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OverviewAetiologyPathophysiologyClinical features and red flagsInvestigationsDifferential diagnosisManagementComplicationsMonitoring and follow-upSpecial situationsCommon pitfallsQuestionsSources
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Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

Perforated peptic ulcer

Gastroenterology and hepatology · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

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Time-critical presentation

Perforated peptic ulcer is an emergency general-surgical diagnosis. Sudden severe epigastric pain, generalised guarding, shock or CT evidence of free perforation requires immediate senior surgical and anaesthetic involvement, nil by mouth status, venous access, analgesia, fluid resuscitation, broad-spectrum intravenous antimicrobials and urgent planning for source control. Do not wait for an erect chest radiograph to show free air, and do not delay theatre in an unstable patient for non-essential tests.

Overview

Recognise gastroduodenal perforation before physiological collapse, resuscitate and treat intra-abdominal infection while arranging urgent source control, then address ulcer aetiology and nutritional recovery after the emergency.

Perforation allows gastroduodenal contents and gas to escape, causing chemical peritonitis followed by bacterial contamination and sepsis. An anterior duodenal ulcer is a classic free perforation; a posterior ulcer more often penetrates adjacent structures or bleeds. Gastric ulcer perforation carries the additional concern of underlying cancer. The opening may be small and temporarily sealed by omentum, so the volume of free gas does not measure the severity of systemic illness.

Initial assessment focuses on shock, sepsis and competing emergencies such as ruptured aortic aneurysm, pancreatitis, mesenteric ischaemia, myocardial infarction and lower thoracic disease. Obtain an early senior surgical opinion, FBC, renal and liver profiles, clotting, group-and-save or crossmatch, blood gas and lactate. CT with intravenous contrast should be rapid when physiology permits; a plain erect chest film is less sensitive and a negative film cannot close the diagnosis.

Practice

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Gastroenterology and hepatologyOriginal SBA

Immediate perforation management

A 68-year-old taking naproxen develops sudden epigastric pain, a rigid abdomen, hypotension and free intraperitoneal gas on CT. Which management bundle is most appropriate?

Choose one answer, then submit
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Sources and review status4 sources · checked 27 Aug 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

  • Royal College of Surgeons emergency surgery standardsUK standards for recognition, escalation and consultant-led care of high-risk emergency surgical patients.
  • Royal College of Anaesthetists National Emergency Laparotomy AuditCurrent UK emergency-laparotomy audit, standards and peri-operative quality framework.
  • NICE NG253: Suspected sepsis in people aged 16 or overCurrent national assessment, antimicrobial timing, escalation and source-control recommendations.
  • NICE CG184: Peptic ulcer investigation and managementH. pylori, NSAID, acid-suppression and gastric-ulcer follow-up standards after emergency recovery.

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom
Definitive treatment is source control. Common operations include laparoscopic or open closure with or without an omental patch and washout, but large, malignant-looking or anatomically complex gastric defects may need biopsy or resection. Operative risk should be assessed without creating delay, with consultant surgeon and anaesthetist involvement and appropriate postoperative critical care. A genuinely non-operative course requires antibiotics, acid suppression, fasting, decompression when appropriate and repeated examination, laboratory and imaging review.

Key points

  • A duodenal or gastric ulcer can perforate freely into the peritoneum or leak in a contained fashion into adjacent tissue, producing very different early examination findings.
  • Pain classically starts abruptly in the epigastrium and becomes generalised, but older, frail, immunosuppressed and steroid-treated patients may have muted tenderness despite severe contamination.
  • NSAIDs, aspirin, H. pylori, smoking, previous ulcer and delayed presentation increase probability; absence of previous dyspepsia does not protect against a first perforation.
  • Contrast-enhanced CT is the most informative test in a patient stable enough for imaging, showing free gas, focal wall defect, fluid and alternative causes of an acute abdomen.
  • Resuscitation and diagnosis must proceed in parallel with antibiotics and surgical decision-making because delay to control of an infected leak worsens outcome.
  • Most free perforations require operative repair and peritoneal washout; laparoscopic or open access and the exact repair depend on physiology, site, size, tissue quality and expertise.
  • Non-operative treatment is exceptional and belongs to close consultant-led observation of a stable patient with evidence that the leak has sealed and immediate access to surgery if deterioration occurs.
  • Survival from the operation is not the endpoint: test and eradicate H. pylori, remove ulcerogenic exposure, ensure gastric pathology is not malignant, and rebuild nutrition and function.

Aetiology

01

Helicobacter pylori ulcer

Untreated H. pylori-associated gastric or duodenal ulcer can deepen through the wall, sometimes without preceding dyspepsia.

02

NSAID and aspirin injury

Prescription or non-prescription NSAIDs and aspirin weaken mucosal protection, with age, steroids and antithrombotics increasing severity or masking symptoms.

03

Smoking and delayed recognition

Smoking impairs healing, while frailty, immunosuppression and analgesic use may blunt warning symptoms until contamination is advanced.

Pathophysiology

  1. 1
    Transmural ulcer extension

    Acid-peptic injury and inflammation progress from mucosa through muscle to breach the gastric or duodenal serosa.

  2. 2
    Chemical peritonitis

    Escaping air, acid, bile and digestive contents cause abrupt sterile peritoneal irritation, pain and guarding within minutes.

  3. 3
    Bacterial contamination and shock

    Enteric organisms proliferate as leakage continues, driving sepsis, capillary leak, hypovolaemia and multiorgan dysfunction without source control.

Clinical features and red flags

Sudden peritoneal painRed flag

Abrupt epigastric pain that spreads across the abdomen, with involuntary guarding, percussion tenderness or rigidity, should be treated as a perforated viscus until urgent assessment proves otherwise.

Physiological collapseRed flag

Tachypnoea, cool peripheries, confusion, oliguria, hypotension or raised lactate suggests sepsis and hypovolaemia. Tachycardia may be absent with beta-blockade, pacing or advanced frailty.

Contained leak

Persistent focal epigastric or right-upper-quadrant pain with a small collection and limited peritonism can represent a sealed perforation; apparent localisation does not make it benign.

Masked abdomen

Systemic corticosteroids, immunosuppression, neuropathy, older age and critical illness can reduce guarding or fever. Unexplained deterioration and a compatible history should lower the threshold for CT.

Gastric malignancy concern

Weight loss, anaemia, early satiety, irregular gastric thickening or a large gastric defect raises cancer probability and affects biopsy, resection and later follow-up planning.

Post-repair deteriorationRed flag

Persistent tachycardia, fever, pain, ileus, rising inflammatory markers or enteric drain output after repair may signal leak, abscess or missed pathology and requires urgent reassessment.

Investigations

  1. 01
    Contrast CT abdomen and pelvisFirst step
    Why
    Locate perforation, assess contamination and identify an alternative surgical emergency.
    Interpretation and limitations
    Extraluminal gas, focal gastroduodenal discontinuity, adjacent inflammatory change and free fluid support perforation. Small or sealed leaks may show little gas; oral contrast is not routinely necessary and must not delay care.
  2. 02
    Blood gas and lactate
    Why
    Quantify perfusion disturbance and provide a serial resuscitation marker.
    Interpretation and limitations
    Raised lactate or metabolic acidosis suggests physiological stress but can have several causes. A normal initial lactate does not exclude early perforation, particularly in a contained leak.
  3. 03
    FBC and inflammatory markers
    Why
    Assess anaemia, leukocyte response and a baseline for postoperative trend.
    Interpretation and limitations
    Leukocytosis supports inflammation, while leukopenia can indicate severe sepsis or immunosuppression. Haemoglobin guides bleeding assessment but does not determine whether perforation is present.
  4. 04
    U&E, LFT and coagulation
    Why
    Identify dehydration, organ dysfunction and correctable peri-operative risk.
    Interpretation and limitations
    Renal impairment and electrolyte loss influence fluid, contrast and antimicrobial plans. Abnormal clotting requires cause-specific correction without delaying life-saving source control.
  5. 05
    Group-and-save or crossmatch
    Why
    Prepare for emergency operation and possible associated ulcer bleeding.
    Interpretation and limitations
    The quantity reserved follows physiology, operative expectation and local protocol. Communicate antibodies and active haemorrhage directly with transfusion staff.
  6. 06
    Operative specimen and ulcer follow-up
    Why
    Exclude malignant gastric perforation and establish the preventable ulcer cause.
    Interpretation and limitations
    Biopsy suspicious gastric tissue when safe and ensure pathology ownership. After recovery, obtain valid H. pylori testing and interval endoscopy where gastric ulcer or incomplete visualisation leaves uncertainty.

Differential diagnosis

01

Acute pancreatitis

Back-radiating pain and diagnostic enzyme elevation support pancreatitis, whereas free gas and a focal gastroduodenal wall defect favour perforation.

02

Acute cholecystitis

Right-upper-quadrant focal inflammation and gallbladder ultrasound findings favour cholecystitis over free upper-GI contamination on targeted imaging.

03

Mesenteric or aortic emergency

Pain out of proportion, vascular risk, pulse deficit or shock requires CT angiographic assessment for bowel ischaemia or aneurysmal rupture.

Management

01ActTreat suspected perforationFirst stepSudden severe abdominal pain, peritonism, sepsis or imaging suggests a gastroduodenal leak.+
  1. 1Keep nil by mouth, call senior general or upper-GI surgery and anaesthesia, obtain venous access, bloods and crossmatch, and begin monitored resuscitation with analgesia and antiemesis.
  2. 2Give broad-spectrum intravenous antimicrobial treatment using the current intra-abdominal sepsis protocol and arrange urgent contrast CT if stability permits without creating a source-control delay.
  3. 3Assess operative risk and destination early, but prioritise timely theatre for free perforation or deterioration, with consultant-delivered surgery and planned postoperative critical care when risk is high.
02ControlRepair and drain contaminationDefinitiveFree perforation, generalised peritonitis, unsealed leak or failed conservative observation requires definitive intervention.+
  1. 1Choose laparoscopic or open access according to physiology, previous surgery, defect anatomy and team capability; lavage and close the defect using an appropriate technique.
  2. 2For gastric perforation, evaluate malignant features and obtain tissue or resect as safely appropriate, balancing oncological adequacy against emergency physiology.
  3. 3Document site, size, repair, contamination and drain rationale, then provide critical-care, antimicrobial, thromboprophylaxis and nutrition plans with explicit leak-surveillance triggers.
03RecoverPrevent another ulcer emergencySource control has succeeded and oral or enteral recovery is being planned.+
  1. 1Review H. pylori, NSAIDs, aspirin, smoking and other ulcer risks; eradicate active infection and verify cure after the correct PPI and antibiotic washout.
  2. 2Continue acid suppression for the planned healing interval, select nutrition progression with the surgical and dietetic team, and recognise refeeding risk after prolonged poor intake.
  3. 3Ensure pathology and interval endoscopy are completed for gastric disease, and give written advice on recurrent pain, bleeding, vomiting or fever that warrants urgent return.
Key medicines and prescribing safety2 treatments · regimens, roles and cautions+
Treats polymicrobial peritoneal contamination while urgent operative or radiological source control is achieved.

Broad-spectrum intravenous treatment for gastroduodenal perforation

Start the current local complicated intra-abdominal infection regimen promptly; select agent and dose for allergy, renal function, sepsis severity, prior colonisation and local resistance, then review after source control and cultures.

Antibiotics cannot close an unsealed perforation. Obtain cultures when useful without delaying treatment, adjust for organ dysfunction, document review and stop dates, and narrow therapy when microbiology and clinical response allow.

Reduces acid exposure across the repaired or sealed ulcer while H. pylori and ulcerogenic medicines are addressed.

Proton-pump inhibitor after perforated ulcer

Use the named intravenous or oral product and dose in the surgical ulcer protocol, changing route as enteral function returns and defining duration from site, cause, repair and follow-up findings.

Do not allow PPI administration to delay source control. Review interactions and long-term indication, and plan a temporary washout before later active H. pylori testing when clinically safe.

Complications

01

Generalised peritonitis and sepsis

Ongoing contamination causes diffuse inflammatory response, bacteraemia, shock and a rapidly narrowing window for safer surgery.

02

Intra-abdominal abscess or leak

Incomplete source control or repair failure leaves infected collections, fistulation and prolonged need for drainage and nutritional support.

03

Multiorgan and nutritional failure

Acute kidney, respiratory and circulatory failure combine with postoperative ileus and catabolism to prolong recovery and worsen frailty.

Monitoring and follow-up

  • Trend consciousness, respiratory status, pulse, blood pressure, capillary refill, urine output and lactate through resuscitation and the postoperative period.
  • Review pain, abdominal findings, temperature, inflammatory markers and organ function for evidence of continuing contamination, repair leak or intra-abdominal collection.
  • Monitor fluid, chloride, potassium, magnesium, phosphate, glucose and nutritional intake, particularly after vomiting or prolonged fasting.
  • Reassess antimicrobial spectrum and duration after source control and microbiology rather than continuing an open-ended broad regimen.
  • Track pathology, H. pylori result and test of cure, NSAID or aspirin decisions and planned gastric endoscopy through to completion.
  • Use postoperative functional, frailty and nutrition review to support rehabilitation after a high-risk emergency laparotomy.

Special situations

Free gas may be small

A tiny or sealed defect can release little visible air, so CT and clinical trajectory outweigh a negative erect chest radiograph.

Pain can briefly ease

Chemical irritation may change as contents distribute, and temporary symptom improvement does not prove that a perforation has sealed safely.

Gastric needs tissue

A perforated gastric cancer can resemble a benign ulcer emergency; pathology and later mucosal review must not be lost after successful repair.

Resuscitation is concurrent

Correcting shock is essential, but repeated fluid cycles must not become a reason to postpone definitive control of ongoing peritoneal contamination.

Conservative means intensive

Non-operative care is not simple observation; it requires convincing sealing, physiological stability, serial senior examinations and immediate surgical rescue capacity.

Common pitfalls

  1. 01

    Excluding perforation because no subdiaphragmatic air appears on a plain chest radiograph.

  2. 02

    Delaying surgical referral until CT is formally reported in a patient with shock and rigid peritonism.

  3. 03

    Giving antibiotics and PPI while leaving an uncontrolled free leak without a source-control decision.

  4. 04

    Choosing non-operative care for frailty alone without evidence of sealing or a rescue plan.

  5. 05

    Failing to biopsy or follow a gastric ulcer because emergency closure appeared technically successful.

  6. 06

    Discharging after repair without H. pylori eradication, NSAID review or test-of-cure ownership.