Boerhaave Syndrome
A life-threatening, complete rupture of the esophagus, typically caused by forceful vomiting, allowing stomach contents to leak into the chest cavity.
Emergency Management: Boerhaave syndrome itself is a catastrophic surgical emergency requiring immediate activation of thoracic surgery and ICU teams.
Boerhaave syndrome is a full-thickness transmural spontaneous rupture of the esophagus, most commonly occurring at the left posterolateral aspect of the distal esophagus, usually secondary to a sudden increase in intraesophageal pressure.
Detailed Overview
Unlike a Mallory-Weiss tear (which is a partial-thickness mucosal tear), Boerhaave syndrome is a full-thickness rupture. It allows gastric contents, acid, and bacteria to spill into the mediastinum and pleural space, rapidly leading to chemical mediastinitis, bacterial infection, sepsis, and septic shock. It is a highly lethal surgical emergency.
Epidemiology & Demographics
Rare condition, accounting for ~15% of all esophageal perforations (iatrogenic is more common). Typically affects males in their 50s-70s. High mortality rate (20-40%) even with treatment.
Etiological Mechanism
Barotrauma to the esophagus. A sudden, massive rise in intra-abdominal and intraesophageal pressure against a closed glottis (most classically due to severe vomiting/retching).
Primary Causes
Severe vomiting/retching (often post-binge drinking or heavy eating), weightlifting, childbirth, or severe coughing.
A sudden, uncoordinated rise in intragastric pressure against a contracted cricopharyngeus muscle transmits massive barometric pressure into the esophagus. The left posterolateral wall of the distal third of the esophagus (3-5 cm above the gastroesophageal junction) lacks support from surrounding structures and is the weakest anatomical point. It tears, causing a full-thickness perforation. Gastric contents heavily contaminate the mediastinum, causing a severe inflammatory systemic response syndrome (SIRS).
Diagnostic Criteria & Guidelines
Diagnosis is established by an esophagram using water-soluble contrast showing extravasation of contrast, or by a CT scan of the chest with IV and oral contrast showing esophageal wall defect, pneumomediastinum, and mediastinal fluid.
Immediate NPO status, aggressive IV fluid resuscitation, and broad-spectrum IV antibiotics (e.g., Piperacillin-Tazobactam 4.5 g Q6H + Vancomycin 15-20 mg/kg Q8-12H). IV Proton Pump Inhibitor (e.g., Pantoprazole 40 mg IV BID).
Second-Line & Adjunctive Therapy
Emergent surgical intervention is the cornerstone of therapy for tears diagnosed <24 hours: Primary closure via left thoracotomy with pleural flap reinforcement and mediastinal drainage. For patients unfit for surgery with a contained leak, endoscopic stent placement may be attempted.
Surgical & Procedural Management
Primary repair via left thoracotomy (for lower esophageal tears). If the diagnosis is delayed (>24 hours) and tissue is highly friable/necrotic, primary repair fails. These require esophageal exclusion, cervical esophagostomy (spit fistula), feeding jejunostomy, and delayed reconstruction (gastric pull-up).
Patient Counseling & Advice
Counsel the family that the patient is in critical condition and prolonged ICU stay, multiple surgeries, and long-term feeding tubes are highly likely. The mortality risk is substantial.
Follow-Up & Monitoring Schedule
Repeat water-soluble contrast esophagram after 7-14 days to confirm no leak before initiating oral intake. Long-term monitoring for esophageal stricture formation.
Preventive Strategies
Early antiemetic therapy (e.g., Ondansetron) in patients presenting with severe, intractable vomiting.
Mortality is 10-20% if treated within 24 hours, but climbs to >50% if treatment is delayed beyond 24 hours. Without surgery/treatment, mortality is nearly 100%.