Give a comprehensive, well detailed, extensive note on the following surgery topics in all simplicity of understanding: 11. Colorectal tumours 12. Blunt abdominal injuries 13. Blunt chest injuries 14. Penetrating abdominal injuries 15. Multiply injured patients 16. Ulcers 17. Fractures 18. Intestinal obstructions 19. Acute appendicitis 20. External hernias

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colorectal tumours blunt abdominal chest injuries fractures hernias appendicitis surgery notes comprehensive

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COMPREHENSIVE SURGERY NOTES

Topics 11–20


11. COLORECTAL TUMOURS

What Are They?

Colorectal tumours are abnormal growths (neoplasms) arising from the lining (mucosa) of the colon or rectum. They may be benign (polyps) or malignant (colorectal carcinoma — CRC), and CRC is the 3rd most common cancer worldwide and the 2nd leading cause of cancer death.

Types of Colorectal Tumours

A. Benign Polyps (Pre-cancerous)

TypeFeatures
Tubular adenomaMost common; small, pedunculated (on a stalk); low malignant potential
Villous adenomaSessile (flat-based); high malignant potential; may secrete mucus causing hypokalemia
Tubulovillous adenomaMixed type
Hyperplastic polypNo malignant potential
Juvenile/hamartomatous polypIn children; rarely malignant
Key rule: The larger the polyp, the more villous it is, and the higher the risk of malignancy.

B. Malignant Tumours

  • Adenocarcinoma — accounts for 95% of all colorectal cancers
  • Carcinoid tumours — arise from neuroendocrine cells; mostly in rectum
  • Lymphoma — rare
  • Leiomyosarcoma — rare, from smooth muscle

Risk Factors

  • Dietary: High red/processed meat, low fibre, low fruit/vegetables, high fat intake
  • Lifestyle: Obesity, physical inactivity, smoking, alcohol
  • Genetic/Hereditary:
    • FAP (Familial Adenomatous Polyposis) — hundreds of polyps; APC gene mutation; near 100% cancer risk by age 40
    • HNPCC / Lynch Syndrome — DNA mismatch repair gene mutation; high risk of right-sided colon cancer
  • Inflammatory Bowel Disease: Ulcerative colitis and Crohn's disease increase risk (longer duration = higher risk)
  • Personal/family history of colorectal cancer or adenomas
  • Age > 50 years

Pathogenesis — The Adenoma–Carcinoma Sequence

Most colorectal cancers develop from adenomatous polyps over 10–15 years through accumulation of genetic mutations:
  1. APC gene mutation → polyp formation
  2. K-RAS mutation → polyp growth
  3. Loss of DCC (Deleted in Colorectal Cancer) gene
  4. TP53 mutation → invasion and carcinoma

Clinical Features (Symptoms)

Symptoms depend on the location of the tumour:
LocationTypical Features
Right colon (caecum/ascending)Occult bleeding → iron-deficiency anaemia, fatigue, weight loss; often presents late as lumen is wide
Left colon (descending/sigmoid)Change in bowel habit (alternating constipation/diarrhoea), bright red rectal bleeding, colicky pain, pencil-thin stools
RectumFresh rectal bleeding, tenesmus (feeling of incomplete evacuation), mucus per rectum
General (systemic) symptoms: Weight loss, anorexia, anaemia, fatigue
Complications: Obstruction, perforation, fistula formation, haemorrhage

Staging — Duke's Classification (Simplified)

StageDescription5-Year Survival
Duke's AConfined to bowel wall mucosa/submucosa~90%
Duke's BThrough bowel wall, no nodal spread~70%
Duke's CRegional lymph node involvement~30–40%
Duke's DDistant metastases (liver, lung, peritoneum)<5%
Modern staging uses the TNM system (Tumour, Node, Metastasis).

Diagnosis

  1. History and physical examination — including digital rectal examination (DRE)
  2. Faecal occult blood test (FOBT) — screening tool
  3. Colonoscopy — gold standard; allows biopsy and polypectomy
  4. Sigmoidoscopy — for left-sided lesions
  5. Barium enema — "apple-core" appearance of annular carcinoma
  6. CT colonography (virtual colonoscopy) — non-invasive
  7. CT scan (abdomen/pelvis/chest) — staging, liver metastases
  8. MRI — especially for rectal cancer (assesses local spread)
  9. CEA (Carcinoembryonic Antigen) — tumour marker; useful for monitoring recurrence, not for diagnosis
  10. Biopsy — histological confirmation

Treatment

Surgery (Curative Intent)

  • Right hemicolectomy — for right colon tumours
  • Left hemicolectomy / sigmoid colectomy — for left colon tumours
  • Anterior resection — for upper rectal tumours
  • Abdominoperineal resection (APR) — for very low rectal tumours; requires permanent colostomy
  • Hartmann's procedure — for emergency obstruction/perforation (end colostomy + rectal stump)
  • Aim for clear resection margins and adequate lymph node harvest (≥12 nodes)

Adjuvant (Post-operative) Treatment

  • Chemotherapy: FOLFOX (5-FU + Oxaliplatin) for stage III (Duke's C)
  • Radiotherapy: For rectal cancer — pre-operative (neoadjuvant) or post-operative
  • Targeted therapy: Bevacizumab, Cetuximab for metastatic disease

Palliative Care (Metastatic Disease)

  • Liver resection if solitary hepatic metastases
  • Palliative chemotherapy
  • Stenting for obstructing tumours

Screening

  • Average risk: Colonoscopy from age 50 every 10 years; FOBT annually
  • High-risk (FAP): Colonoscopy from age 10–12
  • Lynch syndrome: Colonoscopy from age 20–25

12. BLUNT ABDOMINAL INJURIES

Definition

Blunt abdominal injury is trauma to the abdomen without penetration of the abdominal wall. It results from compression, shearing, or deceleration forces.

Causes

  • Road traffic accidents (RTAs) — most common cause (steering wheel, seat belt)
  • Falls from a height
  • Sports injuries, assault (punches, kicks)
  • Explosions (blast wave)
  • Industrial accidents

Mechanism of Injury

Three main mechanisms:
  1. Compression/crushing — direct blow squeezes hollow organs against the spine (e.g., bowel rupture)
  2. Deceleration/shearing — sudden stopping tears organs at fixed attachment points (e.g., liver laceration at the hepatic veins, bowel tear at ligament of Treitz)
  3. Burst injury — sudden increase in intra-abdominal pressure ruptures hollow viscera

Organs Commonly Injured (in order of frequency)

  1. Spleen — most commonly injured solid organ (vulnerable due to poor protection)
  2. Liver — 2nd most common
  3. Small bowel — most commonly injured hollow organ
  4. Kidney
  5. Mesentery
  6. Pancreas — rare but serious
  7. Duodenum — protected retroperitoneally but can rupture
  8. Bladder — especially if full at time of impact

Clinical Features

History:
  • Mechanism (seatbelt use, speed of collision, height of fall)
  • Time of last meal (bowel contents affect contamination)
Symptoms:
  • Abdominal pain (may be diffuse or localised)
  • Nausea, vomiting
  • Signs of shock (tachycardia, hypotension, pallor) if significant haemorrhage
Signs:
  • Abdominal tenderness — guarding, rigidity (peritonism)
  • Bruising: "Seatbelt sign" — transverse bruising across abdomen = high index of suspicion for bowel/mesenteric injury
  • Grey Turner's sign — flank bruising = retroperitoneal haematoma (e.g., pancreatic or renal injury)
  • Cullen's sign — periumbilical bruising = intraperitoneal blood
  • Shoulder-tip pain — diaphragmatic irritation by blood (Kehr's sign for splenic injury)

Assessment — ATLS Approach

Primary Survey: ABCDE
  • Airway, Breathing, Circulation (control haemorrhage), Disability (neurological status), Exposure (full examination)
Key investigations:
  1. FAST Scan (Focused Assessment with Sonography for Trauma) — rapid bedside ultrasound; detects free fluid (blood) in peritoneum; quick and repeatable
  2. Diagnostic Peritoneal Lavage (DPL) — inject saline into peritoneum; positive if >100,000 RBC/mm³ in effluent; largely replaced by FAST
  3. CT scan (abdomen/pelvis with contrast) — gold standard for stable patients; identifies organ injuries, grading, retroperitoneal injuries
  4. Plain X-ray — erect CXR (free gas under diaphragm = bowel perforation), pelvic X-ray
  5. FBC, U&E, amylase, LFTs, group and crossmatch, coagulation
  6. Urinalysis — haematuria suggests renal/bladder injury

Splenic Injury — Grading

GradeDescription
ISubcapsular haematoma <10%, capsular laceration <1 cm
IIHaematoma 10–50%, laceration 1–3 cm
IIIHaematoma >50%, laceration >3 cm, or involving trabecular vessels
IVLaceration of segmental or hilar vessels
VTotally shattered spleen / hilar avulsion

Management

Haemodynamically Unstable:

  • Emergency laparotomy — immediate damage control surgery
  • Pack and control bleeding, repair perforations
  • Damage Control Surgery: Abbreviated initial operation → ICU resuscitation → definitive repair at 24–48 hours

Haemodynamically Stable:

  • Non-operative management (NOM) — preferred for solid organ injuries (spleen, liver, kidney) when patient is stable
  • Admit, close monitoring (pulse, BP, serial abdominal examinations, serial Hb)
  • Angioembolisation — for ongoing bleeding from solid organs (interventional radiology)
  • If patient deteriorates → laparotomy
Splenectomy post-op care:
  • Vaccinate against encapsulated organisms: Pneumococcus, Meningococcus, Haemophilus influenzae (before surgery if elective, after if emergency)
  • Life-long penicillin prophylaxis in children

Key Surgical Procedures in Blunt Abdominal Trauma

  • Splenectomy / splenorrhaphy (splenic repair)
  • Hepatorraphy / packing for liver lacerations
  • Bowel resection and anastomosis (or stoma if contaminated)
  • Nephrectomy for severe renal injury
  • Distal pancreatectomy for pancreatic injuries

13. BLUNT CHEST INJURIES

Definition

Blunt (closed) chest injury involves trauma to the thorax without penetration of the chest wall. It is common, present in up to 25% of trauma deaths.

Causes

  • Road traffic accidents
  • Falls
  • Sports injuries
  • Assault
  • Crush injuries

Types of Blunt Chest Injuries

A. RIB FRACTURES

Most common blunt chest injury.
  • Simple rib fractures: Pain on breathing; risk of pneumonia (splinting)
  • Multiple rib fractures (≥3 ribs): More serious; risk of pneumo/haemothorax
  • Flail chest: ≥3 consecutive ribs fractured in ≥2 places → "floating" segment moves paradoxically (inward on inspiration, outward on expiration). Causes severe respiratory failure. Management: mechanical ventilation, analgesia
Management of rib fractures:
  • Adequate analgesia (key!) — epidural, intercostal nerve block, NSAIDs, opioids
  • Incentive spirometry
  • Physiotherapy to prevent pneumonia

B. PNEUMOTHORAX

Air in the pleural space → lung collapse.
TypeFeaturesManagement
Simple pneumothoraxReduced breath sounds, tympanic percussionChest drain (intercostal drain)
Tension pneumothoraxMediastinal shift, tracheal deviation, distended neck veins, severe hypotensionImmediate needle decompression (2nd intercostal space, midclavicular line) → then chest drain
Open pneumothoraxSucking chest woundSeal wound (three-sided dressing) → chest drain → surgical closure

C. HAEMOTHORAX

Blood in the pleural space.
  • Causes: Intercostal vessel or lung laceration
  • Features: Dullness to percussion, reduced breath sounds, signs of haemorrhage
  • Management:
    • Chest drain (large-bore, 28–32 Fr)
    • If initial drainage >1,500 mL OR ongoing >200 mL/hr for 2–4 hours → thoracotomy (massive haemothorax)
    • Retained haemothorax → fibrothorax (trapped lung) → VATS evacuation

D. PULMONARY CONTUSION

  • Bruising of lung parenchyma → oedema, haemorrhage → impaired gas exchange → hypoxia
  • Most common cause of respiratory failure after blunt chest trauma
  • Features: Hypoxaemia, crepitations, CXR shows patchy infiltrates
  • Management: Supportive — oxygen, ventilation, fluid restriction, analgesia; may need mechanical ventilation

E. CARDIAC TAMPONADE

  • Blood in pericardial sac compresses the heart
  • Beck's Triad: Hypotension + Distended neck veins + Muffled heart sounds
  • ECG: low-voltage complexes, electrical alternans
  • Echocardiogram confirms
  • Management: Emergency pericardiocentesis (needle aspiration) → Surgical drainage (pericardial window)

F. AORTIC INJURY

  • Traumatic aortic rupture (deceleration injury) — most at the aortic isthmus (where aorta is tethered at ligamentum arteriosum)
  • Often fatal at scene; those who survive have contained haematoma
  • CXR: widened mediastinum, obliteration of aortic knuckle, left pleural effusion
  • Confirmed by: CT aortogram or angiography
  • Management: Endovascular aortic repair (EVAR/TEVAR) or open surgery

G. TRAUMATIC DIAPHRAGMATIC RUPTURE

  • Usually left-sided (liver protects right)
  • Bowel/stomach herniates into chest
  • CXR: nasogastric tube in chest, bowel loops in thorax
  • Management: Surgical repair

H. TRACHEOBRONCHIAL INJURY

  • Rare; airway disruption near carina
  • Features: Massive air leak, surgical emphysema, persistent pneumothorax despite drain
  • Management: Bronchoscopy → surgical repair/bronchial sleeve resection

Immediately Life-Threatening Chest Injuries — "ATOM FC"

LetterInjury
AAirway obstruction
TTension pneumothorax
OOpen pneumothorax
MMassive haemothorax
FFlail chest
CCardiac tamponade
These must be identified and treated in the primary survey.

Management Approach

  1. Primary survey (ABCDE) — identify and treat immediate threats
  2. Supplemental O₂, monitoring, IV access
  3. Analgesia — critical for respiratory effort
  4. CXR (portable in trauma bay)
  5. ECG, cardiac enzymes (troponin for myocardial contusion)
  6. CT chest — for stable patients; details all injuries
  7. Definitive management per injury type above

14. PENETRATING ABDOMINAL INJURIES

Definition

Penetrating abdominal injuries involve disruption of the abdominal wall integrity by an external object passing through it. The peritoneal cavity may or may not be entered.

Causes

  • Stab wounds (SW) — most common in civilian practice
  • Gunshot wounds (GSW) — higher energy; more destructive; 80–95% cause significant intra-abdominal injury
  • Impalement injuries — industrial, MVA
  • Blast injuries (fragmentation)

Mechanism

  • Stab wounds: Low-velocity; injure structures directly in the path; less collateral damage
  • Gunshot wounds (low-velocity, <600 m/s): Cause damage along missile path
  • Gunshot wounds (high-velocity, >600 m/s — military weapons): Cause massive cavitation injury well beyond the bullet path (shock wave effect)

Organs at Risk

  • Liver — most commonly injured (right-sided wounds)
  • Small bowel — large surface area; most commonly injured in GSWs
  • Stomach
  • Colon
  • Major vessels (aorta, IVC, mesenteric vessels) — most lethal

Clinical Features

  • History: Type of weapon, direction of stab, calibre of firearm
  • Symptoms: Abdominal pain, haemorrhage symptoms (hypotension, tachycardia, pallor)
  • Signs:
    • Entry/exit wound (note: anterior vs. posterior; tangential vs. direct)
    • Evisceration (bowel or omentum protruding from wound)
    • Peritonism (guarding, rigidity, rebound tenderness)
    • Haemodynamic instability

Indications for Immediate Emergency Laparotomy

Based on the Mulholland/Greenfield Surgery principles and WTA guidelines:
  1. Haemodynamic instability despite resuscitation
  2. Peritonitis (diffuse guarding, rigidity) — 97% chance of significant injury
  3. Evisceration of bowel/omentum
  4. Uncontrolled haemorrhage
  5. Unevaluable patient (head injury, spinal cord injury)
  6. Air under diaphragm on X-ray

Selective Non-Operative Management (NOM)

For stable patients without peritonitis, selective management is now standard:
  • Stab wounds: Up to 64% of anterior stab wounds do not require laparotomy
  • Gunshot wounds: 47% can be managed without laparotomy
  • Back/flank wounds: Even lower rates of significant injury; NOM preferred
  • Requirements: Serial clinical examination, FAST scan, CT scan with contrast, observation in hospital

Investigations

  1. FAST ultrasound — rapid assessment for free fluid
  2. CT scan (abdomen/pelvis) — essential for stable patients; plots missile trajectory, identifies injuries; use IV contrast
  3. Plain X-rays — identifies bullet position and trajectory
  4. Diagnostic Laparoscopy — can assess peritoneal penetration but NOT mandatory for this alone
  5. Local wound exploration — can determine if anterior fascia is violated

Management Principles

Resuscitation

  • IV access (two large-bore IVs or central line), IV fluids
  • Permissive hypotension (target SBP 80–90 mmHg) until haemorrhage controlled in unstable patients
  • Massive transfusion protocol if needed (1:1:1 ratio of packed RBC:FFP:platelets)

Surgical Management

  • Laparotomy (midline incision) — systematic exploration of all quadrants
  • Damage control surgery in unstable patients:
    1. Control haemorrhage (packing, ligation)
    2. Control contamination (staple bowel ends, not formal anastomosis)
    3. Temporary abdominal closure
    4. ICU resuscitation
    5. Return to OR at 24–48 hours for definitive repair

Specific Injuries

  • Liver: Packing, hepatorrhaphy, or formal resection
  • Bowel: Primary repair (small injuries) or resection + anastomosis/stoma
  • Vascular injuries: Vascular control, repair or ligation (mesenteric vessels)

Wound Care

  • Antibiotics (broad-spectrum, e.g., cephalosporins + metronidazole) — prophylactic, single dose or short course
  • Tetanus prophylaxis
  • Wound not primarily closed if contaminated

15. MULTIPLY INJURED PATIENTS (POLYTRAUMA)

Definition

A multiply injured patient (polytrauma) is one with injuries to two or more body regions, at least one of which is life-threatening. Defined by an Injury Severity Score (ISS) ≥ 16.

Epidemiology

  • Trauma is the leading cause of death in ages 1–44 years worldwide
  • Trimodal distribution of trauma deaths:
    1. Immediate (seconds–minutes): Unsurvivable injuries (brain/aorta rupture)
    2. Early (minutes–hours): Preventable — hypoxia, haemorrhage ← golden hour
    3. Late (days–weeks): SIRS, sepsis, multi-organ failure

Principles of Management — ATLS (Advanced Trauma Life Support)

Primary Survey — ABCDE (treat threats immediately as found)

StepAction
A — AirwayClear and protect airway (chin-lift, jaw-thrust, suction, intubation); C-spine control
B — BreathingAssess ventilation; O₂; treat pneumothorax, haemothorax
C — CirculationControl haemorrhage; IV access; fluid resuscitation; FAST scan
D — DisabilityNeurological status (GCS, pupils); blood glucose
E — ExposureFully expose patient; prevent hypothermia

Resuscitation

  • Two large-bore IV cannulas (14G or 16G) in antecubital fossae
  • Warm IV fluids — avoid hypothermia (part of the lethal triad)
  • Massive Transfusion Protocol (MTP): Blood products in 1:1:1 ratio (RBC:FFP:Platelets)
  • Avoid excessive crystalloids (worsens coagulopathy and tissue oedema)
  • Tranexamic acid (TXA) — given within 3 hours of injury; reduces mortality from haemorrhage (CRASH-2 trial)

The "Lethal Triad" of Trauma

Three conditions that spiral into death if not corrected:
  1. Hypothermia (core temp <35°C)
  2. Acidosis (base deficit >6, pH <7.35)
  3. Coagulopathy (INR >1.5)
Damage Control Resuscitation (DCR) aims to break this triad.

Secondary Survey (Head-to-Toe)

After primary survey and resuscitation:
  • Complete head-to-toe physical examination
  • Full history (AMPLE: Allergies, Medications, Past medical history, Last meal, Events)
  • Identify all injuries missed in primary survey

Key Investigations

  • Full blood count, coagulation, group & crossmatch
  • ABG (oxygenation, base deficit, lactate)
  • Trauma CT ("pan-scan"): Whole body CT (head, cervical spine, chest, abdomen, pelvis) — standard for haemodynamically stable polytrauma
  • Pelvis X-ray — in primary survey for haemodynamic instability
  • FAST scan — bedside, repeated

Damage Control Surgery (DCS)

For the unstable polytrauma patient — prioritise survival over perfection:
  1. Phase 0: Prehospital haemorrhage control (tourniquets, wound packing)
  2. Phase 1: Abbreviated surgery — stop bleeding, stop contamination, temporary closure
  3. Phase 2: ICU — warm, correct coagulopathy, treat acidosis
  4. Phase 3: Definitive repair (24–72 hours later)
  5. Phase 4: Abdominal closure, rehabilitation

Priorities in Polytrauma

Hierarchy of life-threatening conditions:
  1. Airway obstruction
  2. Tension pneumothorax
  3. Haemorrhagic shock (external haemorrhage > internal)
  4. Open chest wound
  5. Cardiac tamponade
  6. Head injury
Key concept: Fix the C-spine (assume injury until proven otherwise) — log-roll, cervical collar throughout.

Complications of Polytrauma

  • Acute Respiratory Distress Syndrome (ARDS)
  • Systemic Inflammatory Response Syndrome (SIRS)
  • Multi-organ dysfunction syndrome (MODS)
  • Sepsis/infection
  • Deep vein thrombosis (DVT) / pulmonary embolism
  • Pressure injuries
  • Psychological trauma (PTSD)

16. ULCERS

Definition

An ulcer is a break in the continuity of an epithelial surface that extends through the mucosa into deeper layers, and fails to heal normally.

Types of Ulcers in Surgery

A. PEPTIC ULCER DISEASE (PUD)

The most important type in surgical practice.
Definition: Ulceration of the gastric or duodenal mucosa due to an imbalance between aggressive (acid, pepsin, H. pylori) and defensive (mucus, bicarbonate, prostaglandins, blood flow) factors.

Causes and Risk Factors:
  • H. pylori infection — present in 95% of duodenal ulcers, 70% of gastric ulcers (most important cause)
  • NSAIDs/Aspirin — inhibit prostaglandins → impair mucosal barrier → 2nd most common cause
  • Smoking — impairs healing, increases acid, reduces prostaglandins
  • Steroids — reduce mucus production
  • Zollinger-Ellison Syndrome — gastrinoma (tumour of G cells) → massive acid hypersecretion → severe refractory ulcers
  • Stress ulcers — Curling's ulcer (burns), Cushing's ulcer (head injury)
  • Blood group O — higher risk of duodenal ulcer

Location:
TypeSiteAcidH. pylori
Duodenal ulcer (DU)1st part of duodenum (anterior wall)High/normal95%
Gastric ulcer (GU)Lesser curve, antrumLow/normal70%
Key difference: Duodenal ulcers are more common; gastric ulcers have higher risk of malignancy (must biopsy).

Clinical Features:
  • Epigastric pain — burning, gnawing
  • Duodenal ulcer: Pain relieved by food ("hungry ulcer"); wakes patient at night; 2–3 hours after meals
  • Gastric ulcer: Pain worsened by food; may have weight loss
  • Nausea, vomiting, heartburn, bloating

Diagnosis:
  1. Endoscopy (OGD/gastroscopy) — gold standard; visualise, biopsy (exclude malignancy in gastric ulcers), test for H. pylori (CLO test/rapid urease test)
  2. H. pylori testing:
    • Urea breath test (non-invasive, most accurate non-invasive)
    • Stool antigen test
    • Serology (IgG) — less accurate
    • Biopsy (CLO test, histology, culture)
  3. Barium meal — "niche" (crater) appearance; largely replaced by endoscopy

Treatment:
  1. H. pylori eradication (triple therapy):
    • PPI (e.g., omeprazole 20 mg) + amoxicillin 1 g + clarithromycin 500 mg — all twice daily for 7–14 days
    • Test of cure with urea breath test 4–6 weeks after completion
  2. Stop NSAIDs/aspirin (if possible) or add PPI cover
  3. Acid suppression: PPI or H₂ antagonist for 4–8 weeks
  4. Lifestyle: Stop smoking, reduce alcohol, avoid trigger foods

Complications of PUD (and surgical management):
ComplicationFeaturesManagement
Haemorrhage (most common)Haematemesis, melaena, falling Hb; Rockford/Forrest gradingEndoscopic haemostasis (adrenaline injection, clipping, diathermy); if fails → surgery (underrunning the vessel)
PerforationSudden severe epigastric pain, "peritonism", free gas under diaphragm on erect CXREmergency laparotomy → omental patch (Graham patch), peritoneal lavage; add anti-H. pylori treatment
Obstruction (gastric outlet)Persistent vomiting, weight loss, succession splashEndoscopic dilatation; surgery: pyloroplasty or gastrojejunostomy
PenetrationUlcer erodes into adjacent structure (pancreas)Surgical resection
Malignant changeGastric ulcers onlyGastrectomy

B. LEG ULCERS (Chronic)

TypeCauseFeaturesManagement
Venous (most common, 70%)Chronic venous insufficiency; post-phlebitic limbMedial malleolus; gaiter area; irregular margins, sloping edges, shallow; lipodermatosclerosis, haemosiderin stainingCompression bandaging (4-layer); wound care; treat underlying venous disease
ArterialPeripheral arterial disease (PAD); atherosclerosisPunched-out, deep, painful; toes/heel; poor/absent pulses; ABI <0.9Vascular reconstruction (angioplasty, bypass); wound care; no compression
NeuropathicDiabetes, leprosy, syphilisPainless; pressure points (sole of foot); "punched-out" appearance; normal pulsesOffloading; wound care; control diabetes
Marjolin's ulcerMalignant change in chronic ulcer/scarRaised everted edges, bleeds, fixed baseExcision biopsy; wide local excision

17. FRACTURES

Definition

A fracture is a break in the continuity of bone, occurring when the force applied exceeds the bone's strength.

Classification

By Skin Integrity

TypeDescription
Closed (simple)No communication with external environment
Open (compound)Bone communicates with outside through wound — risk of infection
Gustilo-Anderson classification of open fractures:
  • Grade I: <1 cm wound, clean
  • Grade II: 1–10 cm wound, moderate contamination
  • Grade IIIA: >10 cm, adequate soft tissue cover
  • Grade IIIB: >10 cm, periosteal stripping, needs flap
  • Grade IIIC: Associated vascular injury requiring repair

By Pattern

TypeDescriptionCommon Cause
TransversePerpendicular to bone axisDirect blow
ObliqueDiagonal to bone axisAngulatory force
SpiralSpirals along boneTwisting/rotational force
ComminutedMultiple fragmentsHigh-energy trauma
GreenstickIncomplete, one cortex onlyChildren (bone is more flexible)
ImpactedFragments driven into each otherAxial loading
PathologicalThrough diseased bone (tumour, osteoporosis)Minimal/no trauma
StressRepeated micro-traumaAthletes, military recruits
AvulsionFragment pulled off by muscle/ligamentSudden muscle contraction

Clinical Features

  • Pain — at fracture site, worse on movement
  • Tenderness — point tenderness over the fracture
  • Swelling — due to haematoma and oedema
  • Deformity — angulation, shortening, rotation
  • Loss of function — inability to use the limb
  • Abnormal mobility — movement where there should be none
  • Crepitus — grating sensation (do NOT elicit deliberately)
  • Neurovascular compromise — check distal pulse, sensation, motor function

Diagnosis

  1. X-ray — at least two views (AP and lateral); include the joint above and below
  2. CT scan — for complex fractures (pelvis, spine, intra-articular)
  3. MRI — for soft tissue, occult fractures, spinal cord assessment
  4. Bone scan — for stress fractures

Fracture Healing Stages

  1. Haematoma formation (immediate, hours)
  2. Inflammatory phase (days 1–5) — inflammatory cells clean the area
  3. Soft callus formation (weeks 1–3) — fibrocartilage bridges the gap
  4. Hard callus formation (weeks 3–12) — woven bone formed
  5. Remodelling (months–years) — woven bone replaced by lamellar bone; fracture line disappears

Principles of Fracture Management — "The 3 Rs"

  1. Reduction — restore bone alignment
    • Closed reduction: Manual manipulation under anaesthesia
    • Open reduction: Surgical exposure
  2. Immobilisation (Fixation) — hold the fracture reduced
    • External: Cast/splint/traction/external fixator
    • Internal: Plates & screws, intramedullary nail, wires
  3. Rehabilitation — restore function
    • Physiotherapy, exercises to prevent stiffness and muscle wasting

Specific Important Fractures

FractureKey Features
Colles' fractureDistal radius; "dinner-fork" deformity; fall on outstretched hand; elderly women (osteoporosis)
Scaphoid fractureMost commonly missed; snuffbox tenderness; X-ray often negative; risk of AVN if untreated
Neck of femur (NOF)Elderly; osteoporosis; shortened, externally rotated leg; needs surgical fixation/hip replacement
Supracondylar fractureChildren; risk of brachial artery and radial nerve injury; "Volkmann's contracture" if ischaemia
Clavicle fractureMost common in young; middle-third; most treated conservatively
Pott's fractureAnkle; fibula ± medial malleolus; eversion injury
MonteggiaProximal ulna fracture + radial head dislocation
GaleazziRadial shaft fracture + distal radio-ulnar joint dislocation

Complications of Fractures

Immediate:
  • Haemorrhage (internal or external)
  • Neurovascular injury
  • Organ injury (e.g., lung from rib, spinal cord from vertebral fracture)
Early:
  • Compartment syndrome — raised pressure within osteofascial compartment → ischaemia → 4 P's: Pain (disproportionate), Paraesthesia, Pallor, Pulselessness; Treatment: Emergency fasciotomy
  • Fat embolism syndrome
  • Deep vein thrombosis
  • Wound infection (open fractures)
Late:
  • Malunion — heals in wrong position
  • Delayed union — takes longer than expected
  • Non-union — fails to heal (atrophic/hypertrophic)
  • Avascular necrosis (AVN) — scaphoid, femoral head
  • Osteoarthritis (if intra-articular)
  • Osteomyelitis (infection in bone, especially open fractures)
  • Contractures, myositis ossificans

18. INTESTINAL OBSTRUCTION

Definition

Intestinal obstruction is the impairment of the normal forward movement of intestinal contents. It may be mechanical (physical blockage) or functional (absent/abnormal peristalsis = ileus).

Types

A. Mechanical Obstruction

A physical block in the intestinal lumen. Can be:
  • Simple — one point of obstruction, blood supply intact
  • Strangulated — blood supply compromised → ischaemia, necrosis, perforation → EMERGENCY

B. Adynamic Ileus (Paralytic Ileus)

No physical obstruction but peristalsis is absent.
Causes of ileus:
  • Post-operative (most common)
  • Peritonitis
  • Electrolyte imbalances (especially hypokalemia)
  • Retroperitoneal haematoma
  • Medications (opioids, anticholinergics)
  • Spinal cord injury

Causes of Mechanical Obstruction (Rosen's Emergency Medicine classification)

External to intestinal wall (most common causes):
  • Adhesions — #1 cause of small bowel obstruction (SBO); post-operative scarring
  • Hernias (inguinal, femoral, incisional) — #2 cause of SBO; most common cause in patients with no previous surgery
  • Volvulus — twisting of bowel around its mesenteric axis
Intrinsic to intestinal wall:
  • Carcinoma of the colon — #1 cause of large bowel obstruction (LBO)
  • Crohn's disease (strictures)
  • Diverticular disease (strictures)
  • Intussusception — telescoping of bowel into itself (most common in children 6–18 months)
Intraluminal:
  • Gallstone ileus
  • Bezoars
  • Foreign bodies
  • Ascaris infestation (common in developing countries)

Pathophysiology

  1. Obstruction → bowel distension proximal to block (gas + fluid accumulation)
  2. Bowel wall becomes oedematous → loss of absorptive function
  3. Bacterial overgrowth in normally sterile small bowel → feculent vomiting
  4. Fluid loss into lumen and peritoneal cavity → dehydration, electrolyte imbalance
  5. If strangulation: venous occlusion → arterial occlusion → ischaemia → gangrene → perforation → peritonitis → septic shock

Clinical Features

FeatureSmall Bowel ObstructionLarge Bowel Obstruction
OnsetRapidGradual
VomitingEarly, frequent; may be feculentLate or absent
Abdominal painColicky, centralColicky, lower abdomen/colonic framing
DistensionModerate, centralMarked, peripheral (flanks)
ConstipationLate (absolute constipation)Early, prominent
Bowel soundsHigh-pitched, tinklingReduced or absent
Signs of strangulation (surgical emergency):
  • Constant (not colicky) severe pain
  • Fever, tachycardia
  • Localised tenderness, peritonism
  • Raised WBC
  • Acidosis

Investigations

  1. Plain abdominal X-ray (erect + supine)
    • SBO: Dilated loops of small bowel (central, valvulae conniventes crossing entire lumen), fluid levels
    • LBO: Peripheral colonic distension (haustral folds don't cross entire lumen), "coffee bean sign" in sigmoid volvulus
    • Free gas under diaphragm if perforated
  2. CT abdomen — gold standard; identifies cause, level, and strangulation
  3. Gastrografin/barium follow-through — for partial SBO (can be therapeutic for adhesions)
  4. Blood tests: FBC (raised WBC in strangulation), U&E (electrolytes), LFTs, lactate, group & save

Management

General (All Types):

  • "Drip and suck": IV fluids (correct dehydration) + nasogastric tube (decompress stomach)
  • Urinary catheter (monitor output)
  • NBM (nil by mouth)
  • Analgesia
  • Correct electrolytes (especially K⁺)
  • Monitor closely for signs of strangulation

Small Bowel Obstruction — Adhesional (Most Common):

  • Conservative management first — 70–80% resolve with drip and suck
  • Water-soluble contrast study (Gastrografin) — therapeutic (reduces adhesions) and diagnostic
  • Surgery if: No improvement in 48–72 hours, strangulation suspected, complete obstruction with closed loop

Large Bowel Obstruction:

  • Most require urgent surgery
  • Sigmoid volvulus: First attempt colonoscopic/sigmoidoscopic decompression (pass flatus tube)
  • Caecal volvulus: Requires surgery
  • Carcinoma causing obstruction:
    • Hartmann's procedure — sigmoid colectomy with end colostomy (safest in emergency)
    • Primary resection and anastomosis (in specialist centres)
    • Self-expanding metallic stents (SEMS) — bridge to elective surgery

Strangulation → Emergency Laparotomy

  • Resect non-viable bowel
  • Assess viability (colour, peristalsis, Doppler signal)
  • If uncertain: second-look laparotomy at 24–48 hours

19. ACUTE APPENDICITIS

Definition

Acute appendicitis is inflammation of the vermiform appendix. It is the most common surgical emergency worldwide, accounting for ~17% of acute abdominal pain presentations.

Anatomy

  • The vermiform appendix is a blind-ended diverticulum arising from the posteromedial wall of the caecum at the confluence of the taenia coli
  • Length: 2–20 cm (average 9 cm)
  • Blood supply: Appendicular artery (branch of ileocolic artery)
  • Position varies: Retrocaecal (most common, 65%), pelvic, subcaecal, pre-ileal, post-ileal

Epidemiology

  • Lifetime risk: 8.6% males, 6.7% females
  • Peak age: 10–30 years (but occurs at any age)
  • Accounts for 30% of acute surgical emergencies under 50 years
  • ~318,000 hospital admissions per year in the USA

Pathogenesis

  1. Luminal obstruction — most common cause: faecolith (hardened faeces), lymphoid hyperplasia (in children, following viral illness), tumour, foreign body, worm (Oxyuris/Ascaris)
  2. Obstruction → continued mucus secretion → rising intraluminal pressure
  3. Venous congestion → mucosal ischaemia
  4. Bacterial invasion of wall (E. coli, Bacteroides, Klebsiella)
  5. Inflammation → transmural infection → gangrene → perforation

Clinical Features

Classic Presentation:
  1. Prodromal symptoms: Anorexia, nausea, low-grade fever (up to 38°C)
  2. Pain migration: Initially periumbilical (visceral pain via T10) → within 6–8 hours migrates to right iliac fossa (RIF) as parietal peritoneum is involved
  3. Vomiting — usually after pain onset (distinguishes from gastroenteritis)
  4. Low-grade fever (>38.5°C suggests perforation)
  5. Constipation (occasionally diarrhoea with pelvic appendix)
Physical Examination Signs:
SignDescription
McBurney's point tendernessMaximum tenderness at 1/3 from anterior superior iliac spine to umbilicus
Rovsing's signPalpation of LIF causes pain in RIF (peritoneal irritation)
Psoas signPain on extension of right hip (retrocaecal appendix irritating psoas muscle)
Obturator signPain on internal rotation of flexed right hip (pelvic appendix)
Guarding and reboundPeritonism suggesting localised or generalised peritonitis
Dunphy's signWorsening pain on coughing

Alvarado Score (MANTRELS)

(From Sleisenger & Fordtran's Gastrointestinal and Liver Disease)
FeaturePoints
Migration of pain to RLQ1
Anorexia1
Nausea/vomiting1
Tenderness in RLQ2
Rebound tenderness1
Elevated temperature (>37.3°C)1
Leukocytosis (WBC >10,000)2
Shift to left (neutrophilia)1
Total10
  • Score 1–4: Appendicitis unlikely
  • Score 5–6: Possible appendicitis — further investigation
  • Score 7–8: Probable appendicitis — consider surgery
  • Score 9–10: Appendicitis very likely — operate

Investigations

  1. FBC — leucocytosis (WBC >10,000 in 70–90%); neutrophilia
  2. CRP — elevated; rises more slowly than WBC
  3. Urinalysis — to exclude UTI/renal colic (may have mild pyuria with appendicitis — pelvic appendix)
  4. Beta-hCG — in all women of childbearing age (exclude ectopic pregnancy)
  5. Ultrasound (USS) — operator-dependent; visualises non-compressible appendix >6 mm diameter; free fluid; useful in children and pregnant women
  6. CT scan (abdomen/pelvis) — most accurate (sensitivity/specificity >95%); used in adults when diagnosis uncertain; shows thickened appendix with periappendiceal fat stranding
  7. MRI — preferred in pregnancy

Differential Diagnosis

  • Mesenteric adenitis (children)
  • Ovarian pathology (ectopic pregnancy, ovarian cyst/torsion) — in women
  • Urinary tract infection/renal colic
  • Crohn's disease
  • Meckel's diverticulitis
  • Pelvic inflammatory disease (PID)
  • Testicular torsion (referred RIF pain)

Complications

  1. Perforation — 20–30% of cases; higher in elderly and very young (atypical presentation)
  2. Appendix mass — contained perforation with omentum walling off; managed conservatively initially (Ochsner-Sherren regimen), elective appendicectomy 6–8 weeks later
  3. Appendix abscess — requires drainage (radiological or surgical) + antibiotics, then interval appendicectomy
  4. Generalised peritonitis — free perforation → emergency surgery
  5. Pylephlebitis — portal vein thrombosis (rare but serious)

Treatment

Non-Perforated Appendicitis

  • Appendicectomy — definitive treatment; laparoscopic approach preferred (shorter hospital stay, less pain, quicker return to work)
  • Open appendicectomy — Gridiron (McBurney's) incision in RIF, or Lanz incision
  • Antibiotic therapy alone — emerging evidence (APPAC trial) that antibiotics alone may treat uncomplicated appendicitis in some patients; however, recurrence rate ~39% at 10 years; not yet standard in most settings

Perforated Appendicitis / Peritonitis

  • Emergency laparotomy or laparoscopy
  • Appendicectomy + peritoneal lavage
  • IV antibiotics (broad-spectrum: e.g., cefuroxime + metronidazole; or piperacillin-tazobactam)
Pre-operative preparation:
  • IV fluids, analgesia (does NOT mask signs)
  • IV antibiotics (prophylactic dose at induction)
  • Catheter if needed
  • NBM

20. EXTERNAL HERNIAS

Definition

A hernia is the protrusion of part of the contents of a body cavity through a weakness or defect in its wall, covered by a hernial sac (derived from peritoneum).
An external hernia protrudes to the outside of the body (as opposed to internal hernias which herniate within body cavities).

Anatomy of a Hernia

ComponentDescription
SacPeritoneal covering; has a neck, body, and fundus
ContentsFat, omentum, small bowel, large bowel, ovary, bladder
CoveringsLayers of abdominal wall overlying the sac
DefectThe actual weakness/gap in the abdominal wall

Types of External Hernias

TypeSiteKey Features
Inguinal (indirect)Through deep inguinal ring → inguinal canal → superficial ringMost common (75% of all hernias); follows path of spermatic cord; can descend into scrotum; common in young males
Inguinal (direct)Through Hesselbach's triangle (medial to inferior epigastric vessels)Acquired (weakness of posterior wall); older males; rarely strangulates
FemoralThrough femoral canal (below and lateral to pubic tubercle)More common in women; high risk of strangulation; often presents with strangulation
UmbilicalThrough umbilicusIn adults: acquired (obesity, ascites, pregnancy); in infants: congenital (closes by 2 years)
ParaumbilicalJust above or below umbilicus (through linea alba)Adults; common in obese females
IncisionalThrough previous surgical scarRisk factors: wound infection, obesity, poor nutrition, steroids
EpigastricThrough midline linea alba between umbilicus and xiphoidSmall, often just fat; usually symptomatic
SpigelianThrough semilunar line (lateral border of rectus abdominis)Rare; interparietal (between muscle layers) — difficult to diagnose
ObturatorThrough obturator foramenRare; elderly thin women; "Howship-Romberg sign" (medial thigh pain on hip extension/rotation)
LumbarThrough lumbar triangles (Petit or Grynfeltt)Rare

Inguinal Hernia — In Detail

Boundaries of Inguinal Canal:
  • Anterior wall: External oblique aponeurosis (reinforced laterally by internal oblique)
  • Posterior wall: Transversalis fascia (reinforced medially by conjoint tendon)
  • Floor: Inguinal ligament
  • Roof: Arching fibres of internal oblique + transversus abdominis
Deep ring: Lateral to inferior epigastric vessels Superficial ring: Above pubic tubercle
Indirect vs Direct:
  • Indirect: Lateral to inferior epigastric vessels; through deep ring; congenital (patent processus vaginalis) or acquired; can strangulate
  • Direct: Medial to inferior epigastric vessels; through Hesselbach's triangle; acquired weakness; rarely strangulates
Clinical distinction: At reduction and re-applying pressure over deep ring — indirect hernia is controlled; direct is not.

Clinical Features of Hernia

Symptoms:
  • Lump in the groin/abdomen/scrotum
  • Aching discomfort (especially on standing, straining, or coughing)
  • May be asymptomatic
Examination:
  • Reducible lump that becomes prominent on coughing/straining
  • Expansile cough impulse
  • Inguinal canal examination: Finger invagination into superficial inguinal ring

States of a Hernia — Critical Definitions

StateDescriptionManagement
ReducibleContents return to abdominal cavity spontaneously or with gentle pressureElective surgical repair
Irreducible (Incarcerated)Contents cannot be returned; but blood supply intactUrgent surgical repair
ObstructedBowel within sac is obstructed (no passage) but blood supply intactEmergency surgery
StrangulatedBlood supply to hernial contents is compromised → ischaemia → gangreneEmergency surgery — most dangerous
Signs of strangulation:
  • Sudden increase in pain (constant, not intermittent)
  • Tense, tender, irreducible swelling
  • Vomiting, features of bowel obstruction
  • Absent cough impulse
  • Systemic upset (fever, tachycardia)

Investigations

  • Usually clinical diagnosis
  • Ultrasound — if diagnosis uncertain, impalpable hernia
  • CT scan — for complex/recurrent hernias, to identify Spigelian or obturator hernias
  • Herniogram — rarely used now

Treatment

Conservative (Observation)

  • Asymptomatic inguinal hernias (especially in elderly/high surgical risk): "watchful waiting" is safe in the short term
  • Truss (external support): Rarely used; does not cure hernia

Surgical Repair — Principles

The aim: close the defect and reinforce the abdominal wall
Open Repairs:
ProcedureTechniqueIndication
Bassini repairApproximation of conjoint tendon to inguinal ligamentSimple inguinal hernia (historical)
Shouldice repairMulti-layer repair of posterior wallLow recurrence rate; still used
Lichtenstein tension-free repairMesh placed over defectGold standard for inguinal hernia; low recurrence
Darn repairPolypropylene suture darningLow-tension repair
Laparoscopic Repairs:
ProcedureApproach
TAPP (Trans-Abdominal Pre-Peritoneal)Enter peritoneal cavity, reduce hernia, place mesh preperitoneally
TEP (Totally Extraperitoneal)Operate entirely in preperitoneal space; no peritoneal entry
Laparoscopic advantages: Less pain, quicker recovery, better for bilateral or recurrent hernias
Femoral hernia repair:
  • Low approach (Lockwood): Through groin
  • High approach (McEvedy): Through abdomen; better for strangulation
  • Laparoscopic: TEP/TAPP

Complications of Hernia Repair

  • Immediate: Haemorrhage, injury to bowel/bladder/vas deferens/femoral vessels
  • Early: Wound infection, haematoma, urinary retention, ileus
  • Late: Chronic groin pain (most common after Lichtenstein), mesh infection, mesh migration, recurrence (most important — approximately 1–5% with mesh, higher with non-mesh repairs), testicular atrophy (injury to testicular vessels), hydrocele

Special Situations

  • Strangulated hernia with gangrenous bowel: Resect bowel, primary anastomosis vs. stoma; delayed mesh placement (contaminated field)
  • Paediatric inguinal hernia: All require surgery (high rate of incarceration); herniotomy (ligation of sac) without mesh
  • Femoral hernia: Repair should be prompt even if asymptomatic (high strangulation rate)

QUICK SUMMARY TABLE

TopicKey ConceptSurgical Emergency
Colorectal tumoursAdenoma-carcinoma sequence; CEA for monitoring; Duke's stagingObstruction/perforation → Hartmann's
Blunt abdominalSpleen most injured; FAST scan; NOM for stableHaemodynamic instability → laparotomy
Blunt chest"ATOM FC" life threats; tension PTX = needle decompressionTension PTX, cardiac tamponade, massive haemothorax
Penetrating abdominalPeritonitis/instability → immediate laparotomy; NOM for stable SW/GSWPeritonitis, instability, evisceration
PolytraumaLethal triad (hypothermia+acidosis+coagulopathy); ATLS ABCDE; damage controlAll of primary survey threats
UlcersH. pylori + NSAIDs; triple therapy; perforation = Graham patchPerforation, bleeding
FracturesOpen > closed; compartment syndrome = fasciotomy; 3Rs (reduce, immobilise, rehab)Open fractures, compartment syndrome
Intestinal obstructionAdhesions #1 SBO; carcinoma #1 LBO; drip and suck; strangulation = emergencyStrangulation
Acute appendicitisAlvarado score; RIF pain + fever + leukocytosis; laparoscopic appendicectomyPerforation with peritonitis
External herniasLichtenstein mesh = gold standard; femoral = high strangulation riskStrangulated hernia

*Sources: Mulholland & Greenfield's Surgery (7e), Sleisenger & Fordtran's GI & Liver Disease, Rosen's Emergency Medicine, Roberts & Hedges' Clinical Procedures in Emergency Medicine, Robbins & Kumar Basic Pathology — all cross-referenced from the Medical Textbook Library.*Your credits are exhausted. Your daily credits reset tomorrow, or you can purchase a top-up for more.
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