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  Abdominal compartment syndrome (ACS) is caused by an acute increase in intra-abdominal pressure resulting from a number of medical and surgical conditions.

  
  
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  Abdominal compartment syndrome and intra-abdominal hypertension are often unrecognized causes of organ dysfunction in critically ill patients.

  
  
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  The reference standard for measurement of intra-abdominal pressure is via bladder catheter using a standardized protocol.

  
  
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  Primary ACS results from direct, abdominopelvic pathology, whereas secondary ACS does not.

  
  
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  By elevating the diaphragm and decreasing respiratory system compliance, ACS causes a restrictive respiratory defect. However, ACS affects a number of other organs, especially the kidneys, and may cause multiorgan system failure.

  
  
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  Diagnosis relies on maintaining a high degree of clinical suspicion, measurement of intra-abdominal bladder pressure, and identification of organ dysfunction.

  
  
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  The abdomen should be decompressed before critical organ dysfunction develops.

  
  
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  Failure to recognize and treat ACS portends a poor prognosis.

Compartment syndrome occurs when tissue pressure within a confined compartment threatens perfusion within and through the compartment. Compartment syndrome can be seen in upper and lower extremities, where there are multiple fascial compartments, as well as the abdomen. Abdominal compartment syndrome (ACS) was first described in 1863 by the French surgeon Etienne-Jules Marey, who described the relationship between respiratory function and intra-abdominal pressure.¹ The abdominal compartment is delineated by the pelvis, lumbar spine, abdominal musculature and soft tissues, diaphragm, and ribs. As described further below, ACS is defined by the World Congress on Abdominal Compartment Syndrome as sustained intra-abdominal hypertension (above 20 mm Hg; IAH) with attendant organ dysfunction.^2,3

The diagnosis of ACS should be considered in any patient with a tense or distended abdomen who also has hemodynamic instability, a falling urine output, mental status changes, progressive organ failure, or lactic acidosis. Development of ACS during ICU stay is an independent predictor of mortality, with high mortality in established ACS.⁴ Failure to recognize that IAH can occur without abdominal distension, or that multiorgan failure is a manifestation of ACS, is a potentially lethal error.

Paramount to defining IAH or ACS is how intra-abdominal pressure (IAP) is measured. Clinical examination has been shown to be inaccurate at indicating increased IAP.^5,6 Although there are clues to IAH on abdominal CT, definitive diagnosis requires estimation of IAP.⁷ Several techniques have been described,^8,9 but the most widely adopted method is to transduce the bladder pressure, a simple, safe, and inexpensive procedure.^3,9 The patient should be supine and the bladder catheter connected to a pressure transducer zeroed at the level of the superior iliac crest in the midaxillary line.² The catheter is instilled with 25 mL of sterile saline and the detrusor muscle is allowed to relax for 30 to 60 seconds. IAP is estimated as the bladder pressure at end expiration, although a case has been made to instead approximate the mean IAP by accounting for the impact of ventilation.¹⁰ Erroneous values can be obtained in the presence of abdominal muscle contraction, active expiration (common in ventilated patients, especially those with airflow obstruction),¹¹ bladder pathology, or if the bladder contains more than its unstressed volume. With careful attention to methodology, interrater reliability is quite good.¹² Methods for measuring IAP continuously have been described, relying on specialized bladder or gastric devices.¹³

Normally, IAP is roughly 0 mm Hg; however, pressures may be slightly higher in the obese.¹⁴ During critical illness, IAP is often mildly increased to 5 to 7 mm Hg due to volume resuscitation, positive pressure ventilation, fluid redistribution, or recent abdominal surgery.³ IAH is defined as sustained or repeated elevations of IAP of at least 12 mm Hg and graded by severity: Grade I (IAP 12-15 mm Hg), Grade II (IAP 16-20 mm Hg), Grade III (IAP 21-25 mm Hg), and Grade IV (IAP >25 mm Hg). Grade III or IV IAH with concurrent organ dysfunction defines ACS, which is classified as primary (when due to injuries or disease in the abdomen or pelvis such as acute pancreatitis, retroperitoneal hemorrhage, or abdominal trauma) and secondary, when associated with systemic inflammation from a nonabdominal cause, such as sepsis. A single, isolated measure of IAP greater than 20 mm Hg is not necessarily diagnostic of ACS, and serial measurements demonstrating sustained or repeated elevations are required for the diagnosis.^3,15 Recurrent IAH or ACS describes the redevelopment of IAH or ACS after treatment of the initial primary or secondary episode of IAH or ACS.

In health, the volume of abdominal contents is less than the unstressed volume of the abdominal cavity, so that IAP merely reflects atmospheric pressure. IAH results when the contents (normal structures plus edema, hematoma, ascites, gas, feces, fat, tumor, intravascular blood, etc) exceed the unstressed volume. Beyond this point, IAP rises in inverse relationship to the abdominal compliance. Conditions that increase compliance of the abdominal wall such as obesity, prior pregnancy, and cirrhosis appear to protect against ACS, whereas inflexible scars or burns increase the risk.^16,17 IAP can also be raised by extra-abdominal factors, such as retroperitoneal or pelvic hemorrhage, prone position,^18-20 and the effects of ventilation and positive end-expiratory pressure (PEEP),^21,22 which all reduce the unstressed volume of the abdomen.

Rising abdominal pressure has effects within and beyond the peritoneal contents. Since the driving pressure for visceral blood flow is the difference between arterial pressure and IAP, organ function is threatened as IAP rises.^23-27 This effect is amplified by decreased cardiac output, hemorrhage, and hypovolemia.²⁸ Thus, the abdominal perfusion pressure (APP; mean arterial pressure minus IAP) has been proposed as a superior measure of visceral perfusion, with a goal APP of 60 mm Hg,²⁹ but this has not yet been widely adopted. With IAH, gut mucosal blood flow is impaired as a function of both pressure and duration. When pressure is sufficiently high, intestinal permeability increases, translocation is facilitated, mitochondria are damaged, and the mucosa becomes necrotic.^30,31 A vicious cycle ensues in which IAH produces gut dysfunction, leading to more edema and inflammation, causing IAP to rise further. Direct compression of mesenteric veins increases venous pressure, promoting visceral edema and further increases in IAP that decrease gut perfusion.³²

RENAL EFFECTS

One of the hallmarks, and often the earliest sign, of ACS is oliguric acute kidney injury. IAH directly compresses the renal veins, increasing venous resistance and lowering glomerular filtration rate.^27,33,34 Direct pressure on the renal parenchyma may also play a role, as may ureteral compression at the renal pelvis. Further, because ACS depresses cardiac output, global and renal perfusion fall. Activation of the sympathetic nervous system and renin-angiotensin may compound the impact on the kidneys. Finally, the rise in central venous pressure (CVP) typically seen in ACS causes back pressure and reduced renal perfusion in a manner similar to the cardiorenal syndrome of acute decompensated heart failure.³⁵ In fact, the kidneys are particularly susceptible to IAH, 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 reduction in IAP often results in rapid improvement in urine output and GFR.^36-38 In addition to direct hemodynamic effects, injury may be mediated through primed neutrophils, endothelial cells, and macrophages and by elaborating proinflammatory cytokines in the systemic circulation.³⁹ These humoral mechanisms may also explain other extra-abdominal effects, such as those on the pulmonary circulation and intracranial pressure.

CARDIOVASCULAR EFFECTS

Elevation of the diaphragm by ACS raises pleural and juxtacardiac pressure, limiting right heart filling. At the same time, direct compression 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, right atrial and pulmonary artery occlusion pressures are often elevated because the juxtacardiac pressures are high. Thus, ACS is one of the causes of diastolic dysfunction. In addition, ACS raises left ventricular afterload, further depressing stroke volume.⁴¹ Hypotension is common in ACS, though blood pressure may not fall if sustained by systemic vasoconstriction. In normovolemia, mild increases in IAP to 15 mm Hg centralize blood, raising CVP and left ventricular end-diastolic pressure; greater IAP impedes cardiac filling.⁴⁰ Fluid loading may succeed in boosting cardiac output,⁴² although the rise in central venous pressures and creation of even greater abdominal hypertension may lead to a net negative effect on abdominal organ perfusion.

IAH has been reported to produce false-negative results when using passive leg raising to predict fluid responsiveness.⁴³ Presumably this reflects the fact that leg raising normally augments flow from the legs and splanchnic circulation through the vena cava, but this is impaired in ACS.

PULMONARY EFFECTS

As IAP rises, cephalad displacement of the diaphragm compresses the thorax, reducing functional residual capacity, increasing the work of breathing, and causing atelectasis, ventilation/perfusion inequality, shunt, and a rise in dead space.²⁶ In spontaneously breathing patients, IAH produces rapid, shallow breathing, hypoxemia, hypercapnia, and ventilatory failure.⁴² In mechanically ventilated patients, both peak and plateau pressures are elevated (with volume-preset modes) or tidal volumes fall (with pressure-preset modes). Pulmonary edema is also seen, in part due to systemic inflammation. In a group of burn patients undergoing decompressive laparotomy for ACS, relief of the abdominal pressure led to prompt improvement in peak airway pressures, static respiratory system compliance, ratio of PaO2 to FiO2, and airway resistance.⁴⁴

CENTRAL NERVOUS SYSTEM EFFECTS

There is a strong association between IAH and increased intracranial pressure, largely mediated by the effects of intra-abdominal pressure on central venous pressure.^45,46 In addition, intracranial hypertension may rely on nonhemodynamic mechanisms in some patients, and systemic inflammation may also play a role in central nervous system dysfunction. When systemic hypotension and increased intracranial pressure combine to decrease cerebral perfusion pressure, brain function may be critically compromised.

CLINICAL MANIFESTATIONS

ACS presents in myriad ways and affects multiple organ systems, making it difficult to detect on a background of sepsis, polytrauma, or systemic inflammation. Many of the signs can be predicted based on the pathophysiology described above and are summarized in Table 114-1. Foremost among these are oliguria, shock, and falling respiratory system compliance. Recalling that the inspiratory rise in pleural pressure depends largely on the chest wall compliance (for passively ventilated patients; see Chap. 48), an additional clue to IAH is a larger than normal rise in central venous (similarly pulmonary artery, pulmonary artery occlusion, and esophageal) pressure during inspiration (see Fig. 114-1).⁴⁷