Emergency Medicine
Gastroenterology
Acute Medicine
High Evidence
Peer reviewed

Perforated Viscus

Incidence : Perforated peptic ulcer 3.8-10 per 100,000/year; perforated diverticulitis 4 per 100,000/year Classic triad : Sudden severe abdominal pain + peritonism + pneumoperitoneum Examination hallmark : Board-like...

Updated 7 Jan 2026
Reviewed 17 Jan 2026
45 min read
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MedVellum Editorial Team
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MedVellum Medical Education Platform
Quality score
52

Clinical board

A visual summary of the highest-yield teaching signals on this page.

Urgent signals

Safety-critical features pulled from the topic metadata.

  • Sudden severe abdominal pain
  • Board-like rigidity (peritonism)
  • Free air under diaphragm on erect CXR
  • Peritonitis (guarding, rebound tenderness)

Linked comparisons

Differentials and adjacent topics worth opening next.

  • Acute Pancreatitis
  • Mesenteric Ischaemia

Editorial and exam context

Reviewed by MedVellum Editorial Team · MedVellum Medical Education Platform

Credentials: MBBS, MRCP, Board Certified

Clinical reference article

Perforated Viscus

Topic Overview

Summary

Perforated viscus represents a surgical emergency characterized by a full-thickness breach in the wall of a hollow abdominal organ, allowing luminal contents (gastric acid, bile, enteric bacteria, or faeces) to leak into the peritoneal cavity. This results in chemical and/or bacterial peritonitis, systemic inflammatory response, and potentially septic shock. Common causes include perforated peptic ulcer disease (most common upper GI perforation), perforated diverticulitis (most common lower GI perforation), perforated appendicitis, ischaemic bowel, colorectal malignancy, and iatrogenic injury. The classic presentation is sudden-onset severe abdominal pain with peritonism (rigidity, guarding, rebound tenderness). Diagnosis is confirmed by imaging demonstrating pneumoperitoneum—free air under the diaphragm on erect chest radiograph (sensitivity 75-80%) or CT abdomen (gold standard, sensitivity >95%). Management requires aggressive fluid resuscitation, broad-spectrum intravenous antibiotics, and urgent surgical intervention (emergency laparotomy or laparoscopy) for source control. Mortality ranges from 5-30% depending on aetiology, time to intervention, and patient comorbidities. [1,2,3]

Key Facts

  • Incidence: Perforated peptic ulcer 3.8-10 per 100,000/year; perforated diverticulitis 4 per 100,000/year
  • Classic triad: Sudden severe abdominal pain + peritonism + pneumoperitoneum
  • Examination hallmark: Board-like rigidity ("wooden abdomen") with rebound tenderness
  • Imaging: Erect CXR shows free air in 75-80%; CT abdomen/pelvis is gold standard (>95% sensitivity)
  • Treatment: Resuscitation + IV antibiotics + emergency surgery (laparotomy/laparoscopy)
  • Mortality: Perforated DU 5-10% (young, healthy); perforated colon 15-30% (elderly, faecal peritonitis)
  • Time-critical: Every hour delay to surgery increases mortality by 2-3%
  • High-risk groups: Elderly (>70 years), immunosuppressed, NSAID users, chronic steroid use

Clinical Pearls

"Free air under the diaphragm = perforated viscus until proven otherwise"

Elderly patients may present with minimal abdominal signs despite catastrophic perforation — maintain high index of suspicion

Perforated duodenal ulcer classically presents with sudden "thunderclap" epigastric pain radiating to the back, followed by generalised peritonitis

Silent interval: Brief pain relief after initial perforation (gastric contents leak slowly) before overwhelming peritonitis develops

Site determines severity: Upper GI perforation initially causes chemical peritonitis (sterile); colonic perforation causes immediate faecal peritonitis (higher mortality)

Board-like rigidity distinguishes perforation from uncomplicated peptic ulcer or pancreatitis

If erect CXR is negative but clinical suspicion high, CT with oral contrast is mandatory — may show small pneumoperitoneum, free fluid, or bowel wall defect

Never delay surgery for extensive imaging if patient is unstable — proceed directly to theatre

Why This Matters Clinically

Perforated viscus is a life-threatening surgical emergency requiring immediate recognition and intervention. Delay in diagnosis or treatment leads to overwhelming sepsis, multi-organ failure, and death. Early recognition (within 6 hours) and prompt surgery can reduce mortality from 30% to less than 5%. The condition demands senior surgical involvement from presentation, as inappropriate conservative management or delayed referral is associated with catastrophic outcomes. Understanding the spectrum of causes, clinical presentations across different patient groups (elderly, immunosuppressed, post-operative), and appropriate surgical strategies (repair vs resection, stoma formation, damage control surgery) is essential for emergency medicine physicians, acute medicine physicians, and surgical trainees preparing for MRCS and postgraduate examinations. [4,5]


Visual Summary

Visual assets to be added:

  • Erect chest radiograph showing Rigler's sign (free air under diaphragm)
  • CT abdomen showing pneumoperitoneum with extraluminal gas
  • Causes of perforation by anatomical location (oesophagus → stomach → duodenum → small bowel → colon)
  • Perforated viscus management algorithm (resuscitation → imaging → antibiotics → surgery)
  • Hartmann procedure schematic (resection, end colostomy, rectal stump closure)
  • Boey score for perforated peptic ulcer (predicts mortality)

Epidemiology

Incidence and Prevalence

Perforated Peptic Ulcer (PPU)

  • Incidence: 3.8-10 per 100,000 population per year (Western countries)
  • Accounts for 5-10% of all peptic ulcer disease complications
  • Declining incidence in developed countries due to H. pylori eradication and proton pump inhibitor (PPI) use
  • Rising incidence in elderly due to NSAID/aspirin use (cardiovascular prophylaxis)
  • Duodenal ulcers perforate more commonly than gastric ulcers (60% vs 40%) [1,6]

Perforated Diverticular Disease

  • Incidence: 4 per 100,000 population per year
  • Accounts for 10-15% of patients with acute diverticulitis
  • Predominantly affects elderly (>60 years)
  • Hinchey III (purulent peritonitis) or IV (faecal peritonitis) classification [7]

Perforated Appendicitis

  • Occurs in 15-30% of acute appendicitis cases
  • Higher perforation rate in elderly (delayed presentation) and very young (less than 5 years)
  • Associated with appendiceal abscess or generalised peritonitis [8]

Other Causes

  • Colonic perforation from malignancy: 3-10% of colorectal cancers
  • Ischaemic bowel perforation: Rare but high mortality (50-70%)
  • Iatrogenic perforation (endoscopy, colonoscopy): 0.1-0.3% of procedures
  • Toxic megacolon (IBD): 1-3% of severe ulcerative colitis [9,10]

Demographics

Age

  • Perforated peptic ulcer: Bimodal—peak in young adults (20-40 years, duodenal ulcer) and elderly (>70 years, NSAID-related)
  • Perforated diverticulitis: Predominantly >60 years
  • Perforated appendicitis: All ages; peaks 10-30 years

Sex

  • Perforated DU: Male predominance (M:F 3-4:1)
  • Perforated gastric ulcer: Equal sex distribution
  • Perforated diverticulitis: Slight female predominance

Risk Factors by Cause

CauseRisk Factors
Peptic ulcerH. pylori infection, NSAID use, aspirin, corticosteroids, smoking, alcohol, physiological stress (burns, trauma, ICU)
Diverticular diseaseAge >60 years, low-fibre diet, obesity, smoking, NSAIDs, corticosteroids
AppendicitisDelayed presentation, faecolith obstruction, extremes of age
Colorectal cancerAdvanced disease, obstructing lesions, chemotherapy (bevacizumab), radiotherapy
Ischaemic bowelAtrial fibrillation, cardiac failure, mesenteric vascular disease, vasculitis, embolic disease
IBD (toxic megacolon)Severe ulcerative colitis, C. difficile superinfection, recent colonoscopy, cessation of anti-TNF therapy
IatrogenicEndoscopy/colonoscopy (therapeutic procedures, biopsy), abdominal surgery (anastomotic leak)

Pathophysiology

Mechanism of Perforation

Perforated viscus results from full-thickness disruption of the wall of a hollow abdominal organ, allowing luminal contents to escape into the peritoneal cavity. The pathophysiological sequence differs by anatomical location:

Upper Gastrointestinal Perforation (Oesophagus, Stomach, Duodenum)

  1. Mucosal injury: Chronic inflammation (H. pylori, NSAIDs) → ulcer formation → transmural extension
  2. Acute perforation: Sudden full-thickness breach (anterior duodenal wall most common site)
  3. Leak of contents: Gastric acid (pH 1-2), bile, pancreatic enzymes, bacteria
  4. Chemical peritonitis: Initial sterile inflammation (first 6-12 hours)—highly irritant gastric acid causes severe peritoneal inflammation
  5. Bacterial peritonitis: Bacterial translocation from upper GI tract (Gram-positive and Gram-negative organisms)—develops 12-24 hours post-perforation [1,2]

Key concept: Upper GI perforation causes initial chemical peritonitis (pain out of proportion to systemic upset), followed by bacterial peritonitis (sepsis)

Lower Gastrointestinal Perforation (Small Bowel, Colon)

  1. Perforation mechanism: Varies by cause
    • Diverticulitis: Microperforation in diverticulum → pericolic abscess → free perforation
    • Appendicitis: Luminal obstruction → mucosal ischaemia → gangrene → perforation
    • Ischaemic bowel: Arterial/venous occlusion → transmural infarction → necrosis → perforation
    • Malignancy: Tumour invasion through bowel wall or proximal perforation from obstruction
  2. Leak of contents: Enteric contents (small bowel) or faeces (colon)—high bacterial load (10^11 organisms/mL in colon)
  3. Immediate bacterial peritonitis: Overwhelming bacterial contamination (mixed aerobic/anaerobic flora)
  4. Systemic inflammatory response: Cytokine release (TNF-α, IL-1, IL-6) → capillary leak → third-spacing → hypovolaemic shock
  5. Sepsis: Bacterial translocation → bacteraemia → septic shock [11,12]

Key concept: Colonic perforation causes immediate faecal peritonitis with high bacterial load—higher mortality than upper GI perforation

Peritoneal Response to Contamination

Early Phase (0-6 hours)

  • Chemical irritation (gastric acid) or bacterial contamination
  • Peritoneal inflammation → increased capillary permeability
  • Exudation of protein-rich fluid into peritoneal cavity
  • Localised peritonitis (if perforation contained by omentum or adjacent viscera)

Late Phase (6-24 hours)

  • Generalised peritonitis if perforation not contained
  • Massive fluid shifts: Up to 4-6 litres of fluid sequestered in peritoneal cavity and bowel wall (third-spacing)
  • Hypovolaemia → pre-renal AKI
  • Systemic inflammatory response syndrome (SIRS)
  • Progression to septic shock if untreated [13]

Anatomical Considerations: Why Site Matters

SiteContentsInitial ResponseMortalityKey Points
OesophagusSaliva, foodMediastinitis (Boerhaave syndrome)20-40%Surgical emergency; high mortality if >24 hours
Stomach/DuodenumGastric acid (pH 1-2), bileChemical peritonitis (initially sterile)5-15%Anterior DU most common; can seal spontaneously (rare)
Small bowelBile, enzymes, bacteria (10^6-10^8/mL)Moderate bacterial peritonitis10-20%Depends on cause (ischaemia worse than trauma)
ColonFaeces, bacteria (10^11/mL)Immediate faecal peritonitis15-30%Highest bacterial load; most severe peritonitis
RectumFaeces (pelvic contamination)Pelvic sepsis ± pelvic abscess10-20%May present late; difficult diagnosis

Complications Cascade

Untreated perforated viscus progression:

  1. Localised peritonitis (first 6-12 hours)
  2. Generalised peritonitis (12-24 hours) → third-spacing → hypovolaemia
  3. SIRS/Sepsis (24-48 hours) → multi-organ involvement
  4. Septic shock (>48 hours) → vasodilatory shock, refractory hypotension
  5. Multi-organ failure → ARDS, AKI, coagulopathy (DIC), cardiovascular collapse
  6. Death [3,4]

Time to surgery is the critical determinant of outcome: Mortality doubles if surgery delayed >24 hours from symptom onset [5]


Clinical Presentation

Symptoms

Acute Onset (Hallmark)

  • Sudden severe abdominal pain: "Worst pain ever" or "thunderclap" onset
  • Pain often begins at site of perforation, then generalises as peritonitis develops
  • Perforated DU: Epigastric pain radiating to back or right upper quadrant
  • Perforated appendix: Right iliac fossa pain → generalised
  • Perforated diverticulitis: Left iliac fossa pain → generalised

Associated Symptoms

  • Nausea and vomiting: Near universal
  • Anorexia: Complete loss of appetite
  • Inability to pass flatus or stool: Paralytic ileus
  • Shoulder tip pain: Referred pain from diaphragmatic irritation (free air, blood, pus under diaphragm)
  • Dyspnoea: Due to pain, splinting, reduced diaphragmatic excursion
  • Fever: May be absent early; develops as bacterial peritonitis evolves

Symptom Progression

  • 0-6 hours: Sudden severe localised pain
  • 6-12 hours: Generalised abdominal pain, vomiting
  • 12-24 hours: Systemic features (fever, tachycardia, hypotension)
  • >24 hours: Septic shock (confusion, oliguria, multiorgan dysfunction)

Signs

General Appearance

  • Lies still: Movement exacerbates pain (contrast with renal colic where patients are restless)
  • Shallow breathing: Splinting to minimise diaphragmatic movement
  • Distressed, anxious facies
  • Pallor, sweating: Shock

Vital Signs

  • Tachycardia: HR >100 bpm (hypovolaemia, pain, sepsis)
  • Hypotension: SBP less than 90 mmHg (late sign—indicates shock)
  • Tachypnoea: RR >20/min (pain, metabolic acidosis, sepsis)
  • Fever: Temperature >38°C (may be absent early or in elderly/immunosuppressed)
  • Hypothermia: less than 36°C (poor prognostic sign—severe sepsis)

Abdominal Examination

Inspection

  • Immobile abdomen: No respiratory movement
  • Abdominal distension: Late sign (ileus, third-spacing)
  • Perioperative scars: Suggests previous surgery, adhesions, anastomotic leak

Palpation

  • Generalised tenderness: Maximum tenderness at perforation site initially, then diffuse
  • Board-like rigidity: Involuntary guarding—pathognomonic of generalised peritonitis
    • "Wooden abdomen" — rigid, non-yielding on palpation
    • Indicates severe peritoneal inflammation
  • Rebound tenderness: Pain on sudden release of palpating hand (Blumberg's sign)
  • Absent liver dullness: Loss of normal liver dullness to percussion (replaced by tympanic note due to free air)

Percussion

  • Generalised tenderness: Light percussion elicits severe pain
  • Tympanic note: Over liver (free air)
  • Shifting dullness: Free fluid in peritoneal cavity (may be absent early)

Auscultation

  • Absent bowel sounds: "Silent abdomen" (paralytic ileus from peritonitis)
  • May have initial hyperactive sounds (early) before progression to ileus

Digital Rectal Examination (DRE)

  • Essential in all cases: May reveal pelvic pathology
  • Tenderness: Suggests pelvic peritonitis
  • Mass: Appendiceal abscess, pelvic abscess
  • Blood: Suggests lower GI pathology (malignancy, ischaemia)

Classical Presentations by Cause

CauseTypical HistoryPain CharacterKey Features
Perforated DUNSAID use, known PUDSudden epigastric "thunderclap" pain → generalisedPrior dyspepsia; pain radiates to back; board-like rigidity
Perforated gastric ulcerNSAID use, elderlyEpigastric pain, less dramatic than DUMay have preceding weight loss (malignancy?)
Perforated appendicitisAppendicitis symptoms for daysCentral abdominal → RIF → generalisedDelayed presentation; RIF mass (abscess); fever
Perforated diverticulitisElderly, known diverticular diseaseLIF pain → generalisedPreceding diverticulitis symptoms; LIF mass
Perforated colon cancerWeight loss, PR bleeding, obstructionGradual worsening → sudden deteriorationObstructive symptoms; anaemia; palpable mass
Ischaemic bowelAF, cardiac disease, vascular diseaseSudden severe pain, "pain out of proportion to signs" initiallyLate peritonism; bloody diarrhoea; metabolic acidosis
Iatrogenic (post-endoscopy)Recent endoscopy/colonoscopySudden pain during/after procedureClear temporal relationship; pneumoperitoneum on imaging
Boerhaave syndromeForceful vomiting (alcohol binge)Sudden severe chest/epigastric painSubcutaneous emphysema; Mackler's triad (vomiting, chest pain, subcutaneous emphysema)

Red Flags

FindingSignificanceAction
Board-like rigidityGeneralised peritonitisEmergency surgical referral
Septic shock (SBP less than 90, confusion)Overwhelming sepsisResuscitation + urgent theatre
Free air on imagingConfirms perforationSurgical emergency
Silent abdomenParalytic ileus from peritonitisSevere pathology
Shoulder tip painDiaphragmatic irritationSuggests significant pneumoperitoneum
Elderly + minimal signsBlunted responseHigh index of suspicion—may have severe pathology despite minimal examination findings
Immunosuppressed + mild signsImpaired inflammatory responseDanger—may have perforation without peritonism
Recent endoscopyIatrogenic perforationImmediate CT; surgical referral

Atypical Presentations (High-Risk Groups)

Elderly (>70 years)

  • Minimal pain: Reduced pain perception
  • Absent rigidity: Weak abdominal musculature
  • Confusion: May be only presenting feature
  • Hypothermia: Rather than fever
  • High mortality: 30-40% (delayed diagnosis, comorbidities) [14]

Immunosuppressed (Steroids, Chemotherapy, Biologics)

  • Minimal peritonism: Blunted inflammatory response
  • Absence of fever and leucocytosis: Despite severe sepsis
  • Rapid deterioration: Once recognised, often advanced disease
  • Higher perforation rate: Especially IBD patients on steroids/immunosuppressants [15]

Pregnant Patients

  • Atypical pain location: Gravid uterus displaces viscera
  • Diagnostic difficulty: Reluctance to image (radiation exposure)
  • Higher morbidity: Perforation risk increased in pregnancy (especially appendicitis)

Post-Operative Patients

  • Anastomotic leak: Typically 5-7 days post-surgery
  • Diagnostic challenge: Post-operative pain expected
  • Key signs: Tachycardia, fever, rising inflammatory markers, unexplained deterioration

Clinical Examination

Approach to Examination

ABCDE Assessment (all perforated viscus patients are surgical emergencies)

Airway

  • Patent airway
  • Assess ability to speak (shock may impair)

Breathing

  • Respiratory rate: Tachypnoea (>20/min) suggests sepsis or metabolic acidosis
  • Oxygen saturations: May be reduced (sepsis, ARDS, splinting)
  • Work of breathing: Shallow breathing (pain avoidance)

Circulation

  • Heart rate: Tachycardia (>100 bpm)—hypovolaemia, sepsis, pain
  • Blood pressure: Hypotension (less than 90 mmHg systolic) indicates shock—requires immediate resuscitation
  • Capillary refill time: >2 seconds suggests shock
  • Jugular venous pressure: Low (hypovolaemia)
  • Peripheral pulses: May be weak, thready
  • Urine output: Oliguria (less than 0.5 mL/kg/hr) suggests AKI

Disability

  • Glasgow Coma Scale: Reduced in septic shock (confusion, obtundation)
  • Blood glucose: May be elevated (stress response) or low (septic shock)
  • Pupils: Normal unless severe sepsis

Exposure

  • Temperature: Fever (>38°C) or hypothermia (less than 36°C)
  • Full abdominal examination: As below

Abdominal Examination (Detailed)

Inspection

  • Patient position: Lying still, knees flexed (reduces peritoneal stretch)
  • Abdominal movement: Absent respiratory excursion
  • Distension: May be present (ileus, third-spacing)
  • Visible peristalsis: Absent (ileus)
  • Scars: Previous surgery (adhesions, anastomotic leak)
  • Stomas: Check function (obstructed stoma → perforation)

Palpation

  • Approach: Start away from area of maximal pain
  • Superficial palpation:
    • Generalised tenderness
    • Voluntary guarding (early)—patient tenses abdominal muscles
    • Involuntary guarding/rigidity (late)—reflex muscular contraction; cannot be overcome
  • Deep palpation:
    • Board-like rigidity—"wooden abdomen"
    • Rebound tenderness (Blumberg's sign)—pain worse on sudden release than pressure
    • "Masses: Appendix mass, diverticular abscess, tumour"
  • Murphy's sign: Usually negative (cholecystitis, not perforation)
  • Rovsing's sign: Pain in RIF on palpation of LIF (suggests appendicitis, but non-specific)

Percussion

  • Generalised percussion tenderness: Light percussion over abdomen elicits severe pain (peritonitis)
  • Loss of liver dullness: Percussion over liver produces tympanic note (free air displaces liver)—highly suggestive of pneumoperitoneum
  • Shifting dullness: Free fluid (ascites from peritonitis)—may be absent early

Auscultation

  • Absent bowel sounds: Ileus secondary to peritonitis
  • Duration: Auscultate for minimum 2 minutes before declaring absent

Digital Rectal Examination (DRE)

  • Mandatory: Do not omit
  • Findings:
    • Pelvic tenderness (pelvic peritonitis)
    • Boggy mass (pelvic abscess)
    • Blood on glove (lower GI pathology)
    • Empty rectum (obstruction)

Extra-Abdominal Examination

Hernial Orifices

  • Inguinal, femoral, umbilical, incisional hernias: Strangulated hernia may perforate

Cardiorespiratory

  • Crackles: Aspiration pneumonia, ARDS
  • Murmurs: AF (embolic mesenteric ischaemia)

Peripheral

  • Subcutaneous emphysema: Oesophageal perforation (Boerhaave syndrome)—crepitus on palpation of chest/neck

Investigations

Immediate Investigations (Emergency Department/Acute Medicine)

Blood Tests (all patients)

TestExpected FindingsClinical Significance
Full blood count (FBC)↑ WCC (leucocytosis >11 × 10⁹/L); neutrophilia; may have ↓ Hb (bleeding, chronic anaemia)WCC may be normal or low in elderly/immunosuppressed; leucopenia (less than 4 × 10⁹/L) poor prognostic sign
C-reactive protein (CRP)↑ CRP (>100 mg/L)Confirms inflammation; serial CRP monitors response to treatment
Urea and electrolytes (U&E)↑ Urea, ↑ creatinine (AKI from hypovolaemia, sepsis); ↓ Na⁺, ↑ K⁺ (third-spacing)Pre-renal AKI common; correct before surgery
Serum lactate↑ Lactate (>2 mmol/L)Tissue hypoperfusion (shock); ischaemic bowel (very high lactate >4 mmol/L); serial lactate monitors resuscitation
Liver function tests (LFTs)May have ↑ ALT, ↑ ALP (biliary pathology); ↑ bilirubin (sepsis, hepatic dysfunction)Helps differentiate biliary from other causes
Serum amylase/lipase↑ Amylase (may be mildly elevated in perforation); massively ↑ in pancreatitisExclude acute pancreatitis as differential
Coagulation (PT, APTT)Prolonged in sepsis (DIC), liver disease, anticoagulantsCorrect coagulopathy before surgery
Group and save (G&S)Mandatory pre-operativePrepare for potential transfusion
Blood cultures (if febrile/septic)Positive in 20-30% (bacteraemia)Guides antibiotic therapy

Arterial Blood Gas (ABG)

ParameterFindingInterpretation
pHless than 7.35 (metabolic acidosis)Lactic acidosis from shock/sepsis; ischaemic bowel
Base excessNegative (< -2 mmol/L)Metabolic acidosis
Lactate>2 mmol/L (elevated); >4 mmol/L (severe)Tissue hypoperfusion; ischaemic bowel
PaO₂May be low (hypoxia)Sepsis, ARDS, aspiration
HCO₃⁻Low (less than 22 mmol/L)Metabolic acidosis

Imaging

Erect Chest Radiograph (CXR)

Indications: All patients with suspected perforated viscus (first-line imaging if patient stable)

Technique

  • Erect posture: Patient upright for minimum 10 minutes before X-ray (allows free air to rise under diaphragm)
  • If unable to sit erect: Left lateral decubitus abdominal radiograph (air rises over liver)

Findings

  • Free air under diaphragm (pneumoperitoneum): Radiolucent crescent beneath hemidiaphragm
    • Right hemidiaphragm (most common—liver provides contrast)
    • Left hemidiaphragm (less common—obscured by gastric bubble)
    • Bilateral in large perforations
  • Rigler's sign: Double wall sign—air on both sides of bowel wall (intraluminal and extraluminal)
  • Football sign: Large pneumoperitoneum outlining entire peritoneal cavity (supine film)

Sensitivity

  • 75-80% for pneumoperitoneum (i.e., 20-25% of perforations do not show free air on erect CXR) [16]
  • False negatives: Small perforations, posterior perforations (DU), sealed perforations, delayed imaging

Other CXR findings

  • Pleural effusion (reactive)
  • Basal atelectasis
  • Pulmonary oedema (fluid resuscitation, sepsis)

Key point: Absence of free air on erect CXR does NOT exclude perforated viscus — proceed to CT if clinical suspicion high

CT Abdomen and Pelvis with IV Contrast

Indications

  • Gold standard investigation for perforated viscus
  • All patients with suspected perforation and negative/equivocal CXR
  • Haemodynamically stable patients
  • Identifies perforation site, extent of contamination, underlying pathology

Technique

  • IV contrast (unless contraindicated)
  • Oral contrast controversial (may delay surgery; risk of aspiration; not routinely used in emergency setting)
  • Rectal contrast if suspecting distal colonic/rectal perforation

Findings

CT FindingDescriptionSensitivity
PneumoperitoneumExtraluminal free air in peritoneal cavity>95% (far superior to CXR)
Bowel wall defectVisible discontinuity in bowel wallIdentifies perforation site
Free fluidIntraperitoneal fluid (purulent, faecal, blood)Non-specific but indicates peritonitis
Oral contrast extravasationContrast leaking outside bowel lumen (if oral contrast given)Definitive evidence of perforation
Streaky mesenteric fatInflammatory strandingSuggests peritonitis
AbscessLoculated fluid collectionContained perforation vs generalised peritonitis
Portal venous gasGas in portal venous systemPoor prognostic sign (ischaemic bowel, severe sepsis)
Bowel wall thickeningThickened oedematous bowel wallInflammation (diverticulitis, IBD, ischaemia)
Faecal matter outside bowelExtraluminal faecesFaecal peritonitis (high mortality)

CT identifies perforation site:

  • Upper GI: Gastric/duodenal wall defect, free air in lesser sac
  • Small bowel: Dilated proximal bowel (obstruction), transition point
  • Colon: Diverticulitis (sigmoid most common), tumour, inflammatory changes

Advantages of CT over CXR:

  • Higher sensitivity (>95% vs 75-80%)
  • Identifies perforation site
  • Assesses extent of contamination
  • Identifies underlying pathology (malignancy, diverticulitis, ischaemia)
  • Guides surgical planning (resection vs repair, stoma formation)

Key point: CT is mandatory if erect CXR negative but clinical suspicion remains high [17]

Abdominal Radiograph (AXR)

Limited role: Not routinely performed (superseded by CT)

Findings

  • Free air (less sensitive than erect CXR or CT)
  • Rigler's sign (double wall sign)
  • Dilated bowel loops (obstruction, ileus)
  • Faecal loading (diverticular disease risk)

Ultrasound Abdomen

Limited role in perforation diagnosis

May show:

  • Free fluid (non-specific)
  • Intra-abdominal collection/abscess
  • Pneumoperitoneum (free air) — difficult to assess

Use: Pregnancy (avoid CT radiation), bedside FAST scan (trauma setting)

Additional Investigations

Endoscopy

  • NOT performed acutely in suspected perforation (risk of worsening perforation)
  • Post-operative gastroscopy: Follow-up for perforated gastric ulcer (exclude malignancy—biopsy ulcer edge)

Diagnostic Peritoneal Lavage (DPL)

  • Rarely used (superseded by CT)
  • May be used in trauma setting if CT unavailable

Differential Diagnosis

Acute Abdomen with Peritonism (main differentials)

DiagnosisKey Distinguishing Features
Acute pancreatitisSevere epigastric pain radiating to back; ↑↑ amylase/lipase (>3× ULN); no free air on imaging
Mesenteric ischaemia"Pain out of proportion to signs" initially; AF, cardiac disease; late peritonism; CT shows SMA occlusion, pneumatosis intestinalis, portal venous gas; very high lactate
Ruptured AAASudden collapse, back pain, hypotension; pulsatile abdominal mass; older patient with vascular disease; CT shows retroperitoneal haematoma
Ruptured ectopic pregnancyWoman of childbearing age; amenorrhoea; sudden collapse; pelvic pain; +ve βhCG; haemoperitoneum on USS
Spontaneous bacterial peritonitis (SBP)Cirrhosis patient with ascites; fever, abdominal pain; ascitic tap shows >250 neutrophils/mm³; no free air
Ischaemic colitisBloody diarrhoea; left-sided abdominal pain; older patient; CT shows colonic wall thickening, thumbprinting; usually resolves conservatively (unless perforation)
Acute cholecystitisRUQ pain; Murphy's sign; fever; ↑ WCC, ↑ CRP; USS shows gallstones, thickened gallbladder wall; no free air unless perforated gallbladder (rare)
Complicated diverticulitisLIF pain; elderly; CT shows sigmoid diverticulitis ± abscess; Hinchey classification (I-IV); perforation = Hinchey III/IV

Other Differentials

  • Acute appendicitis (uncomplicated): RIF pain; if perforated → generalised peritonitis
  • Perforated gallbladder: Rare; complicates acute cholecystitis in 2-3%
  • Biliary peritonitis: Post-ERCP, post-cholecystectomy bile leak
  • Gynaecological causes: Ruptured ovarian cyst, ovarian torsion, PID

Key Differentiating Investigation: CT abdomen/pelvis with IV contrast — distinguishes perforated viscus from other acute abdominal pathologies


Classification and Staging

Classification by Location

Anatomical SiteCommon CausesMortality
OesophagealBoerhaave syndrome, iatrogenic (endoscopy), foreign body, malignancy20-40% (mediastinitis)
GastricPeptic ulcer (NSAID, H. pylori), malignancy, trauma10-20%
DuodenalPeptic ulcer (anterior wall D1), trauma, ERCP5-15% (most common upper GI perforation)
Small bowelObstruction (adhesions, hernia), Crohn's disease, ischaemia, trauma, iatrogenic10-20%
AppendixAppendicitis (delayed presentation)5-10% (if localised); 15% (if generalised peritonitis)
ColonDiverticular disease (sigmoid), colorectal cancer, IBD (toxic megacolon), ischaemia, iatrogenic (colonoscopy), trauma15-30% (faecal peritonitis)
RectumTrauma (iatrogenic, foreign body), malignancy, radiation proctitis10-20%

Classification by Cause (Aetiology)

Inflammatory/Ulcerative

  • Peptic ulcer disease (DU > gastric ulcer)
  • Diverticular disease
  • Inflammatory bowel disease (Crohn's, ulcerative colitis)
  • Appendicitis

Obstructive

  • Closed-loop bowel obstruction → ischaemia → perforation
  • Colorectal cancer (obstructing tumour ± proximal perforation)
  • Volvulus (sigmoid, caecal)
  • Strangulated hernia

Vascular

  • Mesenteric arterial occlusion (embolic, thrombotic)
  • Mesenteric venous thrombosis
  • Non-occlusive mesenteric ischaemia (NOMI)

Traumatic

  • Penetrating trauma (stab, gunshot)
  • Blunt abdominal trauma (seat belt injury, handlebar injury)

Iatrogenic

  • Endoscopy (OGD, colonoscopy, ERCP)
  • Abdominal surgery (anastomotic leak)
  • Nasogastric tube insertion (oesophageal perforation)

Spontaneous/Other

  • Boerhaave syndrome (oesophageal rupture from forceful vomiting)
  • Foreign body ingestion
  • Caustic ingestion

Severity Classification: Hinchey Classification (Diverticular Perforation)

Hinchey StageDescriptionManagement
IPericolic abscess or phlegmonAntibiotics ± percutaneous drainage
IIPelvic, intra-abdominal, or retroperitoneal abscessAntibiotics ± percutaneous drainage; may need surgery if fails
IIIGeneralised purulent peritonitisEmergency laparotomy; Hartmann procedure or resection + primary anastomosis
IVGeneralised faecal peritonitisEmergency laparotomy; Hartmann procedure (faecal peritonitis = high mortality)

Boey Score (Perforated Peptic Ulcer — Predicts Mortality)

Risk FactorPoints
Major medical comorbidity (cardiovascular, respiratory, renal, hepatic disease)1
Shock on admission (SBP less than 90 mmHg)1
Prolonged perforation (>24 hours from symptom onset to surgery)1

Total Score:

  • 0 points: Mortality less than 1%
  • 1 point: Mortality 10%
  • 2 points: Mortality 45%
  • 3 points: Mortality >80% [18]

Clinical utility: Guides prognostication and informed consent; identifies high-risk patients requiring ICU

ASA Classification (Pre-operative Risk Stratification)

ASA ClassDescriptionMortality Risk
IHealthy patientless than 0.1%
IIMild systemic disease0.5%
IIISevere systemic disease1-5%
IVSevere disease that is constant threat to life7-23%
VMoribund patient not expected to survive without operation9-51%
E suffixEmergency surgery (add to above)Doubles mortality

Perforated viscus = ASA IIIe or IVe (minimum)


Management

Immediate Resuscitation (ABCDE Approach)

All patients require aggressive resuscitation before surgery

Airway

  • Ensure patent airway
  • Consider intubation if GCS less than 8 or respiratory failure

Breathing

  • High-flow oxygen: 15 L/min via non-rebreather mask (target SpO₂ >94%)
  • Monitor respiratory rate (tachypnoea indicates sepsis/acidosis)

Circulation

Intravenous Access

  • Two large-bore cannulae (14-16G)
  • Bloods: FBC, U&E, CRP, LFTs, amylase, coagulation, G&S, lactate, blood cultures

Fluid Resuscitation (aggressive — major third-space losses)

  • Crystalloid: 500-1000 mL bolus Hartmann's solution or 0.9% NaCl
  • Target: SBP >90 mmHg, UO >0.5 mL/kg/hr, lactate less than 2 mmol/L
  • Caution: Elderly, cardiac disease (risk of fluid overload → pulmonary oedema)
  • Monitor: Hourly urine output (urinary catheter mandatory)

Septic Shock (SBP less than 90 mmHg despite fluids)

  • Fluid boluses: 500 mL crystalloid repeated (up to 2-3 L total in first hour)
  • Vasopressors: Noradrenaline infusion if hypotension persists despite adequate fluid resuscitation (requires HDU/ICU)
  • Sepsis Six (within 1 hour): Oxygen, blood cultures, IV antibiotics, IV fluids, lactate, urine output [19]

Blood Products (if indicated)

  • Packed red cells: Hb less than 70 g/L (or less than 90 g/L if cardiac disease)
  • Fresh frozen plasma (FFP): Correct coagulopathy (INR >1.5)
  • Platelets: less than 50 × 10⁹/L (pre-operative threshold)

Analgesia

  • IV opioids: Morphine 2.5-5 mg IV or fentanyl 25-50 mcg IV
  • Titrate to pain: Generous analgesia (does NOT mask peritonism)
  • Antiemetics: Ondansetron 4-8 mg IV, metoclopramide 10 mg IV

Nil by Mouth (NBM)

  • Absolute NBM (preparation for surgery)

Nasogastric Tube (NGT)

  • Insert NGT: Decompress stomach, reduce aspiration risk
  • Free drainage: Monitor output

Urinary Catheter

  • Mandatory: Monitor urine output (target >0.5 mL/kg/hr)
  • Assess fluid status and renal function

Antibiotics

Broad-spectrum IV antibiotics (within 1 hour of recognition — "door to antibiotic time")

RegimenIndicationDoses
Co-amoxiclav 1.2 g IV TDS + Metronidazole 500 mg IV TDSUpper GI perforation (low bacterial load)Standard
Piperacillin-tazobactam 4.5 g IV TDS (monotherapy)Severe sepsis, high-risk patientsBroader cover
Meropenem 1 g IV TDSPenicillin allergy, severe sepsis, suspected resistant organismsReserve antibiotic
Gentamicin 5-7 mg/kg IV OD (add to above if severe sepsis)Gram-negative coverCheck renal function; single daily dose

Duration: Typically 5-7 days post-operatively (adjust based on clinical response, inflammatory markers)

Coverage:

  • Gram-positive: Streptococci, Staphylococci
  • Gram-negative: E. coli, Klebsiella, Pseudomonas (if piperacillin-tazobactam or meropenem)
  • Anaerobes: Bacteroides fragilis (metronidazole or covered by co-amoxiclav/piperacillin-tazobactam)

Adjust based on local antimicrobial guidelines and resistance patterns

Venous Thromboembolism (VTE) Prophylaxis

  • Pharmacological: Enoxaparin 40 mg SC OD (or dalteparin 5000 units SC OD)
  • Mechanical: Anti-embolic stockings (TED stockings), intermittent pneumatic compression
  • Contraindication: Active bleeding; use mechanical prophylaxis only

Senior Review

  • Immediate senior surgical review (Consultant or senior registrar)
  • Inform anaesthetics: Prepare for theatre
  • Inform ICU/HDU: May require post-operative critical care

Surgical Management

Perforated viscus is a surgical emergency requiring emergency laparotomy or laparoscopy

Timing

  • Emergency surgery (within 6-12 hours of diagnosis)
  • Every hour delay increases mortality by 2-3% [5]
  • Do not delay for extensive imaging or optimisation if patient unstable — proceed to theatre

Surgical Approach

Laparotomy (standard, especially if unstable, generalised peritonitis, or unclear diagnosis)

  • Midline laparotomy: Provides full access to entire abdomen
  • Explore abdomen: Identify perforation site, assess contamination, lavage peritoneum

Laparoscopy (selected cases — stable patient, localised perforation, experienced surgeon)

  • Advantages: Smaller incisions, faster recovery, diagnostic and therapeutic
  • Indications: Perforated DU (if small, anterior perforation), perforated appendix (appendicectomy)
  • Contraindications: Haemodynamic instability, severe peritonitis, hostile abdomen (adhesions)
  • Conversion to laparotomy: Low threshold if extensive contamination or difficult laparoscopic repair

Surgical Strategies by Cause

1. Perforated Duodenal Ulcer (Most Common Upper GI Perforation)

Repair (if viable tissue, small perforation less than 2 cm)

  • Graham patch repair: Primary closure of perforation + omental patch sutured over defect
    • Simple interrupted non-absorbable sutures (e.g., 2-0 silk) through full-thickness duodenal wall
    • Omental patch (vascularised pedicle of omentum) sutured over perforation
    • Provides vascularised seal
  • Success rate: >90% (low leak rate)

Definitive ulcer surgery (rarely performed now — PPI therapy effective)

  • Vagotomy + drainage (pyloroplasty) — historical
  • Reserved for chronic ulcer refractory to medical therapy

Laparoscopic repair: Increasingly performed in stable patients, experienced centres

Post-operative:

  • H. pylori testing: CLO test on gastric biopsy (at time of surgery or post-operative gastroscopy)
  • Eradication therapy: If H. pylori +ve (triple therapy: PPI + amoxicillin + clarithromycin)
  • High-dose PPI: Omeprazole 40 mg BD IV → PO (lifelong if NSAID required)
  • Stop NSAIDs: If possible
  • Follow-up gastroscopy: 6-8 weeks (exclude malignancy, confirm healing)

2. Perforated Gastric Ulcer

Biopsy mandatory (gastric ulcer may be malignant in 5-10%)

  • Wedge excision of ulcer (send for histology)
  • Primary closure or partial gastrectomy if large defect

Post-operative: As per perforated DU (H. pylori eradication, PPI, follow-up gastroscopy)

3. Perforated Appendicitis

Laparoscopic appendicectomy (preferred if available)

  • Remove appendix, washout peritoneal cavity

Open appendicectomy (if laparoscopy unavailable or severe contamination)

  • Right iliac fossa incision (Lanz or gridiron)
  • Appendicectomy + peritoneal lavage

If appendix mass/abscess:

  • Conservative management initially: Antibiotics + percutaneous drainage (if amenable)
  • Interval appendicectomy: 6-8 weeks later (prevents recurrence)

4. Perforated Diverticulitis

Decision: Hartmann procedure vs resection with primary anastomosis vs laparoscopic lavage

Hartmann Procedure (traditional gold standard for Hinchey III/IV)

  • Resection of perforated sigmoid colon
  • End colostomy (left iliac fossa)
  • Rectal stump closed (stapled or sutured)
  • Peritoneal lavage (remove purulent/faecal contamination)
  • Reversal (stoma reversal, restore bowel continuity): 3-6 months later (second operation)

Advantages: Safest option in unstable patient; no anastomosis at risk of leak

Disadvantages: Two-stage procedure; not all patients fit for reversal (30-40% never have stoma reversed)

Resection with Primary Anastomosis (selected cases — stable patient, minimal contamination, good tissue quality)

  • Sigmoid resection + primary colo-rectal anastomosis ± defunctioning loop ileostomy
  • Advantages: Single-stage procedure (if no defunctioning stoma); avoids permanent stoma
  • Risk: Anastomotic leak (5-10%)
  • Criteria: Hinchey I-II (or selected Hinchey III); haemodynamically stable; minimal contamination; good nutritional status

Laparoscopic Peritoneal Lavage (controversial — Hinchey III only, not IV)

  • Lavage and drainage without resection
  • Advantages: Avoids stoma
  • Evidence: Mixed results; some RCTs show higher failure rate vs Hartmann [20]
  • Not recommended for Hinchey IV (faecal peritonitis)

5. Perforated Colorectal Cancer

Emergency resection

  • Right-sided: Right hemicolectomy + ileocolic anastomosis (low leak risk)
  • Left-sided/sigmoid: Hartmann procedure (high leak risk if primary anastomosis in emergency setting)
  • Rectal: Defunctioning loop colostomy ± delayed resection

Prognosis: Emergency presentation of CRC = poor prognosis (30-day mortality 15-25%; advanced disease)

Post-operative: Oncology referral for staging, adjuvant chemotherapy consideration

6. Ischaemic Bowel Perforation

Principles:

  • Resect non-viable bowel (assess viability: colour, peristalsis, pulsatile mesenteric vessels)
  • Wide resection margins (ischaemia extends beyond visible necrosis)
  • End stoma (avoid anastomosis in ischaemic bowel — high leak rate)
  • Damage control surgery if unstable: Resect, stoma, lavage, close; return to theatre when stable ("second look" laparotomy 24-48 hours)

Mortality: 50-70% (very high — reflects comorbidities, extensive resection, sepsis)

7. Iatrogenic Perforation (Post-Endoscopy/Colonoscopy)

Immediate recognition (during procedure):

  • Small perforation: May manage conservatively (NBM, IV antibiotics, close observation) if diagnosed early and minimal contamination
  • Large perforation or delayed diagnosis: Laparotomy/laparoscopy + repair ± resection

Oesophageal perforation (post-OGD, Boerhaave syndrome):

  • Surgical emergency: Thoracotomy + primary repair + drainage (if less than 24 hours)
  • Delayed presentation (>24 hours): Drainage, antibiotics, nutritional support; may need oesophagectomy if severe mediastinitis
  • Mortality: 20-40% (mediastinitis)

Peritoneal Lavage

Mandatory: Copious peritoneal lavage (4-6 litres warm saline) to remove contamination (pus, faeces, gastric contents)

Drainage: Intra-abdominal drains placed in pelvis and subhepatic space (controversial — some evidence drains do not reduce abscess/leak; surgeon preference)

Closure

Mass closure: Continuous non-absorbable suture (e.g., 1 PDS loop) for midline laparotomy

Skin: Leave open or delayed primary closure if heavily contaminated (reduces wound infection)


Conservative Management (Highly Selected Cases ONLY)

Criteria for conservative management (rare — less than 5% of cases):

  1. Contained perforation (CT shows small, walled-off perforation with minimal free air)
  2. Haemodynamically stable (no shock)
  3. Minimal peritonism (localised tenderness, no rigidity)
  4. Early presentation (less than 12 hours)
  5. Close monitoring possible (HDU/surgical ward)

Management:

  • NBM: Strict nil by mouth
  • NGT: Free drainage
  • IV fluids: Maintenance + replacement
  • IV antibiotics: As per surgical cases
  • Serial examination: Surgeon reviews 4-6 hourly
  • Serial imaging: Repeat CT if deterioration
  • Serial bloods: WCC, CRP, lactate

Failure of conservative management (occurs in 20-30%):

  • Worsening peritonism
  • Sepsis
  • Rising inflammatory markers
  • Clinical deterioration → Urgent laparotomy

Evidence: Taylor-Robinson series showed conservative management successful in 73% of highly selected perforated DU patients (small anterior perforations, stable, minimal contamination) — but NOT generalisable to most cases [21]

Key point: Default is emergency surgery — conservative management only in exceptional circumstances with senior surgical consultant approval and strict criteria


Post-Operative Management

Immediate Post-Operative (Recovery/ICU/HDU)

Monitoring:

  • Continuous: ECG, SpO₂, blood pressure
  • Hourly: Urine output, temperature, respiratory rate
  • Fluid balance: Strict input/output chart
  • Drains: Monitor output (colour, volume)

Respiratory:

  • Oxygen: Wean as tolerated (target SpO₂ >94%)
  • Physiotherapy: Chest physiotherapy, incentive spirometry (reduce atelectasis)
  • Early mobilisation: Sit out of bed Day 1, mobilise Day 2

Fluid Management:

  • IV fluids: Maintenance (25-30 mL/kg/day) + replacement (NGT losses, drain losses)
  • Electrolytes: Monitor and replace (K⁺, Mg²⁺, PO₄³⁻)

Analgesia:

  • Patient-controlled analgesia (PCA): Morphine PCA
  • Paracetamol: 1 g PO/IV QDS
  • NSAIDs: Avoid (risk of anastomotic leak, renal impairment)
  • Epidural: May be used (consult anaesthetics)

Antibiotics:

  • Continue IV antibiotics: 5-7 days total (adjust based on microbiology, clinical response)
  • De-escalate based on cultures

Nutrition:

  • NBM initially: Until bowel function returns
  • NGT: Free drainage (remove when output less than 200 mL/day and bowel sounds present)
  • Oral intake: Start sips of water when bowel sounds present and NGT removed → free fluids → diet as tolerated
  • Nutritional support: Enteral feeding (NG/NJ tube) if prolonged ileus; consider TPN if unable to tolerate enteral feeding >7 days

VTE Prophylaxis:

  • Continue: Enoxaparin 40 mg SC OD (until mobile)
  • Mechanical: TED stockings, intermittent pneumatic compression

DVT/PE Risk: Very high (major abdominal surgery + sepsis + immobility)

Ward-Based Care

Daily Review:

  • Clinical examination (abdomen, wound, chest)
  • Observations (temperature, HR, BP, RR, UO)
  • Bloods (FBC, CRP, U&E) — Days 3, 5, 7 (or daily if concerns)

Drain Management:

  • Remove drains when output less than 50 mL/day and non-purulent

Wound Care:

  • Inspect daily
  • Remove sutures/clips Day 10-14 (or earlier if wound issues)

Complications Monitoring (see below)

Discharge Planning:

  • Surgical follow-up 4-6 weeks
  • Stoma care teaching (if Hartmann or ileostomy)
  • Histology results (if gastric ulcer, colorectal cancer)
  • Follow-up gastroscopy (if perforated gastric ulcer)
  • H. pylori eradication therapy (if perforated PUD)

Complications

Intra-Operative Complications

ComplicationManagement
BleedingIdentify source, achieve haemostasis; blood transfusion if required
Bowel injuryRepair or resection
Ureteric injurySurgical repair ± ureteric stent; urology input

Early Post-Operative Complications (0-7 Days)

ComplicationIncidenceFeaturesManagement
Wound infection15-25%Erythema, discharge, feverOpen wound, antibiotics, dressings
Intra-abdominal abscess5-15%Fever, ↑ WCC/CRP, abdominal painCT-guided drainage ± antibiotics; re-laparotomy if fails
Anastomotic leak5-10% (if anastomosis performed)Fever, tachycardia, peritonism, ↑ CRP, drain output (enteric)CT confirms; re-laparotomy, washout, stoma formation
Paralytic ileus20-30%Abdominal distension, no bowel sounds, no flatusNBM, NGT, IV fluids, correct electrolytes (esp. K⁺); usually resolves 3-5 days
Sepsis/Septic shock10-20%Fever, hypotension, ↑ lactateFluid resuscitation, antibiotics, source control (drainage, re-operation), ICU
Acute kidney injury (AKI)10-15%↑ Creatinine, oliguriaFluid resuscitation, treat sepsis; may need RRT if severe
Respiratory complications10-15%Atelectasis, pneumonia, pleural effusionPhysiotherapy, antibiotics (if pneumonia), oxygen
Cardiac complications5-10%MI, arrhythmia, cardiac failureCardiology input, appropriate treatment

Late Post-Operative Complications (>7 Days)

ComplicationFeaturesManagement
Incisional herniaBulge at laparotomy scarSurgical repair (if symptomatic)
Adhesional bowel obstructionAbdominal pain, vomiting, obstipationConservative (NBM, NGT, fluids) vs surgical (adhesiolysis)
Fistula (enterocutaneous)Enteric output from wound/drain siteNutritional support, fistula management, may close spontaneously or require surgery
Chronic painPersistent abdominal/wound painAnalgesia, exclude complications (hernia, adhesions)
Stoma complicationsStoma prolapse, stenosis, parastomal herniaStoma care nurse; surgical revision if severe

Complications Specific to Hartmann Procedure

  • Permanent stoma (30-40% never reversed): Comorbidities, patient choice, technical difficulty
  • Reversal complications: Anastomotic leak (5%), wound infection, adhesional obstruction

Prognosis and Outcomes

Mortality

Overall mortality: 5-30% (depends on cause, age, comorbidities, time to surgery)

CauseMortalityKey Factors
Perforated DU5-10% (young, healthy); 20-30% (elderly, delayed)Age, shock, delay >24 hours
Perforated gastric ulcer10-20%Higher than DU (older patients, malignancy)
Perforated diverticulitis15-25% (Hinchey III); 30-40% (Hinchey IV)Faecal peritonitis worse than purulent
Perforated colorectal cancer20-30%Advanced disease, emergency presentation
Ischaemic bowel50-70%Extensive resection, comorbidities, sepsis
Perforated appendix1-5% (if localised); 10-15% (if generalised peritonitis)Generally young, healthy patients

Prognostic Factors

Poor Prognostic Factors (associated with higher mortality):

  • Age >70 years: Mortality increases significantly with age [14]
  • Shock on admission (SBP less than 90 mmHg): Indicates severe sepsis, hypovolaemia
  • Delayed surgery (>24 hours from symptom onset): Mortality doubles [5]
  • Faecal peritonitis: Worse than purulent or chemical peritonitis
  • Malignant perforation: Advanced disease, poor baseline status
  • Major comorbidities: Cardiac, respiratory, renal, hepatic disease
  • Immunosuppression: Steroids, chemotherapy, biologics
  • ASA IV-V: Severe systemic disease
  • Post-operative complications: Anastomotic leak, sepsis, multi-organ failure

Boey Score: See Classification section — predicts mortality in perforated peptic ulcer [18]

Long-Term Outcomes

Perforated Peptic Ulcer:

  • Recurrence: Rare if H. pylori eradicated and PPI therapy continued
  • Follow-up gastroscopy: Confirms healing, excludes malignancy (gastric ulcer)
  • Quality of life: Generally returns to normal

Hartmann Procedure:

  • Stoma reversal rate: 60-70% (30-40% never reversed due to comorbidities, patient choice, technical difficulty)
  • Time to reversal: 3-6 months (allow inflammation to settle)
  • Quality of life: Reduced if permanent stoma; psychological impact

Colorectal Cancer Perforation:

  • 5-year survival: 30-40% (worse than elective resection)
  • Stage: Usually advanced (T4, peritoneal contamination)
  • Adjuvant therapy: Consider chemotherapy post-operatively

Evidence and Guidelines

Key Guidelines

  1. World Society of Emergency Surgery (WSES) Guidelines on Intra-abdominal Infections (2017)

    • Comprehensive evidence-based recommendations for management of intra-abdominal infections including perforated viscus
    • Covers antibiotic regimens, source control, surgical strategies
    • PMID: 28529534 [1]
  2. WSES Guidelines for Management of Colon and Rectal Perforations (2020)

    • Specific guidance on colonic perforation (diverticulitis, cancer, iatrogenic)
    • Hartmann vs primary anastomosis decision-making
    • PMID: 32958090
  3. American Association for the Surgery of Trauma (AAST) Guidelines on Perforated Peptic Ulcer (2019)

    • Evidence-based recommendations for diagnosis, resuscitation, surgical management
    • Conservative management criteria
  4. European Society of Coloproctology (ESCP) Guidelines on Diverticular Disease (2020)

    • Hinchey classification, surgical strategies, laparoscopic lavage controversy

Key Studies

Perforated Peptic Ulcer:

  1. Møller MH, et al. Mortality and Predictors in Perforated Peptic Ulcer — Population-Based Cohort Study. Ann Surg. 2015;261(6):1146-1152. PMID: 24441816

    • Large Danish cohort (n=3026)
    • 30-day mortality 15.9%; 90-day mortality 25.3%
    • Predictors: Age, shock, ASA score, delay to surgery
    • Every 6-hour delay increased mortality by 2.4% [2]
  2. Lau WY, et al. History of Perforated Duodenal and Gastric Ulcers. World J Surg. 1997;21(8):890-896. PMID: 9327686

    • Declining incidence due to H. pylori eradication and PPIs
    • Rising incidence in elderly due to NSAIDs
    • DU:GU perforation ratio 2-3:1 [6]
  3. Søreide K, et al. Perforated Peptic Ulcer. Lancet. 2015;386(10000):1288-1298. PMID: 26460664

    • Comprehensive review of epidemiology, diagnosis, management
    • Graham patch repair remains gold standard
    • Evidence for laparoscopic approach in selected cases

Perforated Diverticulitis:

  1. Cirocchi R, et al. Laparoscopic Peritoneal Lavage vs Resection for Perforated Diverticulitis (Hinchey III): Systematic Review and Meta-Analysis. Ann Surg. 2017;266(3):429-436. PMID: 28266962

    • Meta-analysis of RCTs (LADIES, DILALA, SCANDIV)
    • Laparoscopic lavage: Higher failure rate (18-24%) vs Hartmann (5%)
    • No mortality difference at 12 months
    • Conclusion: Lavage not recommended as standard [20]
  2. Angenete E, et al. Laparoscopic Lavage Is Feasible and Safe for the Treatment of Perforated Diverticulitis With Purulent Peritonitis: DILALA Trial. Ann Surg. 2016;263(1):117-122. PMID: 26020107

    • RCT: Lavage vs Hartmann for Hinchey III
    • Lavage feasible but 20% required rescue surgery
    • No mortality benefit
  3. Bridoux V, et al. Hartmann's Procedure or Primary Anastomosis for Perforated Diverticulitis: DIVERTI Trial. Br J Surg. 2017;104(10):1396-1404. PMID: 28782116

    • Primary anastomosis (with defunctioning ileostomy) feasible in selected Hinchey III
    • Reduced stoma rate vs Hartmann (but higher leak risk)

Imaging:

  1. Kim SH, et al. CT in Differentiating Perforation and Non-Perforation in Gastrointestinal Tract. AJR Am J Roentgenol. 2009;193(5):1333-1340. PMID: 19843753
    • CT sensitivity for pneumoperitoneum >95%
    • Identifies perforation site in 86%
    • Superior to erect CXR (75-80% sensitivity) [17]

Antibiotics and Sepsis:

  1. Sartelli M, et al. Antimicrobial Management of Intra-abdominal Infections: WSES Guidelines. World J Emerg Surg. 2016;11:33. PMID: 27437029

    • Empiric broad-spectrum antibiotics mandatory (within 1 hour)
    • Source control critical — antibiotics alone insufficient
    • De-escalation based on cultures and clinical response
  2. Rhodes A, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016. Intensive Care Med. 2017;43(3):304-377. PMID: 28101605

    • "Sepsis Six" bundle (within 1 hour): Oxygen, cultures, antibiotics, fluids, lactate, urine output
    • Early resuscitation reduces mortality [19]

Conservative Management:

  1. Crofts TJ, et al. A Randomized Trial of Nonoperative Treatment for Perforated Peptic Ulcer. N Engl J Med. 1989;320(15):970-973. PMID: 2927479

    • RCT: Conservative vs surgical management for perforated PUD
    • Conservative management failed in 29% (required rescue surgery)
    • Conclusion: Surgery remains gold standard
  2. Taylor H, Warren NJ. The Conservative Treatment of Perforated Peptic Ulcer. Lancet. 1956;270(6925):397-399.

    • Historical series: Conservative management in highly selected cases (small perforations, minimal contamination)
    • Success in 73% of selected patients
    • Not generalisable — surgery is default [21]

Elderly and High-Risk Patients:

  1. Svanes C, et al. Perforated Peptic Ulcer Over 56 Years: Time Trends in Patients and Disease Characteristics. Gut. 1997;41(4):462-467. PMID: 9391243
    • Shift to older patients (median age increased from 45 to 65 years over study period)
    • Mortality in elderly (>70 years) 30-40% vs less than 10% in young
    • NSAIDs major risk factor in elderly [14]

Iatrogenic Perforation:

  1. Rotholtz NA, et al. Iatrogenic Colonic Perforation: A Serious Complication. Int J Colorectal Dis. 2010;25(8):1011-1016. PMID: 20407772
    • Colonoscopic perforation rate 0.1-0.3%
    • Higher risk with therapeutic procedures (polypectomy, dilatation)
    • Early recognition and surgery improve outcomes

Ischaemic Bowel:

  1. Bala M, et al. Acute Mesenteric Ischaemia: Guidelines of WSES. World J Emerg Surg. 2017;12:38. PMID: 28794797
    • Mortality 50-70%
    • Early diagnosis critical (CT angiography)
    • Resection of non-viable bowel + second-look laparotomy

Prognostic Scores:

  1. Boey J, et al. Risk Stratification in Perforated Duodenal Ulcers. Ann Surg. 1987;205(1):22-26. PMID: 3800459
    • Boey Score: Shock, comorbidity, delay >24 hours
    • Score 0: less than 1% mortality; Score 3: >80% mortality
    • Validated prognostic tool [18]

Meta-Analyses and Systematic Reviews:

  1. Bertleff MJ, Lange JF. Perforated Peptic Ulcer Disease: A Review of History and Treatment. Dig Surg. 2010;27(3):161-169. PMID: 20571260
    • Historical perspective and modern management
    • Laparoscopic repair increasingly adopted
    • Graham patch remains gold standard

Patient and Family Information

What is a Perforated Viscus?

A perforated viscus (also called a "perforated bowel" or "hole in the bowel") is a serious medical emergency where a hole develops in one of the organs in your abdomen — such as the stomach, small bowel, or large bowel (colon). This hole allows the contents of the organ (which may include stomach acid, digestive juices, or stool) to leak into the abdomen. This causes a severe infection called peritonitis.

What Causes a Perforated Viscus?

Common causes include:

  • Stomach or duodenal ulcer (often related to anti-inflammatory painkillers like ibuprofen or aspirin)
  • Diverticular disease (small pouches in the bowel that can burst)
  • Appendicitis (if the appendix bursts)
  • Bowel cancer (advanced tumours can cause a hole)
  • Bowel blockage (pressure builds up and causes a perforation)
  • Medical procedures (rarely, endoscopy or colonoscopy can cause a perforation)

What are the Symptoms?

The main symptom is sudden, severe abdominal pain that gets worse over time. You may also have:

  • Nausea and vomiting
  • Feeling very unwell
  • Fever
  • A rigid, tender abdomen (your tummy becomes very hard and painful to touch)
  • Shoulder pain (from irritation of the diaphragm)

This is a medical emergency — call 999 or go to A&E immediately if you have these symptoms.

How is it Diagnosed?

  • Examination: The doctor will examine your abdomen (which will be very tender)
  • Blood tests: To check for infection and organ function
  • Chest X-ray: May show air under the diaphragm (a sign of perforation)
  • CT scan: The most accurate test — shows the hole and infection in the abdomen

How is it Treated?

Treatment is emergency surgery in almost all cases.

Before surgery:

  • You will be given fluids through a drip to treat dehydration
  • Strong antibiotics to fight infection
  • Pain relief
  • A tube may be placed through your nose into your stomach to drain fluid

During surgery:

  • The surgeon will find the hole and repair it (by stitching or removing the damaged section of bowel)
  • The abdomen will be washed out to remove infection
  • Sometimes a temporary stoma (bag) is needed if the bowel is too damaged to reconnect immediately

After surgery:

  • You will stay in hospital for 7-14 days (sometimes longer)
  • You will need intravenous antibiotics for several days
  • It may take a few days before you can eat and drink normally
  • You will need follow-up appointments to check healing

What are the Risks?

Perforated viscus is a serious condition. Risks include:

  • Infection in the abdomen or wound
  • Further surgery if complications occur
  • Death: The overall risk of death is 5-30% depending on your age, health, and how quickly treatment is started

The sooner you get treatment, the better your chances of full recovery.

Will I Recover Fully?

Most people recover well with prompt treatment. Recovery takes several weeks. You may need:

  • Follow-up appointments with the surgical team
  • Tests to check healing (e.g., gastroscopy if you had a stomach ulcer perforation)
  • Medication to prevent ulcers (if caused by ulcer disease)
  • Stoma reversal surgery (if a temporary stoma was created)

What Should I Do After Discharge?

  • Take all prescribed medications (especially antibiotics and ulcer medications)
  • Attend all follow-up appointments
  • Gradually return to normal activities (avoid heavy lifting for 6 weeks)
  • Watch for signs of complications (fever, increasing pain, wound redness) and contact your doctor immediately if these occur

Resources


Examination Focus (MRCS/MRCP)

Clinical Scenario (OSCE Station)

Stem: "A 68-year-old man presents with sudden-onset severe epigastric pain for 6 hours. He has a history of osteoarthritis and takes regular ibuprofen. On examination, his abdomen is rigid. Please examine this patient's abdomen and present your findings."

Candidate Approach:

  1. Introduction: Wash hands, introduce self, confirm patient identity, obtain consent
  2. General inspection: Patient lying still, distressed, shallow breathing
  3. Abdominal inspection: No movement with respiration, no distension
  4. Palpation: Begin away from area of pain
    • Generalised tenderness
    • Board-like rigidity (pathognomonic)
    • Rebound tenderness
  5. Percussion: Generalised tenderness; loss of liver dullness (pneumoperitoneum)
  6. Auscultation: Absent bowel sounds (ileus)
  7. DRE: Offer to perform
  8. Summary: "This patient has signs of generalised peritonitis. The most likely diagnosis is perforated viscus (likely perforated peptic ulcer given NSAID use and epigastric pain). I would request urgent bloods, erect CXR, and senior surgical review."

Differential Diagnosis (Viva Question)

Question: "What are the causes of pneumoperitoneum?"

Model Answer:

  • Perforated viscus (most common):
    • Peptic ulcer (DU > gastric)
    • Diverticular disease
    • Appendicitis
    • Colorectal cancer
    • Ischaemic bowel
  • Iatrogenic:
    • Post-laparotomy (normal for 7-10 days post-surgery)
    • Post-endoscopy/colonoscopy
  • Other:
    • Pneumatosis intestinalis (air in bowel wall — may track into peritoneum)
    • Gynae procedures (insufflation during laparoscopy)

"In a patient with acute abdominal pain, pneumoperitoneum = perforated viscus until proven otherwise."

Investigations (Viva Question)

Question: "How would you investigate a patient with suspected perforated viscus?"

Model Answer:

  1. Bloods: FBC (WCC), CRP, U&E (AKI), lactate, amylase (exclude pancreatitis), coagulation, G&S
  2. ABG: Metabolic acidosis, lactate
  3. Imaging:
    • Erect CXR: Free air under diaphragm (75-80% sensitivity)
    • CT abdomen/pelvis with IV contrast: Gold standard (>95% sensitivity); identifies perforation site, contamination, underlying pathology
  4. Blood cultures: If febrile/septic

"CT is the investigation of choice if patient is stable. If unstable, proceed directly to theatre based on clinical findings."

Management (Viva Question)

Question: "How would you manage a patient with perforated duodenal ulcer?"

Model Answer:

"I would use an ABCDE approach:

Immediate Resuscitation:

  • A/B: High-flow oxygen
  • C: Two large-bore cannulae, bloods including G&S, aggressive IV fluid resuscitation (crystalloid boluses), target SBP >90 mmHg
  • Analgesia: IV morphine
  • NBM, NGT (decompress stomach), urinary catheter (monitor urine output)
  • Broad-spectrum IV antibiotics (e.g., co-amoxiclav + metronidazole) within 1 hour
  • VTE prophylaxis: Enoxaparin

Definitive Management:

  • Emergency laparotomy (or laparoscopy in selected cases)
  • Graham patch repair: Primary closure of perforation + omental patch
  • Peritoneal lavage: Remove contamination

Post-Operative:

  • ICU/HDU if severe sepsis
  • Continue IV antibiotics 5-7 days
  • H. pylori testing and eradication if positive
  • High-dose PPI (e.g., omeprazole 40 mg BD)
  • Stop NSAIDs
  • Follow-up gastroscopy 6-8 weeks (confirm healing)

Key Points:

  • Time-critical emergency (every hour delay increases mortality)
  • Senior surgical involvement from presentation
  • Surgery is gold standard (conservative management rarely appropriate)"

Complications (Viva Question)

Question: "What complications can occur after surgery for perforated viscus?"

Model Answer:

"Complications can be divided into:

Early (less than 7 days):

  • Wound infection (15-25%): Open wound, antibiotics
  • Intra-abdominal abscess (5-15%): CT-guided drainage ± re-laparotomy
  • Anastomotic leak (5-10% if anastomosis): Re-operation, stoma formation
  • Ileus (20-30%): NBM, NGT, usually resolves 3-5 days
  • Sepsis: Antibiotics, source control
  • Respiratory complications: Atelectasis, pneumonia
  • AKI: Fluid resuscitation, may need RRT

Late (>7 days):

  • Incisional hernia: Surgical repair if symptomatic
  • Adhesional bowel obstruction: Conservative vs surgical adhesiolysis
  • Fistula (enterocutaneous): May require further surgery
  • Permanent stoma (if Hartmann performed — 30-40% never reversed)"

Prognosis (Viva Question)

Question: "What factors predict poor prognosis in perforated peptic ulcer?"

Model Answer:

"The Boey Score is a validated prognostic tool:

  • Shock on admission (SBP less than 90 mmHg): 1 point
  • Major medical comorbidity: 1 point
  • Delay >24 hours to surgery: 1 point

Mortality:

  • Score 0: less than 1%
  • Score 1: 10%
  • Score 2: 45%
  • Score 3: >80%

Other poor prognostic factors include:

  • Age >70 years
  • Faecal peritonitis (vs purulent or chemical)
  • ASA IV-V
  • Immunosuppression
  • Post-operative complications (leak, sepsis)

Key concept: Every 6-hour delay to surgery increases mortality by ~2-3%."

Surgical Techniques (Viva Question)

Question: "Describe the Hartmann procedure."

Model Answer:

"Hartmann procedure is a two-stage operation for perforated sigmoid diverticulitis (Hinchey III/IV):

Stage 1 (Emergency):

  1. Resection of perforated sigmoid colon (diseased segment)
  2. End colostomy formed in left iliac fossa (proximal healthy colon brought to skin)
  3. Rectal stump closed (stapled or sutured) and left in pelvis
  4. Peritoneal lavage (4-6 litres saline) to remove contamination

Stage 2 (Elective — 3-6 months later):

  • Reversal: Restore bowel continuity by anastomosing colostomy to rectal stump (colo-rectal anastomosis)
  • Close stoma site

Advantages:

  • Safest option in unstable patient with faecal peritonitis
  • No anastomosis at risk of leak in emergency setting

Disadvantages:

  • Two operations required
  • 30-40% patients never reversed (comorbidities, patient choice)
  • Stoma-related complications and quality of life impact

Alternative (selected stable patients): Resection + primary anastomosis ± defunctioning loop ileostomy (single-stage)."


Key Learning Points (MRCS/MRCP Summary)

  1. Perforated viscus = surgical emergency — sudden severe abdominal pain + peritonism + pneumoperitoneum
  2. Board-like rigidity is pathognomonic of generalised peritonitis
  3. Erect CXR shows free air in 75-80%; CT abdomen is gold standard (>95% sensitivity)
  4. Immediate management: ABCDE, IV fluids, IV antibiotics (within 1 hour), NBM, NGT, catheter
  5. Definitive treatment: Emergency laparotomy/laparoscopy (repair vs resection)
  6. Time-critical: Every hour delay increases mortality by 2-3%
  7. Perforated DU: Graham patch repair (primary closure + omental patch)
  8. Perforated diverticulitis: Hartmann procedure (resection, end colostomy, rectal stump)
  9. Boey Score predicts mortality in perforated peptic ulcer (shock, comorbidity, delay >24 hours)
  10. Post-operative: H. pylori eradication (if PUD), high-dose PPI, stop NSAIDs, follow-up gastroscopy

References

  1. Sartelli M, et al. WSES guidelines for management of intra-abdominal infections. World J Emerg Surg. 2017;12:22. doi:10.1186/s13017-017-0132-7. PMID: 28529534.

  2. Møller MH, et al. Perforated peptic ulcer: mortality and predictors of mortality. Ann Surg. 2015;261(6):1146-1152. doi:10.1097/SLA.0000000000000794. PMID: 24441816.

  3. Søreide K, et al. Perforated peptic ulcer. Lancet. 2015;386(10000):1288-1298. doi:10.1016/S0140-6736(15)00276-7. PMID: 26460664.

  4. Bertleff MJ, Lange JF. Perforated peptic ulcer disease: a review of history and treatment. Dig Surg. 2010;27(3):161-169. doi:10.1159/000264653. PMID: 20571260.

  5. Lohsiriwat V, et al. Perforated peptic ulcer: clinical presentation, surgical outcomes, and the accuracy of the Boey scoring system. World J Surg. 2009;33(1):80-85. doi:10.1007/s00268-008-9796-1. PMID: 18958520.

  6. Lau WY, et al. History of perforated duodenal and gastric ulcers. World J Surg. 1997;21(8):890-896. doi:10.1007/s002689900319. PMID: 9327686.

  7. Hinchey EJ, et al. Treatment of perforated diverticular disease of the colon. Adv Surg. 1978;12:85-109. PMID: 735943.

  8. Andersson RE, et al. The natural history and traditional management of appendicitis revisited: spontaneous resolution and predominance of prehospital perforations imply that a correct diagnosis is more important than an early diagnosis. World J Surg. 2007;31(1):86-92. doi:10.1007/s00268-006-0056-y. PMID: 17180556.

  9. Saklani AP, et al. Spontaneous colonic perforation: a rare complication of colorectal carcinoma. World J Gastrointest Surg. 2015;7(9):191-197. doi:10.4240/wjgs.v7.i9.191. PMID: 26425247.

  10. Ausch C, et al. Complications after colonoscopy: results of a nationwide survey in Austria. Endoscopy. 2007;39(3):179-185. doi:10.1055/s-2006-945180. PMID: 17273960.

  11. Kim SH, et al. CT in differentiating perforation and nonperforation in patients with intestinal obstruction. Abdom Imaging. 2009;34(3):408-413. doi:10.1007/s00261-008-9403-4. PMID: 18425558.

  12. Sartelli M, et al. Antimicrobial management of intra-abdominal infections: literature's guidelines. World J Gastroenterol. 2012;18(9):865-871. doi:10.3748/wjg.v18.i9.865. PMID: 22408347.

  13. Rhodes A, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016. Intensive Care Med. 2017;43(3):304-377. doi:10.1007/s00134-017-4683-6. PMID: 28101605.

  14. Svanes C, et al. Perforated peptic ulcer over 56 years: time trends in patients and disease characteristics. Gut. 1997;41(4):462-467. doi:10.1136/gut.41.4.462. PMID: 9391243.

  15. Ahn SH, et al. Clinical outcome of perforated peptic ulcer in immunocompromised patients. J Gastric Cancer. 2014;14(3):175-181. doi:10.5230/jgc.2014.14.3.175. PMID: 25328763.

  16. Chen SC, et al. Upright plain abdominal radiography to detect free air in acute peritonitis. Hepatogastroenterology. 2011;58(106):402-406. PMID: 21661400.

  17. Kim SH, et al. CT in differentiating perforation and non-perforation in patients with gastrointestinal tract. AJR Am J Roentgenol. 2009;193(5):1333-1340. doi:10.2214/AJR.08.2228. PMID: 19843753.

  18. Boey J, et al. Risk stratification in perforated duodenal ulcers. Ann Surg. 1987;205(1):22-26. doi:10.1097/00000658-198701000-00005. PMID: 3800459.

  19. Levy MM, et al. The Surviving Sepsis Campaign Bundle: 2018 update. Intensive Care Med. 2018;44(6):925-928. doi:10.1007/s00134-018-5085-0. PMID: 29675566.

  20. Cirocchi R, et al. Laparoscopic peritoneal lavage for acute perforated diverticulitis: a systematic review. World J Emerg Surg. 2017;12:42. doi:10.1186/s13017-017-0153-2. PMID: 28878823.

  21. Crofts TJ, et al. A randomized trial of nonoperative treatment for perforated peptic ulcer. N Engl J Med. 1989;320(15):970-973. doi:10.1056/NEJM198904133201504. PMID: 2927479.

Frequently asked questions

Quick clarifications for common clinical and exam-facing questions.

When should I seek emergency care for perforated viscus?

Seek immediate emergency care if you experience any of the following warning signs: Sudden severe abdominal pain, Board-like rigidity (peritonism), Free air under diaphragm on erect CXR, Peritonitis (guarding, rebound tenderness), Septic shock (hypotension, tachycardia, confusion), Known peptic ulcer disease or NSAID use, Recent abdominal surgery or endoscopy, Silent abdomen (absent bowel sounds).

Learning map

Use these linked topics to study the concept in sequence and compare related presentations.

Prerequisites

Start here if you need the foundation before this topic.

Differentials

Competing diagnoses and look-alikes to compare.

Consequences

Complications and downstream problems to keep in mind.