01OverviewDefinition, clinical context and the essential points that orientate the chapter.
Perforation begins as focal mucosal injury but becomes a contamination problem once the ulcer crosses the serosa. Initial peritoneal irritation is chemical; bacterial sepsis follows. Patients may present with abrupt pain, guarding and shoulder-tip irritation, yet older, immunosuppressed or steroid-treated people can have muted signs. Tachycardia, hypotension, oliguria, raised lactate and organ dysfunction indicate physiological consequence rather than ulcer size.
Resuscitation includes oxygen as needed, vascular access, balanced crystalloid guided by response, blood tests, analgesia, urinary monitoring, nasogastric decompression and antibiotics that cover Gram-positive, Gram-negative and anaerobic organisms. CT with IV contrast maps free gas and collections; water-soluble oral contrast may demonstrate an active leak when the diagnosis or suitability for observation is uncertain. Endoscopy is not a routine diagnostic test for free perforation because insufflation can worsen contamination.
Surgery washes out contamination, closes or resects the defect and obtains tissue when gastric malignancy is possible. A selected sealed perforation can be managed with nil by mouth, decompression, IV therapy and continuous surgical observation only where immediate rescue operation is available. Failure is signalled by pain, fever, tachycardia, inflammatory rise, organ dysfunction or contrast leak. Long-term prevention addresses H pylori, NSAIDs, smoking and gastric-ulcer histology.
Key points
- CT abdomen is the preferred imaging test because it detects free gas, fluid, the likely site and an alternative diagnosis more sensitively than an erect chest radiograph.
- WSES advises against routine non-operative management; consider it only in an exceptionally selected stable patient whose perforation is sealed on water-soluble contrast and who has no sepsis or peritonitis.
- Operate promptly when there is contrast leak, peritonitis, pneumoperitoneum with clinical deterioration or failed observation; delay increases mortality.
- Laparoscopic repair is reasonable for a stable patient with appropriate expertise, while an unstable patient generally needs the fastest safe open source-control approach.
- For a small perforation, primary closure with or without an omental patch is selected by tissue quality and surgical judgement; large or malignant gastric defects may require resection.
- After survival, test and eradicate H pylori, stop NSAIDs where possible and confirm healing or biopsy of a gastric ulcer so the emergency does not recur.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Helicobacter-associated ulcer
Chronic bacterial inflammation and altered acid regulation create a mucosal defect that can progressively penetrate the full duodenal or gastric wall.
NSAID-associated ulcer
Loss of prostaglandin-mediated mucosal defence permits deep acid-peptic injury, sometimes without preceding pain in older or steroid-treated patients.
Malignant gastric ulcer
An ulcerated gastric adenocarcinoma can necrose through serosa and present as perforation, requiring tissue diagnosis and later oncological staging.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Chemical peritonitis
Escaped acid, bile and digestive enzymes abruptly inflame the peritoneum, producing severe pain, guarding and intravascular fluid shift.
- 2Bacterial contamination
Ongoing luminal leakage seeds polymicrobial infection, converting the early chemical insult into peritonitis, sepsis and organ dysfunction.
- 3Temporary omental sealing
Adjacent omentum can plug a small defect and limit contrast escape, but movement or pressure may disrupt this fragile containment.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Sudden severe epigastric pain rapidly generalises as gas and acidic contents contact the parietal peritoneum.
Tachycardia, hypotension, confusion, oliguria and rising lactate mark systemic consequence and demand rapid source control.
Older age, immunosuppression, steroids and analgesia can blunt guarding despite substantial contamination.
Localised pain and a small adjacent collection may reflect temporary sealing by omentum rather than benign disease.
Irregular gastric thickening, weight loss or nodal disease raises an ulcerated cancer and changes resection and tissue strategy.
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 CT abdomen and pelvisFirst step - Why
- Confirm perforation, locate the likely defect and quantify contamination.
- Interpretation and limitations
- Free gas, focal wall discontinuity, extraluminal contrast and fluid guide operation; small sealed defects can lack dramatic pneumoperitoneum.
- 02
Erect chest radiograph - Why
- Rapidly identify subdiaphragmatic free gas when CT is not immediately available.
- Interpretation and limitations
- A negative film cannot exclude perforation and must not delay CT in a convincing presentation.
- 03
Blood gas and lactate - Why
- Measure perfusion failure and response to resuscitation.
- Interpretation and limitations
- Persistent acidosis or lactate elevation supports urgent source control and critical-care involvement.
- 04
Full blood count, renal, liver and coagulation profile - Why
- Assess inflammation, organ injury and operative readiness.
- Interpretation and limitations
- A normal early white count does not negate peritonitis; renal impairment changes antimicrobial dosing.
- 05
Water-soluble contrast study - Why
- Demonstrate whether a suspected small perforation remains open in a rare observation candidate.
- Interpretation and limitations
- Any extravasation removes the basis for non-operative management and prompts surgery.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Acute pancreatitis
Pancreatitis causes severe epigastric pain and systemic inflammation, but lipase and pancreatic imaging replace the perforation pattern of extraluminal gas and contrast.
Mesenteric ischaemia
Intestinal hypoperfusion can cause pain, lactate elevation and later peritonism without an initial gastroduodenal wall defect or pneumoperitoneum.
Perforated diverticulitis
Colonic diverticular perforation produces free gas and sepsis but CT localises sigmoid or right-colonic inflammation away from the gastroduodenal source.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01Free perforationMove from shock to source controlFirst stepA 61-year-old NSAID user has sudden generalised pain, rigid guarding, lactate 4.1 mmol/L and CT showing free gas with contrast leaking from the anterior duodenal bulb. Initial pressure is 88/54 mmHg with pulse 118/min; there is no beta-lactam allergy and renal function permits the standard antibiotic dose.+
- 1Keep nil by mouth, call surgery and anaesthesia, establish IV access, resuscitate perfusion and decompress the stomach. In this DBTH-protocol example, start co-amoxiclav 1.2 g IV every eight hours, infused over 30–40 minutes, alongside urgent source-control planning.
- 2After resuscitation, blood pressure is 116/72 mmHg, pulse 92/min, urine output exceeds 0.5 mL/kg/hour and lactate has fallen to 2.0 mmol/L. Active leak and generalised peritonitis still require urgent operation; his restored stability permits the experienced team to choose laparoscopy. Persistent instability would favour an open approach.
- 3At urgent laparoscopy, close the 6 mm duodenal defect with an omental patch, wash out contamination and send appropriate cultures.
- 4After closure and washout, lactate falls to 1.2 mmol/L, urine output remains adequate and abdominal tenderness improves. At 48 hours he tolerates oral intake with stable renal function, allowing reviewed stepdown to co-amoxiclav 625 mg orally every eight hours with meals to complete five days under this local protocol. The NSAID is stopped and H pylori assessment after appropriate medication washout is booked rather than lost after the emergency admission.
02Exceptionally selected observationProve sealing and retain rescueA stable patient presents early with localised pain, no sepsis, and CT shows a tiny perigastric air pocket without diffuse fluid.+
- 1Obtain senior surgical review and water-soluble contrast imaging to test whether the defect is sealed.
- 2If there is no leak, use nil by mouth, decompression, IV therapy and repeated examination in a unit able to operate immediately.
- 3Treat new tachycardia, fever, worsening pain, rising inflammatory markers or contrast leak as failure.
- 4Investigate gastric histology and ulcer cause even if emergency surgery is avoided.
03Gastric perforationPreserve oncological optionsCT suggests perforation through a thick irregular distal gastric ulcer in a patient with weight loss.+
- 1Resuscitate and involve an upper-GI surgeon because malignancy affects the operation.
- 2Choose closure, biopsy or resection according to stability, contamination, tissue and resectability.
- 3Send adequately oriented tissue and stage confirmed cancer after emergency recovery.
- 4Verify that pathology and MDT review are not lost during transfer from emergency to elective care.
Key medicines and prescribing safety1 treatment · regimens, roles and cautions+
Co-amoxiclav example for perforated-ulcer intra-abdominal infection
This is the September 2025 DBTH adult complicated intra-abdominal infection example. Give co-amoxiclav 1.2 g IV every eight hours by infusion over 30–40 minutes; the selected product also permits slow injection over 3–4 minutes. Review at 48–72 hours and, when improving and absorbing, change to 625 mg orally every eight hours with a meal, completing five days according to response and source control. For age over 65 AND co-amoxiclav or cephalosporin exposure in the preceding two weeks, DBTH instead uses piperacillin/tazobactam 4.5 g IV every eight hours, infused over 30 minutes, followed by culture-led oral de-escalation.Co-amoxiclav is contraindicated with penicillin hypersensitivity, a previous severe immediate reaction to another beta-lactam, or prior co-amoxiclav-associated jaundice/hepatic dysfunction. After an initial IV 1,000/200 mg dose, reduce to 500/100 mg every 12 hours at CrCl 10–30 mL/min or every 24 hours below 10. The oral 500/125 mg tablet frequency is twice daily at CrCl 10–30 or once daily below 10, not the normal-function three-times-daily schedule. Piperacillin/tazobactam is contraindicated with penicillin hypersensitivity or a previous acute severe other beta-lactam reaction; its maximum is 4 g/0.5 g every eight hours at CrCl 20–40 and every 12 hours below 20. Send cultures and monitor renal/hepatic function and electrolytes. Reassess dosing as AKI changes; antibiotics support but cannot replace closure and washout.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Septic shock
Uncontrolled peritoneal contamination causes vasodilation, capillary leak, myocardial dysfunction and progressive renal, respiratory and circulatory failure.
Intra-abdominal abscess
Residual infected fluid can organise after repair, causing persistent fever, ileus, inflammatory rise and a need for image-guided or operative drainage.
Repair leak
Friable tissue or continuing distal obstruction can disrupt closure, recreating peritonitis and requiring urgent imaging and repeat source control.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Reassess pressure, pulse, lactate, urine output, mental state and oxygen need during resuscitation.
- Repeat abdominal examination because a contained leak can become free contamination.
- Track drain character, inflammatory markers and oral tolerance after repair.
- Review cultures and narrow or stop antibiotics when source control and progress permit.
- Complete H pylori eradication, NSAID review and gastric histology follow-up after discharge.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
A sealed defect is demonstrated
Clinical stability alone cannot prove closure; the rare non-operative pathway requires no water-soluble contrast leak.
Free gas may be small
A tiny duodenal perforation can cause severe peritonitis before a large pneumoperitoneum accumulates.
Source control changes antibiotics
A five-day local course assumes effective closure and washout; persistent contamination requires renewed anatomical assessment.
Gastric tissue has future value
Emergency repair without adequate malignancy assessment can delay diagnosis of an ulcerated gastric cancer.
11Common pitfallsFrequent interpretation and management errors.
- 01
Using a normal chest radiograph to exclude a convincing perforation.
- 02
Choosing observation without proof of sealing or immediate access to rescue surgery.
- 03
Continuing broad-spectrum antibiotics while a free leak remains uncontrolled.
- 04
Discharging after repair without H pylori, NSAID and gastric-histology plans.