Oesophageal Perforation

Oesophageal perforation is full thickness disruption of the oesophageal wall with leakage of oesophageal and gastric contents into the neck, mediastinum, pleural cavity or peritoneum.

Common causes are endoscopic instrumentation, dilation, surgery, spontaneous rupture, foreign bodies and trauma.

The absence of a protective serosal layer and proximity to the mediastinum allow rapid contamination, mediastinitis, pleural sepsis and shock.

Outcome is determined by location, size, underlying oesophageal disease, extent of contamination, physiological state and speed of source control.

Thoracic perforation commonly produces severe chest or upper abdominal pain, dyspnoea and systemic toxicity.

Cervical perforation may present with neck pain, dysphagia, odynophagia, cervical tenderness or subcutaneous emphysema.

Abdominal oesophageal perforation produces epigastric pain and peritonitis.

Tachycardia may be the earliest physiological abnormality. Progressive fever, respiratory distress, hypotension and organ dysfunction indicate uncontrolled contamination.

Contrast enhanced CT chest and upper abdomen with CT oesophagography where available: preferred investigation; identify the leak and determine whether contamination is contained or has entered the mediastinum or pleural cavity.

Diagnostic endoscopy is reserved for persistent diagnostic uncertainty or when an endoscopic treatment is planned because insufflation can enlarge a perforation.

Keep strictly fasting.

Establish IV access, correct hypovolaemia and begin broad spectrum antimicrobial therapy immediately.

A practical adult regimen is:

Piperacillin tazobactam 4.5 g IV every 8 hours by extended infusion, adjusted for renal function.

Add antifungal treatment only when there is a specific risk such as prolonged critical illness, immunosuppression, established Candida infection or another strong clinical indication. Routine empirical antifungal therapy is not required for every perforation.

Give acid suppression, for example:

Pantoprazole 40 mg IV every 12 hours.

Establish early nutrition, preferably distal enteral feeding when feasible.

A stable patient with an early, contained perforation, minimal contamination and no sepsis may be managed without open surgery provided intensive surgical, endoscopic and radiological support is immediately available. This still requires antibiotics, fasting, nutritional support and drainage of any collection.

Small iatrogenic defects, particularly below approximately 2 cm, may be closed with endoscopic clips when recognised early.

Larger defects can be treated with fully covered self expanding oesophageal stents or endoscopic vacuum therapy in selected patients. Endoscopic therapy must be combined with drainage of contaminated mediastinal or pleural spaces where necessary.

Operate urgently for:

• Haemodynamic instability
• Free uncontained leak
• Extensive pleural or mediastinal contamination
• Established sepsis not controlled by drainage
• Necrotic oesophageal tissue
• Failed endoscopic treatment
• Underlying pathology that cannot be adequately treated conservatively

Primary repair is preferred when tissue can hold sutures. Debride devitalised margins, close the defect without tension, reinforce the repair with vascularised tissue where appropriate and provide generous external drainage.

Extensive destruction, delayed presentation with nonrepairable tissue or severe underlying oesophageal disease may require exclusion, diversion or oesophagectomy.

Delay should not be accepted simply because the perforation is more than 24 hours old. Viable repairable tissue can still be primarily repaired in selected delayed cases, but contamination control becomes increasingly important.