Boerhaave Syndrome

Boerhaave syndrome is spontaneous full thickness oesophageal rupture caused by a sudden rise in intraoesophageal pressure, usually during forceful vomiting against a closed upper oesophageal sphincter.

The classic tear occurs in the distal thoracic oesophagus, most often along the left posterolateral wall.

It differs from Mallory Weiss syndrome, which is a mucosal tear causing bleeding without transmural perforation.

Boerhaave syndrome is particularly dangerous because gastric and oesophageal contents rapidly contaminate the mediastinum and pleural cavity.

The classic history is severe chest or epigastric pain immediately after forceful vomiting or retching.

Patients may develop dyspnoea, dysphagia, tachycardia and rapid systemic deterioration.

Subcutaneous emphysema may occur but is not sufficiently sensitive to exclude the diagnosis when absent.

A left pleural effusion, hydropneumothorax or rapidly developing septic picture after vomiting should strongly raise suspicion.

The historical Mackler triad of vomiting, chest pain and subcutaneous emphysema is present in only a minority.

Contrast enhanced CT chest and upper abdomen with CT oesophagography: preferred emergency investigation; demonstrate the oesophageal defect and determine the degree of mediastinal and pleural contamination.

Do not perform a routine diagnostic endoscopy before CT simply because chest pain followed vomiting.

Resuscitation and source control begin immediately.

Keep fasting.

Start:

Piperacillin tazobactam 4.5 g IV every 8 hours by extended infusion, with renal adjustment.

Give:

Pantoprazole 40 mg IV every 12 hours.

Drain associated pleural collections promptly, usually with image guided or operative thoracic drainage.

A very small contained rupture in a stable patient without sepsis and with minimal contamination can occasionally be treated with intensive nonoperative management plus endoscopic closure. Most spontaneous thoracic ruptures presenting with significant mediastinal or pleural contamination require aggressive source control.

Primary operative repair is appropriate when the oesophagus remains viable and the defect can be safely closed. Debride necrotic edges, close the mucosal and muscular defect securely and reinforce with vascularised tissue such as intercostal muscle, pleura, diaphragm or gastric fundus according to location.

Thoracic contamination requires extensive drainage and debridement in addition to closure of the hole.

Endoscopic fully covered stenting can be used in selected stable patients and as an adjunct when a persistent leak remains after repair. Stents are less suitable for very proximal defects, defects crossing the gastroesophageal junction or extremely large disruptions.

Endoscopic vacuum therapy is increasingly useful for contained leaks and infected cavities when local expertise exists.

Extensive oesophageal necrosis, malignancy or nonrepairable destruction may require oesophagectomy or diversion.

Provide early enteral nutrition through a feeding jejunostomy or another route distal to the injury when prolonged fasting is expected.