Oesophageal perforation

Overview

Oesophageal perforation is a life-threatening emergency - full-thickness breach of the oesophageal wall allowing luminal contents to leak into surrounding structures. The oesophagus lacks a serosa, so mediastinitis develops within hours. Mortality approximately doubles when treatment is delayed beyond 24 hours.

Causes

Iatrogenic - most common (~60%); upper GI endoscopy, dilatation, TOE, intubation, surgery
Boerhaave syndrome - spontaneous full-thickness tear from forceful vomiting; left posterolateral distal oesophagus; highest mortality
Foreign body - sharp objects at natural narrowing points; common in children and elderly
External trauma - penetrating neck/chest injuries
Tumour-related - erosion or complication of malignant stenting

Presentation

Mackler's triad (Boerhaave): forceful vomiting → sudden severe chest/epigastric pain → subcutaneous emphysema in neck/chest wall
Chest pain - severe, sudden, tearing or pleuritic; may radiate to back, shoulder, or epigastrium
Subcutaneous emphysema - crepitus in neck or supraclavicular fossae; pathognomonic when present
Hamman's sign - mediastinal crunch on auscultation synchronous with heartbeat (pneumomediastinum)
Left-sided pleural effusion - dyspnoea, dullness at left base
Systemic sepsis - fever, tachycardia, hypotension develop rapidly; may be absent early
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Classic mimic of aortic dissection, MI, and PE. The discriminating feature is the history of forceful vomiting or recent oesophageal instrumentation immediately before the pain. Always ask: "What were you doing just before the pain started?"

Investigations

🥇 First-line

Chest X-ray - pneumomediastinum, left pleural effusion, pneumothorax, surgical emphysema, widened mediastinum. Normal CXR does NOT exclude perforation (up to 12% normal initially)

🏆 Gold standard

CT chest and neck with IV contrast - identifies site, extent, and complications (mediastinal fluid/gas, pleural collections); also excludes aortic dissection

🥈 Second-line

Water-soluble contrast swallow (e.g. Gastrografin) - demonstrates leak directly; used when CT equivocal or to confirm before conservative management
Blood tests: FBC, CRP, U&E, LFTs, clotting, group and save, blood cultures - raised WCC/CRP indicate mediastinitis/sepsis; supportive rather than diagnostic
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Barium swallow must be avoided - barium mediastinitis is extremely harmful if contrast extravasates. Use water-soluble contrast (Gastrografin) only.

Differential diagnosis

Key differentials for sudden severe chest pain after vomiting
ConditionDistinguishing features
Aortic dissectionTearing chest/back pain; CT angiography shows aortic flap, no mediastinal contamination
Acute MIECG changes, troponin rise, no mediastinal air
Pulmonary embolismPleuritic pain + dyspnoea; CTPA shows filling defect, no mediastinal contamination
Mallory-Weiss tearMucosal (partial thickness) only; presents with haematemesis, not mediastinitis; managed conservatively
Perforated peptic ulcerFree air under diaphragm; epigastric peritonism; no pneumomediastinum
Hamman syndromeBenign spontaneous pneumomediastinum; young thin male after straining; no full-thickness tear, no sepsis

Management

Immediate resuscitation: nil by mouth, IV access, fluid resuscitation, analgesia, oxygen
IV broad-spectrum antibiotics and antifungals - cover mediastinal contamination
Nasogastric tube insertion - for decompression and enteral feeding
Urgent senior surgical/upper GI input - all patients
Surgical repair (primary closure + mediastinal washout) - Boerhaave syndrome, large/freely communicating perforations, or contaminated mediastinum; ideally within 24 hours
Endoscopic stenting - selected iatrogenic or contained perforations in specialist centres
Conservative management - small, contained iatrogenic perforations with no systemic sepsis; requires close observation and low threshold to escalate
Chest drain - for pleural effusion/empyema (typically left-sided)
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Patients managed conservatively who progress to sepsis must be escalated to surgery without delay - failure to recognise conservative management failure is a major avoidable harm.

Complications

Mediastinitis - most feared; bacteria and digestive enzymes cause fulminant inflammation and necrosis
Empyema/pleural effusion - usually left-sided; may need chest drain or surgical decortication
Sepsis and multiorgan failure - end-result of uncontrolled contamination
Oesophageal fistula - oesophagopleural or oesophagobronchial; more likely with delayed diagnosis
Stricture - late complication causing dysphagia requiring dilatation

Prognosis

Overall mortality 10-25% with prompt treatment
Boerhaave syndrome: mortality up to 40% even with treatment; untreated approaches 100%
Iatrogenic perforation diagnosed immediately: mortality <5% in some series
Poor outcome predictors: delayed diagnosis (>24 h), distal perforation, mediastinitis, septic shock, malignant oesophagus, advanced age