Management of Abdominal Compartment Syndrome with Acute Kidney Injury
This patient has abdominal compartment syndrome (ACS) requiring immediate surgical decompression via decompressive laparotomy, as the IAP >25 mmHg with new organ failure (acute kidney injury with oliguria) meets definitive criteria for ACS and medical management alone will not reverse this life-threatening condition. 1, 2, 3
Immediate Recognition and Diagnosis
Your patient meets diagnostic criteria for ACS based on:
- IAP >25 mmHg (threshold is ≥20 mmHg) 1, 3
- New organ dysfunction: acute kidney injury with urine output dropping from 55 mL/hr to 10 mL/hr over 2 hours (oliguria defined as <0.5 mL/kg/hr) 1, 4
- Cardiovascular dysfunction: hypotension (BP 100/60) with tachycardia (HR 118) despite elevated CVP of 14 mmHg 5
The elevated CVP paradoxically suggests hypovolemia in the context of ACS—the massively increased IAP compresses the inferior vena cava and increases intrathoracic pressure, falsely elevating filling pressures while actual intravascular volume and cardiac output remain inadequate. 5
Stepwise Management Algorithm
Step 1: Initiate Medical Management Immediately (While Preparing for Surgery)
These interventions buy time but will NOT resolve ACS at this pressure level—they are temporizing only: 1, 2, 3
- Optimize sedation and analgesia to reduce abdominal wall muscle tone 1, 2, 3
- Consider brief neuromuscular blockade as a temporizing bridge to surgery 1, 2, 3
- Insert nasogastric tube (if not already present) and place on continuous suction 1, 2
- Insert rectal tube and administer enemas for colonic decompression 1, 2
- Discontinue enteral nutrition immediately 2
- Adjust body position to supine (avoid head-down positioning which worsens IAP) 1, 3
Step 2: Hemodynamic Support During Resuscitation
Cautious fluid resuscitation is critical—avoid aggressive volume loading which will worsen IAP and bowel edema: 1
- Target MAP ≥65 mmHg with vasopressors rather than excessive fluids 1
- Initiate norepinephrine as first-line vasopressor for hypotension 1
- Limit crystalloid administration—the elevated CVP of 14 mmHg in the setting of hypotension reflects the confounding effect of elevated IAP on filling pressures, not true volume overload, but additional fluids will worsen abdominal edema 1, 5
- Do NOT use diuretics at this stage—while the guidelines note no recommendation for diuretics in hemodynamically stable patients with IAH, this patient is hemodynamically unstable with hypotension and tachycardia, making diuresis contraindicated 1, 6
Step 3: Assess for Percutaneous Drainage (Rarely Applicable)
- Perform urgent bedside ultrasound to identify free intraperitoneal fluid collections 2, 3
- If large ascites or fluid collection present: consider percutaneous catheter drainage (PCD) as it may temporarily reduce IAP and potentially avoid or delay laparotomy 1, 2
- However, at IAP >25 mmHg with organ failure, PCD alone is unlikely to be sufficient—proceed directly to surgical decompression 1, 2
Step 4: Definitive Treatment—Decompressive Laparotomy
Surgical decompression is mandatory and should not be delayed: 1, 2, 3
- Indication: IAP ≥20 mmHg with new organ dysfunction (this patient has IAP >25 mmHg with acute kidney injury and cardiovascular compromise) 1, 3
- Perform full midline decompressive laparotomy with complete fascial opening 2
- Leave abdomen open with temporary abdominal closure using negative pressure wound therapy 2
- Expect immediate improvement in urine output, blood pressure, and oxygenation within 15 minutes of decompression 5
Step 5: Post-Decompression Management
After surgical decompression, the focus shifts to preventing recurrent IAH and achieving abdominal closure: 2, 3
- Continue IAP monitoring at least every 4-6 hours to detect recurrent IAH 3
- Target IAP <15 mmHg with ongoing medical management 3
- Implement strict fluid balance protocols aiming for zero to negative fluid balance by day 3 post-decompression 1, 2, 3
- Plan re-exploration within 24-48 hours for reassessment and potential staged closure 2
- Initiate early enteral nutrition once gastrointestinal function returns (open abdomen patients are hypermetabolic) 2
- Protocolized efforts for early fascial closure (same-hospital-stay if possible) to minimize complications 1, 2, 3
Expected Outcomes After Decompression
- Urine output typically improves within 15 minutes of decompression 5
- The acute kidney injury is primarily due to reduced renal blood flow from elevated IAP compressing renal vasculature and reducing cardiac output 4, 7
- Restoration of normal IAP allows recovery of glomerular filtration rate 4
Cardiovascular improvement: 5
- Cardiac output increases as venous return is restored 5
- Filling pressures (CVP) decrease to more physiologic levels 5
- Vasopressor requirements typically decrease 5
Critical Pitfalls to Avoid
- Do not delay surgery waiting for medical management to work—at IAP >25 mmHg with organ failure, medical therapy alone is insufficient 1, 2, 3
- Do not aggressively fluid resuscitate—this worsens bowel edema and IAP, creating a vicious cycle 1, 8
- Do not interpret elevated CVP as volume overload—in ACS, elevated filling pressures reflect increased intrathoracic pressure from the elevated IAP, not true hypervolemia 5
- Do not use diuretics in the acute hypotensive phase—this will worsen hypotension and renal perfusion 6
- Do not attempt primary fascial closure at initial laparotomy—leave the abdomen open to prevent recurrent ACS 2, 3
Prognosis
Mortality remains 40-50% even with appropriate decompression, emphasizing the importance of early recognition and intervention. 2 The combination of hypotension, tachycardia, oliguria, and IAP >25 mmHg represents advanced ACS with multi-organ dysfunction, requiring immediate surgical intervention to optimize survival. 1, 7, 8