Boerhaave syndrome and oesophageal perforation

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Spontaneous rupture most often involves the distal thoracic oesophagus on the left posterolateral side, where a sudden intraluminal pressure surge tears through all wall layers. Cervical perforations more often follow instrumentation or foreign bodies and may remain locally contained, whereas thoracic and abdominal leaks can spread quickly through the mediastinum, pleura or peritoneum. The resulting illness is determined by the site, size, time to recognition, underlying oesophageal disease, physiological reserve and amount of contamination rather than by the label alone.

Diagnostic delay is common because the presentation mimics acute coronary syndrome, aortic dissection, pulmonary embolism, pneumothorax, pancreatitis or perforated peptic ulcer. Pneumomediastinum, hydropneumothorax and a new left pleural effusion are useful clues but are not uniformly present. A Mallory-Weiss tear is mucosal and usually presents with bleeding; Boerhaave rupture is transmural and usually presents with pain and sepsis, although haematemesis can occur in either. Appropriate cardiac or aortic imaging can proceed within a coordinated CT strategy when those diagnoses remain plausible.

There is no single procedure suitable for every perforation. Recent Royal College of Surgeons literature continues to support prompt primary repair where viable tissue and anatomy permit, ideally early, while documenting expanding endoscopic approaches in selected patients. A covered stent can divert luminal contents but may migrate and still requires drainage; vacuum therapy needs serial procedures; surgery can debride, close and drain but is physiologically demanding. Decisions belong to a specialist multidisciplinary team with the capability to change strategy quickly when the leak persists or sepsis worsens.

Key points

Boerhaave syndrome is a spontaneous full-thickness oesophageal rupture produced by a sharp pressure rise, classically after forceful vomiting against a closed upper sphincter.
Iatrogenic endoscopy, dilation, surgery, foreign bodies, cancer and caustic injury cause more oesophageal perforations overall than spontaneous rupture in many services.
The classic combination of vomiting, severe chest pain and subcutaneous emphysema is insensitive; tachycardia or an unexplained pleural effusion may appear first.
Thoracic leakage rapidly contaminates the mediastinum and pleural cavity with saliva, gastric contents and mixed organisms, driving sepsis and organ failure.
Keep nil by mouth, obtain large-bore IV access, give analgesia and early broad-spectrum IV antibacterials, and involve critical care, radiology and specialist surgeons at presentation.
Contrast-enhanced CT of the neck, chest and upper abdomen, with carefully selected water-soluble oral contrast, is the practical first-line map of leak and contamination.
A normal chest radiograph, absence of fever or early normal inflammatory markers does not safely exclude perforation.
Treatment may use primary surgical repair, resection, drainage, endoscopic clipping, covered stenting or endoluminal vacuum therapy according to site, delay, contamination and expertise.
Non-operative care is reserved for rigorously selected stable patients with a contained leak, minimal contamination and close expert monitoring, not simply for those presenting late.
Source control includes drainage of pleural or mediastinal sepsis and a nutrition plan; sealing the luminal defect alone can fail when infected collections remain.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Spontaneous pressure rupture

Forceful vomiting or retching against a closed upper sphincter can create a sudden transmural tear, classically in the distal thoracic oesophagus.

Iatrogenic injury

Endoscopy, dilation, surgery and therapeutic oesophageal procedures cause many perforations, with risk influenced by tissue disease and intervention complexity.

Traumatic or pathological rupture

Foreign bodies, blunt or penetrating trauma, caustic injury, cancer and severe inflammation can disrupt an already vulnerable oesophageal wall.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Full-thickness disruption
A pressure spike or direct injury tears mucosa, muscle and adventitia, opening the oesophageal lumen to surrounding compartments.
2
Chemical and microbial contamination
Saliva, gastric contents and mixed organisms rapidly enter the mediastinum, pleura or neck, causing intense tissue inflammation.
3
Sepsis and tissue necrosis
Uncontrolled leakage produces mediastinitis, pleural infection, shock and organ failure, while oedema and devitalisation enlarge the defect.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Post-emetic thoracic ruptureRed flag

Sudden severe lower chest or epigastric pain follows repeated vomiting and is accompanied by breathlessness, painful swallowing, tachycardia or rapidly developing systemic illness.

Iatrogenic perforationRed flag

Persistent pain, fever, hypoxia, crepitus or haemodynamic change begins after dilation, difficult endoscopy, transoesophageal procedure or upper-GI surgery and exceeds expected discomfort.

Cervical leakRed flag

Neck pain, dysphagia, odynophagia, voice change, local swelling or palpable gas follows instrumentation or a sharp foreign body and can track into the mediastinum.

Pleural presentationRed flag

Acute dyspnoea, unilateral reduced air entry, pleuritic pain or a new hydropneumothorax may dominate when a thoracic defect decompresses into the pleural cavity.

Evolving mediastinal sepsisRed flag

Fever, confusion, oliguria, rising oxygen need, acidosis and shock develop as contaminated collections spread, sometimes after a deceptively mild initial period.

Contained limited perforationRed flag

A small localised contrast leak may occur in a stable patient without diffuse contamination, but apparent containment requires specialist imaging review and serial reassessment.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

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
Continuous physiological assessmentFirst step
Why
Detect shock, respiratory failure and deterioration while diagnosis proceeds.
Interpretation and limitations
Trend early-warning score, mental state, oxygen requirement, urine output and response to fluid or vasopressor support. Clinical worsening mandates escalation even if imaging initially called the leak small.
02
Full blood count, organ profile, coagulation and lactate
Why
Define sepsis burden, organ dysfunction and procedural risk.
Interpretation and limitations
Leucocytosis, acidosis, kidney injury and coagulopathy support severe illness but may be absent early. Serial lactate helps assess perfusion; a normal value cannot rule out a fresh rupture.
03
Contrast-enhanced CT neck, chest and upper abdomen
Why
Locate the defect and map mediastinal, pleural and abdominal contamination.
Interpretation and limitations
Extraluminal air or oral contrast, wall discontinuity, mediastinal fluid, pleural effusion and collections support perforation. The anatomic scan range follows symptom level and suspected cause.
04
Water-soluble oral contrast protocol
Why
Increase demonstration of active leakage when the patient can swallow safely.
Interpretation and limitations
Administer only after radiology and surgical discussion because aspiration and delay matter. A negative study does not overrule compelling CT or clinical findings, and thin barium is a specialist second-line option in selected cases.
05
Chest radiography
Why
Rapidly detect pleural gas, effusion, mediastinal air or another thoracic emergency.
Interpretation and limitations
Findings can guide immediate drainage in an unstable patient, but sensitivity is insufficient to exclude a leak and CT should not be withheld after a normal film.
06
Diagnostic endoscopy
Why
Define or treat a defect when cross-sectional imaging is incomplete or endoscopic therapy is planned.
Interpretation and limitations
Insufflation may enlarge contamination, so endoscopy is undertaken by an expert after multidisciplinary agreement with minimal gas and source-control readiness, not as an automatic first test.
07
Pleural fluid analysis and culture
Why
Characterise contaminated effusion and direct antimicrobial therapy after drainage.
Interpretation and limitations
Food debris, low pH or raised salivary amylase can support an oesophageal source; mixed bacterial or fungal growth informs microbiology review but treatment cannot await culture.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Acute coronary syndrome

Retrosternal pain, diaphoresis and vomiting overlap; ECG and cardiac biomarkers requires assessment while imaging investigates perforation clues such as pleural fluid or mediastinal gas.

Aortic catastrophe

Abrupt tearing pain, pulse or neurological deficit and aortic imaging abnormalities favour dissection or rupture, another time-critical diagnosis.

Pneumothorax or perforated ulcer

Unilateral absent breath sounds suggest pneumothorax, while free subdiaphragmatic gas and epigastric peritonism favour gastroduodenal rather than oesophageal perforation.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01First responseTreat suspected perforation before collapseFirst stepA compatible trigger is followed by severe pain, respiratory findings or systemic deterioration.

1Keep nil by mouth, assess airway and breathing, give oxygen when indicated, obtain large-bore IV access and begin careful resuscitation, analgesia and continuous monitoring.
2Call the on-call upper-GI or thoracic surgeon, anaesthetist or critical-care team and radiologist immediately, and arrange transfer to a specialist centre if capability is absent.
3Take blood cultures without delaying treatment and start broad-spectrum intravenous antibacterials covering oral and upper-GI organisms under the local perforation or sepsis regimen.
4Obtain urgent contrast-enhanced CT with an agreed oral contrast component and decompress or drain life-threatening pleural tension only through senior specialist direction.

02Source controlMatch closure and drainage to the leakImaging confirms free or contained oesophageal perforation.

1Define cervical, thoracic or abdominal site, time from injury, defect size, tissue viability, underlying obstruction or cancer, contamination and current organ support.
2Use early primary repair with debridement and drainage when anatomy and viable tissue permit, adding buttress or diversion according to surgical judgement.
3Consider expert endoscopic clipping, covered stenting or vacuum therapy for suitable defects while planning active drainage of pleural and mediastinal collections.
4Choose resection, diversion or staged reconstruction when tissue is non-viable, malignancy obstructs the lumen or primary closure cannot control the source.

03Contained leakApply conservative care only under tight criteriaA small well-contained perforation is found in a stable patient without diffuse sepsis or distal obstruction.

1Have the specialist team confirm containment, free drainage back into the lumen, minimal contamination and the ability to deliver immediate rescue intervention.
2Continue nil by mouth, IV antimicrobials, acid suppression where indicated, thrombosis prevention and a jejunal or parenteral nutrition plan agreed by nutrition specialists.
3Monitor in a high-acuity setting with serial examination, bloods and repeat CT or contrast study at a planned interval and after any clinical change.
4EscalationEscalate promptly to endoscopic or operative source control for fever, pain, rising inflammatory markers, organ dysfunction, enlarging collection or continuing leak.

04After interventionProve control and rebuild safelyThe defect has been repaired, covered, drained or managed non-operatively.

1Track drains, sepsis physiology, respiratory function, kidney function and nutritional status, obtaining culture-guided microbiology advice.
2Confirm closure and downstream patency with the imaging method and timing chosen by the treating team before reintroducing oral intake.
3Advance nutrition in stages with dietetic input and assess swallowing, aspiration and reflux rather than relying on absence of drain output alone.
4Arrange follow-up for stricture, recurrent leak, stent removal, underlying malignancy or motor disease and the psychological impact of critical illness.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Treats polymicrobial mediastinal, pleural or abdominal contamination while definitive drainage and defect control are arranged.

Broad-spectrum intravenous antibacterial regimen

Give immediately using the hospital's current oesophageal perforation and sepsis doses, adjusted for allergy, kidney function, prior colonisation and local resistance; obtain urgent microbiology advice and narrow when cultures and source control allow.

Antibacterials cannot substitute for source control. Review renal and hepatic function, allergy, Clostridioides difficile risk and interactions; consider antifungal cover only from clinical risk and microbiology advice rather than automatically.

Reduces acid exposure across a distal repair or leak and treats coexisting acid injury; it is adjunctive rather than definitive therapy.

Intravenous proton pump inhibitor

Use a licensed intravenous preparation and dose from the current BNF or local upper-GI perforation protocol while enteral dosing is impossible, then reassess the indication and oral conversion after source control.

Do not allow PPI administration to delay CT, antimicrobial treatment, drainage or surgery. Review interactions and stop unnecessary prolonged high-intensity therapy once the specialist plan changes.

Relieves severe pain and facilitates ventilation, imaging and procedural care while the source is controlled.

Intravenous analgesia

Titrate a licensed opioid or non-opioid analgesic through the acute-pain and critical-care protocol, accounting for haemodynamics, renal or hepatic function and the need for repeated examination.

Avoid oral medicines, monitor sedation and respiratory rate, and do not mask deterioration without continuous reassessment. Non-steroidal anti-inflammatory medicines may be unsuitable with sepsis, kidney injury or bleeding.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Mediastinitis and shock

Ongoing oesophageal leakage causes rapidly progressive polymicrobial sepsis, circulatory collapse and a need for urgent source control.

Pleural empyema and respiratory failure

Thoracic contamination often enters a pleural cavity, producing effusion, empyema, lung compression and hypoxaemic respiratory deterioration.

Stricture or fistula

Healing after drainage, stenting or surgery may leave fibrosis, dysphagia, persistent leak or abnormal communication to airway or pleura.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Use continuous cardiorespiratory monitoring and serial perfusion assessment, urine output and lactate in a high-acuity environment during the unstable period.
Trend inflammatory markers, haemoglobin, kidney and liver function, coagulation and electrolytes, interpreting results alongside physiology rather than waiting for thresholds.
Measure drain amount and character and reassess pleural or mediastinal collections with planned cross-sectional imaging and after any new fever or oxygen need.
Review antimicrobial spectra and duration daily with microbiology, culture results and evidence of source control, including fungal risk when clinically relevant.
Verify defect closure and oesophageal patency before oral feeding, using the operative or endoscopic team's chosen contrast protocol and dietetic progression.
After discharge monitor dysphagia, weight, reflux, chest pain and recurrent infection and ensure removal or exchange of any temporary stent is not missed.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Do not wait for Mackler

Vomiting, pain and subcutaneous emphysema rarely arrive as a complete triad; unexplained tachycardia and pleural change after emesis may be enough to act.

Contained is not harmless

A locally sealed perforation can reopen or seed a collection, so conservative treatment is an active monitored strategy with a rescue plan.

Closure needs drainage

A technically sealed lumen can coexist with infected pleural or mediastinal material; both the hole and contaminated spaces determine recovery.

Iatrogenic recognition can help

A defect seen during the procedure may be clipped or covered before extensive contamination, provided the endoscopy and surgical teams coordinate immediately.

Delay changes options, not urgency

Late presentation may make primary repair harder but never justifies passive observation; it heightens the need for expert individualised source control.

11Common pitfallsFrequent interpretation and management errors.

01
Waiting for subcutaneous emphysema or a dramatic chest radiograph before considering oesophageal rupture.
02
Requesting a routine swallow study before contacting surgeons and beginning sepsis treatment in an unstable patient.
03
Performing unplanned diagnostic endoscopy with vigorous insufflation when perforation and free contamination are suspected.
04
Calling a leak contained from one early image without serial clinical and radiological reassessment.
05
Using a stent to cover the defect while leaving pleural or mediastinal sepsis undrained.
06
Restarting oral intake from symptom improvement alone without specialist confirmation of closure and downstream patency.