Peritonitis

Definition

Peritonitis refers to inflammation of the peritoneum — the serous membrane lining the abdominal cavity and covering the abdominal viscera ^[1][2][3]. The word itself breaks down from Greek: "peri" = around, "tonaion" = stretched (referring to the membrane), "-itis" = inflammation. So literally: inflammation of the membrane stretched around the abdominal contents.

It is one of the commonest surgical emergencies ^[1][2] and can rapidly become life-threatening. When the peritoneum is inflamed, it becomes oedematous, hyperaemic, and covered with fibrinous exudates ^[1][2]. This triggers a cascade of sequestration of large amounts of protein-rich fluid into the peritoneal cavity (third-spacing), leading to septicaemia, endotoxaemia, hypovolaemia and shock ^[1][2]. Left unchecked, this progresses to multi-organ failure and death.

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Epidemiology and Risk Factors

Epidemiology

• Peritonitis is a leading cause of emergency surgical admissions worldwide.
• Spontaneous bacterial peritonitis (SBP) affects approximately 10–30% of hospitalized patients with cirrhotic ascites — highly relevant in Hong Kong given the prevalence of hepatitis B-related cirrhosis.
• CAPD-associated peritonitis is the leading cause of technique failure in peritoneal dialysis patients. Hong Kong has one of the highest rates of peritoneal dialysis utilization globally (>70% of dialysis patients are on PD), making this a particularly high-yield topic locally.
• Secondary peritonitis from perforated peptic ulcer (PPU), perforated appendicitis, and perforated diverticular disease constitutes the bulk of emergency surgical peritonitis cases.
• In the elderly, peritonitis is particularly dangerous because they are poor historians, may be confused or have dementia, history may be inaccurate (rely on care-provider), and peritoneal signs may be mild ^[1]. This demands a high index of suspicion in any elderly patient with abdominal pain, abdominal distension, fever, leucocytosis, acidosis, or sepsis of unexplained cause ^[1].

Risk Factors

The following are established risk factors for developing peritonitis ^[1][2]:

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Anatomy and Function of the Peritoneum

Understanding peritoneal anatomy is essential to understanding patterns of fluid collection, infection spread, and surgical approach.

Structure

The peritoneum is a continuous serous membrane consisting of:

• Parietal peritoneum: Lines the inner surface of the abdominal and pelvic walls. Innervated by somatic nerves (intercostal nerves T7–T12, subcostal, iliohypogastric, ilioinguinal) → produces sharp, well-localised pain when inflamed.
• Visceral peritoneum: Covers the abdominal viscera. Innervated by autonomic (visceral) nerves → produces dull, poorly-localised, midline pain when inflamed.

This dual innervation explains a classic clinical pattern: early visceral peritoneal irritation (e.g., early appendicitis) causes vague periumbilical pain, but once the parietal peritoneum is involved, pain becomes sharp and localised to the right iliac fossa.

Key Peritoneal Spaces

Knowing peritoneal spaces helps you predict where fluid/pus collects:

• Morison's pouch (hepatorenal recess): The most dependent part of the peritoneal cavity in a supine patient. This is where you look for free fluid on FAST ultrasound ^[3].
• Right and left subphrenic spaces: Subdiaphragmatic abscesses collect here (e.g., post-splenectomy, perforated peptic ulcer).
• Right and left paracolic gutters: The right paracolic gutter communicates directly with the pelvis and the right subphrenic space — this is why a perforated appendix can cause a right subphrenic abscess (pus tracks up the right paracolic gutter).
• Left infra-mesocolic and right infra-mesocolic spaces: Divided by the root of the small bowel mesentery.
• Pelvis (pouch of Douglas / rectovesical pouch): The most dependent part when the patient is upright. Digital rectal examination can detect pelvic peritonitis as tenderness or a boggy mass here.

Retroperitoneal Organs (NOT covered by peritoneum — important for differential)

These structures, when inflamed, do not cause classical peritoneal signs initially ^[3]:

• Kidneys, adrenals, ureters
• Aorta / IVC
• Duodenum (D2, D3), ascending and descending colon
• Pancreas (except the tail)

Function of the Peritoneum

1. Friction reduction: Mesothelial cells secrete a thin layer of serous fluid (~50–100 mL) that lubricates visceral surfaces.
2. Immune defence: Contains macrophages, lymphocytes, and mast cells; the omentum ("policeman of the abdomen") migrates to sites of inflammation to wall off infection.
3. Fluid and solute exchange: The large surface area (~1.7 m²) allows significant absorption — this is why peritoneal dialysis works, but also why toxins/bacteria are rapidly absorbed systemically.
4. Support and compartmentalization: Mesenteries and ligaments suspend organs and create compartments that can temporarily localise infection.

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Etiology

Classification-Based Approach to Etiology

Peritonitis is classified in different ways ^[1][2]:

• Localized vs. generalized (diffuse) — based on extent
• Bacterial vs. chemical — based on etiology
• Primary vs. secondary vs. tertiary — based on source

This last classification is the most clinically useful and exam-relevant:

1. Primary Peritonitis

Definition: Ascitic fluid infection without a surgically treatable intra-abdominal source of infection ^[1][2][3]

The infection reaches the peritoneum via haematogenous spread, lymphatic spread, or transmural migration (bacterial translocation) from the gut — there is NO perforation or breach in the GI tract.

Usually monomicrobial ^[1][2]

a) Spontaneous Bacterial Peritonitis (SBP)

• Who gets it: Patients with cirrhosis and ascites (especially decompensated liver disease) ^[2][3]
• Pathophysiology:
  • Portal hypertension → intestinal mucosal oedema → impaired mucosal barrier → bacterial translocation (bacteria cross from gut lumen into mesenteric lymph nodes and portal blood)
  • Cirrhosis → decreased hepatic reticuloendothelial function (Kupffer cells cannot clear bacteria) → bacteraemia
  • Low complement and low opsonic activity in ascitic fluid (ascitic fluid protein < 1 g/dL has poor opsonic capacity) → bacteria proliferate unchecked in ascites
• Organisms: Strep. pneumoniae, Group A Streptococcus, Enteric organisms (especially E. coli, Klebsiella pneumoniae) ^[1][2]
• Typically Gram-negative enteric organisms predominate, followed by Gram-positive cocci

b) Tuberculous Peritonitis

• Considered rare in developed countries but relevant in Hong Kong (intermediate TB burden) ^[1]
• Presentation may be non-specific: low-grade fever, weight loss ^[1]
• Insidious onset of abdominal pain; peritoneal signs not florid ^[1]
• Peritoneal fluid: AFB smear often negative; culture takes 4–6 weeks (could be falsely negative) ^[1]
• Diagnosis is often made by laparoscopy and biopsy of peritoneum — showing caseating granulomata ^[1]
• Pathophysiology: Haematogenous spread from pulmonary or extrapulmonary TB; can also result from direct spread from infected mesenteric lymph nodes or fallopian tubes
• The ascitic fluid typically has high protein ( > 2.5 g/dL), high lymphocyte count (lymphocyte-predominant), and elevated adenosine deaminase (ADA > 39 U/L)

c) CAPD-Associated Peritonitis

• Primary peritonitis presenting with fever, abdominal pain and turbid PD fluid ^[2]
• Organisms ^[1][2]:
  • Gram +ve: Staphylococcus sp. (particularly coagulase-negative Staphylococci — from skin flora around catheter exit site), S. aureus
  • Gram -ve: E. coli, Campylobacter, Pseudomonas aeruginosa
  • Mycobacterium tuberculosis
  • Fungal species
• Risk factors for CAPD peritonitis ^[2]:
  • Catheter-associated infection (exit-site and tunnel infections)
  • Lack of sanitary conditions / unhygienic home environment
  • Poor dexterity (e.g., diabetic retinopathy → poor hand-eye coordination during exchanges)
  • Underlying GI pathology
  • Recent invasive procedures (colonoscopy, cystoscopy)
  • Nasal carriage of S. aureus
  • Constipation (increased bacterial translocation)
  • Smoking

2. Secondary Peritonitis

Definition: Ascitic fluid infection with a surgically treatable intra-abdominal source of infection ^[1][2][3]

This accounts for most peritonitis cases ^[1]. The peritoneal cavity is contaminated by GI contents, bile, urine, or pancreatic juice through a breach in a hollow viscus or direct spread from an infected organ.

Could be localised (e.g., intra-abdominal abscess) or diffuse ^[1]

Could be preceded by chemical peritonitis (e.g., gastric juice, bile, pancreatic juice, urine & blood) — chemical irritation then becomes secondarily infected ^[1][2]

Causes (by mechanism)

Microbiology

Polymicrobial (mixed aerobic + anaerobic flora reflecting GI tract contents) ^[1][2]:

• Gram-negative: E. coli, Enterobacter, Proteus, Pseudomonas ^[1]
• Gram-positive: Streptococci, Enterococci ^[1]
• Anaerobes: Bacteroides ^[1]

The microbiological profile depends on the level of GI tract perforation:

• Stomach/duodenum: Low bacterial load (acid environment); chemical peritonitis predominates initially. Organisms: Streptococci, Lactobacilli, Candida
• Small bowel: Intermediate bacterial load. Organisms: Gram-negatives + some anaerobes
• Perforation of small bowel is specifically highlighted as having the polymicrobial profile listed above ^[1]
• Colon: Highest bacterial load (10¹¹ organisms/mL). Heavily polymicrobial including abundant anaerobes (Bacteroides fragilis)

3. Tertiary Peritonitis

Definition: Persistent peritonitis after adequate initial therapy ^[3] — i.e., peritonitis that persists or recurs > 48 hours after apparently adequate surgical source control and antibiotic therapy.

• Caused by opportunistic infections with normally non-pathogenic gut flora ^[2][3]:
  • Staphylococcus infection
  • Enterococcus infection
  • Candida infection
  • Other: coagulase-negative Staphylococci, Enterobacter, Pseudomonas
• Associated with prolonged use of antibiotics in persistent intra-abdominal infection ^[2] → selects for resistant/opportunistic organisms
• Typically occurs in ICU patients, immunocompromised hosts, or those with ongoing source of contamination
• Carries the worst prognosis of all three types (mortality 30–60%)

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Pathophysiology

Understanding the pathophysiology of peritonitis is crucial because it explains every clinical feature and guides treatment:

Sequence of Events

Detailed Pathophysiology

1. Initial insult: Bacteria, chemical irritants (gastric acid, bile, pancreatic enzymes), or both contact the peritoneal mesothelium.

2. Inflammatory response: Mesothelial cells release cytokines (IL-1, IL-6, TNF-α) and chemokines → recruitment of neutrophils and macrophages → peritoneal hyperaemia and oedema.

3. Fibrinous exudate formation: Increased vascular permeability leads to exudation of protein-rich fluid containing fibrinogen. Fibrinogen is converted to fibrin, creating fibrinous adhesions. These serve a dual purpose:

   • Beneficial: Wall off infection (localised peritonitis / abscess formation — the omentum contributes as the "abdominal policeman")
   • Detrimental: Can cause bowel obstruction (adhesions), trap bacteria in pockets inaccessible to antibiotics

4. Third-space fluid losses: The inflamed peritoneal surface (1.7 m²) leaks massive amounts of protein-rich fluid into the peritoneal cavity → intravascular volume depletion → hypovolaemia → tachycardia → hypotension → shock.

5. Paralytic ileus: Peritoneal inflammation → reflex inhibition of intestinal motility via:

   • Sympathetic overactivation (splanchnic nerves)
   • Local inflammatory mediators (prostaglandins, nitric oxide)
   • Direct irritation of bowel serosa → Bowel distension → further fluid sequestration within the bowel lumen (yet more third-spacing)

6. Systemic absorption: The peritoneum's vast surface area rapidly absorbs bacteria and endotoxins → bacteraemia / endotoxaemia → systemic inflammatory response syndrome (SIRS) → sepsis → septic shock → multi-organ dysfunction.

7. Metabolic consequences:

   • Massive protein loss (albumin leaks into peritoneal cavity) → hypoalbuminaemia
   • Metabolic acidosis (tissue hypoperfusion + lactate production)
   • Respiratory compromise (diaphragmatic splinting from pain + abdominal distension pushing diaphragm up → basal atelectasis)

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Classification

Summary Table of Classification Systems

Hinchey Classification (for Diverticulitis-Related Peritonitis)

This is specifically geared towards choosing the surgical approach for complicated diverticulitis ^[4]:

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Clinical Features

The clinical features of peritonitis are a direct reflection of the underlying pathophysiology. I'll separate them into symptoms (what the patient tells you) and signs (what you find on examination), with the pathophysiological basis explained inline.

Symptoms

Signs

General / Systemic Signs

Abdominal Signs

Special Considerations

Peritonitis in the elderly deserves special mention ^[1]:

• Poor historian — may be confused or have dementia
• History may be inaccurate → rely on care-provider
• Peritoneal signs may be mild — elderly patients have thinner abdominal musculature (less guarding), reduced inflammatory response, and may be on analgesics/steroids that mask signs
• Need a high index of suspicion: any elderly patient with abdominal pain, abdominal distension, fever, leucocytosis, acidosis, or sepsis of unexplained cause should be investigated for peritonitis ^[1]

Symptoms and Signs of the Primary Pathology

Peritonitis clinical features include symptoms and signs of the primary pathology ^[1]. This means you will also see features specific to whatever caused the peritonitis:

• PPU: Sudden-onset epigastric pain, preceding dyspepsia, NSAID/steroid use
• Appendicitis: Migratory RIF pain, anorexia, Rovsing's/psoas/obturator signs
• Diverticulitis: LIF pain (or RIF in Asian right-sided diverticular disease), altered bowel habit
• Cholecystitis: RUQ pain, Murphy's sign, jaundice
• Pancreatitis: Epigastric pain radiating to back, raised amylase/lipase
• SBP: History of liver disease, jaundice, ascites, encephalopathy
• CAPD peritonitis: Turbid PD fluid, catheter exit-site erythema/discharge

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Peritoneal Fluid Analysis

Peritoneal fluid analysis is critical for distinguishing the type and cause of peritonitis ^[1][2]:

↑ Amylase / bile-stained / faeculent peritoneal fluid indicates perforated GI tract ^[3]

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Summary: Connecting Pathophysiology to Clinical Features

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Active Recall - Peritonitis (Definition, Epidemiology, Anatomy, Etiology, Pathophysiology, Classification, Clinical Features)

1. What are the three classifications of peritonitis by source, and what distinguishes each?

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Primary = no surgically treatable intra-abdominal source (e.g. SBP, CAPD, TB); Secondary = surgically treatable source present (e.g. perforation, ischaemia, inflammation) - accounts for most cases; Tertiary = persistent peritonitis after adequate initial therapy - opportunistic organisms (Candida, Enterococcus, Staph).

2. Why does peritonitis cause hypovolaemia and shock? Explain the pathophysiological cascade.

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Inflamed peritoneum (surface area ~1.7 m2) becomes hyperaemic, oedematous, covered with fibrinous exudates. Massive protein-rich fluid sequestered into peritoneal cavity (third-spacing). Intravascular volume depleted. Also paralytic ileus causes further fluid sequestration in dilated bowel. Combined with sepsis-induced vasodilation leads to hypovolaemic + distributive shock.

3. What is the classic peritoneal triad on examination, and what is the pathophysiological basis of guarding?

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Tenderness + Guarding + Rebound (T+G+R). Guarding = involuntary contraction of abdominal wall muscles via spinal reflex arc: inflamed parietal peritoneum stimulates somatic afferents (intercostal nerves) to spinal cord, which sends efferent motor signals causing overlying muscle contraction as a protective reflex.

4. SBP is monomicrobial while secondary peritonitis is polymicrobial. Name the common organisms for each and explain why this distinction matters clinically.

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SBP: monomicrobial - E. coli, Klebsiella, Streptococcus pneumoniae, Group A Strep. Secondary: polymicrobial - Gram-neg (E. coli, Enterobacter, Proteus, Pseudomonas), Gram-pos (Streptococci, Enterococci), Anaerobes (Bacteroides). If multiple organisms cultured from ascitic fluid in a cirrhotic patient, suspect secondary peritonitis (bowel perforation) rather than SBP - changes management from antibiotics alone to surgery.

5. Why are elderly patients with peritonitis particularly dangerous? List the clinical pitfalls.

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Poor historians, may be confused or demented. History may be inaccurate, need to rely on care-providers. Peritoneal signs may be mild (thinner abdominal muscles, reduced inflammatory response, may be on steroids/analgesics). Need high index of suspicion: look for abdominal pain, distension, fever, leucocytosis, acidosis, unexplained sepsis. Delayed diagnosis leads to higher morbidity and mortality.

6. In peritoneal fluid analysis, what does bile-stained fluid, raised amylase, and raised creatinine each indicate?

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Bile-stained = biliary perforation or gallbladder injury. Raised amylase = perforated duodenum/small bowel or pancreatitis. Raised creatinine (higher than serum) = bladder perforation or urinary tract injury.

References

^[1] Lecture slides: GC 195. Lower and diffuse abdominal pain RLQ problems; pelvic inflammatory disease; peritonitis and abdominal emergencies.pdf (p34–43) ^[2] Senior notes: felixlai.md (Peritonitis section, p738–743; CAPD peritonitis section, p866) ^[3] Senior notes: maxim.md (Section 2.5 Peritonitis) ^[4] Senior notes: felixlai.md (Hinchey classification, diverticular disease section, p637)

Differential Diagnosis of Peritonitis

Why Is the Differential Diagnosis of Peritonitis Important?

Peritonitis is not a single disease — it is a clinical syndrome (inflammation of the peritoneum) that can be caused by dozens of different conditions. When a patient presents with peritoneal signs (tenderness, guarding, rebound) ^[1], your job is twofold:

1. Confirm peritonitis — could the peritoneal signs be mimicked by something else (e.g., abdominal wall pathology, retroperitoneal disease, medical causes)?
2. Identify the underlying cause — because management differs dramatically (e.g., SBP = antibiotics alone vs. perforated viscus = emergency surgery).

The DDx is best approached systematically by thinking about what can irritate the peritoneum from first principles: (a) things that perforate/leak into the peritoneal cavity, (b) organs that inflame and involve the adjacent peritoneum, (c) primary peritoneal disease, and (d) "mimics" — conditions that look like peritonitis but aren't.

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Framework for Differential Diagnosis

I'll organize this in two layers:

Layer 1 — Differentiating BETWEEN the causes of peritonitis (i.e., once you know the peritoneum is inflamed, what's the aetiology?)

Layer 2 — Differentiating peritonitis FROM its mimics (i.e., conditions that present similarly but the peritoneum is not the primary problem)

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Layer 1: Causes of Peritonitis — Differential by Type

This is essentially the aetiological differential: "What caused the peritonitis?"

A. Primary Peritonitis

B. Secondary Peritonitis — The Main Differentials

Accounts for most peritonitis ^[1]. The differential here is essentially: which organ has perforated, become ischaemic, or is severely inflamed?

By Mechanism: Perforation

By Mechanism: Severe Inflammation

By Mechanism: Ischaemia

By Mechanism: Other

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Layer 2: Conditions That Mimic Peritonitis ("Pseudo-peritonitis")

These are critical because they can present with abdominal pain and even some degree of abdominal tenderness/guarding, but the peritoneum itself is NOT the primary site of pathology. Operating on these patients is either unnecessary or harmful.

Retroperitoneal Conditions

Retroperitoneal organs are NOT covered by peritoneum ^[3], so inflammation of these structures does not directly cause classical peritoneal signs — but the pain may be severe and can be confusing:

Gynaecological Conditions (Critical DDx in Women of Reproductive Age)

These are extremely important — several of these present almost identically to appendicitis or pelvic peritonitis:

Medical Causes ("Non-Surgical Abdomen" Mimicking Peritonitis)

These are conditions where laparotomy is not indicated — operating on these patients causes harm:

Abdominal Wall Pathology

Extra-abdominal Conditions

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Systematic Approach — Decision Diagram

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Key Clinical Clues to Narrow the Differential

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Special Consideration: Differentiating Diverticulitis from CRC

This is specifically highlighted in the senior notes ^[2] and worth emphasising:

• Similar clinical features and bowel wall thickening on abdominal CT scan ^[2]
• Features suggestive of acute diverticulitis include: presence of pericolonic and mesenteric inflammation, involvement of > 10 cm of colon, and absence of enlarged pericolonic lymph nodes on CT ^[2]
• CRC can only be excluded with colonoscopy after resolution of acute inflammation ^[2] — you should NEVER do a colonoscopy during the acute episode (risk of perforation)
• In Asian populations, right-sided diverticulitis is significantly more common and is OFTEN confused with acute appendicitis ^[2]

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Special Consideration: DDx of RIF Pain (Appendicitis vs. Everything Else)

Since appendicitis progressing to peritonitis is so common, and RIF pain has a broad differential ^[2]:

GI: Acute appendicitis, right-sided diverticulitis (more common in Asians), Meckel's diverticulitis, acute ileitis (Yersinia, Campylobacter, Salmonella), Crohn's disease, caecal carcinoma, mesenteric adenitis

O&G: Ruptured ectopic pregnancy, PID, tubo-ovarian abscess, ruptured ovarian cyst, ovarian/fallopian tube torsion, endometriosis ^[2]

Urological: Ureteric colic, UTI/pyelonephritis

Other: Strangulated inguinal/femoral hernia, psoas abscess

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Active Recall - Differential Diagnosis of Peritonitis

1. A cirrhotic patient with ascites develops fever and abdominal pain. Ascitic fluid culture grows 3 different organisms. Is this SBP or secondary peritonitis, and why does the distinction matter?

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This is secondary peritonitis, not SBP. SBP is monomicrobial; polymicrobial culture suggests a breach in the GI tract (e.g. perforation). The distinction matters because SBP is treated with antibiotics alone (3rd-gen cephalosporin), whereas secondary peritonitis requires surgical intervention. Runyon's criteria can further support secondary peritonitis: protein > 1 g/dL, glucose < 50 mg/dL, LDH > ULN for serum.

2. Name 3 medical (non-surgical) conditions that can mimic peritonitis and explain why DKA is the classic trap.

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DKA, acute inferior MI, Addisonian crisis (also: porphyria, herpes zoster, hypercalcaemia, sickle cell crisis, FMF). DKA mimics peritonitis because severe metabolic derangement causes gastric dilatation, mesenteric ischaemia from dehydration, and metabolic irritation of the peritoneum, producing genuine abdominal tenderness and even board-like rigidity. Performing a laparotomy on a DKA patient is harmful; checking glucose and ABG reveals the diagnosis.

3. A 28-year-old woman presents with acute RIF pain, fever, and localised peritonitis. List 4 important differential diagnoses and state the single most important bedside test you must not forget.

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DDx: Acute appendicitis, ruptured ectopic pregnancy, PID/tubo-ovarian abscess, ruptured ovarian cyst, right-sided diverticulitis (more common in Asians), ovarian torsion, ureteric colic. The single most important test is a urine pregnancy test (beta-hCG) to exclude ruptured ectopic pregnancy, which is life-threatening.

4. How do you differentiate TB peritonitis from SBP based on clinical presentation and peritoneal fluid analysis?

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TB peritonitis: insidious onset, low-grade fever, weight loss, peritoneal signs not florid. Ascitic fluid is LYMPHOCYTE-predominant (vs. neutrophil-predominant in SBP), high protein > 2.5 g/dL, elevated ADA > 39 U/L. AFB smear often negative, culture takes 4-6 weeks and may be falsely negative. Diagnosis often requires laparoscopy and peritoneal biopsy showing caseating granulomata. SBP: acute onset, neutrophil-predominant ascites (PMN >= 250), usually in context of decompensated cirrhosis.

5. What peritoneal fluid findings indicate a perforated GI tract rather than primary peritonitis?

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Bile-stained fluid (biliary perforation), faeculent fluid (colonic perforation), raised amylase (duodenal/small bowel perforation or pancreatitis), raised creatinine above serum level (bladder perforation). Also: polymicrobial culture, and Runyon's criteria positive (protein > 1 g/dL, glucose < 50 mg/dL, LDH > ULN).

References

^[1] Lecture slides: GC 195. Lower and diffuse abdominal pain RLQ problems; pelvic inflammatory disease; peritonitis and abdominal emergencies.pdf (p34–43) ^[2] Senior notes: felixlai.md (Peritonitis section p738–743; Acute appendicitis DDx p728–729; Diverticulitis DDx p641; CAPD peritonitis p866; SBP p449–450) ^[3] Senior notes: maxim.md (Section 2.5 Peritonitis; Acute abdomen DDx p44–46; Appendicitis p179; Diverticulitis p194) ^[4] Senior notes: maxim.md (Acute abdomen DDx — medical causes: DKA, hypercalcaemia, herpes zoster, porphyria, p44) ^[5] Senior notes: felixlai.md (Ruptured AAA DDx p910–911) ^[6] Senior notes: felixlai.md (Hinchey classification p637)

Diagnostic Criteria

The diagnosis of peritonitis is fundamentally clinical — you see a sick patient with peritoneal signs and you act. However, to classify the type of peritonitis (primary vs. secondary) and guide the correct treatment pathway (antibiotics alone vs. surgery), you need specific diagnostic criteria for each subtype. Let me walk through each one and explain the logic behind every threshold.

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1. Spontaneous Bacterial Peritonitis (SBP)

Diagnosis requires ALL of the following ^[2]:

Important Variants of SBP [2]

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2. CAPD-Associated Peritonitis

Diagnosis requires at least 2 of 3 criteria ^[2]:

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3. Secondary Bacterial Peritonitis (Distinguishing from SBP in a Cirrhotic Patient)

This uses Runyon's criteria — at least 2 of 3 in the ascitic fluid ^[2]:

Additional clues for secondary peritonitis (not part of Runyon's criteria but highly useful):

• Polymicrobial culture (vs. monomicrobial in SBP) ^[1][2]
• Amylase level ↑ — suggests pancreatitis or gut perforation (every segment of gut except gallbladder leaks amylase into fluid when it perforates ^[2])
• Bilirubin level ↑ — suggests perforation of gallbladder into peritoneum (measured if fluid is dark orange or brown ^[2])

Summary Comparison Table: SBP vs. Secondary Peritonitis Ascitic Fluid

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Investigation Modalities

Investigations for peritonitis serve three purposes: (1) confirm peritonitis, (2) identify the cause, and (3) assess severity/guide resuscitation. I'll organise these by modality.

A. Bedside Tests

B. Blood Tests

Blood tests: CBC, LRFT, amylase, ABG, clotting, T&S ^[3]

C. Peritoneal Fluid Analysis

This is the cornerstone investigation for primary peritonitis (SBP and CAPD). For secondary peritonitis, peritoneal fluid is often obtained intra-operatively rather than pre-operatively.

Ascitic fluid analysis by paracentesis ^[2]

Peritoneal fluid analysis ^[1]:

D. Imaging

Imaging: ECG, Erect CXR, erect/supine AXR, USG, CT A+P ^[3]

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Diagnostic Algorithm

The clinical approach follows a logical sequence: resuscitate → clinical assessment → bedside tests → blood tests → imaging → peritoneal fluid analysis → decide: operate or treat medically.

Step-by-Step Walkthrough

Step 1 — Resuscitate and Assess Simultaneously

You never wait for investigation results before starting resuscitation. A patient with peritonitis is losing fluid into the peritoneal cavity (third-spacing) and may be septic. IV fluid replacement, nasogastric tube, urinary catheter, oxygen ^[1] should be started immediately while you take the history, examine, and order tests.

Step 2 — Bedside Tests

• Urinalysis — excludes UTI, detects haematuria (ureteric colic), sterile pyuria (peri-ureteric inflammation) ^[1]
• Pregnancy test — mandatory in reproductive-age women ^[1]
• ECG — excludes inferior MI ^[3]
• Blood glucose — excludes DKA

Step 3 — Blood Tests

Blood count, renal and liver function, amylase, clotting profile, arterial blood gas, type and screen ^[1][3]. Blood cultures before antibiotics. The ABG with lactate is critical — a raised lactate > 2 mmol/L suggests tissue hypoperfusion or bowel ischaemia.

Step 4 — Initial Imaging (Erect CXR + AXR)

Erect CXR is the first imaging — looking for free gas. If present, you have a perforated viscus and may proceed directly to surgery. Erect and supine AXR — look for dilated bowels (obstruction), air-fluid levels, calculi.

Step 5 — Decision Point: Free Gas?

If free gas + florid peritoneal signs → proceed to exploratory laparotomy ^[3]. Do NOT delay with further imaging in an unstable patient.

If no free gas but peritoneal signs present → further investigation needed to identify the source.

Step 6 — Further Imaging / Fluid Analysis

• Cirrhotic with ascites: Diagnostic paracentesis → ascitic fluid analysis (cell count, culture, protein, glucose, LDH, albumin for SAAG, ± amylase/bilirubin/ADA/cytology) ^[2]
• PD patient: Collect PD effluent for cell count + culture ^[2]
• All others: USG abdomen for RUQ/pelvic pathology; CT abdomen + pelvis with contrast for most other scenarios ^[1][2][3]
• If diagnosis remains elusive: diagnostic laparoscopy ^[1]

Step 7 — Classify and Treat

Based on the above, classify as primary (SBP/CAPD/TB) vs. secondary (surgical source) vs. tertiary (persistent/opportunistic) and institute appropriate management.

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Investigation Selection by Site of Pain

This is a practical guide from the clinical approach ^[3]:

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Special Investigation Scenarios

TB Peritonitis

Peritoneal fluid: AFB smear often negative, culture would take 4–6 weeks (could be falsely negative) ^[1]. This makes diagnosis challenging. Key investigations:

• Ascitic fluid: Lymphocyte-predominant, high protein ( > 2.5 g/dL), ↑ ADA level ^[2], low SAAG ( < 1.1 g/dL)
• Diagnosis often made by laparoscopy and biopsy of peritoneum ^[1] — looking for caseating granulomata and "millet seed" tubercles studding the peritoneal surface
• Interferon-gamma release assay (IGRA) / Mantoux can support but not confirm peritoneal TB
• PCR for M. tuberculosis DNA in ascitic fluid — increasing role

Diverticulitis-Related Peritonitis

CT scan helps to confirm diagnosis and assess the severity ^[1]. CT findings include:

• Colonic diverticula, localised bowel wall thickening ( > 4 mm), pericolonic fat stranding
• Abscess (fluid collection with air/debris), free gas (perforation), fistula tracks
• Hinchey classification applied based on CT findings to guide management ^[6]

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Active Recall - Diagnosis and Investigations of Peritonitis

1. State the diagnostic criteria for SBP and explain why the PMN threshold is 250/mm3 rather than 500/mm3.

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SBP requires ALL of: (1) Ascitic fluid PMN >= 250 cells/mm3, (2) Positive peritoneal fluid culture, (3) Secondary causes excluded. The threshold is lower at 250 (not 500) because cirrhotic patients are immunosuppressed and mount a weaker inflammatory response; waiting for 500 would miss early SBP and delay life-saving antibiotics. The 250 cut-off has ~93% sensitivity.

2. Why is the WBC threshold for CAPD peritonitis (100/mm3) lower than for SBP (250/mm3)?

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PD fluid contains dextrose which provides an excellent growth medium for bacteria, leading to rapid bacterial proliferation. Even a lower WBC count indicates significant infection in this environment. Without antibiotic therapy, bacteria multiply quickly in the dextrose-rich PD fluid, so a lower threshold ensures early detection.

3. A cirrhotic patient with ascites develops peritonitis. Ascitic fluid shows: protein 1.5 g/dL, glucose 30 mg/dL, LDH above ULN, polymicrobial culture. Is this SBP or secondary peritonitis? Justify using Runyon's criteria.

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This is secondary peritonitis. Runyon's criteria met (all 3 of 3, need >= 2): protein > 1 g/dL (1.5), glucose < 50 mg/dL (30), LDH > ULN. Additionally polymicrobial culture confirms secondary peritonitis. This patient needs CT to identify source and likely surgical intervention, not just antibiotics.

4. What does a SAAG > 1.1 g/dL indicate and how is it calculated? What does SAAG < 1.1 indicate?

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SAAG = Serum albumin minus ascitic fluid albumin (difference, NOT ratio). SAAG > 1.1 g/dL indicates portal hypertension (cirrhosis, heart failure, Budd-Chiari) and thus SBP is a likely cause of peritonitis. SAAG < 1.1 indicates no portal hypertension - think TB peritonitis, malignancy, nephrotic syndrome, pancreatic ascites.

5. When should you proceed directly to exploratory laparotomy without further imaging in suspected peritonitis?

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When there is free gas under the diaphragm on erect CXR AND/OR florid peritoneal signs (diffuse tenderness, guarding, rigidity, rebound) with haemodynamic instability. Do not delay with CT or other imaging in an unstable patient with clear signs of perforated viscus and generalised peritonitis.

6. List 3 ascitic fluid findings that specifically point to a perforated GI tract rather than SBP.

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(1) Raised amylase - every segment of gut except gallbladder leaks amylase when perforated; also pancreatitis. (2) Bile-stained fluid - suggests gallbladder/biliary perforation. (3) Faeculent fluid - perforated bowel (colonic). Also: raised bilirubin (dark orange/brown fluid = GB perforation), polymicrobial culture, Runyon's criteria positive (high protein, low glucose, high LDH).

References

^[1] Lecture slides: GC 195. Lower and diffuse abdominal pain RLQ problems; pelvic inflammatory disease; peritonitis and abdominal emergencies.pdf (p12, p19, p34–43) ^[2] Senior notes: felixlai.md (Peritonitis diagnosis section p740–742; Ascitic fluid analysis p740–741, p448–449; SBP diagnosis and variants p449–450; CAPD peritonitis diagnostic criteria p866–867; Case study p743) ^[3] Senior notes: maxim.md (Section 2.5 Peritonitis p46; Acute abdomen investigations p45; Imaging by site of pain p45) ^[6] Senior notes: felixlai.md (Hinchey classification p637)

Management Overview

The management of peritonitis is fundamentally dictated by one question: is there a surgically treatable source? If yes (secondary peritonitis), surgery is the definitive treatment. If no (primary peritonitis), the treatment is medical. Everything else — resuscitation, antibiotics, supportive care — is built around this central decision.

Think of it as three simultaneous streams happening in parallel:

1. Resuscitate the patient (they are losing fluid and becoming septic)
2. Treat the infection (antibiotics)
3. Eliminate the source (surgery if secondary; antibiotics alone if primary)

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Management Algorithm

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Immediate Resuscitation (All Types of Peritonitis)

Before you even know the cause, start resuscitation. The patient is dying from two things simultaneously: hypovolaemia (third-space losses) and sepsis (bacterial/endotoxin absorption). Both must be addressed urgently.

Supportive Measures

These are directly from the lecture slides for acute secondary bacterial peritonitis — treatment ^[1]:

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Treatment by Type of Peritonitis

1. Primary Peritonitis — Medical Management

Primary peritonitis has no surgical source — there is nothing to cut out. Treatment is antibiotics ± addressing the underlying predisposition.

A. Spontaneous Bacterial Peritonitis (SBP)

Indications for antibiotic therapy (any of the following) ^[2]:

• Fever > 37.8°C
• Abdominal pain or tenderness
• Altered mental status
• Ascitic fluid PMN count ≥ 250 cells/mm³

Empirical Antibiotic Choice:

3rd generation cephalosporin should be used ^[2]:

• Cefotaxime 2 g IV Q8h OR
• Ceftriaxone 2 g IV daily

Why 3rd-gen cephalosporins? "Ceph" = cephalosporin (β-lactam antibiotic that inhibits cell wall synthesis). The "3rd generation" designation means it has expanded Gram-negative coverage (especially E. coli, Klebsiella) while retaining some Gram-positive activity. These are the predominant organisms in SBP. They also have good peritoneal penetration.

Duration: 5 days — treatment can be stopped when PMN < 250 cells/mm³ ^[2]. A repeat paracentesis at 48 hours is recommended to confirm response (expect ≥ 25% decrease in PMN count).

Adjunctive therapy — IV Albumin:

• IV albumin (1.5 g/kg on day 1, then 1 g/kg on day 3) is given alongside antibiotics in SBP patients with renal impairment (creatinine > 88 μmol/L or BUN > 10.7 mmol/L) or bilirubin > 68 μmol/L to prevent hepatorenal syndrome.
• Why? Albumin expands intravascular volume and prevents the renal vasoconstriction that occurs during SBP due to splanchnic arterial vasodilation and cytokine-mediated renal injury. Reduces mortality from ~30% to ~10%.

Prevention of Recurrence (Secondary Prophylaxis):

Fluoroquinolones for lifelong selective intestinal decontamination (unless patient receives liver transplant with normalisation of liver function) ^[2]:

• Norfloxacin 400 mg PO daily OR
• Levofloxacin 250 mg PO daily

Why fluoroquinolones work for prophylaxis ^[2]:

• Incomplete absorption by gut leading to high concentration in the intestinal lumen
• High activity against Gram-negative bacilli (the organisms causing SBP)
• Low bacterial resistance
• Fewer side effects

The mechanism is "selective intestinal decontamination" — the fluoroquinolone stays in the gut lumen at high concentrations, killing the Gram-negative bacteria that would otherwise translocate across the gut wall to cause SBP, while preserving anaerobic flora (which actually prevents colonisation by pathogenic organisms).

Primary Prophylaxis (preventing first episode of SBP):

• Indicated in cirrhotic patients with ascitic fluid protein < 1.5 g/dL (low opsonic activity → high risk)
• Same agents: Norfloxacin or Levofloxacin
• Also indicated short-term (7 days) in any cirrhotic patient with acute GI bleeding (high risk of SBP during variceal bleed)

B. CAPD-Associated Peritonitis

As early as possible if the diagnosis of peritonitis is certain clinically — do not wait for laboratory confirmation or culture result since delayed treatment carries a worse outcome ^[2].

Empirical Antibiotic Regimen (Intraperitoneal — IP):

1st generation cephalosporin + aminoglycoside ^[2]:

• Gram-positive cover: 1st generation cephalosporin (cefazolin) — covers Staphylococcal species (the most common cause from skin flora around the catheter)
• Gram-negative cover: Aminoglycoside (e.g., gentamicin) OR 3rd or 4th generation cephalosporin (ceftazidime / cefepime)

General rules ^[2]:

• Use less broad-spectrum drugs — start narrow and escalate if needed
• Avoid vancomycin as initial treatment — to minimise emergence of resistant strains (VRE — vancomycin-resistant enterococci). Reserve vancomycin for MRSA or when 1st-gen cephalosporin fails.

Why IP (intraperitoneal) route? Because the infection is IN the peritoneal cavity. IP antibiotics achieve much higher local concentrations than IV antibiotics. The drug is dissolved in the PD fluid and instilled directly into the peritoneum during a regular exchange.

Modification ^[2]:

• Replacing aminoglycoside with 3rd generation cephalosporin is advocated to preserve residual renal function and avoid ototoxicity — aminoglycosides are nephrotoxic and ototoxic; PD patients often have some residual renal function that is important to preserve.

Continuation of PD:

• Continuous peritoneal dialysis should be continued unless peritonitis is refractory to treatment ^[2]. Stopping PD would mean the patient loses their dialysis modality and needs temporary haemodialysis.

Adjust According to Culture:

• Adjust antibiotic therapy according to culture result and sensitivity ^[2] once results are available (usually 48–72 hours).

Success Rate:

• Success rate > 90% ^[2]
• Lower success rate for Gram-negative organisms ^[2]
• Much lower success rate for fungal peritonitis ^[2]

Indications for Tenckhoff Catheter Removal ^[2]:

Post-removal plan ^[2]:

• Tenckhoff catheter should be removed and reinserted for peritoneal dialysis few weeks later after total subsidence of peritonitis signs and symptoms
• Patient maintained on haemodialysis in the interim

C. Tuberculous Peritonitis

• Standard anti-TB therapy: RIPE regimen (Rifampicin, Isoniazid, Pyrazinamide, Ethambutol) for 2 months intensive phase, followed by Rifampicin + Isoniazid for 4–7 months continuation phase (total 6–9 months)
• Consider adding pyridoxine (vitamin B6) to prevent isoniazid-induced peripheral neuropathy
• Surgery is NOT indicated unless complications arise (e.g., bowel obstruction from TB strictures, perforation)
• Response to treatment is monitored clinically (resolution of symptoms, weight gain) and by serial ascitic fluid analysis

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2. Secondary Peritonitis — Surgical Management

Accounts for most peritonitis ^[1]. The fundamental principle is source control — you must eliminate the source of contamination. Antibiotics alone are insufficient because bacteria will continue to pour into the peritoneal cavity from the uncontrolled source.

Surgical correction of underlying pathology — laparotomy if surgically treatable source of infection is documented ^[2]

Indications for Emergency / Urgent Surgery

From the lecture slides on indications for urgent surgery ^[7]:

• Incarcerated, strangulated hernia
• Suspected or proven strangulation
• Peritonitis
• Pneumoperitoneum
• Pneumatosis cystoides intestinalis (gas within bowel wall — indicates transmural ischaemia/necrosis)
• Close-loop obstruction
• Volvulus with peritoneal signs

The overarching rule: proceed to exploratory laparotomy if free gas / florid peritoneal signs ^[3]

Surgical Approach

The management has two components, performed simultaneously or sequentially:

Component 1: Source Control (stop the contamination)

Component 2: Peritoneal Toilet (clean up the contamination)

• Thorough peritoneal lavage with warm normal saline (litres)
• Removal of fibrinous debris, pus, faecal matter
• Ensure all quadrants and paracolic gutters are irrigated
• Drains may be placed in dependent areas (pelvis, subphrenic spaces) if ongoing contamination is expected

Operative Approaches

Laparoscopic surgery / Laparotomy ^[1]:

Non-Operative Source Control

Drainage — percutaneous drainage of abdominal abscess ^[1]:

For localised secondary peritonitis (contained abscess), percutaneous drainage under imaging guidance (CT or USG) can achieve source control without major surgery:

• Indications: Well-defined, unilocular abscess accessible to percutaneous route; patient stable
• Technique: CT-guided or USG-guided catheter placement into the abscess cavity; leave drain in situ until output minimal and clinical improvement
• When it fails: If the abscess does not resolve, or the patient deteriorates, proceed to surgery

This is particularly relevant in diverticular disease ^[3][6]:

Hartmann's procedure: Resection of the affected sigmoid colon with creation of an end-colostomy (the proximal end is brought out as a stoma) and closure of the distal rectal stump. Why? In the presence of gross faecal contamination, performing a primary anastomosis (joining the two bowel ends together) carries a very high risk of anastomotic leak because the tissues are inflamed, oedematous, and contaminated. The stoma is reversed electively months later once the patient has recovered.

Antibiotic Therapy for Secondary Peritonitis

Broad-spectrum antibiotics ^[1] — must cover Gram-negatives, Gram-positives, AND anaerobes (reflecting the polymicrobial nature of secondary peritonitis):

Timing of surgical prophylaxis ^[8]:

• At the induction of GA — to achieve high tissue concentration of antibiotics upon skin incision
• Additional dose if OT > 2× half-life (usually 3 hours for Augmentin/cefuroxime)
• Additional dose if blood loss > 1.5 L

Duration:

• Uncomplicated source (e.g., non-perforated appendicitis): Continue until 24h post-op ^[3]
• Complicated source (e.g., perforated appendicitis with abscess, generalised peritonitis): Continue 3–7 days post-op ^[3], guided by clinical response (resolution of fever, normalising WCC, improving clinically)

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3. Tertiary Peritonitis

Tertiary peritonitis = persistent peritonitis after adequate initial therapy ^[3]. This is the most difficult to manage:

• Re-evaluate source control: Is there an ongoing source that was missed? Undrained abscess? Anastomotic leak? CT abdomen + pelvis to look for residual collections.
• Adjust antibiotics: Culture-guided — these patients often harbour resistant or opportunistic organisms (Staphylococcus, Enterococcus, Candida ^[2]):
  • MRSA → Vancomycin or Linezolid
  • VRE → Linezolid or Daptomycin
  • Candida → Echinocandin (Caspofungin/Anidulafungin) or Fluconazole
  • Pseudomonas → Piperacillin-tazobactam, Ceftazidime, or Carbapenem + Aminoglycoside
• Re-laparotomy / planned re-look laparotomy: May need repeat washouts every 24–48 hours
• Open abdomen management (laparostomy): In severe cases, the abdomen is left open with a temporary abdominal closure (vacuum-assisted closure / negative-pressure wound therapy) to allow ongoing drainage and repeated washouts
• ICU care: These patients are invariably in the ICU with multi-organ support

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4. Specific Scenarios

Emergency Surgery for Diverticulitis-Related Peritonitis [6]

Indications for emergency surgery in diverticulitis ^[6]:

• Frank (free) perforation
• Failure of medical treatment with IV antibiotics
• Colonic obstruction
• Abscess failing non-operative intervention

Elective surgery (sigmoid colectomy with primary anastomosis — "interval colectomy") ^[6]:

• Previous complicated diverticulitis
• Immunocompromised patients
• Inability to exclude malignancy
• Recurrent episodes of uncomplicated diverticulitis — Previously thought that risk of complications increases with recurrent disease but is now proven to be wrong ^[6]. Current guidelines no longer recommend elective surgery based on number of episodes alone.

Appendicitis with Peritonitis

Immediate surgery (present within 72h and fit for surgery) ^[3]:

• Laparoscopic appendicectomy is preferred — lower infection risk, less post-operative pain, shorter hospital stay
• Open surgery if gross sepsis or generalised peritonitis with haemodynamic instability
• Antibiotics: IV ceftriaxone + metronidazole (anaerobic coverage) ^[3]
  • Non-complicated: continue until 24h post-op
  • Complicated (abscess, phlegmon): continue 3–7 days post-op

Interval surgery (present > 72h and stable — walled-off appendix) ^[3]:

• IV antibiotics (~90% success rate) ± image-guided drainage of abscess
• Laparoscopic appendicectomy 6–8 weeks later
• Colonoscopy if > 40 years old to exclude caecal carcinoma ^[3]

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Summary: Decision Framework

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Active Recall - Management of Peritonitis

1. What is the empirical antibiotic regimen for SBP, what is the duration, and what is the criterion for stopping treatment?

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3rd-generation cephalosporin (Cefotaxime 2g IV Q8h or Ceftriaxone 2g IV daily). Duration: 5 days. Stop when ascitic fluid PMN < 250 cells/mm3. Also give IV albumin (1.5 g/kg day 1, 1 g/kg day 3) if renal impairment or bilirubin > 68 umol/L to prevent hepatorenal syndrome.

2. In CAPD peritonitis, what is the empirical antibiotic regimen, why is vancomycin avoided initially, and what are the 3 indications for Tenckhoff catheter removal?

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Empirical: IP 1st-generation cephalosporin (cefazolin) + aminoglycoside (or 3rd-gen cephalosporin like ceftazidime to preserve residual renal function and avoid ototoxicity). Vancomycin avoided to minimise emergence of vancomycin-resistant strains (VRE). Catheter removal indications: (1) Refractory peritonitis with failure of effluent to clear after 5 days of antibiotics, (2) Peritonitis due to hydrophilic Gram-negative rods (e.g. Pseudomonas) - forms biofilms, (3) Fungal peritonitis (e.g. Candida) - antimicrobials insufficient with catheter in situ.

3. What are the 6 immediate resuscitative measures for a patient presenting with peritonitis, as listed in the lecture slides?

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(1) IV fluid replacement (correct hypovolaemia from third-space losses), (2) Nasogastric tube (decompress stomach, prevent aspiration - paralytic ileus), (3) Urinary catheter (monitor urine output for fluid resuscitation), (4) Oxygen (prevent hypoxia from diaphragmatic splinting and sepsis), (5) Pain relief (IV opioids), (6) Broad-spectrum antibiotics (start empirically, do not wait for cultures). Plus close monitoring for change of condition.

4. Explain why Hartmann's procedure is preferred over primary anastomosis in Hinchey III/IV diverticular peritonitis.

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In Hinchey III (generalised purulent peritonitis) and IV (faecal peritonitis), the peritoneal cavity is grossly contaminated. Performing a primary anastomosis (joining bowel ends together) in this environment carries a very high risk of anastomotic leak because tissues are inflamed, oedematous, and contaminated. Hartmann's procedure resects the affected segment, creates an end-colostomy (proximal stoma), and closes the distal rectal stump. The stoma can be reversed electively months later when the patient has recovered and inflammation has settled.

5. What is secondary prophylaxis for SBP, which agents are used, and what is the mechanism by which they prevent recurrence?

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Lifelong fluoroquinolone prophylaxis (Norfloxacin 400mg PO daily or Levofloxacin 250mg PO daily) unless patient receives liver transplant with normalisation of liver function. Mechanism: selective intestinal decontamination - fluoroquinolones are incompletely absorbed by the gut, achieving high intraluminal concentrations. They have high activity against Gram-negative bacilli (the organisms that translocate to cause SBP) while preserving anaerobic flora, low bacterial resistance, and fewer side effects.

6. List 4 indications for emergency surgery in diverticulitis-related peritonitis and state one indication that is NO LONGER considered valid for elective sigmoid colectomy.

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Emergency: (1) Frank free perforation, (2) Failure of medical treatment with IV antibiotics, (3) Colonic obstruction, (4) Abscess failing non-operative intervention. No longer valid: recurrent episodes of uncomplicated diverticulitis - previously thought risk of complications increases with recurrent disease but now proven wrong. Current guidelines do not recommend elective surgery based on number of episodes alone.

References

^[1] Lecture slides: GC 195. Lower and diffuse abdominal pain RLQ problems; pelvic inflammatory disease; peritonitis and abdominal emergencies.pdf (p34, p39, p41, p42) ^[2] Senior notes: felixlai.md (Peritonitis treatment p741–743; SBP treatment and prophylaxis p449–450; CAPD peritonitis treatment p866–867; Case study p743) ^[3] Senior notes: maxim.md (Section 2.5 Peritonitis p46; Appendicitis management p181; Diverticulitis Hinchey classification and management p95, p194) ^[6] Senior notes: felixlai.md (Diverticulitis treatment p645–647; Emergency surgery indications p645; Hinchey staging p637) ^[7] Lecture slides: GC 194. Intestinal obstruction colorectal cancer.pdf (p25 — Indications for urgent surgery) ^[8] Senior notes: maxim.md (Surgical antibiotic prophylaxis p49)

Complications of Peritonitis

Peritonitis is dangerous not only because of the acute episode itself, but because it triggers a cascade of local and systemic complications that can kill the patient even after the source is controlled. Think of complications in two categories: systemic (the whole body is affected) and local (problems within the peritoneal cavity). I'll also cover complications specific to each subtype (SBP, CAPD, secondary) and post-operative complications.

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A. Systemic Complications

These arise because the inflamed peritoneum (1.7 m² surface area) acts as a massive absorption surface for bacteria and endotoxins, while simultaneously sequestering litres of protein-rich fluid. The result is the simultaneous insults of hypovolaemia and sepsis.

1. Sepsis and Septic Shock

• Pathophysiology: Bacteria and endotoxins (lipopolysaccharide from Gram-negative cell walls) are absorbed across the inflamed peritoneum into the systemic circulation → activate the innate immune system → massive release of pro-inflammatory cytokines (TNF-α, IL-1, IL-6) → SIRS → if uncontrolled, progresses to sepsis → septic shock (persistent hypotension despite adequate fluid resuscitation, requiring vasopressors)
• Septicaemia, endotoxaemia leading to hypovolaemia & shock ^[1]
• Septic shock involves distributive shock (nitric oxide-mediated vasodilation → decreased SVR) superimposed on hypovolaemic shock (third-space losses)
• Mortality of septic shock from intra-abdominal source: 30–50%

2. Multi-Organ Failure (MOF)

When the sepsis cascade is not controlled, individual organ systems begin to fail sequentially. This is the terminal pathway of untreated peritonitis:

3. Hypovolaemic Shock

• Sequestration of large amounts of protein-rich fluid into the peritoneal cavity ^[1]
• Paralytic ileus compounds this by causing further fluid sequestration within distended bowel loops
• If not aggressively resuscitated with IV fluids, the patient develops profound intravascular depletion → end-organ hypoperfusion → metabolic acidosis → cardiac arrest
• Associated electrolyte derangements: hypokalaemia (vomiting, NGT losses), metabolic acidosis (tissue hypoperfusion, lactate accumulation), hypoalbuminaemia (protein leak into peritoneal cavity)

4. Electrolyte and Metabolic Derangements

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B. Local (Intra-Abdominal) Complications

1. Intra-Abdominal Abscess

• The most common local complication of peritonitis
• Pathophysiology: The body's attempt to wall off infection is both protective and problematic. The omentum ("policeman of the abdomen") and fibrinous adhesions seal off pockets of infection, creating localised collections of pus. While this prevents generalised spread, the abscess itself becomes a persistent source of sepsis inaccessible to systemic antibiotics (poor penetration into the abscess cavity).
• Common sites: Subphrenic spaces (right and left), Morison's pouch, paracolic gutters, pelvis (pouch of Douglas), interloop collections
• Clinical features: Persistent fever (swinging/spiking pattern) despite appropriate antibiotics, persistent abdominal pain, leucocytosis, failure to improve. Should be suspected in patients with no improvement in abdominal pain or a persistent fever despite 3 days of antibiotic treatment ^[6]
• In appendicitis: Walled off → form appendiceal abscess → obstruction ^[3]. Not walled off → generalised peritonitis ^[3]
• Diagnosis: CT abdomen with contrast — rim-enhancing fluid collection ± air/debris
• Management: Percutaneous drainage of abdominal abscess ^[1] (CT-guided or USG-guided) + continued IV antibiotics. Surgical drainage if percutaneous approach fails or is not technically feasible.
• A special variant: pyogenic liver abscess — may develop due to spread of infection through the portal circulation ^[6] (e.g., from diverticulitis or appendicitis via pylephlebitis)

2. Paralytic Ileus

• Already present during peritonitis (reflex sympathetic inhibition + local mediators), but may persist after source control
• Prolonged ileus → continued third-space losses, inability to feed, risk of aspiration
• Differentiating prolonged ileus from early adhesive mechanical obstruction post-operatively can be challenging (CT with oral contrast helps)

3. Adhesion Formation

• Fibrinous exudates deposited during peritonitis organise into fibrous adhesions between bowel loops, omentum, and parietal peritoneum
• These adhesions are the most common cause of small bowel obstruction in the developed world
• Can cause obstruction weeks, months, or years after the original peritonitis episode
• Post-operative complications of surgery for peritonitis include: adhesive intestinal obstruction ^[2]
• Why does peritonitis cause MORE adhesions than a clean operation? Because the massive fibrin deposition overwhelms the normal fibrinolytic capacity of the peritoneal mesothelium

4. Fistula Formation

• Chronic inflammation/abscess adjacent to a hollow viscus can erode through the wall and create an abnormal communication (fistula)
• Particularly relevant in diverticulitis-related peritonitis ^[6]:
  • Most commonly involve the bladder (colovesical fistula) — presents with pneumaturia, faecaluria, recurrent dysuria/UTI ^[3][6]
  • Followed by vagina (colovaginal fistula) — especially in post-hysterectomy patients — presents with passage of faeces and flatus per vagina ^[6]
  • Colocutaneous fistula — uncommon, usually easy to identify (faecal discharge from skin) ^[6]
  • Coloenteric fistula — uncommon, may be asymptomatic or cause corrosive diarrhoea ^[6]
• Post-appendicectomy: Enterocutaneous fistula — result from an intraperitoneal abscess that fistulises to the skin ^[2]
• Management of fistula ^[6]: control sepsis by antibiotics and drainage → resection of affected segment of colon with primary anastomosis → simple repair of the secondarily involved organ (primary closure of bladder or vagina)

5. Intestinal Obstruction

Peritonitis can cause obstruction through multiple mechanisms:

• Partial colonic obstruction occurs because of relative luminal narrowing due to pericolonic inflammation or compression from a diverticular abscess ^[6]
• Complete colonic obstruction occurs because recurrent attacks of acute diverticulitis result in progressive fibrosis and scarring leading to formation of intestinal strictures ^[6]
• LBO due to fibrosis and stricture, SBO due to adhesion to inflamed bowel ^[3]

6. Wound Complications (Post-Operative)

Patients operated on for peritonitis have grossly contaminated surgical fields:

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C. Complications Specific to Each Subtype

SBP-Specific Complications

CAPD Peritonitis-Specific Complications

Secondary Peritonitis-Specific Complications

These depend on the underlying cause but include all the local complications above plus:

Diverticulitis-Specific Complications Leading to/From Peritonitis

The progression of diverticulitis complications is well-characterised ^[6][7]:

Complicated diverticulitis — perforation ^[7]:

• Resuscitation with IVF + antibiotics
• Percutaneous drainage for abscess
• Consider emergency surgery if:
  • Unresponsive to antibiotics
  • Septic shock (high fever, tachycardia, hypotension, oliguria)
  • Generalised peritonitis (Hinchey III & IV)

The Hinchey classification stages represent progressive complications ^[7]:

Note how mortality escalates dramatically from stage II to IV — this underscores the importance of early diagnosis and intervention to prevent progression.

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D. Summary of Complications by Time Course

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Active Recall - Complications of Peritonitis

1. Explain the pathophysiological cascade from peritonitis to multi-organ failure, naming at least 4 organ systems affected and the mechanism for each.

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Peritonitis → bacterial/endotoxin absorption → SIRS → sepsis → MOF. (1) Lungs: ARDS from cytokine-mediated pulmonary capillary leak → non-cardiogenic pulmonary oedema. (2) Kidneys: AKI from hypovolaemia + sepsis-induced renal vasoconstriction + direct tubular injury. (3) Liver: septic hepatitis from hypoperfusion + endotoxin-mediated cholestasis. (4) Coagulation: DIC from diffuse activation of coagulation cascade → consumption of factors and platelets. (5) Brain: septic encephalopathy from cytokines crossing BBB. (6) Heart: septic cardiomyopathy from TNF-alpha and IL-1 causing myocardial depression.

2. What are the 3 SBP-specific complications, and why is IV albumin given alongside antibiotics in SBP?

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SBP-specific complications: (1) Hepatorenal syndrome - SBP causes splanchnic vasodilation → effective hypovolaemia → renal vasoconstriction → functional renal failure. (2) Hepatic encephalopathy - infection increases ammonia production + impairs hepatic clearance. (3) Variceal haemorrhage - increased portal pressure and worsened coagulopathy. IV albumin (1.5 g/kg day 1, 1 g/kg day 3) is given to expand intravascular volume and prevent the renal vasoconstriction that causes HRS. Reduces mortality from ~30% to ~10%.

3. Why does repeated CAPD peritonitis lead to PD failure, and what is encapsulating peritoneal sclerosis?

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Repeated peritonitis damages the mesothelial layer of the peritoneal membrane and promotes submesothelial fibrosis. Combined with chronic exposure to dextrose-containing PD fluid, this causes progressive peritoneal membrane fibrosis → reduced transport capacity → PD failure (most common reason for conversion to long-term haemodialysis). EPS is a rare but devastating complication where the peritoneum becomes encased in a thick fibrous cocoon encasing the bowel → intestinal obstruction. Presents with anorexia, nausea, abdominal pain, ascites, bowel obstruction. CT shows peritoneal calcification and bowel tethering. Treatment: tamoxifen + surgical enterolysis. Mortality 25-50%.

4. Why is primary anastomosis avoided in diffuse peritonitis, and what operation is performed instead for Hinchey IV diverticular peritonitis?

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Primary anastomosis is avoided in diffuse peritonitis because the tissues are inflamed, oedematous, and contaminated → very high risk of anastomotic leak, which would re-establish peritoneal contamination. Hartmann's procedure is performed instead: resection of affected sigmoid with end-colostomy (proximal end brought out as stoma) and closure of distal rectal stump. The stoma is reversed electively months later. Hinchey IV (faecal peritonitis) carries 50% mortality.

5. A patient develops persistent spiking fever 5 days after laparotomy for perforated appendicitis despite appropriate antibiotics. What is the most likely complication and how would you investigate and manage it?

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Most likely: intra-abdominal abscess. Suspect if no improvement in abdominal pain or persistent fever despite 3 days of antibiotics. Investigate with CT abdomen with contrast (rim-enhancing fluid collection with air or debris). Manage with CT-guided percutaneous drainage + continued IV antibiotics. If drainage fails or collection is not amenable to percutaneous approach, surgical drainage (re-laparotomy) is needed.

References

^[1] Lecture slides: GC 195. Lower and diffuse abdominal pain RLQ problems; pelvic inflammatory disease; peritonitis and abdominal emergencies.pdf (p41–42) ^[2] Senior notes: felixlai.md (Peritonitis p738–743; SBP p449–450; CAPD peritonitis complications p865–867; Appendicitis complications p736–737; CRC anastomosis principles p695–696) ^[3] Senior notes: maxim.md (Appendicitis complications p179; Diverticulitis complications p194–195; Peritonitis p46) ^[6] Senior notes: felixlai.md (Diverticulitis complications p647; Fistula management p647; Obstruction mechanism p647) ^[7] Lecture slides: Diverticular diseases - Dr. J Tsang.pdf (p12–13 — Hinchey classification and complicated diverticulitis perforation management)