Peritonitis in Adults

Quick Reference Card

PERITONITIS SUSPECTED
        |
        v
RESUSCITATION (concurrent with workup)
- IV access x2, crystalloid bolus 30 mL/kg if septic
- Blood cultures, lactate, FBC, U&E, coagulation
- Broad-spectrum IV antibiotics WITHIN 1 HOUR
        |
        v
IMAGING + SOURCE IDENTIFICATION
- Erect CXR (free air) → CT if stable
- Paracentesis if ascites present
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        v
    +----------------+----------------+
    |                                 |
    v                                 v
SECONDARY PERITONITIS            PRIMARY SBP
(Perforation/leak)               (Cirrhosis + ascites)
    |                                 |
    v                                 v
EMERGENCY LAPAROTOMY             MEDICAL MANAGEMENT
- Source control                 - Ceftriaxone 2g IV daily
- Peritoneal lavage              - Albumin 1.5g/kg D1, 1g/kg D3
- Consider damage control        - Duration: 5-7 days
                                 - NO surgery unless secondary

Overview

Peritonitis is inflammation of the peritoneum, the serosal membrane lining the abdominal cavity and covering the visceral organs. [1] It represents one of the most time-critical surgical emergencies, with mortality rates ranging from 10% in uncomplicated cases to over 50% in patients with delayed source control or multi-organ failure. [2] The condition may be primary (spontaneous bacterial peritonitis, SBP, occurring without an identifiable intra-abdominal source), secondary (resulting from perforation, ischemia, or contamination of the peritoneal cavity), or tertiary (persistent or recurrent infection despite adequate initial treatment). [3]

The cardinal clinical feature of generalised peritonitis is abdominal rigidity - the involuntary contraction of abdominal wall muscles creating a "board-like" abdomen that reflects severe peritoneal irritation. [4] This finding, along with free intraperitoneal air on imaging, mandates emergent surgical exploration in secondary peritonitis. In contrast, SBP in cirrhotic patients is managed medically with antibiotics and albumin, making accurate differentiation between primary and secondary peritonitis essential for appropriate management. [5]

Early recognition, aggressive resuscitation, broad-spectrum intravenous antibiotics, and timely source control form the pillars of management. The Surviving Sepsis Campaign guidelines emphasise antibiotic administration within one hour of sepsis recognition and source control within 6-12 hours as key determinants of survival. [6] This topic covers the complete spectrum of peritonitis from pathophysiology through emergency surgical management, with emphasis on examination-relevant clinical decision-making.

Epidemiology

Incidence and Prevalence

Peritonitis remains a significant cause of morbidity and mortality worldwide. The epidemiology varies considerably between primary SBP and secondary peritonitis. [7]

Mortality Rates

Mortality from peritonitis depends critically on aetiology, timing of intervention, and patient comorbidities. [2,8]

Risk Factors

For Secondary Peritonitis:

• Peptic ulcer disease (NSAIDs, H. pylori)
• Diverticular disease
• Appendicitis (delayed presentation)
• Recent abdominal surgery (anastomotic leak)
• Abdominal trauma
• Inflammatory bowel disease
• Mesenteric ischemia

For Spontaneous Bacterial Peritonitis:

• Cirrhosis with ascites (Child-Pugh B/C)
• Ascitic fluid protein less than 1.0 g/dL [9]
• Prior episode of SBP (1-year recurrence: 40-70%)
• Gastrointestinal haemorrhage
• Urinary tract infection
• Hepatocellular carcinoma
• Malnutrition

Aetiology and Classification

Classification by Source

Classification by Distribution

Causes of Secondary Peritonitis

Exam Detail: By Anatomical Region:

Pathophysiology of Contamination:

The severity of peritonitis correlates with:

1. Volume of contamination: Larger spills worsen outcome
2. Nature of contents: Colonic > small bowel > gastric (higher bacterial load distally)
3. Time since perforation: > 24 hours significantly increases mortality
4. Underlying pathology: Malignancy, ischemia worsen prognosis

Microbiology

Secondary Peritonitis - Typical Organisms: [10]

SBP Microbiology: [9]

Key Point: SBP is typically monomicrobial with enteric organisms. Polymicrobial growth strongly suggests secondary (surgical) peritonitis. [5]

Pathophysiology

Peritoneal Anatomy and Defence Mechanisms

The peritoneum is a serous membrane with a surface area of approximately 1.7-2.0 m2, comparable to skin. It comprises:

• Parietal peritoneum: Lines abdominal wall, innervated by somatic nerves (sharp, localizable pain)
• Visceral peritoneum: Covers organs, innervated by autonomic nerves (dull, poorly localized pain)

Normal Peritoneal Defences:

1. Mesothelial cell barrier function
2. Lymphatic drainage (especially diaphragmatic)
3. Omental "wrapping" of inflammation
4. Resident macrophages and mast cells
5. Antimicrobial properties of peritoneal fluid

Secondary Peritonitis - Mechanism

Exam Detail: Stage 1: Contamination

• Breach of GI tract barrier (perforation, ischemia, anastomotic leak)
• Spillage of luminal contents: bacteria, bile, gastric acid, pancreatic enzymes, faeces
• Peritoneal contamination with > 10^6-10^10 CFU/mL of GI content

Stage 2: Local Inflammatory Response

• Mesothelial injury triggers cytokine release (IL-1, IL-6, TNF-alpha)
• Complement activation (C3a, C5a)
• Neutrophil recruitment to peritoneal cavity
• Increased vascular permeability and protein-rich exudate
• Fibrin deposition (attempts to localize infection)

Stage 3: Systemic Response

• Cytokines enter systemic circulation
• Endothelial activation and capillary leak
• Third-spacing of fluid into peritoneal cavity and bowel wall
• Hypovolemia and cardiovascular compromise
• Paralytic ileus from peritoneal inflammation

Stage 4: Sepsis and Organ Dysfunction

• Persistent inflammatory response
• Septic shock (vasodilatory, hypotension)
• Multi-organ dysfunction syndrome (MODS)
• Acute kidney injury (AKI)
• Acute respiratory distress syndrome (ARDS)
• Disseminated intravascular coagulation (DIC)

Factors Determining Outcome:

Spontaneous Bacterial Peritonitis - Mechanism

The pathogenesis of SBP involves: [9,11]

1. Intestinal bacterial overgrowth: Common in cirrhosis due to decreased gut motility
2. Increased intestinal permeability: Portal hypertension causes bowel wall oedema
3. Bacterial translocation: Bacteria cross intestinal epithelium to mesenteric lymph nodes
4. Impaired reticuloendothelial function: Portosystemic shunting bypasses hepatic clearance
5. Bacteremia: Bloodstream seeding from translocated bacteria
6. Ascitic fluid colonization: Low ascitic fluid protein (less than 1.0 g/dL) reduces opsonic activity
7. SBP development: Bacteria multiply in ascites with impaired local defences

Why Ascitic Fluid is Vulnerable:

• Low protein content (less than 1.0 g/dL) in 15-20% of cirrhotic ascites
• Low complement levels (C3, C4)
• Impaired neutrophil function
• Decreased opsonization capacity

Consequences of Peritonitis

Clinical Presentation

Symptoms

Secondary Peritonitis - Classic Presentation:

Historical Clues to Aetiology:

SBP - Presentation in Cirrhosis: [5,9]

Clinical Pearl: SBP May Be Subtle: In cirrhotic patients, the classical signs of peritonitis may be attenuated due to immunosuppression, malnutrition, and chronic illness. A change in mental status or unexplained clinical deterioration should prompt diagnostic paracentesis regardless of abdominal findings.

Physical Examination

Abdominal Examination in Secondary Peritonitis:

Exam Detail: Testing for Peritoneal Signs:

1. Guarding assessment: Palpate gently, asking patient to breathe deeply. True guarding persists through respiration and cannot be voluntarily overcome.

2. Rigidity: The abdomen is hard and fixed, described as "board-like" or comparable to a wooden table. This indicates severe generalised peritonitis.

3. Rebound tenderness: Press slowly and deeply, then release quickly. Pain on release indicates peritoneal inflammation. Note: This test is painful and can be replaced by:

   • Percussion tenderness: Gentle tapping produces pain
   • Cough test: Ask patient to cough - positive if produces abdominal pain

4. Rovsing's sign: RLQ pain on LLQ palpation (suggests appendicitis)

5. Obturator sign: Pain on internal rotation of flexed right hip (pelvic appendix)

6. Psoas sign: Pain on hip extension (retrocecal appendix)

Systemic Signs:

Signs in SBP/Cirrhosis:

• Signs of chronic liver disease (spider naevi, palmar erythema, gynaecomastia)
• Ascites (shifting dullness, fluid thrill)
• Hepatic encephalopathy (asterixis, confusion)
• Jaundice
• Often minimal abdominal findings despite infection

Red Flags and Warning Signs

Life-Threatening Features Requiring Immediate Action

High-Risk Patients

Differential Diagnosis

Systematic Approach to Acute Abdomen

Distinguishing SBP from Secondary Peritonitis

This distinction is critical as SBP is managed medically while secondary peritonitis requires surgery. [5,12]

Runyon's Criteria for Secondary Bacterial Peritonitis:

Two or more of the following suggest secondary peritonitis in a cirrhotic patient:

• Total protein > 1 g/dL
• Glucose less than 50 mg/dL
• LDH > upper limit of serum normal

Clinical Pearl: Treatment Test: If a cirrhotic patient with presumed SBP does not show improvement in ascitic fluid PMN count by > 25% at 48 hours despite appropriate antibiotics, consider secondary peritonitis and obtain CT imaging. [5]

Investigations

Initial Laboratory Studies

Imaging

Erect Chest X-Ray:

CT Abdomen and Pelvis with IV Contrast (Gold Standard):

Exam Detail: CT Findings in Specific Conditions:

Ultrasound:

Paracentesis for SBP

Technique:

1. Position: Supine with slight left lateral tilt
2. Site: LLQ (lateral to rectus muscle, avoiding inferior epigastric vessels)
3. Ultrasound guidance recommended (reduces complications)
4. Aspirate 20-30 mL for analysis

Ascitic Fluid Analysis for SBP: [5,9]

When to Perform Paracentesis:

• All cirrhotic patients with ascites admitted to hospital [5]
• Any suspicion of infection (fever, abdominal pain, encephalopathy)
• GI haemorrhage in cirrhosis
• Unexplained deterioration
• Before starting prophylactic antibiotics

Management

Principles of Treatment

The management of peritonitis follows four key principles: [2,6,13]

1. Resuscitation: Aggressive fluid resuscitation and haemodynamic stabilisation
2. Empirical broad-spectrum antibiotics: Administered within 1 hour of sepsis recognition
3. Source control: Surgical or interventional elimination of infection source
4. Supportive care: Organ support, nutrition, VTE prophylaxis

Initial Resuscitation

Simultaneous with diagnostic workup - do not delay for imaging:

Clinical Pearl: "Resuscitate en route to theatre": In patients with secondary peritonitis and septic shock, surgical source control should not be delayed for prolonged resuscitation. Damage control surgery with planned re-look is preferred over attempting complete correction of physiological derangement pre-operatively. [6,13]

Antibiotic Therapy

Principles: [10,14]

• Cover Gram-negative aerobes, anaerobes, and consider Enterococcus in high-risk patients
• Administer within 1 hour of sepsis recognition
• Adjust based on source, severity, and local resistance patterns
• De-escalate once culture results available

Empirical Regimens for Secondary Peritonitis:

Duration: [14]

• With adequate source control: 4-7 days
• Without source control: Continue until source controlled
• Clinical improvement should occur within 48-72 hours

SBP Antibiotic Therapy: [5,9]

SBP Prophylaxis: [5,9]

Albumin in SBP

Intravenous albumin significantly reduces the incidence of hepatorenal syndrome and mortality in SBP. [15]

Indication: All patients with SBP and creatinine > 1 mg/dL, BUN > 30 mg/dL, or bilirubin > 4 mg/dL. [5,15]

Surgical Source Control

Indications for Emergency Laparotomy: [2,13,16]

• Free intraperitoneal air on imaging
• Generalised peritonitis with haemodynamic instability
• Failure of non-operative management
• Clinical deterioration despite resuscitation
• CT evidence of perforation requiring operative intervention
• Anastomotic leak with sepsis

Timing of Surgery:

Exam Detail: Emergency Laparotomy - Surgical Principles:

Pre-operative:

• Informed consent (may be rapid/documented post-operatively)
• Pre-operative antibiotics
• VTE prophylaxis
• Nasogastric tube, urinary catheter
• Prepare for damage control if unstable

Incision:

• Midline laparotomy preferred (maximum access)
• Consider muscle-sparing approaches if source known

Intra-operative Steps:

1. Identify source: Four-quadrant examination
2. Control contamination: Clamp/pack source
3. Debride necrotic tissue: Remove all devitalised tissue
4. Definitive repair: Depends on source and patient physiology
5. Peritoneal lavage: Warm saline irrigation
6. Assess for damage control: If unstable → temporise
7. Drain placement: Controversial; for abscess cavities

Source-Specific Procedures:

Damage Control Surgery

For critically unstable patients, damage control principles apply: [16,17]

Indications ("Lethal Triad"):

• Temperature less than 35°C (hypothermia)
• pH less than 7.2 (acidosis)
• PT/APTT not correctable (coagulopathy)

Damage Control Steps:

1. Abbreviated laparotomy: Control contamination, no definitive repair
2. Temporary abdominal closure: Bogota bag, VAC dressing
3. ICU resuscitation: Correct physiology (warm, correct coagulopathy, optimise)
4. Planned re-look: 24-72 hours when stable
5. Definitive surgery: When patient can tolerate

Percutaneous Drainage

Indications: [13]

• Well-defined, accessible abscess
• Patient stable
• No need for operative source control
• Diverticular or appendicular abscess as bridge to interval surgery

Contraindications:

• Free perforation with ongoing contamination
• Multiple/loculated collections
• Inability to access safely

Complications

Early Complications

Late Complications

SBP-Specific Complications

Prognosis

Prognostic Factors

Poor Prognostic Indicators: [2,8,17]

Scoring Systems

Mannheim Peritonitis Index (MPI): [18]

Interpretation:

• MPI less than 21: Mortality ~2-3%
• MPI 21-29: Mortality ~20-30%
• MPI > 29: Mortality ~50-60%

Outcomes

Special Populations

Cirrhotic Patients

• Always consider SBP: Low threshold for paracentesis
• Distinguish from secondary peritonitis: Runyon's criteria
• Albumin is essential: Prevents hepatorenal syndrome
• Prophylaxis after first episode: Long-term antibiotics
• Consider transplant evaluation: SBP indicates advanced liver disease
• Avoid nephrotoxins: NSAIDs, aminoglycosides, contrast (if possible)

Immunocompromised Patients

• Atypical presentations: Blunted inflammatory response
• Unusual organisms: Fungal, opportunistic infections
• Lower threshold for imaging: Clinical examination unreliable
• Broad empirical coverage: Include antifungals if high-risk
• Higher mortality: Aggressive management required

Elderly Patients (> 70 years)

• Atypical presentations: Minimal pain, no fever
• Reduced physiological reserve: Decompensate rapidly
• Comorbidities: Cardiac, renal impairment
• Polypharmacy: Anticoagulation, steroids may mask signs
• Higher mortality: Need for prompt diagnosis and treatment
• Goals of care discussions: May be appropriate

Post-Operative Patients

• Anastomotic leak: Usually POD 5-10
• Clinical deterioration: Tachycardia, fever, rising WCC
• Low threshold for CT: Especially with drain output changes
• Re-laparotomy: May be required
• Consider damage control: If unstable

Pregnant Patients

• Enlarged uterus: Displaces organs, alters examination findings
• Physiological changes: Increased WCC, altered vital signs
• Appendicitis most common cause: Location changes with gestation
• MRI preferred over CT: Avoid radiation if possible
• Multidisciplinary management: O&G involvement essential
• Fetal monitoring: Continuous monitoring peri-operatively

Exam Focus

Common FRCS/MRCS Viva Questions

Viva Point: Opening Statement: "Peritonitis is inflammation of the peritoneum, classified as primary (spontaneous bacterial peritonitis in cirrhosis), secondary (from GI perforation or contamination), or tertiary (persistent infection after treatment). Secondary peritonitis is a surgical emergency requiring source control, while SBP is managed medically."

Key Points to Mention:

1. Abdominal rigidity is the hallmark sign of peritonitis
2. Free air on imaging confirms perforation and mandates surgery
3. Source control within 6-12 hours is critical for survival
4. SBP: PMN > 250/mm3, treat with ceftriaxone + albumin
5. Mannheim Peritonitis Index predicts mortality

Likely Examiner Questions:

Model Answer: Management of Perforated Duodenal Ulcer

"I would manage this as a surgical emergency, following an ABC approach. I would resuscitate the patient with IV fluids and broad-spectrum antibiotics covering GI flora - piperacillin-tazobactam is my first choice. I would ensure the patient has IV access, crossmatch, catheter, and NG tube.

After confirming the diagnosis with erect CXR showing free air or CT, I would proceed to emergency laparotomy via midline incision. Intra-operatively, I would perform peritoneal lavage, identify the perforation, and perform an omental patch repair (Graham patch). I would consider definitive ulcer surgery only in stable patients with known ulcer disease, which is rare today.

Post-operatively, I would continue antibiotics for 3-5 days, commence PPI therapy, test and treat for H. pylori, and stop any NSAIDs. I would follow up to ensure ulcer healing with endoscopy at 6-8 weeks if concerning features."

Common Examination Mistakes

Errors That Fail Candidates:

Key Clinical Pearls

Diagnostic Pearls

• Board-like rigidity = perforation: This finding alone mandates surgical exploration
• Free air on erect CXR: 70-80% sensitive; absence does not exclude perforation
• CT is gold standard: For identifying source and planning intervention
• SBP can be silent: Always paracentesis in cirrhotic with any clinical change
• PMN > 250/mm3 = SBP: Even with negative culture
• Polymicrobial ascites = secondary peritonitis: Requires surgical evaluation

Treatment Pearls

• Time is critical: Every hour of delay increases mortality
• Antibiotics within 1 hour: Non-negotiable in sepsis
• Source control within 6-12 hours: Optimal window for surgery
• Albumin saves lives in SBP: NNT = 6 to prevent one death
• Damage control in the unstable patient: Abbreviated surgery, ICU resuscitation, re-look
• No surgery for uncomplicated SBP: Medical management only

Prognostic Pearls

• MPI score predicts mortality: Score > 29 = > 50% mortality
• Faecal peritonitis has highest mortality: Colonic source worst prognosis
• SBP survival depends on liver function: Consider transplant evaluation
• Recurrence is common in SBP: 40-70% at 1 year without prophylaxis

Guidelines Summary

Imaging Interpretation

Plain Radiography: Free Air Detection

Erect Chest X-Ray Interpretation:

Free intraperitoneal air (pneumoperitoneum) is best detected on an erect chest X-ray, where air rises to the highest point in the abdomen - under the diaphragm. [4]

Alternative Imaging if Patient Cannot Stand:

Rigler's Sign (Double Wall Sign):

• Air visible on both sides of bowel wall
• Indicates pneumoperitoneum
• Requires > 1000 mL of free air to detect on supine film
• Much less sensitive than erect CXR

Clinical Pearl: Causes of Pneumoperitoneum Without Perforation:

• Recent abdominal surgery (normal for 3-7 days)
• Laparoscopy (may persist for days)
• Peritoneal dialysis
• Pneumatosis cystoides intestinalis
• Vaginal insufflation (rarely)

Always correlate with clinical picture - free air in a patient with peritonitis = perforation until proven otherwise.

CT Abdomen: Detailed Interpretation

Systematic Approach to CT in Suspected Peritonitis:

1. Free air: Location, volume, proximity to likely source
2. Free fluid: Distribution, density (blood vs ascites vs pus)
3. Bowel assessment: Wall thickening, enhancement, discontinuity
4. Source identification: Appendix, diverticula, ulcer, anastomosis
5. Complications: Abscess, phlegmon, vascular involvement
6. Staging information: Malignancy if suspected

CT Signs by Condition:

CT Grading of Severity:

Surgical Anatomy for Peritonitis

Peritoneal Cavity Divisions

Understanding peritoneal anatomy is essential for predicting contamination spread and planning surgical drainage. [4]

Greater Sac:

• Main peritoneal cavity
• Divided by transverse mesocolon into supramesocolic and inframesocolic compartments

Lesser Sac (Omental Bursa):

• Posterior to stomach
• Communicates with greater sac via epiploic foramen (of Winslow)
• Posterior gastric ulcer perforations may be contained here initially

Paracolic Gutters:

• Right paracolic gutter: Continuous superiorly with hepatorenal recess (Morrison's pouch)
• Left paracolic gutter: Separated from left subphrenic space by phrenicocolic ligament

Fluid Flow Pathways:

Exam Detail: Surgical Access and Incisions:

Peritoneal Lavage Technique:

1. Irrigate all four quadrants with warm saline (3-6 liters or more)
2. Aspirate thoroughly
3. Pay attention to paracolic gutters, pelvis, subphrenic spaces
4. Continue until effluent is clear
5. Evidence on saline vs antiseptic lavage: No difference in outcomes; saline preferred

Vascular Considerations

Mesenteric Blood Supply:

SMA Occlusion Signs:

• Pain out of proportion to examination
• Rapid progression to gangrene
• "Thumbprinting" on imaging (mucosal oedema)
• Metabolic acidosis, elevated lactate

Clinical Scenarios

Scenario 1: Perforated Duodenal Ulcer

Presentation: A 45-year-old man presents with sudden-onset severe epigastric pain for 4 hours. He has a history of NSAID use for chronic back pain. On examination, he has a rigid abdomen, tachycardia (110 bpm), and is febrile (38.2°C).

Key Management Steps:

1. Resuscitation: IV access, crystalloid bolus, analgesia
2. Investigations:
   • Erect CXR → free air under diaphragm
   • Bloods: WCC 18, Lactate 3.2
3. Antibiotics: Piperacillin-tazobactam 4.5g IV
4. Surgical consultation: Emergency laparotomy
5. Operative management:
   • Midline laparotomy
   • Identify anterior D1 perforation
   • Graham patch repair (omental plug)
   • Peritoneal lavage
6. Post-operative: PPI, H. pylori testing, stop NSAIDs

Examiner Follow-up Questions:

• "What if you can't find the perforation?" → Systematic exploration, inject air via NG tube with saline in abdomen to identify bubbles
• "When would you do a definitive ulcer procedure?" → Rarely indicated now; only in massive bleeding or obstruction

Scenario 2: SBP in Decompensated Cirrhosis

Presentation: A 62-year-old woman with known alcoholic cirrhosis (Child-Pugh C) presents with confusion and low-grade fever. She has tense ascites. Abdominal examination reveals mild diffuse tenderness without rigidity.

Key Management Steps:

1. High suspicion for SBP: Altered mental status in cirrhotic
2. Diagnostic paracentesis:
   • PMN count: 850 cells/mm³ → Confirms SBP
   • Protein: 0.8 g/dL (low)
   • Culture: Sent (often negative)
3. Antibiotic therapy: Ceftriaxone 2g IV daily
4. Albumin:
   • Day 1: 1.5 g/kg IV
   • Day 3: 1.0 g/kg IV
5. Monitor: Renal function (hepatorenal syndrome risk)
6. Repeat paracentesis at 48 hours: Confirm > 25% reduction in PMN
7. Duration: 5-7 days antibiotics
8. Secondary prophylaxis: Norfloxacin 400mg PO daily long-term

Examiner Follow-up Questions:

• "What if PMN count doesn't improve at 48 hours?" → Consider secondary peritonitis, obtain CT
• "What is the long-term plan?" → SBP prophylaxis, transplant evaluation, nutritional support

Scenario 3: Post-Operative Anastomotic Leak

Presentation: A 68-year-old man is post-operative day 6 following anterior resection for sigmoid cancer. He develops fever (38.8°C), tachycardia, and increasing abdominal pain. His drain output has changed from serous to purulent.

Key Management Steps:

1. Recognize the presentation: Classic timing for anastomotic leak (POD 5-10)
2. Investigations:
   • Bloods: Rising WCC, CRP
   • CT with rectal contrast: Extraluminal contrast at anastomosis
3. Resuscitation: IV fluids, broad-spectrum antibiotics
4. Management options:
   • Stable, localized leak: Percutaneous drainage + antibiotics
   • Generalized peritonitis/unstable: Re-laparotomy
5. Surgical options:
   • Takedown anastomosis + end colostomy (Hartmann's)
   • Proximal diversion + drainage
   • Repair if clean and viable (rarely possible)
6. Post-operative: Prolonged antibiotics, nutritional support

Key Points:

• High index of suspicion in post-operative patients
• Change in drain output is an early warning sign
• CT is essential for diagnosis and planning
• Lower threshold for re-operation than for primary peritonitis

Quality Metrics and Documentation

Performance Indicators for Peritonitis Management

Documentation Checklist

For Emergency Presentations:

• Time of symptom onset
• Time of presentation
• Time of antibiotic administration
• Imaging findings (free air, source)
• Surgical consultation time
• Time of source control procedure
• Resuscitation volumes and response

For SBP:

• Indication for paracentesis
• Ascitic fluid results (PMN, protein, culture)
• Antibiotic and albumin administration
• 48-hour follow-up paracentesis planned
• Prophylaxis plan documented

References

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