Surgical Decompression for Abdominal Compartment Syndrome
This patient requires immediate surgical decompression for abdominal compartment syndrome (ACS). The clinical picture—massive fluid resuscitation (10 L IV fluids), rising plateau pressures (30 cm H2O), hypotension, tachycardia, oliguria, and hypoxemia—represents a surgical emergency requiring decompressive laparotomy.
Clinical Reasoning
Why Surgical Decompression is the Priority
Abdominal compartment syndrome is present: This patient received 10 L of fluid resuscitation following multiple intra-abdominal injuries (bowel resection, splenectomy, pancreatic injury, pelvic fracture). The combination of massive crystalloid administration, intra-abdominal bleeding, tissue edema, and surgical packing creates elevated intra-abdominal pressure 1.
Rising plateau pressures indicate respiratory compromise: Plateau pressures of 30 cm H2O reflect transmitted intra-abdominal pressure compressing the diaphragm and reducing lung compliance. This mechanical restriction prevents adequate ventilation despite high PEEP (12 cm H2O) and FiO2 (60%), resulting in hypoxemia (SpO2 90%) 1.
Oliguria despite massive fluid resuscitation: Persistent oliguria after 10 L of IV fluids indicates renal compression from elevated intra-abdominal pressure, not hypovolemia. Additional fluid will worsen ACS 2.
Hemodynamic instability from venous compression: The hypotension (84/48 mmHg) and tachycardia (120 bpm) result from inferior vena cava compression reducing venous return, not from inadequate fluid resuscitation 1, 2.
Why Other Options Are Incorrect
Vasopressors (Option A) would be harmful without addressing the underlying ACS. Vasopressors cannot overcome mechanical venous compression and would worsen end-organ perfusion by increasing afterload against an already compromised cardiac output 3. The FDA label for norepinephrine explicitly warns that "prolonged administration of any potent vasopressor may result in plasma volume depletion" and can cause "severe peripheral and visceral vasoconstriction with diminution in blood flow and tissue perfusion" 3.
Protective lung strategy (Option C) is already being attempted (PEEP 12, which is appropriate) but cannot overcome the mechanical restriction from elevated intra-abdominal pressure. While lung-protective ventilation is important, it addresses the wrong problem here 1, 4.
Continuous renal replacement therapy (Option D) would not address the mechanical cause of oliguria and would delay definitive treatment. The kidneys are failing due to compression, not intrinsic renal disease 2.
Management Algorithm
Immediate Actions (Within Minutes)
Notify surgery immediately for emergent decompressive laparotomy 1.
Measure bladder pressure if time permits (>20 mmHg confirms ACS, though clinical diagnosis is sufficient here) 1.
Prepare for OR transfer with continued mechanical ventilation and hemodynamic monitoring 1.
Intraoperative Considerations
Anticipate hemodynamic collapse upon abdominal decompression as venous pooling occurs. Have vasopressors ready (norepinephrine first-line) but only after decompression 1, 3.
Expect improved ventilation immediately after decompression as chest wall compliance improves 1.
Plan for temporary abdominal closure (vacuum-assisted or Bogota bag) as primary fascial closure will be impossible with bowel edema 1.
Post-Decompression Management
Initiate vasopressors judiciously: After decompression, if hypotension persists despite improved venous return, start norepinephrine targeting MAP ≥65 mmHg 1, 3.
Implement lung-protective ventilation: Use low tidal volumes (6 mL/kg ideal body weight), appropriate PEEP, and target plateau pressures <30 cm H2O 1, 4.
Balanced fluid resuscitation: Use crystalloids (lactated Ringer's preferred) or albumin, avoiding further massive fluid administration that contributed to ACS 1.
Monitor for reperfusion injury: Serial lactate measurements and assessment for acute kidney injury following restoration of perfusion 2.
Critical Pitfalls to Avoid
Delaying surgery while attempting medical management: ACS is a surgical emergency. Every minute of delay worsens end-organ damage 1, 2.
Administering more IV fluids: This patient has already received 10 L—additional fluid will worsen ACS and increase mortality 2, 5.
Starting vasopressors before decompression: Vasopressors cannot overcome mechanical obstruction and will worsen mesenteric and renal ischemia 3.
Attempting primary fascial closure: The abdomen must remain open temporarily to prevent recurrent ACS 1.