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Parathyroid Adenoma

Definition and Epidemiology

• Robbins Pathologic Basis of Disease, p. 1010
• Schwartz's Principles of Surgery, p. 1665

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Etiology and Molecular Pathogenesis

1. Cyclin D1 (CCND1) gene inversion - A pericentromeric inversion on chromosome 11 relocates the CCND1 gene adjacent to the PTH gene promoter, causing overexpression of cyclin D1 (a cell cycle regulator), driving cell proliferation. Even without this inversion, cyclin D1 is overexpressed in up to 40% of adenomas.
2. MEN1 gene mutation - ~15% of sporadic tumors carry somatic mutations of the MEN1 tumor suppressor gene (chromosome 11q13), with loss of heterozygosity (LOH) at the second allele.
3. CDC73 mutation - Encodes parafibromin; mutated in ~70% of sporadic parathyroid carcinomas and occasionally in adenomas. Germline CDC73 mutations cause the rare hyperparathyroidism-jaw tumor (HPT-JT) syndrome.

• Robbins Pathologic Basis of Disease, p. 1010

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Pathology

Gross Appearance

• Almost always solitary (double adenomas occur in only 1.7-12% of PHPT cases)
• Weight averages 0.5-5 g (mean ~0.55 g; tumours up to 53 g recorded)
• Well-circumscribed, soft, tan to reddish-brown (or yellow-red to orange-brown) nodule
• More severe hypercalcemia correlates with larger adenoma size
• The remaining glands are normal or shrunken due to feedback suppression (helps distinguish from hyperplasia)

Microscopic Appearance

• Sheets of uniform, polygonal chief cells with small, centrally placed nuclei and pale/vacuolated cytoplasm
• Nests of larger oxyphil cells are also present; rarely, adenomas are composed entirely of oxyphil or water-clear cells
• A rim of compressed, non-neoplastic parathyroid tissue may be visible at the edge
• Mitotic figures are rare; bizarre/pleomorphic nuclei (endocrine atypia) may be present - this is NOT a criterion for malignancy
• Stromal fat is inconspicuous (unlike normal parathyroid)

• Robbins Pathologic Basis of Disease, p. 1011
• Scott-Brown's Otorhinolaryngology, p. 2113

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Variants of Parathyroid Adenoma (WHO 4th Ed, 2017)

• Scott-Brown's Otorhinolaryngology, p. 2207

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Clinical Presentation

Asymptomatic (most common today)

Symptomatic

• Robbins Pathologic Basis of Disease, p. 1012
• Schwartz's Principles of Surgery, p. 1667

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Biochemical Diagnosis

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Localization Imaging

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Treatment

Surgery (definitive)

• Minimally invasive parathyroidectomy (MIP): Focused unilateral exploration guided by preoperative localization studies. Suitable when both sestamibi and ultrasound concordantly identify the same gland (~95% success).
• Bilateral neck exploration: Standard when localization fails, multiglandular disease is suspected, or IOPTH is unavailable.
• Intraoperative PTH monitoring (IOPTH): PTH has a 3-5 minute half-life; a >50% drop from baseline at 10 minutes confirms curative resection (the Miami criterion).
• Radio-guided parathyroidectomy: Uses pre-injected Tc-99m sestamibi and a handheld gamma probe; rarely used now as it offers little advantage over preoperative scanning.

Non-surgical management (for asymptomatic, ineligible patients)

• Adequate hydration, avoid thiazides and immobilization
• Cinacalcet (calcimimetic): Reduces serum calcium by increasing sensitivity of the CaSR to extracellular calcium; does not improve bone density
• Bisphosphonates: Improve bone density
• Schwartz's Principles of Surgery, p. 1670-1701
• Scott-Brown's Otorhinolaryngology, p. 2086

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Familial Associations

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Recent Evidence (2024-2026)

• A 2024 systematic review in JCEM (PMID 38739762) confirms that parathyroidectomy has a significant positive skeletal effect in PHPT patients.
• A 2026 meta-analysis in ANZ J Surg (PMID 41721481) shows minimally invasive parathyroidectomy under locoregional anaesthesia is a safe and effective alternative to general anaesthesia.

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Varicose Veins - Complete Clinical Overview

Definition

• Telangiectasias / spider veins (C1): intradermal dilated vessels <1 mm
• Reticular veins (C1): dilated blue subdermal veins 1-3 mm

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Epidemiology & Risk Factors

• Adult prevalence of visible varicose veins: 30-50%
• More common in women; increases markedly with age (Edinburgh Vein Study: 11.5% at 18-24 years up to 55.7% at 55-64 years)

• Bailey and Love's Short Practice of Surgery, 28th Ed, p. 1051

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Classification

1. Primary vs Secondary

2. CEAP Classification (2020 Updated)

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Pathophysiology

1. Valvular incompetence - valve leaflets fail to coapt, allowing reflux
2. Primary wall weakness - defective connective tissue (reduced collagen/elastin ratio) causes vein dilatation, which stretches and separates valve cusps
3. Calf muscle pump failure - ineffective muscle contraction fails to propel blood centrally
4. Perforator incompetence - bidirectional flow in perforators allows high-pressure deep system blood to enter low-pressure superficial system

• Great Saphenous Vein (GSV) joins the femoral vein at the Saphenofemoral Junction (SFJ) in the groin - responsible for ~60% of varicose veins (medial thigh and calf distribution)
• Small Saphenous Vein (SSV) joins the popliteal vein at the Saphenopopliteal Junction (SPJ) - responsible for ~20% (posterolateral calf)
• Anterior Accessory GSV (AAGSV) - anterolateral thigh/calf distribution

• Fitzpatrick's Dermatology, p. 2185; Bailey and Love, p. 1052

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Clinical Features

Presenting Symptoms (Subjective)

• Aching, heaviness, throbbing, burning, bursting sensation in affected leg
• Itching over varicosities
• Ankle swelling (oedema), especially in the evening
• All symptoms worsen with prolonged standing and are relieved by elevation and compression
• Cosmetic concern (most common complaint)
• Symptoms may be disproportionate to the severity of visible veins - a trial of compression helps confirm venous aetiology

Signs (Objective)

• Tortuous, dilated subcutaneous veins - visible and palpable
• Saphena varix - large dilated veins at SFJ, presents as a soft groin lump disappearing on lying (can mimic inguinal hernia; has a cough impulse)
• Oedema of ankle (pitting - venous)
• Haemosiderin pigmentation (brown staining) at medial gaiter area
• Venous eczema / stasis dermatitis - dry, scaly, itchy skin
• Lipodermatosclerosis - woody induration and fibrosis of the skin
• Atrophie blanche - white, scarred plaques
• Varicose (venous) ulcer - typically medial gaiter area (over medial malleolus), shallow, sloping edges, granulating base, painful

Complications

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Clinical Tests (Bedside Examination)

Note: Tourniquet tests (Trendelenburg/Perthes) and handheld Doppler are now largely abandoned in favour of duplex ultrasound, which provides definitive anatomical and physiological information.

• Bailey and Love, p. 1052

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Investigations

1. Duplex Ultrasound Scan (DUS) - MANDATORY before any intervention

• Confirm reflux in the deep and superficial venous systems
• Define the exact distribution and extent of reflux and affected junctions (SFJ, SPJ, perforators)
• Assess deep vein patency (exclude obstruction/DVT)
• Assess suitability for treatment (diameter, extent, tortuosity)
• Detect thrombus within superficial veins
• Identify pelvic source of reflux

• High-frequency linear array transducer: 7.5-13 MHz
• Patient examined standing for diameter/reflux measurements
• Reflux definition: retrograde flow lasting ≥0.5 seconds (superficial/perforator veins) or ≥1 second (proximal deep veins)
• Elicited by calf/foot squeeze release, manual compression, or Valsalva

2. Other Investigations (Selected Cases)

• Bailey and Love, p. 1052; Schwartz's Surgery, p. 1670

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Management

Framework (SVS/AVF/AVLS 2022/2023 CPG + NICE CG168)

Step 1 - Conservative Management

• British Classification: Class 1 (14-17 mmHg), Class 2 (18-24 mmHg), Class 3 (25-35 mmHg)
• Improves symptoms but does NOT prevent progression or occurrence
• Compliance is universally poor
• CPG (NICE/SVS): Compression is an adjunct, NOT a substitute for definitive treatment; interventional treatment is superior and cost-effective
• ABI must be checked before prescribing; contraindicated if ABI <0.8

• Leg elevation
• Weight loss
• Exercise / calf muscle pump activation
• Avoid prolonged standing

Step 2 - Interventional Treatment (for symptomatic C2-C6)

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A. Endothermal Ablation - First-line treatment (CPG Grade 1A)

• Both are equivalent in efficacy; associated with faster recovery and less morbidity than open surgery
• Bailey and Love, p. 1051-1058; Schwartz's Surgery, p. 1671

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B. Non-Thermal, Non-Tumescent (NTNT) Ablation

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C. Open Surgical Treatment (still used, less commonly)

• Oblique groin incision at pubic tubercle level
• Dissect and ligate SFJ (flush ligation with all six tributaries)
• GSV stripped retrogradely to the knee (not ankle - reduces saphenous nerve injury risk)
• Followed by phlebectomy of residual varicosities

• Popliteal fossa incision at skin crease
• Duplex marking of SPJ essential pre-operatively (very variable anatomy)
• SSV can be ligated or stripped; risk of sural nerve injury with stripping
• Bailey and Love, p. 1052-1658

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D. Phlebectomy (Ambulatory / Stab Phlebectomy)

• Removal of varicose tributaries through multiple small (2-3 mm) stab incisions using phlebectomy hooks
• Performed as sole treatment (isolated tributary incompetence) or concurrently with truncal ablation
• Concomitant phlebectomy gives more rapid QOL improvement and allows single-visit treatment
• Superior to powered transilluminated phlebectomy for bruising and pain

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E. Sclerotherapy (Liquid / Foam)

• Sclerosing agents: sodium tetradecyl sulphate (STS), polidocanol, hypertonic saline
• Liquid sclerotherapy for telangiectasias/reticular veins (C1)
• Foam sclerotherapy for larger varicosities and truncal veins
• Compression bandaging applied post-procedure for 3-5 days, then stockings for 2 weeks
• Complications: pigmentation, thrombophlebitis, DVT, skin necrosis, allergic reaction, visual disturbance (rare, with foam)

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CPG Summary Table (SVS/AVF/AVLS 2022/2023 - Key Recommendations)

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Special Situations

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Surgical Complications

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• Bailey and Love's Short Practice of Surgery, 28th Ed - Chapter 62 (Varicose Veins), pp. 1050-1058
• Schwartz's Principles of Surgery, 11th Ed - Chapter 23, pp. 1669-1672
• Mulholland & Greenfield's Surgery, 7th Ed - Chapter on Chronic Venous Insufficiency
• SVS/AVF/AVLS CPG Part I (Gloviczki et al., J Vasc Surg Venous Lymphat Disord 2023;11:231-261) - Duplex & Truncal Reflux Treatment
• SVS/AVF/AVLS CPG Part II (Gloviczki et al., J Vasc Surg Venous Lymphat Disord 2024;12:101670) - Compression, Tributaries & Complications
• NICE CG168 - Varicose veins: diagnosis and management (2013, reviewed 2016)

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Clinical Features of Intestinal Obstruction + Neonatal Causes

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PART 1 - ACUTE INTESTINAL OBSTRUCTION: Clinical Features

Definition & Types

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Cardinal Clinical Features (The "Big Four")

"Pain, Vomiting, Distension, Absolute Constipation"

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HISTORY

1. Abdominal Pain

• First and most prominent symptom - occurs suddenly and is usually severe
• Character: Colicky (intermittent, wave-like) - coincides with peristaltic contractions
• Proximal (jejunum/high ileum): Colic in waves every 3-5 minutes, lasting ~30 seconds; centred at the umbilicus/epigastrium; vomiting often terminates the pain
• Distal (terminal ileum): Longer intervals between cramps, 8-10 minutes; more distension, less vomiting
• Colonic obstruction: Pain in the lower abdomen (hypogastrium)
• With increasing distension: colicky pain becomes constant, diffuse aching
• Severe unrelenting pain = strangulation until proven otherwise; beware the patient whose pain is not controlled with IV opiates

2. Vomiting

• The more proximal the obstruction, the earlier and more frequent the vomiting
• Character changes with time:
  • Early: Ingested food/gastric contents
  • Intermediate: Bilious (bile-stained, duodenal content)
  • Late (days): Faeculent vomiting - grave sign (bacterial overgrowth of intestinal content; takes ~3-4 days in complete obstruction)
• In high duodenal/proximal small bowel obstruction: vomiting is early, profuse, relieves pain
• In low/colonic obstruction: vomiting is late, distension is pronounced
• Bilious vomiting in a neonate = mechanical obstruction until proven otherwise

3. Distension

• Depends on site and duration of obstruction
• Small bowel (proximal): Less distension, central (umbilical)
• Small bowel (distal): Pronounced central distension
• Large bowel: Peripheral (flank) distension, appears later
• Visible peristalsis: Pathognomonic when present; can be provoked by gently flicking the abdominal wall; seen in thin patients
• Volvulus: Regional distension

4. Absolute Constipation

• Defined as failure to pass both faeces AND flatus - absolute feature of complete obstruction
• Important caveat: Takes at least 24 hours to develop as a sign; early cases may still pass stool evacuated from below the obstruction
• Diarrhoea may occur instead of constipation in:
  • Mesenteric vascular occlusion
  • Richter's hernia
  • Pelvic abscess with adhesion obstruction
  • Partial obstruction

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EXAMINATION

A. Inspection

B. Palpation

• Muscle guarding: Conspicuously absent in simple obstruction (differentiates from peritonitis)
• Local tenderness: Impending or established ischaemia
• Localised tenderness over surgical scar: Adhesion obstruction
• Generalised tenderness + rigidity: Indicates need for early laparotomy (perforation/infarction)
• Shock (tachycardia, hypotension): Suggests strangulation/ischaemia

C. Bowel Sounds

• High-pitched tinkling rushes: Classic of mechanical obstruction; coincide with colic, may precede vomiting
• Normal bowel sounds: Negative predictive value (do NOT exclude obstruction)
• Scanty or absent: Long-standing obstruction; bowel has become inactive
• Ominously quiet bowel: Strangulation/peritonitis developing - bowel becomes atonic

D. Dehydration

• Seen predominantly in small bowel obstruction (repeated vomiting + fluid sequestration into obstructed loops)
• Up to 6 litres/day of salt-rich fluid secreted into small intestine normally; in obstruction, this accumulates
• Signs: dry mucous membranes, sunken eyes, poor venous filling, oliguria, tachycardia
• Labs: raised urea, raised haematocrit, electrolyte disturbance

E. Other Findings

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Features Distinguishing Simple vs Strangulating Obstruction

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PART 2 - NEONATAL INTESTINAL OBSTRUCTION: Classification & Clinical Features

General Features of Obstruction in the Newborn

• Bilious vomiting in a neonate = mechanical intestinal obstruction until proven otherwise
• Non-bilious persistent vomiting may indicate: gastro-oesophageal reflux, pyloric stenosis, or high duodenal (pre-ampullary) obstruction
• Additional features:
  • Abdominal distension (degree directly related to level of lesion)
  • Failure to pass meconium (98% of full-term infants pass meconium within 24 hours)
  • Hyperactive bowel sounds
• Distension confined to upper abdomen = high (duodenal/jejunal) obstruction
• Massive distension (may cause respiratory embarrassment) = lower level
• Erythema/oedema of anterior abdominal wall = peritonitis (perforation or ischaemia)

Classification of Neonatal Intestinal Obstruction

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1. INTESTINAL ATRESIA

Definition

Incidence

Aetiology

Sites (frequency order)

1. Duodenal atresia - most common form of neonatal intestinal obstruction; associated with Down syndrome (trisomy 21) in 30%
2. Jejunal atresia - second most common
3. Ileal atresia
4. Colonic atresia - rare

Types (Grosfeld Classification)

Clinical Features

• Bilious vomiting - dominant in jejunal atresia (onset within hours of birth)
• Abdominal distension - more prominent in ileal atresia (lower level)
• Failure to pass normal meconium - small amounts of pale meconium may be passed even with complete atresia
• Possible antenatal history of polyhydramnios (failure to swallow amniotic fluid)
• Associated malformations common (assess whole bowel intraoperatively for multiple atresias)

Investigations

• Plain abdominal X-ray (supine + erect): Variable number of dilated loops with air-fluid levels; number of dilated loops reflects level of obstruction
• "Double bubble" sign (duodenal atresia): Gas in stomach + duodenum; no distal bowel gas
• Contrast enema: In stable infants for distal obstructions; identifies microcolon (distal ileal atresia), meconium plug, Hirschsprung's, or meconium ileus

Management

• Resuscitate with IV fluids, NGT decompression
• Duodenal atresia: Duodenoduodenostomy
• Jejunal/ileal atresia: Resection of dilated proximal segment (poor motility) + primary end-to-end anastomosis (end-to-back "fish-mouth" technique for disparity in lumen size)
• Tapering of proximal bowel if extremely dilated
• Temporary stoma if primary anastomosis not safe (unstable infant, ischaemia)

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2. MECONIUM ILEUS

Definition

Pathophysiology

• Cystic fibrosis (autosomal recessive, CFTR gene mutation) causes:
  • Pancreatic enzyme deficiency → meconium not liquefied
  • Abnormal chloride secretion → dehydrated, viscous intestinal contents
• Thick meconium becomes impacted in terminal ileum → progressive intestinal obstruction

Types

Clinical Features

• Presents shortly after birth
• Progressive abdominal distension - visibly dilated loops of bowel often palpable
• Failure to pass meconium
• Bilious vomiting (intermittent)
• Family history of CF may be present (autosomal recessive)

Investigations

• Plain X-ray: Dilated loops of small intestine; characteristic "ground glass" appearance (gas bubbles trapped in inspissated meconium in distal ileum); no air-fluid levels (meconium too viscous to separate from gas)
• Contrast enema: Shows microcolon (unused, underdeveloped colon); terminal ileum filled with meconium pellets; in uncomplicated cases, no abrupt termination of gas
• Gene mutation analysis (CFTR)
• Sweat test (beyond neonatal period): elevated sodium and chloride levels >70 mmol/L
• In complicated cases: eggshell calcifications on X-ray (intraperitoneal calcification from meconium peritonitis)

Management

• Hyperosmolar Gastrografin enema (water-soluble contrast): Draws fluid into gut lumen + detergent properties liquefy meconium; may be repeated at 12-hourly intervals
• N-acetylcysteine (Mucomyst) enema: Alternative/adjunct
• Patient requires extra IV fluids to compensate for fluid shifts
• If contrast cannot be refluxed into dilated ileum: suggests associated atresia → laparotomy

• Laparotomy + enterotomy + bowel irrigation
• Resection + primary anastomosis
• Resection + end ileostomy + mucus fistula
• Bishop-Koop anastomosis (end-to-side ileoileostomy with irrigating stoma - now rarely used)
• CF management long-term: pancreatic enzyme replacement, physiotherapy, nutritional support

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3. MECKEL'S DIVERTICULUM

Definition

The "Rule of 2's"

Ectopic Tissue

• Present in ~50% of cases
• Gastric mucosa (80-85% of ectopic tissue) → acid secretion → peptic ulceration of adjacent ileal mucosa
• Also: pancreatic tissue, duodenal mucosa

Clinical Presentations (Complications)

Investigations

• Meckel's scan (Tc-99m pertechnetate scintigraphy): Investigation of choice for bleeding; ectopic gastric mucosa takes up isotope; sensitivity ~85% in children
• Plain X-ray: Usually unhelpful; occasionally dilated bowel loops with air-fluid levels within the diverticulum
• CT scan: May show tubular blind-ending structure from antimesenteric border of terminal ileum; CT enterography has improved detection
• Barium contrast studies: Generally unhelpful

Management

• Symptomatic Meckel's: Diverticulectomy or segmental small bowel resection + anastomosis (preferred if base is wide, inflamed, or contains ectopic tissue)
• Do NOT amputate at base and invaginate (risk of stricture, leaving ectopic tissue)
• Incidental finding at surgery: Leave if wide-mouthed and not thickened; remove if in doubt

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4. FOREIGN BODY

Mechanisms of Obstruction

• Direct luminal obstruction: Large or irregularly shaped foreign body (e.g., ingested toy part, bezoar)
• Obstruction is most common at anatomical narrowings: pylorus, terminal ileum, ileocaecal junction
• In neonates: rare; more often iatrogenic (feeding tube, calcified meconium fragments)
• Gallstone ileus: Erosion of gallstone from gallbladder into intestine → obstruction of terminal ileum; gas in biliary tree on X-ray (Rigler's triad: pneumobilia + small bowel obstruction + ectopic gallstone)
• Bezoar: Phytobezoar (vegetable matter) or lactobezoar (milk) in neonates/infants

Clinical Features

• Symptoms of small bowel obstruction (pain, vomiting, distension, constipation)
• Foreign body may be visible on plain X-ray if radio-opaque

Management

• Plain X-ray first: identifies radio-opaque foreign bodies
• CT abdomen: Identifies level and nature of obstruction; gas in biliary tree if gallstone ileus
• Endoscopic retrieval if in accessible location
• Surgical removal if causing complete obstruction/perforation

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SUMMARY TABLE: Neonatal Causes Compared

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• Bailey & Love's Short Practice of Surgery, 28th Ed, Ch. 78 - pp. 1399-1410
• Schwartz's Principles of Surgery, 11th Ed, Ch. 39 - pp. 1752-1755
• Pye's Surgical Handicraft, 22nd Ed, Ch. 27 - pp. 408-410
• S. Das - Manual on Clinical Surgery, 13th Ed, pp. 479-481
• Robbins & Kumar Basic Pathology - p. 561
• Robbins, Cotran & Kumar Pathologic Basis of Disease - pp. 1490-1503
• Sleisenger & Fordtran's GI and Liver Disease - pp. 1396-1420

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Dr. Rashide's Week 3 - Complete Study Notes

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TOPIC 1 - PANCREATITIS

Definition

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Aetiology ("GET SMASHED")

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Pathophysiology

• Obstruction/injury → premature activation of trypsinogen → trypsin within acinar cells
• Trypsin activates other zymogens (phospholipase A2, elastase, lipase)
• Autodigestion → pancreatic oedema, haemorrhage, fat necrosis, parenchymal necrosis
• Release of inflammatory mediators (cytokines, bradykinin, PAF) → systemic effects: SIRS → MODS

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Clinical Presentation (Bailey & Love)

Symptoms

• Pain: Cardinal symptom - epigastric, sudden onset reaching maximum within minutes (not hours), severe, constant, lasts hours to days; radiates to back in 50%; relieved by leaning forward; does NOT improve with vomiting
• Nausea and vomiting: Marked, persistent retching; vomiting does not relieve pain (unlike peptic ulcer)
• Hiccoughs: Due to gastric distension or diaphragmatic irritation

Signs

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Investigations

1. Is the diagnosis correct?
2. How severe is the attack?
3. What is the aetiology?

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Severity Scoring (Revised Atlanta Classification 2013)

• Mild AP: 80-90% of cases; mortality ~1%
• Severe AP: 5-10% of cases; mortality 20-50%

Ranson & Glasgow Scoring (Score ≥3 = Severe)

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TOPIC 2 - COMPLICATIONS OF PANCREATITIS

Systemic Complications (First Week)

1. Hypovolaemic Shock

• Massive third-space fluid loss into retroperitoneum and peritoneal cavity (up to 6-8L)
• Vomiting and nasogastric losses
• Vasodilation from inflammatory mediators (bradykinin, PAF)
• Haemorrhage from erosion of peripancreatic vessels
• Result: reduced circulating volume → decreased cardiac output → shock

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2. Septic SIRS (Systemic Inflammatory Response Syndrome)

• Heart rate >90/min
• Core temperature <36°C or >38°C
• Respirations >20/min or pCO₂ <32 mmHg
• WBC <4000 or >12,000/mm³

• Early SIRS = sterile inflammatory mediator release (cytokines, IL-1, IL-6, TNF-α)
• Late septic SIRS = infection superimposed (translocation of gut bacteria into necrotic pancreas)
• Infected pancreatic necrosis = bacteraemia → septic shock → MODS; mortality up to 50%
• Organisms: E. coli, Klebsiella, Pseudomonas, Enterococcus (gut flora translocation)

• Early: supportive (no prophylactic antibiotics routinely - controversial)
• Late infected necrosis: CT/USS-guided fine needle aspiration → if purulent: drainage (endoscopic transgastric or percutaneous) + targeted antibiotics (imipenem/meropenem)
• Pancreatic necrosectomy as last resort

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3. DIC (Disseminated Intravascular Coagulation)

• Activated pancreatic enzymes (trypsin, elastase, phospholipase A2) enter systemic circulation
• Trigger the extrinsic coagulation pathway → widespread microthrombi
• Consumption of clotting factors (V, VIII, fibrinogen) and platelets
• Secondary activation of fibrinolysis → uncontrolled bleeding

• Simultaneous thrombosis (multi-organ ischaemia) AND bleeding (skin petechiae, GI bleed, haematuria, oozing from venepuncture sites)
• Labs: ↓ platelets, ↓ fibrinogen, ↑ PT/APTT, ↑ D-dimer, ↑ FDPs (fibrin degradation products)

• Treat underlying cause (pancreatitis resuscitation)
• Fresh frozen plasma (FFP) for coagulopathy
• Platelet transfusion if <50,000/mm³ and bleeding
• Cryoprecipitate for fibrinogen replacement
• Heparin rarely used (controversial)

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4. Gastrointestinal Haemorrhage / Bleeding

• Erosion of peripancreatic vessels (splenic artery most common) → haemorrhage into pseudocyst = "sentinel bleed" → potentially catastrophic
• Stress ulceration of gastric/duodenal mucosa (Curling's ulcer) due to shock and impaired mucosal perfusion
• Haemorrhagic pancreatitis - Grey Turner's sign, Cullen's sign
• Splenic vein thrombosis → gastric varices → haematemesis
• Portal hypertension from splenic vein compression

• Haemodynamic resuscitation
• Stress ulcer prophylaxis (PPI/H2 blocker)
• CT angiography to identify bleeding vessel → interventional radiology (embolisation)
• Surgery if refractory

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5. Perforation

• Rare direct complication of acute pancreatitis
• Occurs secondary to enzymatic digestion of adjacent viscera (duodenum, transverse colon)
• More often: perforation is in the differential diagnosis (perforated peptic ulcer can simulate pancreatitis and vice versa)
• Also: infected pancreatic necrosis can erode into adjacent bowel → internal fistula or free perforation
• Colon (transverse colon) is most susceptible to enzymatic injury → colonic fistula
• Management: surgical repair; colostomy if colon involved

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Systemic Complications Table (Bailey & Love)

Local Complications Table

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TOPIC 3 - LIVER SEGMENTS (Couinaud Classification)

Concept

Anatomical Landmarks

• Cantlie's line: Plane through the middle hepatic vein and the IVC - divides liver into right and left hemilobes
• The right and left hepatic veins subdivide each hemilobe into two sectors
• Portal pedicles further divide sectors into segments

Couinaud Segments

Functional Divisions

Key Portal Anatomy

• Portal vein = confluence of superior mesenteric vein + splenic vein (at the neck of pancreas)
• Left portal vein is longer, more horizontal; right portal vein shorter
• Common hepatic artery → from coeliac axis → proper hepatic artery → right and left hepatic arteries (arterial variation in 40%)
• Replaced right hepatic artery arises from SMA (13% of patients) - must be identified at surgery

Clinical Relevance of Segments

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TOPIC 4 - INFLAMMATORY BOWEL DISEASE (IBD)

Definition

Extra-intestinal Manifestations (Both)

Complications

Management Overview

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TOPIC 5 - COLORECTAL CARCINOMA (CRC)

Epidemiology

• 3rd most common cancer worldwide; 2nd most common cause of cancer death
• Peak incidence: 60-70 years; males slightly more than females
• Incidence increasing in young adults with IBD or Lynch syndrome

Risk Factors

Adenoma-Carcinoma Sequence

Clinical Features

Symptoms vary by location:

Staging

Dukes Classification (Modified):

TNM Staging (AJCC 8th Edition - current standard):

Investigations

• Colonoscopy + biopsy: Gold standard; identifies synchronous lesions (~50% of patients)
• CT colonography (virtual colonoscopy): For patients unable to tolerate colonoscopy
• CT chest/abdomen/pelvis: Staging for metastases
• MRI pelvis: Rectal cancer staging - T-stage, circumferential resection margin (CRM)
• CEA (carcinoembryonic antigen): Not for diagnosis; used for post-operative surveillance (rising CEA = recurrence)
• FBC: Anaemia (iron deficiency)
• LFTs: Liver metastases

Surgical Management

• Right hemicolectomy: Caecal, ascending colon, hepatic flexure
• Left hemicolectomy: Descending colon
• Anterior resection: Sigmoid and upper rectum
• Abdominoperineal resection (APR): Low rectal; permanent colostomy
• Hartmann's procedure: Emergency obstruction/perforation; colostomy + rectal stump
• Total mesorectal excision (TME): Standard for rectal cancer; reduces local recurrence

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TOPIC 6 - LIVER PATHOLOGIES

A. HEPATOCELLULAR CARCINOMA (HCC)

Epidemiology

• Most common primary liver tumour globally; 5th most common cancer worldwide
• M:F = 4-8:1; peak in 5th-6th decade (earlier in endemic areas)

Risk Factors

• Cirrhosis (any cause) - most important; 70-90% of HCC arises in cirrhotic liver
• Hepatitis B (HBsAg carriers - risk even without cirrhosis via direct oncogenic mechanisms; HBx protein)
• Hepatitis C (cirrhosis required for carcinogenesis)
• Aflatoxin B1 (Aspergillus-contaminated food - endemic in Africa/Asia)
• Alcohol-related cirrhosis
• NAFLD/NASH-related cirrhosis
• Haemochromatosis, Wilson's disease, α1-antitrypsin deficiency

Clinical Features

• Often silent until advanced (pre-existing cirrhosis masks symptoms)
• Right upper quadrant pain / dull ache
• Hepatomegaly - hard, nodular liver; hepatic bruit in 25%
• Weight loss, anorexia, malaise
• Jaundice - late feature
• Ascites - usually haemorrhagic
• Decompensation of previously stable cirrhosis
• Paraneoplastic syndromes: Hypoglycaemia (insulin-like factors), hypercalcaemia, erythrocytosis, polycythaemia

Investigations

Staging (BCLC - Barcelona Clinic Liver Cancer):

• Stage 0/A: Very early/early - resection or transplantation curative
• Stage B: Intermediate - TACE (transarterial chemoembolisation)
• Stage C: Advanced - Sorafenib/Lenvatinib
• Stage D: Terminal - palliative

Milan Criteria for Transplantation:

• Single tumour ≤5 cm OR up to 3 tumours each ≤3 cm, no vascular invasion, no extrahepatic spread

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B. LIVER ABSCESS

Two main types:

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C. HEPATITIS

Viral Hepatitis Overview

Hepatitis B Serology

Acute Hepatitis - Clinical Features (all types)

• Pre-icteric phase: Malaise, anorexia, nausea, vomiting, fever, myalgia, RUQ discomfort; smokers lose desire to smoke; dark urine (bilirubinuria)
• Icteric phase: Jaundice (yellow sclera first), pale stools, dark urine, pruritus, hepatomegaly (tender), splenomegaly (25%)
• Resolution phase: Symptoms improve, jaundice fades

Fulminant Hepatic Failure (FHF)

• Encephalopathy within 8 weeks of onset in previously healthy liver
• Features: coagulopathy (INR >1.5), encephalopathy, cerebral oedema
• Most common causes: Hep B, paracetamol toxicity (in UK), Wilson's disease
• Management: ICU, liver transplantation if criteria met (King's College Criteria)

Chronic Hepatitis - Consequences

• Fibrosis → Cirrhosis → Portal hypertension, varices, ascites, encephalopathy, hepatorenal syndrome, HCC

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• Bailey & Love's Short Practice of Surgery, 28th Ed, Ch. 72 (Pancreatitis), pp. 1290-1300
• Mulholland & Greenfield's Surgery, 7th Ed, Ch. 57 (Liver Anatomy), pp. 2775-2780
• Sleisenger & Fordtran's GI and Liver Disease - IBD and CRC chapters
• Robbins & Kumar Basic Pathology / Pathologic Basis of Disease
• Schwartz's Principles of Surgery, 11th Ed, Ch. 39/15

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Intestinal Obstruction - Complete Notes

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DEFINITION

• Tintinalli's Emergency Medicine: "Intestinal obstruction is the inability of the intestinal tract to allow for regular passage of food and bowel contents secondary to mechanical obstruction or adynamic ileus."
• Pye's Surgical Handicraft: Intestinal obstruction may result from vascular occlusion, mechanical, or neuromuscular factors - all preventing the normal aboral flow of bowel contents.

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CLASSIFICATION

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TYPE 1: DYNAMIC (MECHANICAL) OBSTRUCTION

Peristalsis is present and active - it is working against a physical block. Also called mechanical obstruction.

• Initially shows increased peristalsis (attempt to overcome the block → produces colicky pain and audible bowel sounds)
• With time, dilates, then undergoes flaccidity and paralysis (due to fatigue)
• The bowel distal to the obstruction continues normal peristalsis and absorption until it empties and collapses

Sub-classification by location of the block:

Sub-classification by urgency/blood supply:

Further classification by onset:

• Acute: Sudden complete blockage
• Chronic / Subacute: Gradual narrowing (tumour, stricture) - incomplete or intermittent obstruction

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TYPE 2: ADYNAMIC (NON-MECHANICAL) OBSTRUCTION

There is no physical block. Instead, peristalsis is absent or inadequate due to failure of neuromuscular transmission in the bowel wall.

Sub-types:

A. Paralytic Ileus

• Clinically significant if at 72 hours post-laparotomy: no return of bowel sounds AND no passage of flatus
• Abdominal distension - tympanic, progressive
• Effortless vomiting (no colic - distinguishes from mechanical obstruction)
• Absent bowel sounds (silent abdomen)
• Absolute constipation
• Diffuse, mild abdominal discomfort (not colicky)
• X-ray: gas-filled loops of both small and large bowel with fluid levels; no single point of transition

• Nasogastric suction (not routinely post-elective surgery but needed if prolonged)
• Nil by mouth until bowel sounds return and flatus passed
• IV fluid replacement and electrolyte correction (especially K⁺)
• Treat underlying cause (infection, metabolic)
• Neostigmine 0.5 mg subcutaneously: acetylcholinesterase inhibitor → increases acetylcholine → stimulates peristalsis (especially for colonic pseudo-obstruction)
• CT scan if paralytic ileus prolonged (to exclude mechanical cause or intra-abdominal sepsis)

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B. Pseudo-obstruction (Ogilvie's Syndrome)

• Conservative first: NBM, IV fluids, electrolytes, encourage mobility, stop offending drugs
• Colonoscopic decompression (first-line intervention)
• IV Neostigmine 2mg IV over 3-5 minutes: highly effective for acute colonic pseudo-obstruction; requires cardiac monitoring (risk of bradycardia)
• Surgery (caecostomy or colostomy) only if above fails or perforation occurs

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COMPARISON: DYNAMIC vs ADYNAMIC OBSTRUCTION

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OVERVIEW OF IMPORTANCE AND COMPLICATIONS

Why Intestinal Obstruction Matters

1. Common surgical emergency - accounts for ~3% of all acute abdominal pain admissions
2. Progressive and potentially lethal - mortality rises with each passing hour; untreated complete obstruction is fatal
3. May mask serious underlying pathology (malignancy, hernia, ischaemia)
4. Mimics many other conditions: pancreatitis, perforated peptic ulcer, MI, pneumonia

1. Adhesions (~60%) - post-surgical
2. Hernias (~20%)
3. Neoplasms (~5%)
4. Inflammatory (Crohn's, diverticulitis)
5. Others (volvulus, intussusception, gallstone ileus)

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PATHOPHYSIOLOGY (How Complications Arise)

1. Gas accumulation: bacterial overgrowth produces gas (90% nitrogen after O₂/CO₂ reabsorption); swallowed air
2. Fluid accumulation: digestive secretions (saliva 500 mL + bile 500 mL + pancreatic 500 mL + gastric 1 L/day = ~2.5 L/day minimum) accumulate as absorption fails

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COMPLICATIONS

A. Fluid and Electrolyte Complications

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B. Strangulation and Ischaemia

• Hernial orifices (direct compression)
• Volvulus (twisted mesenteric vessels)
• Intussusception (trapped mesentery)
• Closed-loop obstruction (elevated intraluminal pressure)

1. Venous return compromised first (low pressure) → venous congestion → oedema
2. Raised capillary pressure → impaired local perfusion
3. Arterial supply compromised → haemorrhagic infarction → necrosis
4. Bacterial translocation from ischaemic bowel → endotoxaemia → sepsis

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C. Perforation

• Bowel wall necrosis → full-thickness gangrene → perforation
• Most dangerous site: caecum in large bowel obstruction (thinnest wall + largest diameter)
• Caecal perforation risk when diameter >12 cm
• Perforation → faecal peritonitis → septicaemia → mortality >50%

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D. Septic Complications

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E. Systemic / Multi-organ Complications

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F. Complications Specific to Treatment/Surgery

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Summary of Key Points

Intestinal Obstruction
│
├── DYNAMIC (Mechanical) ─── Peristalsis present, fighting a block
│     ├── Intraluminal (faeces, FB, gallstone, bezoar)
│     ├── Intramural (CA, stricture, intussusception, volvulus)
│     └── Extramural (adhesions, hernia)
│           ├── Simple (blood supply intact)
│           └── Strangulated (blood supply compromised - EMERGENCY)
│
└── ADYNAMIC (Non-mechanical) ─── Peristalsis absent/inadequate
      ├── Paralytic ileus (post-op, sepsis, metabolic, reflex)
      └── Pseudo-obstruction / Ogilvie's syndrome (colonic)

Complications (untreated):
Dehydration → Hypovolaemic shock
Distension → Ischaemia → Strangulation → Gangrene → Perforation
Bacterial translocation → Septicaemia → SIRS → MODS → Death

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• Bailey & Love's Short Practice of Surgery, 28th Ed, Ch. 78, pp. 1394-1412
• Tintinalli's Emergency Medicine: A Comprehensive Study Guide, Ch. 83, pp. 685-727
• S. Das - Manual on Clinical Surgery, 13th Ed, pp. 478-484
• Pye's Surgical Handicraft, 22nd Ed, pp. 9001-9061
• Robbins & Kumar Basic Pathology, p. 561