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CHAPTER 114: Abdominal Compartment Syndrome 1085

a manner similar to the cardiorenal syndrome of acute decompensated TABLE 114-1 Signs Suggestive of intra-abdominal Hypertension and Abdominal
heart failure. In fact, the kidneys are particularly susceptible to IAH, Compartment Syndrome, Unexplained by Other Causes
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often suffering at levels of IAP (10-15 mm Hg) that do not cause other
organ failures. In cases of acute renal failure secondary to ACS, prompt Cardiovascular
reduction in IAP often results in rapid improvement in urine output Low cardiac output
and GFR. 36-38 In addition to direct hemodynamic effects, injury may Hypotension
be mediated through primed neutrophils, endothelial cells, and macro-
phages and by elaborating proinflammatory cytokines in the systemic Elevated CVP
circulation. These humoral mechanisms may also explain other extra- Exaggerated rise in CVP during inspiration
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abdominal effects, such as those on the pulmonary circulation and Pulmonary
intracranial pressure. Respiratory failure
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■ CARDIOVASCULAR EFFECTS Reduced respiratory system compliance
Elevation of the diaphragm by ACS raises pleural and juxtacardiac pres- Falling tidal volume (in pressure preset modes)
sure, limiting right heart filling. At the same time, direct compression Increased peak and plateau pressure (in volume preset modes)
of the vena cava also impedes blood return to the heart, so that preload
and cardiac output are greatly reduced. 24,34,40 Although preload is low, Renal
right atrial and pulmonary artery occlusion pressures are often elevated Oliguric acute kidney injury
because the juxtacardiac pressures are high. Thus, ACS is one of the Neurologic
causes of diastolic dysfunction. In addition, ACS raises left ventricular Intracranial hypertension
afterload, further depressing stroke volume. Hypotension is common
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in ACS, though blood pressure may not fall if sustained by systemic Metabolic
vasoconstriction. In normovolemia, mild increases in IAP to 15 mm Hg Lactic acidosis
centralize blood, raising CVP and left ventricular end-diastolic pres-
sure; greater IAP impedes cardiac filling. Fluid loading may succeed in
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boosting cardiac output, although the rise in central venous pressures depends largely on the chest wall compliance (for passively ventilated
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and creation of even greater abdominal hypertension may lead to a net patients; see Chap. 48), an additional clue to IAH is a larger than normal
negative effect on abdominal organ perfusion. rise in central venous (similarly pulmonary artery, pulmonary artery
IAH has been reported to produce false-negative results when using occlusion, and esophageal) pressure during inspiration (see Fig. 114-1). 47
passive leg raising to predict fluid responsiveness. Presumably this
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reflects the fact that leg raising normally augments flow from the legs
and splanchnic circulation through the vena cava, but this is impaired EPIDEMIOLOGY
in ACS. While ACS has long been described in trauma patients, particularly
■ PULMONARY EFFECTS those receiving large volumes of resuscitation, 48-51 all ICU patients can
develop ACS. For example, in a mixed ICU population, approximately
As IAP rises, cephalad displacement of the diaphragm compresses the 35% of ventilated patients develop IAH or ACS, and approximately 65%
thorax, reducing functional residual capacity, increasing the work of of those are primary. 52,53
breathing, and causing atelectasis, ventilation/perfusion inequality, shunt, ACS is now recognized as a significant cause of severe organ dys-
and a rise in dead space. In spontaneously breathing patients, IAH pro- function and an independent predictor of mortality. Secondary ACS
26
4,52
duces rapid, shallow breathing, hypoxemia, hypercapnia, and ventilatory portends a worse outcome than primary cases. Some of the causes of
failure. In mechanically ventilated patients, both peak and plateau ACS are listed in Table 114-2.
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pressures are elevated (with volume-preset modes) or tidal volumes fall
(with pressure-preset modes). Pulmonary edema is also seen, in part TREATMENT
due to systemic inflammation. In a group of burn patients undergoing
decompressive laparotomy for ACS, relief of the abdominal pressure Traditionally, decompressive laparotomy has been the treatment of
led to prompt improvement in peak airway pressures, static respiratory choice in patients with primary IAH or ACS; however, patients with
52
, and airway resistance. 44 secondary IAH or ACS are often considered poor surgical candidates.
system compliance, ratio of Pa O 2 to Fi O 2 Secondary IAH and ACS are caused by heterogeneous pathology, so mul-
■ CENTRAL NERVOUS SYSTEM EFFECTS tiple therapies can be considered; however, few have been shown in large
There is a strong association between IAH and increased intracranial trials to demonstrate consistent benefit in lowering IAP. Nonsurgical
therapies for IAH or ACS are often condition specific: patients with
pressure, largely mediated by the effects of intra-abdominal pressure on tense ascites may benefit from paracentesis, 50,54 ultrafiltration, 38,55,56 or
central venous pressure. 45,46 In addition, intracranial hypertension may aggressive diuresis; those with gastric or colonic distention may benefit
rely on nonhemodynamic mechanisms in some patients, and systemic from gastric or colonic decompression 57,58 or limiting enteric feeding.
inflammation may also play a role in central nervous system dysfunc- Two nonsurgical treatments deserve special mention. First, a subset
tion. When systemic hypotension and increased intracranial pressure of ACS is iatrogenic, provoked by exuberant fluid resuscitation. It is
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combine to decrease cerebral perfusion pressure, brain function may be increasingly clear that many critically ill patients in shock do not respond
critically compromised. to fluid administration ; in these patients, fluids cannot help and may
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■ CLINICAL MANIFESTATIONS cause harm, in part by contributing to IAH. Dynamic predictors of
fluid responsiveness (but not passive leg raising as discussed above) are
ACS presents in myriad ways and affects multiple organ systems, superior to central venous and pulmonary artery occlusion pressures
making it difficult to detect on a background of sepsis, polytrauma, or and may help reduce the burden of ineffective fluid therapy. Secondly,
systemic inflammation. Many of the signs can be predicted based on the paracentesis may be more effective than previously recognized. Large-
pathophysiology described above and are summarized in Table 114-1. volume paracentesis for ascites secondary to decompensated heart
Foremost among these are oliguria, shock, and falling respiratory failure both reduces IAP and improves renal function. In a series of
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system compliance. Recalling that the inspiratory rise in pleural pressure 31 patients with free intraperitoneal blood or fluid, paracentesis

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