Abdominal compartment syndrome in burns
Key Points
- ACS occurs in 4-17% of severely burned patients and carries mortality rates averaging 75% across published series [2]
- Bladder pressure monitoring should be routine in patients receiving large-volume resuscitation, particularly burns exceeding 30% TBSA [1][4]
- Protocol-driven fluid restriction and colloid use are the primary prevention strategies for burn-related ACS [6][2]
- Decompressive laparotomy is definitive treatment for refractory ACS but should be performed early to prevent irreversible organ damage [2][5]
- Non-surgical interventions including neuromuscular blockade and percutaneous drainage can effectively reduce IAP in selected patients [1]
Overview
Abdominal compartment syndrome (ACS) is defined as sustained intra-abdominal pressure (IAP) greater than 20 mmHg with associated new-onset organ dysfunction [4]. Burn patients are at high risk for secondary ACS due to the massive capillary leak and large-volume fluid resuscitation characteristic of the first 24 hours after major injury. The prevalence of intra-abdominal hypertension (IAH, defined as IAP greater than 12 mmHg) in mechanically ventilated burn patients ranges from 65-75%, while ACS occurs in 4-17% of this population [1][2]. Mortality rates for ACS in burn patients average 74.8% across published series, making prevention and early recognition critical [2].
Pathophysiology
Burn-induced ACS results from the convergence of visceral and retroperitoneal edema, massive fluid resuscitation, and restricted abdominal wall compliance from circumferential trunk burns. The capillary leak that drives burn shock produces edema in the intestinal wall, mesentery, and retroperitoneum. Resuscitation volumes exceeding those predicted by formula ("fluid creep") amplify this effect [6]. Circumferential full-thickness trunk burns restrict abdominal wall expansion, further increasing IAP. As pressure rises, it compresses the inferior vena cava (reducing venous return and cardiac output), compromises renal perfusion (producing oliguria), elevates the diaphragm (impairing ventilation), and reduces mesenteric blood flow (threatening gut viability) [2].
Risk Factors
Wise et al. found that patients who developed ACS had significantly higher TBSA burns (35.8% vs 20.6%) and higher cumulative fluid balances at 48 hours (13.6 L vs 7.6 L) compared with those who did not [1]. The percentage of TBSA burned correlated with mean IAP (R = 0.34, P = 0.01) [1]. Boehm et al. conducted a multicenter matched-pair analysis of 38 burn patients who developed ACS and found that fluid therapy was a fundamental risk factor for late-onset ACS (after 4 days), while early-onset ACS was influenced by additional factors beyond fluid volume alone [3]. Burke and Latenser surveyed US burn physicians and found that only 31% routinely measured bladder pressure, and most did not differentiate between IAH and ACS [4].
Monitoring
Intravesical (bladder) pressure measurement is the standard method for monitoring IAP [4]. The World Society of the Abdominal Compartment Syndrome defines IAH as IAP greater than or equal to 12 mmHg and ACS as IAP greater than 20 mmHg with new organ dysfunction. Serial IAP measurements should be obtained in all patients receiving large-volume resuscitation, particularly those with burns exceeding 30% TBSA [1][2]. Clinical signs of ACS include tense distended abdomen, difficulty ventilating (elevated peak inspiratory pressures), oliguria, and hemodynamic instability [4].
Management
Prevention focuses on limiting resuscitation volumes through protocol-driven algorithms. Peters et al. demonstrated that modifying the Parkland formula to target lower volumes reduced average resuscitation from 11.8 L to 9.4 L (P = .03), with a non-significant reduction in ACS from 16% to 10% [6]. Colloid use, particularly rescue albumin, has been advocated as a volume-sparing strategy [2].
Non-surgical interventions for established IAH include neuromuscular blockade to improve abdominal wall compliance, nasogastric and rectal decompression, diuretics, and continuous renal replacement therapy for fluid removal [1]. Wise et al. found that non-surgical interventions (24 instances) effectively reduced IAP and improved oxygenation and urine output [1].
Escharotomy of circumferential trunk burns may relieve the restrictive component of elevated IAP. Percutaneous catheter drainage of ascites can reduce IAP in selected patients [4].
Decompressive laparotomy is the definitive treatment for ACS refractory to medical management. Nguyen et al. described a case of ACS developing after only 6 L of lactated Ringer's in a patient with 45% TBSA and inhalation injury, requiring emergent decompressive laparotomy in the emergency department [5]. The systematic review by Strang et al. confirmed that decompressive laparotomy effectively reduces IAP but carries significant morbidity, and timing is essential: decompression should prevent progression to ACS rather than treat established multiorgan failure [2].
Controversies and Evidence Gaps
The optimal threshold for decompressive laparotomy in burn patients is not firmly established. Survey data show wide variation in practice, with physicians citing IAP thresholds ranging from 15 to 40 mmHg [4]. Whether routine IAP monitoring improves outcomes compared with clinically driven monitoring has not been tested in a randomized trial. The relative contributions of fluid volume, burn size, inhalation injury, and abdominal wall compliance to ACS risk are difficult to disentangle in retrospective studies. Non-resolution of IAH is independently associated with mortality, but it is unclear whether this reflects the severity of the underlying injury or a modifiable treatment factor [1].
References
[1] Wise R et al. "Incidence and prognosis of intra-abdominal hypertension and abdominal compartment syndrome in severely burned patients." Anaesthesiol Intensive Ther 2015;48(2):95-109. PMID: 26588479 [2] Strang SG et al. "A systematic review on intra-abdominal pressure in severely burned patients." Burns 2014;40(1):9-16. PMID: 24050978 [3] Boehm D et al. "Fluid Management as a Risk Factor for Intra-abdominal Compartment Syndrome in Burn Patients." J Burn Care Res 2019;40(4):500-506. PMID: 30918949 [4] Burke BA, Latenser BA. "Defining intra-abdominal hypertension and abdominal compartment syndrome in acute thermal injury: a multicenter survey." J Burn Care Res 2008;29(4):580-4. PMID: 18535480 [5] Nguyen A et al. "Development of Early Abdominal Compartment Syndrome Leading to Emergent Decompressive Laparotomy in Full-Thickness Burn Injury." J Med Cases 2022;13(9):438-442. PMID: 36258705 [6] Peters J et al. "Using a Fluid Resuscitation Algorithm to Reduce the Incidence of Abdominal Compartment Syndrome in the Burn Intensive Care Unit." Crit Care Nurse 2023;43(6):58-66. PMID: 38035617