01Approach to the Critical Patient/attcp45

Immediate stabilization

›Time-critical actions

›Airway and breathing assessment

›Risk of aspiration from vomiting or NGT placement

›Supplemental oxygen for SpO2 < 94%

›Intubation if airway unprotected or hemodynamic collapse imminent

›Circulatory resuscitation

›Two large-bore IV lines

›Crystalloid bolus 1–2 L immediately for hypotension

›Foley catheter for urine output monitoring target >= 0.5 mL/kg/hour

›NPO immediately upon suspicion

›Reduces ongoing peritoneal contamination

›NGT to suction for gastric decompression

›Immediate general surgery consultation

›Do not delay for imaging if frank peritonitis present

›Every hour of delay associated with 2.4% decreased probability of survival

Hemodynamic monitoring and targets

›Resuscitation targets

›MAP >= 65 mmHg

›Vasopressors if refractory to fluids

›Norepinephrine first-line vasopressor

›Urine output >= 0.5 mL/kg/hour

›Monitor hourly via Foley

›Reassess fluid responsiveness

›Lactate clearance

›Repeat lactate at 2–4 hours

›Target clearance >= 10% per hour in septic shock

›Continuous cardiac monitoring

02History/hx79

Onset and character of pain

›Classic presentation

›Sudden-onset severe epigastric pain

›Hallmark presentation in 66–88% of patients

›Pain rapidly becomes generalized within hours

›Prior dyspepsia or known PUD history

›Only ~30% have known PUD diagnosis at time of perforation

›Prior epigastric burning, nocturnal pain, belching

›Duration of symptoms

›Symptoms > 24 hours worsen outcomes significantly

›Delay to surgery > 12 hours independently increases mortality

Risk factors and triggers

›Pharmacologic triggers

›NSAID and aspirin use

›Responsible for ~36% of PUD cases

›Can cause ulcers within 7 days of initiation

›Corticosteroid use

›Risk amplified when combined with NSAIDs

›Can blunt peritoneal signs masking severity

›Bevacizumab and VEGF inhibitors

›Increased GI perforation risk

›Recent chemotherapy

›Behavioral and environmental triggers

›Alcohol binge drinking

›Acute heavy alcohol use

›Chronic heavy use as background risk

›Crack cocaine and amphetamine use

›Intense vasoconstriction leading to mucosal ischemia and necrosis

03Physical Exam/exam50

Vital signs

›Stability snapshot

›Heart rate

›Tachycardia early sign of pain and volume depletion

›Persistent tachycardia suggests ongoing peritoneal contamination

›Blood pressure

›Hypotension late and ominous sign indicating septic shock

›SBP < 90 mmHg triggers resuscitation escalation

›Temperature

›Fever suggests established peritonitis and sepsis

›Hypothermia in severe sepsis is ominous

›Respiratory rate

›Tachypnea from pain splinting and developing sepsis

›>= 22/minute as qSOFA sepsis marker

›Oxygen saturation

›Hypoxemia from aspiration, sepsis, or atelectasis

›Diaphragmatic splinting reduces tidal volume

Abdominal exam

›Classic peritonitis findings

›Board-like rigidity

›Chemical peritonitis from acid exposure is hallmark

›Most specific exam finding for perforation

›Diffuse tenderness

›Rebound tenderness indicating peritoneal irritation

›Guarding both voluntary and involuntary

›Absent bowel sounds

›Ileus from peritoneal irritation

›Loss of hepatic dullness on percussion (pneumoperitoneum sign)

04Differential Diagnosis/ddx45

Life-threatening mimics requiring immediate exclusion

›Vascular emergencies

›Ruptured abdominal aortic aneurysm

›ICD-10 I71.3

›Pulsatile mass, back and flank pain, haemodynamic collapse

›Acute mesenteric ischemia

›ICD-10 K55.0

›Pain out of proportion to exam, lactic acidosis, atrial fibrillation

›Cardiac mimics

›Acute myocardial infarction inferior wall

›ICD-10 I21.1

›ST elevation in inferior leads, troponin rise

›Epigastric pain from inferior MI is a classic trap

Intra-abdominal surgical emergencies

›Pancreatic and biliary pathology

›Acute pancreatitis

›ICD-10 K85.9

›Epigastric pain radiating to back, elevated lipase, managed non-operatively

›Acute cholecystitis

›ICD-10 K81.0

›RUQ pain, Murphy sign, fever, ultrasound confirmation

›Acute cholangitis

›ICD-10 K83.0

›Charcot triad: fever, jaundice, RUQ pain

›Hollow viscus perforation

›Perforated diverticulitis

›ICD-10 K57.20

›LLQ predominance, older adults, pneumoperitoneum possible

05Laboratory Tests/lt52

Core resuscitation labs

›Haematologic assessment

›Complete blood count

›Leukocytosis common but non-specific

›Leukopenia in severe sepsis or immunosuppression

›Haematocrit for baseline before transfusion decisions

›Type and screen

›Mandatory preoperative preparation

›Crossmatch if concurrent bleeding suspected

›Coagulation profile

›PT/INR and PTT for perioperative coagulopathy

›Elevated INR in liver disease or anticoagulated patients

›Metabolic and organ function

›Basic metabolic panel

›Renal function for antibiotic dosing adjustment

›Electrolytes deranged from vomiting and NGT suction

›Glucose as sepsis stress marker

›Liver function tests

›Liver cirrhosis increases perioperative mortality

›Bilirubin and coagulation factor context

›Albumin

›Hypoalbuminaemia independent risk factor for releak and poor outcomes

›Target correction if severely low before elective surgery

Sepsis and perfusion markers

›Lactate

›>= 2 mmol/L as organ hypoperfusion marker

›Repeat at 2–4 hours to assess clearance

›Lactate >= 4 mmol/L with septic shock mandates ICU

06Diagnostic Tests/dt72

Scoring Systems

›Operative risk and mortality prediction

›Boey Score

›Three risk factors: major medical illness, preoperative shock, duration of perforation > 24 hours

›Score 0: mortality < 1%

›Score 1: mortality ~10%

›Score 2: mortality ~45%

›Score 3: mortality ~100%

›PULP Score (Peptic Ulcer Perforation Score)

›Incorporates age, comorbidities, shock, delay to presentation, and lab values

›More granular than Boey for risk stratification

›Used in WSES 2020 guidelines for NOM candidate selection

›AAST Grading System 2016

›Grades PPU 1–5 using clinical, radiographic, operative, and pathologic criteria

›Grade 1–2: contained, low complexity

›Grade 4–5: free perforation with vascular involvement, highest mortality

›ASA Physical Status Score

›High ASA score independently associated with poor prognosis

›ASA IV–V patients have significantly elevated perioperative mortality

›qSOFA score

›Respiratory rate >= 22/min

›SBP <= 100 mmHg

›Altered mental status

›Score >= 2 indicates high risk of adverse outcomes

MRI

›MRI role in perforated peptic ulcer

›Limited acute utility for PPU

›Availability constraints in emergency setting

›Time required incompatible with surgical emergency

›Problem-solving indications in stable patients

›Suspected gastric malignancy masquerading as benign ulcer

›Complex post-operative complications

›Contraindications in acute setting

›Haemodynamically unstable patient

›Inability to lie flat due to pain

›Non-compatible implants

CT

›CT abdomen and pelvis with IV contrast

›Gold standard imaging modality

›98% diagnostic accuracy for PPU

›Identifies perforation site, free air, free fluid, bowel wall thickening

›Key CT findings of PPU

›Pneumoperitoneum: extraluminal free air

›Unexplained intraperitoneal free fluid

›Bowel wall thickening at perforation site

›Mesenteric fat stranding adjacent to ulcer

›Extraluminal contrast extravasation if oral contrast administered

›Clinical decision on CT timing

›In frank peritonitis, sepsis, and free air on CXR: proceed directly to OR

›Up to 12% of perforations may have normal CT

›Water-soluble oral contrast study via NGT if CT negative with high suspicion

›Exclusion of alternative diagnoses

›AAA, pancreatitis, mesenteric ischaemia, diverticulitis

›Valuable when diagnosis uncertain

›CT limitations

›Sealed or contained perforation may appear subtle

›Small pneumoperitoneum missed on axial views without lung windows

›Radiologist review with PPU clinical context mandatory

Ultrasound

›POCUS and FAST examination

›Detection of free intraperitoneal fluid

›Hepatorenal space, splenorenal space, pelvis

›Lacks specificity for hollow-organ perforation

›Pneumoperitoneum detection

›Enhanced peritoneal stripe sign

›Limited sensitivity compared to CT and CXR

›Adjunctive role in haemodynamically unstable patients

›Bedside when CT not immediately available

›Cardiac function assessment for shock differential

›Bedside lactate as point-of-care adjunct

›Immediate perfusion assessment

›Results within minutes at bedside

›Guides resuscitation aggressiveness

›Paired with POCUS for unstable patient

›Combined assessment within 5–10 minutes of arrival

›ACEP Level B recommendation for lactate in sepsis assessment

07Disposition/dispo53

Inpatient admission (all PPU patients)

›Universal admission requirement

›All confirmed or suspected PPU requires inpatient surgical admission

›No outpatient management for any PPU

›Direct to operative suite or surgical ward

›ICU admission indications

›Sepsis or septic shock

›Vasopressor requirement

›Multi-organ dysfunction

›Post-operative unstable patients

Surgical consultation and OR activation

›Immediate general surgery consultation triggers

›Clinical peritonitis

›Immediate consultation without waiting for imaging

›Frank peritonitis: direct to OR

›Pneumoperitoneum on any imaging modality

›CXR free air under diaphragm

›CT free air confirmed

›Free fluid with clinical peritonitis

›FAST positive with peritoneal signs

›Diagnostic uncertainty does not delay consultation

›Time-sensitive thresholds

›Surgery within 6–12 hours of diagnosis for optimal outcomes

›Every hour of delay reduces survival by 2.4%

›Operating room must be notified immediately upon diagnosis

Nonoperative management observation (highly selected)

›NOM candidate criteria

›Age < 70 years

08Treatment/t100

Initial emergency department stabilization

›Resuscitation bundle

›Crystalloid resuscitation

›Normal saline or Ringer's lactate

›1–2 L bolus in first 30 minutes for hypotension

›Reassess after each bolus for fluid responsiveness

›NGT insertion to suction

›Reduces ongoing gastric acid leak into peritoneum

›Aspiration risk reduction

›Water-soluble contrast study via NGT if needed for diagnosis

›Analgesia

›IV opioids as needed; do not withhold for diagnostic purposes

›Morphine 2.5–5 mg IV titrated to pain relief

›Evidence supports analgesia does not mask diagnosis

›VTE prophylaxis

›Pneumatic compression devices immediately

›Pharmacological prophylaxis after haemostasis confirmed post-operatively

Antibiotic therapy

›Broad-spectrum IV antibiotics

›Gram-negative and anaerobic coverage mandatory

›Initiate within 1 hour of diagnosis in septic patients

›Class I recommendation (WSES Guidelines 2020)

›Piperacillin-tazobactam

›4.5 g IV every 6 hours

›First-line for confirmed perforation with peritonitis

›Extended infusion over 3–4 hours if available

›Ceftriaxone plus metronidazole alternative

›Ceftriaxone 2 g IV daily

›Metronidazole 500 mg IV every 8 hours

›Acceptable alternative to piperacillin-tazobactam

›Carbapenem for severe sepsis or healthcare-associated perforation

›Meropenem 1 g IV every 8 hours

›Imipenem-cilastatin 500 mg IV every 6 hours

›Reserve for resistant organism risk

›Duration

›4–7 days post-operatively if source control achieved

›Extend if ongoing infection signs or intra-abdominal abscess

Proton pump inhibitor therapy

›IV PPI initiation

›Pantoprazole IV

›80 mg IV bolus then 8 mg/hour continuous infusion

›Alternative: 40 mg IV every 12 hours

›Reduces acid secretion and ongoing mucosal injury

›Transition to oral PPI post-operatively

›Once tolerating oral intake

›Long-term PPI therapy indicated

Surgical treatment (definitive)

›Laparoscopic omental patch repair (Graham patch)

›Preferred approach for most perforations

›Non-inferior to open repair with lower morbidity

›WSES 2020 recommendation for stable patients

›Technical considerations

›Thorough peritoneal lavage with warm saline

›Biopsy ulcer edges mandatory for gastric perforations

›Drain placement per surgeon preference

›Conversion to open repair if

›Laparoscopic approach not feasible

›Haemodynamic instability deteriorating on table

›Extensive contamination limiting visualisation

›Open repair indications

›Haemodynamically unstable patients

›Cannot tolerate pneumoperitoneum

›Damage control surgery with peritoneal packing if severe contamination

›Large perforations or pyloric location

›May require distal gastrectomy or pyloroplasty

›Suspicion of malignancy in gastric corpus perforations

›Distal gastrectomy

›Large perforations near pylorus

›Gastric corpus perforations with malignancy concern

›Biopsy all gastric perforations without exception

›Damage control surgery

›Severely unstable patients with diffuse contamination

›Abbreviated procedure: lavage and closure

›Planned return to OR at 24–48 hours

›Bridge to ICU stabilisation

Post-operative management

›H. pylori eradication

›Test all patients for H. pylori

›Histology from biopsy or rapid urease test intraoperatively

›Urea breath test or stool antigen >= 4 weeks post-antibiotics

›Triple therapy first-line (if low clarithromycin resistance)

›Clarithromycin 500 mg PO twice daily

›Amoxicillin 1 g PO twice daily

›Omeprazole 20 mg PO twice daily

›Duration 14 days

›Quadruple therapy (bismuth-based) for second-line or high resistance

›Bismuth subcitrate 120 mg PO four times daily

›Tetracycline 500 mg PO four times daily

›Metronidazole 250–500 mg PO four times daily

›PPI standard dose twice daily for 10–14 days

›NSAID and aspirin management

›Discontinue NSAIDs immediately and permanently when possible

›Substitute acetaminophen 325–1000 mg PO every 4–6 hours

›If NSAIDs medically necessary, co-prescribe PPI

›Low-dose aspirin for cardiovascular indications

›Weigh risk versus benefit with cardiology input

›PPI co-prescription mandatory if continued

›Follow-up endoscopy

›Gastric ulcer perforations: repeat endoscopy at 4–6 weeks

›Confirm ulcer healing

›Biopsy to exclude malignancy

›H. pylori eradication confirmation

›Duodenal ulcer perforations

›Endoscopy if clinically indicated

›H. pylori eradication testing mandatory

09Special Populations/sp64

Pregnancy

›Pregnancy-specific considerations

›Epidemiology in pregnancy

›PPU extremely rare in pregnancy

›H. pylori infection is a risk factor as in general population

›Diagnostic approach

›CXR with abdominal shielding when pneumoperitoneum suspected

›CT abdomen/pelvis: foetal radiation risk balanced against diagnostic urgency

›Ultrasound first-line but insensitive for free air

›Physiologic changes affecting presentation

›Uterine enlargement displaces abdominal organs

›Peritoneal signs may be blunted or atypical

›Delayed gastric emptying increases aspiration risk

›Surgical management

›Emergency surgery not delayed for foetal concerns

›Laparoscopic repair feasible in first and second trimester

›Foetal monitoring during and after surgery

›Obstetrics consultation mandatory

›Antibiotic safety in pregnancy

›Piperacillin-tazobactam: generally considered safe, Category B

›Metronidazole: avoid in first trimester if possible

›Fluoroquinolones: avoid in pregnancy

›Maternal oxygenation target SpO2 >= 95%

Geriatric

›Older adult-specific features

›Atypical presentation

›Peritoneal signs absent in up to 40% of elderly patients

›Steroid use and reduced pain perception blunt exam

10Background/b72

Epidemiology

›Incidence and burden

›PPU accounts for 2–10% of all peptic ulcer disease complications

›Short-term mortality up to 30% and morbidity up to 50%

›Overall mortality approximately 9% but up to 30% with delayed presentation

›Location distribution

›Proximal duodenum (anterior wall): 35–65% of cases

›Pylorus: 25–45% of cases

›Stomach: 5–25% of cases

›Geographic and temporal trends

›Declining incidence with H. pylori eradication programs

›NSAID-associated perforation increasing as aging population grows

›PPU in patients < 75 years more likely associated with smoking and H. pylori

›Time-sensitivity data

›Every hour of surgical delay: 2.4% decreased probability of survival

›Delay > 12 hours independently worsens outcomes

›Symptoms > 24 hours correlate with increased morbidity and mortality

Pathophysiology

›Mucosal injury mechanisms

›H. pylori infection

›Colonises gastric antrum and corpus

›Causes chronic active gastritis, disrupts mucosal defence

›Responsible for 50–80% of perforated PUD cases

›Urease production neutralises acid locally; toxins disrupt epithelium

›NSAID-mediated injury

›COX-1 inhibition reduces prostaglandin E2 synthesis

›Prostaglandins maintain mucus secretion, bicarbonate barrier, mucosal blood flow

›Can cause ulcers within 7 days of initiation

›Gastric ulcers predominate with NSAID use

›Acid hypersecretion

›Zollinger-Ellison syndrome: gastrin-secreting tumour drives ulcerogenesis

›Stress ulcers in critically ill from mucosal ischaemia

›Crack cocaine and amphetamines: intense vasoconstriction causing ischaemic necrosis

›Perforation mechanism

›Progressive full-thickness mucosal erosion

›Anterior duodenal wall most common site

›Chemical peritonitis from gastric acid, bile, pancreatic enzymes

›Contamination spectrum

›Free perforation: immediate generalised peritonitis

›Contained perforation: omentum or adjacent organs seal the defect

›Sealed perforation: may present as attenuated syndrome

›Sepsis cascade

›Bacterial translocation from peritoneal soiling

›Mixed flora including gram-negatives and anaerobes

›Endotoxin release drives SIRS and septic shock

›Multi-organ failure in delayed presentations

›Acute kidney injury from sepsis and hypoperfusion

›ARDS from systemic inflammatory response

Therapeutic Considerations

›Surgical strategy evidence

›Laparoscopic versus open repair

›Laparoscopic non-inferior to open for morbidity and mortality

›Shorter hospital stay and lower wound complication rate with laparoscopic

›WSES 2020 guidelines support laparoscopic as preferred approach

›NOM evidence base

›NOM failure rate 28–46% across studies

›Highest failure in elderly, delayed presentation, or haemodynamically unstable

›Requires strict criteria and 24-hour surgical backup

›Definitive ulcer treatment versus patch repair

›Most guidelines recommend patch repair plus H. pylori eradication

›Definitive acid reduction surgery rarely performed in acute setting

›Follow-up endoscopy and medical management preferred

›H. pylori eradication evidence

›Reduces recurrence risk substantially after repair

›Eradication reduces 1-year recurrence from 70% to < 5%

›Testing and treating is Class I recommendation

›Confirmation testing essential

›Urea breath test or stool antigen >= 4 weeks post-antibiotics and >= 2 weeks off PPI

›NSAID management after PPU

›Avoid NSAIDs permanently when possible

›Substitute acetaminophen for pain management

›If cardiovascular NSAID or aspirin needed: PPI co-prescription mandatory

›Long-term PPI therapy

›Standard dose PPI for minimum 4–8 weeks post-repair

›Indefinite if NSAID continuation unavoidable

11Patient Discharge Instructions/pdi69

copy discharge instructions

›What happened to you

›A hole formed in the lining of your stomach or small bowel (peptic ulcer perforation)

›This required emergency surgery to repair the hole and clean the abdomen

›You received antibiotics to treat the infection caused by stomach contents leaking out

›Medications to take at home

›Proton pump inhibitor (acid-reducing medication)

›Take exactly as prescribed, usually once or twice daily

›Do not stop without speaking to your surgeon or family doctor

›H. pylori antibiotic course if prescribed

›Complete the full course even if feeling better

›All three or four medications must be taken together

›Pain medications

›Use acetaminophen as directed for pain

›Avoid ibuprofen, aspirin, and all anti-inflammatory pills

›Activity and diet

›Diet advancement

›Start with clear fluids and advance slowly to soft foods

›Small frequent meals; avoid large meals

›Avoid spicy foods, alcohol, and carbonated drinks initially

›Activity restrictions

›No heavy lifting > 5 kg for 6 weeks

›Gradually increase walking each day

›No driving while taking opioid pain medications

›Wound care

›Keep incision clean and dry

›Remove dressings per surgeon instruction

›No soaking in baths or pools until incision healed

12References/r36

Guidelines and key sources

›Primary evidence sources

›Soreide K, Thorsen K, Harrison EM, et al. Perforated Peptic Ulcer. Lancet. 2015. PMID 26460663

›Comprehensive review of epidemiology, pathophysiology, management

›Time-to-surgery survival data: 2.4% decreased survival per hour delay

›Tarasconi A, Coccolini F, Biffl WL, et al. Perforated and Bleeding Peptic Ulcer: WSES Guidelines. World Journal of Emergency Surgery. 2020. PMC6947898

›WSES 2020 current guidelines for management of PPU

›Laparoscopic approach recommendation, NOM criteria, antibiotic guidance

›Arshad SA, Murphy P, Gould JC. Management of Perforated Peptic Ulcer: A Review. JAMA Surgery. 2025

›Contemporary review of NOM criteria and outcomes

›NOM failure rates 28–46%, selection criteria

›Vakil N. Peptic Ulcer Disease: A Review. JAMA. 2024

›Comprehensive PUD review including perforation pathophysiology

›NSAID and H. pylori mechanisms

›Almadi MA, Lu Y, Alali AA, Barkun AN. Peptic Ulcer Disease. Lancet. 2024. PMID 38885678

›Updated epidemiology and H. pylori eradication data

›Recurrence reduction with eradication from 70% to < 5%

›Coccolini F, Sartelli M, Sawyer R, et al. Source Control in Emergency General Surgery: WSES, GAIS, SIS-E, SIS-A Guidelines. World Journal of Emergency Surgery. 2023. PMC10362628

›Source control principles including peritoneal lavage

›Damage control surgery indications

›Yadlapati RH, Shaheen NJ. Gastro-Esophageal Disorders of the Geriatric Population. American Journal of Gastroenterology. 2025

›Geriatric-specific NSAID and PUD burden

›Management considerations in older adults

Scoring and classification tools

›Risk stratification references

›Boey Score: 3-variable mortality prediction tool for PPU

›Major medical illness, preoperative shock, perforation duration > 24 hours

›Validated across multiple international cohorts

Evidence & Review