01OverviewDefinition, clinical context and the essential points that orientate the chapter.
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.
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.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Helicobacter pylori ulcer
Untreated H. pylori-associated gastric or duodenal ulcer can deepen through the wall, sometimes without preceding dyspepsia.
NSAID and aspirin injury
Prescription or non-prescription NSAIDs and aspirin weaken mucosal protection, with age, steroids and antithrombotics increasing severity or masking symptoms.
Smoking and delayed recognition
Smoking impairs healing, while frailty, immunosuppression and analgesic use may blunt warning symptoms until contamination is advanced.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Transmural ulcer extension
Acid-peptic injury and inflammation progress from mucosa through muscle to breach the gastric or duodenal serosa.
- 2Chemical peritonitis
Escaping air, acid, bile and digestive contents cause abrupt sterile peritoneal irritation, pain and guarding within minutes.
- 3Bacterial contamination and shock
Enteric organisms proliferate as leakage continues, driving sepsis, capillary leak, hypovolaemia and multiorgan dysfunction without source control.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
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.
Tachypnoea, cool peripheries, confusion, oliguria, hypotension or raised lactate suggests sepsis and hypovolaemia. Tachycardia may be absent with beta-blockade, pacing or advanced frailty.
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.
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.
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.
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.
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
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Acute pancreatitis
Back-radiating pain and diagnostic enzyme elevation support pancreatitis, whereas free gas and a focal gastroduodenal wall defect favour perforation.
Acute cholecystitis
Right-upper-quadrant focal inflammation and gallbladder ultrasound findings favour cholecystitis over free upper-GI contamination on targeted imaging.
Mesenteric or aortic emergency
Pain out of proportion, vascular risk, pulse deficit or shock requires CT angiographic assessment for bowel ischaemia or aneurysmal rupture.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01ActTreat suspected perforationFirst stepSudden severe abdominal pain, peritonism, sepsis or imaging suggests a gastroduodenal leak.+
- 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.
- 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.
- 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.+
- 1Choose laparoscopic or open access according to physiology, previous surgery, defect anatomy and team capability; lavage and close the defect using an appropriate technique.
- 2For gastric perforation, evaluate malignant features and obtain tissue or resect as safely appropriate, balancing oncological adequacy against emergency physiology.
- 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.+
- 1Review H. pylori, NSAIDs, aspirin, smoking and other ulcer risks; eradicate active infection and verify cure after the correct PPI and antibiotic washout.
- 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.
- 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+
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.
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.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Generalised peritonitis and sepsis
Ongoing contamination causes diffuse inflammatory response, bacteraemia, shock and a rapidly narrowing window for safer surgery.
Intra-abdominal abscess or leak
Incomplete source control or repair failure leaves infected collections, fistulation and prolonged need for drainage and nutritional support.
Multiorgan and nutritional failure
Acute kidney, respiratory and circulatory failure combine with postoperative ileus and catabolism to prolong recovery and worsen frailty.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- 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.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
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.
11Common pitfallsFrequent interpretation and management errors.
- 01
Excluding perforation because no subdiaphragmatic air appears on a plain chest radiograph.
- 02
Delaying surgical referral until CT is formally reported in a patient with shock and rigid peritonism.
- 03
Giving antibiotics and PPI while leaving an uncontrolled free leak without a source-control decision.
- 04
Choosing non-operative care for frailty alone without evidence of sealing or a rescue plan.
- 05
Failing to biopsy or follow a gastric ulcer because emergency closure appeared technically successful.
- 06
Discharging after repair without H. pylori eradication, NSAID review or test-of-cure ownership.