General Surgery

• Abdominal cutaneous nerve entrapment syndrome: localised abdominal wall pain from an entrapped anterior cutaneous nerve branch.
• A diagnosis of exclusion — but USS-guided local anaesthetic injection is both diagnostic and therapeutic.

• Diagnosis needs ≥5 attacks: midline/periumbilical dull pain ± nausea, vomiting, anorexia, pallor.
• Attacks last 2–72 hours with complete freedom between attacks.
• Treatment: paracetamol, ibuprofen, and sumatriptan for attacks.

• Watch for hyponatraemia from associated diarrhoea/fluid loss — in an elderly patient this can cause confusion that muddies the clinical picture.
• Investigate with CT mesenteric angiography; pneumatosis intestinalis + shock are late, ominous findings.

Causes in order of frequency: diverticulitis (1) > malignancy (2) > Crohn's disease (3). Suspect with pneumaturia, faecaluria or recurrent polymicrobial UTIs.

• Structural: mass / tumour, stricture, extrinsic compression.
• Neurological: stroke, brainstem pathology, motility disorder.
• Infective/inflammatory: candidiasis, oesophagitis.

• Hydatid cyst — look for a calcified rim.
• Pyogenic liver abscess — heterogeneous collection; a gas–fluid interface points to gas-producing bacteria.

• Copper deposition disease: low caeruloplasmin; diagnosis scored by the Leipzig criteria.
• Triad to recognise: Kayser–Fleischer rings (vision/eye finding), jaundice/liver disease, and neurology — dystonia, tremor, rigidity.

• High post-op risk of biliary disease — rapid weight loss drives gallstone formation.
• A classic setting for thiamine deficiency and Wernicke's encephalopathy — supplement early if intake is poor or vomiting. Screen for B1, B6, B12 and folate deficiency long-term, plus iron and fat-soluble vitamins.
• Hepatic decompensation is more likely after malabsorptive bypass than after sleeve gastrectomy — monitor liver function, especially with rapid weight loss.

• Densities: white = bone and calcification; grey = soft tissue; black = air.
• Poor soft-tissue discrimination — it cannot properly evaluate the bowel wall, and it may show obstruction without revealing the cause.
• For suspected free gas the erect CXR is the better first film.

• Normal: gas in the stomach, a small amount in small bowel, and almost always gas in the sigmoid and rectum. Scattered bowel gas is normal.
• Rectal gas absent + paucity of gas in the transverse colon → think obstruction around the splenic flexure.
• RIF tenderness in large bowel obstruction = the caecum may be compromised — escalate.
• Trace the psoas margin and the line of the ureters when hunting renal tract stones.

The more fixed a segment is and the larger its diameter, the harder it is for it to get stuck — which is why mobile, narrow small bowel obstructs most readily.

• Opiates (slowed transit), dehydration, immobility.
• Undiagnosed Hirschsprung disease (aganglionic bowel — faeces and air proximally; rarely perforates because the bowel has adapted over time).

• Sigmoid > caecal.
• A classic “coffee bean” sigmoid volvulus may not need CT — involve surgery early.
• Endoscopic decompression is both diagnostic and therapeutic; recurrence is common, so subsequent resection of the involved colon is usually needed.

• Free gas is usually right-sided under the diaphragm (don't confuse with the gastric bubble on the left).
• Supine signs: Rigler's sign (gas on both sides of the bowel wall — “double wall”), football sign (large central lucency — classically necrotising enterocolitis in neonates), falciform ligament sign (the ligament outlined as a tissue density).
• A benign cause to remember: jejunal diverticulitis can produce free gas without catastrophe — but treat every pneumoperitoneum as surgical until proven otherwise.

• Staghorn calculus — check the renal pelvis outline.
• Bladder stones.
• Gastric band — confirm the band has not slipped (check its angle and position).
• Ureteric stents and other hardware — confirm position.

• Overt: abdominal pain and hypotension.
• Subclinical: a rising CRP when it should be falling — trend it, and record drain outputs.

• No routine early CT — the diagnosis is clinical + lipase; early scans understate severity.
• Watch over time; CT if deteriorating — looking for necrosis, vascular complications (ischaemia) or perforation as alternative diagnoses.
• Always ask: is there a luminal/biliary obstruction driving this (gallstones → USS ± MRCP)?
• Meanwhile: fluids, analgesia, early enteral nutrition.