MSC - F. Surgery Answers 2025

oEntire abdomen becomes "board-like" (generalized peritonitis).

Distension:

oParalytic ileus → no bowel sounds, tympanic percussion.

Vomiting:

oProgresses from reflexive → bilious → fecaloid (late sign of obstruction).

2.Systemic Signs (Early Decompensation)

Fever:

oHigh (39–40°C) or hypothermia (in severe sepsis).

Tachycardia (>120 bpm):

oWeak, thready pulse (poor peripheral perfusion).

Hypotension:

oEarly septic shock (systolic BP <90 mmHg, responsive to fluids).

Tachypnea (>24 breaths/min):

oRespiratory alkalosis → metabolic acidosis (lactic buildup).

Altered Mental Status:

oRestlessness → confusion → lethargy (cerebral hypoperfusion).

3.Laboratory & Imaging Findings

Leukocytosis (>20,000/mm³) or leukopenia (bad prognostic sign).

Elevated lactate (>2 mmol/L) → tissue hypoxia.

CT Abdomen:

oFree fluid, air, abscess formation, dilated bowel loops.

Pathophysiological Changes

Management Priorities

1. Immediate Surgery

oLaparotomy (source control: resection, drainage, lavage).

2.Aggressive Resuscitation

oIV fluids (crystalloids ± vasopressors if BP remains low).

oBroad-spectrum antibiotics (e.g., meropenem + vancomycin + metronidazole).

3.ICU Monitoring

oCentral venous pressure (CVP), urine output, lactate clearance.

4.Supportive Care

oMechanical ventilation (if respiratory failure).

o Dialysis (if acute kidney injury).

Why This Stage Is Critical

Reversible with treatment, but delay leads to:

o Decompensated shock (refractory hypotension). o Multi-organ failure (mortality >50%).

Clinical Red Flags:

o Fecaloid vomiting → advanced ileus.

o Cold, clammy skin → peripheral shutdown.

o Anuria → renal failure.

Prognosis: Mortality jumps to 20–30% in this stage.

Takeaway

"The calm before the storm"—patients may transiently stabilize before rapid deterioration.

Every minute counts—outcome depends on speed of surgical intervention.

6.Clinical picture of peritonitis of decompensation stage. Abdominal sepsis.

Abdominal Sepsis with Multi-Organ Failure

The decompensation stage represents end-stage peritonitis, where the body's compensatory mechanisms completely fail, leading to severe sepsis, shock, and irreversible organ damage. Mortality exceeds 50–70% even with aggressive treatment.

Key Clinical Features

1.Abdominal Signs (Paradoxical Deterioration)

"Silent Abdomen":

o Loss of pain (due to necrotic nerve endings). o No bowel sounds (complete paralytic ileus).

oDistended, dough-like on palpation (no rigidity).

Fecaloid vomiting (intestinal contents stagnate).

Free fluid on percussion (massive exudation).

2.Systemic Collapse (Septic Shock)

Hypotension (refractory to fluids/vasopressors).

Tachycardia → Bradycardia (terminal sign).

Hypothermia (<36°C, worse prognosis than fever).

Cutis marmorata (mottled skin from microthrombi).

3.Multi-Organ Dysfunction Syndrome (MODS)

4.Laboratory Findings

Leukopenia (<4,000/mm³) or leukemoid reaction (>50,000/mm³).

Lactic acidosis (>4 mmol/L).

Hyperbilirubinemia (>2 mg/dL).

Acute kidney injury (creatinine >2 mg/dL).

Thrombocytopenia (<50,000/mm³).

Pathophysiology of Abdominal Sepsis

1.Bacterial Toxins (LPS, superantigens) → cytokine storm (TNF-α, IL-6).

2.Endothelial Damage → capillary leak, microthrombi.

3.Mitochondrial Dysfunction → cellular energy failure.

4.Immunoparalysis → inability to clear infection.

Management (Last-Ditch Efforts)

1. Source Control

oEmergency laparotomy (if not already done) with bowel resection, ostomy.

oOpen Abdomen (laparostomy) for repeated lavage.

2.ICU Support

oVasopressors (norepinephrine + vasopressin).

o Mechanical ventilation (low tidal volume for ARDS).

oRenal replacement therapy (CVVH).

3.Antibiotics

oCarbapenems + antifungals (e.g., meropenem + caspofungin).

4.Adjuvant Therapies

oIV immunoglobulins (for immunoparalysis).

o Corticosteroids (if refractory shock).

Prognostic Indicators of Irreversibility

Lactate >8 mmol/L.

INR >3.

pH <7.2.

No response to 3 vasopressors.

Clinical Pearl

"The point of no return": Once liver failure + DIC develop, mortality approaches 90%.

Families should be prepared for poor outcomes—palliative care may be appropriate.

7.Clinical diagnosis of peritonitis.

Peritonitis is a surgical emergency requiring rapid diagnosis. A combination of history, physical exam, labs, and imaging is essential.

1.History (Key Clues)

Sudden, severe abdominal pain (localized → generalized).

Nausea/vomiting (progressing to fecaloid in late stages).

Fever, chills (signs of systemic infection).

Risk factors:

o Recent abdominal surgery.

o Peptic ulcer disease, diverticulitis, appendicitis.

oCirrhosis (for spontaneous bacterial peritonitis).

2.Physical Exam (Critical Findings)

A.Inspection

Distended abdomen (paralytic ileus).

Shallow breathing (avoiding diaphragmatic movement).

B.Palpation

Rebound tenderness (Blumberg’s sign) → most reliable indicator.

Guarding (voluntary) → Rigidity (involuntary, "board-like" abdomen).

Percussion tenderness (especially over McBurney’s point in appendicitis).

C.Special Signs

D.Rectal/Vaginal Exam

Cul-de-sac tenderness (pelvic peritonitis).

Bulging Douglas pouch (abscess).

8. Instrumental diagnosis of peritonitis.

4. Imaging

X-ray (Erect)

Free air under diaphragm (perforation), dilated loops (ileus)

CT (Gold

- Free air, fluid collections.

Standard)

- Fat stranding (inflammation).

- Source identification (e.g., appendicitis, diverticulitis).

5. Diagnostic Algorithm

1. Suspicion: Sudden abdominal pain + fever + vomiting. 2. Physical Exam: Rebound tenderness/rigidity.

3. Labs: Leukocytosis, elevated lactate.

4. Imaging: CT confirms diagnosis/localizes source.

5. Ascitic Tap (if ascites present): Diagnose SBP.

Differential Diagnosis

Early peritonitis vs. colic (renal/biliary).

Localized peritonitis vs. abscess.

SBP (no surgical cause) vs. secondary peritonitis.