Special Feature

Abdominal Compartment Syndrome

By Grant E. O’Keefe, MD

In recent years, an important manifestation of shock, resuscitation, and critical illness has become more evident in the intensive care unit. Elevated intra-abdominal pressure (intra-abdominal hypertension) leading to critical pulmonary, renal, or cardiac dysfunction has been dubbed the "abdominal compartment syndrome" (ACS). The ACS is associated with a high case-fatality rate, with death, according to most authors, almost certain if the increased pressure is not somehow relieved.1 Increased attention to the diagnosis and earlier, aggressive treatment of ACS has been suggested to reduce the associated mortality.2

Our understanding and treatment based on observations from case reports and small case series have been improved by data obtained from cohort studies—leading to a reliable body of evidence regarding predisposing clinical conditions, important risk factors, and expected outcomes from ACS. Nevertheless, even the seemingly simple task of establishing consistent definitions remains a challenge. Furthermore, treatment concepts are less clearly defined because they are based upon these same observational studies. This review is meant to summarize the important clinical features of the ACS in order to provide clinicians with contemporary information to assist in diagnosis and treatment of this serious complication of critical illness.

Definitions, Clinical Presentation, and Epidemiology

In order to discuss the incidence, associated risk factors, and outcomes, it is necessary to define both intra-abdominal hypertension and ACS. Although this is a task more complicated than might be expected, acceptable definitions can be gleaned from existing literature. Intra-abdominal hypertension can be defined as an intra-abdominal pressure of ³ 20 cm H2O.3 Other pressure thresholds, ranging from 15 to 25 cm H2O, have been used, but there is little objective evidence from clinical studies to select one threshold over others. Resorting to experimental data, it seems that alterations in hepatic arterial, portal venous, and hepatic microcirculatory blood flow are markedly reduced when intra-abdominal pressure is increased to ³ 20 cm H2O, lending some rationale for the use of this threshold and remembering that the observations in the laboratory setting may not translate perfectly to the clinical situation.4

The ACS can be defined as respiratory, renal, or cardiovascular dysfunction, associated with intra-abdominal hypertension that responds to reduction of intra-abdominal pressure (most often by decompressive celiotomy).3 This fairly restrictive definition, incorporating response to treatment (decompressive celiotomy) as part of the definition of ACS is not universally accepted, but seems appropriate. Other causes of lung, kidney, and cardiac dysfunction commonly exist (and often co-exist) in these critically ill patients and will not respond to reduction of elevated intra-abdominal pressure.

The incidence of ACS reported in the literature thus varies with the definitions used and also with the nature of the cohort studied. Using the above definition, the ACS was found to be rare in a cohort of 706 consecutive trauma victims admitted to a single intensive care unit. Hong and colleagues identified a total of 15 (2%) with intra-abdominal hypertension (using a threshold definition of ³ 20 mm Hg) and 6 of these (1% of the 706) developed ACS.3 Although using a relatively liberal pressure threshold to define intra-abdominal hypertension, most of the patients with the ACS, in fact, had much higher intra-abdominal pressures (as estimated by bladder pressure), which averaged 40 mm Hg.

ACS has been most often reported in association with severe abdominal trauma. However, it has been observed and reported in conjunction with a wide range of clinical situations (see Table). Typically, ACS was observed after severe abdominal trauma that required celiotomy and control of intra-abdominal hemorrhage.5,6 Observations of the ACS in cases of nontraumatic intra-abdominal catastrophes, initially postoperative hemorrhage, followed its description in critically ill patients with intra-abdominal injuries.7 Aggressive attempts to primarily close the fascia, in the presence of marked intestinal edema or intra-abdominal packing to control nonsurgical bleeding leads to a number of physiological alterations and the consequences of ACS.8 More recently, the ACS has been described in the setting of intra-abdominal injuries that were initially managed nonoperatively (severe liver or kidney injuries, for example).9 Trauma and burn victims without intra-abdominal injuries also seem to be at risk for ACS.10-12 Taken together, severe injury, resulting in shock and associated with large volume resuscitation, regardless of the specific injuries sustained, is the most common scenario in which ACS develops.

Diagnosis of Abdominal Compartment Syndrome

A triad of clinical findings including: (1) tense, distended abdomen; (2) increased end-inspiratory (plateau) airway pressures; and (3) oliguria despite appropriate volume resuscitation, when seen together, is a reliable indicator of ACS. In the appropriate clinical situation, this triad may be sufficient to mandate surgical decompression. However, the diagnosis is often not so obvious. Additional clinical measurements, particularly those that reflect poor cardiac performance, may be helpful in making the diagnosis. Typical signs consistent with ACS are a reduced cardiac output, elevated systemic vascular resistance, and elevated pulmonary capillary wedge pressure with simultaneous low or normal calculated estimates of end-diastolic volume. The addition of corroborative findings from invasive hemodynamic monitoring may help clarify the diagnosis and direct the appropriate treatment.

Most clinicians indirectly measure intra-abdominal pressure to determine more definitively whether the observed physiologic changes are associated with intra-abdominal hypertension and therefore reflect ACS. Bladder pressure is the most widely used estimate of intra-abdominal pressure. The technique of measuring bladder pressure is well described but is presented here because of its importance in the diagnosis and management of these patients. Approximately 100 mL of saline, a clamp capable of occluding the bladder catheter drainage system, an 18-gauge needle and a pressure transducer, such as an intra-arterial catheter system and monitor, are needed.

With the patient supine, the bladder is distended with 100 mL of sterile saline, injected through the aspiration port (found in the proximal part of the bladder catheter drainage system), which is then allowed to drain until a continuous column of fluid is visible in the tubing. The tubing is then occluded and the 18-gauge needle, connected to the pressure transducer, is inserted through the aspiration port into the catheter tubing. An adequate pressure "tracing" is indicated by visible respiratory variation, which is usually less than 5-10 mm Hg. The mean pressure should be used as an estimate of the intra-abdominal pressure, although this aspect of the procedure is not well characterized. Bladder pressure measurements have been observed to correlate well with direct intraperitoneal pressure measurements under a variety of circumstances and across a wide range (5-50 mm Hg) of pressure levels. A simpler method (although not validated) involves filling the bladder with 100 mL of sterile saline and elevating the clear tubing vertically above the pubic symphysis. The height of the fluid column is measured and converted to mm Hg (1.3 cm H2O = 1 mm Hg).


Clinical Conditions Associated with Acute Abdominal Compartment Syndrome

• Intra-abdominal trauma with solid organ injury

• Pelvis fracture with retroperitoneal hematoma

• Severe nonabdominal trauma

• Ruptured abdominal aortic aneurysm

• Severe burns

• Sepsis

• Pancreatitis

Treatment of Abdominal Compartment Syndrome

Established ACS (intra-abdominal hypertension, progressively increasing end-inspiratory airway pressures, declining urine output, and persistent shock) is treated with surgical decompression of the abdomen. This recommendation is based upon the high fatality rate reported in patients who are not decompressed, and not based upon clear evidence that decompression increases survival per se.13 As indicated above, there is little objective information upon which to base decisions regarding the timing of surgery, particularly what thresholds should be used to mandate abdominal decompression. However, some recommendations can be made.

First, elevated intra-abdominal pressures, regardless of the actual measured value, in the absence of clinical evidence of ACS should never be an indication for decompressive celiotomy. Second, based upon the observation that the first cases of ACS were described in postoperative patients in whom the abdominal fascia was closed, it is appropriate not to close the fascia in the case of moderate-to-marked visceral edema, particularly in patients requiring ongoing resuscitation—in whom the edema will increase postoperatively. This intra-operative decision is often difficult and requires the surgeon to be attentive to the presence of ongoing resuscitation needs, the patient’s acid-base status and the end-inspiratory pressures needed to achieve adequate oxygenation and ventilation during any attempts to close the abdominal fascia.

Beyond these 2 recommendations of (1) when decompression is not indicated and (2) when fascial closure should be avoided to prevent ACS, it is not possible to provide precise recommendations concerning when decompression should be undertaken. The following suggestions are based upon the author’s compilation of the literature and experience in treating these patients. High intrathoracic pressures, marked FiO2, and PEEP requirements are probably not sufficient to warrant decompression. Although the elevated pressures, PEEP, and FiO2 needs can often be dramatically decreased after decompressive celiotomy, these physiological improvements may not translate into relevant clinical benefits. Often the elevated intrathoracic pressures, as well as PEEP and FiO2 needs, decline (relatively more gradually) after resuscitation is complete without abdominal decompression.

On the other hand, the addition of progressive renal dysfunction (oliguria, rising creatinine) despite adequate preload and ongoing resuscitation to the clinical scenario should warrant abdominal decompression. Similarly, persistent shock (elevated base deficit or arterial lactate concentration) particularly when vasopressor agents are used to supplement fluid resuscitation also warrants decompressive celiotomy. There are no airway pressure, hourly urine output, or arterial lactate concentration thresholds that indicate or contraindicate decompressive celiotomy. Finally, in the absence of rapid and progressive clinical deterioration, it seems wise to observe the patient’s course for 2-4 hours (perhaps longer) before deciding to undertake decompression. This observation period should be active and must include determining whether fluid and vasoactive drug requirements are increasing or stabilizing and whether indices of shock (arterial base deficit or lactate concentrations) are improving. Until we have more comprehensive evidence upon which to base treatment decisions, these recommendations will provide a reasonable foundation upon which the decision to operate can rest.

The exact nature of the operative procedure depends on the underlying cause and extent of intestinal edema after decompression, and few authors define which physiologic derangements prompted or responded to abdominal decompression. It is important to recognize that ACS can occur in patients whose fascia has not been definitively closed, but some other technique of temporary abdominal closure has been performed. It seems that techniques including temporary skin closure or those that incorporate suturing prosthetic material to the fascia may place the patient at risk for recurrence of ACS. One strategy for managing the open abdominal wound incorporates: (1) temporary coverage of the viscera with a nonadherent material; (2) overlying absorbent dressings and suction drains; and followed by (3) an occlusive drape to prevent seepage of peritoneal fluid.14 This approach may be less likely to result in subsequent ACS as resuscitation continues, although ACS has been described after this mode of temporary closure and critical care physicians must therefore have a continued high level of suspicion.15

One factor that seems common to all cases of ACS is the use of aggressive crystalloid resuscitation. However, no study has adequately assessed the role and amount of crystalloid resuscitation as a risk factor for ACS. Therefore, it is not presently appropriate to recommend or criticize any particular approach to resuscitation in order to minimize the risk or avoid the development of ACS. It is possible, however, that attempts to achieve "supranormal" resuscitation end points, such as an oxygen delivery index of ³ 600 mL/min/m2 rather than more modest end points, which do not seem to improve clinical outcomes, may contribute to ACS.10,16

Summary and Conclusions

It is interesting to consider whether intra-abdominal hypertension and ACS are the necessary consequences of our ability to save more critically ill patients who, in previous years, might have succumbed to their injuries and therefore not been at risk for ACS. We must, however consider whether our aggressive approach to volume resuscitation with crystalloid solutions has contributed to the emergence of this complication.16 Interesting experimental data suggest that lactated ringer’s solution activates circulating neutrophils, tissue macrophages and endothelial cells, raising the possibility that our treatment, at least in part, contributes to this serious complication of shock and reperfusion.17 Sorting out the exact pathophysiology will be important to potentially avoiding, reducing the consequences of, and treating the ACS. Presently our clinical armamentarium involves the unsophisticated tasks of early recognition and surgical decompression of the abdomen.

Dr. O'Keefe is Department of Surgery Harborview Medical Center University of Washington, Seattle, WA.


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