MSC - F. Surgery Answers 2025

Primary (spontaneous bacterial peritonitis, ~1%): Hematogenous/lymphatic spread (e.g., cirrhosis, nephrotic syndrome).

Secondary (most common): Due to abdominal pathology:

o Hollow organ perforation (peptic ulcer, appendicitis, diverticulitis).

o Postoperative infection (anastomotic leak, contamination).

o Trauma (penetrating/blunt abdominal injury).

oIschemia (mesenteric thrombosis, strangulated hernia).

Tertiary: Persistent/recurrent infection despite treatment (immunocompromised patients).

Pathogenesis:

1. Inflammatory Response:

oMicrovascular changes → exudation (serous → fibrinous → purulent).

oLeukocyte migration → release of lysosomal enzymes → tissue damage.

oKinin system activation → hemodynamic instability.

2.Intestinal Dysfunction:

oParalytic ileus → bacterial translocation → sepsis.

oFluid sequestration → hypovolemia, electrolyte imbalance.

3.Systemic Effects:

oEndotoxemia → septic shock.

o Metabolic disturbances (acidosis, hypoproteinemia).

oPolyorgan Dysfunction Syndrome (PODS) → multi-organ failure.

2.Classification of peritonitis. Primary, secondary, tertiary peritonitis.

Classification of Peritonitis

1. By Origin:

Primary (spontaneous): Rare, from hematogenous spread (e.g., pneumococcal, tuberculous).

Secondary: Due to abdominal pathology (most common).

Tertiary: Persistent infection after initial treatment.

2.By Exudate Type:

Serous

Fibrinous

Purulent

Fecal

Enzymatic (e.g., pancreatic)

3.By Spread:

Localized (abscess, confined to one region).

Generalized (diffuse).

4.By Clinical Course:

Acute (most common).

Chronic (e.g., tuberculous peritonitis).

1.Primary Peritonitis (Spontaneous Bacterial Peritonitis, SBP)

Definition: Infection of the peritoneal fluid without an obvious intraabdominal source (no perforation or abscess).

Pathogenesis:

o Hematogenous or lymphatic spread of bacteria.

oCommon in patients with:

Cirrhosis (due to portal hypertension and bacterial translocation).

Nephrotic syndrome (low IgG levels).

Immunocompromised states (HIV, chemotherapy).

Microbiology:

oUsually monomicrobial (e.g., E. coli, Streptococcus pneumoniae, Klebsiella).

Clinical Features:

oDiffuse abdominal pain, fever, ascites.

oDiagnosis: Ascitic fluid analysis (PMN >250 cells/mm³).

Treatment:

oAntibiotics (cefotaxime, fluoroquinolones).

oAlbumin infusion (to prevent hepatorenal syndrome).

2.Secondary Peritonitis (Most Common Type)

Definition: Infection due to direct contamination from a perforated or inflamed abdominal organ.

Causes:

oPerforation (peptic ulcer, appendicitis, diverticulitis, trauma).

o Postoperative leakage (anastomotic breakdown).

oIschemic necrosis (strangulated hernia, mesenteric thrombosis).

Microbiology:

oPolymicrobial (Gram-negative rods, anaerobes like Bacteroides fragilis).

Clinical Features:

oSevere abdominal pain, guarding, rigidity, vomiting, sepsis.

Diagnosis:

oCT scan (identifies source, free air, abscess).

oLaparotomy (definitive diagnosis & treatment).

Treatment:

oEmergency surgery (source control: resection/repair).

oBroad-spectrum antibiotics (e.g., piperacillin-tazobactam, carbapenems + metronidazole).

3.Tertiary Peritonitis (Persistent/Recurrent Infection)

Definition: Persistent or recurrent peritonitis after initial treatment of secondary peritonitis.

Risk Factors:

oImmunosuppression (diabetes, steroids, chemotherapy).

o Inadequate source control (undrained abscess, necrotic tissue).

oResistant organisms (e.g., Candida, MRSA, Pseudomonas).

Microbiology:

oOften nosocomial, multidrug-resistant (MDR) pathogens.

Clinical Features:

oLow-grade fever, ongoing ileus, organ dysfunction.

oNo clear focus on imaging (occult infection).

Treatment:

oRe-exploration (if localized abscess).

o Culture-directed antibiotics (e.g., vancomycin, antifungals). o Immunonutrition, ICU support (for sepsis).

Clinical Stages of Peritonitis

1.Reactive Stage (First 24 Hours)

Pathology: Local inflammation, no systemic toxicity.

Symptoms:

oSevere localized abdominal pain (e.g., right iliac fossa in appendicitis).

o Muscle rigidity (guarding), rebound tenderness.

oNausea/vomiting (reflexive).

Systemic Signs:

oTachycardia (~100–120 bpm).

o ARDS (lung failure).

oComa (cerebral hypoxia).

Prognosis:

oMortality >70% even with treatment.

Key Takeaways

Localized peritonitis → better prognosis if treated early.

Generalized peritonitis → surgical emergency (high mortality if delayed).

Exudate type helps identify cause (e.g., fecal = perforated colon).

Three stages:

1.Reactive (localized pain, treatable).

2.Toxic (sepsis, needs urgent surgery).

3.Terminal (MOF, often fatal).

Management Principle:

Early diagnosis + source control (surgery) + antibiotics = best chance of survival.

4.The clinical picture of peritonitis of compensation stage.

Clinical Picture of Peritonitis: Compensation Stage

*(Early/Reactive Phase, First 24 Hours)*

The compensation stage represents the initial phase of peritonitis, where the body's compensatory mechanisms (inflammatory response, hemodynamic adjustments) are still able to maintain stable organ function despite the developing infection.

Key Features:

1. Local Symptoms (Dominant in This Stage)

oSudden, sharp abdominal pain:

Initially localized to the affected area (e.g., right lower quadrant in appendicitis, epigastrium in perforated ulcer).

Gradually becomes more diffuse as inflammation spreads.

o Muscle guarding & rigidity:

Involuntary contraction of abdominal muscles ("board-like abdomen" in generalized peritonitis).

oRebound tenderness (Blumberg’s sign):

Pain worsens upon sudden release of palpation.

oShallow breathing (to minimize diaphragmatic movement).

2.Gastrointestinal Symptoms

oNausea & vomiting (initially reflexive, later due to ileus).

o Loss of appetite, thirst (early dehydration).

oConstipation/absent bowel sounds (developing paralytic ileus).

3.Systemic Signs (Compensated, Not Yet Critical)

oTachycardia (100–120 bpm) → sympathetic activation.

oNormal or slightly elevated BP (early vasoconstriction compensates for fluid loss).

o Low-grade fever (37.5–38.5°C).

oLeukocytosis (12,000–15,000/mm³ with left shift).

4.Laboratory Findings

oElevated CRP, procalcitonin (markers of inflammation).

o Mild metabolic acidosis (lactic acid buildup from tissue hypoxia).

oNormal/mildly elevated creatinine (early renal compensation).

5.Imaging

oX-ray: May show free air under diaphragm (if perforation present).

oUltrasound/CT: Localized fluid, thickened peritoneum, possible abscess.

Why Is This Stage Called "Compensation"?

The body maintains blood pressure via vasoconstriction & tachycardia.

Renal function is preserved (urine output normal or slightly reduced).

No overt organ failure (brain, liver, lungs still functional).

Danger Signs (Progression to Toxic Stage Imminent)

Pain shifts from localized → generalized.

Vomiting becomes bilious/fecaloid (sign of ileus).

Tachycardia worsens (>120 bpm), BP begins to drop.

Oliguria develops (kidney hypoperfusion).

5.The clinical picture of peritonitis of subcompensation stage. *(Intermediate/Toxic Phase, 24–72 Hours After Onset)*

The subcompensation stage marks the transition from localized inflammation to systemic toxicity, where the body's compensatory mechanisms begin to fail. This is a critical period—rapid intervention is needed to prevent progression to irreversible septic shock.

Key Clinical Features

1.Abdominal Symptoms (Worsening Peritoneal Irritation)

Pain:

o Initially localized → now diffuse, constant, and severe.

oMay paradoxically decrease due to nerve-ending necrosis (ominous sign).

Muscle Rigidity: