Abdominal compartment syndrome in burn resuscitation

Overview

Abdominal compartment syndrome is the burn-resuscitation complication that turns a survivable injury into a fatal one. In the severely burned patient it is almost always a secondary process: there is no primary intraperitoneal injury, yet massive interstitial swelling and capillary leak combine with the crystalloid load given to maintain perfusion, and intra-abdominal pressure climbs until the kidneys, the lungs, and the heart begin to fail ^[16]. The condition was first recognized in burns in pediatric patients, and for years was thought not to occur in burned adults ^[1]. That view changed when adults with very large burns requiring extraordinary resuscitation volumes were described developing ACS during the resuscitation phase itself ^[1].

The clinical importance is twofold. First, ACS is lethal: once intra-abdominal hypertension progresses to organ dysfunction, reported mortality is extreme ^[21]. Second, it is at least partly iatrogenic. The fluid given to rescue burn shock is also the agent that raises intra-abdominal pressure, which makes ACS a complication that resuscitation strategy can influence ^[4]. The remainder of this page covers how often it occurs, the mechanism, the grading scheme used to define it, how it is detected through serial pressure monitoring, the medical and surgical management ladder, and where the evidence remains thin.

Epidemiology

ACS is uncommon but not rare in major burns, and its frequency tracks burn size and resuscitation volume. Prevalence of ACS in severely burned patients has been estimated at 4% to 17% ^[8]. Intra-abdominal hypertension, the precursor state, is far more common: in patients with at least 15% total body surface area burned, 53% developed intra-abdominal hypertension in one cohort ^[9]. A pooled analysis found an overall intra-abdominal hypertension prevalence of 57.8%, and reported that roughly one in two patients with severe burns exceeding 20% in children or 25% in adults developed the condition ^[6].

The injury threshold matters. In a prospective burn protocol, intra-abdominal hypertension occurred commonly in major burns, while overt ACS was seen regularly only in patients with more than 70% body surface area burns ^[2]. An early adult series reported that three patients with burns of more than 70% who each required more than 20 L of crystalloid developed ACS during resuscitation ^[1]. Eight of 48 patients with more than 30% total burn surface area developed ACS within roughly 18 hours in another cohort, at intra-abdominal pressures far above normal ^[3].

Pathophysiology

ACS in burns is the end point of a process in which massive interstitial swelling in the abdomen raises pressure inside a fixed compartment ^[15]. Severe burns drive capillary leak and third-spacing ^[42], and the large-volume fluid resuscitation needed to support the circulation ^[43] compounds visceral and bowel-wall edema ^[44]. Recognized contributors are diminished abdominal wall compliance, increased intraluminal and intraperitoneal contents, and edema from capillary leak and resuscitation [32, 16]. Ascites, bowel distention, and hemoperitoneum add to the intra-abdominal volume ^[38].

As intra-abdominal pressure rises, perfusion to the kidneys and abdominal viscera falls and cardiac output drops, while the diaphragm is splinted and ventilation becomes difficult ^[15]. Elevated pressure reduces venous return, raises intrathoracic pressure, and impairs both preload and contractility ^[31]. The fluid relationship is direct: a large intravenous fluid volume decreases abdominal perfusion during resuscitation because of the rise in intra-abdominal pressure ^[4]. Resuscitation volume and intra-abdominal pressure correlate, and most patients who developed ACS in one series had required more than 300 mL/kg of fluid in the first 24 hours ^[3]. The Parkland-formula "fluid creep" phenomenon is named as a driver of this complication ^[37]. The mechanism is not uniform, however: in late-onset ACS fluid therapy is a fundamental risk factor, whereas in early-onset ACS other factors appear to tip the balance even when fluid administration contributes ^[25].

Classification

The contemporary framework comes from the World Society of the Abdominal Compartment Syndrome. ACS is defined as a sustained intra-abdominal pressure above 20 mmHg, with or without an abdominal perfusion pressure below 60 mmHg, that is associated with new organ dysfunction or failure ^[13]. The bladder-pressure gold standard is used to operationalize these definitions: a pressure above 12 mmHg is consistent with intra-abdominal hypertension, and the burn literature has used a pressure above 25 mmHg as consistent with ACS ^[14], somewhat above the 20 mmHg WSACS definitional threshold.

A clinically important distinction is primary versus secondary ACS. Severe burns are the prototype of secondary ACS, in which there is no primary inciting intraperitoneal injury yet severe intra-abdominal hypertension develops from aggressive fluid resuscitation ^[21]. Secondary intra-abdominal hypertension behaves differently from the primary form: it is less frequent, has a different time course, and carries a worse outcome ^[24]. In one comparison, patients with secondary intra-abdominal hypertension had significantly higher ICU mortality than those with primary disease ^[24]. In trauma cohorts, prehospital and emergency-department crystalloid volume predicted secondary ACS, underscoring that resuscitation volume drives the secondary form ^[22].

Assessment

Diagnosis is clinical but cannot rest on examination alone, because the sensitivity of physical examination is low and at-risk patients are monitored with intra-abdominal pressure measurement ^[28]. The criterion standard is intravesical pressure measurement performed through a urinary catheter ^[17]. The standard technique measures pressure in the bladder filled with about 25 mL of sterile saline ^[18]. The classic presentation that should trigger measurement is the triad of high peak airway pressures, oliguria despite adequate filling pressures, and intra-abdominal pressures above 25 mmHg ^[1].

Serial measurement is what makes the diagnosis, and timing is anchored to resuscitation volume. One protocol recommended bladder-pressure measurement after infusion of more than 0.25 L/kg during acute resuscitation and for peak inspiratory pressures above 40 cmH2O ^[2]. Another suggested measuring every 6 hours in patients with more than 40% burns, escalating to hourly once the Ivy resuscitation score reaches 200 mL/kg ^[19]. A practical caution from the burn literature is that secondary ACS in burned adults is commonly unsuspected and can compromise the reliability of urine output as a resuscitation guide ^[21]. Consensus recommendations support intra-abdominal pressure measurement and protocolized management of sustained intra-abdominal hypertension ^[12]. Abdominal perfusion pressure, calculated as mean arterial pressure minus intra-abdominal pressure, has been proposed as a resuscitation endpoint ^[40]; whether it should serve in that role is taken up under Controversies and Evidence Gaps.

Management

Management proceeds as a ladder from medical measures to surgical decompression, escalating with the degree of organ dysfunction. Medical management is instigated early to prevent progression and works along several axes: increasing abdominal wall compliance with analgesia, sedation, and neuromuscular blocking agents, and evacuating gastrointestinal contents ^[16]. Deeper sedation and muscle relaxation, evacuation of gastric and bowel contents, and diuretics or ultrafiltration form the conservative core ^[18]. In one burn case, cisatracurium and increased sedation reduced intra-abdominal pressure to 9 mmHg and prevented progression to ACS ^[33]. Negative fluid balance is a parallel lever: in a controlled comparison in a non-burn severe-acute-pancreatitis cohort, a negative-fluid-balance strategy lowered intra-abdominal pressure and reduced the new mechanical ventilation rate compared with a positive-balance group ^[23].

When medical measures fail, percutaneous catheter drainage of ascites is the next step. Percutaneous drainage of ascites is described as a simple and potentially effective tool to reduce intra-abdominal pressure once organ dysfunction develops, especially in burn patients ^[10]. Decompressive laparotomy is the definitive therapy, but consensus guidance positions it for established disease: surgical decompression followed by temporary abdominal closure is considered in patients with signs of organ dysfunction ^[38]. Decompressive laparotomy improves respiratory compliance and stabilizes hemodynamic parameters, but it is morbid, and its complications are especially severe in the burn population [38, 8]. Decompression leaves an open abdomen, and primary fascial closure becomes the next goal; closure rates may be improved by early return to the operating room and by limiting crystalloid during the surgical interval ^[26].

Complications

Beyond the abdomen, the same over-resuscitation physiology produces compartment syndromes elsewhere. Orbital compartment syndrome risk factors mirror those for ACS: total body surface area burned, resuscitation above the Ivy index of more than 250 mL/kg, and the calculated Parkland volume ^[29]. Orbital congestion can develop within the first 24 hours of admission, when resuscitation volumes are greatest ^[29]. Orbital compartment syndrome is a rare but devastating complication of over-resuscitation that may cause permanent visual loss, described in a series of twelve burn patients with a mean total body surface area burn of 63.7% ^[41]. Decompressive laparotomy for ACS itself generates complications, including the morbidity of the open abdomen, which is especially pronounced in burn patients ^[8].

Special Considerations

Children are a distinct population. Pediatric thresholds are lower than adult cutoffs: an intra-abdominal pressure above 10 mmHg with new organ dysfunction should be considered ACS in children until proven otherwise, because ACS may occur at pressures below the adult 20 mmHg threshold ^[11]. In children, normal intra-abdominal pressure in mechanically ventilated patients is approximately 7 mmHg, lower than in adults ^[11]. ACS in burns was in fact first described in pediatric patients, while for years it was thought not to occur in burned adults ^[1].

Outcomes

Outcomes are poor once intra-abdominal hypertension progresses to organ failure. In severe burns, mortality associated with intra-abdominal hypertension has been estimated above 74.5% once organ dysfunction occurs ^[6]. Historically, survival of burn patients with ACS was reported as poor, averaging just 16% after laparotomy, but timing of intervention changes that picture ^[5]. In a series where decompression was managed proactively, overall survival was 56%, and immediate laparotomy gave 70% survival versus 33% when ACS was treated later in the hospital course (p=0.03); fascial closure within 48 hours was associated with 100% survival ^[5]. Immediate laparotomy produced much higher survival than previously reported in burn patients with ACS ^[5]. The earliest adult burn series reported a mortality rate of 100% among the patients who developed ACS during resuscitation, confirming the grave consequences of the syndrome ^[1]. ACS is a serious complication of burn injury that carries high morbidity and mortality ^[30], and is described as a devastating complication in burn patients with a high mortality ^[7].

Controversies and Evidence Gaps

The largest open question is the resuscitation endpoint. There is currently insufficient evidence to recommend abdominal perfusion pressure as a resuscitation endpoint in patients with intra-abdominal hypertension ^[34]. Consensus guidance made no recommendation on using abdominal perfusion pressure as a resuscitation endpoint, and no recommendations on diuretics, albumin, or renal replacement therapy ^[35].

Prevention strategy is also contested. Limiting fluid intake with colloids, hypertonic saline, or hyperoncotic albumin solutions has been associated with favorable effects on intra-abdominal pressure ^[27]. In a burn protocol, hypertonic lactated saline reduced the intravenous volume needed to maintain urine output and lowered peak intra-abdominal and inspiratory pressures relative to lactated Ringer's, and the authors concluded it could reduce the risk of secondary ACS with a lower fluid load ^[4]. By contrast, a colloid comparison found that hydroxyethyl starch and 5% albumin had comparable effects on intra-abdominal hypertension in severely burned patients ^[39]. Awareness is a further gap: surveys show bladder pressure is not routinely measured by most burn physicians, with many centers waiting until the abdomen is tense ^[20]. Finally, the timing of de-resuscitation is acknowledged as important, but clear indicators to guide the decision are lacking ^[36].

References

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