Perforation and mesenteric ischaemia

Perforated Peptic Ulcer: Recognition and Emergency Repair

Perforation represents the most lethal complication of peptic ulcer disease, carrying an overall 30-day mortality between 10% and 25%. Most perforations occur on the anterior wall of the first part of the duodenum (anterior duodenal ulcers perforate, whereas posterior duodenal ulcers erode into the gastroduodenal artery, causing massive upper gastrointestinal haemorrhage).

Risk Factors

• Regular use of Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) or selective COX-2 inhibitors.
• Helicobacter pylori infection.
• Tobacco smoking and heavy alcohol consumption.
• Systemic corticosteroids and concurrent anticoagulants/antiplatelets.
• Physiological shock, severe burns (Curling ulcer), or intracranial trauma (Cushing ulcer).

Clinical Presentation and Evolution

1. Initial Perforation Phase (0–2 hours): Abrupt, explosive onset of agonizing, knife-like, epigastric pain. The patient can frequently recall the precise minute the pain struck. Escape of acidic gastric juice and bile into the lesser and greater peritoneal sacs triggers violent chemical peritonitis.
2. Intermediate Phase (2–12 hours): Chemical peritonitis is temporarily diluted by peritoneal transudate. Pain may subjectively soften slightly, creating a false sense of improvement (the "illusion of relief"), but physical examination reveals persistent profound involuntary guarding and tachycardia. Peritoneal fluid tracks down the right paracolic gutter into the RIF, mimicking acute appendicitis (Valentino sign).
3. Late Phase (> 12–24 hours): Secondary bacterial invasion establishes diffuse purulent peritonitis, marked abdominal distension, septic shock, hypovolaemia, and multi-organ dysfunction syndrome.

Examination Hallmarks

• The patient lies entirely stationary, breathing shallowly, as any diaphragmatic descent or trunk movement causes intolerable pain.
• Board-like abdominal rigidity across all four quadrants.
• Complete absence of bowel sounds.
• Loss of normal liver dullness on percussion over the right mid-axillary line due to subdiaphragmatic free air.

Diagnostic Investigations

• Suspected perforation: Urgent surgical assessment and CT are usually preferred in a patient stable enough for imaging. A plain erect chest radiograph can show free air where CT is unavailable, but a negative film does not exclude perforation and should not delay definitive assessment.
• Abdominal CT with IV Contrast: The definitive diagnostic modality if the CXR is negative or equivocal despite high clinical suspicion. Demonstrates extraluminal free gas, free fluid tracking throughout the gutters, discontinuity of the gastroduodenal wall, and mesenteric stranding.
• Absolute Contraindication: Upper gastrointestinal endoscopy and barium swallow are strictly contraindicated in suspected perforation, as endoscopic air insufflation and chemical barium leakage cause catastrophic peritoneal contamination.

Emergency Surgical Management

1. Resuscitation: Aggressive crystalloid fluid loading, NGT decompression on continuous suction, Foley catheter placement, and strict NBM.
2. Initial treatment: Analgesia, nil by mouth, measured crystalloid resuscitation, acid suppression where indicated and prompt antibiotics selected for intra-abdominal infection, allergy and renal function. A bleeding-ulcer PPI infusion is not a mandatory perforation regimen. Source control is urgent.
3. Operative Repair: Emergency exploratory laparotomy or laparoscopy. The defect is identified, ulcer edges biopsied (mandatory for gastric ulcers to rule out ulcerated adenocarcinoma), irrigated with copious warm saline, and closed using an omental patch repair (Graham patch), in which a pedicled tongue of vascularized greater omentum is placed over the perforation and secured with absorbable sutures.

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Acute Mesenteric Ischaemia: Time-Critical Vascular Emergency

Acute mesenteric ischaemia (AMI) is a life-threatening abdominal catastrophe characterized by sudden interruption of blood flow to the mesenteric arterial or venous vascular beds, leading to rapid intestinal ischaemia, gangrene, and death. Overall mortality exceeds 50% to 70%, with survival fundamentally dependent upon early diagnosis before full-thickness transmural bowel infarction develops.

Pathophysiological Subtypes

1. Acute Superior Mesenteric Artery (SMA) Embolism (~50%): Most common subtype. Cardiogenic emboli (dislodged from the left atrium or left ventricle) travel down the aorta into the SMA. Because the SMA branches off the aorta at an acute angle, emboli typically lodge $3-10\text{ cm}$ distal to the origin, sparing the proximal jejunum (middle colic and inferior pancreaticoduodenal arteries) but compromising the remaining small bowel and right colon.
2. Acute SMA Thrombosis (~25%): Occurs at the site of severe pre-existing atherosclerotic narrowing, usually at the very origin of the SMA from the aorta. Patients often have a prior history of "intestinal angina" (postprandial dull pain, weight loss, food fear).
3. Non-Occlusive Mesenteric Ischaemia (NOMI, ~15%): Splanchnic vasoconstriction in response to severe systemic hypoperfusion, cardiogenic shock, cardiac arrest, septic shock, or high-dose vasopressor therapy (adrenaline, noradrenaline) in critically ill ICU patients.
4. Mesenteric Venous Thrombosis (MVT, ~10%): Thrombus formation within the superior mesenteric vein and portal venous system. Driven by prothrombotic states (Factor V Leiden, protein C/S deficiency, antiphospholipid syndrome), portal hypertension, pancreatitis, or malignancy.

Clinical Presentation and Diagnosis

• Cardinal Clinical Hallmark: Severe, agonizing, unremitting central abdominal pain disproportionate to minimal or absent physical examination findings. In the early stages, the abdomen remains soft, non-distended, and non-tender or only mildly tender without guarding, because the mucosal ischaemia has not yet penetrated to irritate the parietal peritoneum.
• Late Signs of Gangrene: As full-thickness transmural bowel infarction occurs, the patient develops abdominal distension, severe involuntary guarding, board-like rigidity, "red-currant jelly" bloody diarrhoea (mucosal sloughing), profound diaphoresis, and refractory septic shock.
• Mesenteric ischaemia: Elevated lactate is concerning but neither specific nor proof of irreversible bowel necrosis; early ischaemia may have normal lactate. Severe pain out of proportion, embolic risk or shock warrants urgent surgical assessment and CT angiography without waiting for a late biochemical sign.
• Definitive Diagnostic Investigation: Biphasic CT Mesenteric Angiography (CTMA)—incorporating non-contrast, early arterial, and portal venous phases—is the diagnostic gold standard (sensitivity $> 93\%$, specificity $> 95\%$). It demonstrates SMA vessel cut-off, filling defects, non-enhancing bowel wall segments, bowel wall thickening, mesenteric stranding, and late features such as pneumatosis intestinalis (gas within the bowel wall) and portal venous gas.
• Plain Films: Plain abdominal X-rays are completely normal in early disease and must never be used to rule out mesenteric ischaemia.

Emergency Management

• Immediate Resuscitation: Rapid intravascular volume loading with balanced crystalloids to restore splanchnic perfusion, correction of electrolyte disturbances, and immediate therapeutic anticoagulation with an intravenous unfractionated heparin bolus and infusion (titrated to APTT $1.5-2.5$ times control) to halt propagation of thrombus.
• Broad-Spectrum Antibiotics: Intravenous piperacillin-tazobactam or meropenem to combat bacterial translocation through damaged intestinal mucosa.
• Time-Critical Surgical Revascularization: Emergency vascular and general surgical intervention. Endovascular therapies (catheter-directed embolectomy, balloon angioplasty, or stenting) may be attempted in centres with immediate interventional radiology availability for non-peritonitic patients. In patients with peritonitis or suspected bowel necrosis, emergency exploratory laparotomy is mandatory to revascularize the SMA (surgical embolectomy or mesenteric bypass grafting) and resect necrotic bowel, followed by a planned second-look laparotomy at 24 to 48 hours to reassess bowel viability.

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Clinical comparison: Acute Abdominal Emergencies Comparison

• Perforated ulcer: Primary Pathophysiology: Sudden pain, guarding or generalised peritonism; no single sign excludes it; Classic Pain Evolution: CT where feasible, urgent surgical assessment and source control; High-Yield Bedside Sign: Resuscitation, analgesia and appropriate antibiotics
• Acute Mesenteric Ischaemia: Primary Pathophysiology: Embolic or thrombotic occlusion of SMA causing acute gut ischaemia; Classic Pain Evolution: Sudden, agonizing, severe unremitting periumbilical colic; High-Yield Bedside Sign: Pain entirely disproportionate to physical findings on palpation; Definitive Investigation of Choice: Biphasic CT Mesenteric Angiography (CTMA); Immediate Management Priority: Crystalloid resuscitation, therapeutic IV heparin, urgent revascularization and bowel resection

Primary references (checked 7 October 2026): WSES perforated-ulcer guidance.