01OverviewDefinition, clinical context and the essential points that orientate the chapter.
A sudden pressure rise against a closed cricopharyngeus during vomiting commonly tears the distal left posterolateral oesophagus in Boerhaave syndrome. Instrumentation can injure anywhere, particularly across strictures or after therapeutic dilation. Leakage causes chemical injury followed by polymicrobial infection. Pain may radiate to the back or shoulder, and dyspnoea or sepsis can dominate; a normal early chest radiograph does not exclude disease.
CT shows extraluminal gas, wall disruption, pleural effusion and collections and can demonstrate active oral-contrast leak. A water-soluble contrast swallow adds dynamic localisation when the patient is stable and CT is equivocal, but a negative study does not overrule convincing clinical and CT evidence. Endoscopy can inspect or treat but insufflation may worsen contamination and should occur only within the definitive expert plan.
Management pairs defect control with drainage. Endoscopic clips, covered stents or vacuum therapy suit selected defects with viable tissue and accessible anatomy. Surgery may debride, repair with vascularised buttress, divert or resect when contamination is extensive, tissue is non-viable or cancer or end-stage oesophagus underlies rupture. Non-operative care is an active monitored pathway with serial imaging, drainage, nutrition and a low threshold to intervene.
Key points
- Boerhaave syndrome is spontaneous full-thickness rupture after forceful vomiting; iatrogenic injury after endoscopy or dilation is a common alternative mechanism.
- The classical triad is insensitive, so use the event and physiological trajectory rather than waiting for vomiting, pain and subcutaneous emphysema together.
- Contrast-enhanced CT of neck, chest and upper abdomen with oral contrast when appropriate identifies air, fluid, leak site and pleural or mediastinal contamination.
- Initial treatment includes nil by mouth, immediate resuscitation, broad intravenous antibacterial cover for aerobic and anaerobic organisms, analgesia, organ support, drainage and nutrition planning; obtain cultures only when doing so does not delay treatment.
- A promptly recognised small iatrogenic perforation may be closed endoscopically within a planned expert pathway. A free thoracic Boerhaave rupture with contamination generally needs urgent operative source control and primary repair when feasible, plus debridement and drainage.
- Time matters because tissue oedema, necrosis and sepsis worsen the chance of primary repair, but treatment selection still depends on location, cause, viability and underlying disease.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Pressure rupture
Forceful vomiting against a closed upper sphincter abruptly raises intraluminal pressure and can tear the distal oesophagus.
Iatrogenic injury
Endoscopy, dilation, mucosal resection, difficult tube passage and thoracic or upper gastrointestinal surgery can perforate either normal wall or tissue weakened by disease.
Pathological wall failure
Cancer, caustic injury, severe inflammation or retained foreign material weakens tissue and can cause spontaneous or procedural breach.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Chemical contamination
Saliva, gastric acid, digestive enzymes and food enter mediastinal tissues and pleural spaces, causing immediate chemical inflammation before established bacterial infection.
- 2Polymicrobial sepsis
Oral and gastrointestinal organisms multiply in devitalised mediastinal tissue and undrained pleural collections, producing capillary leak, septic shock and multiorgan failure.
- 3Progressive tissue loss
Delay permits oedema, necrosis and enlargement of the defect, reducing the feasibility of simple primary closure.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Abrupt severe chest or epigastric pain after forceful vomiting is the key Boerhaave context, even without palpable crepitus.
New pain, tachycardia, fever or breathlessness after dilation, endoscopic resection or foreign-body removal demands urgent investigation.
Neck pain, dysphagia, voice change and cervical emphysema may follow proximal perforation and can spread into the mediastinum.
Pleural fluid, hypoxaemia and shock suggest free mediastinal and pleural soilage rather than a tiny contained defect.
Temporary analgesic improvement does not prevent progressive infection; unexplained sepsis after vomiting or instrumentation should reopen the diagnosis.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Contrast-enhanced CTFirst step - Why
- Map perforation, extraluminal gas, collections and pleural contamination.
- Interpretation and limitations
- Scan the relevant neck, chest and upper abdomen; oral contrast can show active leakage, while absence of visible extravasation does not exclude a contained tear.
- 02
Water-soluble contrast swallow - Why
- Demonstrate dynamic leak site in a stable cooperative patient.
- Interpretation and limitations
- A negative initial study may miss a small perforation and should not delay treatment when CT and physiology are convincing.
- 03
Pleural fluid analysis - Why
- Identify oesophageal contamination when an effusion is drained.
- Interpretation and limitations
- Food debris, very low pH or high salivary amylase supports communication, but source control should not wait for every laboratory result.
- 04
Endoscopy in a planned setting - Why
- Define mucosa and provide clip, stent or vacuum therapy in selected defects.
- Interpretation and limitations
- Insufflation and passage can enlarge injury, so diagnostic endoscopy is not a casual substitute for CT and should involve the treating team.
- 05
Serial sepsis and organ assessment - Why
- Determine response to drainage and closure.
- Interpretation and limitations
- Track perfusion, lactate, oxygenation, urine output, inflammatory markers and drain character; a technically placed stent does not prove control.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Acute coronary syndrome
Chest pain with vomiting and autonomic symptoms still requires ECG and troponin while perforation is assessed from context and imaging.
Aortic catastrophe
Abrupt chest or back pain and shock may reflect dissection or rupture; contrast CT protocol must address the plausible vascular emergency.
Spontaneous pneumothorax
Dyspnoea and pleuritic pain can arise from pleural air without an oesophageal leak, distinguished by history and CT findings.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01Emergency source controlOperate on a free contaminated thoracic rupture when feasibleFirst stepAfter repeated vomiting, an adult develops shock; CT shows a free distal thoracic leak and a large left pleural collection.+
- 1Begin ABCDE resuscitation, keep nil by mouth, obtain blood and pleural cultures only if this causes no treatment delay, and start the hospital’s verified oesophageal-rupture antimicrobial regimen with immediate microbiology input.
- 2Assemble upper-GI surgery, endoscopy, radiology, anaesthesia and critical care and drain pleural contamination promptly; shock and free leakage make simple endoscopic clipping inappropriate even though CT cannot directly certify tissue-edge viability.
- 3At urgent operation, direct inspection finds devitalised rupture edges; debride back to viable tissue, perform tension-free primary repair with buttress and drain mediastinal and pleural spaces. Reserve stent, vacuum therapy, diversion or resection for anatomy, tissue or underlying disease that makes primary repair unsuitable.
- 4In critical care, provide specialist-directed enteral feeding distal to the repair or parenteral support as appropriate while swallowing remains unsafe. Verify source control through falling vasopressor and oxygen requirements, controlled drain character and interval contrast assessment before reintroducing oral intake across the repair.
02Contained cervical injuryUse monitored non-operative careA small cervical perforation is contained, the patient is stable and there is no distal obstruction.+
- 1Admit under specialist care, keep nil by mouth initially and provide intravenous antimicrobials and nutrition.
- 2Drain any collection and use repeat clinical and imaging assessment to confirm containment.
- 3EscalationEscalate to endoscopic or operative therapy for worsening pain, leak, sepsis or loss of containment.
- 4Demonstrate safe healing before oral intake is advanced.
03Underlying diseaseTreat beyond the holeA perforation occurs through an obstructing oesophageal cancer.+
- 1Resuscitate physiological collapse and control pleural or mediastinal contamination immediately.
- 2Obtain tissue and staging information only as safely feasible without delaying sepsis treatment.
- 3Choose stenting, resection, diversion or palliation through the cancer and emergency MDT according to fitness and goals.
- 4Confirm nutrition, symptom control and oncology ownership after the acute episode.
Key medicines and prescribing safety1 treatment · regimens, roles and cautions+
Dated North Bristol oesophageal-rupture antimicrobial example (current status unconfirmed)
North Bristol NHS Trust antimicrobial guideline v7.3 is dated October 2022, was due for review in July 2023 and had no issuing-body confirmation of current validity when checked on 8 September 2026. Its historical adult oesophageal-rupture example is co-trimoxazole 960 mg IV twice daily plus metronidazole 500 mg IV three times daily plus fluconazole 400 mg IV once daily. Although the site table prints five days, the same document directs oesophageal-rupture duration to a medical microbiologist, so duration must follow current receiving-hospital policy and microbiology advice. Co-trimoxazole 960 mg is 10 mL of 16 mg/80 mg per mL concentrate, usually added to 250 mL compatible infusion fluid such as sodium chloride 0.9% and infused over 60–90 minutes. At creatinine clearance 15–30 mL/min use 480 mg every 12 hours; below 15 mL/min this product is not recommended. Infuse metronidazole 500 mg/100 mL at about 5 mL/min. Infuse fluconazole 2 mg/mL at no more than 10 mL/min; for multiple dosing at creatinine clearance 50 mL/min or less in a non-dialysis patient, give the initial dose then 50% of the maintenance dose.Do not use this dated example as a live prescription without current local confirmation and pharmacy/microbiology review of the entire combination. Co-trimoxazole is contraindicated in the first trimester of pregnancy, acute porphyria and previous drug-induced immune thrombocytopenia caused by trimethoprim or a sulfonamide; also exclude relevant hypersensitivity and severe liver impairment. Review renal function, potassium, sodium, blood counts, rash risk and interactions including warfarin, methotrexate, ACE inhibitors, ARBs and potassium-sparing diuretics. The usual 10 mL concentrate-in-250 mL dilution must be checked against fluid status and the exact compatible-fluid table; do not invent a concentrated alternative for fluid restriction. With metronidazole, avoid alcohol, review coumarin anticoagulants and neurological toxicity, and reduce the daily dose to one third in hepatic encephalopathy. With fluconazole, review QT interactions, electrolytes, liver toxicity and sodium/fluid load. Reassess all agents after source control and culture results.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Mediastinitis
Infected mediastinal tissues can progress rapidly to abscess, pleural empyema, vascular erosion, refractory septic shock, respiratory failure and death.
Pleural empyema
Leakage into the chest creates a contaminated effusion requiring effective drainage in addition to luminal control.
Late stricture
Healing by fibrosis after repair, stenting or caustic inflammation can produce recurrent dysphagia requiring careful reassessment.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Repeat observations, lactate, oxygen requirement and urine output through the early source-control period.
- Measure drain quantity and content and correlate with oral intake and imaging.
- Provide enteral feeding distal to the leak or parenteral nutrition according to anatomy and duration.
- Reimage persistent fever, pain, respiratory failure or inflammatory rise for undrained contamination or device migration.
- After healing, assess stricture, reflux, swallowing, nutrition and the underlying cause of rupture.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Mackler triad is insensitive
Absence of emphysema does not make severe post-emetic chest pain safe.
Location changes contamination
Cervical leaks may remain contained, while thoracic tears rapidly soil mediastinum and pleural cavities.
Closure alone can fail
A perfectly covered defect remains dangerous if infected pleural and mediastinal collections are not drained.
Stents require ownership
Migration, pressure injury and removal timing are active clinical issues, not administrative afterthoughts.
11Common pitfallsFrequent interpretation and management errors.
- 01
Treating post-vomiting chest pain as reflux without imaging when physiology is abnormal.
- 02
Relying on a normal early chest radiograph to exclude perforation.
- 03
Performing unplanned diagnostic endoscopy that enlarges the defect or delays CT.
- 04
Closing the lumen while leaving pleural or mediastinal contamination undrained.