Acute Abdomen, GI Bleeding & Abdominal Compartment Syndrome

Gastrointestinal Physiology in Critical Illness

The gastrointestinal tract depends on adequate perfusion, coordinated motility, mucosal integrity, and functioning hepatic and pancreatic systems. Shock and vasoconstriction can reduce splanchnic perfusion; opioids, immobility, electrolyte disorders, and autonomic injury impair motility. These mechanisms explain common feeding intolerance, but they do not establish that a new distended abdomen is benign ileus.

The official outline includes acute abdomen, upper and lower bleeding, adynamic and obstructive ileus, perforation, mesenteric ischemia, and abdominal compartment syndrome. A patient unable to describe pain needs serial examination and attention to distension, stool and gastric output, blood loss, ventilation pressures, urine output, and systemic perfusion. New deterioration should trigger diagnostic reassessment rather than automatic escalation of prokinetics or laxatives.

Recognize and Stabilize Gastrointestinal Hemorrhage

Upper GI bleeding may present with hematemesis, coffee-ground material, melena, or shock. Lower GI bleeding often causes hematochezia, but brisk upper bleeding can also do so. Assess circulation, airway protection, hemoglobin trend, coagulation, platelets, medications, and the possibility of portal hypertension. A normal initial hemoglobin does not exclude acute major blood loss.

Resuscitate and obtain urgent gastroenterology assessment for endoscopic diagnosis and hemostasis. Antithrombotic interruption or reversal depends on bleeding severity, drug, timing, and competing thrombotic indications. A recent intracranial event or coronary stent changes the decision. Suspected variceal hemorrhage requires a portal-hypertension-specific pathway, including appropriate vasoactive therapy and antimicrobial coverage, rather than acid suppression alone.

A transfusion threshold is not a substitute for treating shock or active hemorrhage. General restrictive strategies may need modification in acute brain injury, ischemia, or substantial ongoing loss. Monitor calcium, temperature, and coagulation during major transfusion. Pharmacologic stress-ulcer prophylaxis prevents selected bleeding risk; it does not replace investigation and treatment of established bleeding.

Ileus Versus Mechanical Obstruction

Adynamic ileus is impaired propulsion without a fixed mechanical blockage. Common contributors include surgery, opioids, electrolyte abnormalities, systemic illness, and immobility. Mechanical obstruction can involve a transition point, closed loop, hernia, adhesion, mass, or volvulus. Bowel sounds alone do not distinguish them reliably, and the usual pain pattern may be absent under sedation.

Hold or modify enteral feeding when obstruction, bowel ischemia, or another acute surgical problem is suspected. Treat electrolyte problems and reduce contributory drugs when possible, but do not use empiric motility treatment to postpone assessment of a mechanical lesion. Persistent distension with fever, shock, peritoneal findings, or worsening metabolic abnormalities warrants urgent imaging and surgical involvement.

Perforation and Mesenteric Ischemia

GI perforation can cause contamination, peritonitis, sepsis, and rapid circulatory deterioration. Obtain appropriate imaging when the patient is stable enough and initiate resuscitation, antimicrobial treatment, and urgent source-control assessment. Free air is a major clue, but postoperative context and the clinical syndrome matter. A normal or initially nondiagnostic plain radiograph cannot reliably exclude perforation.

Acute mesenteric ischemia may be arterial embolic, arterial thrombotic, venous, or nonocclusive. Atrial fibrillation, atherosclerotic disease, hypercoagulability, shock, and high vasopressor requirements provide different mechanisms. Pain out of proportion is a classic clue in an awake patient; its absence in coma is meaningless. Lactate can rise late or for other reasons, so a normal early concentration does not rule out the diagnosis.

CT angiography is important when ischemia is suspected and should not be deferred reflexively because of kidney dysfunction when the diagnosis is life threatening. Treatment combines resuscitation, bowel-viability assessment, antimicrobial therapy, and revascularization or surgery as appropriate. Nonocclusive ischemia requires correcting the low-flow state and assessing the bowel, not assuming that escalating vasoconstriction alone will solve the problem.

Intra-Abdominal Hypertension and Compartment Syndrome

Increasing abdominal pressure can impair renal perfusion, venous return, and ventilation and can hinder cerebral venous drainage. Abdominal compartment syndrome is sustained pressure above 20 mm Hg with new organ dysfunction, with or without a low abdominal perfusion pressure. A tense abdomen alone is insufficient, and organ dysfunction can occur before all classic signs appear.

Measure pressure using a standardized technique, commonly through the bladder, when the syndrome is suspected. Reassess fluid accumulation, abdominal contents, positioning, muscle tone, and reversible causes. Gastric or colonic decompression, drainage of fluid collections, and carefully selected medical measures may help, while overt refractory syndrome can require surgical decompression. In a patient with rising airway pressures, oliguria, and falling CPP after major resuscitation, consider an abdominal mechanism alongside primary pulmonary and intracranial causes.

Sources checked October 17, 2026: WSES mesenteric ischemia guideline, IDSA intra-abdominal infection guidance, and WSACS consensus definitions.