention precipitated by
o Postponement of micturition o Overindulgence in beer
 Chronic retention
o In patients in whom the residual volume is >250ml or so
o Causes bilateral hydronephrosis, UTI, renal impairment
o Present with over flow incontinence enuresis and renal insufficiency.
 Impaired bladder emptying predisposing to UTI and stone formation
 Hematuria and renal failure P a g e 198 | 548
 4. 2. Urolithiasis
 Case Discussion…………………………………………199
 Introduction……………………………………………..199
 Epidemiology…………………………………………….200
 Risk factors……………………………………………….200
 History………………………………………………………200
 Physical Examination………………………………..201
 Complication…………………………………………….201
 Differential Diagnosis……………………………….202
 Investigation…………………………………………….202
 Management……………………………………………202

Case Discussion
 A 60 years old man present to emergency department with sudden onset, sever flank pain
which radiate to his back. He has no associated symptoms and physical examination was
unremarkable except that he was changing his position frequently due to the pain.

Introduction
 Formation stone in urinary tract
 Include nephrolithiasis, ureterolithiasis and bladder stones
 Cause include genetic and environmental factors
 Types of stone
o Oxalate stones (75%) o Cystine stones (2%)
o Phosphate stones (10-15%) o Xanthine stones
o Urate stones
o Most stones are mixed and contain organic matrix

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 Epidemiology

 Urolithiasis is common disease

 It affects 11% of men and 7% of women in their life time.
 Total life time Prevalence renal stone is 15-20%

Risk Factors
 Family history or previous history of urolithiasis
 Dietary risk factors
o Vitamin A deficiency o Diet rich in protein
o Dehydration
 Environmental
o Hot climate
 Inadequate urinary drainage and urinary stasis
 Infection
 Medical history
o Hyperparathyroidism o HTN
o Gout o Obesity
o Hyperoxaluria o Immobilisation from any
o Cystinuria (Autosomal cause, e.g. paraplegia
recessive) o Medication intake
o Low urinary citrate level
 Surgical history such as Gastric by-pass surgery

History
 Asymptomatic
 Pain: depend on position of the stone
o Renal stone: acute renal colic, sudden onset of severe pain originating in
the flank radiating anteriorly and inferiorly
o Stone obstructing ureteropelvic junction:
 Mild to severe flank pain without radiation

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  Irritative voiding symptoms
 Suprapubic pain
o Stone within ureter:
 Abrupt onset of sever, colicky pain in the flank and ipsilateral lower
abdomen radiation to testicle or vulvar area
 Intense nausea with or without vomiting
o Upper ureteral stones: pain radiates to flank or lumbar
o Mid ureteral stone: pain radiate anteriorly and caudally
o Stone in the bladder:
 Mostly asymptomatic  Positional urinary retention
 Hematuria: gross or microscopic
 Nausea and vomiting:
o As a result of compression of renal capsule
 Fever is usually absent in uncomplicated urolithiasis

Physical Examination

 Guarding or rigidity on back and abdominal muscle

 Sign distinguishing renal colic from other causes of pain
o Abdominal exam is unremarkable
o Patients tend to move constantly unlike patients with acute abdomen who
lie absolutely still.

Complications
 Hydronephrosis  Renal loss due to long standing
 Abscess formation obstruction
 Urinary fistula formation  Increased risk of small cell
 Ureteral scarring and stenosis carcinoma
 Ureteral perforation
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 Differential Diagnosis

 Pyelonephritis  RCC
 Pyonephrosis  Bladder ca
 Renal trauma
 Pelvic inflammatory diseases
 Renal TB

Investigations
 Urine analysis, urine culture
 RFT, serum electrolyte, parathyroid hormone and phosphorus.
 CBC
 CRP
 Ultrasound
o Detect stone in kidney and bladder
o Assess obstructive changes
o Assess parenchyma loss
 Plain abdominal x ray (KUB)
o Detect up to 90% of the stones
 IVP
 CT scan

Management
 Expectant treatment
o For stone <5mm
 Extracorporeal shock wave lithotripsy (ESWL)
 Ureteroscopy
 Percutaneous nephrolithotomy (PCNL)
 Open surgery rarely required (<5%); if the non-invasive options are available
 Medical therapy
o Dissolution of calculi through alkalization of urine
 For uric acid and cysteine stones
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 o Chemoprophylaxis
 Limitation of dietary component
 Stone formation inhibitors (intestinal calcium binders)
 Augmentation of fluid intake (goal being a urine output of 2L
per 24 hours)

4.3. Renal Cell Carcinoma

 Case Discussion…………………………………………203
 Introduction……………………………………………..204
 Epidemiology…………………………………………….205
 Risk factors………………………………………………..206
 Clinical Manifestation………………………………..207
 Differential Diagnosis…………………………………208
 Investigation……………………………………………..208
 Staging……….……………………………………………..209
 Management……………………………………………..211

Case Discussion

 A 48 years old women present with flank pain of 1-year duration. She also had fever weight loss
and night sweet of a month duration. She had no LUTS or hematuria and on physical
examination she was febrile and had right renal mass.

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 Introduction

Renal Neoplasms:
 Can be primary or secondary
o Secondary renal neoplasms are usually clinically insignificant and discovered
at postmortem examination
 Primary:
o Arising from/within the renal cortex  80 to 85 %
o Transitional cell carcinomas of the renal pelvis  approximately 8%
o Wilms' tumor  5 to 6 %
o Parenchymal epithelial tumors (oncocytomas, collecting duct tumors, and
renal sarcomas)  occur infrequently
o Renal medullary carcinoma (seen in sickle cell disease)  rare
RCC
 It is an adenocarcinoma arising from renal tubular cells
 The most common site is proximal renal tubule
 RCC types:
 Clear cell (75 to 85 percent of tumors)
o Sporadic  deletion of chromosome 3p or associated with von Hippel-
Lindau disease
o Arise from the proximal tubule
o Macroscopically, they may be solid or less commonly, cystic
o Has abundant lipid and glycogen
 Papillary (chromophilic)  (10 to 15 percent)
o Originates from the proximal tubule
 Type I: Typically presents as stage I or II disease  Favorable
prognosis
 Type II: Typically presents as stage III or IV disease  Aggressive 
poor prognosis
 Chromophobe  (5 to 10 percent)
o Lack abundant lipid and glycogen
o Originate from the intercalated cells of the collecting system
o Early presentation  good prognosis
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 Oncocytic  (3 to 7 percent)
o Consist of a pure population of oncocytes, which are large well-
differentiated neoplastic cells with intensely eosinophilic granular
cytoplasm that is due to a large number of mitochondria
o Benign: well encapsulated, rarely invasive/ metastasize
o Originate from the intercalated cells of the collecting system
 Collecting duct (Bellini's duct)  (very rare)
o Younger patients
o Frequently aggressive
o They commonly present with gross hematuria
o Includes renal medullary carcinoma
 < 5 %  Unclassified
o Includes lymphomas, soft tissue sarcomas (eg, leiomyosarcoma,
liposarcoma) and carcinoids
o Translocation carcinomas:
o Fusion of the TFE3 gene to a number of other genes
o Occur at a younger age compared with other RCCs
 Common in North America

Epidemiology
 Men > than Females by 50%
 6th – 8th decade (mean age is 64)
 Early (<40)  genetic
 Extent:
o Localized  65% o Metastasis  16%
o Regional (LNs)  16% o Unstaged  3%

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 Risk Factors

Established:
 Smoking, HTN, Obesity
 Acquired cystic disease:
o 35 to 50 percent of chronic dialysis patients  RCC in 6%
 Occupational Exposure:
o Cadmium o Petroleum by-products
o Asbestos
 Analgesics:
o Aspirin o Acetaminophen
o NSAIDS
 Cytotoxic chemotherapy in childhood
 Chronic Hepatitis infection  CKD  RCC
 Sickle cell disease
 Stone
 Genetics if:
o Young age
o Treated for previous RCC
o Strong family history (first degree relatives with a tumor, onset before the
age of 40, and bilateral or multifocal disease)
o Chromosome 3 abnormalities
o Inherited PKD.
Factors that modify risk:
 DM
 PKD
 Dietary factors
o Nitrite from processed meat sources
 Prior radiation therapy

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 Clinical Manifestations

Majority are asymptomatic until the disease is advanced

o At presentation, 25% of individuals either have distant metastases or advanced
locoregional disease
Symptoms:
 The classic triad of RCC:
o Flank pain
o Hematuria
o Palpable abdominal renal mass
o Strongly suggests locally advanced disease
 Hematuria:
o Only with tumor invasion of the collecting system.
o When severe, the bleeding can cause clots and "colicky" discomfort.
 An abdominal or flank mass:
o In lower pole tumors.
o The mass is generally firm, homogeneous, nontender, and moves with
respiration
 Scrotal varicosities:
o Obstructed the gonadal vein where it enters the renal vein
 Inferior vena cava involvement:
o Lower extremity edema
o Ascites
o Hepatic dysfunction (possibly related to a Budd-Chiari syndrome)
o Pulmonary emboli
 Dissemination:
o Lungs o Liver
o Lymph nodes o Brain
o Bone
Paraneoplastic Syndromes:
 Anemia:
o Precede the diagnosis of RCC by several months
o Anemia of chronic disease.
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 Hepatic dysfunction / Stauffer syndrome:
o GM-CSF and (IL)-6  Liver dysfunction  Elevated ALP with fever, weight
loss and fatigue
o Poor prognosis
o Nephrectomy may result in the amelioration of hepatic dysfunction
 Fever: intermittent
 Hypercalcemia:
o Lytic bone metastases
o Overproduction of PTHrP
o Increased production of prostaglandins that promote bone resorption
 Cachexia
 Erytrocytosis:
o Elevated EPO
o VHL  HIF-1α  EPO
 Thrombocytosis: poor prognosis

Differential Diagnosis
 Pyelonephritis  Adrenal tumour
 Polycystic kidney disease  Retroperitoneal tumour
 Solitary cyst of kidney  Bladder cancer

Investigation
 Initially Abdominal US: criteria for a simple cyst
o The cyst is round and sharply demarcated with smooth walls
o There are no echoes within the cyst ("anechoic")
o There is a strong posterior wall echo, indicating good transmission through a cyst
 If all of these criteria are fulfilled  No further evaluation is needed
 likelihood of a malignancy is extremely small
 CT before and after injection of iodinated contrast
o Simple cyst: Bosniak category I
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  Hairline thin wall (has a smooth appearance without a clearly
delineated wall)
 Has no enhancement with intravascular contrast
 Does not contain septa, calcification, or solid components
 Has the density of water (less than 20 Hounsfield units)
o Malignancy: Bosniak category IV
 Thickened irregular walls or septa and enhancement after
contrast
 MRI: When,
o US and CT are non-diagnostic
o Radiographic contrast cannot be administered because of allergy or poor
renal function
o Identify the presence and/or extent of involvement of the collecting system
and/or inferior vena cava.
 Biopsy:
o Mostly: Nephrectomy or partial nephrectomy
o Occasionally: biopsy of a metastasis.
o Percutaneous biopsy: more limited except for a small renal mass if there is a
high index of suspicion for a metastatic lesion to the kidney, lymphoma, or a
focal kidney infection.

Staging
 Abdominal CT
 Others:
o Bone scan: only in patients with bone pain and/or an elevated ALP
o Chest CT: pulmonary or mediastinal lymph node metastases.
o MRI: the inferior vena cava and right atrium involvement
o PET or PET/CT
 Solid renal masses less than 3 cm were once thought to represent benign
adenomas; distinctions based upon size are no longer used.

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  Then TNM Staging

Table 4.3: Kidney Cancer TNM staging AJCC UICC 2017

Primary Tumor (T)
T category T criteria
TX Primary tumor cannot be assessed
T0 No evidence of primary tumor
T1 Tumor ≤7 cm in greatest dimension, limited to the kidney
T1a Tumor ≤4 cm in greatest dimension, limited to the kidney
T1b Tumor >4 cm but ≤7 cm in greatest dimension, limited to the kidney
T2 Tumor >7 cm in greatest dimension, limited to the kidney
T2a Tumor >7 cm but ≤10 cm in greatest dimension, limited to the kidney
T2b Tumor >10 cm, limited to the kidney
T3 Tumor extends into major veins or perinephric tissues, but not into
the ipsilateral adrenal gland and not beyond Gerota's fascia
T3a Tumor extends into the renal vein or its segmental branches, or
invades the pelvicalyceal system, or invades perirenal and/or renal
sinus fat but not beyond Gerota's fascia
T3b Tumor extends into the vena cava below the diaphragm
T3c Tumor extends into the vena cava above the diaphragm or invades
the wall of the vena cava
T4 Tumor invades beyond Gerota's fascia (including contiguous
extension into the ipsilateral adrenal gland)
Regional lymph nodes (N)
N category N criteria
NX Regional lymph nodes cannot be assessed
N0 No regional lymph node metastasis
N1 Metastasis in regional lymph nodes
Distant metastasis (M)

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 M category M criteria
M0 No distant metastasis
M1 Distant metastasis
Prognostic stage groups
T N M Stage group
T1 N0 M0 I
T1 N1 M0 III
T2 N0 M0 II
T2 N1 M0 III
T3 NX, N0 M0 III
T3 N1 M0 III
T4 Any N M0 IV
Any T Any N M1 IV

Screening:
 Not recommended because of the low prevalence except for patients with:
o Inherited diseases like VHL syndrome and tuberous sclerosis.
o End-stage renal disease, who have been on dialysis for three to five years
or more.
o A strong family history of RCC
o Prior kidney irradiation.

Management

Localized disease:
 This includes stage I, II, and III
 Surgery is curative in the majority of patients
 May require a radical nephrectomy or a partial nephrectomy
o To preserve renal parenchyma for appropriately selected patients

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  Surgery may be carried out through:
o A conventional approach or
o A minimally-invasive approach such as laparoscopy
 In carefully selected patients who present with a resectable primary tumor and
a concurrent single metastasis:
o Surgical resection of the metastasis, in conjunction with radical
nephrectomy, may be curative
 Other ablative procedures for patients with relatively small renal masses who
are not surgical candidates:
o Cryotherapy
o Radiofrequency ablation [RFA]
Advanced Disease:
 RCC is known to be chemo and radio resistant.
 In general, systemic therapy (immunotherapy, molecularly targeted agents),
surgery, and radiation all may have a role depending upon
o The extent of disease
o Sites of involvement
o Patient-specific factors
 The choice of treatment for patients with advanced disease should consider
prognostic risk factors

o Karnofsky performance status (KPS) <80 %

Patients with:
o Time from diagnosis to treatment <1 year
 0 risks → Good risk
o Hemoglobin concentration <lower limit of normal
 1/2 risks → Intermediate risk
o Serum calcium >upper limit of normal
 > 3 risks → Poor risk
o Neutrophil count >upper limit of normal
o Platelet count >upper limit of normal

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 4.4. Urologic Trauma

 Case Discussion……………………………………….…..213
 Introduction………………………………………….……..213
 Epidemiology……………………………………….………214
 History…………………….………………………….……….214
 Physical Examination……………….………..…………215
 Investigation…………………………………….………….216
 Differential Diagnosis……………………………….….218
 Discussion of the Differentials……………………..219
 Management……………………………………………….229
 Complications…………………………….………………..231

Case Discussion
 A 20-year-old patient was apparently healthy 04 hours back at which time he sustained a motor
vehicle crush accident to his pelvis. He was a passenger sitting in the front seat and sustained
side impact vehicle collision. Since the accident he complains of abdominal pain and inability to
void. On his physical examination he has blood at the urethral meats, suprapubic tenderness
and high riding prostate on digital rectal exam.

Introduction

 Trauma is defined as a physical injury or wound to living tissue caused by extrinsic

agent.
 Genitourinary trauma involves injury to the kidneys, ureters, bladder, and/or urethra.

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 Epidemiology

 It may result in high morbidity if not properly identified and managed. The diagnosis
of genitourinary trauma typically relies on patient history, physical examination,
urinalysis, and imaging (CT, cystoscopy, retrograde urethrogram.
 10% of the 2.8 million trauma patients hospitalized yearly in the US sustaining
genitourinary injuries
 The majority of renal, bladder, and posterior urethral trauma is from blunt
mechanisms, most commonly motor vehicle collisions.
 Most ureteral and anterior urethral injuries are iatrogenic

History
1) What is the mechanism of injury?
 Blunt injuries vs. penetrating?
 motor vehicle collision
o Speed of vehicle
o Crush or not: Crush injury to the pelvis- posterior urethral injury
 Falls
o Height of fall o Landing condition
 Gunshot injury
o Type of gun o Distance of shooting
 Assaults: know type of weapon
 Sports injury
 History of instrumentation:
o TURP o Endoscopic surgery
o Radical prostatectomy
 Self-inflicted: foreign body insertion may damage urethra
2) Chief complaint and associated symptoms
 Hematuria
o Neither specific or sensitive in urologic trauma
o Seen in renal and bladder trauma
o In bladder trauma, 82% have this symptom
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 o Clot in damaged kidney and maybe delayed as clot dislodges
 Flank pain: renal trauma or if ureter has been ligated
 Abdominal mass: urinoma
 Abdominal pain
o Nonspecific in urologic trauma
 Inability to void  Perineal pain- urethral injury
 Prolonged postoperative fever or overt urinary sepsis
 Ileus – due to urine in peritoneal cavity in ureter injury
o Diffuse, persistent abdominal pain
o Nausea and/or vomiting
o Delayed passage of or inability to pass flats
o Inability to tolerate an oral diet
3) Previous medical history
 History of Renal disease
4) Concomitant injury
 Head injury: history of Loss of consciousness
 Spinal cord injury: incontinence  Fracture
5) Assess for complications
 Bleeding  Stricture and recurrent stenosis
 Infection  Urethro-cutaneous fistful
 urinary fistula  Impotence
 hypertension  Uroascites
 Incontinence: common in bladder injury, very rare in urethral injury (2%)

Physical Examination
 General appearance: in distress? Bleeding? Conscious?
 Vital: look for hemodynamic instability and sepsis
 Renal trauma:
 Obvious penetrating trauma and bullet entry or exit at the lower thorax, upper
abdomen, flanks and back
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  Flank tenderness  Fractured ribs
 Flank ecchymosis  Meteiorism
 Abdominal distension 24–48 hours after renal injury is probably as a result of
retroperitoneal hematoma implicating splanchnic nerves
 Ureter injury:
 Abdominal mass (urinoma)
 Signs of ileus (abdominal distention)
 Drainage of fluid from drains, abdominal wound or vagina
 Bladder injury:
 bruises over the suprapubic region
 abdominal distention  Abdominal Tenderness
 Urethral trauma:
 Posterior urethral trauma
o Blood at the urethral meats o Palpable pelvic hematoma
o Suprapubic tenderness o Perianal and suprapubic
o Palpable full bladder contusions
o Pelvic fracture
o DRE: “high-riding” prostate or a “butterfly” perineal hematoma
 Anterior urethral trauma
o Blood may be present at the end of the penis and a hematoma around the
site of the rupture
o Tender perineum
o Scrotum swelling and a ‘butterfly wing’ pattern of bruising

Investigation
1) laboratory
 Urine analysis
o For Hematuria; Gross or microscopic (> 5 rbc/ hpf)
 Serial hematocrit
o For continuous follow up
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  Creatinine measurement
o Indicates preexisting renal abnormality if increased (if taken within 1
hr of trauma)
2) Imaging
 Ultrasound
o For initial evaluation of renal injury
o Can show laceration but can’t assess the renal function status
o Doppler ultrasound or ultrasound with contrast to determine blood
flow to the kidney
 CT scan
o More accurately defines the location of injuries
o Easily detects contusions and devitalized segments
o Visualizes the entire retroperitoneum and any associated
hematomas, also arterial extravasations and pre-existing
abnormalities
 IVP
o Should only be performed when CT scan is not available
o Can be used to confirm function of the injured kidney and presence of
the contralateral kidney.
o Can be used to diagnose ureteral injury
o Incomplete visualization of the entire ureter
o Ureteral deviation or o Urinary extravasation
dilation o Hydronephrosis.
 MRI
o Accurate in finding perirenal hematomas, assessing the viability of
renal fragments, and detecting preexisting renal abnormalities
 Failed to visualize urinary extravasation on initial
examination.
 Not the first choice in managing the patient with trauma
 Radionuclide scan

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 o Helpful to document renal blood flow in the trauma patient with
severe allergy to iodinated contrast material
o In following up repair of renovascular trauma
 CT urography
o Best study for detecting ureteral injuries
o Delayed ipsilateral nephrogram
o Lack of contrast in the distal ureter
o Contrast extravasation o Periureteral urinoma
o Hydronephrosis
 Retrograde ureterogram
o Is the most sensitive radiographic test for ureteral injury.
o Most commonly used to diagnose initially missed ureteral injuries,
because it allows the simultaneous placement of a ureteral stent if
possible.
 Cystography
o Very accurate (>90%) in bladder injury
o Can distinguish intraperitoneal from extra peritoneal rupture.
 CT cystography
o Has the highest sensitivity
o Correctly assess other visceral injuries in a polytraumatized patient
o It has the drawback:
 Of being expensive
 It can’t not differentiate urine from ascites and also adequate distension
 Extravasation of contrast material is an issue leading to high false
positive results
 Retrograde urethrography: gold standard for urethral injury

Differential Diagnosis
 Renal Injury  Bladder Injury
 Ureter Injury  Urethral Injury
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 Discussion of the Differentials

4.4.1. Renal Trauma

 Epidemiology……………………………………………….219
 Etiology………………………………………………………..219
 Clinical Manifestation…………………………………..220
 Investigation…………………………………………………220

Epidemiology
 Kidney is the most commonly injured organ in the genitourinary system.
 Seen in up to 5% of all trauma cases, and in 10% of all abdominal trauma cases.
 Associated with young age and male gender with incidence of about 4.9 per 100,000

Etiology
 Renal trauma is most often an acute condition caused by a blunt abdominal injury
and may, if severe, represent a urological emergency.
 Blunt injury could be:
o Motor vehicle collision
o Falls
o Assault
o Sports injury
 Renal trauma could occur following penetrating injuries: tend to be more severe and
less predictable.
o Stab wounds
o Gunshot wounds

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 Clinical Manifestations

 The classical symptoms of renal trauma are hematuria and pain in the affected
side following injury.
 Associated symptoms
o Bruising o Hematoma
o Possible accompanying injuries
 E.g., rib fracture with motion-dependent pain
o Meteiorism
 Abdominal distension 24–48 hours after renal injury is probably as a
result of retroperitoneal hematoma implicating splanchnic nerves
o Flank tenderness o Abdominal tenderness
o Flank ecchymosis o Palpable mass
 Patients may also be asymptomatic
 Some may have nonspecific symptoms like nausea and vomiting in venous
occlusions.

Investigation
 CT with IV contrast of the abdomen/pelvis
o Is used to assess renal and accompanying injuries or intra-abdominal fluid
retention.
 Mild trauma generally only requires monitoring, while high-grade injury may
require emergency surgery and intensive care

Table 4.4: AAST Grading System

Grade Type Description

1 Contusion Microscopic or gross hematuria, urologic studies

normal
Hematoma Subscapular, nonexpanding without paranchymal
laceration
2 Hematoma Non expanding perirenal hematoma confined to renal
retro peritoneum
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 Laceration <1 cm paranchymal depth of renal cortex without
urinary extravasation
3 Laceration >1 cm paranchymal depth of renal cortex without
urinary extravasation
4 Laceration Paranchymal laceration expanding through renal
cortex, medulla and collecting system
Vascular Main renal artery or vein injury with contained
hemorrhage
5 Laceration Completely shattered kidney
Vascular Avulsion of renal hilum, devascularizing the kidney

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 4.4.2. Ureteral Trauma

 Epidemiology……………………………………………..222
 Etiology………………………………………………………222
 Clinical Manifestation………………………………..223
 Investigation………………………………………………223

Epidemiology

 Of all urologic traumas, roughly 1% to 2.5% is ureteral.

 Injury to the ureters is rare and generally iatrogenic, occurring mostly during
operative procedures.

Etiology

 Penetrating stab and gunshot wounds and external injury from high-speed blunt
mechanisms contribute to the overall incidence; 95% are penetrating and 5%are
blunt injuries
 External trauma
o Ureteral injuries are often subtle and clinicians must maintain a high index of
suspicion to prevent a delay in diagnosis and comorbidity.
o The presence of massive force injuries in the patient with blunt trauma
should increase the level of suspicion for ureteral injury.
 Surgical Injury
o Any abdominopelvic surgical procedure, whether gynecologic, obstetric,
general surgical, or urologic, can potentially injure the ureter
 Crushing from misapplication of a clamp
 Ligation with suture
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  Transection (partial and complete)
 Angulation of the ureter with secondary obstruction
 Ischemia from ureteral stripping
 Resection of ureteral segment (recently one of the common causes
of ureteral injury are perforations, lacerations and avulsions
sustained during ureteroscopy for stones)
 Ureteral injuries are often subtle and clinicians must maintain a high index of

Clinical Manifestations
suspicion to prevent a delay in diagnosis and comorbidity.
 Hematuria is a nonspecific indicator of urologic injury
 Fever, leukocytosis, and local peritoneal irritation are the most common signs and
symptoms of ureteral injury and always should prompt CT examination.

Investigation
 CT urography with delayed images is the best study for detecting ureteral injuries.
 Retrograde ureterogram is the most sensitive radiographic test for ureteral injury

Table 4.5: AAST Grading (American Association for the Surgery of Trauma)
Grade Description
I  Contusion or hematoma without devascularization
II  Laceration; less than 50% transection
III  Laceration; 50% or greater transection
IV  Laceration; complete transection with less than 2cm of devascularization
V  Laceration; avulsion with greater than 2cm of devascularization

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 4.4.3. Bladder Trauma

 Epidemiology……………………………………………..224
 Etiology………………………………………………………224
 Clinical Manifestation…………………………………225
 Investigation………………………………………………226

Epidemiology
 Due to the protected deep-seated position of the urinary bladder in the bony pelvis,
bladder injuries are quite uncommon.
 They constitute less than 2% of abdominal injuries necessitating surgical
intervention.
 However, the incidence of blunt trauma is rising as a result of modern transportation
preferences.
 The presence of a bladder injury signifies the severity of trauma and is usually
associated with serious injuries to various other organ systems.

Etiology
 Blunt trauma
o Accounts for 67%–86% of traumatic bladder ruptures
o The most common cause (90%) of bladder rupture by blunt trauma is motor
vehicle accident followed by falls, industrial trauma/pelvic crush injuries and
blows to the lower abdomen.
o A urine-filled bladder is particularly susceptible in this kind of conditions;
when trauma occurs after drinking alcohol. In contrast, an empty bladder is
usually well protected.
o Approximately 83-95% of patients with bladder injuries from blunt trauma
have associated pelvic fractures.
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  Penetrating trauma
o Most commonly due to gunshot wounds (85%).
o Stab injuries account for (15%) of the cases.
 Iatrogenic trauma
o Rare
o Following gynecological, obstetric and general surgery procedures:
transurethral or pelvic surgery
 Idiopathic
o This type of condition which may result from combination of overdistended
bladder with minimal trauma.

Clinical Manifestations

 Extraperitoneal and/or intraperitoneal injury:

 Is the most common type of bladder injury, accounting for 85% of the cases.
 It is usually the result of pelvic fractures or penetrating trauma.
 The injury is usually caused by distortion of the pelvic ring, with shearing of the
anterolateral bladder wall near the bladder base or by a ‘counter-coup’ that bursts
opposite the fracture site.
 It commonly presents with:
o Gross hematuria (majority of cases)
o Inability to void
o Pain in the lower abdomen
 Intra-peritoneal injury:
 Are caused by a sudden rise in intravesical pressure, secondary to a blow to the
pelvis or lower abdomen.
 Occurs in about 15% of major bladder injury.
 It’s a result of a direct blow to the already distended bladder.
 Peritoneal surface disrupted with urine extravasations

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  It commonly presents with:
o Peritoneal irritation
o Sudden severe pain in the hypogastrium, often accompanied by
syncope.
o Shock subsides, abdomen distended, no desire to micturate
o Rise in serum creatinine through peritoneal resorption of urinary
creatinine

Investigation
 Retrograde cystography or retrograde CT cystography:
o Severity of injury can be graded
o Can distinguish intra peritoneal from extra peritoneal rupture.
o Extra peritoneal bladder injuries usually resolve with catheterization,
while intra peritoneal injury requires surgery, which can help to prevent
peritonitis and urosepsis

Table 4.6: AATS Grading

Grade Injury Description
1 Hematoma Contusion, intramural hematoma
Laceration Partial thickness
2 Laceration Extra peritoneal (EP) <2cm
3 Laceration EP ≥2 cm or intraperitoneal (IP) <2cm
4 Laceration IP ≥ 2cm
5 Laceration EP or IP extending into bladder neck or ureteral orifice (trigone)

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 4.4.4. Urethral Trauma

 Epidemiology……………………………………………….227
 Etiology………………………………………………………..227
 Clinical Manifestation…………………………………..228
 Investigation………………………………………………..228

Epidemiology
 Uncommon
 10% of male patients and up to 6% of female patients with pelvic fractures
 Girls younger than 17 years of age have a higher risk for urethral injury compared
with women, perhaps because of greater compressibility of the pelvic bones
 In children, injuries are less common but are more likely to extend proximally to
the bladder neck because of the rudimentary nature of the prostate.

Etiology
 External blunt
 Pelvic fracture:
o Most common cause of posterior urethral injury
o Road traffic accidents, falls from a height, crush injuries
 Straddle injury:
o E.g. forceful contact of perineum with bicycle cross-bar*), kick to
perineum; penile fracture
o Most common cause of anterior urethral injury
 External penetrating
 Gunshot—rare; stab—rare.
 Internal, iatrogenic:
 Endoscopic surgery  Radical prostatectomy

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  TURP  Penile surgery
 Catheter balloon inflated in
urethra
 Internal, self-inflicted
 Foreign bodies inserted into urethra—rare

Clinical Manifestations
 Patient usually complain of hematuria, Inability to void despite urge and
suprapubic pain
 The common findings on physical examination include:
o Blood at the urethral meatus
o Socrotal hematoma
o Perineal tenderness
o High-riding prostate on PR exam
o Palpably distended bladder

Investigation
 Retrograde urethrography is gold standard to investigate urethral injury.
Table 4.7: AAST classification
Type Description Appearance
1 contusion blood at the urethral meatus; normal urethrogram
2 Stretch injury Elongation of the urethra without extravasation on urethrography.
3 Partial disruption Extravasation of contrast at injury site with contrast visualized in
the bladder
4 Complete disruption Extravasation of contrast at injury site without contrast visualized
in the bladder, <2cm urethral separation
5 Complete disruption >2cm urethral separation or extension to prostate or vagina

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Management of Urologic Trauma

Renal Trauma: Blunt

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 RenalUreteral
Trauma:Trauma
Penetrating

Bladder Trauma
 For extraperitoneal
o Foley catheter drainage
o Rest
o Prophylactic antibiotic
 For intraperitoneal
o Surgical exploration

Urethral Trauma

 Suprapubic Cystostomy with Planned Delayed Reconstruction

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 Complications of Genitourinary Injury

 Early:
o Bleeding
o Infection, abscess
o Urinary extravasation, urinoma
 Cyst containing urine that forms outside the urinary tract following
trauma or a surgical procedure
o Renal hypertension

 Delayed:
o Bleeding
o Hydronephrosis
o Calculus formation
o Chronic pyelonephritis
o Hypertension
o Arteriovenous fistula
o Urethral stricture
o Urinary incontinence
o Sexual dysfunction
o Loss of function in the affected kidney:
 As a result of hydronephrosis or renal artery stenosis

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 Short Case Discussion
 Content By:
 Enas Hassen
 Samuel Mesfin 4.5. Urethral Catheterization………………………………….…………233
 Edited By: 4.6. Suprapubic Cystostomy……………………………….…………….236
 Samuel Mesfin
 Reviewed By: 4.7. Hypospadias…………………………………………………….………..238
 Dr. Abeselom Lemma 4.8. Video QR Codes.………………………………………………………..247
(Urologist)

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 4.5. Urethral Catheterization
 Introduction………………………………………………..233
 Types…………………………………………………….......233
 Indications…………………………………………………..234
 Contraindications………………………………………..234
 Equipment…………………………………………………..234
 Technique……………………………………………………235
 Removal………………………………………………………235
 Complication……………………………………………….235

Introduction
 Urethral catheterization is a routine medical procedure that facilitates direct
drainage of the urinary bladder.
 It may be used for diagnostic purposes (to help determine the etiology of various
genitourinary conditions) or therapeutically (to relieve urinary retention, instil
medication, or provide irrigation).

Types

 Straight tip
 Coude tip
 3-way catheter

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 Indications

 Diagnostic
o To collect uncontaminated urine specimen
o Urine output monitoring
o Imaging of urinary tract
 Therapeutic
o Acute urinary retention
o Chronic obstruction causing hydronephrosis
o Intermittent bladder decompression
 For neurogenic bladder
o Immobilized pt and unconscious pt
o Pt with urinary incontinence
o Intravesical pharmacologic therapy

Contraindications
 Absolute: Urethral injury secondary to pelvic or straddle injury
 Relative:
o Urethral stricture o Recent surgery

Equipment
 Catheter tray with:
o Povidone-iodine
o Sterile cotton ball
o Lubrication gel
o Sterile glove
o Sterile drape
o Urethral catheter
 Catheter type and size
o Adults: Foley catheter 16F-18F
o Adult male with obstruction at the urethra: Coude tip (18F)

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 o Adults with gross hematuria: Foley catheter (20-24F) or 3-way irrigation
catheter (20-30F)
o Children : Foley, to determine size divide child’s age by 2 and then add 8
o Infants younger than 6 months – Feeding tube (5F) with tape
 Drainage bag

Technique
 Consider prophylactic antibiotics: valvular
heart disease or acute prostatitis.
 Consider intraurethral anesthetic.
 Position: supine, frog leg or knees flexed.
 Locate meatus.
 Apply antiseptic.

 Gently insert lubricated tube until urine is obtained

 Inflate retention balloon slowly with 5cc saline.
 Connect to drainage system.
 Secure tube with tape.

Removal
 Deflate the balloon by aspirating contents with 10cc syringe from side port.
 Withdraw catheter gently, taking care not to splash from tip

Complications
 Infection
 Paraphimosis
 Bladder perforation
 Bladder Fistula (urethral injury)

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 4.6. Suprapubic Cystostomy
 Introduction…………………………………………………236
 Indications……………………………………………………236
 Contraindications…………………………………………236
 Technique…………………………………………………….237
 Complication………………………………………………..237

Introduction

 Cystostomy is the general term for the surgical creation of an opening into the bladder;
it may be a planned component of urologic surgery or an iatrogenic occurrence.
 Often, however, the term is used more narrowly to refer to suprapubic cystostomy or
suprapubic catheterization.

Indications
 Acute urinary retention in which urethral catheter can’t be passed. For example:
o Uretral stricture
o Bladder neck contracture secondary to previous surgery.
 Urethral trauma
 Management of complicated genitourinary tract infection

Contraindications
 Requirement for long term urinary diversion (e.g neurogenic bladder)
 Absolute contraindication
o Distended bladder which is not easily palpable and can’t be localized by ultra-
sonographic assistant
o History of bladder Ca
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  Relative contra indication
o Coagulopathy
o Pelvic cancer with or without history of irradiation
o Pervious lower abdominal or pelvic surgery
o Placement of orthopaedic hardware for pelvic fracture repair

Technique

 Percutaneous
 Open

Complications

 Early complication
o Inadvertent bowel injury o Vascular injury
o Bleeding o Post-operative diuresis
 Intraperitoneal extravasation
 Extra peritoneal extravasation
 Latex allergy
 Refractory hematuria
 Wound infection
 Urosepsis
 Bladder stone
 Tube calcification and
 malfunction

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 4.7. Hypospadias
 Introduction………………………………………………….……238
 Risk Factors…………………………………………………….….238
 Classification……………………………………………………..239
 Epidemiology……………………………………………………..240
 Physical Examination………………………………………...240
 Diagnosis……………………………………………………………241
 Discussion of the Case………………………………………..242
 Management……………………………………………………..244
 Complications…………………………………………………….246

Introduction
 Hypospadias is a congenital anomaly of the male urethra that results in abnormal
ventral placement of the urethral opening. The location of the displaced urethral
meatus may range anywhere within the glans, the shaft of penis, the scrotum, or
perineum
 Hypospadias is defined as a combination of any or all of the following associated
penile anomalies:
o Ectopic urethral meatus
o Penile curvature (chordee)
o Ventral foreskin deficiency with incomplete foreskin closure around the glans,
leading to the appearance of a dorsal hooded prepuce

Risk Factors
 In most cases of hypospadias the cause is unknown.
 Reported risk factors include the following
o Advanced maternal age
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 o Preexisting maternal diabetes mellitus
o Gestational age before 37 weeks
o History of paternal hypospadias
o Exposure to smoking and pesticides
o Placental insufficiency (low placental weight and pathology)
o Prematurity o In-vitro fertilization
o Fetal growth restriction

Classification
 Based on the examination, the penile anatomy can be classified into the following
categories for hypospadias based on the appearance of the foreskin, urethral
location, and the presence and degree of penile curvature
o Normal
o Forme fruste of hypospadias (incomplete or partial presence of hypospadias)
 Approximately 10 percent of hypospadias
o Standard hypospadias
 Ectopic urethral meatus that is accompanied by a classic dorsal
hooded foreskin without fusion of the foreskin to the scrotum with a
normal penile length
 Normal glans size (≥14 mm at maximal diameter)
 Variable penile curvature (approximately 65 percent of hypospadias).
o Severe hypospadias
 Ectopic urethral meatus located in the scrotum or perineum and/or an
abnormally small glans size (<14 mm at maximal diameter) and severe
curvature (approximately 20 percent of hypospadias)
o Less common variants:
 Chordee without hypospadias and megameatus with a normal
appearing foreskin (approximately 5 percent of hypospadias).

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 Epidemiology

 Hypospadias is one of the most common congenital anomalies

 Incidence varies from 0.3 to 0.7 percent in live male births
 The incidence varies with ethnicity

Physical Examination
General
 The newborn examination begins with an overall assessment of the child and
identification of any associated congenital anomalies that would suggest a possible
syndromic cause of hypospadias. Examples include:
o Anridia associated with Wilms tumor
o Hand-foot-mouth anomalies
o Ocular telorism, asymmetry of the skull and laryngoesophageal defects
o Cryptophthalmos and cutaneous syndactyly are features of Fraser syndrome
that is also associated with genitourinary anomalies.
o Other findings that have been associated with hypospadias include:
 Ear tags/deformities  Club feet
 Digit abnormalities  Spinal abnormalities
 Cardiac anomalies  Imperforate anus
Genital examination
 The key aspect of the genital examination is direct visualization of the penis and
glans, hence adequate lighting is obligatory. The examination includes:
o Assessment of the stretched penile length, which should be 2.5 to 3.5 cm in a
full term male.
 To measure the penile length, the glans penis is held with the thumb
and forefinger and the penis is fully stretched until point of increased
resistance is reached.
 The measurement is taken using a ruler or caliper from the pubic
ramus (making sure the suprapubic fat pad is depressed) to the distal
tip of the glans penis over the dorsal side.

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 o Assessment regarding any evidence of penile curvature, and if so, the degree
of curvature.
 The severity of curvature is classified by the assessment of the
curvature when the penis is fully erected as follows:
 Normal  No curvature to 15 degrees
 Mild  15 to 40 degrees
 Moderate  40 to 80 degrees
 Severe  80 degrees
o Assessment of the foreskin to ensure complete and circumferential
development of the foreskin without any ventral asymmetry or deficiency.
 If the foreskin is normally circumferential, it is unlikely that a
significant hypospadias requiring surgery is present.
 If the foreskin is not properly formed, the presence of an ectopic
urethral meatus along the ventral shaft of the penis should be sought
after and identified.
o Determination of the presence of both testicles in the normal dependent
position in the scrotum.

Diagnosis
 The diagnosis of hypospadias is generally made during the newborn genital
examination
 Physical findings consistent with the diagnosis include:
o Abnormal foreskin resulting in an incomplete closure around the glans
leading to the appearance of a dorsal hooded prepuce.
o Abnormal penile curvature (chordee).
o The appearance of "two urethral openings":
 The first in the normal position at the end of the glans
 The second, the abnormally located true urethral meatus.

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 Discussion of the Case

4.7.1. Forme Fruste (incomplete or partial presence) of Hypospadias

 Forme fruste of hypospadias (incomplete or partial presence

of hypospadias) is characterized by clinically insignificant
meatal abnormalities, occasionally asymmetric foreskin, and
no penile curvature.
 The urethral defect is typically manifested as a blind ending
urethral pit or a slightly ectopic urethral meatus, which is
usually located 1 to 2 mm from the normal terminal position of
the urethral meatus on the ventral tip of the glans penis.
 These patients do not have any impairment of voiding or
sexual function, and surgical reconstruction is rarely required.
 In most patients, the foreskin is normal or only slightly
deficient on the ventral aspect.
 However, circumcision may be difficult to perform in more
severe forms of foreskin asymmetry due to the inability to
properly place either a Plastibell or Gomco device over the glans
and have sufficient foreskin to complete the circumcision.
 A less common variation is a normally positioned urethral meatus with incomplete
fusion or separation of the glans with a bridge of ventral skin. These patients may
also have a dorsal hooded foreskin. However, there are no voiding issues with this
variant, and reconstruction of the glans is not necessary.

4.7.2. Standard Hypospadias

 Standard hypospadias is characterized by an ectopic urethral meatus that is
accompanied by a classic dorsal hooded foreskin without fusion of the foreskin to
the scrotum, and a penis of normal length and curvature that varies from none to
mild or moderate
 Standard hypospadias is further subdivided by the location of the ectopic urethral
meatus

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 The severity of hypospadias increases as the position of the displaced urinary
meatus increases from the normal position at the tip of the glans and with increasing
penile curvature.
o Distal – The most common location for an ectopic urethral meatus is at the
proximal glans, coronal margin, or just below the coronal margin
 Patients with distal standard hypospadias typically have a normal-size
penis and glans, and dorsal hooded foreskin due to deficient ventral
foreskin with or without mild penile curvature.
o Proximal – The more severe variant of standard hypospadias occurs when the
urethral meatus is proximally located along the penile shaft, at the
penoscrotal junction or within the scrotum.
 These patients often have moderate amounts of penile curvature. They
have a normal size penis and glans, and a classic dorsal hooded foreskin
without fusion of the foreskin to the scrotum, which distinguishes them
from patients with the more severe hypospadias variant.

4.7.3. Severe Hypospadias

 Severe hypospadias is characterized by an ectopic
urethral meatus located in the scrotum or
perineum, and/or an abnormally small glans (<14 mm
at maximal diameter), and severe penile curvature,
often associated with a ventral penile foreskin tethering
(referred to as short urethral plate) or fusion of the
foreskin to the scrotum
 There is often associated penoscrotal transposition
(where the scrotum inserts above the penis and the
penis is abnormally located well below the scrotum)

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 4.7.4. Uncommon Hypospadias

 Hypospadias with intact foreskin (megameatus intact prepuce)

o In this uncommon variant (approximately 5 percent of cases), the foreskin is
normal, and the urethral abnormality only becomes apparent during or after
circumcision when the glans of the penis is visualized.
o Patients with this form of hypospadias typically have an abnormally large
urethral meatal opening at the coronal margin, referred to as megameatus
intact prepuce
o The clinician and family should be aware that the hypospadias is not caused
by the circumcision and can be repaired whether the circumcision is
completed or aborted.
o As a result, we would recommend the circumcision be completed.
 Chordee with normal urethral meatus
o Patients with this variation of hypospadias have a normal glans and normal
terminal urethral meatus but with atretic urethral spongiosum manifested by
a thin urethra on the penile shaft resulting in penile curvature

Management
 Urologic referral and correction are reserved for those patients in whom there is a
potential functional issue including:
o Significant deflection of the urinary stream
o Inability to urinate from a standing position
o Erectile dysfunction due to penile curvature leading to intercourse difficulties
o Fertility issues due to sperm deposition difficulties
 Urologic referral is not needed for patients with mild defects; this includes patients
with:
o Forme fruste of hypospadias (incomplete or partial presence of hypospadias)
o Standard distal hypospadias (eg, urethral opening at the proximal glans,
coronal margin, or just below the coronal margin) and without penile
curvature.
o Neonatal circumcision should be avoided in patients with:
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  Hypospadias where the foreskin is asymmetric with abnormal
development on the ventral aspect of the penis:
 This anatomical configuration is not conducive to a safe
neonatal circumcision
 Standard and severe forms of hypospadias:
o The foreskin needs to be preserved and reserved for use during
the hypospadias reconstruction to prevent fistula formation
 In severe cases: to reconstruct the new urethra.

 Surgery: indications include:

 Patients with hypospadias who are at-risk for voiding or sexual dysfunction
 The operations used to correct hypospadias include:
o Primary tubularization – Tubularized urethroplasty, with or without incision
of the urethral plate (tubularized incised plate [TIP]):
 It is commonly used for glandular and penile shaft hypospadias repair
 This procedure consists of making a new urethra by rolling a ventral
strip of penile shaft skin
o Onlay island flap:
 For more severe hypospadias
 The urethra is created by transferring a vascular strip of inner foreskin
onto the ventral skin (urethral plate)
o Two-stage hypospadias repair:
 For the most extreme or severe forms of hypospadias, including cases
with significant penile curvature
 It is used to straighten the penis and create a new urethral opening
 In the first operation, performed at six months of age, the curved
penis is corrected by the insertion of dorsal midline plication sutures in
the nerve-free zone at the 12 o'clock position, which straightens the
penis
 This technique allows preservation of sexual function as it does
not affect penile innervation.

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  Excess dorsal foreskin is transferred to the ventral side of the
penis, as this tissue is required for the second stage.
 The second operation is performed at least six months later, after
healing is complete from the first procedure.
 In this stage, the urethra is reconstructed using the transferred
dorsal skin that is now on the ventral aspect of the penis in a
manner similar to the primary tubularization.
o In any of the procedures, the addition of a complete covering layer over the
newly constructed urethra is recommended, as this reduces the risk of
developing a urethral fistula
o Choice of surgical procedure — for standard hypospadias, the procedure of
choice is primary tubularization, and when necessary, incision of the urethral
plate.

Complications
 Urethral fistula
o The most common complication following hypospadias surgery is
urethrocutaneous fistula, which is characterized as two urinary streams
because of the extra urethral opening.
o It is reported in approximately 4 to 20 percent of patients, depending on the
severity of their hypospadias
o Fistula correction requires a second operation that is performed six months
after the initial procedure.
 Urethral stricture:
o It is due to tightening of the reconstructed urethra within the glans, which is
referred to as meatal stenosis.
o These children will have symptoms of straining or pushing on urination and a
thin or fine urinary stream.
o Correction of a urethral stricture requires a second operation at least six
months following the prior surgery.

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 Urethral diverticulum:
o Urethral diverticulum is due to outpouching of the reconstructed urethra.
o These children can have ballooning of the ventral aspect of the penis on
urination and dribbling from retained urine after they void.
o Correction of a urethral stricture requires a second operation, ideally, at least
six months following the prior surgery, unless recurrent infection requires
more immediate intervention.

4.8. Video QR Codes

Urinary Catheterization

Suprapubic Cystostomy

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 Part 5: Gastrointestinal Surgery

Long Case Discussion

5.1. Liver Abscess.………………………..………………..…….249

 Content By: 5.2. Obstructive Jaundice (OJ).………………………...……262
 Nanati Jemal
 Zemichael Getu 5.3. Colorectal Cancer.………………………..………….…….282
 Samuel Mesfin
5.4. Gastric Outlet Obstruction (GOO)…………………..294
 Thomas Mesfin
5.5. Small Bowel Obstruction (SBO)………………….…..318
 Edited By:
 Samuel Mesfin 5.6. Large Bowel Obstruction (LBO)………………………328
5.7. Acute Abdomen …………………………………………...338
5.8. Perianal Emergency.………………………..……….……369
5.9. Abdominal Trauma.………………………..…………….381

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 5.1. Liver Abscess
 Case Discussion………………………………………………….249
 History …………………………………………….……………….249
 Physical Examination…………………………………………251
 Investigation……………………………………………………..252
 Differential Diagnosis………………………………………..253
 Discussion of the Case……………………………………….254

Case Discussion
 A 50-year-old male patient complains of gradual onset dull aching RUQ pain of 1-month
duration with radiation to the right shoulder. He has associated high grade intermittent
fever, chills and rigors. In addition, he developed productive cough of blood tinged
sputum, SOB and pleuritic chest pain. He has history of drinking areke for >20 years. On
physical examination there were signs of pleural effusion and tender hepatomegaly.

History
1) Describe the pain (PQR^2ST)
2) Duration: if acute more likely – pyogenic, if chronic- amoebic, hydatid
3) Ask for Associated symptoms:
 Fever, chills – if high grade fever (pyogenic)
 Loss of appetite, weight loss
 Yellow discoloration
 Symptoms of anemia (blurring of vision, palpitations)
 Change in bowel habit – prior hx of dysentery (amoebic in 3-9%)
 Respiratory symptoms (cough, chest pain) due to diaphragm irritation
4) Asses for risk factors
 Low socioeconomic, immune suppression -amoebic
 Age, sex – older male risk of HCC and abscess
 Alcohol, cigarette history- HCC
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  Contact with jaundiced person, blood transfusion or MSP- Hepatitis for HCC
 Travel history and history of ingestion water or food contaminated with dog
feces- hydatid cyst
 Abdominal trauma or prior history of surgery- pyogenic
 Fever and jaundice (ascending cholangitis) – pyogenic
 DM, underlying pancreatic or hepato-biliary disease-pyogenic, DM for HCC
 OCP use- adenoma of the liver
 Symptoms of cirrhosis(hematemesis, tarry stool, jaundice) - HCC
5) Rule out differential
 Contact with chronic coughed or previous TB treatment -TB
 Hemoptysis, bone pain, bleeding from other site – HCC
 Constitutional symptoms of malignancies (weight loss, fever, loss of appetite) –
HCC
 Jaundice, pale stool, dark urine, itching sensation -biliary disease or hydatid
 Urinary complaints (dysuria, hematuria)- pyelonephritis?
6) Rue out complications
 Cough, SOB, pleuritic chest pain- pleural effusion and pneumonia
 Secondary infection
 Generalized abdominal pain – peritonitis
 Copious brown sputum – rupture to bronchus
 Symptoms of OJ-hydatid cyst complication
 Headache, dizziness & decreased level of consciousness – hydatid cyst cerebral
involvement
7) Ask Treatment in between the symptoms:
 Route of treatment
 Frequency per day
 For how long it was taken

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 Physical Examination

General appearance:

 Comment on nourishment, color- jaundice may be seen in 1/3 of pyogenic abscess

due to biliary causes

Vital:

 Especial attention to BP, RR, Temp to rule out septic shock

HEENT:

 Pallor, icterus, edema (hepatorenal syndrome)

Lymphoglandular System:

 LN enlargement – HCC
 Parotid enlarged, testicular atrophy, gynecomastia – HCC on top of cirrhosis

Respiratory:

 Follow the steps and do detailed examination to check for signs of pleural effusion
and pneumonia as complication

Table 5.1: Pleural effusion Vs. Consolidation

Pleural effusion Pneumonia (consolidation)
 Reduced chest wall movement  Reduced chest wall movement
 Trachea deviation to opposite side  Trachea central
 Stony dullness  Relatively dull on percussion
 Absent/ reduced breath sounds  Reduced breath sounds
 May have bronchial breath sound above  Bronchial sounds
the effusion

CVS:

 Precordial knock, friction rub, p2 accentuation due to RHF in cirrhosis

GI:

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  Perform a detailed and meticulous abdominal examination, which includes:
inspection, auscultation, palpation and percussion.
 Note the Site, Size, shape, surface, edge, consistency, mobility and attachments,
bimanual palpability and pulsatile nature of any palpable mass.
 Also look for stigmata of cirrhosis (spider angioma), stigmata of HCC (bruit over the
liver, friction rub, liver will be irregular, nodular and hard in consistency).
 In liver abscess you will appreciate: tender hepatomegaly: soft, smooth, regular,
mobile
 In hydatid: non tender, round border, smooth surface and enlarged liver with
typical hydatid thrill

Integumentary:

 Look for stigmataof cirrhosis (palmar erythema, duptryne-contracture, jaundice,

clubbing, leukonychia and alopecia)

CNS:

 Look for evidence of cirrhosis, spread of HCC or hydatid cyst spread

Investigation
 CBC: increased total WBC in abscess and hydatid cyst
o Eosinophilic: hydatid
o Neutrophil count increased if pyogenic
 Raised ESR and CRP
 Abdominal ultrasound & US guided aspiration: establishes diagnosis
o Pyogenic:
 Round or oval hypoechoic lesions with well-defined borders and a variable
number of internal echoes.
o Hydatid cysts
 Are well-defined hypodense lesions with a distinct wall.
 Ring-like calcifications of the pericysts are present in 20% to 30% of cases.
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  As healing occurs, the entire cyst calcifies densely, and a lesion with this
appearance is usually dead or inactive.
 Daughter cysts generally occur in a peripheral location within the main cyst
and are typically slightly hypodense compared with the mother cyst.
 CT followed by FNAC: when in doubt
o Pus for gram stain, culture and sensitivity
o Pyogenic: hypodense with peripheral enhancement and may contain air-fluid
levels indicating a gas-producing infectious organism.
 CXR: for empyema thoracic, perforated viscous
 Stool exam:
o Amoebic cyst, culture and sensitivity for typhoid bacilli
 Serologic testing (indirect hemagglutinin test):
o 90-95% amoebic abscesses
 Sigmoidoscopy:
o Shows flask shaped ulcer in amoeba
 AFP and metastasis workup: HCC
 Plain x-ray:
o Speckled calcification of hydatid cyst
 ERCP:
o If there is OJ following hydatid cyst

Differential Diagnosis

1. Pyogenic liver abscesses

2. Amoebic liver abscesses
3. Hydatid cyst
4. HCC
5. Abdominal TB

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 Discussion of the Differentials

5.1.1. Pyogenic Liver Abscess

 Introduction …………………………………………..……….254
 Epidemiology……………………………………………………254
 Risk Factors………………………………………………………255
 Microbiology……………………………………………………255
 Clinical Manifestation………………………………………256
 Diagnosis………………………………………………………….256
 Management……………………………………………………256

Introduction

 Pyogenic liver abscesses usually develop following peritonitis due to leakage of

intraabdominal bowel contents that subsequently spread to liver via the portal
circulation or via direct spread from biliary infection.
 May also result from arterial hematogenous seeding  Systemic infection
 They may be single or multiple and are more frequently found in the right lobe of
the liver due togreater blood supply.
 The abscess cavities are variable in size and, when multiple, may coalesce to give a
honeycomb appearance.

Epidemiology
 Liver abscesses are the most common type of visceral abscess
 The annual incidence of liver abscess has been estimated at 2.3 cases per 100,000
populations and is higher among men than women (3.3 versus 1.3 per 100,000).

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 Risk Factors

 Diabetes
 Underlying hepatobiliary or pancreatic disease
 Liver transplant
 Geographic and host factors may also play a role:
o For example, a primary invasive liver abscess syndrome due to K.
pneumoniae has been described in East Asia.
 Independent risk factors for mortality include:
o Need for open surgical drainage
o The presence of malignancy
o The presence of anaerobic infection

Microbiology
 Approximately 40% of abscesses are monomicrobial, an additional 40% are
polymicrobial, and 20% are culture-negative.
 The most common infecting agents are gram-negative bacteria:
o Escherichia coli is found in two thirds of cases
o Other common organisms include:
 Streptococcus  Klebsiella
faecalis  Proteus vulgaris
 Anaerobic organisms such as Bacteroidesfragilisalso are seen frequently.
 In patients with endocarditis and infected indwelling catheters:
o Staphylococcus and Streptococcus species are more commonly found.
 Arise from:
- Ascending infection-infected and obstructed biliary tree
- Haematogenous
- Localized liver necrosis-trauma, local ablative therapies
- Cryptogenic
- Impaired biliary drainage
- Subacute bacterial endocarditis
- Infected indwelling catheters
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 - Dental work
- The direct extension of infections such as diverticulitis or Crohn’s disease into
the liver.

Clinical Manifestations
 Fever
 Abdominal pain and tenderness,
o Usually localized to the right upper quadrant and may include pain, guarding,
rocking tenderness (pain caused by gently rocking the patient's abdomen), and
even rebound tenderness
 Nausea and vomiting
 Anorexia and weight loss
 Hepatomegaly and Jaundice

 Lab: ↑ WBC, Bilirubin, enzymes, ↓ HCT and Albumin

 G-stain and culture of the pus, blood culture

Diagnosis
 Imaging
o CXR  Elevated diaphragm, pleuraleffusion, atelectasis, sub-diaphragmatic
air-fluid level
o U/S and CT –localize the abscess and guide percutaneous treatment

Management
 The Goal
1) Complete drainage of pus and infected debris.
2) Initiation of adequate antibiotic therapy.
3) Resolution of the underlying cause.

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 Treatment options ranges from antibiotic therapy alone to major operative
interventions.
 Blood samples should be obtained before starting antibiotics if possible.
 Broad-spectrum parenteral therapy must begin as soon as possible.
o Antibiotics – 4-6 weeks  ceftriaxone [G +ve and -ve] plus metronidazole
[anaerobe]
o Drain: indication failure to respond to antibiotics, abscess> 6cm, impending
rupture
 Percutaneous
 Laparoscopic
 Open-drainage /resection [when most part of liver affected]
 Treat the underlying cause- e.g biliary obstruction
 PCD is performed when:
o The pus is too thick to be aspirated
o The abscess is greater than 5 cm in diameter
o The wall is thick and non-collapsible
o The PLA is multi-loculated
o Failure of PCD may occur in as many as 10% of patients.

 Surgical therapy is indicated

o Intraperitoneal rupture.
o Rx. of complications of the PD (bleeding or intraperitoneal leakage of pus.)
o Patients with an underlying pathology that needs surgical inter.
o Large, multiloculated abscesses containing thick pus.

 Procedure  Aspiration of pus  Open the

abscess cavity  Break loculation 
Debride the abscess cavity

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 5.1.2. Amoebic Liver Abscess
 Introduction …………………………………………………………….258
 Epidemiology…………………………………………………………...258
 Risk Factors………………………………………………………………259
 Clinical Manifestation……………………………………………….259
 Diagnosis………………………………………………………………….260
 Management……………………………………………………………261

Introduction
 Amebic liver abscess is the most common extra intestinal manifestation of
amebiasis.
 Amebae establish hepatic infection by ascending the portal venous system

Epidemiology
 Amebic liver abscess (and other extra intestinal disease) is 7 to 10 times more
common among adult men than other demographic groups, despite equal gender
distribution of colonic amebic disease.
 It is observed most frequently in the fourth and fifth decades of life.
 The reasons for these observations are not fully understood; suggested mechanisms
include hormonal effects and a potential role of alcoholic hepatocellular damage in
creating a nidus for portal seeding.
 In developed countries, amebiasis is generally seen in migrants from and travelers to
endemic areas.
 Amebiasis is relatively uncommon among short-term travelers, but amebic liver
abscesses can occur after travel exposures as short as four days.

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 Risk Factors

 Use of steroid  Advanced age

 Malignancy  Malnutrition
 Homosexuals
 Heavy alcohol consumption
 It has been suggested that immunosuppression secondary to HIV may increase the
likelihood of presenting with an amebic liver abscess

Clinical Manifestations
 One to two weeks of right upper quadrant pain and fever (38.5 to 39.5ºC).
o Pain may be referred to the epigastrium, the right chest, or the right
shoulder.
o The pain is usually dull but may be pleuritic or aching.
 Cough  Malaise
 Sweating  Hiccoughs
 Anorexia and weight loss
 Concurrent diarrhea is present in less than one-third of patients
o Some patients report history of dysentery within the previous few months.
 Jaundice occurs in less than 10 percent of patients
 Physical examination reveals hepatomegaly and point tenderness over the liver in
approximately 50 percent of cases.
 Rupture of liver abscess can occur into any adjoining space or organ; extension into
the chest occurs almost four times as often as extension into the peritoneal cavity.
o In up to 7 percent of cases peritonitis and hepatic vein and inferior vena cava
thrombosis
 Patients with secondary cardiac or pulmonary involvement may present with
symptoms primarily due to these complications.
 Occasionally patients have a more chronic presentation:
o Fever o Abdominal pain
o Weight loss o Hepatomegaly

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 Diagnosis

 Lab
o A leukocytosis (>10,000/mm3) without eosinophilia.
o Alkaline phosphatase
 Elevated (80 percent of cases)
o Hepatic transaminases
 May also be elevated.
o Amebic Serology:
 Highly sensitive and specific in the differentiation b/n PLA and ALA.
 An indirect hemagglutinin test (IHAT)  90% sensitive.
 EIA detects antibodies specific for E. histolytica in ~ 95% of pnts with
extraintestinalamebiasis.
 Currently: ELISA and IHATappear to be the most reliable tests, with
sensitivity and specificity > 95%
 Imaging
o CXR
 Elevation of the right dome of the diaphragm
 Atelectasis of the right lung
 Pleural effusion
 Gas in the biliary tree or liver parenchymal.
o US:
 Preferable diagnostic test (90% accuracy).
 Round or oval, with well-defined margins.
 Single:
 80%: right lobe  6%: caudate lobe
 10%: left lobe
 The remaining are multiple abscesses.
 CT scan:
o Does not add to the diagnostic accuracy
o Is helpful in differentiating amebic from pyogenic abscesses and in identifying
simple cyst & necrotic tumor.

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 Management

Chemotherapy
 Metronidazole is the drug of choice for ALA (500-750 mg TID for 7 -10 days) with
cure rate >90%.
 Luminal agent:  Paromomycin, iodoquinoldiloxanide furoate.
 Emetine hydrochloride reaches amebicidal concentrations in tissues rather than
intestine.
Aspiration or PCD indicated
1. Age older than 55 years,
2. Abscess greater than 10 cm in diameter, and
3. Failure of medical therapy after 7 days
4. Failure to differentiate PLA from ALA
5. Abscesses that extended into the peritoneal cavity.
Open laparotomy indicated
1. Doubtful diagnosis
2. Concomitant hollow viscus perforation with fistulation: in life-threatening
hemorrhage or sepsis
3. Failure of conservative management.
Treat the complications
1) Pulmonary complications:
o Thoracocentesis
o Pulmonary decortication  If amebic empyema complicated by secondary
infection.
o Lung abscess:  Postural drainage, bronchodilators, and anti- amebic drugs
may suffice.
2) Vascular and Pericardial Involvement
o Pericardial thickening or pericardial effusion: Aspiration of a left-sided ALA.
o Cardiac Tamponade: Pericardiocentesis + drainage of liver abscess & anti-
amebic drugs

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 5.2. Obstructive Jaundice (OJ)
 Case Discussion……………………………………………..262
 History ………………………………………………………….262
 Physical Examination…………………………………….264
 Investigation…………………………………………………265
 Differential Diagnosis……………………………………267
 Discussion of the Case…………………………………..267
 Discussion of the Differentials……………………….272

Case Discussion
 A 55-year-old male soldier who presented with dull aching generalized abdominal pain of
2-month duration. He has associated nausea, vomiting and loss of appetite. He had yellow
discoloration of the eye and palm. In addition, he had clay colored stool, dark urine and
itching at night. He also had alcohol and smoking habit.

History
1) Chief complaints and associated symptoms

 Jaundice: Duration, Onset, Progression, Associated with pain or not

 Fever: ask if Intermittent/continuous, Duration, Association with chills and rigors
 Dark urine, Pale stool, pruritus: mostly with pancreatic head Ca
 Weight loss: CBD stone, malignancy
 GI bleeding: OJ can cause cirrhosis resulting in anorectal varices and hemorrhoids
or the bleeding can be due to periampulary tumor
 Steatorrhea, bleeding tendencies: fat malabsorption
 Fat intolerance: bloating and stomach distention, diarrhea, gas, steatorrhea,
greasy stool
2) Asses for risk factors

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  Age and sex: Cholelithiasis-30-50 of age and usually female, 50-70 years
periampulary cancer more likely
 Previous history of malignancy
 History of previous gallbladder surgery- may lead to bile strictures and jaundice, also
endo prosthesis or stents cold be risk factors
 Look for the 5 F’s – risk for stone
 Alcohol, drugs and medication:
o OCP, hormone replacement therapy are a risk factor for cholelithiasis
o Alcohol abuse risk for pancreatic cancer
 Past history of DM
 Known gallstone disease
3) Rule out differential
 Pain
o Colicky: sharp RUQ pain which occurs after having a heavy meal or during the
night usually waking the patient from sleep. It may radiate to the right
scapular area or the chest. It may last from 15 minutes to a few hours –
choledocholithiasis
o Painless or dull aching persistent pain: pancreatic head cancer back pain-
retroperitoneal extension of PCa
 Acuteness of symptoms: perampullary ca has shorter duration (1-3) months
 Color of jaundice: deep yellow (choledocholithiasis), greenish yellow (perampullary
Ca)
 Anemia symptoms: light headedness, malaise, dizziness, fatigue, palpitations -
perampullary Ca
 Early satiety, vomiting, belching: pancreatitis or biliary stricture
 Family history of jaundice
 Round worm infestation: Ascaris
 History of contact with a jaundiced patient, transfusion, drug abuse/needle sharing,
needle-stick injuries, sexual contact – rule out pre-hepatic and hepatic cause of
jaundice

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4) Rule out complication
 Chariots triad and Reynolds pentad
 Encephalopathy following liver decompensation
 Diarrhea of recent onset- liver failure
 Bone pain, neck lump, dyspnea: periampulary cancer metastasis
 Urinary symptoms and edema: renal failure

Physical Examination
 General appearance

o In distress? Cachectic? Any abdominal distension?

 Vital signs
o In Shock? Any Fever? Dehydration?
 HEENT
o Icterus? (Yellow discoloration of sclera, skin, nail bed, under surface of tongue,
soft palate)
 Lymph glandular system
o Supraclavicular, periumbilical,axillary, inguinal lymph nodes, testis
 Peripheries
o Stigmata of chronic liver disease
o Scratch marks
 Abdomen
o Surgical scars, scratch marks
o Generalized distension, dialated periumbilical veins: cirrhosis, portal
hypertension and liver decompensation (Could be due to metastatic disease, or
primary liver pathology)
o Movement with respiration
o Look for fullness in right hypochondrium due to distended gallbladder (Can be
seen in very thin patients).

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 o Hepatomegaly: is common in both hepatic and post hepatic jaundice. Palpation
of an enlarged irregular liver suggests cancer and a shrunken nodular liver is
likely to be due to cirrhosis.
o Murphy’s sign

Palpable Gallbladder When distended it can be felt as tense globular swelling

– Mucocele projecting downwards and forwards from below the liver just

– Empyema lateral to the outer border of rectus muscle (Below the 9th rib

– Carcinoma of pancreas tip) and it moves with respiration.

– Carcinoma of gall bladder

Courvoisier’s law: Exception to the law:

 Double impaction by stone
 If the gall bladder is palpable in a person with painless
 Oriental cholangiohepatitis
obstructive jaundice, the cause is unlikely to be stones. A
 Pancreatic calculus obstructing
non-tender, palpable gallbladder in a jaundiced patient
ampulla of vater
suggests malignant common duct obstruction, but absence
 Mucocele due to stone in cystic duct
of a palpable gallbladder does not rule out cancer.

 Intrgumentary system: - bruising, scratch marks, dryness, hyper-pigmentation,

xanthomas, spider angioma, petichae, palmar pallor
 Nervous system: -personality changes, flapping tremor

Investigation
Laboratory Studies

 CBC: Hb, Hct and WBC

 Serum electrolytes
 LFT
o Billrubin, Albumin and PT (Increased direct bilirubin suggests OJ)
 Liver enzymes – AP, AST, GGT and ALT
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 o Elevated alkaline phosphatase > 10 times normal is strongly suggestive of
obstruction and simultaneous elevation of gamma-glutamyltransfers(40
times) confirms obstruction
 Serum Amylase
 Urine analysis and RFT:
o 0.05mg/dl bilirubin can be seen on the urine with strip test
 Hepatitis serology
 Stool examination
 Coagulation profile:
o Prolonged prothrombin time which can be normalized with injection of vitamin
K.
 ANA and Ant mitochondrial AB:
o Primary sclerosing cholangitis

Table 5.2: Normal value of Tests

Test Normal Range
Bilirubin 5-17 µmol/l
Alkaline phosphatase 35-130 IU/l
Aspartate transaminase 5-40 IU/l
Alanine transaminase 5-40 IU/l
Gamma-glutamyltranspeptidase 10-48 IU/l
Albumin 35-50 g/l
Prothrombin time 12-16 sec

Imaging:

 Plain x-ray:
o Shows radiopaque gallstones in 10% of the patients  Mercedzbenz sign
 Ultrasonography: Initial imaging modality of choice; shows
o Biliary calculi
o Size and thickness of Gall bladder
o Presence of inflammation around GB
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 o Size of Common Biliary Duct
o Stones within the biliary tree
 Preferred for GB stones rather than CBD stones
 CT:
o The modality of choice in the staging of cancers of the liver, gall bladder, bile
ducts and pancreas.
o It is inferior to u/s to diagnose stones
 MRCP: replaced ERCP
 ERCP: gold for CBD stone removal
 PTC: to diagnose pathologies in higher level above cystic duct
 Barium meal follow through:
o Periampulary ca - inverted 3 sign
o Pancreatic head tumor – pad sign

Differential Diagnosis
1. Congenital: Biliary atresia, choledochal cyst
2. Inflammatory: Ascending cholangitis, sclerosing cholangitis
3. Obstructive: Common bile duct (CBD) stones, biliary stricture, parasitic infestation
4. Neoplastic: Carcinoma of head of pancreas, periampulary carcinoma, cholangio-
carcinoma, Klatskin tumor
5. Extrinsic compression: Compression by lymph nodes

Discussion of the Case

 Jaundice is a generic term, which describes yellow pigmentation of the skin, mucous
membrane or sclera. It can be caused by pre-hepatic, hepatic and post hepatic
causes.

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  Obstructive jaundice is strictly defined as a condition occurring due to a block in the
pathway between the site of conjugation of bile in liver cells and the entry of bile
into the duodenum through the ampulla
 Normal serum bilirubin level is from 0.3-1.0 mg/dL.
o Conjugated: 0.1- 0.3mg/dl
o Unconjugated: 0.2-0.7mg/dl
 Jaundice is clinically detected in sclera when serum bilirubin is greater than 2.5-
3mg/dl.
 Jaundice is clinically detected in skin/mucus membrane when serum bilirubin is
greater than 6.0mg/.

Globin Fe2+, CO
HO Bilirubin
Hemoglobin Heme Biliverdin
(insoluble) Spleen
O2, H2O,
NADPH NADP+

Bilirubin-albumin
conjugate Blood

Bilirubin

Liver

Bilirubin diclucorinide

Excreted

Physiology
 Normal secretory pressure of bile is 15-25cm of water.
 At 35cm of water, there is suppression of bile flow.
 High pressure leads to cholangiovenous and cholangiolymphatic reflux of bile.
 Dilation of bile duct and intra hepatic biliary radicals (IHBR)
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 Pathophysiology
 Increase in biliary pressure leads to
o Disruption of tight junctions between hepatocytes and bile duct cells with
increased permeability
o Reflux of bile contents in liver sinusoids
o Neutrophil infiltration, increased fibro genesis and deposition of reticulin fibers in
portal triad
o Reticulin fibers get converted to type 1 collagen
o Laying down of collagen fibers leads to hepatic fibrosis obstruction of sinusoids and
secondary biliary cirrhosis and portal hypertension
o Fibrosis can also lead to atrophy of obstructed liver.

Causes:
A. In the lumen of duct C. Outside the wall
B. In the wall of duct 1. Benign
1. Congenital 2. Malignant
2. Acquired

Clinical Classification:
Table 5.3: Clinical Classification
Type 1 (Complete) Type 2 (Intermittent)
 Malignancy of Head of Pancreas  Choledocholithiasis
 Ligation of Common Bile Duct  Periampulary tumor
 Cholangiocarcinoma  Duodenal diverticula
 Parenchymal Liver Disease  Choledochal Cyst
 Papillomas of the bile duct
 Intrabiliary parasites
 Hemobilia

Clinical Presentation:

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  Pruritus
 Clay colored stools, High colored urine
 RUQ pain and tenderness
 Biliary colic
 Steatorrhea, Bleeding tendency
 Icterus
 Nausea/Vomiting, Anorexia, Weight loss
 High grade fever with chills

Diagnosis:
 The sensitivity of history, physical examination, and blood tests alone range from
70% to 95%, whereas the specifity is approximately 75%.
 The overall accuracy of clinical assessment of hepatic and post-hepatic causes of
jaundice ranges from 87%-97%.

Complications:
 Can be due the underlying pathologies or due to procedures for management.
 Cholangitis  Renal failure
 Cholecystitis  Liver failure
 Hypoprotenemia and Malnutrition  Acute pancreatitis
 Liver abscess  Reccurent stone
 Septicemia  Coagulation factor defect
 Biliary cirrhosis

Management:
1) Pre-op:
 Fluid and electrolyte:
o Intravenous administration of 5% dextrose saline followed by 10% mannitol
or loop diuretics to prevent renal failure (12-24 hours prior to surgery)
 Nutrition:

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 o High protein high carbohydrate and low fat diet through enteral route to
increase the glycogen reserve
 Coagulopathy:
o Intramuscular vitamin K(1-10mg), Fresh frozen plasma
 Endotoximia:
o Broad spectrum Antibiotic prophylaxis, Lactose, Early enteral nutrition
 Pain management
 Cholestyramine and antihistamine for symptomatic relief of pruritus
 Antiemetics are given to minimize nausea and vomiting

2) Surgical
 Cholidocolithiasis
o Sphincterotomy & ductal clearance, followed by laparoscopic
cholecystectomy or
o Found with intraoperative cholangiogram during cholecystectomy,
laparoscopic CBD exploration via the cystic duct or with formal
choledochotomy
 Pancreatic ca
o Palliative
o Pain>narcotic
o Jaundice and pruritus
 Endoscopic sphincterotomy
+
Stenting with percutaneous trans-hepatic biliary drainage
 Cholidochoduodenostomy
 Cholidochojejunostomy
 Cholecystojejunostomy
o Surgical resection > whipple’s resection
o Adjuvant therapy: Chemotherapy, Radiotherapy
 Cholangiocarcinoma
o Biliary decompression + cholecystectomy (to prevent cholecystitis)
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 Discussion of the Differentials

5.2.1. Choledocholithiasis

 Introduction …………………………………………………………….272
 Epidemiology……………………………………………………………272
 Risk Factors………………………………………………………………272
 Clinical Manifestation…………………………………………….…272
 Diagnosis……………………………………………………………….…274

Introduction
 It refers to the presence of gallstones within the common bile duct (CBD).

Epidemiology
 The exact incidence and prevalence of Choledocholithiasis are not known, but it has
been estimated that 5 to 20 percent of patients have CBD stones at the time of
cholecystectomy, with the incidence increasing with age.

Risk Factors
 In the setting of bile stasis (eg, patients with cystic fibrosis)
 Elderly patients with large bile ducts and periampullary diverticular
 Patients with recurrent or persistent infection involving the biliary system

Clinical Manifestations
 Patients with CBD stones may be asymptomatic or present with pain and liver test
abnormalities with or without evidence of complications.
o Asymptomatic presentation

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  In such patients, the diagnosis is typically made when imaging studies are
obtained for unrelated reasons, when a patient is being evaluated for
abnormal liver tests, or when an intraoperative cholangiogram is obtained
during cholecystectomy.
o Pain and liver test abnormalities
 Patients with uncomplicated CBD stones typically have pain and abnormal
liver tests, but are afebrile and do not have other abnormal laboratory tests.
Symptoms
 Right upper quadrant or epigastric pain
o The pain is often more prolonged than is seen with typical biliary colic and
resolves with either spontaneous passage or removal of the CBD stone.
o Some patients have intermittent pain due to transient blockage of the CBD
(ball-valve effect).
 nausea, and vomiting
Complicated Choledocholithiasis
 Acute cholangitis
o Charcot's triad:
 Fever
 Right upper quadrant pain
 Jaundice
o Leukocytosis
o Bacteremia and sepsis may lead to hypotension and altered mental status
(Reynolds' pentad)
 Biliary pancreatitis
o Pain o Vomiting
o Nausea o Elevated liver tests
o Elevations in serum amylase and lipase (by definition >3 times the upper limit
of normal)
o Imaging findings suggestive of acute pancreatitis.

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 Diagnosis

 In a 2010 guideline, the American Society for Gastrointestinal Endoscopy (ASGE)

proposed a strategy to stratify patients based upon their risks of having CBD stones.
Patients were stratified using the following predictors.

"Very strong" Predictors

 The presence of a CBD stone on transabdominal ultrasound
 Clinical ascending cholangitis
 A serum bilirubin greater than 4 mg/dL (68 micromol/L)
"Strong" Predictors
 A dilated CBD on u/s (> 6 mm in a patient with a gallbladder in situ)
 A serum bilirubin of 1.8 to 4 mg/dL (31 to 68 micromol/L)
"Moderate" Predictors
 Abnormal liver biochemical test other than bilirubin
 Age older than 55 years
 Clinical gallstone pancreatitis

 Patients with at least one very strong predictor or both strong predictors are considered high-risk.
Patients who do not qualify as high-risk, but who have at least one of the strong or moderate
predictors are considered intermediate-risk. Patients with no predictors are considered low-risk.

 High-risk
o Proceed directly to ERCP
 Intermediate-risk
o If the patient is a surgical candidate, proceed to laparoscopic
cholecystectomy with intraoperative cholangiography or ultrasonography.
o If the patient refuses surgery, is not a surgical candidate, or is post-
cholecystectomy, further imaging with an MRCP or EUS is recommended.
o If no CBD stones are seen on MRCP but suspicion remains for bile duct
stones, proceed to EUS.

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 o If no CBD stones are seen by EUS, proceed to laparoscopic cholecystectomy in
patients who are surgical candidates (assuming cholelithiasis has been
confirmed by transabdominal or endoscopic ultrasound).
o If a stone is seen on MRCP or EUS proceed to ERCP, followed by laparoscopic
cholecystectomy (in surgical candidates) either during the same
hospitalization or electively.
 Low-risk
o If stones or sludge are present within the gallbladder and the patient is a
good surgical candidate, proceed to laparoscopic cholecystectomy without
imaging of the CBD preoperatively or intra-operatively.

5.2.2. Exocrine Pancreatic Cancer

 Introduction ……………………………………………………….……275
 Epidemiology……………………………………………………………276
 Risk Factors………………………………………………………………276
 Pathology………………………………………………………………...276
 Clinical Manifestation………………………………………….……276
 Diagnosis…………………………………………………………….……278

Introduction
 The commonly used term "pancreatic cancer" usually refers to a ductal
adenocarcinoma of the pancreas (including its subtypes), which represents about
85 percent of all pancreatic neoplasms.
 Approximately 60 to 70 percent of exocrine pancreatic cancers are localized to the
head of the pancreas, while 20 to 25 percent are in the body/tail and the remainder
involve the whole organ.

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 Epidemiology

 Pancreatic cancer is the fourth leading cause of cancer-related death in the among
both men and women.
 The majority of these tumors (85 percent) are adenocarcinomas arising from the

Risk Factors
ductal epithelium.

 Hereditary  Diabetes mellitus

 Cigarrate smoking  NSAIDS and aspirin
 Coffee and alcohol use
 Obesity and physical inactivity

Pathology
 History of partial gastrectomy or cholecystectomy
 Helicobacter pylori and Hepatitis B virus

 Of the several subtypes of ductal adenocarcinoma, most share a similar poor long-
term prognosis, with the exception of colloid carcinomas, which have a somewhat
better prognosis.
 The more inclusive term "exocrine pancreatic neoplasms" includes all tumors that

Clinical Manifestations
are related to the pancreatic ductal and acinar cells and their stem cells (including
pancreatoblastoma), and is preferred.

 The initial presentation of pancreatic cancer varies according to tumor location.

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 Pancreatic head tumors more often present with jaundice, steatorrhea, and weight
loss
 The most common presenting symptoms are pain, jaundice, and weight loss.
o The pain
 Insidious in onset, and has been present for one to two months at the
time of presentation.
 Rarely, pain develops very acutely, as a result of an episode of acute
pancreatitis due to tumor occlusion of the main pancreatic duct
 Typical gnawing visceral quality is generally epigastric, radiating to the
sides and/or straight through to the back.
 Severe back pain should raise suspicion for a tumor arising in the body
and tail of the pancreas
 Intermittent and made worse by eating or lying supine.
 It is frequently worse at night. Lying in a curled or fetal position may
improve the pain.
o Jaundice
 Usually progressive,
 May be accompanied by pruritus, darkening of the urine, and pale stools.
 Painless jaundice has been more favorable prognosis
 Early sign in tumors arising from the pancreatic head
 Jaundice secondary to a tumor in the body or tail typically occurs later in
the course of the disease, and may be secondary to liver metastases.
 Unexplained superficial thrombophlebitis, which may be migratory (classic
Trousseau’s syndrome) is sometimes present.
o It reflects the hypercoagulable state that frequently accompanies pancreatic
cancer (more commonly in tumors of tail or body of the pancreas).
 Atypical diabetes mellitus may be noted
 Signs of metastatic disease
o An abdominal mass or ascites
o Left supraclavicular lymphadenopathy (Virchow's node)

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 Diagnosis

o A palpable periumbilical mass (Sister Mary Joseph’s node) or a palpable rectal

shelf are present in some patients with widespread disease.

1) Transabdominal ultrasound (US)

 Transabdominal US has high sensitivity for detecting biliary tract dilation and
establishing the level of obstruction.
 It also has high sensitivity (>95 percent) for detecting a mass in the pancreas,
although sensitivity is lower for tumors<3 cm.
2) Abdominal CT scan
 If a pancreatic mass is seen on transabdominal US
 Typically obtained to confirm the presence of the mass and to assess disease
extent.
3) ERCP
 Indicated if choledocholithiasis remains in the differential diagnosis after initial
evaluation or if biliary decompression is required.
 Stent placement should be avoided in patients who have not yet undergone CT
o It may cause artifact in the pancreatic head that can mask the lesion
o The trauma of stent insertion may induce inflammatory changes that
might be indistinguishable from tumor
4) CA 19-9
 The reported sensitivity and specificity rates of CA 19-9 for pancreatic cancer
range from 70 to 92, and 68 to 92 percent, respectively.
 However, sensitivity is closely related to tumor size.
 CA 19-9 levels are of limited sensitivity for small cancers.
 Serum levels of CA 19-9 do have some value as prognostic markers
5) Biopsy
 Histologic confirmation is required to establish a diagnosis of pancreatic cancer

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 5.2.3. Cholangiocarcinoma
 Introduction ………………………………………………….…………279
 Epidemiology……………………………………………………………279
 Pathophysiology……………………………………………………….279
 Risk Factors………………………………………………………………280
 Clinical Manifestation………………………………………….……280
 Diagnosis…………………………………………………………….……281

Introduction
 Cholangiocarcinomas arise from the intrahepatic or extrahepatic biliary epithelium.
 More than 90% are adenocarcinomas, and the remainders are squamous cell
tumors.
 The etiology of most bile duct cancers remains undetermined.

Epidemiology
 Incidence in most Western countries ranges from 2 to 6 cases per 100,000 people
per year.
 The highest annual incidences are in Japan, at 5.5 cases per 100,000 people

Pathophysiology

 Cholangiocarcinomas tend to grow slowly and to infiltrate the walls of the ducts,
dissecting along tissue planes.
 Local extension occurs into:
o The liver/ porta-hepatis
o Regional lymph nodes of the celiac and pancreatico-duodenal chains.

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 Risk Factors

 Infections:

o Liver flukes
o Ascaris
o H.pylori
 IBD
o Cholangiocarcinoma generally develops in patients with long-standing
ulcerative colitis and primary sclerosing cholangitis.
 Chemical exposure:
o Workers of aircraft, wood and rubber industires
 Miscellaneous: choledochal cyst
 Bile duct adenoma
 Obesity

Clinical Manifestations

Signs and symptoms of cholangiocarcinoma include the following:

 Jaundice
o Best detected in direct sunlight
o Occurs early if the tumor is located in the common bile duct or common hepatic
duct.
o Occurs later in perihilar or intrahepatic tumors and is often a marker of advanced
disease.
 Clay-colored stools
 Bilirubinuria (dark urine)
 Pruritus
 Weight loss
 Abdominal pain
o Relatively common in advanced disease. It often is described as a dull ache in
the right upper quadrant.
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 A palpable gallbladder:
o If the cholangiocarcinoma is located distal to the cystic duct takeoff
 An abdominal mass or palpable lymphadenopathy: uncommon
 Hepatomegaly may be noted in as many as 25% of patients.

Diagnosis

1. Ultrasound
 May demonstrate biliary duct dilatation and larger hilar lesions.
 Patients with underlying primary sclerosing cholangitis (PSC) may have limited
ductal dilatation secondary to ductal fibrosis.
 Doppler ultrasound may show vascular encasement or thrombosis.
2. CT
 Resembles ultrasound in that it may demonstrate ductal dilatation and large mass
lesions.
 Evaluates for pathologic intra-abdominal lymphadenopathy.
 Helical CT scans are accurate in diagnosing the level of biliary obstruction.
3. Magnetic resonance imaging (MRI)
 Demonstrates hepatic parenchyma
 MR cholangiography enables:
o Imaging of bile ducts
o In combination with MR angiography, permits staging (excluding vascular
involvement)
o Hepatic involvement can also be detected.
4. Biopsy

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 5.3. Colorectal Cancer
 Case Discussion…………………………………………………..282
 History …………………………………………………………..…..282
 Physical Examination…………………………………….…….284
 Investigation…………………………………………………….…285
 Differential Diagnosis………………………………………….285
 Discussion of the Case…………………………………….…..287

Case Discussion
 A 70-year-old man was seen in the surgical outpatient clinic complaining of a 3-month
history of loose stools. He normally opens his bowels once a day, but has recently been
passing loose motions up to four times a day. The motions have been associated with the
passage of blood clots and fresh blood mixed within the stools. His appetite has been
normal, but he reports a 2-stone weight loss. The past history was otherwise
unremarkable. His father died from cancer at the age of 45 years, but he is unsure of the
origin. On physical exam, there was no pallor or lymphadenopathy is present. The
abdomen is soft and non-tender with no palpable masses. Digital rectal examination is
normal.

History

1) Asses risk factors

 Family history of colorectal cancer ( first degree relative or >2 relatives)
 Diet (high fat, low fiber, low fruit) and those high in calcium, selenium, vitamins A,
C, and E, carotenoids, and plant phenols are thought to be protective
 Past history of IBD
 Age (>50), jews ethnicity
 Sex (right sided colonic ca more common in female and left in male)
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  Obesity
 Smoking and alcohol
 Pelvic radiation
 Other: acromegaly patient and with history of ureterosigmoidostomy
2) Look for symptoms
 Right sided colonic Ca
o Melena/ maroon colored stool
o Anemia symptom (dizziness, palpitation, blurring of vision, fatigue)
o Right sided abdominal swelling/mass
 Left sided colonic ca
o Change in bowel habit
o Change in stool calibre (pencil-thin stool)
o Cramping abdominal pain
o Red blood per rectum
 Rectal ca
o tenesmus (straining during defecation)
o sense of incomplete defecation
o heamatochezia (blood in the stool)
o early spurious diarrhoea
o constipation : Annular type of growth
o Bloody slime: Blood stained mucus
 Patients may be asymptomatic and/or present with unexplained anemia, weight
loss, or poor appetite.
3) Look for differentials
 Raw milk consumption, contact with a smear +ve case, previous TB hx (TB)
 LLQ pain, chills, fever, nausea, vomiting (diverticulitis)
 Chronic abdominal pain, mucus in stool, diarrhea, systemic symptoms (IBD)
 Chronic diarrhea amenable to therapy, always painful, never bloody or fatty,
never constitutional symptoms or weight loss (irritable bowel syndrome)
 Rectal bleeding, pain, pruritus or prolapse (hemorrhoids)

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4) Look for complications
 urinary complaints (pneumaturia, fecaluria, recurrent UTI, hematuria)
 jaundice, ascites, difficulty breathing (metastasis)
 Intestinal obstruction symptoms (constipation, vomiting, abdominal distension,
pain)
 Generalized peritonitis

Physical Examination
Physical examination may usually be unrevealing except in advanced disease.
 General appearance:
o chronically sick looking, acutely sick looking if there is obstruction
 vital signs:
o BP low &HR high if there is excessive bleeding,
o temp high if there is secondary infection or pericolic abscess
 HEENT
o EYE: pale, icteric
 Lymphadenopathy- supraclavicular
 Chest
o Sign of metastasis (pleural effusion)
 Abdomen
o abdominal mass due to the tumour and/or hepatomegaly,
o signs of ascites
o abdominal tenderness
o PR: mass,blood,fixation (a sigmoid tumour may prolapse into the pouch of
Douglas)
o GU
o Faecal matter coming out of vagina or urethra(in case of fistula)
 Locomotor system
o Edema (hypoalbuminaemia)
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 Investigation

Lab:
 CBC: WBC, Hb&Hct  ESR stool exam: occult blood
 Electrolytes  LFT,RFT,
 BUN & Cr  CEA- diagnostic if >1000IU

Imaging
 ECG
 CXR
 US for liver secondary
 CT of abdomen
 Double contrast barium enema
 Colonoscopy(gold standard)
 Flexible sigmoidoscopy: useful in supplementing barium investigations where
diagnosis is difficult due to diverticular disease.

Differential Diagnosis
1. Ulcerative colitis
2. Diverticular disease
3. Intestinal TB
4. Irritable bowel syndrome
5. Other dynamic and adynamic causes of bowel obstruction (volvulus, band, adhesion,
intussusception, ileus, etc…)
6. AVM (arterio venous malformation)
7. Ischemic bowel disease
8. Hemorrhoids
9. Dysenteries and other causes of diarrhea and change in bowel habit

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 Table 5.4: Causes of Constipation
Organic Painful anal cause Adynamic bowel Drugs Habit and diet
obstruction
 Carcinoma of  Fissure in ano  Hirschsprung’s  aspirin  Dyschezia
colon  Prolapsed piles disease  Opiate analgesics  Dehydration
 Diverticular  Senility  Anticholinergics  starvation
disease  Spinal cord  Ganglion blockers  Lack of bulk in diet
injury/ disease
 myxoedema
 Parkinson
disease

Table 5.5: Causes of Diarrhea

Specific Inflammatory drugs Loss of Pancreatic Postgastrect General diseases
infections /irritative absorptive dysfunction omy and
surface vagotomy
 Food  Ulcerative  Antibiotic  Bowel    Anxiety
poisoning colitis induced resection  Hyperthyroidism
 Dysentery  Tumours of colitis  Sprue and  Uremia
 Cholera large bowel  purgatives celiac disease  Carcinoid syndrome
 Viral  Diverticular  Idiopathic  Zollinger Ellison
enterocolitis disease steatorrhoea
 Crohn’s
disease

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 Discussion of the Case

 Introduction ……………………………………………………….……287
 Epidemiology……………………………………………………….……287
 Risk Factors…………………………………………………………….…287
 Pathology………………………………………………………………...289
 Clinical Manifestation……………………………………………….289
 Spread of the disease..……………………………………………..290
 Staging……………………………………………………………………..290
 Management……………………………………………………………293

Introduction
 Colorectal carcinoma is the most common malignancy of the gastrointestinal tract.

Epidemiology

 The incidence is similar in men and women and has remained fairly constant over
the past 20 years; however, the widespread adoption of current national screening
programs is gradually decreasing the incidence of this common and lethal disease

Risk Factors

 Aging
o It is the dominant risk factor for colorectal cancer, with incidence rising
steadily after age 50 years.
o However, individuals of any age can develop colorectal cancer, so symptoms
such as a significant change in bowel habits, rectal bleeding, melena,
unexplained anemia, or weight loss require a thorough evaluation.
 Hereditary risk factors

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 o Approximately 80% of colorectal cancers occur sporadically, while 20% arise
in patients with a known family history of colorectal cancer.
 Environmental dietary factors
o The observation that colorectal carcinoma occurs more commonly in
populations that consume diets high in animal fat and low in fibre
o A diet high in saturated or polyunsaturated fats increases risk of colorectal
cancer while a diet high in oleic acid (olive oil, coconut oil, fish oil) does not
increase risk.
o In contrast, a diet high in vegetable fibreappears to be protective.
o A correlation between alcohol intake and incidence of colorectal carcinoma
has also been suggested.
o Ingestion of calcium, selenium, vitamins A, C, and E, carotenoids, and plant
phenols may decrease the risk ofdeveloping colorectal cancer.
o Obesity and sedentary lifestyle seems to increase
 Inflammatory Bowel Disease.
o It is hypothesized that chronic inflammation predisposes the mucosa to
malignant changes, and there is some evidence that degree of inflammation
influences risk.
o In general, the duration and extent of colitis correlate with risk.
 Primary sclerosing cholangitis
 Family history of colorectal cancer.
 Other Risk Factors
o Cigarette smoking is associated with an increased risk of colonic adenomas,
especially after more than 35 years of use.
o Patients with:
 History of uretero-sigmoidostomy
 Acromegaly
 History of pelvic radiation

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 Pathology

 Microscopically:

o The neoplasm is a columnar cell carcinoma originating in the colonic

epithelium.
o It is likely that all carcinomas start as a benign adenoma, the so called
‘adenoma–carcinoma sequence’.
 Macroscopically:
o The tumour may take one of four forms: Annular, tubular, ulcer and
cauliflower.
o The annular variety tends to give rise to obstructive symptoms, whereas the
others will present more commonly with bleeding.
o Type 4 /cauliflower/ is the least malignant form.

Clinical Manifestations

1. Local effects
 Change in bowel habit is the most common symptom, either constipation or
diarrhoea or the two alternating with each other.
o The diarrhoea may be accompanied by mucus (produced by the excessive
secretion of mucus from the tumour) or bleeding, which may be bright,
melaena or occult.
 Intestinal obstruction due to a constricting neoplasm commonly found in the left.
 Perforation of the tumour, either into the general peritoneal cavity or locally with
the formation of a pericolic abscess, or by fistulae into adjacent viscera
2. Effect of secondary deposit:
 Jaundice,
 Abdominal distension due to ascites and hepatomegaly.
3. Malignant features
 Weight loss
 Anemia
 Loss of appetite
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 Spread of the Disease

 Local spread
o Tumour can spread in a longitudinal, transverse or radial direction.
o It spreads round the intestinal wall and usually causes intestinal obstruction
before it invades adjacent structures.
 Lymphatic spread
o Lymph nodes draining the colon are grouped as follows:
 N1: nodes in the immediate vicinity of the bowel wall;
 N2: nodes arranged along the ileocolic, right colic, midcolic, left colic and
sigmoid arteries;
 N3: the apical nodes around the superior and inferior mesenteric vessels.
 Bloodstream spread
o Accounts for a large proportion (30–40%) of late deaths.
o Metastases are carried to the liver via the portal system, sometimes at an early
stage before clinical or operative evidence is detected (occult hepatic
metastases).

Staging
 Transcoelomic spread: Rare
Duke’s Classification
A: confined to the bowel wall
B: through the bowel wall but not involving the free peritoneal serosal surface;
C: lymph nodes involved.
D: implies either advanced local disease or metastases to the liver.

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 Table 5.6: Colorectal Cancer TNM staging AJCC UICC 2017
Primary Tumor (T)
T category T criteria
TX  Primary tumor cannot be assessed
T0  No evidence of primary tumor
Tis  Carcinoma in situ: intramucosal carcinoma (involvement of lamina propria with no
extension through muscularis mucosae)

T1  Tumor invades the submucosa (through the muscularis mucosa but not into the
muscularis propria)
T2  Tumor invades the muscularis propria
T3  Tumor invades through the muscularis propria into pericolorectal tissues
T4  Tumor invades the visceral peritoneum or invades or adheres to adjacent organ or
structure
T4a  Tumor invades through the visceral peritoneum (including gross perforation of the bowel
through tumor and continuous invasion of tumor through areas of inflammation to the
surface of the visceral peritoneum)
T4b  Tumor directly invades or adheres to adjacent organs or structures
Regional lymph nodes (N)
N category N criteria
NX  Regional lymph nodes cannot be assessed
N0  No regional lymph node metastasis
N1  One to three regional lymph nodes are positive (tumor in lymph nodes measuring ≥0.2
mm), or any number of tumor deposits are present and all identifiable lymph nodes are
negative
N1a  One regional lymph node is positive
N1b  Two or three regional lymph nodes are positive
N1c  No regional lymph nodes are positive, but there are tumor deposits in the
o Subserosa
o Mesentery

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 o Non-peritonealized pericolic, or perirectal/mesorectal tissues
N2  Four or more regional nodes are positive
N2a  Four to six regional lymph nodes are positive
N2b  Seven or more regional lymph nodes are positive
Distant metastasis (M)
M category M criteria
M0  No distant metastasis by imaging, etc, no evidence of tumor in distant sites or organs.
(This category is not assigned by pathologists.)
M1  Metastasis to one or more distant sites or organs or peritoneal metastasis is identified
M1a  Metastasis to one site or organ is identified without peritoneal metastasis
M1b  Metastasis to two or more sites or organs is identified without peritoneal metastasis
M1c  Metastasis to the peritoneal surface identified alone/with other site or organ metastases
Prognostic Stage Groups
T N M Clinical Stage group
Tis N0 M0 0
T1, T2 N0 M0 I
T3 N0 M0 IIA
T4a N0 M0 IIB
T4b N0 M0 IIC
T1, T2 N1/N1c M0 IIIA
T1 N2a M0 IIIA
T3, T4a N1/N1c M0 IIIB
T2, T3 N2a M0 IIIB
T1, T2 N2b M0 IIIB
T4a N2a M0 IIIC
T3, T4a N2b M0 IIIC
T4b N1-N2 M0 IIIC
Any T Any N M1a IVA
Any T Any N M1b IVB
Any T Any N M1c IVC
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 Management

Preoperative:
 The bowel is cleared by enemas and oral stimulant laxatives (e.g. Picolax).
 Metronidazole and gentamicin (or a cephalosporin) is given at the time of surgery.
 The haemoglobin level is checked and blood transfusion given if necessary.

1. Operative:
 Principle  wide resection of the growth with regional lymphatics.
 In the unobstructed case, the bowel can be prepared beforehand and primary
resection with restoration of continuity can be achieved.
 In the obstructed case, in which bowel preparation is contraindicated, the primary
goal is to relieve obstruction.
 It may be possible to achieve primary resection with restoration of continuity at the
same time, but the poor vascularity and high incidence of colonic anastomotic
breakdown means that this is undertaken only after serious consideration.
 The options would be to use an extended right colonic resection round to the splenic
flexure, or bring out a defunctioning colostomy or ileostomy.

2. Postoperative
 Adjuvant chemotherapy with 5 - fluorouracil (5 - FU), in combination with folinic
acid, may reduce the risk of recurrent disease.
 For metastatic disease:
o The combination of 5 - FU together with folinic acid and irinotecan may
prolong survival.
 Follow - up cross - sectional imaging is performed to detect local recurrence and
liver metastases:
o If there is metastasis to one lobe of the liver in the absence of other disease
 resect the affected liver lobe.
 Follow - up surveillance colonoscopy is undertaken at intervals to detect new
tumors and local recurrence.

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 5.4. Gastric Outlet Obstruction (GOO)
 Case Discussion……………………………….………..……294
 History……………………………………………………………294
 Physical Examination……………………………………..295
 Investigation………………………………………………….296
 Differential Diagnosis…………………………………….298
 Management…………………………………………………298
 Discussion of the Case……………………………………299

Case Discussion
 This is a 65-year-old, male who came with of vomiting of 8 months duration. The Vomiting
was projectile, non-bilious and non-blood tinged. There was associated burning epigastric
pain of 2 years duration along with nausea, weight loss, easy fatigability and anorexia. On
physical examination, the patient was chronically sick looking with pale conjunctiva and
palms. Abdominal examination showed a decreased bowel sounds in addition to a 7x7,
tender, hard mass in the epigastric area that moves with respiration.

History
 The cardinal symptoms a patient with GOO are:
o Nausea and vomiting

 Patients usually come with these cardinal symptoms as a chief complaint.

 So the first thing to do is asking about the chief complaint, vomiting:
o Content: It is non-bilous and undigested food taken several hours ago.
o Timing and frequency: It may be intermittent and usually occurs within 1 hour
of a meal.
o Nature and quantity: It is copious, projectile and unpleasant.
 we should ask for any associated symptoms like:
o Epigastric pain: is severe and persistant.
 It is related to underlying causes like PUD and pancreatic cancer.
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 o Early satiety o Gastric retention
o Abdominal distension o Indigestion
o Bloating o Anorexia
o Epigastric fullness
o Weight loss:
 Common in chronic cases.
 Is most significant in malignant diseases, tuberculosis, and chronic
obstruction due to benign causes.
o They are frequently malnourished and dehydrated and have a metabolic
insufficiency.
 The onset of symptoms of GOO varies depending upon the etiology of the
obstruction.
 The Symptoms generally occur abruptly in:
o Gallstone impaction o PEG tube migration
o Prolapse of a large gastric polyp o Gastric volvulus
 Other causes tend to follow a more indolent course.
 The symptoms in malignant disease may have a shorter duration than those with
benign disease.

Physical Examination
 General Appearance
o Chronically ill looking
o Malnourished with evidence of weight loss
o Dehydrated with signs like:
 Oliguria  Confusion
 Dry skin  Irritability
 Sunken eye ball  Fainting
 Rapid heartbeat
 Rapid breathing On Vital sign
 Decreased BP
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  Lymphoglandular system:
o The left supraclavicular lymph node can be enlarged (Virchow's node) in cases
of a metastatic gastric cancer.
o Periumbilical lymph node might also be palpable (Sister Mary Joseph's node) in
cases of metastatic gastric cancer.
 Abdominal examination
o Visible gastric peristalsis: This can be elicited by asking the patient to drink a
glass of water.
o A distended abdomen with tympanitic mass may be appreciated in the
epigastric area and/or left upper quadrant as the stomach dilates.
o Succussion splash can also be experienced.
 It is a sloshing sound heard with a stethoscope rested over the upper
abdomen during a sudden movement of the patient.
 It is reflective of retained gastric material.
 Is done after 3 hrs.
 A palpable abdominal mass is noted in a minority of patients.

Investigation
Laboratory studies
 May be normal or nonspecifically abnormal.
 Serum electrolyte:
o Hypokalemic hypochloremic metabolic alkalosis:
 Prolonged vomiting leads to loss of hydrochloric acid.
 Bicarbonate is increased in the plasma to compensate the loss.
 Potassium shifts to the extracellular compartment due to alkalosis.
 With continued vomiting, sodium is preserved while potassium is
excreted by the kidneys  hypokalemia.
 CBC:
o Anemia may be seen in patients with:

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  Peptic ulcer disease  Large gastric polyps
 Primary or metastatic malignant diseases
 Serum tumor markers:
o CA 19-9 and/or CEA:
 Can be elevated in patients with pancreatic cancer.
 Can also be elevated in other malignancies involving the gastrointestinal
tract, as well as some benign conditions.
Imaging
 Plain abdominal X-ray:
o The gastric bubble and the proximal duodenum can be enlarged.
o Air may be absent in the small bowel.
 Contrast studies:
o With water-soluble contrast or barium studies.
o In complete GOO the contrast won’t pass to the small bowel.
o Although not specific it can give clues to the underlying etiology.
o The stomach should be decompressed first to minimize risks of aspiration.
 Abdominal CT scan:
o Can show gastric distention o Air-fluid level
o The retained contents in the o Can suggest the specific causes
gastric lumen
 Endoscopy:
o Useful to identify a specific cause and in therapeutic procedures.
o The stomach should be decompressed first to decrease risk of aspiration.
o Patients should fast for at least 4 hrs.
o Parenteral PPIs should be given to reduce gastric secretions and inflammation.
o Endoscopic biopsy:
 Can confirm a diagnosis and exclude malignant diseases.
 It can show false negative results if the tumor is extraluminal or does not
involve the mucosa.
 Surgical specimens are better to diagnose gastroduodenal tuberculosis.

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 Differential Diagnosis

Table 5.7: Differentials for GOO

Benign Conditions Malignant Conditions
 PUD  Pancreatic Pseudocyst  Distal Gastric cancer  Duodenal cancer
 Gastric polyp  Pancreatitis  Pancreatic cancer  Gallbladder cancer
 Caustic injury  Gastric volvulus  Gastric lymphoma  Cholangiocarcinoma
 Gastric Tuberculosis  Pyloric stenosis  Ampullary cancer  Gastric carcinoid
 Gastric bezoars  Crohn disease

Management

 Principles of management:
o Correcting the metabolic abnormality.
o Treating the mechanical cause.
 Correcting the metabolic abnormality:
o Rehydration with an IV isotonic saline:
 To allow kidney to correct the acid-base abnormality.
o Replacement of K, Ca, and Mg.
 In anemic patient blood transfusion may be considered.
 Gastric decompression
o Should be done with nasogastric tube or large bore nasogastric tubes.
 IV proton pump inhibitors should be administered to:
o Decrease gastric secretion.
o Improve inflammatory response.
 Definitive treatment is based on the underlying etiology.
 It includes:
o Stenting o Endoscopic balloon dilation
o Chemotherapy o Surgery

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 Discussion of the Differentials

5.4.1. Peptic Ulcer Disease

 Introduction ……………………………………………………………299
 Epidemiology…………………………….……………………………..299
 Etiology…………………………………….………………………………300
 Clinical Manifestation……………………………………………….301
 Diagnosis………………………………………………………………….303
 Management……………………………………………………………305

Introduction
 Peptic ulcers are defects in the gastrointestinal mucosa that extend through the
muscularis mucosae.
 Corrosive effect of acid & proteolytic effect of pepsin are responsible.
 Common sites are:
o First part of duodenum o Stoma after gastric resection
o Lesser curvature of stomach
 Less common:
o Distal esophagus
o Meckel’s diverticulum, which contains ectopic gastric epithelium
 It can be an acute or chronic ulceration.

Epidemiology
 H. pylori infection determines the disease burden.
o The ulcer incidence in H. pylori-infected individual ulcer incidence is around
1% per year, which is 6-10x higher than for uninfected individual.
 In developing countries:
o Most children get infected before the age of 10.

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 o More than 80% of adults are infected before the age of 50.
 In developed countries:
o Infection before the age of 10 is uncommon.
o It is around 10% in those between 18 and 30 years of age.
o It is around 50% in those older than age 60.
 The peak age incidence in gastric ulcer is older than duodenal ulcer.
 The sex incidence is equal for gastric ulcers unlike duodenal ulcers with a slight
predilection of men.
 Gastric ulceration is substantially less common than duodenal ulceration.

Etiology
 There are 2 major factors:
o Helicobacter pylori infection, and
o Non-steroidal anti-inflammatory drugs (NSAIDs): The risk of PUD is dependent
on factors like:
 Prior history of ulcer  Genetic predisposition
 Dose  Comorbidities: cardiovascular
 Duration of action disease
 Duration of therapy
 Co-therapy with drugs that enhance toxicity
 Advanced age of the patient (generally above 75 years)
 Other unusual causes include:
o Drugs other than NSAIDs:
 Acetaminophen  Sirolimus
 Bisphosphonates  Spironolactone
 Glucocorticoids  SSRIs
 Clopidogrel  Chemotherapy
o Hormonal or mediator-induced:
 Gastrinoma  Carcinoid syndrome
 Systemic mastocytosis  Myeloproliferative disorders
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  Antral G-cell hyperfunction
o Postgastric surgery and postprocedure ulceration
o Other infections like:
 Herpes simplex virus type I  Candidiasis
 Cytomegalovirus
o Radiation therapy
o Inflammatory and infiltrating disease like:
 Sarcoidosis  Crohn disease
o Idiopathic

Clinical Manifestations
 Patients with PUD usually come with a complaint of dyspepsia which is an upper
abdominal pain or discomfort.
o It is seen in almost 80% of patients.
o It is described as gnawing or burning in nature and may radiate to the back.
o It is intermittent.
o Duodenal ulcer pain:
 It is considered to occur 2-5 hrs after a meal and at night (between
about 11 PM and 2 AM).
 It is relieved by eating food or taking antacids.
 It is aggravated by hunger.
 Gastric ulcer pain occurs immediately after a meal.
o The Symptoms are periodical which may be related to the spontaneous
healing of the ulcer.
o They may disappear for weeks or months to return again.
 Other possible manifestations include:
o Vomiting: becomes more prominent with stenosis occurrence.
o Heart burn
o Bleeding:

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  It may be acute which may present with nausea, hematemesis, or
melena. In rare cases, with hematochezia and orthostatic
hypotension if it is massive.
 It may be chronic which may present with microcytic anemia.
o Alteration in weight:
 Patients with gastric ulcer are often underweight unlike duodenal
ulcer patients.
o Gastric outlet obstruction: occurs as a complication of PUD located in the
pyloric channel or duodenum.
o Penetration and fistulization: is one of the complications of PUD in which the
peptic ulcers penetrate through the bowel wall without a free perforation.
 The pain typically becomes more intense with longer duration
 Is frequently referred to the lower thoracic or upper lumbar spine
region.
 It is not relieved by food or antacids.
 This change in symptom pattern may be gradual or sudden.
 Gastrocolic or duodenocolic fistulas can present with halitosis,
feculent vomiting, postprandial diarrhea, dyspepsia, and weight loss.
o Perforation: present with sudden severe, diffuse abdominal pain.
 Occurs in 2-10% of patients.
 Duodenal perforations are the commonest next to prepyloric
ulcerations.
Stages of perforation:
 Stage 1:
 Chemical peritonitis on the first 2-4 hrs after a leak of duodenal and gastric
contents especially HCl followed by agonizing pain +/_ coffee ground
vomitus, Melina.
 Pale & anxious pt, increase pulse, Normal BP
 Guarding and rigidity of abdomen
 Rebound tenderness all over the abdomen.
 Absent liver dullness & often bowel sound
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  Stage 2:
 It is also called stage of reaction/stage of delusion/illusion.
 It lasts for 3 to 6 hrs.
 There is improvement of symptoms.
 But signs are worse feeble pulse, hypotensive, shifting dullness plus
guarding, absent bowel sounds.
 Stage 3
 Bacterial peritonitis
 Severely ill ,dehydrated, toxic with Hippocratic face in shock
 Hypovolemic and septicemic
 Distended abdomen with guarding and generalized tenderness.
On physical exam:
o For uncomplicated PUD findings are few and non-specific.
o Patients might present with signs of GOO mentioned above.
o In perforation patient might appear with:
 Fever  Dehydration
 Tachycardia  Ileus
o Abdominal examination reveals
 Exquisite tenderness  Guarding
 Rigidity  Rebound tenderness

Diagnosis
H pylori testing: is essential in all patients with peptic ulcer.
 Endoscopic or invasive tests for H pylori include:
o A rapid urease test: is test of choice.
 Tests the bacterial product urease on the biopsy specimen.
o Histopathology
 Sensitivity is about 95% and specificity 99%.
o Culture:

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  Sensitivity is about 80% and specificity 100%.
 Non-invasive tests:
o Serology/ Fecal antigen test: detects H pylori antigens in stool.
 It lacks specificity when blood is present in the stool due to cross
reactivity with blood constituents.
 This test cannot be used to assess eradication after therapy because
the antibody titers can remain high for a year or more.
o Urea breathe test:
 It is based on the ability of H. pylori to hydrolyze urea.
 Its sensitivity and specificity are both greater than 95%.
 In the presence of H pylori infection, after ingestion of the carbon
isotope- labeled urea, urea will be metabolized to ammonia and
labeled bicarbonate which is excreted in the breath as labeled carbon
dioxide.
 False-negative results can occur if the test is done too soon after
treatment, so it is usually best to test 4 weeks after therapy is finished.
 It is the method of choice to document eradication.
 Upper endoscopy:
o It is the most accurate diagnostic test.
o Benign ulcers features:
 Smooth, regular, rounded edges, with a flat, smooth ulcer base often
filled with exudate.
o Malignant ulcer features:
 An ulcerated mass protruding into the lumen.
 Folds surrounding the ulcer crater are nodular, clubbed, fused, or stop
short of the ulcer margin.
 Overhanging, irregular, or thickened ulcer margins.
o Biopsy should be taken of ulcers with malignant features.
 Upper Gastrointestinal Radiography:
o It requires the demonstration of barium within the ulcer crater.
o With single-contrast: 50% of duodenal ulcers may be missed.
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 o With double-contrast studies: 80% to 90% of ulcer craters can be detected.
o Malignant ulcers appear: large, interrupted, fused, or nodular mucosal folds
approaching the margin of the crater, irregular filling.

Management
 Principles:
o Relieve symptoms o Prevent recurrence
o Heal ulcer o Prevent cause
 Lifestyle modifications:
o Avoiding cigarette smoking
 It retards ulcer healing.
o Discontinuation of aspirin or NSAIDs, if possible.
o Decreasing usage of alcohol
 It damages the mucosa
o Decreasing usage of coffee
 It strongly stimulates acid secretion.
 Medical management:
o H2 -receptor antagonists:
 Most ulcers can be healed within few weeks.
 Some patients are relatively refractory to the conventional dose.
o Proton pump inhibitors:
 Majority of benign ulcers heal within 2 weeks.
 Most patients become asymptomatic within few days.
 They are safe to use.
 Relapse after therapy cessation occurs.
o Antacids:
 Most effective when ingested 1 hour after a meal.
 If taken on an empty stomach, the antacids are emptied rapidly and
have only a transient buffering effect.

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 o Eradication of Helicobacter pylori:
 It is associated with higher healing rates of ulcer.
 Eradication of infection should be confirmed four or more weeks after
the completion of therapy.
 In patients with risk factors for macrolide resistance, we use bismuth
quadruple therapy including:
 PPI
 Bismuth subcitrate or Bismuth subsalicylate
 Tetracycline (500 mg)
 Metronidazole (250 to 500 mg)
 In patients without risk factors for macrolide resistance, we use
clarithromycin-based triple therapy including:
 PPI
 Clarithromycin(500mg) and
 Amoxicillin (1 gram) or Metronidazole (500 mg)
Surgical management:
 The four classic indications for surgery are:
o Intractability o Perforation
o Hemorrhage o Obstruction
 The surgical procedures used are:
1. Vagotomy +/- drainage: includes:
 Truncal vagotomy:
o Is the most common operation performed for duodenal ulcer disease.
o It is usually done together with a drainage procedure.
 Selective vagotomy
 Highly selective/parietal cell vagotomy
o Preserves the vagal innervation of the gastric antrum so that there is
no need for routine drainage procedures.
2. Gastric resection:

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A. Truncal Vagotomy and Antrectomy:
 The most common indication is gastric ulcer.
 Relative contraindications include cirrhosis, extensive scarring of the
proximal duodenum, and previous operations on the proximal duodenum.
 It is far more effective at reducing acid secretion and recurrence.
 It requires reconstruction of GI continuity:
o Gastroduodenostomy/ Billroth I procedure or
o Gastrojejunostomy/ Billroth II procedure
B. Subtotal Gastrectomy :
 Rarely performed today.
 Done in patients with:
o Underlying malignancies
o Recurrent ulcerations after truncal vagotomy and antrectomy.
 Restoration of GI continuity is done with:
 Billroth II anastomosis
 Roux-en-Y gastrojejunostomy

5.4.2. Gastric Cancer

 Introduction ……………………………………………………………308
 Epidemiology……………………………………………………………308
 Risk Factors………………………………………………………………309
 Clinical Manifestation………………………….……………………311
 Diagnosis…………………………………………….……………………312
 Staging…………………………………………………....………………313
 Management……………………………………………………………315

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 Introduction

 It is classified by the Lauren classification in to:

 Intestinal gastric cancer:
o Forms polypoid tumors or ulcers
o Is common in an elderly male
o Has a better prognosis
 Diffuse gastric cancer:
o Infiltrates deeply into the stomach without forming obvious mass
lesions.
o Is common in young and female.
o It has a much worse prognosis.
 Mixed morphology: a small proportion.
 It can also be classified into:
 Early gastric cancer:
o Limited to the mucosa and submucosa with or without lymph node
involvement.
 Advanced gastric cancer:
o Involves the muscularis.

Epidemiology
 4th most common cancer in men
 5th most common cancer in women
 Globally:
o 8% of all cancers and 10% of deaths.
o Peak age is around 60-84 years.
o Male : Female=2:1
o Blacks are affected twice as whites
o High incidence in low socioeconomic status
o 95% are Adenocarcinomas.
o Over all declining is related to distal stomach; however, proximal is
increasing.

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 o Fatality to case ratio 70%
o Incidence highest
 Eastern Asia  South America
 Eastern Europe
o Lowest:-Northern and Southern Africa
 In Ethiopia:
o TAH 1992-96: 96pts operated, 437 GIT Cancer patients
 22% of GIT Cancers  M:F = 2.4:1
 Mean age 48 yrs
o World Health Ranking:
 6th most common cancer  3rd cause of ca death

Risk Factors
 Environmental factors:
o Diet:
 Salt and salt-preserved foods:
 A potential synergistic effect of salt and H. pylori.
 By damaging stomach mucosa and increasing the risk of
carcinogenesis.
 Nitroso compounds
o Obesity
o Smoking
o Occupational exposures:
 Coal and tin mining
 Steel and iron processing
 Rubber manufacturing industries
o Helicobacter pylori:
 Triggers inflammation at the corpus mucosa that results in atrophy and
intestinal metaplasia.
 Six fold increase in the risk of adenocarcinomas distal to the cardia.

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 o Regular use of NSAIDs
 It has been inversely associated with the risk of distal gastric
adenocarcinoma.
o Epstein-Barr virus
o Alcohol
o Socioeconomic status:
 Distal gastric cancer is high in low socioeconomic status.
 Proximal gastric cancer is high in higher socioeconomic class.
o Gastric surgery
o Cancer survivors who received abdominal irradiation
o Reproductive hormones:
 Gastric ca is lower in women suggesting a protective role of reproductive
hormones in women.
 Host-related factors
o Blood group:
 Blood group A has 20% increased risk than those of group O, B, or AB.
o Familial predisposition:
 Hereditary (familial) gastric cancer accounts for 1-3% of the global
burden.
 It comprises:
 Hereditary diffuse gastric cancer (HDGC)
 Gastric adenocarcinoma and proximal polyposis of the stomach
(GAPPS)
 Familial intestinal gastric cancer (FIGC).
o Gastric polyps: many have malignant potential.
o Gastric ulcer:
 Approximately 25% of patients have a history of gastric ulcer.
 All gastric ulcers should be followed to complete healing
 Those that do not heal should undergo resection.
o Pernicious anemia:
 2-6 fold increased risk.
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 Clinical Manifestations

Symptoms:
 It lacks specific symptoms early in the course of the disease.
 The most common symptoms are:
o Weight loss:
 Is due to decreased intake, which may be attributed to anorexia,
nausea, abdominal pain, early satiety, and dysphagia.
o Persistent abdominal pain:
 Epigastric area
 It is non-radiating
 It is not relieved by food ingestion
 Early in the disease: vague and mild
 As it progresses: severe and constant
 Dysphagia
o Occurs in proximal gastric ca.
 Nausea and early satiety:
o Due to tumor mass
o Due to poor distensibility in linitis plastica with diffuse mural involvement.
 Gastric outlet obstruction:
o Occurs in an advanced distal tumor.
 Occult GI bleeding is frequently seen
o Results in iron deficiency anemia.
 Overt bleeding occurs in 20% of cases.
Physical signs:
 Most commonly associated with locally advanced or metastatic disease.
o Patient may present with signs of anemia:
 Pale conjunctivae, skin pallor and the like.
o Virchow's node:
 Palpable left supraclavicular lymph nodes.
 Is the most common finding of metastatic disease.
o Irish node:
 A left axillary node.
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 o Sister Mary Joseph's node:
 A periumbilical nodule
o Palpable abdominal mass:
 Present in long-standing and advanced disease.
o Blumer's shelf:
 Peritoneal metastasis to the pouch of douglas which is palpable by
rectal examination.
o Krukenberg's tumor:
 Metastasis to ovary leading to an enlarged ovary.
o A metastasis to the liver can lead to hepatomegaly.
 Other clinical features like jaundice, ascites, and cachexia can also
occur.
o If peritoneal carcinomatosis occurs ascites can be a manifestation.
o Signs GOO mentioned above can occur is there is obstruction.
 Paraneoplastic syndromes such as:
o Dermatomyositis
o Acanthosis nigricans Poor prognostic features.
o Circinate erythemas

Diagnosis
 Laboratory Tests:
o CBC: to look for anemia and for the need of pre-operative blood transfusion.
o Liver function test: if there is metastasis to the liver.
 Endoscopy:
o Helps to determine the anatomic location and extent of a lesion.
o Biopsy can be taken.
 During endoscopy adds to its clinical utility.
 A single biopsy has a sensitivity of 70% seven biopsies from the ulcer
margin and base has a sensitivity of greater than 98%.
 A combination of strip and bite biopsy techniques: to diagnose linitis plastica.

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 o Brush cytology:
 Increases the sensitivity of single biopsies
 If bleeding with biopsy is a concern.
 Barium studies:
o Shows irregular filling defect and infiltrating lesions.
o False-negative results can occur in as many as 50% of cases.
o It has 14% sensitivity in early gastric ca.
o “Leather-flask" appearing stomach: can be seen in case of linitis plastica.
 Ultrasound and CT-scan:
o Useful to rule out secondaries on liver, ovaries and other sites.
o To look for an enlarged nodes, and detect ascites.
 Laparoscopy:
o To stage disease.
o Picks up peritoneal secondaries; detect occult metastases, organ
invasion.
o Can be used to take :
 Biopsy of peritoneum and  Peritoneal lavage for cytology
nodes  Laparoscopic US
o It will avoid unnecessary laparotomy.
o It is more accurate than CT.

Staging
 There are two major classification systems currently in use for gastric cancer:
o The Japanese classification
 The most elaborate; it is based upon refined anatomic location,
particularly of the lymph node stations
o The American Joint Committee on Cancer (AJCC) and the Union for
International Cancer Control (UICC) classification:
 The more widely used staging system, It is based upon tumor, node,
and metastasis (TNM) classifications, refer the table below

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 Table 5.8: Stomach Cancer TNM staging AJCC UICC 2017
Primary Tumor (T)
T category T criteria
TX  Primary tumor cannot be assessed
T0  No evidence of primary tumor
Tis  Carcinoma in situ: Intraepithelial tumor without invasion of the lamina propria, high-
grade dysplasia

T1  Tumor invades the lamina propria, muscularis mucosae, or submucosa

T1a  Tumor invades the lamina propria or muscularis mucosae
T1b  Tumor invades the submucosa
T2  Tumor invades the muscularis propria
T3  Tumor penetrates the subserosal connective tissue without invasion of the visceral
peritoneum or adjacent structures
T4  Tumor invades the serosa (visceral peritoneum) or adjacent structures
T4a  Tumor invades the serosa (visceral peritoneum)
T4b  Tumor invades adjacent structures/organs
Regional lymph nodes (N)
N category N criteria
NX  Regional lymph nodes cannot be assessed
N0  No regional lymph node metastasis
N1  Metastasis in one or two regional lymph nodes
N2  Metastasis in three to six regional lymph nodes
N3  Metastasis in seven or more regional lymph nodes
N3a  Metastasis in 7 to 15 regional lymph nodes
N3b  Metastasis in 16 or more regional lymph nodes
Distant metastasis (M)
M category M criteria
M0  No distant metastasis
M1  Distant metastasis

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 Prognostic stage groups
T N M Clinical Stage group
Tis N0 M0 0
T1 N0 M0 I
T2 N0 M0 I
T1 N1, N2, or N3 M0 IIA
T2 N1, N2, or N3 M0 IIA
T3 N0 M0 IIB
T4a N0 M0 IIB
T3 N1, N2, or N3 M0 III
T4a N1, N2, or N3 M0 III
T4b Any N M0 IVA
Any T Any N M1 IVB

Management

 Aims of surgery:
o Palliative resection or bypass:
 For bleeding or obstruction
o Curative resection when possible.
 Resection is considered curative if:
 No evidence of gross or residual tumor.
 No involvement of serosa, no T3 or T4 tumor.
o No evidence of metastatic tumor.
 Management of gastric ca is a multidisciplinary Approach:
o Surgery o Radiotherapy
o Chemotherapy
 Surgery:
o It is the treatment of choice for carcinoma stomach.

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 o The most common procedure is gastrectomy (total, subtotal or distal)
 Signs of in-operability:
o Distant metastasis o Hard nodular liver (secondaries)
o Malignant ascites o Peritoneal seedling like
o Sr. Mary joseph’s nodes krukenberg
o Fixed to pancreas and retro peritoneum
o Celiac, para-aortic, supraclavicular LNs
 Endoscopic:
o Excision of early gastric Ca
o Haemostatic for bleeding lesions
o Endoscopic palliation (stent placement)
o Recannalization of neoplastic obstruction
 Surgical treatment; gastric resection:
o The most important determinant of resectability is the stage of the disease
o Type of procedure is determined by:
 Growth pattern on biopsy  Location of LN metastasis
 Site and macroscopic size of lesion in stomach
o Type of procedure
 Subtotal gasterectomy:
 For an early or well circumscribed T2 Ca
 If the proximal edge is>2cm from esophagogastric junction
 A 5cm clearance is required for more infiltrative lesions.
 Total gasterectomy:
 If the proximal distance from the junction is<5cm or
 If it is diffuse with submucosal infiltration.
o Recommendations of UIAC &Japanese Research Society:
 Proximal 3rd:
 Extended gasterectomy + distal esophagectomy.
 Distal 3rd:
 Subtotal gasterectomy (intestinal) & Total gasterectomy (diffuse).
 Middle 3rd:
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  Total gasterectomy
o In all cases:
 Excision of the greater and lesser omentum is undertaken with the
anterior leaf of the omental bursa (lesser sac).
 Duodenum should be divided at least 2cm beyond the pylorus.
o If it is adherent to adjacent structures removal of part or whole of the organs
en block is necessary to obtain a macroscopically free margin.
o Reconstruction GI continuity is by Roux-en Y jejunal loop.
o Jejunal interposition pouches to improve nutritional intake.
 Lymphadenectomy:
o Extended to reduce regional recurrence
o Allows more accurate staging and better prediction of survival.
o Radicality of dissection D1,D2,D3 is categorized by level of complete node
groups excised:
 D1 resection:
 Removal of perigastric lymph nodes.
 Done when nodes are not involved (N0).
 D2 resection:
 Removal of group N1&N2 Nodes (left gastric/ common
hepatic/splenic/retropancreatic)
 Adjuvant and Neoadjuvant therapies
o Surgery is principal Rx
o Advanced disease has limited outcome.
o Chemo and Radiotherapy does not prolog 5yr survival (used for palliation).
o Neoadjuvant chemotherapy:
 Allow downstaging of disease to increase respectability.
 Decrease micrometastatic disease burden prior to surgery.
 Determine chemotherapy sensitivity.
 Reduce the rate of local and distant recurrences.
 Palliative treatment:
o Radiotherapy:
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  Relief from bleeding, obstruction, and pain in advanced disease.
o Surgery:
 Wide local excision  Gastrointestinal bypass
 Partial gasterectomy
o Combined chemo radiation o Endoscopic laser therapy
o Endoluminal stenting and Feeding jejunostomy

5.5. Small Bowel Obstruction (SBO)

 Case Discussion……………………………………………………318
 History……………………….…………………………………………319
 Physical Examination…………………………………………….320
 Etiology…………………………………………………………………321
 Investigation…………………………………………………………321
 Differential Diagnosis……………………………………………323
 Management………………………………………………………..323
 Discussion of the Differentials………………………………325

Case Discussion
 A 54-year-old man presents to the emergency department with a 4-day history of abdominal
distension, central colicky abdominal pain, vomiting and constipation. On further questioning
he says he has passed a small amount of flatus yesterday but none today. He has had a previous
right-sided hemicolectomy 2 years ago for colonic carcinoma. He lives with his wife and has no
known allergies. On physical exam His blood pressure and temperature are normal. The pulse is
irregularly irregular at 90/min. He has obvious abdominal distension, but the abdomen is only
mildly tender centrally. The hernia orifices are clear. There is no loin tenderness and the rectum
is empty on digital examination. The bowel sounds are hyperactive and high pitched. Chest
examination finds reduced air entry basally. P a g e 318 | 548
 History

Cardinal features (asses for level of obstruction)

 Pain
o sudden and severe which is centered on the umbilicus or lower abdomen –
small bowel
o colicky type initially (paroxysms of pain occurring every four or five minutes)
but diffuse and constant later
o Mild in large bowel obstruction
o The more severe and constant indicates strangulation
 Vomiting (type, duration)
o Prominent symptom with proximal obstructions than distal.
o As obstruction progresses it changes from digested matter to feculent mater
as a result of enteric bacteria
 Abdominal distention
o In small bowel it is greater the more distal the lesion
o Early and pronounced in large bowel obstruction
 Constipation
o Complete (obstipation) vs relative
o Obstipation is cardinal feature of complete obstruction- may not be present
in high obstruction
o Its absence doesn’t exclude obstruction
Asses for etiology
 Age
 Sex
o Female: due to PID adhesion
 Address
o Northern Ethiopia: sigmoid volvulus
o Southern: SBO
 Past illness and state of health
o Tumor o Crohn’s Disease
o TB
 Previous surgery: adhesion
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 o Appendectomy
o Previous surgery for obstruction
 One must assume the presence of a small bowel tumor until proven
otherwise in a patient with a de-novo SBO.
 Change in bowel habit
o Per rectal bleeding- colorectal tumor
 Fever, cough, night sweats [peritoneal TB]
 Intussusception:
o Intermittent drawing up leg and screaming in a previous well patient
o Gradual bile stained vomiting and red currant jelly stool
Asses for gangrene or impending gangrene
 Dehydration (oliguria)  Respiratory embarrassment
 Pyrexia, constant pain  Peritonitis

Physical Examination
 Vital signs
o Fever and tachycardia- strangulating obstruction.
o Hypotension- dehydration and strangulation
 HEENT
o Dry mucous membranes – dehydration
 Abdomen
o surgical scars
o Look for hernia sites
o Auscultation may reveal high-pitched or hypoactive bowel sounds- not very
helpful.
o Tenderness to light percussion, rebound, guarding, and localized tenderness-
peritonitis
o Tympany is usually present due to air-filled loops of bowel or stomach.
o Abdominal mass
 An abscess  Volvulus  Tumor

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 o Central lump which hardens on pulsation- intussusception
o DRE:
 Empty rectal vault, but occasionally a rectal mass can be the cause of
obstruction.
 Gross or occult blood- with intestinal neoplasm, ischemia, and
intussusception

Etiology
 In our setup: volvulus and hernia
 In western setup: adhesion
1. Adhesions 6. Inflammatory bowel disease
o Common after previous 7. Radiation enteritis
abdominal/gynaecological 8. Intussusception
surgery 9. Trauma
2. Malignancy 10. Early post op obstruction
3. Strictures 11. Superior mesenteric artery
4. Incarcerated hernia syndrome: unusual cause
5. Gallstone ileus

Investigation
Lab
 The urea nitrogen and creatinine and the hematocrit- degree of dehydration.
 CBC
o Leukocytosis with leftward shift may indicate the presence of strangulation.
o Hb- low in malignancy and dehydration
 Serum electrolyte:
o Metabolic alkalosis can be seen in patients who have frequent emesis
o Lactic Acidosis can result if the bowel becomes ischemic or if dehydration is
severe enough to cause hypoperfusion of the gut and other tissues.

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 o Serum lactate: is elevated in mesenteric ischemia and is a sensitive, though
not specific, marker of strangulation in SBO
Imaging:
 Plain abdominal X-ray: upright chest film
o Dilated small bowel loops (>3 cm in diameter)
o Multiple air-fluid levels seen on upright films
o Paucity of air in the colon.
 Small bowel series
o Standard for determining whether an obstruction is partial or complete
o Inferior to CT in the detection of closed-loop obstruction or ischemic
o Rarely offer any indication of the etiology of the obstruction
 CT scan
o Abdominal pathology can be detected
o Closed-loop or strangulating obstruction detected in some cases
o The diagnosis of obstruction is made when
 There is a discrepancy in the caliber of proximal and distal small bowel
 Absence of air or fluid in the distal small bowel or colon- complete
obstruction.
 Distended, fluid-filled, sometimes C-shaped or U-shaped loop of bowel
with prominent mesenteric vessels converging on the point of torsion
or incarceration- Closed-loop obstruction
o Advanced small bowel ischemia can be recognized by intestinal pneumatosis
and hemorrhagic mesenteric changes.
 Ultrasonography:
o Is more sensitive and specific than plain films for the diagnosis of small
bowel obstruction but not as accurate as CT
o For pregnant patients or as a bedside test for the critically ill

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 Differential Diagnosis

1. Paralytic ileus
 Paralytic ileus occurs to some degree after almost all open abdominal operations
and can also be caused by peritonitis, trauma, and intestinal ischemia.
 It is exacerbated by electrolyte disorders, particularly hypokalemia.
 As the intestine becomes distended, the patient experiences many of the symptoms
of obstruction described above, despite the absence of a mechanical obstruction.
 On radiologic examination there is air in the colon and rectum, and by CT or small
bowel series there is no demonstrable obstruction.
2. Intestinal pseudo-obstruction
 It is a chronic condition characterized by symptoms of recurrent abdominal
distention.
 The colon is generally affected more than the small intestine.
 No mechanical cause can be demonstrated in these patients, and they frequently
have a history of several previous operations for bowel obstruction during which no
cause for obstruction could be found.
 Laparotomy should be avoided in these patients; once diagnosed, the preferred
treatment is nasogastric suction, correction of any metabolic abnormalities, and in
some cases parenteral nutrition

Management
 Aims of treatment
o To relieve obstruction
o To correct dehydration
o To prevent recurrence
o To control peritonitis and to save life
1. Supportive management: partial SBO due to metastatic intraabdominal malignancy,
recurrent adhesive obstruction, obstructing radiation enteritis, or during the early
postoperative period.
 Limiting oral intake

P a g e 323 | 548
  Nasogastric decompression is achieved by the passage of a non-vented (Ryle)
or vented (Salem) tube.
 Fluid and electrolyte replacement -Hartmann’s solution or normal saline
 Antibiotics: if complicated

2. Surgical treatment
 Relief of obstruction -- delayed until resuscitation is complete (no sign of
strangulation or evidence of closed-loop obstruction)
 Adequate exposure is best achieved by a midline incision (If the site of
obstruction is unknown, see diagram below)
 Incarcerated inguinal hernia- an inguinal incision even if bowel resection is
required
 Operative treatment of most other types of small bowel obstruction requires
laparotomy or laparoscopy for exploration.

Long Midline Incision

Cecum is collapsed Cecum is distended

Small intestinal Obstruction Large intestinal Obstruction

Growth/gangrene
Viable Bowel Gangrene No gangrene

Treat the cause Resection Treat the cause Treat accordingly

(e.g. perforation)

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 Table 5.9: Difference between Viable and Non-viable Bowel
Viable Non-viable
Circulation  Dark changes to lighter color  Dark color
 Visible pulsation in mesenteric arteries  No detectable pulsation
General Appearance  Shiny  Dull and lustreless
Intestinal Musculature  Firm  Flabby, thin and friable
 Peristalsis maybe observed  No peristalsis

Discussion of the Case

 Small bowel obstruction (SBO) occurs when the normal flow of intestinal contents is
interrupted

Table 5.10: Common etiologies of Small bowel obstruction

 Adhesions
 Neoplasm  Primary small bowel neoplasm
 Secondary (e.g melanoma derived metastasis)
 Local invasion (e.g desmoid tumors)
 Hernias  External (e.g inguinal and femoral)
 Internal
 Crohn’s disease  Foreign body  Meckel’s diverticulum
 Volvulus  Post ischemic strictures  Hematoma
 Intussusception  Gallstone ileus  Congenital abnormalities (webs,
 Radiation induced stricture  Diverticulitis duplication and malrotation)

Pathogenesis
 The hallmark of SBO is dehydration and its sequelae.

P a g e 325 | 548
 When normal luminal flow of intestinal contents is interrupted, the small intestine
proximal to the obstruction begins to dilate as intestinal secretions are prevented
from passing distally.
 This has a number of consequences that depend, in part, upon the site and the
degree of obstruction.
o Patients with proximal obstruction (jejunum) experience repeated bouts of
nausea and emesis and typically cease taking in food or liquids orally.
o These features are less prominent in patients with distal obstruction (ileum).
 Swallowed air and gas from bacterial fermentation accumulates, adding to the
dilatation.
 Bacterial overgrowth occurs in the proximal small bowel, the contents of which are
normally nearly sterile, and therefore the emesis can become feculent due to
bacterial overgrowth.
 As the process continues, the bowel wall becomes edematous and the intestine's
normal absorptive function is lost so that even more fluid is sequestered in the
bowel lumen.
 Secretion of fluid into the lumen of the proximal dilated bowel increases. With
worsening edema of the intestine, there is transudative loss of fluid into the
peritoneal cavity.
o The end result is increasing dehydration with concomitant electrolyte
derangements and decreased urine output.
o Tachycardia, oliguria, azotemia, and hypotension can result from progressive
dehydration.
 In more proximal obstruction, emesis causes the loss of fluid containing Na, K, H, and
Cl, resulting in metabolic alkalosis.
 Strangulation complicates from 7 to 42% of bowel obstruction and occurs when
bowel wall edema and increasing intraluminal pressure compromise perfusion to a
segment of intestine.
o Necrosis ensues, with concomitant fever and leukocytosis, which will
eventually lead to perforation unless the process is interrupted.

P a g e 326 | 548
 o Necrosis of the small bowel during obstruction is most commonly caused by
twisting of the mesentery (such as in volvulus) from an adhesive band acting
as the point of fixation.
o Mortality is significantly increased in the setting of strangulation.
o Strangulation of the intestine almost always occurs in the setting of complete
obstruction.
o Obstruction of the small intestine can be complete or partial.
o One exception to that rule is a Richter's hernia, a condition in which only part
of the circumference of a segment of intestine passes through a hernia
orifice.
 In such cases strangulation can occur without complete obstruction of
the lumen.
 A closed-loop obstruction occurs when a segment of intestine is obstructed in two
locations, creating a segment with no proximal or distal outlet.
o If undetected, closed-loop obstruction can rapidly progress to strangulation.
o In this setting, there may only be a short segment of intestine that is
distended, making the diagnosis difficult because of minimal abdominal
distention.
 It is therefore of utmost importance to determine whether a bowel obstruction is
complete or partial, and whether strangulation of the intestine is impending or has
occurred.
 The location and cause of obstruction are of secondary importance, although in rare
circumstances this information may affect subsequent management decisions.

Diagnosis:
 The diagnosis of SBO is generally made based upon clinical and radiographic features
 It must be distinguished from non- obstructing causes of bowel dilatation.
 See above for more.

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 5.6. Large Bowel Obstruction (LBO)
 Case Discussion……………………….………………………….…328
 History……………………………………………….…………….……328
 Physical Examination………………………….…………….……329
 Investigation……………………………………………….….……..330
 Management………………………………………………..……….332
 Differential Diagnosis……………………………………….……333
 Discussion of the Differentials…………………………..……334

Case Discussion
 This is a 77 years old male patient who presented with inability to pass feces and flatus for
7 days duration which was accompanied by abdominal distension. He had the same
complaint starting 10 years back with 3-month recurrence with one episode lasting for not
more than a day. He also has history of abdominal pain, nausea and vomiting. The patient
is conscious and chronically ill looking. The vitals are within normal range. There is a
sagittal scar extending from the umbilicus till the pubic symphysis.

History
 Risk factors:
o Ask risk factors for malignancy (colonic cancer or non-colonic like pancreatic
cancer, ovarian cancer, and lymphoma )
o Prior abdominal surgery  adhesive large bowel obstruction
o Repeated bouts of intestinal inflammation  strictures; examples include:
diverticulitis, sequelae of ischemic colitis and inflammatory bowel disease.
o Benign conditions that lead to rectal stenosis like inflammatory bowel
disease, tuberculosis, suppository use, radiotherapy, fibrosis due to
endometriosis, lymphogranuloma venereum, and postoperative stricture.

P a g e 328 | 548
 Clinical Features:
o Acute Obstruction:
 Abdominal Pain:
- Infraumbilical and cramping type with paroxysms of pain occurring
every 20 to 30 minutes.
- Pain in the low pelvis may be due to rectal tenesmus as a sign of
rectal obstruction.
- Focal abdominal pain may indicate peritoneal irritation due to
ischemia or colonic necrosis, whereas a sudden relief of pain followed
by a progressive worsening of pain may relate to intestinal
perforation.
 Nausea and/or vomiting: particularly with proximal colonic obstruction
 Bloating
 Obstipation
o Chronic obstruction:
 Progressive change in bowel habits, typically over weeks to months.
 A change in bowel habits associated with unintentional weight loss over
the same period is suggestive of malignancy.

Physical Examination
 Patients with colorectal obstruction, particularly those with a delayed presentation,
may have signs of dehydration, shock, or even abdominal compartment syndrome
from severe colonic distention.
 Check features of toxemia or septicemia: tachycardia, tachypnea, fever
 Abdominal examination:
o Inspection: check for abdominal distention, which can be particularly
dramatic for distal complete obstructions.
o Auscultation: increased/high pitched metallic sounds; if fatigue occurs or
gangrene develops, bowel sounds are not heard—silent abdomen.

P a g e 329 | 548
 o Palpation: check for abdominal tenderness, initially localized but later
becomes diffuse
o PR Examination: Shows empty, dilated rectum, often with tenderness. If
rectal growth is the cause for obstruction, it may be palpable.

Investigation
 Lab studies
o Serum electrolytes
 There is derangement of most of the electrolytes (hypokalemia,
hyponatremia, hypochloremia) in case of intestinal obstruction which
needs to be corrected preoperatively.
 Strangulation may be associated with deranged potassium, amylase or
lactate dehydrogenase.
o Complete blood count
 Low hemoglobin indicates underlying malignancy.
 Increases total WBC count indicates infection and sepsis (perforation).
Definitive diagnosis
1. Plain abdominal X-ray  Gas shadows appear earlier than fluid
 Upright position: Air fluid levels:
levels, so if fluid levels are pronounced,
 Multiple in small bowel obstruction
the obstruction is advanced.
 Two big in sigmoid volvulus
 Isolated air fluid level at the area of left colon suggests malignant
obstruction at the recto sigmoid bowel.
 Supine position:
 Indicates the distal limit of the obstruction
 Central distension indicates small bowel obstruction
 Peripheral distention indicates large bowel obstruction
 Valvulae Conniventes in small bowel
 Haustrations in large bowl.

P a g e 330 | 548
  Caecum has no haustrations:- It appears as a round gas shadow in the
right iliac fossa.
 Lateral erect X Ray:
 To see gas in the rectum, absence of gas in the rectum is suggestive of
complete mechanical obstruction
 Anteriorly located bowel distension is suggestive of small bowel
obstruction.
 Posteriorly located distension is suggestive of large bowel obstruction
2. Sigmoidoscopy  If the obstruction is in the distal segment
 When large amount of colonic air of the colon it usually does not give rise to
extends down to the rectum, flexible or small bowel fluid levels unless advanced,
rigid sigmoidoscopy will readily exclude whereas in proximal colonic obstruction
a rectal or distal sigmoid obstruction. may do so in the presence of an income-
petent ileocaecal valve.
3. Barium Enema: With water soluble contrast material.
 Bird’s beak appearance in sigmoid volvulus.
 Apple core appearance in colonic malignancy.
 To differentiate large bowel obstruction from pseudo-obstruction, which is a
severe impairment in the ability of the intestines to push food through, is by
using a limited water soluble enema should be undertaken.
 But contrast studies with enema are contraindicated in case of perforation.
4. Ultrasound
 Sonographic evidence has been established for small bowel and colonic
obstruction.
o Simultaneous observation of distended and collapsed bowel
segments.
o Free peritoneal fluid
o Inspissated intestinal content
o Paradoxical pendulating peristalsis
o Highly reflactive fluid within the bowel lumen
o Bowel wall edema between serosa and mucosa
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 o A fixed mass of aperistaltic, fluid filled, dilated intestinal loops.
 Advantages of US includes:
o Is well suited to critically ill patients, because it can be performed at
the bedside
o Is relatively inexpensive
o Is easy and quick to perform
o Can provide a great deal of information about the location, nature,
and severity of the obstruction
5. CT Scan of the Abdomen:
 It can ascertain level of obstruction
 It can assess the severity of the obstruction and determine its cause.
 It can detect closed loop obstruction and early strangulation.
 It can detect inflammatory and neoplastic processes both outside and inside
peritoneal cavity.
 Can visualize small amounts of intraperitoneal air or pneumatosis cystoides
intestinalis not seen in the conventional films.
 Accuracy higher than 95% sensitivity and more than 94% specificity.
 When CT Scanning is not diagnostic, small bowel follow through examination
with dilute barium is often useful.

Management
 Preoperative management includes correction of dehydration and electrolytes as
well as relief of symptoms ones the diagnosis is settled.
A- Aspiration: - With Ryle’s tube (NGT)
 This is the most important step in the management of intestinal obstruction.
 It helps in decreasing the distension
 Prevents vomiting
 Prevents respiratory complications, such as aspiration during and following general
anesthesia.
B- Bowel care: - No Purgatives
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  Nothing is given by mouth because purgation can cause perforation
C- Charts
 Temperature
 Pulse
 Respiration rate
 Intake and output measurement
o In cases of conservative management such as obstruction due to adhesion,
change in temperature and increasing pulse rate, suggest perforation and
gangrene.
o These patients have to be operated immediately.
D- Drugs
 To cover gram-positive, gram negative & anaerobic microorganisms.
E- Exploratory Laparotomy
 To check and treat the obstruction depending on the
F- Fluids
 Should be given before, during and after surgery.
 It forms the most the most important treatment of intestinal obstruction.

Differential Diagnosis
1. Volvulus
2. Neoplasm
a. Benign b. Malignant
3. Stricture
a. Diverticular disease b. Ischemic
4. Congenital
a. Anorectal malformation b. Congenital megacolon
5. Impaction Bands

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 Discussion of the Differentials

5.6.1. Volvulus

 Introduction ……………………………………………………………334
 Epidemiology…………………………………………………………..334
 Risk Factors………………………………………………………………334
 Clinical Manifestation………………………………………………335
 Diagnosis………………………………………………………………….336
 Management……………………………………………………………336

Introduction
 A volvulus is a twisting or axial rotation of a portion of bowel about its mesentery.
o >180° torsion- obstruction of lumen.
o >360°torsion-vascular occlusion of mesentery  Thrombosis  Ischemia.

Epidemiology
 Sigmoid volvulus accounts for two thirds to three fourths of all cases of colonic
volvulus.
o Cecal and transverse colon volvulus cover the rest.
 It usually occurs in older adults with a mean age of 70 years at presentation.
 It has been reported in patients with
o Crohn disease o Chagas disease
o Pregnancy

Risk Factors
 Older age
 Loaded colon due to high residue diet.
 Diverticulitis with a band or adhesion

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 Chronic constipation
 Anatomic factors
o A long redundant and pendulous colon
o Long mesentery
o Narrow attachment at the base

Clinical Manifestations
 Majority of patients present with:
o Insidious onset of slowly progressive abdominal pain which is usually
continuous and severe, with a superimposed colicky component during
peristalsis.
o Nausea
o Abdominal distension which starts from the left iliac fossa and extends to the
rest.
o Constipation.
o Vomiting usually occurs several days after the onset of pain.
 A distended tympanic abdomen with tenderness on palpation is a common physical
finding.
 Rarely, compromise of the blood supply to the sigmoid colon may result in gangrene,
peritonitis, and sepsis.
 If perforation and/ or peritonitis develop EXPECT:
o Fever o Abdominal guarding
o Tachycardia o Rigidity
o Hypotension o Rebound tenderness

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 Diagnosis

 Plain abdominal X-ray

o The dilated sigmoid loop extends from the pelvis to the right upper quadrant
as high as the diaphragm
 It is described as bent inner tube sign, omega sign and/or coffee-bean
sign.
 CT scan
o The dilated sigmoid colon around its mesocolon and vessels causes a whirl
pattern, and a bird-beak appearance of the afferent and efferent colonic
segments.
o Absence of rectal gas
o If there is bowel necrosis pneumatosis intestinalis, portal venous gas, or loss
of bowel wall enhancement are present.
 Contrast enema
o The contrast tapers to the point of obstruction giving the characteristic
appearance a twisted taper or a bird's beak configuration.
o Contrast enemas should not be performed in patients with possible
peritonitis.

Management

 The goal of treatment of sigmoid volvulus is to reduce the sigmoid volvulus and to
prevent recurrent episodes.
o First we have to perform the aforementioned principles of management.
o Then deflation of the gut should be done with a flexible sigmoidoscopy or
rigid sigmoidoscopy and insertion of a flatus tube which should be secured
for 24 hours:
 To reduce the chance of recurrent volvulus in the acute setting.
o Take X-ray to make sure that the decompression has occurred.
o In the elderly there is a high death rate
 ~80 per cent at two years
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  If further surgical management is done unlike young patients who
require an elective surgical intervention after week to avoid
recurrence.
o If this method fails, the volvulus is untwisted at laparotomy and the bowel
is decompressed via a rectal tube threaded upwards from the anus and if
viable, it can be fixed to the lateral wall of abdomen or pelvis—
sigmoidopexy.
 But resection of the segment and anastomosis is preferable.

 If the segment is gangrenous we can perform:

o Paul-Mikulicz Operation:
 The gangrenous segment is resected and the proximal cut end is
brought out as colostomy and the distal end is brought out as mucous
fistula, from the rectum.
 Continuity is maintained after 6 weeks.
o Hartmann’s procedure:
 Sigmoid colectomy is done and the proximal cut is brought out as end
colostomy where the distal end is closed.
 Colorectal anastomosis is done after 6-12 weeks.
o Resection with primary anastomosis is not advisable because of the
contamination and anastomotic leak risks.
 Immediate laparotomy:
o When endoscopic detorsion is unsuccessful or in patients with signs and
symptoms suggestive of peritonitis.

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 5.7. Acute Abdomen
 Case Discussion……………………………………………………….338
 Introduction…………………………………………………………….338
 History ……………………………………………………………………338
 Physical Examination…………………………………………….…342
 Investigation……………………………………………………………343
 Management…………………………………………………………..346
 Discussion of the Differentials…………………………………346

Case Discussion

 A 22-year-old male presents to the emergency room with abdominal pain, anorexia,
nausea, and low-grade fever. Pain started in the mid-abdominal region 6 hours ago and is
now in the right lower quadrant of the abdomen. The pain is steady in nature and
aggravated by coughing. Physical examination reveals a low-grade fever (100.5°F [38°C])
and pain on palpation at right lower quadrant (McBurney sign).

Introduction
 It refers to signs and symptoms of abdominal pain and tenderness.
o Previously undiagnosed pain that arises suddenly.
o Less than 7 days duration usually less than 48 hrs.
o If the abdominal pain persists for more than 6 hours it is most likely surgical.

History
 Age
o Infants and children: Intussusceptions, Mid gut Volvulus, Incarcerated
hernia, Hirschsprung's disease
o Young: Appendicitis, ovarian/Testicular torsion
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 o Adult: Acute pancreatitis, acute cholecystitis, perforation
o Elderly: intestinal ischemia and infarction, diverticulitis, and sigmoid volvulus
and carcinoma of the colon causing obstruction.
 Sex
o Ectopic pregnancy, PID, and twisted ovarian cyst are only seen in females.
o Acute cholecystitis and primary peritonitis are common in females.
o Volvulus, intussusception, and perforated peptic ulcer are common in males.
 Elaborate the chief complaint
o Pain is the most common compliant of patients with acute abdomen.
o Onset and duration
 Sudden onset(within seconds): perforation, rupture, infarction, stone,
and torsion
 Rapidly accelerating pain (within minutes):
- Colic syndromes: biliary colic and ureteral colic.
- Inflammatory processes: acute appendicitis, pancreatitis, and
diverticulitis.
- Ischemic processes: mesenteric ischemia, strangulated intestinal
obstruction, and volvulus.
 Gradual onset with increasing in intensity(over several hours):
- Inflammatory conditions: appendicitis and cholecystitis.
- Obstructive processes: nonstrangulated bowel obstruction and
urinary retention.
- Other mechanical processes: ectopic pregnancy and penetrating
or perforating tumors.
 Quality of pain
o Colicky: gripping in nature which starts and stops abrubtly and occurs due to
spasm of hollow viscus.
o Dull: deep ache felt in an area, but does not stop the patient from daily
activity.
 Initial periumblical pain of appendicitis
o Burning: peritonitis.
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 o Lancinating: piercing or stabbing sensation.
 Acute pancreatitis
o Tearing: causing continued or repeated pain or distress.
 Dissecting aneurysm
 Timing
o Intermittent Colicky/Crampy/ pain: SBO, ureteric stone
 biliary colic is an exception
o Persistent, sharp and steadily increasing: infectious or inflammatory process
(e.g., appendicitis).
 Location and radiation
o Solid organ visceral pain: generalized in the involved quadrant.
o Appendicitis: diffuse periumbilical pain later shifts to the right lower
abdomen.
o Perforated ulcer, ruptured aortic aneurysm or pancreatitis: may radiate to
the back.
o Genitourinary pain: starts at the flank and radiates to the groin.
 Alleviating and aggravating factors
o Diffuse peritonitis:
 Worsened by any movement, deep breathing, coughing, or sneezing;
relieved by lying still.
o Intestinal obstruction:
 Transient relief after vomiting. Eating may worsen it.
o Acute pancreatitis:
 Exacerbated by lying down and relieved by sitting up.
o Non-perforated duodenal ulcer:
 Relieved by eating or taking antacids.
o Eating worsens the pain of bowel obstruction, biliary colic, pancreatitis,
diverticulitis, or bowel perforation.
 Ask for any associated symptoms:
o Nausea and vomiting.

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  It occurs before the onset of pain in non-surgical conditions like

Murphy’s syndrome: the gastroenteritis or food poisoning.

classic presentation of  It occurs after the onset of pain in surgical conditions like appendicitis,
acute appendicitis which pancreatitis, colics.

has been described as pain  It is repetitive and profuse in acute pancreatitis and acute intestinal
first, vomiting next and obstruction.

fever last.  It is periodical and infrequent in duodenal ulcer perforation.

 Bilious emesis: a process distal to the duodenal ampulla.
 Hematemesis: conditions like peptic ulcer or gastritis.
o Fever - inflammatory & infectious process
 High grade fever, chills & mental status change- bacteremia &
impending septic shock.
o Anorexia is present in many patients with acute peritonitis.
o Constipation, obstipation, distention:
 Certain for some degree of intestinal obstruction.
o Diarrhea: medical causes like infectious enteritis, IBD, and parasitic
contamination.
 Incomplete obstruction ↑ secretions
 Bloody diarrhea can be seen in these conditions as well as in colonic
ischemia.
 Ask past medical and surgical history:
o Previous abdominal surgery, which is important in intestinal obstruction.
o Peripheral vascular disease or coronary artery disease.
o Previous history of same illness (recurrence).
o History of trauma
o If there is any history of medication intake.
 Ask gynecologic history:
o Ask for LMP and missed menstrual periods to rule out ectopic pregnancy.
o Abnormal vaginal bleeding or discharge
o Risk factors for ectopic pregnancy:
 PID
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  Use of an intrauterine device, or
 Previous tubal surgery

Physical Examination
 General appearance
o Acute peritonitis: Patient stays still in the bed in supine position without
moving.
o Colic: restless and unable to find a comfortable position.
 Patients with ureteral colic may writhe in pain or walk around the
examination room.
o Biliary obstruction: jaundice
o Septic: weak and lethargic
 Vital
o Fever: once patient develops septicemia fever might not be present.
o Hypotension or tachycardia:
 It remains normal during the initial phases of appendicitis,
pancreatitis, and peritonitis and develops when sepsis occurs.
 In intestinal obstruction it is due to dehydration.
 Abdominal examination
o Inspection- Look for any:
 Distention: is gradually progressive in acute intestinal obstruction and
acute peritonitis.
 Hernia: because they are common causes of intestinal obstruction.
 Surgical scars, Bulging masses
 Areas of erythema, ecchymosis: bruising around the umbilicus
(cullen’s sign) and around the flank (Grey Turner’s sign) is a feature of
acute hemorrhagic pancreatitis.
 Movement with respiration: a diffuse restriction of movement is seen
in a diffuse peritonitis unlike appendicitis and cholecystitis with
localized limitation of movement.

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  Visible peristalsis: step ladder peristalsis is a typical feature of small
bowel obstruction.
o Auscultation-
 Hyperactive: in early phases of intestinal obstruction.
 Absent bowel sound: is a typical feature of diffuse peritonitis.
o Palpation
 Tenderness:
McBurney’s tenderness  McBurney’s tenderness
is typical of acute  Rebound tenderness indicates an inflamed parietal
appendicitis which is of peritoneum.
spinoumbilical line at  Mass
rd
junction of medial 2/3  Guarding and rigidity: indicates an inflamed parietal peritoneum.
rd
and lateral 1/3 .  Organomegally
 Thoroughly search for hernias
o Percussion:
 Tympanic Vs dull,
 Signs or fluid collection,
 Obliteration of liver dullness: due to bowel perforation.
 Rectal examination
o Tenderness or a mass on the right pelvic side wall is sometimes seen in
appendicitis.
o Look for a mass in the rectum and occult blood in the stool specimen.
 Other
o Pelvic examination o Testicular/scrotal

Investigation
Laboratory studies
 CBC (with differentials):
o Leukocytosis typically suggests an infectious or inflammatory process like
peritonitis.
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  Acute appendicitisis is not ruled out with a normal WBC count.
o Anemia suggests either acute or acute on chronic bleeding.
o Increase in hematocrit may indicate hemoconcentration due to dehydration.
 Serum electrolyte:
o Hypochloremic hypokalemic metabolic alkalosis occurs in recurrent vomiting.
o Metabolic acidosis (lactic acidosis) and hyperkalemia can occur in bowel
ischemia.
 LFT and Liver enzymes:
o Conjugated hyperbilirubinemia, mildly elevated transaminases is expected in
choledocholithiasis, cholangitis, and gallstone pancreatitis.
o Highly elevated transaminases and mild cholestasis can be seen in hepatic
abscess.
 Pancreatic enzymes (Lipase and amylase):
o A three-fold elevation in lipase is diagnostic of acute pancreatitis. Amylase is
less specific and may be elevated in other conditions like bowel obstruction
and PUD.
 Urinalysis:
o The presence of hematuria, nitrates, and/or urinary crystals should raise
suspicion for a UTI and/or nephrolithiasis.
o Mild pyuria may be present in acute appendicitis because of relationship of
appendix with the right ureter.
 β-hCG urine and serum test:
o Should be performed in every woman of reproductive age, regardless of
current contraception use to rule out undiagnosed intrauterine pregnancy
and ectopic pregnancy.
 RFT:
o Elevated urea may indicate prerenal azotemia.
o Elevated creatinine is a relative contraindication for IV contrast
administration.
 Serum Lactate:

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 o Elevated in hypotension/shock like in acute pancreatitis and bowel infarction
due to bowel obstruction/mesenteric ischemia.
 Cultures:
o If urinalysis indicates a UTI we do urine cultures.
o Blood cultures in patients with suspected sepsis.
NB. Patients with obvious signs of diffuse peritonitis do not require further diagnostic
imaging and should proceed straight to surgical management.
Imaging studies:
 Plain abdominal X-ray:
o Gas under diaphragm is visible in case of perforation.
o Multiple air fluid levels can be seen in intestinal obstruction.
o In the presence of acute peritonitis ground glass appearance can be seen.
o Shows abnormal calcifications:
 About 5% of appendicoliths, 10% of gallstones, and 90% of renal
stones contain sufficient amounts of calcium to be radiopaque.
 Pancreatic calcifications can be seen in many patients with chronic
pancreatitis.
 Ultrasonography:- is preferred for:
o The bedside evaluation of unstable patients.
o Suspected pregnancy and to evaluate for other acute gynecologic disorders
such as:
 tubo-ovarian abscess,
 ruptured corpus luteum cyst, or
 Ovarian torsion.
o It is also preferred for the initial evaluation of suspected acute cholecystitis
and ureteral stones with hydronephrosis
 CT-scan:
o It is preferred and can provide a definitive diagnosis in up to 90% of patients
with acute severe abdominal pain

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 o It can be falsely negative early in the course of acute pancreatitis, mesenteric
ischemia, cholecystitis, appendicitis, and diverticulitis, especially if performed
without contrast.
 MRI imaging:
o It is not widely used yet in the diagnostic work-up of patients who present
with acute abdominal pain.
o Its main advantage is that it lacks ionizing radiation exposure.

Management

 Establish a DDX and a plan to confirm the DX

 Prioritize
 Determine whether operative intervention is necessary
 Pre OP- Preparation to minimize morbidity and mortality

Discussion of the Differentials

5.7.1. Acute Appendicitis

 Introduction ………………………………………………………….347
 Epidemiology…………………………………………………………347
 Etiology………………………………………………………………….347
 Clinical Manifestation…………………………………………….348
 Diagnosis……………………………………………………………… 351
 Management…………………………………………………………353
 Differential Diagnosis…………………………………………….356

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 Introduction

 It i s acute inflammation of the vermiform appendix.

 It is today recognized as one of the most common and significant causes of severe
acute abdominal pain worldwide.

Epidemiology
 It is common in the second and third decades of life.
 The incidence is approximately 233/100,000 population and is highest in the 10 to
19 year-old age group.
 Male to female ratio is 3:2.
 The lifetime incidence is around 8.6% in male and 6.7% in women.

Etiology
 The etiology of appendicitis still doesn’t have a unifying hypothesis.
 Although it is associated with the growth of both aerobic and anaerobic organisms,
the initiating event is controversial.
 Obstruction of the appendix lumen:
o The lumen of the appendix is small in relation to its length, and this
configuration may predispose to closed-loop obstruction and gives a fertile
ground for overgrowth of bacteria.
o And the continued secretion of mucus leads to intraluminal distention and
increased wall pressure which produces the visceral pain sensation
experienced by the patient as periumbilical pain.
o Subsequent impairment of lymphatic and venous drainage leads to mucosal
ischemia.
o These findings in combination promote a localized inflammatory process that
may progress to gangrene and perforation.
o Inflammation of the adjacent peritoneum gives rise to localized pain in the
right lower quadrant.This can occur due to:
 Faecolith (Appendicolith): is composed of inspissated faecal
material, calcium phosphates, bacteria and epithelial debris.
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  A fibrotic stricture
 Neoplasm of caecum near the base.
 Intestinal parasites, particularly Oxyuris vermicularis (pinworm), can
proliferate in the appendix and occlude the lumen.
 Non obstructive theory:
o Diffuse inflammation of the appendix due to different kinds of bacteria.
 Dietary factors:
o Decreased intake of dietary fiber and increased consumption of refined
carbohydrate.
 Familial susceptibility:
o A long retrocecal appendix is more susceptible to appendicitis since there
is a decreased blood flow to the tip.
 Abuse of purgatives

Clinical Manifestations
 Clinical syndromes of acute appendicitis:
o Acute catarrhal (non-obstructive) appendicitis and
o Acute obstructive appendicitis:
 Is characterized by a more acute course.
 There may be a generalized abdominal pain from the start.
 The temperature may be normal and vomiting is common.
 The classic symptoms of acute appendicitis are:
o Abdominal pain: is the most common symptom.
 The pain at first is a periumblical colicky type of abdominal pain which
is a visceral pain and later it is shifted to the right iliac fossa which is
more intense, constant and somatic in nature as the inflammation
progresses.
 It is aggravated by coughing or sudden movement.
 It is known as a migratory pain and is the most reliable symptom; but
is present in only about half of the patients.

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  Atypical pain is more common in the elderly
o Anorexia: is a useful and constant clinical feature, particularly in children.
o Nausea and vomiting: if they occur, usually follow the onset of pain and is
nonfrequent. It is due to reflex pylorospasm.
 After the first 6 hours, slight pyrexia (37.2– 37.7°C) with a corresponding increase in
the pulse rate to 80 or 90 is usual, but not in 20% of patients.
 In many patients, initial features are atypical or nonspecific, and can include:
o Indigestion
o Flatulence
o Bowel irregularity
o Diarrhea: if the appendix is at post-ileal or pelvic position.
o Generalized malaise
o Urinary frequency: Inflamed appendix may come in contact with bladder and
can cause bladder irritation.
NB. The symptoms of appendicitis vary depending upon the location of the appendix.
Signs:
 McBurney's point tenderness:
o Is described as maximal tenderness at the spinoumbilical line over the
junction of medial 2/3rd and lateral 1/3rd.
o Has a sensitivity of 50-94% and specificity of 75-86%.
 Rovsing's sign:
o It is also called indirect tenderness.
o Refers to pain in the right lower quadrant with palpation of the left lower
quadrant. It is due to displacement of colonic gas and small bowel coils
impinging up on the inflamed appendix.
o Has sensitivity of 22-68% and specificity 58-96%.
 The psoas sign:
o Is associated with a retrocecal appendix.
o This is manifested by right lower quadrant pain with passive right hip
extension due to irritation of the right psoas muscle.
o Has a sensitivity of 13-42% and specificity 79-97%.
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  The obturator sign:
o Is associated with a pelvic appendix.
o Flexion of the right hip and knee followed by internal rotation produces a
right lower quadrant pain due to irritation of obturator internus muscle.
o Has a sensitivity of 8% and specificity of 94%.
 Blumberg’s sign:
o Is rebound tenderness over the right iliac fossa due to inflammation of the
parietal peritoneum.
 Cough tenderness: it is due inflammation of the parietal peritoneum.
o Is usefull in differentiating acute appendicitis form ureteric colic.
 Per rectal examination shows tenderness over the right side of the rectum.
o Often infection gets localized by omentum, dilated ileum and parietal
peritoneum leading to appendicular mass.
o Most often suppuration occurs in the localized area resulting in appendicular
abscess.
Special features:
 Acute Appendicitis in Infancy:
o Is rare, but has a higher chance of perforation with a higher mortality rate.
o Diffuse peritonitis can develop rapidly because of the underdeveloped
greater omentum.
 Acute Appendicitis in Children:
o Peritonitis occurs early due to absence of localization.
o Dehydration and septicemia are common.
o Almost all children have vomiting as a symptom.
 In Elderly
o Gangrene and perforation occur much more frequently.
o Localization is poor and so peritonitis occurs early due to lax abdominal wall.
o Has a higher mortality rate.
 In Pregnancy
o The appendix is pushed to the right upper quadrant during pregnancy.

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 o However, pain in the right lower quadrant of the abdomen remains the
cardinal feature, but can also be localized at mid or even the upper right side
of the abdomen.
o Leads to an increased rate of maternal mortality and also leads to premature
labour and fetal loss.

Diagnosis
 Laboratory tests
o WBC count with differential:
 A very high WBC count suggests a complicated appendicitis with
perforation or gangrene.
 A completely normal leukocyte count and differential is found in about
10% of patients with acute appendicitis.
o Serum C-reactive protein (CRP)
o Serum pregnancy test in women of childbearing age
 Alvarado score:
o The diagnosis of acute appendicitis is essentially clinical.
Table 5.11: Alvarado (MANTRELS) score
Symptoms Points
 Migratory right lower quadrant pain 1 point
 Anorexia 1 point
 Nausea or vomiting 1 point
Signs
 Tenderness in the right lower quadrant 2 point
 Rebound tenderness in the right lower quadrant 1 point
 Elevated temperature >37.5°C (>99.5°F) 1 point
Laboratory values
 Leukocytosis of WBC count >10 x 109/L 1 point
 Shift to Left (>75% neutrophils) 2 point
Total score 10

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  Score less than 5: Not sure.
 Score between 5-6: Compatible. Abdominal ultrasound or contrast-
enhanced CT examination further reduces the rate of negative
appendicectomy.
 Score between 6-9: Probable.
 Score more than 9: Confirmed
 Abdominopelvic CT-scan:
o Is recommended as the preferred test in the imaging evaluation of suspected
appendicitis in adults.
o Intravenous contrast is recommended unless there is contradiction like:
 Renal insufficiency
 History of hypersensitivity reaction to iodinated contrast.
o Demonstrates higher diagnostic accuracy than ultrasound or MRI.
o The imaging features of acute appendicitis on abdominopelvic CT are:
 Enlarged appendiceal double-wall thickness (>6 mm)
 Appendiceal wall thickening (>2 mm)
 Periappendiceal fat stranding
 Appendiceal wall enhancement
 Appendicolith (seen in a minority of patients)
 Ultrasound:
o Useful to rule other causes.
o It is preferred over CT-scan in children and pregnant women.
o Advantages:
 Lack of ionizing radiation and intravenous contrast.
 Can be performed at the bedside.
o Disadvantage:
 Has a lower diagnostic accuracy than CT or MRI.
 Compression over the appendix can cause significant patient
discomfort in patients with appendicitis.
 Rates of indeterminate exams are high.
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 o Imaging features of acute appendicitis on ultrasound include
 Noncompressible appendix with double-wall thickness diameter of >6
mm
 Focal pain over appendix with compression
 Appendicolith
 Increased echogenicity of inflamed periappendiceal fat
 Fluid in the right lower quadrant
 MRI:
o Is preferred over CT in:
 Pregnant women.
 Older children who can cooperate with the exam
 Plain abdominal X-ray:
o Is not recommended in the diagnostic workup of suspected appendicitis.
o The exam does not visualize the appendix.
o It can be used to rule out other causes of acute abdomen like intestinal
obstruction.
 Surgical exploration:
o Is done when clinical suspicion for appendicitis is high but imaging studies are
negative, nondiagnostic, or unavailable.

Management
 Catarrhal(non-obstructive) appendicitis:
o Are now treated with conservative management.
o They should generally be hospitalized for treatment with intravenous
antibiotics, bed rest, intravenous fluids, and bowel rest.
o For outpatient management, antibiotics are administered and the course is
followed closely.
o However there is an approximately 15% recurrence rate within one year.
o This approach should also be considered in patients with high operative risk
(multiple comorbidities).

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  Preoperative preparation:
o They require adequate hydration with intravenous fluids (isotonic saline or
ringer lactate).
o Correction of electrolyte abnormalities.
o Administration of perioperative antibiotics:
 Is important for preventing wound infection and intra-abdominal
abscess following appendectomy.
 Should be given within a 60-minute "window" before the initial
incision for patients proceeding directly from the emergency room to
the operating room.
o The patient's vital signs and urine output should be closely monitored; a Foley
catheter may be required in severely dehydrated patients.

Appendicectomy:
 Gridiron incision:
o Is made at right angles to spinoumblical line, its centre being along the line at
McBurney’s point.
 Rutherford Morison incision:
o Is used when a better access is required. It is an oblique muscle cutting
incision with its lower end over McBurney’s point and extending obliquely
upwards and laterally as necessary.
 Lanz incision:
o Is a transverse skin crease. It has a better exposure and extension is easier to
make.
 Lower midline abdominal incision:
o Is done when the diagnosis is in doubt.

Laparoscopic Appendicectomy
 Is superior over open approach in:
o Management of suspected appendicitis is as a diagnostic tool, particularly in
women of child-bearing age.
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 o Lower rate of wound infections.
o Less pain on postoperative days.
o Shorter duration of hospital stay.
o In obese patients
 But it inferior in:
o Has a higher rate of intra-abdominal abscesses
o It requires a longer operative time.

Management of Appendix abscess

 suggestions for the presence of pus:
o After a conservative treatment of appendix mass, if it fails to resolve.
o Continued spiking pyrexia.
 Ultrasound or abdominal CT scan is used to identify an area suitable for the insertion
of a percutaneous drainage.
 If the percutaneous drainage fails we may consider a laparotomy through a midline
incision rarely.

Management of an appendix mass

 For a patient with appendix mass and good condition, we use a conservative
Ochsner–Sherren regimen.
o IV fluid
o NGT
o Analgesics
o Parenteral antibiotics
o Mark the limits of the mass on the abdominal wall using a skin pencil.
o Monitor vital sign (at 4 hours interval), size of the mass, fluid balance
maintained.
o Clinical improvement is expected in 24-48hrs.
 Clinical deterioration or evidence of peritonitis is an indication for early laparotomy.
 Failure of the mass to resolve should raise suspicion of a carcinoma or Crohn’s
disease.
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 Differential Diagnosis

1. Ischemia:
a. Ovarian torsion
b. Testicular torsion
c. Mesenteric ischemia
d. Strangulated hernia
e. Ischemic colitis
2. Obstruction:
a. Small bowel obstruction
b. Large bowel obstruction
3. Hemorrhage:
a. Solid organ trauma
b. Leaking or ruptured arterial aneurysm
c. Ruptured ectopic pregnancy
d. Hemorrhagic pancreatitis
e. Intestinal ulceration
4. Perforation:
a. Perforated GI ulcer and cancer
b. Boerhaave’s syndrome
c. Perforated diverticulum
5. Infection:
a. Appendicitis
b. cholecystitis
c. Meckel’s diverticulitis
d. Hepatic abscess
e. Diverticular abscess
f. Psoas abscess

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 5.7.2. Acute Cholecystitis
 Introduction …………………………………………………………….357
 Epidemiology……………………………………………………………357
 Etiology…………………………………………………………………...358
 Clinical Manifestation………………………………………………359
 Diagnosis………………………………………………………………… 359
 Management……………………………………………………………361

Introduction
 The term cholecystitis refers to inflammation of the gallbladder.
 It can be:
o Acute cholecystitis:
 Refers to a syndrome of right upper quadrant pain, fever, and
leukocytosis. It can be:
 Calculus cholecystitis:
 Is an obstructive cholecystitis due to gallstones.
 It is more common.
 Acalculous cholecystitis:
 Less often, without gallstones.
 It has a more fulminant course and more commonly
progresses to gangrene, empyema, or perforation.
o Chronic cholecystitis:
 It develops over time and be discovered histologically following
cholecystectomy.

Epidemiology
 The distribution and incidence of acute cholecystitis follow that of cholelithiasis
because of the close relationship between the two.

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  It occurs in approximately 20% of patients with biliary colic if they are left
untreated.
 However incidence is falling likely due to early treatment of symptomatic
gallstones.
 It is 3 times more common in women than in men up to the age of 50 years, and
is about 1.5 times more common in women than in men thereafter.

Etiology
 Cholecystolithiasis accounts for 90%–95% of all causes of acute cholecystitis.
o The “5F ” Risk factors for cholelithiasis can be an indirect factors:
 Female gender  Fat
 Forty  Fair
 Fertile
o Common to all individuals with these “5Fs” are high levels of estrogen and
progesterone which leads to reduction in gallbladder contractility and bile
stasis.
o Hemolytic anemia, surgery, and drugs can also be risk factors.
 Acalculous cholecystitis accounts for the remaining 5%–10%.
 Although the exact etiology is unclear, gallbladder stasis and ischemia have been
implicated as causative factors.
o Risk factors are:
 Older age  Total parentral nutrition
 Diabetes  Prolonged fasting
 HIV infection  Immobility
 Vascular disease  ICU patient
 Critically ill patients after trauma, burns and major operations.

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 Clinical Manifestations

 The most common symptom of acute cholecystitis:

o Steady right upper quadrant pain, similar in severity to but much longer in
duration than pain from previous episodes of biliary colic which is more than
4-6 hrs
 It is colicky in nature and may radiate to the right shoulder or back.
 Other common symptoms include fever, nausea, vomiting, and anorexia.
o There is often a history of fatty food ingestion one hour or more before the
initial onset of pain.
 On physical exam:
o Patient is usually ill appearing, febrile, tachycardic, and lies still on the
examining table:
 Because cholecystitis is associated with true local parietal peritoneal
inflammation that is aggravated by movement.
o Abdominal examination usually demonstrates voluntary and involuntary
guarding distinguishing the episode from simple biliary colic.
 When inflammation spreads to the peritoneum, patients develop
more diffuse tenderness, guarding and rigidity.
o The gallbladder along with adherent omentum occasionally forms a mass
which can be palpated.
o Murphy's sign:
 Is an inspiratory arrest with deep palpation in the right upper
quadrant, which is frequently present in these patients.
o Boas’ sign:
 Is an area of hyperesthesia between 9th and 11th ribs. It is less than 7%
sensitive.

Diagnosis
 Laboratory tests
o WBC count with differential: there is leukocytosis with a left shift which is an
increased number of band forms.

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 Ultrasonography
o Finding calculi on ultrasound in the presence of right upper quadrant
abdominal pain and fever suggests an acute cholecystitis but is not
diagnostic.
o Additional sonographic features include:
 Gallbladder wall thickening (greater than 4 to 5 mm) or edema (double
wall sign).
 A "sonographic Murphy's sign" can be elicited which can confirm that
the inspiratory arrest is indeed due to the gallbladder.
o It has a sensitivity of 84% and specificity of 99%.
 Cholescintigraphy/HIDA scan:
o Is indicated if the diagnosis remains uncertain following ultrasonography.
o A 99mTc-hepatic iminodiacetic acid is injected intravenously and is excreted
into the biliary tree within 30-60 minutes.
o In acute cholecystitis edema of the cystic duct prevents the dye from entering
the gallbladder. The test is positive if the gallbladder is not visualized.
o It has a sensitivity of 90-97% and specificity of 71-90%.
o False positive results occur in:
 Cystic duct obstruction with a stone or tumor.
 Severe liver disease.
 Patients with total parenteral nutrition.
 Biliary sphincterotomy.
 Hyperbilirubinemia.
o False negative results are uncommon but can occur if the obstruction is
incomplete.
 Abdominal CT-scan:
o Is usually unnecessary.
o It can easily demonstrate gallbladder wall edema.
o It is useful when we suspect acute cholecystitis complications like:
 Emphysematous cholecystitis
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  Gallbladder perforation
o It may fail to detect gallstones because many stones are isodense with bile.

Management

 Admit to the hospital

 Give intravenous fluid therapy
 Correction of electrolyte disorders
 Control of pain:
o NSAIDs or opioids are used..
o If the pain progresses, it indicates a clinical progression.
 Antibiotics may also be indicated.
o To protect against sepsis and wound infection.
o Is highly recommended in older patients or those with diabetes or
immunodeficiency.
o Should cover the most common pathogens Enterobacteriaceae family.
 The severity of symptoms and risk for cholecystectomy determine the selection and
timing of definitive therapy.
 Emergency cholecystectomy or gallbladder drainage is required:
o If gangrene or perforation is suspected
o If there is a clinical progression despite the supportive therapy.
 Preferably laparoscopic cholecystectomy at admission:
o Considered in Low-risk patients without emergent indications.
 Gallbladder drainage procedure:
o Done in High-risk patients without emergent indications, if symptoms do not
improve with supportive care.
 Cholecystectomy can be done if the medical status can be optimized.

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 5.7.3. Acute Pancreatitis
 Introduction …………………………………………………………….362
 Epidemiology……………………………………………………………363
 Etiology…………………………………………………………………...363
 Clinical Manifestation………………………………………………364
 Diagnosis…………………………………………………………………365
 Management…………………………………………..………………367

Introduction

 It is an acute inflammatory process of the pancreas.

 It can be classified in to:
o Mild acute pancreatitis:
 Characterized by the absence of organ failure and local or systemic
complications. It has 1% mortality rate.
o Moderately severe acute pancreatitis:
 Characterized by transient organ failure (resolves within 48 hours)
and/or local or systemic complications without persistent organ failure
(>48 hours).
o Severe acute pancreatitis:
 Characterized by pancreatic necrosis and persistent organ failure that
may involve one or multiple organs.
o Interstitial edematous acute pancreatitis:
 Characterized by an inflammation without tissue necrosis.
o Necrotizing acute pancreatitis:
 Associated with pancreatic parenchymal necrosis and/or
peripancreatic necrosis.

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 Epidemiology

 Although rare in kids, it may occur at any age, with a peak in young men and older
women.
 There is no sex predilection.
 The annual incidence is 4.9-35/100,000 population.
 It is the leading gastrointestinal cause of hospitalization in the United States.
 The mortality rate has decreased due to advancement in diagnostic and therapeutic
interventions.

Etiology
 The two major causes are:
o Biliary calculi: accounts for 50–70% of patients, and
o Alcohol abuse: accounts for 25% of cases.
 Other causes include:
o Mechanical ampullary obstruction:
 Biliary sludge  Ampullary stenosis
 Ascariasis  Periampullary diverticulum
 Pancreatic or periampullary cancer
 Duodenal stricture or obstruction.
o Toxic:
 Ethanol  Scorpion venom
 Methanol  Organophosphate poisoning
o Metabolic:
 Hyperlipidemia (types I, IV, V)  Hypercalcemia
o Drugs:
 Corticosteroids  Valproic acid
 Azathioprine  Thiazides
 Asparaginase  Oestrogens
o Infection:
 Viruses: mumps, coxsackie, hepatitis B, CMV, varicella-zoster, HSV,
HIV
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  Bacteria: mycoplasma, Legionella, Leptospira, salmonella
 Fungi: aspergillus
 Parasites: toxoplasma, cryptosporidium, Ascaris
o Hyperparathyroidism: causing hypercalcemia
o Trauma:
 Blunt or penetrating abdominal injury
 Iatrogenic injury during surgery or ERCP (sphincterotomy)
o Congenital: Cholodochocele type V
o Vascular:
 Ischemia  Atheroembolism
 Vasculitis (polyarteritis nodosa, SLE)
o Genetic: CFTR and other genetic mutations
o Miscellaneous:
 Post ERCP  Renal transplantation
 Pregnancy  Alpha-1-antitrypsin deficiency

Clinical Manifestations
 Pain is the cardinal symptom.
o It has an acute onset and is persistent for several hours or days, severe and is
often felt over the epigastric abdominal area, but can also be felt over either
of the upper quadrants.
o The pain radiates to the back in approximately 50% of patients in a” belt like”
manner.
o It may be partially relieved by sitting up or bending forward.
 There is retching, nausea and repeated vomiting which may persist for several hours
in 90% of patients.
o The retching may persist despite the stomach being kept empty by
nasogastric aspiration.

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 There may also be dyspnea and hiccoughs, in case of diaphragm irritation and
pleural effusion.
 On physical exam: it varies with the severity.
o The patient might appear well or in severe cases gravely ill with profound
shock, toxicity and confusion.
o Tachypnoea is common,
o Tachycardia is usual, and hypotension may be present.
o The body temperature is often normal or even subnormal, but frequently
rises as inflammation develops.
o Mild icterus can occur due to obstructive jaundice caused by
choledocholithiasis or edema of the head of the pancreas.
o On abdominal exam:
 There is epigastric tenderness and guarding.
 They may also have abdominal distention and hypoactive bowel
sounds due to an ileus secondary to inflammation.
 An epigastric mass can also be palpated due to inflammation.
 Although not pathognomonic for acute pancreatitis bruising around
the umbilicus (cullen’s sign) and around the flank (Grey Turner’s sign)
can also be present.
o In 10–20 % of patients’ plural effusion, pulmonary edema and pneumonitis
are present.

Diagnosis
 Laboratory tests:
o Serum amylase:
 It rises within 6 to 12 hours of the onset.
 It has a half-life of approximately 10 hours.
 It returns to its normal level within 3-5 days in uncomplicated cases, so
a normal serum amylase level doesn’t exclude acute pancreatitis.
 An elevation of 3-4 times above the normal is indicative of the disease.
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 o Serum lipase:
 It rises within 4-8 hours of the onset.
 It peaks at 24 hours.
 It returns to its normal level within 8-14 days.
 It elevates earlier and last longer as compared with elevations in
amylase
 It is more sensitive and specific test than amylase.
o Trypsinogen activation peptide (TAP):
 Is elevated in acute pancreatitis.
 It useful in detection of early acute pancreatitis and as a predictor of
the severity of acute pancreatitis.
 Plain erect chest and abdominal radiographs:
o Are not diagnostic.
o Non-specific findings in pancreatitis include:
 A generalised or local ileus (sentinel loop),
 A colon cut-off sign: reflects a paucity of air in the colon distal to the
splenic flexure due to functional spasm of the descending colon
secondary to pancreatic inflammation.
 A renal halosign.
 Occasionally, calcified gallstones or pancreatic calcification may be
seen.
o A chest radiograph may show a pleural effusion and, in severe cases, a diffuse
alveolar interstitial shadowing may suggest acute respiratory distress
syndrome.
 Abdominal ultrasound:
o The pancreas appears diffusely enlarged and hypoechoic.
o Gallstones may be visualized in the gallbladder or the bile duct.
o To rule out acute cholecystitis as a differential diagnosis.
 Abdominal CT-scan:
o Findings with the use of an intravenous contrast are:

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  Focal or diffuse enlargement of the pancreas with heterogeneous
enhancement.
 Can distinguish interstitial from necrotising pancreatitis
 If done three or more days after the onset, it can detect the presence
and extent of pancreatic necrosis and local complications and predict
the severity of the disease.
 MRI:
o On contrast-enhanced, failure of the pancreatic parenchyma to enhance
indicates the presence of pancreatic necrosis.
o Can yield similar information to that obtained by CT and has a higher
sensitivity for the diagnosis of early acute pancreatitis and can better
characterize the pancreatic and bile ducts and complications of acute
pancreatitis.
o MRCP is comparable to ERCP for the detection of choledocholithiasis.

Management
 Assessment of severity should be done first.
o Helps to predict the pts course and Complications.
o Identify patients who need admission to the ICU.
o Guides use of prophylactic antibiotics, urgent bile duct imaging and early
ERCP.
o There are different scores like:
 Atlanta criteria and  APACHE II scoring system
MODS score  SIRS score
 Ranson criteria  CT severity index
o They have low specifictiy and positive predictive value but good negative
predictive value.
 Supportive treatment:
o Aggressive fluid and electrolyte replacement (Crystalloids)
o Blood sugar control: Sliding scale insulin
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 Table 5.12: RANSON CRITERIA
At admission Within 24hrs
 Age > 55yrs HCT drop > 10 Number Mortality
<2 1%
 WBC > 16,000 BUN > 5
3-4 16%
 Glucose > 200 Arterial PO2 < 60mmHg
5-6 40%
 LDH > 350IU/L Base deficit > 4mEq/L
7-8 100%
 AST > 250IU/L Serum Ca < 8
Fluid sequestration > 6L
o Pain control:
 Adequate pain control requires the use of intravenous opiates.
o Pancreatic rest / Nutrition:
 For Patients with mild pancreatitis can often be managed with
intravenous hydration alone since recovery occurs rapidly unlike
patients with severe pancreatitis which need nutritional support.
o Organ support
o Antibiotics:
 Are not recommended in acute pancreatitis as a prophylaxis
 Can be given if extra-pancreatic infection is suspected.
o Prompt identification and treatment of Complications.
 In acute pancreatitis that require intervention include:
o Local complications o Infected Pancreatic necrosis
o Pancreatic necrosis with persistent Symptoms
o Persistent /symptomatic Pseudocyst
 The types of intervention are:
o Percutaneous o Surgical (laporascopic or open)
o Endoscopic
 Treatment of Biliary stone associated pancreatitis:
o Early ERCP for selected patients:
 Concomitant cholangitis  Bil >5mg/dl
 Persistent biliary obstruction  Severe biliary pancreatits
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 5.8. Perianal Emeregency
 Case Discussion………………………………………………………….369
 Introduction……………………………………………………………….369
 Differential Diagnosis…………………………………………………369
 Discussion of the Differentials……………………………………370

Case Discussion
 A 28-year-old man presents to the emergency department complaining of anal and lower-
back pain for the previous 36 h. He has tried taking simple analgesics with no benefit. The
pain is progressively getting worse and he is now finding it uncomfortable to walk or sit
down. He is otherwise fit and well and smokes 10 cigarettes a day. On physical
examination, Inspection of the anus reveals a 3cm by 3 cm swelling at the anal margin.
The swelling is warm, exquisitely tender and fluctuant. There is no other obvious
abnormality.

Introduction

 Anorectal/perianal emergencies refer to anorectal disorders presenting with some

alarming symptoms which might require an immediate management such as
o Acute anal pain
o Bleeding

Differential Diagnosis
o Anorectal abscess
o Anal fissure
o Fistula inano
o Thrombosed hemorrhoid

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 Discussion of the Differentials

5.8.1. Anorectal Abscess

 Introduction ……………………………………………………….370
 Epidemiology………………………………………………………370
 Risk Factors…………………………………………………………371
 Clinical Manifestation…………………………………………371
 Investigation……………………………………………………….372
 Management…………………………………………………..….373

Introduction
 Perianal and perirectal abscesses are common anorectal problems.
 The infection originates most often from an obstructed anal crypt gland:
o The resultant pus collects in the subcutaneous tissue, intersphincteric
plane, or beyond (ischiorectal space or supralevator space)  various types
of anorectal abscesses form.
 Once diagnosed, anorectal abscesses should be promptly drained surgically.
 An undrained anorectal abscess can continue to expand into adjacent spaces as well
as progress to generalized systemic infection.

Epidemiology
 The mean age of presentation is 40 years
o Range from 20 to 60
 Adult males are twice as likely to develop an anorectal abscess and/or fistula
compared with females
 30 to 70 % of anorectal abscesses are associated with a concomitant anorectal
fistula
 30 to 40 % of patients develop an anorectal fistula after undergoing treatment for an
anorectal abscess
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 Risk Factors

 Sexually transmitted infections and an infected anal fissure are common cause of
anal abscesses.
 Some other risk factors include:
o Crohn’s disease o Diabetes
o Ulcerative colitis
o A compromised immune system due to illnesses like HIV
o Anal sex
 It can increase the risk of anal abscesses in both men and women
o Use of the medication:
 Prednisone or other steroids
o Current or recent chemotherapy

Clinical Manifestations
History:
 The classic locations of anorectal abscesses, listed in order of decreasing frequency,
are as follows:
o Perianal
o Ischiorectal
o Intersphincteric
o Supralevator
 The clinical presentation correlates with the anatomic location of the abscess.
 Almost all perirectal abscesses are associated with perirectal pain:
o It is indolent in nature.
o It is exacerbated by movement and increased perineal pressure from sitting
or defecation.
o Associated with the pain patients may also complain of dull perianal
discomfort and pruritus
 Those with an ischiorectal abscess often present with:
o Systemic fevers and chills
o Severe perirectal pain and fullness consistent with the more advanced nature
of this process.
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  External signs are minimal and may include
o Erythema
o Induration
o Fluctuance.
Physical Examination:
 Patients with anorectal abscesses usually have normal vital signs on initial evaluation
o Only 21% reporting fevers or chills (most likely to be Ischiorectal)
 Physical examination in case of perianal abscess demonstrates
o A small, erythematous, subcutaneous mass near the anal orifice.
o It is usually well-defined and fluctuant
 On digital rectal examination (DRE):
o A fluctuant, indurated mass may be encountered.
 Optimal physical assessment of an ischiorectal abscess may require anesthesia to
alleviate patient discomfort that would otherwise limit the extent of the
examination.
 Patients with an intersphincteric abscess present with rectal pain and exhibit
localized tenderness on DRE.
 Physical examination may fail to identify an intersphincteric abscess.
 Anal abscesses are most often diagnosed through a physical exam

Investigation
 CBC:
o WBC might be elevated in case of ischiorectal abscess because systemic
symptoms are more manifested.
 Imaging:
o CT, Ultrasound and MRI:
 Imaging studies are not usually necessary in the evaluation of
patients with an anorectal abscess
 Clinical suspicion of an intersphincteric or supralevator abscess may, however,
require confirmation by means of CT, anal ultrasonography, or MRI.
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 o As a rule, use of anal ultrasonography is limited to confirming the presence
of an intersphincteric abscess
 This modality can also be used intraoperatively to help identify a
difficult abscess or fistula.

Management
 Perianal abscesses almost always require surgical drainage, even if they have
spontaneously discharged
 Patients with diabetes
 Immunosuppression
 Evidence of systemic sepsis
 Substantial local cellulitis require urgent drainage
 In uncomplicated cases, offer incision and drainage within 24 hours
 Drainage leads to an open cavity that typically takes 3-4 weeks to heal
 Persistent failure to heal may indicate an underlying fistula
 Antibiotics are only indicated:
o If there is extensive overlying cellulitis
o If the patient is immunocompromised.

5.8.2. Fistula In ano

 Introduction …………………………………………………….……374
 Risk Factors…………………………………………………….………374
 Clinical Manifestation……………………………………….……375
 Investigation……………………………………………………….…375
 Management…………………………………………………………375

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 Introduction

 Fistula in ano is an abnormal tract or cavity with an external opening in the perianal
area by identifiable internal opening.
 Goodsall’s rule to identify the internal opening offistula in ano suggests that:
o Fistulas with an external opening anteriorly  connect to the internal
opening by a short, radial tract.
o Fistulas with an external opening posteriorly  track in a curvilinear fashion
to the posterior midline.
o However, exceptions to this rule often occur if an anterior externalopening
is greater than 3 cm from the anal margin.
 Such fistulas usually track to the posterior midline.

Risk Factors
 Previous anorectal abscess  Radiation therapy for prostatic ca.
 Trauma  Actinomycosis
 CD ( Crohn’s disease)  TB
 Anal fissures  LGV
 Anal carcinoma
Parks classification for fistula in ano
1. Inter sphincteric 3. Trans sphincteric
2. Supra sphincteric 4. Extra sphincteric

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 Clinical Manifestations

History:
 Patients often provide a reliable history of previous pain, swelling, and spontaneous
or planned surgical drainage of an anorectal abscess.
 Signs and symptoms of fistula-in-ano, in order of prevalence, include the following:
o Perianal discharge o Diarrhea
o Pain o Skin excoriation
o Swelling o External opening
o Bleeding
 A review of symptoms may reveal the following in patients with a fistula in ano:
o Abdominal pain o Changes in bowel habit
o Weight loss
Physical examination:
 The examiner should observe the entire perineum, looking for an external opening
that appears as an open sinus or elevation of granulation tissue.
 Spontaneous discharge of pus or blood via the external opening may be apparent or
expressible on digital rectal examination.
 Digital rectal examination (DRE) may reveal:
o A fibrous tract or cord beneath the skin
o It also helps to delineate any further acute inflammation that is not yet drained.

Investigation
 Lateral or posterior induration suggests deep postanal or ischiorectal extension.
 Laboratory or imaging studies are not done in routine fistula in ano
o Physical examination findings remain the mainstay of diagnosis.

Management
 Drainage
 Eradicating the fistulous tract

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 5.8.3. Anal Fissure

 Introduction ……………………………………………………….……376
 Epidemiology……………………………………………………………376
 Risk Factors……………………………………………………………...376
 Clinical Manifestation………………………………………….……377
 Management……………………………………………………………378

Introduction
 An anal fissure is a painful linear tear or crack in the distal anal canal
o In the short term, usually involves only the epithelium
o In the long term, involves the full thickness of the anal mucosa.
 Acute if <6Wks

Epidemiology

 Anal fissure is one of the most common benign anorectal diseases.

 One of the most common causes of anal pain and anal bleeding.
 Anal fissures develop with equal frequency in both sexes
 They tend to occur in younger and middle-aged persons
 Precise incidence cannot be established because anal discomfort is often
misattributed to symptomatic hemorrhoids

Risk Factors

 Primary anal fissures:

o Local trauma
 Passage of hard stool  Chronic diarrhea
 Constipation  Vaginal delivery
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  Anal sex
o Low fiber diet
o Prior anal surgery
 Secondary anal fissures:
o Crohn disease
o Other granulomatous diseases
 Eg: Extrapulmonary tuberculosis, sarcoidosis
o malignancy
 Eg: Squamous cell anal cancer, leukemia
o communicable diseases
 Eg: HIV infection, syphilis, chlamydia

Clinical Manifestations

History:
 The symptoms of an anal fissure are relatively specific, and the diagnosis can often
be made on the basis of the history alone.
 Typically, the patient reports severe pain during a bowel movement
o The pain lasting several minutes to hours afterward.
o The pain recurs with every bowel movement, and the patient commonly
becomes afraid or unwilling to have a bowel movement
 This leads to a cycle of worsening constipation, harder stools, and
more anal pain.
 Patients note bright-red blood on the toilet paper or stool.
o Occasionally, a few drops may fall in the toilet bowl, but significant bleeding
does not usually occur with an anal fissure.
Physical examination:
 Initially, the fissure is just a tear in the anal mucosa and is defined as an acute anal
fissure.

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  If the fissure persists over time, it progresses to a chronic fissure that can be
distinguished by its classic features.
o The fibers of the internal anal sphincter are visible in the base of the chronic
fissure
o An enlarged anal skin tag is present distal to the fissure
o Hypertrophied anal papillae are present in the anal canal proximal to the
fissure.

Management
 Conservative treatment to minimize anal trauma
o Bulk agents
o Stool softeners
o Warm sitz baths
o Analgesic creams
 Surgical treatment for chronic fissures that failed
medical therapy
o Lateral sphincterotomy
o To decrease spasm of internal sphincter by
dividing a portion of the muscle.

5.8.4. Hemorrhoids
 Introduction…………………………………………………….……..379
 Risk Factors…………………………………………………….……….379
 Clinical Manifestation……………………………………….…..…379
 Differential Diagnosis……………………………………….……..380
 Investigation…………………………………………………….….….380
 Management……………………………………………………….….381

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 Introduction

 Hemorrhoids are pathologically

swollen blood vessels in the lower
rectum.
 Classified into internal and external
based on anatomical location i.e
dentate line
 Age (elderly)

Risk Factors
 Constipation  Family history
 Straining  Chronic diarrhea
 Pregnancy  prolonged toilet sitting
o Postpartum hemorrhoids from  Colon malignancy
straining during labor  IBD
 Low fiber diet  Heavy weight lifting

Clinical Manifestation
History

 The most common presentation of hemorrhoids are:

o Rectal bleeding o Pruritus
o Pain o Prolapse
 Ask about
o Familial predisposition o Weight loss
o Diet o Abdominal pain
o History of constipation or o Change in appetite or bowel
diarrhea habits.
o History of prolonged sitting
or heavy lifting

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  The presence of pruritus or any discharge should also be noted.
 Inflammatory bowel diseases need to be ruled out as the cause of symptoms.

Physical Examination

 In addition to the general physical examination, physicians should also perform

visual inspection of the rectum, digital rectal examination, and anoscopy.
 Inspection of the rectum
o Skin tags (redundant tissue o Signs of infection or abscess
from old thrombosed formation
external hemorrhoids) o Rectal /hemorrhoidal
o Fissure prolapse
o Fistula
 DRE (Digital rectal examination) o Rectal tone
o Indurated/ulcerated area o Palpate the prostate in all
o Masses, tenderness, men.
mucoid discharge or blood

Differential Diagnosis
 Condylomaacuminata  Proctitis
 Anal fissure  Rectal prolapsed
 Anal fistula  Colorectal ca
 Anal abscess

Investigation
 Lab Studies
o CBC( infection, anemia)
 Imaging Studies
o Anoscopy o Flexible sigmoidoscopy
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 Management

 Conservative Rx
o Give stool softener
o Advice on
 High fiber diet  Avoidance of straining
 Increasing fluid intake  Good hygiene
 Non-surgical
o Rubber band ligation o Sclerotherapy
o Infrared photo-coagulation
 Surgical
o Excision of thrombosed external hemorrhoids
o Operative hemorrhoidectomy

5.9. Abdominal Trauma

 Case Discussion………………………………………………..……382
 Introduction………………………………………………….………382
 History ………………………………………………………….………382
 Physical Examination……………………………………….……383
 Investigation…………………………………………………………383
 Evaluation of Special Injuries..………………………………385
 Management…………………………………………………………387

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 Case Discussion
18-year-old girl has sustained a falling down and she is now complaining of generalized
abdominal pain and left shoulder-tip pain. Examination of her chest is normal, initially; her pulse
rate is 110/min with a blood pressure of 84/60 mmHg. She is slightly drowsy and her GCS is 14.
On examination of the abdomen, there is an abrasion on the left side beneath the costal margin
with tenderness in the left upper quadrant. There is no evidence of any other injuries. The
patient is given 2 L of intravenous fluids and the blood pressure improves to 130/90 mmHg.

Introduction

 Abdominal trauma is seen quite often in the Emergency Department and can result
from blunt or penetrating mechanisms.
 Blunt abdominal trauma (BAT) is frequently encountered in the form of motor vehicle
crashes (MVCs) (75%), followed by falls and direct abdominal impact.
 There are two main kinds of Penetrating abdominal trauma (PAT):
o Stab Wounds (SW) and Gun Shot Wounds (GSW)
o SWs are more common than GSWs, however they have a lower mortality rate
compared with GSWs.
o The higher energy transfer and missile trajectory with multiple bullet fragments
from GSWs leads to increased morbidity and mortality compared to stab
wounds.

History

 For MVCs speed of collision, position of colliding car to each other, position of patient
in the car, seatbelt use, and extent of damage (intrusion, windshield damage,
difficulty of extrication, air-bag deployment) are important elements to elicit.
 With respect to falls, height of fall is very important.
 In gunshot wounds, the type of gun, distance from the shooter, and number of shots
heard are all relevant.

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  For stab wounds, it is prudent to obtain information on the type of weapon
used.
 AMPLE” history (Allergies, Medications, Past Medical History, Last Oral Intake
and Events Preceding the Incident).
 The AMPLE history can be obtained at the same time as the physical exam
portion of the secondary survey if the patient is alert and cooperative.

Physical Examination
 The abdomen should be examined by inspection, auscultation, palpation, and
percussion.
 The abdominal exam should detail exit and entry wounds, number of wounds,
any evisceration, ecchymosis and deformity, in addition to tenderness.
 The perineum, rectum and genitalia should all be examined at this point.
 A rectal exam can alert the provider to a high riding prostate, lack of rectal
tone, or heme-positive stools.
 The stability of the pelvis should also be assessed during the physical exam.
 When assessing a trauma victim, it is important to be aware of factors that
make a physical exam unreliable.
 These factors include altered mental status, intoxication and distracting
injuries.
 The most important way to make your physical exam reliable is to perform it
serially, noting important changes as the patient is reexamined.

Investigation

 Plain films:
o Will be ordered on all abdominal trauma patients.
o Chest and abdominal X ray should be ordered.
o Cervical and Lumbar spine films may be useful as well.

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 CT Scan:
o The most common and the most accurate diagnostic modalities for
penetrating and blunt abdominal injury.
o Should only be performed if the patient is hemodynamically stable
o If there is an absolute indication for exploratory laparotomy*, don’t
waste time with a CT.
 Focused abdominal sonography for trauma (FAST):
o A series of ultrasound reading looking for bleeding in the abdomen (as
well as in pericardium if there is bleeding can be non-hypovolemic cause
of hypotension.)
o Performed in most patients.
o Ideal for non-stable patients because of its relative efficiency.
 Diagnostic peritoneal lavage:
o DPL is used as a method of rapidly determining the presence of
intraperitoneal blood.
o It is particularly useful if the history and abdominal examination of an
unstable patient with multisystem injuries are either:
 Unreliable (eg, because of head injury, alcohol, or drug
intoxication) or
 Equivocal (eg, because of lower rib fractures, pelvic fractures,
or confounding clinical examination).
o DPL results are considered positive in a blunt trauma patient:
 If 10 mL of grossly bloody aspirate is obtained before infusion
of the lavage fluid or
 If the siphoned lavage fluid contains more than 100,000 red
blood cells (RBCs)/µL, more than 500 white blood cells
(WBCs)/µL, elevated amylase content, bile, bacteria, vegetable
matter, or urine.

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 Evaluation of Specific Injuries

 The liver, spleen, and kidney are the organs predominantly involved following blunt
trauma, although the relative incidence of hollow visceral perforation, and lumbar
spinal injuries increases with improper seat-belt usage.
 Diagnosis of injuries to the diaphragm, duodenum, pancreas, genitourinary system,
and small bowel can be difficult.
 Most penetrating injuries are diagnosed at laparotomy.

5.9.1. Diaphragm Injuries

 Blunt tears can occur in any portion of either diaphragm, although the left
hemidiaphragm is most often injured.
 Abnormalities on the initial chest x-ray include elevation or “blurring” of the
hemidiaphragm, hemothorax, an abnormal gas shadow that obscures the
hemidiaphragm, or a gastric tube positioned in the chest.
 However, the initial chest x-ray can be normal in a small percentage of patients.
 Suspect this diagnosis for any penetrating wound of the thoracoabdominal, and
confirm it with laparotomy, thoracoscopy, or laparoscopy.

5.9.2. Duodenal Injuries

 Duodenal rupture is classically encountered in:

o Unrestrained drivers involved in frontal-impact motor vehicle collisions
o Patients who sustain direct blows to the abdomen, such as from bicycle
handlebars.
 A bloody gastric aspirate or retroperitoneal air on an abdominal radiograph or CT
should raise suspicion for this injury.
 An upper gastrointestinal x-ray series, double-contrast CT, or emergent laparotomy
is indicated for high-risk patients.

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 5.9.3. Pancreatic Injuries

 Pancreatic injuries often result from a direct epigastric blow that compresses the
pancreas against the vertebral column.
 An early normal serum amylase level does not exclude major pancreatic trauma.
 Conversely, the amylase level can be elevated from nonpancreatic sources.
 Double-contrast CT may not identify significant pancreatic trauma in the immediate
postinjury period (up to 8 hours).
o It may be repeated, or other pancreatic imaging performed, if injury is
suspected. Surgical exploration of the pancreas may be warranted following
equivocal diagnostic studies.

5.9.4. Hollow Viscus Injuries

 Blunt injury to the intestines generally results from sudden deceleration with
subsequent tearing near a fixed point of attachment, particularly if the patient’s seat
belt was positioned incorrectly.
 A transverse, linear ecchymosis on the abdominal wall (seat-belt sign) or lumbar
distraction fracture (i.e., Chance fracture) on x-ray should alert clinicians to the
possibility of intestinal injury.
 Although some patients have early abdominal pain and tenderness, the diagnosis of
hollow viscus injuries can be difficult since they are not always associated with
hemorrhage.

5.9.5. Solid Organ Injuries

 Injuries to the liver, spleen, and kidney that result in shock, hemodynamic
abnormality, or evidence of continuing hemorrhage are indications for urgent
laparotomy.
 Solid organ injury in hemodynamically normal patients can often be managed
nonoperatively.

P a g e 386 | 548
  Admit these patients to the hospital for careful observation, and evaluation by a
surgeon is essential.
 Concomitant hollow viscus injury occurs in less than 5% of patients initially
diagnosed with isolated solid organ injuries.

Management

Initial Actions and Primary Survey:

 All trauma patients must be managed in accordance with the Advanced Trauma Life
Support (ATLS) algorithm:
o A: Airway Maintenance with CERVICAL SPINE protection (Is the patient
speaking in full sentences?)
o B: Breathing and Ventilation (Is the breathing labored? Bilateral symmetric
breath sounds and chest rise?)
o C: Circulation with hemorrhage control/shock assessment (Pulses present
and symmetric? Skin appearance: cold & clammy or warm & well
perfused?)
o D: Disability (GCS score? Moving all extremities?)
o E: Exposure/Environmental Control (Completely expose
 If the patient’s primary survey is intact, the adjuncts to the primary survey and
resuscitation begin.
 The adjuncts to the primary survey include any of the following as necessary:
o eFAST exam (see below on investigation), EKG, ABG, chest X-ray, pelvis x-ray,
and/or urinary catheter.
Non operative management:
 Indications:
o Hemodynamically stable
o No signs of acute abdomen
o No signs of severe bleeding
 Support with:
P a g e 387 | 548
 o IV fluid therapy
o Close monitoring of vital signs
o Nasogastric suctioning
o Don’t give prophylactic antibodies or analgesics.
Trauma Laparotomy:
 The aim is to control the bleeding and inspection of the entire abdominal cavity
looking for any specific organ injury
 Indications for trauma laparotomy include the following:
o Hemodynamically unstable patient with abdominal trauma
o Positive findings on objective evaluation necessitating surgical intervention
(FAST or CT scan)
o Penetrating abdominal gunshot injury
o Stab wound to abdomen penetrating the peritoneum
o Evisceration of abdominal viscus
 Trauma laparotomy should follow damage-control approach to avoid further morbidity
and mortality from lethal triad of
o Coagulopathy,
o Hypothermia and
o Acidosis
Damage control approach includes

Table 5.13: Patient Selection

Anatomic Physiologic Environmental
 Unable to achieve hemostasis  To < 34oc  Operating time > 60min
 Complex injury  PH<7.2  Inability to approximate
 Inaccessible major vein injury  Serum lactate >5mmol/l abdominal incision
 Demand non-operative control  PT >165  Desire to reassess
of other injuries  PTT >60sec intraabdominal contents
 Time consuming  >10units blood transfused
 Sys BP <90mmHg for >60 min

P a g e 388 | 548
 3. Patient selection:
4. Control of hemorrhage and contamination
 Simple ligation of blood vessels
 Shunting of major arteries and veins
 Drainage
 Temporary stapling of bowel
 Therapeutic packing
 Closure
5. Resuscitation continued in ICU: to correct the triad
6. Definitive treatment

Table 5.14: Absolute Indications for laparotomy

Blunt Penetrating
 Shock  Shock
 Peritonitis  Peritonitis
 Blood out of NG tube or on rectal exam  Evisceration
 Intraperitoneal bladder rupture  Weapon still in situ
 Diaphragmatic rupture  Blood out of NG tube or
 on rectal exam
 Gross hematuria

Abdominal Compartment Syndrome

 Is a pathologic intra-abdominal hypertension sufficient to produce physiologic
deterioration
 Primary: due to intra-abdominal injury.
 Secondary: may result from any condition requiring extensive crystalloid
resuscitation, including extremity trauma, chest trauma, or even post injury sepsis.
 Operative decompression is the treatment of choice.

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 Short Case Discussion

5.10. Ostomy.………………………..………………..…...391
 Content By:
 Nanati Jemal 5.11. T-Tube.………………………..…..……………..…..397
 Mikiyas Mesay
 Edited By: 5.12. Hernia.………………………..………….……..…...400
 Samuel Mesfin
5.13. Nasogastric Tube (NGT)………………………..420
5.14. Video QRs…………………………………………….425

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 5.10. Ostomy

 Describe what you see………………………………………..391

 Introduction……………………………………………………….391
 Types of Ostomy…………………………………………………392
 Indications………………………………………………………….392
 Complications…………………………………………………….393
 Specific Ostomies..………………..…………………………..393

Describe what you see

 There is pink and fleshy stoma opening through a single circular opening in the Right
lower quadrant. It is not foul smelling and skin irritation wasn’t seen. There is yellow
watery discharge continuously coming out and its amount is not predictable due to
unattached bag. The patient appears emaciated but not dehydrated
 What kind of ostomy is it?
o Ileostomy
 Has watery discharge
 Not foul smelling
 The site is RLQ
 Emaciated

Introduction

 An ostomy is surgery to create an opening (stoma) from an area inside the body to
the outside.
 It treats certain diseases of the digestive or urinary systems.
 It can be permanent, when an organ must be removed.
 It can be temporary, when the organ needs time to heal.
 The organ could be the small intestine, colon, rectum, or bladder.
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  With an ostomy, there must be a new way for wastes to leave the body.
 The part of the bowel that is seen on the abdomen surface is called a stoma.

Types of Ostomy
 Tracheostomy  Cecostomy
 Esophagostomy  Nephrostomy
 thoracostomy  Ureterostomy
 Gastrostomy  Cystostomy
 Jejunostomy  Vesicostomy
 Ileostomy  T-tube
 Colostomy
Classify ostomies
o Based on role
o Permanent o Temporary
o Based on type
o End o Loop
o Spectacle o Double barrel
o Temporary indication

Indications
o Gangrenous LBO o Penetrating injuries
o Hemodynamic instability
 Trauma, sepsis
o Perianal fistfuls
o High risk leak
 Malnourished, immunosuppressed
o Permanent indication
o Rectal excision o Proctocolectomy
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 Complications

o Early
o Leakage o Stromal necrosis
o Skin irritation o Stromal retraction
o Late
o Stromal stenosis o Parastomal hernia
o Stromal prolapse

Specific Ostomies

5.10.1. Colostomy
 Introduction …………………………………………………………….393
 Classification…………………………………………………………….393
 Indication…………………………………………………………………394
 Complication……………..…………………………………………….395
 When to Close..………………………………………………………..395

Introduction
 Colostomy: is an iatrogenic fistula between the colon and the skin:
o colo-cutaneous fistula.

Classification
 Based on surgical construction
o Loop:
o Penetrating abdominal injury o Perianal injury
o Descending colon diverticula o Congenital megacolon
 Double barrel
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  Spectacle:
o In ARM o Fistula
 End:
o In sigmoid volvulus o volvulus
o Gangrenous

 Based on bowel segment  Based on function

o Descending o Diversion colostomy
o Ascending o Decompression colostomy
o Transverse o Exteriorization colostomy

Indications
 Temporary
o Trauma
 Perianal injury with or without sphincter
 Penetrating injury with colonic trauma
o Inflammatory
 IBD
 High type perianal fistula
o Obstruction
 Malignancies
 Sigmoid volvulus
 Pelvic mass
 Congenital:
- ARM
- Hirschsprung’s Disease
 Permanent
o Unresponsive incontinence
o APR
o Perianal fistula

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 Complications

 Early
o Bleeding o Necrotic distal end
 Late
o Prolapse o Fecal impaction
o Retraction o Infection
o Hernia o Irritation of skin (95%bile)
o Diarrhea o Depression

When to Close?
 At 6-12 weeks

5.10.2. Illeostomy

 Introduction …………………………………………………………..396
 Indication……………………………………………………………….396
 Complication……………..…………………………………………..396
 How to differentiate Stomas………………………………….397

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 Introduction

 Ileostomy - the bottom of the small intestine (ileum) is attached to the stoma.
 This bypasses the colon, rectum and anus.

Indications
 Child  Young adult
 Meconium ileus  Cohn’s
 Illeal Artesia  Illeal TB perforation
 Long segment HST  Typhoid perforation
 Complicated volvulus  Malignancy
 Intussusception  Primary volvulus
 Gangrenous volvulus

Complications
 Immediate
 Bleeding’
 Necrosis (if double barrel and it clamped branching vessels)
 Spillage
 Local and adjacent organ injury
 Fluid and electrolyte derangement (ileostomy bypasses the fluid absorbing
capability of the colon)
 Early
 Bleeding  Skin irritation  Hernia
 Infection  Retraction  Malnutrition
 Necrosis  Diarrhea
 Late
 Adhesion  Infection
 Stenosis  Bleeding
 Diarrhea (skin contamin-ation  Fecal Impaction
and GI microflora)  Psychological impact

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 How to Differentiate Stomas

Table 5.15: Differentiating stomas

Criteria Ileostomy Colostomy
content Watery Mucus
Surrounding skin More irritation Pink
Odor Foul smelling
Size of stoma Narrow Wide
Site

 Compared to colostomy, Ileostomy has

 More dehydration with fluid and electrolyte imbalance
 More skin irritation
 Less hernia complications

5.11. T-Tube

 Introduction……………………………………………………………398
 Indications……………………………………………………………..398
 Placement………………………………………………………………398
 Management………………………………………………………….399
 Complications…………………………………………………………400

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 Introduction

 A tubular device in the shape

of a T
 It is inserted through the skin
into a cavity or a wound and
used for drainage.

Indications
 After Laparoscopic /open Choledochotomy
o Access for postoperative stone retrieval or cholangiography or
choledochoscopy
 After biliary tree manipulation
 Injury to the common bile duct
 Drainage of bile in the setting of CBD or papillary edema
 Persistent Duodenal Fistula
 Hepaticojejunostomies in the setting of liver transplantation
 Pancreaticoduodenectomy
 Tracheal stenosis.
 Montgomery T tube in ventilator-dependent patients

Placement
A) Prepare T-tube by cutting two limbs at lengths that will not transverse into the left
or right hepatic duct proximally or into the duodenum distally
 Excise the back wall of the horizontal portion of the T (to minimize the risk
of tube occlusion and to facilitate tube removal).
B) T-tube should be inserted to the supra-duodenal portion of the common bile duct
 The incision on the common bile duct should be vertical.
C) After the incision, the stone is removed followed by T-tube insertion

P a g e 398 | 548
 D) The remainder of the duct is closed with fine
absorbable sutures around the tube.
 Leave enough redundancy in the
intraperitoneal portion of the tube to
avoid tension (and possible tube
disgorgement) in the event of
significant postoperative abdominal
distension.

E) The long segment will be drawn externally in the right upper quadrant and will be
connected to a plastic bag, to be placed under the bed.
 It also important to concomitantly drain the Morrison’s pouch, also known
as the sub-hepatic space.

Post-Operative Management

1) Drainage of bile through T-tube up to 7th POD

2) Position of the T-tube should be maintained
3) Progressive clamping of the T-tube from 8th POD
4) Observation of the patient during clamping for:
 Pain in abdomen  Jaundice
 Fever
5) Daily observation of bile flow:
 Quantity of bile  Any leakage
 Color of bile
6) Post-operative t-tube cholangiography on 11th post OP day
7) Removal of T-tube after 13th or 14th post OP day by slow traction if:
P a g e 399 | 548
  Patient general condition satisfactory
 Urine, stool color and LFT are normal
 The drainage bile looks normal
 Draining amount becomes small enough
 T-tube cholangiography shows clear flow to the duodenum

Complications
 In situ
o Fluid and electrolyte o Tube dislocation
imbalance o Tube retention
o Early dislodgment o bacteremia
 With removal of the T-tube
o Bile leaks o Biliary peritonitisSepsis

5.12. Hernia

 Introduction…………………………………………………………401
 Precipitating Factors……………………………………………402
 Surgical Pathology….……………………………………………403
 Basic Feature………………………………………………………404
 Complications……………………………………………………..404
 Discussion….…………………………………….…………………406

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 Introduction

 It is an abnormal protrusion of the whole or a part of a viscus through an opening in

the walI of the cavity in which it is contained.
 An internal (concealed) hernia:
o It is due to the protrusion of the viscus commonly intestine through an
internal defect or into a peritoneal recess within the abdomen
o Examples:
 Hiatus hernia
 Diaphragmatic hernia
 Hernia through the foramen of Winslow
 Hernia through the peritoneal recess around
 Duodenojejunal junctions
 Caecum: Paracaecal hernia
 Hernia through a defect in the mesentery following bowel resection.
 An external abdominal hernia
o Is protrusion of a viscus from the peritoneal cavity through a weak part of the
abdominal wall, either congenital or acquired
o Common external herniae are:
1. Inguinal 3. Umbilical
2. Incisional 4. Femoral
o Less common types are:
1. Epigastric
2. Para-umbilical
3. Lumbar.
o Rare types are:
1. Spigelian
2. Obturator
3. Gluteal

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 Precipitating Factors

A. Weakness of the abdominal wall

B. Continued or repeated increases in abdominal pressure.

A. Weakness of the abdominal wall

 It may be congenital or acquired.
 Congenital weakness: Due to persistence of congenital peritoneal sac, e.g.,
o Persistence of processus vaginalis may lead to indirect inguinal hernia in
males.
o Patent canal of Nuck may lead to indirect inguinal hernia in females.
o Incomplete obliteration of umbilicus may lead to umbilical hernia.
 Acquired weakness: Weakness of the abdominal wall can result from:
o Muscle weakness following obesity with fatty infiltration of the flat
muscles, repeated pregnancy, wasting disease.
o Poor wound healing leading to weakened wound due to inadequate
closure with or without infection in the early postoperative period.
o Iatrogenic- surgical incision may cause division of the nerves which causes
muscle weakness. E.g., McBurney's incision for appendicectomy may cause
divisions of the subcostal or ilioinguinal nerve leading to right sided direct
inguinal hernia.

B. The increased intra-abdominal pressure

 It becomes continued or repeated in following conditions:
1. Chronic cough
2. Constipation.
3. Bladder neck or urethral obstruction
4. Severe muscular effort
5. Parturition.
6. Vomiting.
7. Ascites

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 Surgical Pathology

 An external abdominal hernia consists of:

o A peritoneal sac o The contents of the sac.

o The coverings of the sac
 The sac is a pouch of stretched peritoneum which comes out through a gap in the
abdominal musculature.
 The sac consists of four parts:
1. The mouth i.e., the opening of the sac through which the contents enter
the sac.
2. The neck of the sac which is the most constricted part and passes through
the abdominal musculature. Neck is narrow in indirect sac but wide in
direct sac.
3. The body i.e., the main part of the sac holding the contents.
4. The fundus which is the most redundant and dependent part of the sac.
 The coverings are the layers of the abdominal wall which cover the hernial sac.
 These depend on the on the site and type of hernia and usually include skin and
muscles of the abdomen
 The contents may comprise one of the following:
1. Omentum (omentocele/epiplocele)
2. A loop of intestine (enterocele)
3. Meckel's diverticulum (Littre's hernia)
4. A part of the circumference of intestinal wal (Richter's hernia)
5. Two loops of intestine in the manner of 'W' (Maydl's hernia)
6. A part of bladder wall (direct/femoral hernia)
7. Ovary with or without fallopian tube
8. Fluid:
 Slight amount of fluid almost always present but it increases in
presence of ascites.
 The fluid may be blood stained when the hernia is strangulated.

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 Basic Features

1. They occur through a weak spot of the abdominal wall.

2. They have an expansile impulse on coughing (both visible and palpable).
3. They are reducible - either on lying down or with manual pressure. A reducible
hernia is one in which the contained viscus can be returned to its original cavity.
4. A reducible hernia expands on coughing or straining - cough impulse positive. In
irreducible hernia - cough impulse is absent.
5. The contents of the hernia - commonly gut or omentum. In presence of gut, the
hernia will feel soft and it may gurgle during reduction. In presence of omentum, the
hernia feels doughy

Complications

1. Irreducibility:
 When the contents of the sac cannot be completely emptied from the sac
because of:
o Adhesion formed between the contents and the sac or between the
contents themselves;
o Growth of the omentum within the sac;
o Narrowing of the neck of the sac because of fibrosis, e.g., following
continuous pressure of truss;
o Retention of faeces in the large intestine occupying the sac.
 In a simple irreducible hernia, though the contents cannot be reduced, the blood
supply remains intact, and there are no symptoms of intestinal obstruction
2. Obstruction:
 Irreducibility+ obstruction of the lumen of the contained bowel leading to
intestinal obstruction. The features are:
o The hernia is irreducible but painless.
o Cough impulse may be present.
o Features of intestinal obstruction are present.
o Can precipitate strangulation if not treated early.
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  Hernia is one of the commonest causes of intestinal obstruction. So, hernial sites
should always be examined in a patient presenting with intestinal obstruction.
3. Strangulation:
 Irreducibility + features of intestinal obstruction + arrest of blood supply to the
contained intestine leading to gangrene.
 The features are:
o The hernia is irreducible and painful.
o The sac is tense and tender.
o Cough impulse absent.
o Features of intestinal obstruction present - pain abdomen, vomiting,
abdominal distension, rebound tenderness.
 Strangulation is more likely to happen in a hernia with a narrow neck.
 Most strangulated herniae are therefore either inguinal or femoral, because
these herniae have narrow necks.
 Often, the sac contains the greater omentum which may become gangrenous
due to arrest of blood supply showing the features of strangulation but without
the features of intestinal obstruction.
 Strangulation without obstruction also noted in Richter's hernia.
4. Reduction-en-masse:
 Sometimes, during forceful manual reduction of irreducible hernia, the
contents together with the covering sac gets pushed forcibly back into the
abdominal cavity; the bowel within the sac may be strangulated by the neck of
the sac.
 Thus, the symptoms of obstruction or strangulation may not be relieved
5. Incarceration:
 Incarcerated hernia is a variety of irreducible hernia where the content of the sac
is large gut containing faeces.
 The large gut is fixed in the sac because of its size or adhesions.
 Here, the hernia can be indented like putty with the fingertip pressure because
of the scybalous content of the gut.

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  Though the hernia is irreducible, obstruction or strangulation rarely occur.
6. Inflammation
 E.g., tuberculosis of the sac
7. Compression or torsion of the omentum within the sac:
 The omentum may become gangrenous due to arrest of blood supply
showing the features of strangulation but without features of intestinal
obstruction.
8. Collection of fluid in the hernial sac-hydrocele of the hernial sac.
9. Maydl's hernia
10. Sliding hernia
11. Recurrent hernia

Discussion of the Differentials

5.12.1. Inguinal Hernia

 Introduction …………………………………………………….……..406
 Surgical Anatomy…………………………………………….………407
 Indirect Inguinal Hernia…………………………………….……..407
 Direct Inguinal Hernia…………………………………….………..409
 Diagnostic Criteria ……………………………………………….….410
 Congenital Inguinal Hernia……………………………………….414

Introduction
 This is the most common type of abdominal hernia in both males and females.
 There are two types:
1. Indirect or oblique inguinal 2. Direct inguinal hernia
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 Surgical Anatomy

 Inguinal canal

o The inguinal canal is an oblique fibromuscular tunnel about 4 cm long in

the lower part of the anterior abdominal wall, a little above and parallel to
the inner half of the inguinal ligament.
o It passes downward and medially and extends from the deep inguinal ring
to the superficial inguinal ring.
o The canal transmits the spermatic cord in males and the round ligament of
uterus in females and ilioinguinal nerve in both sexes.

Indirect Inguinal Hernia

 The hernia sac enters the inguinal canal through the deep inguinal ring lateral to
the inferior epigastric artery.
 The neck of the sac is lateral to the inferior epigastric artery.
 Indirect hernia is usually congenital due to persistence of patent processus
vaginalis; it appears at or soon after birth or may appear in adolescence.
 Indirect hernia may be acquired when the sac is formed as an outpushing of the
abdominal peritoneum through the deep ring.
 The acquired variety may occur at any age in adult life due to increased intra-
abdominal pressure following strenuous exercises, heavy weight lifting, straining
at defaecation (chronic constipation) or at micturition (enlarged prostate,
stricture urethra) or at coughing (chronic bronchitis).
 The indirect hernia may be subdivided into:
1. Incomplete
2. Vaginal or Complete hernia

Incomplete
• Bubonocele
o The processus vaginalis is closed proximal to the superficial inguinal ring.
o The hernia is limited in the inguinal canal and so appears as an inguinal
swelling.
• Funicular Incomplete hernia

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 o Here the processus vaginalis is closed at its lower end, so the sap of the
hernia is separate from the sac of tunica vaginalis.
o The sac is closed and extends beyond the superficial inguinal ring but
stops above the testis.
o The testis lies below the hernia and can be felt separately from the
contents of the hernial sac
o Most of the indirect inguinal herniae belong to this category and are
commonly seen in adults.
o It is usually acquired but may be congenital.

Vaginal or Complete hernia

• Here the processus vaginalis is patent throughout.
• Hence the sac is continuous with the tunica vaginalis of the testis.
• The hernia descends down to the bottom of the scrotum covering the testis in
front and at the sides, so the testis cannot be felt separately before reduction of
hernial contents.
• Both the funicular and vaginal herniae appear as inguino-scrotal swellings.

Coverings of indirect inguinal hernia, from superficial to deep:

1. Skin
2. Superficial fascia. When the hernia comes out through superficial ring and
descends into the scrotum - dartos muscle of the scrotum.
3. External oblique aponeurosis, or external spermatic fascia when the hernia
comes out through the superficial inguinal ring.
4. Cremaster muscle.
5. Internal spermatic fascia.
6. Processus vaginalis or peritoneum - the sac.

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 Direct Inguinal Hernia

 The hernia protrudes directly through the posterior wall of the inguinal canal in
the Hesselbach's triangle.
 The direct hernial sac lies outside the cord (cf indirect inguinal hernia) - behind,
above or below the cord.
 The neck of the sac lies medial to the inferior epigastric artery- a differentiating
point at operation from indirect hernial sac where the neck of the sac lies lateral
to the artery.
 Direct herniae are mostly acquired in nature.
 It is found predominantly in the elderly males due to increased intra-abdominal
pressure leading to increased wear and tear of the conjoined tendon.
 A direct inguinal hernia seldom comes out through the superficial inguinal ring
and thus it is unusual for the sac to descend into the scrotum.
 The neck of the direct hernial sac is wide and therefore the hernia appears
immediately on standing and disappears again immediately when the patient
lies down.
 Moreover; because of this wide neck obstruction or strangulation is extremely
rare.

Coverings of direct inguinal hernia, from superficial to deep:

1. Skin
2. Superficial fascia
3. External oblique aponeurosis
4. Conjoint tendon when the sac passes medial to the lateral umbilical
ligament
5. Fascia transversalis
6. Peritoneum - the sac

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 Diagnostic Criteria

History
1. Age: It occurs in all ages, from birth to elderly. Indirect hernia is more common in
younger and adult life. Direct hernia is more common in elderly people.
2. Sex: Common in males
3. Symptoms:
 History of swellings in the groin – inguinal swelling which is gradually
increasing in size.
o The swelling becomes more prominent on standing or straining and
gets smaller or disappears on lying or on manipulation, unless it is
complicated.
• The swelling may expand and extend down to the scrotum - inguinoscrotal
swelling.
• The swelling may be asymptomatic – the hernia may be accidentally
discovered during a medical checkup.
 Local discomfort or pain which gets worsened on strenuous effort.
o The pain may be aching sensation in the groin due to the stretching
of the deep inguinal ring by the protruding viscus.
o The pain may be dragging indicating omentocele. As the omentum is
attached to stomach and supplied by Tl2 nerve, the pain may be
referred to the umbilicus.
o Sudden severe pain in the hernia with vomiting and irreducibility
indicates obstruction of the hernia.
• History of chronic strain e.g., cough, constipation and difficulty in passing
urine should be enquired as these may be the cause of hernia formation.

Physical examination:
The patient should be examined first in the standing position and then in lying down
position (supine), if necessary.
1. Inguinal swelling- indirect hernia: bubonocele or direct hernia; Inguinoscrotal
swelling - indirect hernia: funicular or vaginal hernia
2. Shape: A bubonocele or direct hernia is globular in shape. A funicular or vaginal
hernia is usually pyriform in shape.
3. Expansile impulse on coughing - visible and palpable: present.

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4. Non-tender if uncomplicated
5. Consistency - depends on the contents of the sac: soft, elastic and fluctuant,
resonant on percussion - if it contains gut. Firm and doughy, non-fluctuant and
dull on percussion - if it contains omentum.
6. Getting above the swelling in presence of inguinoscrotal swelling.
• To differentiate a scrotal swelling from inguinoscrotal swelling.
• With the patient standing, normally the spermatic cord is palpated
between the thumb and the fingers at the root of the scrotum.
o In case of scrotal swelling e.g., hydrocele, the spermatic cord
can also be felt easily, above the swelling= so. getting above the
swelling is possible.
o In inguinoscrotal Swelling. 5micular and complete indirect
hernia the spermatic cord cannot be felt nakedly, because iris
covered anterolaterally by the sac, so getting above the
swelling is not possible. On complete reduction of swelling, one
can feel the cord at the root of the scrotum.
7. Relation of the sac with pubic tubercle: To differentiate inguinal from femoral
hernia.
• Inguinal hernia- the swelling is situated above and medial to the pubic
tubercle.
• Femoral hernia-the swelling is situated below and lateral to the pubic
tubercle.
8. Reducibility: All hernia are reducible unless complicated.
• On lying down - the direct hernia usually reduces immediately and
spontaneously, but indirect hernia usually requires manipulation.
• A direct hernia reduces directly backwards.
• An indirect hernia reduces in an upward, backward and lateral direction.
• During reduction confirm the contents of the sac
o If there is gurgling sound, it is an enterocele; if the sac feels
doughy, it is omentocele.
o In enterocele, during reduction the first part of the content is
difficult to reduce but the latter part is easy to reduce.

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 o In omentocele, during reduction the first part is easy to reduce
while the latter part is difficult to reduce.
• After reduction:
o Note the relation of the sac with the pubic tubercle.
o Note the reappearance of the swelling on straining or coughing:
 ln indirect hernia, the swelling reappears gradually and
steadily in medial and downward directions.
 In direct hernia, the swelling reappears immediately
straightforward exactly where it was observed before.
9. Deep ring occlusion test:
• Identification of deep inguinal ring - it lies1 cm above the femoral pulse
felt below the inguinal ligament.
• After the reduction of hernia, the deep ring is occluded by the pressure of
the thumb and the patient is asked to cough:
o Indirect hernia - the swelling does not reappear, so the test is
positive.
o Direct hernia - the swelling reappears immediately, so the test is
negative.
10. Invagination test:
• After the hernia is reduced, the tip of the index finger can be invaginated
into the neck of the scrotum and then pushed inside the inguinal canal
through the superficial inguinal ring - the patient is then asked to cough
o Indirect hernia - a thrust will be felt at the tip of the finger.
o Direct hernia - a thrust will be felt at the pulp of the finger.
 Invagination test helps to diagnose an early case of incomplete hernia. It also
helps to differentiate bubonocele and direct hernia from femoral hernia.
Invagination test is not a must.
 When necessary, it should be performed very gently not to cause any pain to the
patient.
 This test cannot be done in female as the labial skin is thick and not lax.
11. Examine the opposite side also to exclude hernia. Direct hernia is often
bilateral.

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 12. Examine the testis, epididymis & spermatic cord.
13. Examine the tone of abdominal muscles by head or leg rising test. Also look for
Malgaigne bulging. Valsalva maneuver may be used to check the tone of the
abdominal muscles.
14. Note for any evidence of chronic straining like chronic bronchitis, enlarged
prostate (per rectal examination), stricture urethra (palpation of bulbar urethra
for thickening).

Table 5.16. Differential diagnosis of groin swellings:

 Femoral hernia  Encysted hydrocele of the cord
 Enlarged inguinal lymph nodes  Undescended or ectopic testis
 Saphena varix  Psoas abscess
 Femoral aneurysm  Malgaigne's buldge
 Lipoma of the cord

Table 5.17: Difference between Indirect and Direct Hernia

Indirect Direct
Age At any age but common in infants and Usually in the elderly person
young adults
Site Usually unilateral (30% bilateral) Usually bilateral
Extent Maybe incomplete or complete Usually incomplete
Entrance Through the deep inguinal ring Through the floor of Hesselbach’s
triangle
Exit Through the superficial inguinal ring, can Rarely through superficial ring, doesn’t
descend into the scrotum descend into scrotum
Relation with inferior Inferior epigastric vessels lie medial to Inferior epigastric vessels lie lateral to
epigastric vessels the neck of the sac the neck of the sac
Relation with The sac lies within coverings of The sac lies outside the coverings of the
spermatic cord spermatic cord. The sac is anterior to the spermatic cord. The sac is either behind,
cord below or above the cord.
Shape of the swelling Usually pyriform shape, with narrow end Usually globular with broad base above

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 above and broad base below
Appearance of the Slowly appears on straining or coughing Easily pops out on standing, straining or
swelling coughing
Reducibility Gradually reduces, may need Usually reduces immediately and
manipulation spontaneously on lying down
Direction of reduction Reduces upwards, then laterally and Reduces upwards and backwards
backwards
Deep ring occlusion Positive i.e. the swelling does not appear Negative i.e. swelling reappears
test after reduction when the patient coughs.
Release of occlusion The swelling appears first in the middle The swelling reappears straight forward
followed by coughing of the inguinal region and the follows exactly where it was before
medially and ultimately turns down to
the neck of scrotum
Obstruction/ Common due to narrow neck of the sac Rare due to wide neck of the sac
strangulation

Congenital Inguinal Hernia

 Develops due to failure of obliteration of the processus vaginalis.

 Always indirect type. Usually appears as an inguinoscrotal swelling since birth. It
gradually increases in size.
 The swelling appears on straining or crying, on crawling, sitting and standing.
 The swelling disappears when the child lies down.
 The swelling may transilluminate (cf. congenital hydrocele).
 Reducible with or without gurgling sound.
 The swelling will reappear, if the child is induced to cry.
 In newborn infant, the inguinal canal is not developed and the deep and
superficial inguinal rings lie close or superimposed to each other

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 5.12.2. Femoral Hernia

 Introduction …………………………………………………….………415
 Surgical Pathology…………………………………………………….415
 Diagnostic Criteria ……………………………………………………416

Introduction
 It is the protrusion of the extraperitoneal fat and peritoneum with or without
abdominal contents through the femoral canal. In this hernia the sac passes through
the femoral ring and enters the femoral canal.

Surgical Pathology

1. Majority of femoral hernia are acquired in nature.

2. Femoral hernia is more common in females.
• More common in the middle aged and the
elderly females due to wide pelvis and
repeated pregnancy.
• Repeated pregnancy causes increased
abdominal pressure which is probably an
initiating factor.
• However, inguinal hernia is more common
than femoral hernia in females.
• Femoral hernia is almost unknown in infants.
3. Right-sided hernia is more common than the left sided one.
• The hernia may be bilateral.
4. Course of the hernia:
• The hernial sac enters through the femoral ring and descends vertically
down along the femoral canal up to the lower border of fossa ovalis where
it lies in close relation to the long saphenous vein.

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 • Due to abdomen (fascia of Scarpa) to the fascia lata of the thigh at the
lower border of the fossa ovalis, the sac cannot pass down in the thigh.
• So, the sac courses, and when enlarging it courses upward over the
inguinal ligament and external oblique aponeurosis and thus the distal
part of the sac overlies the inguinal ligament and occupies the inguinal
region.
• The shape of the sac then becomes retort-shaped.

Contents of the sac may contain:

1. A part of the omentum.
2. A loop of small bowel.
3. A part of the circumference of small bowel (Richter's Hernia).

Coverings of the sac from superficial to deep:

1. Skin.
2. Superficial fascia.
3. Cribriform fascia covering the saphenous opening.
4. Fascia transversal is- representing the anterior femoral sheath.
5. Extraperitoneal fat.
6. Peritoneum - the hernial sac.

Diagnostic Criteria
1. Age- middle aged to elderly
2. Sex: More common in females.
3. Symptoms:
• The patient complains of dragging pain in the groin.
• Usually she or he presents with a small globular swelling in the groin. It
becomes more prominent on standing or straining but may disappear on lying
down.
• An obese lady may present with the features of intestinal obstruction or
strangulation of an unnoticed femoral hernia.
• Examination: the femoral hernia should be examined in the similar
manner as in inguinal hernia. Ask the patient to stand up, note the exact
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 position of the lump, try to determine the exact anatomical relations of
the lump to the inguinal ligament and pubic tubercle and then note if the
lump has a cough impulse and whether it is reducible.
4. Position- A round or oval swelling below the medial end of the inguinal ligament-
at or below the groin crease.
5. Palpation: The neck of the lump is situated below and lateral to the pubic
tubercle (cf. Inguinal hernia).
6. Cough impulse: Both visible and palpable, may be absent in many femoral hernias
because the contents are adherent to the peritoneal sac.
7. Reducibility: Often partial. When complete it reduces directly upwards and
backwards.
8. Inguinal canal examination, e.g., invagination test – empty

Table 5.18: Difference between Inguinal and Femoral Hernia

Inguinal Femoral
Age Any age Middle aged or elderly persons
commonly
Sex More common in males More common in females
Side Unilateral, common on the right side Unilateral, common on the right side
Relation with pubic Lies above and medial to pubic Lie below and lateral to pubic tubercle
tubercle tubercle
Cough impulse Usually present Usually absent
Reducibility Usually reducible; reduces in an Often partial; when complete, it reduces
upward, backward and lateral directly upward and backwards.
directions
Invagination test after On coughing by the patient: a thrust On coughing; no thrust will be felt: the
reduction will be felt at the tip of finger inguinal canal felt to be empty

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 5.12.3. Incisional Hernia

 Introduction ……………………………………………………………418
 Predisposing Factors………………………………………………..418

Introduction
• AKA: Postoperative hernia, Ventral hernia
• An abdominal incisional hernia is one where the peritoneal sac herniates through
an acquired scar in the abdominal wall, usually caused by a previous surgical
operation or an accidental trauma.
• Scar tissue is inelastic and can be stretched easily if subjected to constant strain.
• Contents of such hernia are usually bowel and/ or omentum

Predisposing Factors
1. Some subjects:
 Obese individuals with poor musculature.
 Diabetic patients.
 Malnutrition: severe anemia. hypoproteinemia. avitaminosis, e.g., vitamin
C deficiency.Patients with cachexia and advanced malignant disease.
 Patients with any chronic source of straining,
2. Some operations:
 Operation for peptic perforation or appendicular perforation.
 Operation in case of peritonitis.
 Operation for visceral cancer.
 Pancreatic resection operation.
3. Some incisions:
 Kocher’s subcostal incision for cholecystectomy causing injury to the ninth
and tenth thoracic nerves.
 McBurney's incision for appendicectomy causing injury to the ilio-inguinal
nerve.
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  Battle's para-rectal incision for appendicectomy.
 Midline infraumbilical incision e.g., during caesarean section.
4. Some faults during operation:
 Division of motor nerves supplying the muscles around the wound.
 Defective closure of the laparotomy wound, e.g., failure of suturing the
abdominal wounds in anatomical layers; suturing under tension causes
pressure necrosis of intervening tissues.
 Inadequate haemostasis during operation leading to wound haematoma
which becomes more vulnerable if infected.
 Wound closed with non-absorbable suture materials like nylon, prolene
are followed by a lesser incidence of incisional hernia than the wound
closed with absorbable sutme like catgut.
 Drainage tubes brought through the main laparotomy wound and left
behind for a long time. (lntraperitoneal drains should always be brought
out through a separate stab incision.)
5. Some post-operative complications:
 Severe post-operative abdominal distensions causing tension over the
suture line.
 Persistent postoperative cough – causing tension over the suture line.
 Post-operative peritonitis - because there is a chance of wound infection
and abdominal distension.
 Wound infection.
 Wound haematoma.
 Too early removal of sutures.
 Too early resumption of strenuous labour.

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 5.13. Nasogastric Tube (NGT)

 Introduction…………………………………………………………420
 Indications……………………………………………………………420
 Contraindications….…………………………………………… 421
 Equipment……………………………………………………………422
 Placement……………………………………………………………423
 Complications………………………………………………………424

Introduction

 An NG tube is a long, thin polyurethane, silicone, or rubber tube that's

inserted into a patient's nasal or oral passage to administer (gavage) or
remove (lavage) substances in the stomach

Indications

 Comatose or have experienced trauma to their oral pathway

 Hydration
 Nutrition
 Medication administration
 Gastric decompression
 Aspiration of ingested toxic materials
 Bowel rest with a small bowel obstruction
 Traumatic injuries (such as gunshot wounds)
 Mechanical ventilation
 Paralytic ileus
 Metastatic gastric diseases
 Failed swallowing study/high risk of aspiration

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Indication for Pediatric Patients
 Acute gastric dilatation
 Upper GI bleeding
 Decontamination of poisoned children
 Intussusceptions in children
 Growth failure & poor weight gain
 Caustic esophageal injury
 Treatment of appendicitis
 Inpatient Treatment of pneumonia
 DKA in children
 Suckling & swallowing disorders in newborn
 Fluid & electrolyte therapy

Contraindications
 Absolute contraindications
 Severe midface trauma
 With midface trauma, you run the risk of the NG tube going through
the cribriform plate of the ethmoid bone; if this happens, then the
NG tube will be in the cranial vault with fatal results
 Recent nasal, throat, or esophageal surgery.
 NG tubes should only be placed by a surgeon if being used for a
patient who's undergone recent nasal, throat, or esophageal
surgery. The risk of reopening the suture line is too great and can
lead to serious post-op complications.
Relative contraindications
 Coagulation abnormalities
 The mucosal lining of the nasal passages is extremely thin and very
vascular. If your patient has an uncorrected coagulation
abnormality, you run the risk of epistaxis during NG tube insertion.
Severe epistaxis is a true medical emergency; it can lead to airway
compromise and/or aspiration of blood.

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  Esophageal varices
 The fact that the veins are so close to the surface of the esophagus
makes it easy for them to start bleeding upon NG tube insertion.
 Esophageal stricture
 The scar tissue isn't as pliable as normal esophageal tissue, making
it easier to become damaged with the insertion of invasive tubes
 Alkaline ingestion
 With an NG tube in place, the cardioesophageal sphincter can't
completely close, increasing the risk of reflux of the alkaline
substance into the esophagus, causing further damage.
 Contraindications in the pediatric population
 Congenital birth defects affecting the gastrointestinal tract, most specifically
cleft lip and/or cleft palate.
 Recent esophageal or gastric surgery
 Head trauma with possible basilar skull fracture

Equipment

 Glove
 NG tube
 Lubricant
 cup with water
 Syringe & stethoscope

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 Placement

1. Explain the procedure to the patient

and obtain consent.
2. Gather the supplies needed.
3. Place the patient in an upright
position; if unable, lay the patient on
one side.
4. Agree on a signal with the patient that
he or she can use to stop the
procedure (such as raising the hand).
5. Wash your hands and put on gloves.
6. Measure the distance from the tip of
the patient's nose, to his or her
earlobe, and to the bottom of the
xiphoid process (see NG tube
measurement). Mark this length so
you'll know when to stop advancing.
7. Lubricate the first 2 to 4 in of the
tube with water-soluble lubricant.
8. Inspect the patient's nares for a deviated septum or visible nasal polyps; use the
larger nares for your insertion.
9. Wash the patient's nose with warm water and soap, and dry completely.
10. Advance the tube slowly into the nares, aiming the tube horizontally, along the
floor of the nasal cavity. If resistance is met, don't force the tube; withdraw and
attempt at a different angle.
11. As the tube approaches the nasopharynx, ask the patient to swallow; with each
swallowing motion the patient makes, advance the tube a little farther. If able and
cooperative, ask the patient to tuck his or her chin, which causes the opening of the
esophagus to widen.
12. Stop once you've advanced the tube to the mark you made while measuring.
13. Lightly tape the tube to the patient's cheek while you're confirming placement

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 14. Confirm placement per your facility's
policy. Ways to check placement include
aspirating gastric contents and testing it with pH
paper (a pH of 5.5 or less indicates gastric acid), or
obtaining a chest X-ray.
Special consideration: Average gastric pH is 1 to 3;
with patients who are taking medication for acid
reduction, the pH can be higher than 4.
15. Once placement is confirmed, tape the
tube more securely to the patient's nose.

Complications

 Pharyngeal discomfort
 Erosion of the naris
 Sinusitis
 Nasotracheal intubation causing pneumothorax and pulmonary placement
 Gastritis
 Perforation and bleeding

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 5.14. Video QRs

Stoma

NG Tube Insertion

Inguinal Hernia Examination

Groin Hernias

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 Part 6: Pediatric Surgery

Long Case Discussion

 Content By:
 Samuel Mesfin
6.1. Approach to Scrotal Swelling……………………427
 Edited By:
 Samuel Mesfin 6.2. Video QRs………………..………………………………438

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 6.1. Approach to Scrotal Swelling

 Case Discussion………………………………………………….…427
 Introduction………………………………………………………...427
 History………………………………………………………………...428
 Physical Examination……………………………………….....429
 Diagnostic Approach…………………………………………….431
 Discussion of the Differentials………………………………431

Case Discussion
 A 13-year-old boy was presented to the pediatric emergency with a 2-week history of
swelling of the right scrotal contents, of simple evolution. During the previous 48hrs, his
symptoms worsened by the appearance of acute scrotal pain. He had no known testicular
or scrotal abnormalities. There were no fevers, abdominal pain, nausea or vomiting. He
had no significant past medical, past surgical or family history. The examination revealed a
soft abdomen but with an erythematous right hemiscrotum that was swollen, tense and
particularly painful during its palpation

Introduction
 The most common causes of painless scrotal swelling in children and adolescents include
hydrocele and inguinal hernias that are not incarcerated.
 Less common causes are varicocele, spermatocele, localized edema from insect
bites, nephrotic syndrome (swelling is usually bilateral), and rarely, testicular
cancer
 Scrotal swelling and testicular masses warrant prompt evaluation.

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 History

 The essential points include

o Is there history of pain? If so:
 Determine the onset and severity (remember that some
adolescents may not report scrotal pain because of modesty or
embarrassment)
 The major causes of acute scrotal pain in children and adolescents
are testicular torsion, torsion of testicular or epididymal
appendages, and epididymitis
 Testicular torsion is a surgical emergency.
o Is there a history of trauma?
 Blunt scrotal trauma is common in children and adolescents.
 Although severe injury is rare, it can cause unilateral testicular pain
arising from testicular contusion, rupture, or traumatic testicular
torsion.
o Is there a history of change in testicular or scrotal size?
 If so, what is the onset of this change?
 Does scrotal size vary with time of day, position, or Valsalva
maneuver?
 Such changes are suggestive of communicating hydrocele (with or
without an inguinal hernia) or varicocele.
 These conditions and other causes of scrotal swelling are discussed
separately
o Is the patient sexually active?
 Sexual activity may be associated with epididymitis, although
epididymitis also occurs in prepubertal and nonsexually active
males.
o Is the patient having difficulty voiding or painful urination?
 Difficulty voiding suggests a urinary tract infection; intraabdominal,
pelvic or rectal mass; or neurologic problem, including a lesion of
the spinal cord.
o Is there flank pain or hematuria?
 These findings suggest a renal stone, which may cause referred
pain in the scrotum.

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 o Is there abdominal pain associated with decreased appetite,
nausea, and/or vomiting?
 These symptoms can be nonspecific but may represent referred
pain associated with testicular torsion.
o Has the patient had fever?
 Fever suggests orchitis due to infections such as coxsackie virus,
mumps, or brucellosis.
 Fever is also seen in some patients with epididymitis.

Physical Examination
 Inspection
o The first step is to inspect the penis, pubic hair, and inguinal area while
the patient is standing.
o The examiner should notice the presence or absence of any ulcers,
papules, urethral discharge, piercings, tattoos, pubic hair infestation, or
lymphadenopathy.
o Ulcers, papules, discharge, and lymphadenopathy may suggest a sexually
transmitted infection.
o Piercings and tattoos may provide a portal of entry for skin and soft tissue
infection.
o The position of the testicles (eg, high versus low and horizontal versus
vertical) should be evaluated.
 The left testicle usually lies slightly lower than the right testicle.
o Patients with varicoceles should also be examined in the supine position.
 This maneuver will help to differentiate idiopathic from secondary
varicocele.
 Idiopathic varicocele usually is more prominent in the upright
position and disappears when the patient is supine, whereas
secondary varicocele usually does not get much smaller with
change in position from upright to supine.
 Palpation

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 o The examiner should palpate the entire testicular surface by gently rolling
it between his or her thumb and forefingers.
o The testicle should have the consistency of a hard-boiled egg.
o The epididymis should be palpated in the posterolateral position and
followed to the spermatic cord
o The examiner should note any swelling or tenderness along any of these
structures; if swelling is noted, transillumination may help to determine if
it is cystic or solid in nature.
o Transillumination is performed by placing a light source at the base of the
scrotum.
o Fluid-filled masses (eg, hydrocele or spermatocele) will transfer the light
and cause the scrotum to glow; solid masses (eg, torsed testicle) will not.
 Cremasteric reflex
o It should be assessed by stroking the upper thigh while observing
the ipsilateral testis.
o Normal response is cremasteric contraction with elevation of the
testis.
o The reflex is present in the majority of healthy boys between the
ages of 30 months and 12 years
o It is almost always absent in patients with testicular torsion, may
help to distinguish this condition from other causes of scrotal pain
 Prehn sign (testicular elevation)
o Prehn reported that elevation of the scrotal contents relieves the pain in
patients with epididymitis and aggravates or has no effect on the pain in
patients with the emergency condition, testicular torsion.
o However, Prehn sign may not be a reliable distinguishing feature between
testicular torsion, epididymitis, and other diagnoses in children.
 Ancillary studies
o In addition to the genital examination, abdominal and rectal examinations
are indicated if clinical suspicion exists for an abdominal or rectal mass,
metastatic visceral disease, or prostatitis.

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 Diagnostic Approach

 The major considerations in the differential diagnosis of scrotal pain or swelling

can be divided according to the predominant symptom: pain or swelling.
 Pain predominant: the most common causes of acute scrotal pain in children and
adolescents are:
o Testicular torsion (a surgical emergency)
o Torsion of the appendix testis
o Epididymitis
o Incarcerated inguinal hernia (a surgical emergency)
o Torsion of the appendix epididymis
o Trauma
o Immunoglobulin A vasculitis (IgAV; Henoch-Schönlein purpura [HSP])
o Orchitis
o Infection (eg, Fournier's gangrene)
o Referred pain (eg, from a renal stone)
 Swelling predominant — The most common causes of isolated scrotal swelling
(as opposed to the generalized edema seen in conditions such as nephrosis) in
children and adolescents are:
o Hydrocele Spermatocele (epididymal cyst)
o Varicocele Testicular cancer

Discussion of the Differentials

6.2.1. Testicular Torsion

 Generally presents with the abrupt onset of severe
pain.
 The testicle may lie transversely in the scrotum and
be retracted and/or swollen; the cremasteric reflex
typically is absent.
 Testicular perfusion is decreased and can be assessed
on Doppler ultrasound or nuclear scan of the
scrotum.

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 Although the clinical and radiographic evaluations may be normal at the time of
presentation in a boy with an intermittent torsion that has been reduced,
findings may be present to varying degrees on physical examination and imaging.

6.2.2. Torsion of the Appendix Testis

 Also presents with the abrupt onset of pain.
 The pain is initially localized to the region of the appendix
testis (anterosuperior, and is frequently mild.
 With the development of a reactive hydrocele, diffuse
swelling and tenderness that are similar to testicular
torsion may occur.
 A pathognomic "blue dot" sign may be apparent
 Testicular perfusion is normal on imaging studies.

6.2.3. Epididymitis

 It often presents with a subacute onset of pain

and swelling isolated to the epididymis
 Patients with epididymo-orchitis (inflammation
of the epididymis and the testes due to
infection may also have testicular pain as well.
 The patient may have a history of frequency,
dysuria, urethral discharge, and/or fever.
 Testicular perfusion is normal or increased on
imaging studies.
 Pyuria is often present on urinalysis.

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 6.2.4. Scrotal Trauma

 It usually is evident from the history.

 The spectrum of injuries can range from a
hematocele (hematoma in the tunica vaginalis) to
an intratesticular hematoma to disruption of the
tunica albuginea causing testicular rupture.
 Color Doppler ultrasonography can accurately
diagnose the extent of injury.
 Testicular rupture requires surgical repair.
 Lesser injuries are managed according to the
clinical severity and often can be treated
nonoperatively.

6.2.5. Hydrocele
 A hydrocele is a collection of peritoneal fluid between
the parietal and visceral layers of the tunica vaginalis.
 Hydroceles may be communicating or
noncommunicating.
o Communicating hydroceles usually develop as a
result of failure of the processus vaginalis to close
during development; the fluid around the testis is
peritoneal fluid
o Noncommunicating hydroceles have no
connection to the peritoneum; the fluid comes
from the mesothelial lining of the tunica vaginalis
 Hydroceles are common in newborns (whether related to delayed closure of a
patent processus vaginalis or fluid trapped at the time of testicular descent is not
known)
o The majority of hydroceles in neonates resolve spontaneously, usually by
the first birthday
o In older children and adolescents, noncommunicating hydroceles may be
idiopathic or may occur secondary to epididymitis, orchitis, testicular

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 torsion, torsion of the appendix testis or appendix epididymis, trauma, or
tumor (reactive hydroceles).
 Patients with hydroceles present with a cystic scrotal mass.
 A hydrocele that communicates with the peritoneal cavity may increase in size
during the day or with the Valsalva maneuver.
 Noncommunicating hydroceles are not reducible and do not change in size or
shape with crying or straining.
 In patients with testicular pain and scrotal swelling, the hydrocele may arise from
epididymitis, orchitis, testicular torsion, torsion of the appendix testis or appendix
epididymis, testicular rupture, testicular hematoma, or tumor as the primary
etiology (reactive hydroceles);
 Doppler ultrasonography is usually necessary to evaluate these patients further.
 The diagnosis of hydrocele can be made by physical examination and
transillumination of the scrotum that demonstrates a cystic fluid collection.
 Communicating hydroceles are often reducible; noncommunicating hydroceles are
not.
 Doppler ultrasonography may be necessary to evaluate the testicle and rule out a
primary cause.
 Surgical repair is indicated for hydroceles in newborns that persist beyond one year
of age, for communicating hydroceles, and for idiopathic hydroceles that are
symptomatic or compromise the skin integrity.
 The management of hydrocele in a neonate or child younger than one year of age
usually is supportive
 Hydroceles that are present in newborns, whether communicating or
noncommunicating, usually resolve spontaneously by the first birthday, unless they
are accompanied by an inguinal hernia
 Communicating hydroceles in older patients rarely resolve and pose a risk for
development of incarcerated inguinal hernia.
 Surgical repair of communicating hydrocele is usually undertaken on an elective
basis

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 6.2.6. Varicocele

 A varicocele is a collection of dilated and

tortuous veins in the pampiniform plexus
surrounding the spermatic cord in the
scrotum
 The cause of primary or idiopathic
varicoceles, that arise spontaneously and
are not caused by obstruction of the
inferior vena cava, is unknown.
 One etiologic theory is that primary
varicoceles result from increased venous
pressure and incompetent valves
 Varicoceles occur more commonly on the left side (85 to 95 percent):
o Because the left spermatic vein enters the left renal vein at a 90 degree
angle, whereas the right spermatic vein drains at a more obtuse angle
directly into the inferior vena cava, facilitating more continuous flow
 Approximately 10 to 25 percent of all adolescent males and as many as one-third of
all males examined at an infertility clinic have a varicocele.
o However, only 10 to 15 percent of males with varicoceles have fertility
problems
 Patients with varicoceles can be asymptomatic or present complaining of a dull
ache in or fullness of the scrotum upon standing.
 The key task for the examiner is to differentiate primary varicocele from secondary
varicocele caused by obstruction of the inferior vena cava.
o The examination for varicocele initially should be performed with the
patient standing
o The scrotum is inspected for any visible distention around the spermatic
cord (indicative of a grade III varicocele).
o The scrotum, testes, and cord structures are then gently palpated; a
palpable varicocele has the texture of a "bag of worms"
o Grade II varicoceles are palpable, but nonvisible.
o The patient should then be asked to perform the Valsalva maneuver; if the
varicocele is palpable only with the Valsalva maneuver, it is Grade I
 The patient also should be examined in the supine position

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 This maneuver will help to differentiate idiopathic or primary from secondary
varicocele.
o Primary varicocele usually is more prominent in the upright position and
disappears in supine
o Secondary varicocele usually does not get much smaller with change in
position from upright to supine.
 If the varicocele persists in the supine position, has acute onset, or is right-sided
(secondary varicocele), then processes that cause inferior vena caval (IVC)
obstruction must be ruled out with Doppler ultrasonography.
 These processes include:
o IVC thrombus
o Right renal vein thrombosis with clot propagation down the IVC
o Abdominal mass (eg, retroperitoneal tumors, kidney tumors, or
lymphadenopathy)
 Varicocele grade does not correlate well with abnormal semen analysis or infertility
in adults
 Most varicoceles in adolescents are managed conservatively with observation.
o When more aggressive treatment is necessary, varicoceles are repaired
through surgical ligation or testicular vein embolization.
 These procedures should be considered under the following circumstances
o Affected testicular volume is less than that of the unaffected testicle (a
difference in size of >10 to 15 percent or >2 mL when assessed by
ultrasonography);
o Loss of testicular volume is associated with a decreased sperm count
o Testicular growth arrest can be reversed with varicocele repair
 To alleviate symptoms: Pain, heaviness, swelling.

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 6.2.7. Spermatocele (Epididymal Cyst)

 A spermatocele (epididymal cyst) is a painless, fluid-

filled cyst of the head (caput) of the epididymis that
may contain nonviable sperm
 A spermatocele can be palpated as distinct from the
testis and typically transilluminates as a cystic mass.
 In contrast, testicular tumors are palpated within the
testis and do not transilluminate.
 Ultrasonography may be helpful to confirm the
diagnosis of spermatocele. Spermatoceles do not
affect fertility.
 Treatment (eg, surgical excision) is indicated to relieve
discomfort.

6.2.8. Testicular Cancer

 Testicular cancer accounts for 20 percent of

cancer diagnosed in males 15 to 35 years old,
rendering it the most common solid tumor in
males within this age group
 The epidemiology and risk factors for testicular
cancer, which include cryptorchidism, family
history of testicular cancer, cancer of the other
testicle, human immunodeficiency virus (HIV)
infection, germ cell neoplasia in situ (GCNIS,
formerly called intratubular germ cell neoplasia
of the unclassified type), and race, are discussed
in detail separately.
 Clinical presentation
o Testicular cancer usually presents as a painless mass discovered by the
patient or clinician on physical examination, although rapidly growing germ
cell tumors may cause acute scrotal pain secondary to hemorrhage and
infarction.

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 o Other common signs are testicular enlargement or swelling. Many patients
also report an aching feeling in the lower abdomen or scrotum.
o On examination, intrascrotal malignancies usually are firm, nontender
masses that do not transilluminate unless accompanied by a reactive
hydrocele.
o Some patients may have gynecomastia. The clinical presentation of
testicular cancer and advanced or metastatic testicular cancer are discussed
in more detail separately.
 Diagnosis
o Scrotal ultrasound is the initial diagnostic test of choice
o Although pathology is the definitive diagnostic test, scrotal ultrasound may
help to distinguish intrinsic from extrinsic testicular lesions.
o Several conditions may mimic neoplasia on ultrasound, including
inflammation, hematoma, infarct, fibrosis, and tubular ectasia of the rete
testis.
o In cases in which the ultrasound is inconclusive, magnetic resonance
imaging (MRI) may help differentiate benign from malignant lesions.

6.2. Video QRs

Scrotal Swelling

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 Part 7: Neurosurgery

Long Case Discussion

7.1. Head Injury…………………………………………….440

 Content By:
 Eyerusalem Nega 7.2. Peripheral Nerve Injury………………………….460
 Nanati Jemal
 Edited By:
7.3. Spinal Cord Injury…………………………………..472
 Samuel Mesfin 7.4. Brain Tumor………………………….……………….475
 Reviewed By:
 Dr. Kibruyisfaw Zewdie 7.5. Neural Tube Defects (NTDs)……………………485
(Neurosurgeon)
7.6. Hydrocephalus………………………….……………493
7.7. Video QRs……..………………………….…………..499

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 7.1. Head Injury
 Case Discussion……………………………………….…440
 Introduction………………………………………………440
 History..…………………………………………………….441
 Physical Examination…………………………………443
 Investigation……………………………………………..446
 Management…………………………………………….447
 Discussion of Case…………………………………….449

Case Discussion
 A 15-year-old boy is brought to the emergency department by his parents. He had been playing
with his friends and accidentally he was struck on the head by stone by one of his friends
approximately half an hour before admission. He lost consciousness briefly, but was able to walk
from the scene. He is complaining of a severe headache, and has vomited three times. He is mildly
confused. He has no previous medical history, and he is not on any medication. The physical
examination reveals a pulse rate of 58/min and a blood pressure of 180/110 mmHg. During the
course of the examination he becomes drowsy and his Glasgow Coma Score (GCS) drops to 3/15.
He has a ‘boggy swelling’ over the right temple.

Introduction
 Head injury is the leading cause of death and disability from childhood to early
middle age.
 Road traffic accidents are the leading cause of head injury, being responsible for up
to 50 per cent of cases.
 Risk factors include male sex, recreational drugs (including alcohol and substance
abuse) and youth, with a peak at 15–30 years of age.

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 History

Identification:

 Age  tells the prognosis,  Address -tells delay

Mechanism of injury  Source of history
 Handedness  Religion

Chief complaint:

 Duration

HPI:

 Ask Mechanism of injury which could be

o Motor vehicle accident:
 Head on collision  Was the patient
 Car to stationary car ejected out?
 Speed of the car
 Death among the occupant  indicates high risk injuries with
multiple injuries
o Fall from height:
 Significant fall  Fall from 10feets or 3meters high
 Ask the way the patient lands
o Assault or being struck with a falling object
 Have markedly greater likelihood of poorer vocational outcome.
o Gunshot injury
 Military guns – cause  Non-military gun
severe injury  Ask type of gun
 Loss of consciousness:
o The presence of unconciousness
o Duration of unconciousness
o Even questionable loss of consciousness can be a marker of sever
neurological injury
o Level of consciousness at scene and on transfer
o Presence of amnesia

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 Table 7.1: Grading post traumatic amnesia
Grade Duration
 Grade 1 or Slight  less than 1 hour
 Grade 2 or Moderate  1-24hours
 Grade 3 or Severe  1-7days
 Grade 4 or Fatal  more than 7days

 Focal neurologic deficit:

o Weakness o Speech difficulty
o Seizure – Time, type, and duration should be included (In middle
meningeal haemorrhage it is unilateral (Jacksonian) starting from toes
going upwards towards face)
o Cranial nerve deficit
 Probable hypoxia or hypotension
 Amount of blood loss
 Signs of increased intracranial pressure such as
o Vomiting- usually o Visual disturbance
repititive and projectile (diplopia) -due to CN VI
o Global headache o Change in mentation
 Signs for basal skull facture;
o Extravasation of blood o Presence of neckpain
o Watery discharge (CSF) through the ears, nose, mouth
 The presence of prior head injuries
o Particularly concussive episodes in sport can indicate the potential for
more sever long term outcomes
 Pre-existing medical conditions such as:
o DM o History of epilepsy
o Hypertension o Drug allergies
 Medications
o Anticoagulants o Anti-platelets
 illicit drug and alcohol use
 Previous history of surgery

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 Physical Examination

 Starts with resuscitation and primary survey.

 Primary survey include the ABCDE.
o Air way-
o Breathing
o Circulation
o Disability – focus on
 GCS
 Pupillary size and reactivity
 Focal neurologic signs
 Secondary survey then ensues. Detailed physical examination is done here.
o General appearance
o Vital signs:
 Pulse rate
- Tachycardia is seen on concussion
Cushing traid:
- Slow bounding pulse with hypertension indicates
 It is characterized by cereberal compression
o Hypertention - Irregular pulse suggests poor prognosis
o Bradychardia  Blood pressure
o Irregular breathing  Respiatory rate
 It’s a late manifestation - Slow and deep breath in brain compression, shallow in

 It’s due to herination concussion

 Temprature
- Hyperpyrexia – pontine hemmorrhage, brain stem,
injury intraventricular hemorrhage, cerebral
compression.
o HEENT
 Head: look for
- Scalp laceration
- Bleeding
- Scalp hematoma may be subcutaneous (superficial, mobile)
- Subaponeurotic (extends beyond skull bone suture lines)
- Subpericranial (limited to one cranial bone by suture line).
 Head: Palpate the scalp and look for

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 - Skull fracture with or without CSF leak
 Ear
- Bleeding through the - CSF leak
ear - Hearing loss
 Eyes
- Periorbital - Visual difficulty
ecchymoses
 Nose
- Bleeding via the nose - Difficulty in smelling/
- CSF leak Anosmia
 Mouth
- Fluid/blood
o Chest Examination:
Sub conjunctival hemorrhage:
 It is very important to examine the chest since
- It is deep to conjunctiva most head injuries are associated with other life
- Does not move with conjunctiva threatening injuries such as heamothorax,
- Points towards the cornea with tension pneumothorax.
invisible posterior limit  Follow the standard steps:
- Conjunctival edema can occur  Inspection – bruise, symmetry, scar
 Palpation – position of the trachea, tactile
Superficial conjunctival hemorrhage:
fremitus, tenderness
- It is confirmed by its mobility with  Percussion – resonance
the conjunctiva  Auscultation- check breath sounds
- Has visible posterior limit

o Abdomen
 Look for associated injury such as bleeding, Spleenic rupture
 Rectal examination paying special attention to the anal tone (spinal injury)
o GUT
 High ridding prostate (uretheral ruputre)
o MMSE
 Limb fracture, bleeding
o CNS

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  Conciousness – assessed with GCS (refer to table 7.2 below)
 Mental status
 Cranial nerve examination—focus on the following
- Pupillary size and reactivity:
 Asymmetrical sluggish response: may suggest partial third
nerve dysfunction on that side implying uncal herniation as a
result of a mass on the ipsilateral side of sluggish pupil
 As the third nerve becomes increasingly compromised the
ipsilateral pupil will become fixed and dilated.
- Anosmia (CN-I):
 Associated with rhinorrhea ->This pts are @ risk of ascending
meningitis
- CN VI palsy:
 Raised ICP
- CN VII & VIII palsy:
 Basal skull fracture
 A peripheral nerve examination should record…
- Muscle tone - Reflexes
- Muscle strength - Sensory loss
Table 7.2: Glasgow Coma Scale (GCS)
Examination of the whole patient in head
Eye opening injury
 Spontaneous 4
 Cervical spine injury is common in
 Response to verbal command 3 patients with head injuries
 Response to pain 2  Even obtunded patients should move
 No eye Opening 1 all four limbs
Best verbal response  Check and record power, tone and
 Oriented 5 sensation in the peripheral nerves
 Confused 4  Log roll to check the whole spine for
 Inappropriate words 3 steps and tenderness
 Incomprehensible sounds 2  Perform a rectal examination to check
 No verbal response 1 for anal tone and anal wink
Best motor response  Check for priapism

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  Obeys command 6
 Localizing response to pain 5
 Withdrawal response to pain 4
 Flexion to pain 3
 Extension to pain 2
 No motor response 1
Total 15

Clinical Signs of IC-HTN

1. Pupillary dilatation (unilateral or bilateral)

2. Asymmetric pupillary reaction to light
3. Decerebrate or decorticate posturing (usually contralateral to the blown pupil)
4. Progressive deterioration of the neurologic exam not attributable to extra-cranial factors.
 Items 1-3 represent clinical signs of herniation.
 The most convincing clinical evidence of IC-HTN is the witnessed evolution of one or more of
these signs.
 IC-HTN may produce a bulging fontanel in an infant.
 Blown pupil: fixed and dilated pupil

Investigation
 Labratory workup:
o CBC - Haemoglobin, PCV
o Blood type and cross match
o Coagulation study - PT/PTT
o Serum electrolytes
 Hyponatremia which can be due to SIADH or cereberal salt wasting
 Elevated sodium level indicate simple dehydration or DI
o Blood sugar level (RBS)
o Blood gas analysis
o Toxicology screening for drugs
o Blood alcohol level
o Renal function test
 Diagnostic imaging Studies
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 o Plain skull x-ray
o CT scan without contrast
 Is ideal investigation to identify intracranial injuries
 Usually plain CT is done in emergency situation
o MRI is very useful and senstive
o Angiography
o Electromyography and NCS
o Brain tissue oxygen sensor
o Intraparenchymal fiberoptic pressure transducer
 National Institute for Health and Clinical Excellence (NICE)guidelines for computed
tomography (CT) in head injury.
o GCS <13 at any point
o GCS 13 or 14 at 2 hours
o Focal neurological deficit
o Suspected open, depressed or basal skull fracture
o More than one episode of vomiting
o Any patient with a mild head injury over the age of 65 years or with a
coagulopathy, for instance warfarin use, should be scanned urgently
o Dangerous mechanism or injury or antegrade amnesia >30 minutes warrants
CT within 8 hours

Management
Priorities:
 Minimize secondary brain injury
o ABCs
o A = Airway – is he protecting his airway?
 GCS< 9 = unable to protect airway  Intubate
 Hypercapnia causes vasodilation, increasing ICP
o C spine immobilization and avoid head tilt to open the airway
o B = Breathing – is it compromised
 E.g. any secondary lung injuries?
 Administer O2
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  Hypoxemia causes vasodilation, increasing ICP
o C = Circulation – is it adequate?
 Maintain systolic BP> 90 mm Hg
Medical Management:
 ABC’s
o Ensure Adequate Oxygenation/ Ventilation
 PaCO2 – normal (35 mm Hg)
o IV Fluids
 Isotonic – NS or Ringer’s
 Goal: Euvolemia
 Medical Management: Mannitol
 Hyperventilation
 Head Elevation
o Anti-Seizure Medication:
 If severe head injury (GCS ≤ 8)
 Penetrating head injury
 History of seizure disorder
 Antibiotics
 ICP Monitoring and Management
 Surgical Management
o Burrhole o Craniectomy

Discharge criteria in minor and mild head injury

 GCS 15/15 with no focal deficits
 Normal CT brain if indicated (see below)
 Patient not under the influence of alcohol or drugs
 Patient accompanied by a responsible adult
 Verbal and written head injury advice: seek medical attention if:
o Persistent/worsening headache despite analgesia
o Persistent vomiting
o Drowsiness/Visual disturbance
o Limb weakness or numbness

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 Discussion of the Case

 Classification………………………………………….…449
 SCALP Laceration……………………………………..450
 Skull Fracture…………………………………………..451
 Brain Injuries..……………………………………….…453

Classification
 Head injury include any trauma to scalp, skull and brain
 SCALP laceration
 Skull fracture
o Open or closed o Vault or Basal skull
o Linear or depressed fracture
 Intracranial bleeding
o Epidural hematoma
o Subdural hematoma
o Intraparenchymal hematoma/bleeding
 Brain injury could be either
o Primary injury: could be focal or diffuse
o Secondary injury
 Based on GCS
o Minimal – GCS 15/15, no loss of conciousness
o Mild – 13-15/15 , loss of consciousness <5minutes
o Moderate – 9-12/15, loss of consciousness >5 minutes, CT finding-
contussion, laceration, heamatoma , Focal neurologic deficit such as
seizure,weakness, speech difficulty, memory, cranial deficit
o Severe – GCS 5-8/15
o Critical GCS <5
 Based on clinical type
o OPEN – fracture of the skull associated with tear of the dura and the
arachinoid resulting in CSF leakage (either to the external enviroment or
through the base of skull, otorrhea, rhinorrhea)

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  Result in intracranial infection which could be generalised
meningitis or focal infections such as subdural empyema, brain
abcess, osteomyelitis of the skull.
 If intracranial air can be seen on the x-ray, then the dura has
been breached too.
o CLOSED – associated with no leakage
 Subpericranial blood clot infection may result in pott’s puffy tumor
o This classification helps to identify who has the likelyhood of developing
infective complication.
 Based on type of injury
o Blunt:
 Acceleration  Decceleration
o Penetrating:
 Gunshot injury

SCALP Laceration
Introduction:
 The most minor type of head trauma
 Scalp is highly vascular  Profuse bleeding
 Major complication is infection
Physical examination:
 The following attributes of the wound should be noted:
o Length of laceration in centimeters
o Depth of laceration:
 Epidermis
 Dermis
 Subcutaneous fat
 Muscle
 Bone
o Shape of laceration:
 Linear  Stellate
 Curvilinear  Corner

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 o Presence of gross contamination or visible foreign bodies
o The presence of skin loss
Investigation:
 Patients with clinical findings that suggest the presence of a foreign body or
bony injury need appropriate imaging:
o Plain radiograph
o Head CT without contrast
Management:
 Direct pressure initially controls the bleeding, allowing close inspection to the
injury
 Simple laceration  Copiously irrigate & close primarily
 Laceration
o Short or a single layer:
 Percutaneous suture
 Laceration
o Long or has multiple arms:
 Debridement and closure in the OR

Skull Fracture
Introduction:
Skull fracture can be:
 Open or Closed
o A closed fracture:
 Is covered by intact skin
 Do not normally require specific treatment.
o An open, or compound fracture
 Associated with disrupted overlying skin
 Require repair of the scalp and operative debridement.
 Depressed or Non-Depressed
o Depressed fracture
 Inner and outer cortices of the skull are disrupted and fragment is
pressed toward the brain.

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  Occur when trauma of significant force drives a segment of the skull
below the level of the adjacent skull
 The sharp edges of the bones can lacerate dura,brain or vessels
 Increased risk of infection, neurologic deficit, late onset epilepsy
 Craniotomy is required to elevate the fracture.
 However, fractures overlying dural venous sinuses require restraint.
Because surgical exploration leads to life threatening hemorrhage
from lacerated sinuse.
o Llinear fracture
 Mostly skull vault fracture is a single fracture that most often
extends through the entire thickness of the calvarium.
 They occur most often in the temporoparietal, frontal, and occipital
regions.
Location:
 Vault
 Across midline…involve sagittal sinus
 Basilar skull fractures
o Anterior skull base facture
o Middle skull base fracture
o Posterior skull base fracture
Physical signs of skull fractures:
 Anterior cranial fossa
o Nasal bleeding
o Orbital haematoma（Racoon eyes)
o Cerebrospinal fluid rhinorrhea
o Cranial nerve injuries, nerves I – VI
 Middle cranial fossa
o Orbital haematoma o Bleeding from the ear
o Cerebrospinal fluid otorrhoea (rare)
o Cranial nerve injuries, nerves VII and VIII
 Posterior cranial fossa
o Bruising over the suboccipital region, which develops after a day or two
(Battle’s sign)

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 o Cranial nerve injuries – nerves IX, X and XI (rare)
Investigation:
 Halo test
o Is simple test used to detect CSF.
o Allow a drop of the fluid to fall on an absorbent surfaceIf blood is mixed
with CSF
 The drop will form a double ring, with a darker center spot
containing blood components surrounded by a light halo of CSF.
 Beta transferrin test
o Carbohydrate-free isoform of transferrin exclusively found in the CSF
Management:
 Skull base fractures requiring intervention include those with an associated
cranial nerve deficit or CSF leak.
 NG tube insertion is contraindicated in skull base fracture
 Indications for craniotomy include:
o Depression greater than the cranial thickness
o Intracranial hematoma o Frontal sinus involvement

Brain Injuries
 TBI is best understood as a complex process that is composed of overlapping
phases, including primary injury and its evolution, secondary injury, and recovery.

• Occurs at the time of insult; direct and indirect impact to the brain parenchyma
• Shearing secondary to motion of the brai relative to the fixed skull and dura (DAI)
Primary Injury • Vascular injury: torn bridging veins, arterial dissections, etc... and it is not amenable to treatment

• The constellationof cellular and biochemical processses that are set in motion by the primary
injury; evolve over the subsequent hours and days
Secondary
Injury • Significant cause of post traumatic neurological disability

• Rehabilitaion of an injured neurons

• Neuroplacticity
Recovery/
Regeneration • Nerve regeneration

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 Table 7.3 Categorization of Head Injury Severity
Minimal Mild Moderate Severe
 GCS = 15 GCS = 14 GCS = 9-13 GCS = 5-8 Critical TBI
 No loss of Conscious- Or Or GCS = 3-4
ness (LOC) GCS = 15 plus either brief LOC ≥ 5 min
 No amnesia LOC (<5 min) or impaired Or
alertness of memory Focal neurologic deficit

Traumatic Brain
Injury

Non-focal
Focal Lesions
Lesions

Contusions/
Epidural Subdural Diffuse Axonal Diffuse Cerebral
intraparenchym
Hematomas Hematomas Injury (DAI) Edema
al Hematomas

1. Concussion:
 Temporary neuronal dysfunction due to non penetrating trauma
 Clinical features include:
o Confusion o Vertigo
o Amnesia – specially o Nausea and vomiting
amnesia of the event is o Vacant state
very common o Delayed verbal
o Loss of consciousness expression
o Headache o Inability concentrating
o Dizziness o Disorientation
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  Normal head CT; there is no apparent parenchymal damage
 Deficit resolve over minutes to hours
 For grading refer to the table below
 Second-impact syndrome:
o Occurs when the brain swells rapidly, and catastrophically, after a person suffers
a second concussion before symptoms from an earlier one have subsided.
Table 7.4: Concussions grading according to Colorado grading system
Grade 1 Head trauma patients with confusion only
Grade 2 Patients with amnesia
Grade 3 Patients who lose consciousness

2. Contusion:
 Bruise of the brain
 It is due to break down of small vessels and extravasation blood into the brain
 The frontal, occipital and temporal lobes are commonly involved
 On CT scan, the contused areas appear bright
 Edema develops around the contusion and creates mass effect
 Coup injury:
o Occurs under the site of impact with an object
 Countercoup injury:
o Occurs on the side opposite to the area that was hit.
o Occurs with decceleration of the brain against the skull
 Coup and contrecoup injuries can occur individually or together.
 The management for contussion is aimed at preventing or reducing swelling

3. Diffuse axonal injury:

 Damage to the axon throughout the brain
 Caused by rotational acceleration then decceleration
 In more severe cases small hemorrhage can be seen clasically over the corpus
callosum, and the dorsolateral midbrain
 On CT scan: loss of grey-white interface, slit ventricles
 High (50%) mortality rate
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 4. Intracranial haematoma:
 Haemorrhage within the cranium occurs in four main sites:
o Extradural
o Subdural
o Subarachnoid
o Intraparenchyma
A. Extradural Haematoma
 Accumulation of blood between the skull and dura
 Results from rupture of arteries, veins or venous sinuses.
 Typically it is associated with tear in the middle meningeal artery due to
temporal bone fracture
 Has classical three stage clinical presentation (seen only 20%).
o Brief loss of conciousness, then Lucid interval followed by sudden
deterioration.
 Uncal herniation from an EDH classically causes ipsilateral third nerve palsy and
contralateral hemiparesis.
 Head CT reveals:
o Blood clot as bright
o Biconvex (lentiform) in shape
o Doesn’t cross the cranial sutures
o Evident skull fracture
o Compression of the brain and midline shift which indicates mass effect
 EDH is neurosugical emergency.
o Require open cranioctomy for evacuation.
 Conservative management for patients with:
o Clot volume <30 cm3
o Maximum thickness <1.5 cm
o GCS score >8 can be managed
B. Subdural Haematoma
 Accumulation of blood between dura and subarachinoid
 It can be acute or chronic
i. Acute subdural haematoma:
 Results from tear of bridging veins crossing
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  Elderly and alcoholics are at high risk because of the atrophied brain
 On head CT it appears as:
o Bright or mixed density
o Crescent (lunate) shape
o May have less distnict border
o Do not cross the midline
 Inducation for open craniotomy for evacuation
o Thickness >1 cm
o Midline shift >5 mm
o GCS drop by two or more points from the time of injury to
hospitalization.
ii. Chronic subdural haematoma:
 It is a collection of blood breakdown products that is at least 2 to 3 weeks old.
 Risk factors:
o Older age
o Excessive alcohol Intake (alcoholics)
o Anticoagulation therapy
 Could occur with minor trauma
o Therefore, patients may not have clear history of trauma
o Patients could present with:
o Headache
o Seizure
o Confusion
o Hemiparessis
o Coma
 On head CT true chronic SDH appears as black as CSF
 Chronic SDH >1cm or any symptomatic SDH needs to be surgically drained via
burr hole
iii. Acute on chronic SDH :
 Small recurrent hemorrhages into the collection (chronic SDH) lead to
expansion of the collection enough to be symptomatic.
 Source of acute hemorrhage may be the vascularized membranes formed in
the matured hematoma.

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 C. Subarachnoid Hemorrhage
 Is bleeding into the space between subarachnoid membrane and pia matter
 It can occur spontaneously (ruptured cerebral aneurysm which is the most
common cause) or due to head trauma
 Signs and symptom include sudden onset severe headache (thunderclap
headache or the worst headache of my life), loss of consciousness, hemiparesis
seziure, nausea or vomiting, meningismus
 It carries poor prognosis if associated with loss of consciousness
D. Intraparenchymal hemorrhage
 Most often associated with hypertensive hemorrhage or arteriovenous
malformations (AVMs)
 Indications for craniotomy include:
o Any clot volume >50 cm3 or a clot volume >20 cm3 with referable
neurologic deterioration (GCS 6–8)
o Associated midline shift >5 mm or basal cistern compression

Management
 Indications in administration of mannitol in E/ R
1. Evidence of intracranial hypertension
2. Evidence of mass effect (focal deficit, e.g. hemiparesis)
3. Sudden deterioration prior to CT (including pupillary dilatation)
4. After CT, if a lesion that is associated with increased ICP is identified
5. After CT, if going to O.R.
6. To assess “salvageability”: in patient with no evidence of brainstem function,
look for return of brainstem reflexes
 Contraindications:
1. Prophylactic administration is not recommended due to its volume-
depleting e ect. Use only for appropriate indications (see above)
2. Hypotension or hypervolemia: hypotension can negatively influence
outcome. Therefore, when intracranial hypertension (IC-HTN) is present,
first utilize sedation and/or paralysis, and CSF drainage. If further measures
are needed, fluid resuscitates the patient before administering mannitol.
Use Hyperventilation in hypovolemic patients until mannitol can be given

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 3. Relative contraindication: mannitol may slightly impede normal coagulation
4. CHF: before causing diuresis, mannitol transiently increases intravascular
volume. Use with caution in CHF, may need to pre-treat with furosemide
(Lasix®): bolus with 0.25–1 gm/kg over <20 min (for average adult: ˜ 350 ml
of 20% solution). Peak occurs in ˜ 20 minutes.

Table 7.5. General Measure (should be utilized routinely)

Step Rationale/Remedy
 Elevate HOB to 30-45°  Decrease ICP by enhancing venous outflow but
also reduces mean carotid pressure (no net
change in CBF)
 Keep neck straight, avoid neck constrictions (tight  Constriction of jugular outflow causes increase
trach tape, tight cervical collar) in ICP

 Avoid arterial hypotension (SPB < 90 mm Hg)  Hypotension reduces CBF

 Normalize intra vascular volume, use pressors if
needed
 Control hypertension if present  Nicardipine if not tachycardic
 Beta blocker if tachycardic
 Avoid over-treatment (hypotension)
 Avoid hypoxia (PaO2 < 60 mm Hg or O2 sat < 90%)  Hypoxia may cause further ischemic brain
injury: maintain airway and adequate
oxygenation
 Ventilate to normocarbia (PaCO2 = 35-40 mm Hg)  Avoid prophylactic hyperventilation (p.872)

 Light sedation e.g. codeine 30-60mg IM q 4hrs  (Same as heavy sedation, see below)
PRN

 Controversial: prophylactic hypothermia.  Hypothermia →↓ CMRO2 efficacy not

 If used hold at target temp > 48hrs rigorously proven

 Unenhanced head CT scan for ICP problems  Rule out surgical condition

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 7.2. Spinal Injury

 Case Discussion…………………………………………460
 Introduction……………………………………………..460
 History……………………..………………………………461
 Physical Examination………..………………………462
 Investigation………………………………….…………464
 Management……………………………………………465
 Complication……………………………………………466
 Discussion of Case……………………………………466

Case Discussion
 A 35-year-old man came to the hospital by ambulance after gunshot injury to the lumbar spine.
The injury occurred when he was involved in war. He was shot with an AR- 15 rifle, and the bullet
went through the victims back. He has lost consciousness after the accident and remained
unconscious for three hours. After the incident, his bilateral lower limbs showed no muscle
contraction with sensory loss. His vitals are PR- 120, BP- 180/90, RR- 30. Examination of the lumbar
spine shows penetrating wound around L2.

Introduction

 Evaluation of a patient with suspected spinal cord injury begins with primary
survey which focuses on assessment of life threatening conditions ABCs
 Suspected spinal injury:
o High speed o Neurologic deficit
o Unconscious o Spinal tenderness
o Multiple injuries
 On secondary survey detailed history and physical examination is obtained.

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 History

 Mechanism and velocity of injury

o Flexion or extension
o Ask about landing
 Onset of symptoms:
o The rapid onset of symptoms after trauma usually makes the
diagnosis obvious
 Duration of symptoms
 Presence of spinal pain
 Any Trauma especially to the head or neck
 Perivous injury such as Car wrecks? Back Problems? Training Regimen?
 Ask patient presence or absence of
o Pain o Loss of bowel/bladder
o Paralysis or paresthesia control
o Sexual dysfunction
 Autonomic symptoms such as:
o Urinary retention o Hypothermia
o Constipation o Hypotension
o Ileus o Bradycardia
 Motor symptoms such as:
o Hemiplegia and/or hemiparesis
o Tetraplegia and/or tetraparesis
 Sensory synptoms such as:
o Lack of sensation at certain level
o Hemisensory loss
 Unusual sensations?
o Pain description:
 Tingling, burning or numbness
o Pain patterns:
 Localized in neck, down arm, into buttocks or feet
o Loss of strength:
 Trouble sitting, standing or sleeping
 Symptoms of neurogenic shock such as:
o Lightheadedness o Diaphoresis
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 o Bradycardia
 Concomitant medical problem such as:
o Rheumatoid arthritis
o Down syndrome
o Neck dystonia or torticollis
o Cogenital neck abnormalities
 Respiratory symptoms – shortness of breath, cough(moist cough)
 Other comorbidities such as COPD, heart failure
 Starts with ABCD

Physical Examination
 Vital signs:
o Vital signs including heart rate, blood pressure, respiratory status, and
temperature require ongoing monitoring.
o Pulse oximetry is important to identify hypoxia.
 Identification of shock:
o Hypotensive shock
 Low BP, tachycardia, cold clammy skin. Mx- resucitation
o Neurogenic shock:
 Low BP, normal heart rate or bradycardia, warm peripheries
 Occurs in acute spinal cord injuries above T6
 Associated neurologic deficit
 Due to disruption of autonomic pathway(sympathetic)
causing decreased vascuar resistance(unopposed vagal
stimulation)
 Diligent search for source of heamorrhage must be completed
before attributing hypotension to neurogenic shock
 Treated with ionotrops, avoid fliud overload
o Spinal shock:
 Initial loss of all neurological function
 Characterized by hypotonia, paralysis, areflexia
 Usually lasts 24hrs after spinal cord injury

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  Chest examination:
o Carefully evaluate respiratory rate, chest wall expansion,
Degree of respiratory dysfunction abdominal wall movement, cough, chest wall and/or
depends on: pulmonary injuries (such as
pneumothorax,hemothorax).
 Preexisting pulmonary
o Inspection: look for poor chest wall expansion, pallor,
comorbidty
cyanosis, paradoxic movement of the chest wall,
 Level of spinal cord injury
increased accessory muscle use.
 Associated chest wall or lung
o Palpation: look for chest wall tenderness, tracheal
injury
deviation (pneumothorax, hemothorax)
o Percussion: check if there is dullness or hyperresonance
o Auscultaion: check if there is decreased air entry, rales, rhonci
 Abdominal examination:
o Follow the steps and do detailed examination.
o Check for seat belt mark  Indicate high energy injury.
 Spine exam:
o Apply the formal spinal log roll.
o Logrolling the patient to systematically examine each spinous process of
the entire axial skeleton from occiput to the sacrum can help identify
and localize injury.
o “ Skeletal level of injury – level of greatest verteberal damage on
radiograph.”
o Inspection – swelling, erythema, wounds - stabbed site or penetrating
o Palpation- tenderness, swelling, palpable step or gap
 Neurological examination - focus on:
o Motor function (out of 5)
o Sensory function-Sensation, position and vibration
o Deep tendon and superficial abdominal reflexes
o Rectal exam
 Anal tone
 Voluntary anal contraction
 Perianal sensation

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 Investigation

Labratory workup
 CBC ->Hg and/or hematocrit serially taken to dectect or monitor blood loss
 Arterial blood gas-> to evaluate adequacy of oxygenation and vantilation
 Serum lactate -> to monitor perfusion status
 Urine analysis -> to detect any associated genitourinary injury
Diagnostic imaging
 Plain radiograph:
o X-ray Guidelines (cervical) AABBCDS

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 o AP and lateral, open mouth
 Adequacy, Alignment
 Bone abnormality, Base of skull
 Cartilage
 Disc space
 Soft tissue
 CT is better for occult fractures and identifying details of fracture.
 CT scanning remains the most sensitive imaging modality in spinal trauma.
 MRI is good to identify those injuries with no bony involvement.
o Posttraumatic disc prolapse
o Hematoma
o Soft tissue and ligament injury
 Flexion-extension films for stability in patient with no deficit.

Management

Primary goal is to prevent secondary injury:

 Immobilization in the initial assessment
 ATLS
 Log roll patients
Principles:
 Spinal alignment:
o Deformity/subluxation/dislocation  Reduction
o Skull tongs – in cervical subluxation/dislocation
o Open reduction and operative realignment with internal fixation
o Closed realignment – using halo brace in cervical
 Spinal column stability: Unstable  Stabilization
o Unstable fracture – moves abnormally when stressed and carries high risk
of further neurologic damage. As well as post traumatic deformity
o Early stablisation is very important as it allows early moblisation of the
patient.

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 o Many spinal injuries can be managed non opertatively using external
support.
o Absolute indication for surgery in spinal trauma is deteriorating
neurologic function
 Neurological deficit: Deficit >Decompression
o Cord can be compressed by bone or disc. Surgical decompression is
necessary.
o Reduce post traumatic syrnix formation

Complications of Spinal Cord Injury

 Pain and spasticity
 Autonomic dysreflexia
 Syringomyelia causes neurological deterioration in 3–5% of cases
 Thromboembolic events occur in 30% of the cases
o 1–2% of patients develop fatal pulmonary embolus
o low molecular heparin is recommended as prophylaxis
 Heterotopic ossification and contractures
 Bedsores  paraplagic  Infection
 Respiratory problem  Muscle atrophy

Discussion of the Case

 Introduction…………………………………………...467
 Classification ………………………………………….467
 Specific Local Spinal Injuries..………………….471
 M

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 Introduction

 Every trauma patient has spinal injury unless proven otherwise

 Trauma could result in bony fracture or ligamentous disruption, often both
 Spinal trauma may occur with or without neurologic injury
 Common causes of physical trauma:
o Motor vehicle accident o Fall down accident
o Gun shot injuries o Different sport activities
 Non traumatic causes
o Infection o Spinal cord tumors
o Ischemia ( Insufficient
blood flow)
 Morphology—fractures, fracture dislocations, SCIWORA, penetrating injury
 Sites Prone to injury  Sites of greatest movement
o Cervical region  55% o Thoracolumbar  15%
o Thoracic region  15%. o Lumbosacral  15%

Classification
 Spinal cord injuries are classified as
o Primary or Secondary
o Temporary (Spinal shock) or Permanent (Immediate it Delayed)
o Complete or Incomplete
 Primary Injury:
o Direct insult to neural component, which occurs at the time of initial
trauma.
o The injury could be directly from:
 Flexion  Rotation or traction
 Extension  Axial loading
 Compression of the cord by fragment bone or disc material.
 Secondary Injury – due to
o Haemorrhage, oedema and ischaemia
o Hypotension, hypoxia or spinal instability
o Persistent compression of the neural elements.

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 o Management of a spinal cord injury must focus on minimizing secondary
injury
 Complete:
o No function below the level of injury
o Sensation and voluntary movement around S4/5 is absent.
o In the acute phase, the classic syndrome of complete spinal cord
transection at the high cervical level consists:
 Respiratory insufficency
 Quadriplegia with upper and lower
extremity areflexia
 Ansthesia below the affected level
 Neurogenic shock (hypothermia and
hypotension without compensatory
tachycardia)
 Loss of rectal and bladder sphincter tone
 Urinary and bowel retention leading to
abdominal distention, ileus and delayed
gastric empyting.
 This constellation of symptoms is called
spinal shock.
o Horner syndrome is also present with higher lesions, ie:
 Ipsilateral ptosis  Anhydrosis
 Miosis
o Lower cervical level injury spares respiratory muscles
o Higher thoracic lesions lead to paraparesis, but autonomic symptoms are
still marked
o Lower thoracic and lumbosacral cord lesions, hypotension is not present
but urinary and bowel retention are.
o The presence of priapism after spinal shock phase indicates the presence
of complete spinal cord injury and is marker for progression to complete
cord injury.
 Incomplete

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 o Is preservation of sensation around S4/5 distribution and voluntary anal
control?
o Includes phenomenon called Sacral sparing.
o Some of incomplete injuries are the following:

1. Anterior Cord Syndrome:

 Injury to the ventral part of the cord or
reduction in bloodflow through anterior spinal
artery.
 Typically observed with anterior spinal artery
infarction, or acute disc herination.
 It results in paralysis with loss of pain and
temprature sensation below the level of the
lesion and relative sparing of touch, vibration
and proprioception (because posterior
columns recieve their primary blood supply
from the posterior spinal arteries).
 Has the worst prognosis.

2. Central Cord Syndrome:

 Injury to the interior gray matter of the cord in
the cervical spine .
 Typically obsreved in syringomyelia, central
canal epedymoma,and trauma.
 It is associated with more significant arm
weakness than leg weakness and variable
sensory deficits
o Most affected sensory modalities are
pain and temprature because the
lateral spinothalamic tract fibers cross
just ventral to the central canal.
o This is aka dissociated sensory loss and
is present in capelike distibution.

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  Taumatic injury is usually caused by severe neck hyperextension.
o It is characterized by initial quadriplegia replaced over minutes by leg
recovery.
o In addition to the distal morethan proximal arm weakness (man in a barrel
syndrome), bladder dysfunction, patch sensory loss below the level of the
lesion, and considerable recovery occur.
 In older patients neck hyperextension in prexisting cervical stenosis.
 In the young patients neck flexion is common cause.
 Most common causes are falls and vehicle accidents
3. Brown Sequard Syndrome:
 Injury to half the cord at a given level with
loss of motor control and proprioception
ipsilaterally and loss of nociception and
thermoception contralaterally.
 Typically it is due to stab injury or
gunshot.
 Carries good prognosis

4. Posterior Cord Syndrome:

 Dorsal columns of spinal cord are affected.
 Mostly seen in chronic myelopathy, but
can also occur in posterior arterial
infarction.
 Below the level of injury, motor function is
preserved.
 Loss of sensory function pressure, strech
and proprioception.
 Usually posterior cord injuries result from
insults like disease or vitamin deficiency
rather than trauma.

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 Table 7.6: American Spinal Injury Association Scale (ASIA) Impairment Scale (AIS)
Grade Criteria
A  Complete cord injury.
 No motor or sensory function is preserved in the sacral segments S4-5.
B  Sensory incomplete.
 Sensory but not motor function is preserved below the neurologic level and includes the
sacral segments (light touch or pin prick at S4-5 or deep anal pressure)
 No motor function is preserved more than three levels below the motor level on either side
of the body.
C  Motor incomplete.
 Motor function is preserved below the neurologic level and more than half of key muscle
functions below the neurologic level of injury have a muscle grade <3 (Grades 0 to 2).
D  Motor incomplete.
 Motor function is preserved below the neurologic level and at least half (half or more) of
key muscle functions below the neurologic level of injury have a muscle grade ≥3.
E  Normal
 Sensation and motor function are graded as normal in all segments and the patient had
prior deficits.

 Patients without an initial spinal cord injury do not receive an AIS grade.

Specific Local Spinal Injuries

 Upper cerical injuries(skull – C1)
o Craniocervical dislocation:
 Usually due to high energy trauma, fatal
 Dislocation can be anterior, posterior or vertical
o Atlantoaxial instability o Occipital condyle fracture
o Jefferson fracture (C1 ring)
 The most common C1 fracture is a burst fracture (Jefferson
fracture)
 Rarely cause a cord injury
 Usually treated in a halo jacket or rigid collar
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 Odontoid fracture (axis C2 fracture)
o It has a 5-10% chance of neurological deficit
 Subaxial cervical spine (C3-C7)
o Common level of subluxation is C5/C6
 Thoracolumbar fractures:
o Caused by a combination of hyperflexion and rotation injury.
o Mostly high energy trauma due to MVA or falls from a height
o 90% of dislocation above T10 level results in complete paraplegia.
 Chance fracture:
o It is a flexion-distraction injury causing failure of the middle and posterior
columns, sometimes with anterior wedging.
o It is caused by violent forward flexion, causing distraction injury to the
posterior elements.
o Typical in lap seat belt hyperflexion with associated abdominal injury.
o Is often unstable and associated with neurologic deficit.

7.3. Peripheral Nerve Injury

 Introduction …………………..………………….……472
 Types of Injury………….……………………….…….473
 Management………….……………….………………474

Introduction

 The peripheral nervous system extends throughout the body and is subject to
injury from a wide variety of trauma.
 Four major mechanisms of injury to peripheral nerves:

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 o Laceration - Knives, passing bullets, or jagged bone fractures may lacerate
nerves.
o Stretched - Adjacent expanding hematomas or dislocated fractures may
stretch nerves.
o Compression - Expanding hematomas, external orthoses such as casts or
braces, or blunt trauma over a superficial nerve may compress or crush
nerves
o Contusion - Shock waves from high velocity bullets may contuse nerves.
 The following four characteristics make a nerve segment more vulnerable:
o Proximity to a joint o Being fixed in position
o Superficial course
o Passage through a confined space

Types of Injury
According to Seddon classification:
 Neurapraxia:
o Temporary failure of nerve functions
without physical axonal disruption.
o No Axon degeneration
o Recovery occurs in hours to months,
often in the 2- to 4-week range.

 Axonotmesis:
o Disruption of axons and myelin.
o The surrounding connective tissues, including endoneurium, are intact.
o The axons degenerate proximally and distally from the area of injury.
o Distal degeneration is known as Wallerian degeneration.
o Axon regeneration within the connective tissue pathways can occur,
leading to restoration of function.
 Axons regenerate at a rate of 1 mm per day.
 Significant functional recovery may occur for up to 18 months.
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 o Scarring at the site of injury from connective tissue reaction can form a
neuroma and interfere with regeneration.
 Neurotmesis:
o Disruption of axons and endoneurial tubes.
o Peripheral collagenous components, such as the epineurium, may or may
not be intact.
o Proximal and distal axonal degeneration occurs.
o Effective axonal regeneration depends on the extent of neuroma
formation and on the degree of persisting anatomic alignment of the
connective tissue structures.

Management

 The sensory and motor deficits should be accurately documented.

 Deficits are usually immediate.
 Progressive deficit suggests expanding hematoma and require early surgical
exploration.
 Clean, sharp injuries  early exploration and reanastomosis.
 Most other peripheral nerve injuries should be observed.
 EMG/NCS studies should be done 3- to weeks post injury if deficits persist.
 Axon segments distal to the site of injury will conduct action potentials normally
until Wallerian degeneration occurs, rendering EMG/NCS before 3 weeks
uninformative.
 Continued observation is indicated if function improves.
 Surgical exploration
o If no functional improvement occurs over 3 months.
 Anastomoses under tension will not heal.
o A nerve graft may be needed to bridge the gap between the proximal and
distal nerve ends.
o The sural nerve often is harvested, as it carries only sensory fibres and
leaves a minor deficit when resected

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 7.4. Brain Tumor
 Case Discussion……………………………………….475
 Introduction……………………………………………475
 History.……………………………………..…………...476
 Physical Examination………………………………479
 Investigation…………………………………………..480
 Differential Diagnosis……………………………..481
 Management………………………………………….481
 Discussion of Case………………………………….483

Case Discussion
 A 57-year-old male patient complains of progressive visual loss of 8 years duration and complete
blindness of 6years duration. He has associated severe bilateral headache which gets worse at
night and vomiting of ingested matter. In addition, he has had fecal and urinary incontinence of 6-
month duration. Other than that he has no history of ABM, trauma and chronic medical illness. On
physical examination, there was cranial nerve deficit of cranial nerve 2, 3, 4 and 6.

Introduction

 Brain tumors may originate from neural elements within the brain, or they may
represent spread of distant cancers.
 Primary brain tumors arise from CNS tissue and account for roughly half of all
cases of intracranial neoplasms.
 The remainders of brain neoplasms are caused by metastatic lesions.
 In adults, two thirds of primary brain tumors arise from structures above the
tentorium (supratentorial), whereas in children, two thirds of brain tumors arise
from structures below the tentorium (infratentorial).
 Gliomas, metastasis, meningiomas, pituitary adenomas, and acoustic neuromas
account for 95% of all brain tumors.

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 History

Manifestations depend on the cause of the symptoms, which may comprise any of the
following:

 Increased intracranial pressure (ICP)

 Direct compression of essential gray or white matter
 Shifting of intracranial contents
 Secondary cerebral ischemia
1) Ask duration of symptoms
 Insidious onset
 An acute episode may occur with bleeding into the tumor, or when an
intraventricular tumor suddenly occludes the third ventricle.
 Patients with a brain tumor may present with acute neurologic changes
mimicking those associated with stroke.
2) Figure out the chief complaint
 Headache, nausea/vomiting, and gait disturbance are the most common
presenting symptoms
3) Elaborate the chief complaint
 Most headaches in patients with brain tumors are nonspecific and resemble
tension-type headaches
 In patients with a history of headache, a change in the headache pattern may
be cause for concern
 New onset of headaches in middle-aged or older patients is worrisome
 The location of the headache reliably indicates the side of the head affected,
but it does not indicate the precise site of the tumor.
 Headaches are more common with posterior fossa tumors
 Headache which worsens early morning
4) Look for Associated Symptoms
 Altered mental status  Weakness
 Ataxia
 Seizures
o May be the earliest expression of a brain tumor

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 o Seizures are common in patients with supratentorial meningioma,
affecting anywhere from 10% to 50% of individuals with these lesions,
and are frequently the presenting symptom.
o A Jacksonian pattern (ie, one in which a focal seizure begins in one
extremity and then progresses until it becomes generalized) is
distinctive in suggesting a focal structural lesion of the cortex.
o Any middle-aged or elderly patients presenting with a first seizure
should have CNS tumor high in the differential diagnosis
 Fixed visual changes  TIA symptoms
 Speech deficits
 Focal sensory abnormalities
5) Look for Manifestations of brain tumor may reflect the tumor site
 Frontal lobe
o Mental status changes, especially memory loss and decreased alertness
o Sleeping longer, appearing preoccupied while awake, and apathy.
 Temporal lobe neoplasms
o Depersonalization o Emotional changes
o Dejavu sensation o Behavioral disturbances
o Auditory/olfactory
affection
 Partial lobe
o Contralateral loss of motor/sensory
o Homonyms hemianopsia
o Apraxia
 Occipital lobe
o Contralateral loss of vision
 An acoustic neuroma
o Intermittent (then o Disequilibrium
progressive) hearing loss o Tinnitus.
 Posterior fossa tumors
o Irritability o Headache
o Unsteadiness o Vomiting
o Ataxia o Progressive obtundation

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  Supratentorial tumors in children
o Seizures o Speech difficulties
o Hemiparesis o Intellectual disturbance
o Visual field cuts
 Infratentorial symptoms
o Increased ICP due to hydrocephalus
 Headache  Ataxia
 Nausea  Vertigo
 Vomiting  Diplopia
 Papiledema
o Local symptoms
 Cerebllar hemisphere- intention tremor, ataxia
 Cerebllar vermis- truncal ataxia, broad based gait
 Brain stem
 Pituitary adenomas
o Non-functional pituitary adenomas remain asymptomatic until they are
large enough to encroach the optic chiasm and disturb normal vision.
o Most hyper secretory pituitary adenomas secrete prolactin,
 Women noting an amenorrhea galactorrhea syndrome.
 Men with complain of headache, visual problems, and
impotence.
6) Asses for risk factors
 Occupation:
o Agricultural: herbicides, pesticides
o Electrical workers: EMF exposure
 Diets: N-nitroso compounds (NOCs)
 Infection: toxoplasma in astrocytoma and meningioma
 Radiation history
 Family history
 Head trauma: for meningioma
7) Rule out differentials
 History of chronic cough or exposure to a known TB patient- TB
 VDRL status and sexual history- neurosyphilis
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  Travel hx and hx of ingestion water or food contaminated with dog feces, Right
upper quadrant pain - hydatid cyst
 History of cough and bloody vomiting, bone pain, breast lump etc- brain
metastasis
 Stroke in acute settings

Physical Examination
 Based on their location, intracranial tumors may produce a focal or generalized
deficit, but signs may be lacking (especially if the tumor is confined to the frontal
lobe) or even falsely localizing.
 Papilledema:
o More prevalent with pediatric brain tumors, reflects an increase in ICP of
several days or longer.
o Not all patients with CNS tumors develop papilledema.
 Diplopia:
o Result from displacement or compression of the sixth cranial nerve at the
base of the brain.
 Parinaud syndrome:
o May occur with pineal tumors
o Impaired upward gaze
 Tumors of the occipital lobe specifically may produce homonymous hemianopia or
partial visual field deficits.
 Anosmia may occur with frontal lobe tumors.
 Brainstem and cerebellar tumors
o Cranial nerve palsies o Nystagmus
o Ataxia, incoordination o Pyramidal signs
o Sensory deficits on one or both sides of the body.
 Tumors in the region of the cerebellopontine angle:
o May impair the functions of the three cranial nerves that traverse this
region: facial, cochlear, and vestibular.
o Acoustic neuromas most commonly originate from the vestibular nerve
(part of cranial nerve VIII).
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 Investigation

Laboratory
 CBC: for anemia and rule out differentials
 Coagulation studies
 Serum electrolyte: to check for Hypercalcemia
 Metabolic studies: SIADH
 Tumor markers
o Human chorionic gonadotropin (hCG)
o Alpha-fetoprotein
o Carcinoembryonic antigen (CEA)
o S-100 protein
Imaging
 Important information to gain from neuro imaging
o Age
o Location
o Multicentricity
o Architecture
o Contrast enhancement
o Bilateral hemisphere involvement
o Interaction with surrounding tissue
 Gadolinium-enhanced magnetic resonance imaging (MRI):
o It is the preferred modality because of its resolution and enhancement
with contrast agents.
 Head and spine computed tomography (CT):
o If MRI cannot be performed (e.g., in patients with metallic implants,
embedded devices, or claustrophobia)
o It cannot adequately assess lesions in the posterior fossa and spine.
o White areas = areas that absorb or “attenuate” the passage of x-ray beam
(acute hematoma, bone, calcium = hyperdense/ attenuating)
o Black areas = areas that do not absorb or “attenuate” the passage of x-ray
beam (fat, air, CSF, edema = hypodense/ attenuating)

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 Differential Diagnosis

Table 7.7: Differentials of CNS Tumors

Age (<3 years) 3-15 15-65 >65
 Medulloblastoma  Pilocytic astrocytoma  Glioblastoma  Metastatic
carcinoma
 Polycystic  Medulloblastoma  Anaplastic  Glioblastoma
astrocytoma astrocytoma
 Ependymoma  Ependymoma  Astrocytoma  Anaplastic
astrocytoma
 Choroid plexus  Astrocytoma  Meningioma  Meningioma
tumors
 Teratoma  Choroid plexus tumors  Pituitary tumors  Acoustic
schwannoma

WHO classification of CNS tumors:

1. Diffuse astrocytic and oligodendroglial tumors
2. Other astrocytic tumors
3. Ependymal tumors
4. Other gliomas
5. Choroid plexus tumors
6. Neuronal and mixed neuronal tumors
7. Tumors of pineal region
8. Embryonal tumors
9. Tumors of cranial and paraspinal nerves

Management
 Principles:
o Careful history, physical o Chemotherapy
and investigation o Radiotherapy
o steroids o Surgery
o Mannitol

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Craniotomy for supratentorial tumors
 Position: (depends on location of tumor)
 Pre-op embolization (by neuroendovascular interventionalist) for some vascular
tumors including some meningiomas
 Equipment:
o Microscope o Image guidance system
o Ultrasonic aspirator
 Blood availability: type and cross match
 Post-op: ICU
 Consent
o Procedure: surgery through the skull to remove as much of the tumor as is
safely possible
o Alternatives: nonsurgical management, radiation therapy for some tumors
o Complications: usual craniotomy complications plus inability to remove all
of the tumor

Craniotomy for infratentorial tumors:

 Retro mastoid surgery for vestibular schwannomas
 Position: (typically either prone or park bench, depending on tumor type/location
and surgeon preference)
 Pre-op embolization (by neuroendovascular interventionalist) for some vascular
tumors such as hemangioblastoma
 Equipment:
o Microscope o Image guidance system
o Ultrasonic aspirator (optional)
 Blood availability: type and cross 2 U PRBC
 Post-op: ICU
 Consent
o Procedure: surgery through the skull to remove as much of the tumor as is
safely possible
o Alternatives: nonsurgical management, radiation therapy for some tumors
o Complications: usual craniotomy complications plus inability to remove all
of the tumor
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  Consent
o Procedure: surgery through the skull remove as much of the tumor as is
safely possible
o Alternatives: nonsurgical management, radiation therapy for some tumors
o Complications: usual craniotomy complications plus inability to remove all
of the tumor, hydrocephalus, CSF leak
Imaging studies post-surgery
 Non-contrast CT scan within 6–12 hours of surgery
o To assess for acute complications (primarily blood – within brain or
epidural or subdural hematoma, amount of pneumocephalus,
hydrocephalus...).
 Post-op brain CT or MRI with out and with contrast
o Within 2–3 days, or should be delayed at least ≈ 30 days.
o To assess the extent of tumor removal,

Discussion of the Commonest Tumors

1. Astrocytoma:
• Astrocytic tumors are the most common primary
intra-axial brain tumor.
• The best-established causes for brain tumors are
syndromic (familial diseases…) and post-radiation
therapy
• The major cause of morbidity with low-grade
astrocytomas is dedifferentiation to a more
malignant grade.
• GBM is The most common primary brain tumor
• It is also the most malignant astrocytoma

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2. Meningioma:
• Meningiomas are the most common primary
intracranial tumors. They are usually slow
growing, extra-axial tumor, circumscribed (non-
infiltrating), benign lesions.
• Arise from arachnoid cap cells (not dura)
o Most commonly located along falx,
convexity, or sphenoid bone
o Most are cured if completely removed

3. Pituitary tumors:
• Most are benign adenomas arising from the
anterior pituitary (adenohypophysis)
• Presentation: most commonly present due to
hormonal effects (includes: hyperprolactinemia,
Cushing’s syndrome, acromegaly…)
• Mass effect (most commonly: bitemporal
hemianopsia from compression of optic chiasm)
• As an incidental finding, or infrequently with pituitary apoplexy
• Prolactinoma is the only type for which medical therapy (DA agonists) may be the
primary treatment.
• For other tumor types, options primarily consist of surgery (transsphenoidal or
transcranial), or XRT
• Most primary pituitary tumors are benign adenomas which arise from the
anterior pituitary gland
• Microadenoma: A pituitar y tumor < 1 cm diameter.
• Macroadenomas: Tumors >1 cm diameter.
4. Metastasis to brain:
• Those commonly involving brain include:
I. Lung cancer: small-cell IV. Renal cell
II. Breast V. Lymphoma
III. Melanoma VI. GI

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 7.5. Neural Tube Defects (NTDs)
 Case Discussion……………………………….…….485
 Introduction…………………………………….…….485
 History…………………….……………………….…..486
 Physical Examination………………….…….……487
 Investigation……………………………………….…488
 Management………………………………………….489
 Complications………………………………………..489
 Discussion of Case………………………………….490

Case Discussion

 A case of 13 weeks period of gestation with meningomeyelocele came for termination of

pregnancy. The diagnosis was confirmed by ultrasonography. History suggests that patient had
previous neural tube defect baby and non-compliance to folic acid supplements.

Introduction
 Neural tube defects (NTDs) are congenital malformations of the neural tube,
caused by failure of the neural tube to close at the end of the fourth week after
conception. Neural tube defects are typical examples of a multifactorial
congenital malformation.
 The neural tube is the structure from which the skull, brain, spinal cord and
nerves will develop, as well as the spinal column (made up of vertebrae).
 If the neural tube fails to close at the head end, the defect results in
anencephaly or an encephalocoele. If it fails to close lower down along the
spine, the result is spina bifida.
 There are several anatomic types of NTDs, which affect either the spine or
cranium. They can be classified as open (neural tissue exposed) or closed
(neural tissue not exposed). Open NTDs often involve both the spine and
cranium, while closed NTDs are usually localized and confined to the spine.

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 History

1) Asses for risk factors

 Genetic factors
o Chromosomal abnormalities (trisomy 13, 18, 21) are also associated with
NTDs.
o Concordance between monozygotic twins is higher than dizygotic twins.
 Environmental factors
o Low socioeconomic class
o Maternal diabetes
o Maternal age
o Zinc and folate deficiencies
o Maternal alcohol and cocaine abuse during pregnancy
o Maternal use of valproate
o Intrauterine hyperthermia
o Family history of NTDs and a previous pregnancy affected with NTDs
2) Look for Common clinical presentation
 An obvious abnormality along the spine- The most common presentation of a
closed NTD
o A fluid-filled cystic mass
o Area of hypopigmentation or hyperpigmentation
o Cutis aplasia
o Congenital dermal sinus
o Capillary telangiectasia/hemangioma
o Hairy patch (hypertrichosis)
o Skin appendages
o Asymmetrical gluteal cleft.
N.B: A closed NTD can present without a cutaneous marker.
 Asymmetry of the legs and/or feet
o One calf can be thinner, with a smaller foot on the same side, higher
arch, and hammering or clawing of the toes.
 Progressive spinal deformities such as scoliosis.
 Low back pain also can occur, sometimes without neurological deficit.
o Pain is more common in older children or adolescents.
 Low sacral region

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 o Bowel & Bladder incontinence
o Loss of sensation in perianal region
o No motor weakness
 Mid lumbar region –
o weakness of lower limbs
o loss of sensation
 Sudden onset of pain, motor and sensory loss, and bladder dysfunction after an
acute trauma (e.g., fall, motor vehicle accident, placement in lithotomy
position).
o May be related to tethering of the cord (the distal end of the spinal cord
is fixed in position).
 Ask for symptoms of CNS infections
o A patient with a dermal sinus also can present with bacterial meningitis
or spinal abscess.
o Neuro-enteric or dermoid cysts also can present with repeated bouts of
aseptic meningitis due to leaking of the contents into the spinal
subarachnoid space.
 Ask for symptoms of spinal cord compression
o Seen in a patient with a closed NTD such as a congenital dermal sinus
with an intraspinal dermoid cyst or a neuro-enteric cyst
 Ask for medical co morbidities
o The prevalence depends on the level and severity of the lesion
o Urologic abnormalities (i.e., UTI and nephrolithiasis) are the most
common issues among adults with NTDs.
o Scoliosis, pain, epilepsy, and pressure ulcers are also often reported in
adult patients with myelomeningocele.

Physical Examination
1) A complete neurological assessment of the newborn with an open NTD
 Measurement of head circumference
 Assessment of general vigor (especially cry and sucking)

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  Upper extremity motor function, anal sphincter, and urinary stream, as well as
thorough motor and sensory examination of the lower extremities and trunk.
o Observation of muscle bulk
o Spontaneous active movements
o Movements in response to stimulation
o Assessment of muscle tone by palpation.
o Extent of muscle weakness and paralysis
o Deep tendon reflexes and anocutaneous reflex (anal wink)
2) Inspect the spine for:
 The size and site of the lesion: whether it is leaking CSF.
 The shape of the defect
 Health and laxity of the surrounding skin and soft tissue
 The presence of early spinal deformity (eg, kyphosis)
3) Attention to the following features
 Level of the spinal cord neurologic deficit
 Associated SC anomalies, such as split cord malformation
 Signs of hydrocephalus
 Evidence of brainstem compression (from the Chiari II)
4) Evaluation for associated abnormalities
 Clubfeet  Kyphosis
 Flexion or extension contractures of hips, knees, & ankles
 Other congenital abnormalities

Investigation
N.B. postnatal diagnosis is usually done through clinical examination.
 Maternal serum alpha-fetoprotein
o Abnormal MSAFP tests are typically followed by an ultrasound exam to
assess for possible NTD, confirm gestational age, fetal viability, number of
fetuses, and so on.
 Aminocentesis
 Ultrasonography
o Used antenatally for neural tube defect (NTD) screening.

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 MRI
o Study of choice for imaging neural tissue and for identifying contents of
the defect in the newborn
o This allows for visualization of associated anomalies, both intraspinal and
intracranial
o Rarely used
 CT scan
o To determine the presence or absence of hydrocephalus or other
intracranial anomalies
o Usually reserved for adults or older kids with spina bifida occulta due to its
high radiation.

Management
 Medical management:
o keep the newborn warm
o Cover the defect with a sterile wet saline dressing.
o Antibiotics for meningitis & UTI
o Recurrent catheterization o Anticonvulsants
 Surgical management:
o Fetal surgery
o The newborn with an open NTD should undergo prompt closure of the
defect.
o Hydrocephalus- should have a ventriculoperitoneal shunt placed
o Symptomatic Chiari malformations: should undergo suboccipital
craniotomy and decompression of the posterior fossa and tonsils.
o Syrinx- needs a laminectomy and placement of a syringosubarachnoid stent
to divert the CSF out of the central canal.

Complications
 Infection
 Bladder dysfunctions

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 Discussion of the Case

 Classification……………………………………………490
 Anencephaly……………………………………………490
 Encephalocoele……………………………………....491
 Spina Bifida……………………………………………..491

Classification

 Primary neurulation defects :

o 95% of all NTD
o Primary failure of closure/disruption of NT b/n 18-28 days.
 Cranirachischisis  Encephalocele
 Myelomeningocele  Anencephalus
 Secondary (post neurulation ) defects
o 5% of all NTD.
o Abnormal development of lower sacral segment during secondary
neurulation
o Skin is usually intact
o Involves lumbo-sacral region

Anencephaly
 Anencephaly (no brain) is the most
serious of all neural tube defects and
always results in stillbirth or early
neonatal death.
 The top (vault) of the skull is absent,
exposing the brain, which is malformed.
 The cerebral hemispheres do not
develop with anencephaly.

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 Encephalocoele

 An encephalocoele is a failure of closure in the

midline of the skull anywhere from a position
between the eyes (frontal area) to the back of
the skull (occipital area).
 The brain coverings (the meninges), with or
without brain tissue, protrude through the skull
defect into a membranous sac which is covered
by skin. Herniation of meninges without brain
tissue is referred to as a meningocele.
 Most patients with encephaloceles and
meningoceles have impaired cognitive
development
 The most common site of an
encephalocoele is convexity of the skull.
 Encephalocoeles are called closed neural
tube defects because neural tissue is not
exposed as the defect is covered by skin.
 Treatment involves excision of the
herniated tissue and closure of the defect.

Spina Bifida

 Spina bifida (split spine) is an opening in the spinal column due to failure of
closure of the bony vertebral arches. Spina bifida may occur anywhere down the
spinal column. There are three forms of spina bifida:
o Spina bifida with Meningomyelocoele (spina bifida cystica): this is the
most severe form
o Spina bifida with Meningocoele (spina bifida aperta): a less severe than
meningomyelocoele.
o Spina bifida occulta. This is the least severe form as it only involves the
bony spine.
A) Spina bifida with Meningomyelocoele

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  It is an open neural tube defects
 Neural tissue (spinal cord and nerves) and the
coverings of the spinal cord (the meninges) bulge
through the opening.
o The skin over this defect does not close, but
the defect may be covered by a thin
membrane which tears easily.
o The neural tissue that bulges through the bony
defect is usually damaged, resulting in nerve
abnormalities below the level of the defect.
 Myelomeningocele patients often have hydrocephalus and a Chiari II
malformation, an abnormal downward herniation of the cerebellum and brain
stem through the foramen magnum
 Common findings include weakness and atrophy of the lower extremities, gait
disturbance, urinary incontinence, constipation, and deformities of the foot.
o Myelomeningoceles arising from the high lumbar cord usually cause
total paralysis and incontinence, while those arising from the sacral
cord may have only clawing of the foot and partial urinary function
loss
B) Spina bifida with Meningocoele
 Only the coverings of the spinal cord (the meninges)
protrude through the defect, forming a sac which is
filled with cerebrospinal fluid (CSF).
 The spinal cord and nerves are normal and do not
bulge through the opening.
o There is no associated spinal cord or nerve
damage.
o The meningocoele usually is covered on the
outside by skin (closed neural tube defect).

C) Spina bifida occulta

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  Spina bifida occulta is congenital absence of posterior
vertebral
o The spinous process is always missing
o The laminae may be missing to various
degrees, but the underlying neural tissues are
not involved elements
 Spina bifida occulta is a closed neural tube defect.
 Spina bifida occulta is found in 25% of the general
population
 It is asymptomatic unless associated with other developmental abnormalities
 The spinal cord and meninges are normal and do not
protrude through the defect.
o The defect may be covered by an overlying
abnormality such as a midline patch of hair, a
lipoma or a dimple.

7.6. Hydrocephalus
 Case Discussion………………………………………494
 Introduction……………………………………………494
 Clinical Manifestations…………………………...495
 Investigation…………………………………………..496
 Management………………………………………….496
 Complications………………………………………..496
 Discussion of Case………………………………….497

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 Case Discussion

 Baby Aster is delivered by caesarean section and transferred to the pediatric intensive care unit
(PICU). On admission to the nursery: Temperature: 37° C (98.6° F) Pulse: 144 beats/minute,
Respirations: 40 breaths/minute. She has bulging fontanels and a high-pitched cry. Her head
circumference is 42 cm and her chest circumference is 35 cm. In the lumbar region of her spine,
the she has a sac-like projection.

Introduction

 It is an excess CSF in the brain that results in enlarged ventricles is known as

hydrocephalus.
 The total CSF volume is normally about 150mL. Production from the walls of the
ventricles and the choroid plexus is about 20 mL per hour.

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 Clinical Manifestation

Table 7.8: Symptoms of Hydrocephalus

Infants Toddler and older child Young and Middle- aged Older Adults
adults
- An unusually large - Headache - Headache - Loss of bladder
head control or a
- A bulging or tense soft frequent urge to
spot (fontanel) on the urinate
top of the head
- Poor growth - Blurred or double - Lethargy - Memory loss
vision
- Vomiting - Eyes fixed downward - Loss of coordination or - Poor coordination
- Poor feeding (sunsetting of eyes) balance or balance (a
shuffling gait)
- Sleepiness - Abnormal enlargement - Loss of bladder control - Progressive loss of
of a toddler's head or a frequent urge to other thinking or
urinate reasoning skills
- Deficits in muscle tone - Sleepiness or lethargy - Impaired vision
and strength
- Poor responsiveness to - Poor appetite, Nausea - Decline in memory,
touch or vomiting concentration and
other thinking skills that
may affect job
performance
- Irritability - Unstable balance

- Seizures - Poor coordination

- Eyes fixed downward - Seizures

(sunsetting of the - Urinary incontinence
eyes)

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 Investigation

 CT is the first line of investigation

o Ballooning of frontal horns of lateral ventricle ("Mickay Mouse"
Ventricles)
o For communicating hydrocephalus, LP can confirm raised CSF pressure and relieve
it temporarily

Management
 Medical Management: Diuretics
 Surgical management:
o Surgery Principle
 To reduce the CSF production
 To by-pass the blockage to normal CSF flow (ventriculoperitoneal [VP]).
 To drain CSF externally
 To drain CSF to another absorptive viscus
 To treat the cause (remove the obstruction)
o Surgery Contraindication (Lober’s criteria)
 Paraplegia  Congenital anomaly
 Kyphoscoliosis  Intracranial birth injury
 Gross hydrocephalus  Ventriculitis

Complications Following Treatment

 Infection
 Obstruction
 Acute hemorrhages
 Hematoma
 Shunt malfunction & over drainage resulting in low pressure symptoms
 Disconnections
 Seizure  5.5% in the 1st year & drops to 1.1% in the 3rd yr
 Erosion of skin (in infants) and perforation of viscus

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 Discussion of the Case

 Classification……………………………………………….497
 Communicating Hydrocephalus…………….......497
 Non-communicating Hydrocephalus ……….…497
 Congenital Hydrocephalus………………………....498
 Acquired Hydrocephalus……………………………..498

Classification
 Using two methods
o Communicating (non-obstructive) vs. Non-communicating (obstructive)
o Congenital vs. Acquired

Communicating Hydrocephalus
 Obstruction at the level of the arachnoid granulations
constitutes communicating hydrocephalus
 It is caused by:
o Meningitis
o Subarachnoid hemorrhage- may cause
transient hydrocephalus

Non-communicating Hydrocephalus
 It is obstruction of CSF pathways
 The ventricles proximal to the obstruction dilate, while
those distal to the obstruction remain normal in size.
 It can be caused by:
o Intracranial cysts with no evidence of bleed at diagnosis

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 o Triventricular hydrocephalus due to radiologically apparent aqueductal stenosis
o Membranous obstruction of aqueduct
o Asymmetrical hydrocephalus, due to atresia of the foramen of Monro
o Obstruction of fourth ventricle outlets
 They may present precipitously and require urgent shunting to prevent herniation.

Congenital Hydrocephalus
 Congenital is caused by:
o Stenosis of the cerebral aqueduct
o Chiari malformation
o Myelomeningocele
o Intrauterine infections
o Neural tube defects—MM, Chari-malformation
o Isolated hydrocephalus: caused by aqueductal
stenosis
o Dandy-Walker: caused by atresia of the foramina of
Luschka and Magendie
o Choroid plexus papilloma or carcinoma

Acquired Hydrocephalus
 Acquired is caused by:
o Infections
o Post-hemorrhagic hydrocephalus: hemorrhage
into the subarachnoid space or, less commonly,
into the ventricular system, by ruptured
aneurysms, arteriovenous malformations,
trauma, or systemic bleeding disorders.
o Secondary to masses & spinal tumors
o Post op
o Low pressure hydrocephalus

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 7.7. Video QRs

Neurologic Examination

Dermatome and Myotome Dance

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 Part 8: Orthopedics

Long Case Discussion

 Content By:
 Matyas Wondwossen
 Nanati Jemal 8.1. Fracture ………………………………………………501
 Edited By:
 Samuel Mesfin 8.2. Bone Tumor…………………………………………510
 Reviewed By:
 Dr. Matiyas Seid
(Orthopedic Surgeon)

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 8.1. Fracture
 Case Discussion……………………………………………………501
 Clinical Manifestation………………………….………………501
 Investigation……………………………………………………….504
 Discussion of the Case………………………………………...504
 Principles of Management…………………………………..508
 Complications……………………………………………………..509

Case Discussion

 A 23-year-old man is brought into the emergency department by ambulance after coming
off his motorcycle. He was travelling at approximately 45 mph and hit a stationary car.
There is no other history available and he is in significant pain.

Clinical Manifestation

History:
N.B: For patients without apparent life-threatening injuries who appear appropriate for
office management, assessment begins with a focused history. Analgesia is sometimes
needed before a history can be obtained.
 Age
o Both extremes of age have increased tendency for fracture
o Younger age is important for bone healing
 Sex
o Menopausal females at risk of fracture
o Males more prone to accidents and are risk takers
 Assess for chief complaints
o Pain, Swelling, Bruising, Loss of function and deformity

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 o Duration and site of the injury
 Asses for risk factors
o Injuries
o occupation: contraction workers, drivers, high risk sport athletes, ballerinas
o Other Comorbidities: diabetes mellitus, arteriovascular disease, anemia,
hypothyroidism, malnutrition (eg, vitamin C or D deficiencies, inadequate
protein intake),
o Excessive chronic alcohol: intoxication clues to severe due to loss of
protective reflexes.
o Specific medications may also impair fracture healing: nonsteroidal anti-
inflammatory drugs, glucocorticoids, and certain antibiotics (eg,
ciprofloxacin)
 Describe the mechanism and degree of injury in trauma
o Road traffic accident
 Ask if the patient was restrained: airbag + seatbelt
 Was the patient in the front seat or back?
 Was the patient a passenger or pedestrian?
 death in passengers/pedestrians, severe casualties, burn associated
with the accident, rolled car
o Gunshot
 Nature of the incident
 Accident or assault
 Type of gun
 distance
o Falling down accident
 height
 landing condition
 Why?
 Accident at work  Suicide
 Intoxication  pushed
 Look for associated injuries: Did you injure any other part of your body?
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 o Shortness of breath
o Blood in the urine
o Altered sensibility
 Significant past injuries or surgeries in the affected area
 Family history
 Last meal (in case an injury requiring urgent surgery is identified) and medical
care given prior to coming to the hospital

Physical examination
 Follow trauma protocol and Do ABCDE
 General appearance, level of awareness, GCS
 Check vital signs
 Evaluate overlying skin: intact skin, bleeding, bruising,
 Look, feel and move for signs of fracture
o Visible or palpable deformity
o Local swelling
o Visible bruising (ecchymosis) from escape of blood from the fracture
surfaces and periosteum
o Marked local tenderness over bone
o Marked impairment of function
 Is there a wound communicating with the fracture? -skin integrity
 Is there any impairment of circulation distal to the fracture? -color, warmth,
pulse, capillary return, nerve conductivity
 Is there any evidence of nerve injury? Is there any evidence of visceral injury?

N.B: If the symptoms include weakness or incoordination or a change in sensibility, or if

they point to any disorder of the neck or back, a complete neurological examination of the
related part is mandatory.

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 Investigation

 Clinical evidence of fracture must always be confirmed or refuted by radiographic

examination.
o X-ray
o Computed tomography (CT)
o Magnetic resonance imaging (MRI)
o Doppler u/s or arteriography: to look for impairment of circulation distal to
injury site
Table 8.1: Common radiographic views for identifying fractures by location
Anatomic region Plain radiograph fracture views
Wrist  AP, lateral
 Oblique: fracture suspected but AP and lateral negative
 Scaphoid: scaphoid fracture suspected
Elbow  AP, lateral, oblique
Shoulder  AP, scapular Y, axillary
Knee  AP, lateral, oblique, (internal and external rotated)
 Sunrise (axial, tangential): patellar injury
Foot  AP, lateral
 Oblique: if fracture seen on AP or lateral
Tibia, femur, forearm  AP, lateral
Ankle  AP, lateral and mortise

Discussion of the Case

 Introduction……………………..……………………..505
 Stress Fracture…………………………………………505
 Pathologic Fracture………………………………….506
 Open Fracture……………………………………….…507

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 Introduction

 Fracture is a complete or incomplete crack in the

continuity of the bone. We can classify fracture
based on etiology, radiology and clinical diagnosis.
 Based on etiology-
o Sudden injury/Traumatic fracture
o Fatigue/stress fracture,
o Pathological fracture
 Based on radiology
o Transverse, Oblique, Spiral, Comminuted, Segmental, Depressed, Impacted,
Greenstick, Avulsion
 Based on clinical diagnosis
o Open o Closed

Stress Fracture
 Stress fractures are due to loads that stress (either
compress or stretch) a bone but would not individually be
expected to cause it to break.

 Stress fractures may be the result of:

o A small number of repetitions with a relatively large
load (eg, a military recruit marching for several miles
with a heavy backpack)
o A large number of repetitions with a usual load (eg, an athlete training for a
long-distance race), or some intermediate combination of increased load
and number of repetitions.
 The great difference between a fatigue and ordinary ‘traumatic’ fracture is there is
no single causative injury in cases of fatigue fracture.
 It is important to remember that radiologically nothing abnormal may be seen at
first: it is only 2-4wks that radiographic changes appear.

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  Even then the fracture itself may show only as a faint hairline crack, usually more or
less transverse in direction: only rarely is there any displacement of the fragments.
 More striking than the fracture is the zone of callus that surrounds it.
 Faint—seen only as a haze near the bone—this new bone may eventually form a
dense fusiform mass about the site of fracture.

Pathologic Fracture
 It occurs through a bone that is already weakened
by disease.
 Often the bone gives way from trivial violence, or
even spontaneously.
 In many cases the patient, when directly
questioned, will admit to having suffered pain or
discomfort in the region of the affected bone for
some time before fracture.
Causes
 Infections:
o Pyogenic osteomyelitis (usually in chronic form)
 Tumors:
 Miscellaneous: Simple bone cyst
 Congenital disorders:
o Osteogenesis imperfect (fragilitas ossium)
 Diffuse rarefaction of bone:
o Senile osteoporosis o Infantile rickets
o Cushing syndrome
 Disseminated tumors:
o Multiple myeloma
 Miscellaneous:
o Paget’s disease o Gaucher’s disease

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 Open Fracture

 Fractures that are in contact with the outside environment

(ie, open to air)
 Represent orthopedic emergencies requiring immediate
irrigation and debridement in the operating room and
treatment with intravenous antibiotics.
 In addition to infection, open fractures are associated with:
o Higher rates of compartment syndrome
o Neurovascular injury
o Other soft tissue injuries compared with closed
fractures.
 The severity of open fractures may be classified using the following system
o Type 1 – Puncture wound (≤1 cm) with minimal contamination and minimal
muscle injury.
o Type 2 – Laceration (>1 cm) with moderate soft tissue damage.
o Type 3 – Extensive soft tissue damage with severe crush injury of muscle and
massive contamination, including comminuted bone fragments (type 3A),
periosteal stripping (type 3B), or arterial injury requiring repair (type 3C).

Table 8.2: Unique fracture terms

Finger
Mallet finger  Rapture of distal extensor tendon that may involve avulsion
fracture of distal phalanx
Jersey finger  Rapture of distal flexor tendon that may involve avulsion
fracture of distal phalanx
Boxer’s fracture  Fracture of distal fifth metacarpal at the metaphyseal-
diaphyseal junction with apex dorsal angulation
Wrist
Colles fracture  Distal radius fracture with apex palmar angulation
Smith’s fracture  Distal radius fracture with apex dorsal angulation
Styloids fracture  Fracture of the distal radius or distal ulna styloid process

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 Hip
Femoral neck  Proximal femur fracture between the trochanters and the
fracture femoral head
Interochanteric  Proximal femur fracture extending between the greater and
fracture lesser trochanters
Foot
Jones fracture  Acute fracture in the metaphyseal-diaphyseal area of the
proximal 5th meta-tarsal (often confused with avulsion or stress
fractures)

Principles of Management

Initial management
A) Airway and cervical position
B) Breathing
C) Circulation
D) Disability (neurological, GCS)
E) Exposure
F) Open Fracture

Treating uncomplicated closed Fracture

 Reduction
 Immobilization
 Rehabilitation
o To preserve function so far as possible while the fracture is uniting; and
o To restore function to normal when the fracture is united.
III) Treating complicated open fractures
 Wound and, whenever necessary, remove all dead and devitalized tissue and all
extraneous material, leaving healthy well-vascularized tissues that are able to

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 ward off infection from the organisms that must inevitably remain even after the
most meticulous cleansing.
 Supplementary treatment
 Broad-spectrum antibiotic, such 3rd generation cephalosporin
 Prophylaxis against tetanus
 Precautions: - in severe open fractures, with perhaps considerable loss of blood,
there is a greater liability to shock, and appropriate measures of resuscitation are
often required

Complications

 Life-threatening Conditions:
o Femur fractures that disrupt the femoral artery or its branches are potentially
fatal
o Pelvic fractures can damage pelvic arteries or veins causing life-threatening
hemorrhage.
o Hip fractures, particularly in the elderly, may prevent ambulation, resulting in
potentially life-threatening complications, such as pneumonia,
thromboembolic disease, and possibly rhabdomyolysis.
o Patients with multiple rib fractures are at substantial risk for pulmonary
contusion and related complications.
 Arterial injury
 Nerve injury
 Compartment syndrome
 Thromboembolic disease
 Osteomyelitis
 Nonunion
o Incomplete healing of a fracture where the cortices of the bone fragments do
not reconnect
 Malunion
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 o When a fracture heals with a deformity (eg, angulation, rotation, incongruent
joint surface)
 Complex regional pain syndrome:
o Complex Regional Pain Syndrome (CRPS), also known as Reflex Sympathetic
Dystrophy (RSD)
o It is a complex disorder of the extremities characterized by localized pain,
swelling, limited range of motion, vasomotor instability, skin changes, and
bone demineralization.
 Fat embolism syndrome:
o FES typically manifests 24 to 72 hours after injury with dyspnea, tachypnea,
and hypoxemia.
o Neurologic abnormalities and a petechial rash may be present.
o Severe respiratory distress and death can occur.
 Post Traumatic Arthritis

8.2. Bone Tumor

 Case Discussion……………………………………………..511
 Clinical Manifestation…………………………………….511
 Investigation………………………………………………….512
 Differential Diagnosis…………………………………….516
 Discussion of the Case………..…………………………517
 Principles of Management…………………………….520

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 Case Discussion

 A 14-year-old male patient presented with right knee swelling of 03 month duration. The
swelling was initially small in size, later it increase to attend the current size. Associated
with the swelling he has also intermittent Right knee pain for the past 10 weeks, the pain
and swelling has grown more regular in the last week. Further interview reveals that the
patient plays on a youth soccer team, and his knee feels especially painful during practice.
His parents attributed the symptoms to “growing pains,” as the patient’s height and
weight have been increasing appropriately for his age, and he has had no known skeletal
diseases—nor any serious conditions—prior to onset of the pain, no compliant in other
system. On Physical examination, Vital signs were normal on MSK examination there is
8x6 cm, palpable mass on the anterior aspect of the right proximal tibia. Which is tender
to palpation, mobile, not adherent to the adjacent structure.

Clinical Manifestation

History
 Age: you can narrow down your differentials based on age
 Chief complaint
o Localized pain or swelling of a few weeks' or months' duration
 Asymptomatic in most benign tumors
 Mild pain which is aggravated by exercise and is often worse at night:
malignant tumors
 Ask for associated bleeding
o Thyroid and kidney metastasis is highly vascular
 Ask for signs of infection
o Fever
o Tenderness
o discharge
 Rule out Malignant metastasis to Bone
o Ask if there is breast lump, discharge or any prior breast cancer diagnoses
o Ask for anterior neck swelling, heat or cold intolerance- thyroid cancer

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 Investigation

o Shortness of breath, hemoptysis, chest pain-lung cancer

o Hematuria, urinary complaints- prostate and Renal cancer
 Ask history of fracture
 Ask history of Trauma
o Minor trauma, may be the initiating event that calls attention to a benign or
malignant bone tumor.
o Malignancy can cause bone fragility which causes trivial trauma
 Ask history of radiation exposure
 Chronic disease
 Red Flag signs to look out for
o Night pain or non-mechanical pain
o Unintentional weight loss
o Thoracic back pain
o Age (<20 or >50 years old)
o Previous history of malignancy
Physical examination:
 Follow look, feel and move principle
o Characterize the mass:
 Size  Nodularity
 Mobility  Temperature
 Fixity  Surface
 Tenderness
o Neurovascular affection
o Look for joint involvement- loss of motion, effusion
 Examine the spine for stiffness and scoliosis
 Complete the physical examination with special attention to:
o Breast
o Lung
o Thyroid
o Prostate
 CBC:
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 o Haemoglobin o Sodium
o Mean cell volume (MCV) o Potassium
o White cell count (WCC) o Urea
o Platelets o Creatinine
o Erythrocyte Sedimentation o C-reactive protein
Rate (ESR)
 Plain radiograph: first diagnostic test and it will allow us to identify:
 Anatomy  Bone destruction
 Border of the lesion  Matrix formation
 Number of lesions  Periosteal reaction

How to describe bone lesions on radiographs

 Bone & Site:
1. What is included in radiograph (what bone, what joint, side, view)
2. Epiphysis, metaphysis, or diaphysis
3. Mature vs. Immature

 Lesion:
1. Osteoid, chondroid or fibrous (ground glass)
2. What is the lesion doing to the bone? (sclerotic/lytic/mixed/calcification)
3. What is the bone doing to the lesion? (periosteal reaction/Codman’s triangle/onion skinning)

 Margins:
1. Well defined (narrow zone of transition) - slow growing – less aggressive
2. Poorly defined (wide zone of transition – likely progressive (malignant)
3. Cortical breach
 You should be able to comment on radiographs if the likely diagnosis is non-aggressive or
aggressive lesion
 Although a definite diagnosis may not be expected, there should be an appropriate
recognition and work up for a potentially malignant condition.

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 Table 8.3: X-ray features of common tumors
Giant cell tumor Soap bubbles
Osteochondroma Exostosis
Osteosarcoma Sunburst appearance
Ewing sarcoma Onion skin periosteum, moth eaten
Chondrosarcoma Moth eaten butterfly shape
Osteoid osteoma Nidus (hole)<1.5 cm
Osteoblastoma Nidus (hole)>1.5 cm

 CT-scan:
o To evaluate disease extent
 Radionuclide bone scans or total body
positron emission tomography (PET)
o To evaluate the entire skeleton for
the presence of multiple lesions
 MRI
o For nerve conduction test
o For soft tissue tumor
o To look for prognosis
 Tumor markers
 Biopsy: the indications for biopsy are:
o Whenever there is significant doubt as to the diagnosis of a benign or
malignant lesion
o When the histologic distinction among possible diagnoses could alter the
planned course of treatment
o When definitive confirmation of the diagnosis is required before undertaking
a hazardous, costly, or potentially disfiguring treatment

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Work-Up of Suspected Neoplasm

Image whole limb:

 Local staging: MRI of whole limb (to assess spread of tumour, compartments involved, check
for skip lesions and look for neurovascular proximity)
 Systemic workup:
o CT chest
o Abdomen and pelvis to identify primary or metastatic lesions
 Bone scan - to check for skeletal metastases
 Don’t fix fracture until sure of pathology
 Staging vs. Grading:
o Stage – degree of spread of the tumor
o Grade – Degree of cellular differentiation

Biopsy:

 Only after a discussion with bone tumor unit

 Types
o FNAC Not enough
o Core biopsy can be performed under LA
o Can be combined with imaging (US for soft tissue, CT for bone)
o Diagnostic accuracy 85%
o Tru-Cut needle for soft tissue
o Jamshidi needle for bone
o Open biopsy - Diagnostic accuracy 95%
o For soft tissue - place stitches to orientate sample for pathologist

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Principles of biopsy:

 Must be performed by or under direct instruction of surgeon at specialist bone tumor unit
 Tract removable within definitive incision
 Extensile longitudinal incision
 If using LA, then judicious use to avoid seeding
 Tourniquet use only with gravity exsanguination, should be deflated prior to definitive closure
 Direct to bone do not follow planes
 Don’t contaminate > 1 compartment
 Enough tissue from periphery of tumour to avoid area of central necrosis
 Meticulous haemostasis to avoid seeding
 Send in a formalin container
 If a drain is inserted, it should come out through or in line the surgical incision
 Do not forget to biopsy every infection and culture every tumour
 Sutures close to wound margin to allow inclusion for excision of tract later

Differential Diagnosis

1) Bone tumor
2) Abscess
3) Metastasis to the bone
4) Bone cyst
5) Osteomyelitis
6) Fibrous dysplasia

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 Discussion of the Case

 Introduction…………………………………………………..517
 Osteosarcoma…………………………………………….….518
 Chondrosarcoma……………………………………………518
 Ewing Sarcoma……………………………………………….519
 Other Tumors…………………………………………………519

Introduction
 Bone tumors can be classified as primary and secondary.
 Secondary bone tumor is the most common
 Primary bone tumors can be classified into:
o Bone forming
 Osteoma
 Osetoid osteoma
 Osteoblastoma
 Osteosarcooma
o Cartilage forming
 Osetochondroma
 Enchondroma
 Chnodromyxoid fibroma
 Chondroblastoma
 Chondrosarcoma
o Miscellaneous tumors
 Ewing sarcoma
 Giant cell tumor of bone

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 8.2.1. Osteosarcoma

 Osteosarcoma is by far the most common primary

malignant tumor arising in bone (myeloma
excluded).
 It is most common in the second and third
decades of life and is usually a high-grade
malignancy, although the parosteal form is a
notable exception.
 Most often osteosarcoma is located in the
metaphysis of a long bone and usually has
demonstrable internal bone formation.
 Characteristic features of conventional osteosarcomas include:
o Destruction of the normal trabecular bone pattern
o Indistinct margins
o Lack of endosteal bone response
o There is usually a mixture of radio dense and radiolucent areas, with
periosteal new bone formation, and sometimes formation of Codman's
triangle.
o The associated soft tissue mass may be ossified in a radial or "sunburst"
pattern.

8.2.2. Chondrosarcoma
 A condition of middle aged and older adults
 Bones of pelvis, proximal femur, proximal humerus
 Is usually of low or intermediate grade.
 Cartilage can be recognized on imaging because it tends to
grow in nodules, has a very high-water content (making it
bright on T2 weighted MRI and dark on CT scan), and
deposits mineral in dense "rings and arcs" whose density
can focally exceed cortical bone.

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 8.2.3. Ewing Sarcoma

 Has a "permeative" or "moth-eaten" pattern on

imaging with very poorly defined margins.
 The tumors can be large, and frequently involve the
diaphysis.
 The characteristic periosteal reaction produces
layers of reactive bone, deposited in an "onion peel"
appearance.
 The soft tissue component of the tumor rarely shows
any calcification or ossification.
 Sclerosis of bone, if present, represents a secondary bone reaction rather than the
primary bone formation that characterizes osteosarcoma.
 A pathologic fracture is present at diagnosis in 10 to 15 percent of cases.
 Ewing tumors may resemble subacute osteomyelitis on imaging, and the clinical
presentation may also be similar

8.2.4. Differential Diagnosis of Primary Lytic Lesions

Malignant
 Fibrosarcoma: tends to resemble osteosarcoma but without ossification
 Primary lymphoma of bone: in an older age group and is generally associated with
less bone destruction than ES.
 Metastasis from a non-bone tumor.
Benign
 Hemangioma
 various types of cysts
 lipomas
 eosinophilic granuloma: at a younger age and are not associated with a sizable soft
tissue mass.
 Giant cell tumor of bone

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 Management

1. Chemotherapy
 Induces apoptosis
 Targets rapidly dividing cells, such as those found in neoplasms, therefore not
effective against slow dividing cells
o E.g. Cartilage
 Lack of specificity – therefore other rapidly dividing cells also affected
o E.g. lining of gut, bone marrow, hair, and skin
 Eliminates micro-metastases in lungs
 Indications:
o Osteosarcoma
o Ewing's sarcoma
o Metastatic soft tissue sarcoma
 6 – 12 weeks pre-op and 6 – 12 months postop
 Agent specific side effects:
o Doxorubicin (cardiac toxicity)
o Ifosfamide: (neurological toxicity)
o Cyclophosphamide: (myelosuppression and urotoxicity)
o Bleomycin: (pulmonary fibrosis)
2. Radiotherapy
 Production of free radicals leading to direct genetic damage
 Indications:
o Ewing Sarcoma
o Lymphoma of bone
o Multiple Myeloma
o Soft tissue sarcoma
 Metastatic bone disease - breast & prostate
o Radio-resistant: renal & GI metastases
 Complications:
o Delayed bone healing o Sarcoma
o Infection o AVN
o Fracture o Growth arrest
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3. Surgical excision
 Indications for surgery in benign tumors:
 Thinning of >50% of cortex
 Mass effect
 Types of surgery:
o Intralesional: Excisional biopsy for benign lesions
o Marginal:
 Resection passes through reactive zone
 Outside tumour pseudocapsule where inflammatory and tumour
cells are present
 Between cancer and normal tissues, micro-metastasis may persist
o Wide:
 Outside reactive zone with cuff of normal tissue
 Intra-compartmental possibility of skip lesions
 Careful planning of surgical approach to ensure tumour clearance
o Radical:
 En-bloc excision of entire compartment
 Reconstruction endoprosthesis, custom-made or modular
o Amputation: When Vascular/neurological invasion present

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 Short Case Discussion

 Content By:
 Matyas Wondwossen
 Nanati Jemal 8.3. Fracture management…………………………………523
 Edited By:
 Samuel Mesfin
8.4. Talipes Equinovarus
 Reviewed By: (Idiopathic Club-Foot)..…………………………………529
 Dr. Matiyas Seid
(Orthopedic Surgeon)
8.5. Video QRs………………..…………………………………534

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 8.3. Fracture Management

 Principles……………………………………………….523
 Plaster of Paris……………………………………….524
 Continuous Traction……………………………….525
 External Fixation………………………………….…526
 Internal Fixation…………………………………….528

Principles
A. Reduction
 Restoration of fracture fragment to acceptable position
o Aim for adequate apposition and normal alignment
o There are two methods closed or open
 In many fractures reduction is unnecessary, either because there is no displacement
or because the displacement is immaterial to final result.
1. By closed manipulation- most commonly used, under generalized or local
anesthesia,
2. By mechanical traction with or without manipulation
 Closed reduction principles
o All displaced # should be reduced
o Analgesia & muscle relaxation
o Correct length, rotation & angulation
o Use splints initially
o Immobilize it above and below #
3. By open operation
B. Immobilization
 Indication:
1. To prevent displacement or angulation of the fragments
2. To prevent movement that might interfere with union
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 3. To relieve pain
 Methods: -
1. By a plaster of Paris (POP) or another external splint
2. By continuous traction
3. By external fixation
4. By internal fixation

Plaster of Paris (POP)

 Plaster of Paris is still widely used as a splint,
especially for distal limb fractures and for most
children’s fractures.
 It is safe enough, so long as the practitioner is alert
to the danger of a tight cast and provided pressure
sores are prevented.
 The speed of union is neither greater nor less than
with traction, but the patient can go home sooner.

 Holding reduction is usually no problem and patients with tibial fractures can bear
weight on the cast.
 However, joints encased in plaster cannot move and are liable to stiffen.
 Stiffness can be minimized by:
o Delayed splintage – that is, by using traction until movement has been
regained, and only then applying plaster; or
o Starting with a conventional cast but, after a few weeks, when the limb can
be handled without too much discomfort, replacing the cast by a functional
brace which permits joint movement.

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Types of application of POP
 Posterior gutter:
o The POP is applied only posteriorly and the rest
is covered by bandage.
o It allows expansion, thus helping to decrease risk
of compartment syndrome.

 Circular cast:
o The POP spans the whole
circumference of the limb, making it
better at stabilizing the fracture
fragments.
o But it has higher risk for compartment
syndrome.
 Indications
o Undisplaced fractures
o Tolerable displacement
o Closed reduction of displacement possible
o Fracture in children (Upper and lower extremities)
 Complications
o Tight cast
o Pressure sores
o Abrasion or laceration of the skin.

Continuous Traction

 Traction is applied to the limb distal to the fracture, so as to exert a continuous pull
in the long axis of the bone, with a counterforce in the opposite direction (to
prevent the patient being merely dragged along the bed).

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 Traction includes:
o Traction by gravity:
 This applies only to upper limb injuries.
Thus, with a wrist sling the weight of the
arm provides continuous traction to the
humerus.
o Skin traction:
 Skin traction will sustain a pull of no more
than 4 or 5 kg.
 Holland strapping or one-way-stretch
Elastoplast is stuck to the shaved skin and
held on with a bandage.
 The malleoli are protected by Gamgee
tissue, and cords or tapes are used for
traction.
o Skeletal traction:
 A stiff wire or pin is inserted – usually
behind the tibial tubercle for hip, thigh and
knee injuries, or through the calcaneum
for tibial fractures – and cords tied to them
for applying traction.

External Fixation

 A fracture may be held by transfixing screws or tensioned

wires that pass through the bone above and below the
fracture and are attached to an external frame.
 This is especially applicable to the tibia and pelvis, but the
method is also used for fractures of the femur, humerus,
lower radius and even bones of the hand.
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 Indications
o Fractures associated with severe soft-tissue damage (including open
fractures) or those that are contaminated, where internal fixation is risky
and repeated access is needed for wound inspection, dressing or plastic
surgery.
o Fractures around joints that are potentially suitable for internal fixation but
the soft tissues are too swollen to allow safe surgery; here, a spanning
external fixator provides stability until soft-tissue conditions improve.
o Patients with severe multiple injuries, especially if there are bilateral femoral
fractures, pelvic fractures with severe bleeding, and those with limb and
associated chest or head injuries.
o Ununited fractures, which can be excised and compressed; sometimes this is
combined with bone lengthening to replace the excised segment.
o Infected fractures, for which internal fixation might not be suitable.
 Parts of external fixator
1. Pins: are the metals that go through the bone.
2. Bar: is the metal found externally to which the
pins are attached.
3. Clamp: can be of 3 types, pin-to-bar (attach the
pin to the bar), pin-to-pin (attach one pin to
another) and bar-to-bar (attach one bar to
another bar).
 Complications
o As we incise the skin and soft tissue, we can cause a neurovascular damage
o As we drill the bone to insert the pins there may be heat necrosis of the bone
o If we accidentally damage the cortex on the other side of the bone it causes
Iatrogenic fracture
o After the external fixator is placed, we can have Pin site infection, Pin
loosening (technical problems), joint stiffness (if it is joint spanning)

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 Internal Fixation

 Bone fragments may be fixed with screws, a metal

plate held by screws, a long intramedullary rod or
nail (with or without locking screws),
circumferential bands or a combination of these
methods.
 Indications
o Fractures that cannot be reduced except by operation.
o Fractures that are inherently unstable and prone tore-displace after
reduction (e.g. mid-shaft fractures of the forearm and some displaced ankle
fractures).
 Also included are those fractures liable to be pulled apart by muscle
action (e.g. transverse fracture of the patella or olecranon).
o Fractures that unite poorly and slowly, principally fractures of the femoral
neck.
o Pathological fractures in which bone disease may prevent healing.
o Multiple fractures where early fixation (by either internal or external
fixation) reduces the risk of general complications and late multisystem
organ failure.
o Fractures in patients who present nursing difficulties (paraplegics, those with
multiple injuries and the very elderly).
 Parts of internal fixators
o Screws
o Wires
o Plate and screws
o Intramedullary nails
 Complications:
o Infection
o Implant failure
o Non-union
o Re-fracture

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8.4. Talipes Equinovarus (Idiopathic Club-Foot)
 Introduction………………………………………………….529
 Pathological Anatomy…………………………………..529
 Epidemiology………………………………………………..530
 Etiology…………………………………………………….…..530
 Clinical Manifestation……………………………………531
 Deformities…………………………………………….…….532
 Investigation…………………………………………………532
 Management…………………………………………..……533

Introduction
 The term ‘talipes’ is derived from talus (Latin = ankle bone) and pes (Latin = foot).
 Equinovarus is one of several different talipes deformities; others are talipes
calcaneus and talipes valgus.
 In the full-blown equinovarus deformity the heel is in equinus, the entire hindfoot in
varus and the mid and forefoot adducted and supinated.
 The abnormality is relatively common, the incidence ranging from 1–2 per thousand
births; boys are affected twice as often as girls and the condition is bilateral in one-
third of cases.

Pathological Anatomy
 The neck of the talus points downwards and deviates medially, whereas the body is
rotated slightly outwards in relation to both the calcaneum and the ankle mortise.
 The posterior part of the calcaneum is held close to the fibula by a tight calcaneo-
fibular ligament, and is tilted into equines and varus; it is also rotated medially
beneath the ankle.

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 The navicular and entire forefoot are shifted medially and rotated into supination
(the composite varus deformity).
 The skin and soft tissues of the calf and the medial side of the foot are short and
underdeveloped.
 If the condition is not corrected early, secondary growth changes occur in the
bones; these are permanent.

Epidemiology
 Even with treatment the foot is liable to be short and the calf may remain thin.
 The most common birth defect
o 1/1000 Caucasians, 3/1000 Polynesians
o Female: Male = 2: 1
o Bilateral in 50%
 Underlying bone problem are
 Deformed talus, which it is flexed and medially deviated

Etiology
 Calcaneus is in varus and rotated medially around talus
 Navicular and cuboid are displaced medially
 Multifactorial
o Neurogenic theory:
 Histochemical abnormalities secondary to denervation changes in
various muscle groups of the leg/ foot
o Neurogenic imbalance deformity:
 Defect in nerve supply (the incidence of varus and equinovarus
deformity in spina bifida is approximately 35%)
o Myogenic theory:
 Primary muscle defect.
 Predominance in type I muscle fibres and fibre type IIB deficiency
P a g e 530 | 548
 o Congenital constriction bands/rings
o Retracting fibrosis:
 Increased fibrous tissue in muscles and ligaments

Clinical Manifestation
 Examine the whole child to exclude associated abnormalities:
o Myelomeningocele o Polio
o Intraspinal tumour o CP
o Diastematomyelia
 Usually obvious at birth; the foot is both
turned and twisted inwards so that the sole
faces posteromedial.
 The ankle is in equinus, the heel is inverted
and the forefoot is adducted and supinated;
sometimes the foot also has a high medial
arch (cavus), and the talus may protrude on
the dorsolateral surface of the foot.
 The heel is usually small and high, and deep creases appear posteriorly and medially;
some of these creases are incomplete constriction bands.
o In some cases, the calf is abnormally thin.
 The infant must always be examined for associated disorders such as congenital hip
dislocation and spinabifida.
 X-rays are used mainly to assess progress after treatment.
 Look for any associated developmental syndrome:
o Arthrogryposis o Diastrophic dysplasia
 Examine the spine (neurological cause)
 Pulses: Usually present but vascular dysgenesis
is possible (absent dorsalis pedis artery)
 Examine foot creases: Medial, plantar, posterior

P a g e 531 | 548
 Deformities

 Affected limb may be shortened, calf muscle is

atrophic, and foot is short compared to
opposite side
 Midfoot Cavus (tight intrinsic, FHL, FDL)
 Forefoot Adductus (tight tibialis posterior), forefoot supinated in relation to hindfoot
but relative pronation due to 1st MT drop)
 Hindfoot Varus (tight tendoachilles, tibialis posterior)
 Hindfoot Equinus (tight tendoachilles)
Pirani score (maximum score = 6)
 Score severity of hind foot & mid foot contracture and likelihood of success of
treatment 0 – 1 for each
 Normal (0)
 Moderately abnormal (0.5) or
 Severely abnormal (1)
1. Hindfoot 2. Midfoot
 Posterior crease  Severity of medial crease
 Rigidity of equinus  Coverage of lateral head of talus
 Degree of emptiness of heal  Curvature of lateral foot

Investigation
 Radiographs not routinely taken in a newly diagnosed presenting infant but may be
of value if the case is resistant to therapy or other pathologies
o E.g. congenital vertical talus) is suspected
 Dorsiflexion lateral (Turco view):
o Shows hindfoot parallelism between talus and calcaneus
 Lateral:
o Talo-calcaneal angle < 250
o Tibio-calcaneal angle > 900
 AP:
o Talo-calneal (Kite) angle < 200
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 Management

 Aim of treatment: painless functional plantigrade foot without need of orthotic shoe
in the 1st year
 Ponseti – Spanish physician worked in Iowa in 1950s
o 90 % success
o Start at 7 days - can be used in children up to 10 years
o Lasts for 6-8 weeks
o Serial weekly above knee casting with knee in 90 degree flexion
 Cast manipulation using head of talus as fulcrum
o Cavus corrected first by dorsi-flexing first ray, increase supination – foot looks
worse
o Forefoot abducted
o Adduction and varus corrected simultaneously (varus corrected with hindfoot
abduction)
o Finally, equinus corrected – once anterior calcaneum is abducted from under
talus)
 Kite error (Fulcrum at calcaneo-cuboid joint, which prevented correction of hindfoot)
 Post-reduction abduction splinting is required to maintain the position for 23 hours
per day (full-time splinting) for 3 months and then 12 hours per day (night-time
splinting) until age 5 (or as close to this as canrealistically be achieved)
 Traditionally, this involved Denis Browne boots and bar; however, Mitchell boots are
gaining popularity as they are well tolerated by infants (and therefore, their parents)
 Residual equinus requires tendoachilles release in 90 %
 Aim for at least 150 dorsiflexion
 Done under LA (full division)
 Cast for further 3 weeks while tenotomise heals
 Cochrane:
o Ponseti technique produce better short-term outcomes compared to Kite’s
 Posteromedial soft tissue release and Achilles tendon lengthening

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 8.5. Video QRs
Article on Clubfoot Etiology and Treatment

Fracture Management

Bone Remodeling and Repair

Bone Tumor

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P a g e 535 | 548
 Index
Abdomen Renal, 203 Fractures, 501
Acute pancreatitis, 362 Skin, 15 Fracture Management, 523
Colorectal cancer, 282 Cardiac tamponade, 262 Gait, 476
Gallstones, 357 Charcot’s triad, 273 Gallbladder, 265, 274
Intestinal obstruction, 319, 328 Chest trauma, 121 Gallstones (cholelithiasis), 357, 361
Intussusceptions, 338, 441 Cleft lip and palate, 43 Gastric cancer, 307
LUTS, 183, 283 Club foot (congenital talipes Aetiology and risk factors, 309
Abdominal trauma, 381 equinovarus), 529 Chemotherapy, 315
Advanced Trauma Life Support Colorectal cancer, 282 Clinical features, 311
(ATLS), 387 Clinical features, 282 Imaging, 312
Anorectal abscess, 370 Epidemiology, 287 Incidence, 308
Appendicectomy, 354, 419 Investigation, 285 Investigations, 312
Bladder cancer, 179 Management, 293 Radiotherapy, 315
Bladder outflow obstruction, 170 Pathology, 289 Surgery, 316
Bladder cancer, 179 Risk factors, 287 Subtotal gastrectomy, 316
Bladder trauma, 224 Spread, 290 Total radical gastrectomy, 316
BPH, 171 Staging, 290 Gastric outlet obstruction, 294
Neurogenic bladder, 197 Cystoscopy, 188 Gastric ulcers, 309, 310, 319
Prostatic Cancer, 175 Debridement, 12 Glasgow Coma Scale
Urethral stricture, 194 Digital rectal examination (GCS), 443, 444, 445
Brain injury, 440 (DRE), 375 Goitre, 76, 77, 78, 80, 82
Brain tumours, 475 Ductal carcinoma in situ Retrosternal, 75, 89
Breast carcinoma, 65 (DCIS), 67 Toxic, 78
Burns, 24 Dysphagia, 98 Goitrogens, 77
Cancer External fixation, 526 Graves’ disease, 79, 80, 86
Bone, 511 Extradural haematoma, 456 Haematuria, 174, 185
Bladder, 180 Extremity trauma, 398 Haemorrhoids, 369, 378
Colorectal, 282 Compartment Haemothorax, 130, 146, 149
Esophageal, 107 syndrome, 507 Hamartomas, 49
Gastric, 307 Fractures, 501 Hartmann’s procedure, 387
Prostatic, 175 Follicular carcinoma, 82 Head injury, 440
P a g e 536 | 548
Hernias, 400, 406, 415, 418 Lung cancer, 484, 512 Parkland formula, 34
Hydronephrosis, 174, 201 Melanoma, 22 Penetrating injuries, 6, 152, 394, 467
International Prostate Symptom Meningioma, 475, 477 Peptic ulcers, 297, 299
Score (IPSS), 174 Nasogastric tubes, 420 Perforation, 302, 303, 326
Intestinal obstruction, 318, 328 Nephrolithiasis, 199 Plaster of Paris, 524
Intracranial pressure (ICP), 445, 448 Neural tube defects, 485 Pleural effusion, 251, 260, 284
Intussusceptions, 338, 441 Neurogenic shock, 461, 468 Prepuce, 238, 244
Jaundice, 250, 262 Nipple, 60, 63, 64 Priapism, 445, 468
Keloid scars, 10 Nocturia, 170, 185 Primary survey, 387, 443
Liver Osteosarcoma, 518 Prostate
Abscess, 254, 258 Paget’s disease, 68, 92 Prostate cancer, 175
Hydatid cyst, 250, 253 Pancreas Prostatectomy, 174, 175
Metastases, 253, 264 Pancreatic carcinoma, 276 Rectal bleeding, 283, 379
Trauma, 386 Pancreatitis, 362 Renal calculi/stones, 199, 428
Tumours, 249, 250 Papillary carcinoma, 82 Renal cell carcinoma, 203
Lower urinary tract symptoms Paradoxical respiration, 465 Retrograde ureterogram, 218
(LUTS), 174, 203 Paralytic ileus, 30, 323 Urinary catheterization, 233
Screening, 183, 212, 446 Subarachnoid hemorrhage, 458
Skin cancer, 15 Testes, 432, 435 Wound healing
Skin grafts, 12, 34 Thyroid, 71, 86 Abnormal, 10
Skull fractures, 445, 451 Tracheostomy, 160 Burns, 24
Small intestines, 323, 326 Transurethral resection of Contractures, 10
Smoking, 14, 45, 58, 108 Prostate (TURP) Delayed, 12
Spinal cord injury, 460 Complications, 174 Infected wounds, 10
Staging, 21, 111, 177 Tumor, nodes, metastases Primary intention, 9
Strangulation, 321, 326 (TNM) staging, 177, 190, 210 Secondary intention, 9
Strictures, 328, 332, 412 Ureteroscopy, 202, 223 Wound management, 10
Subdural haematoma, 454, 456 Urethra
Tension pneumothorax, 128 Stricture, 231, 234

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