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1084 PART 10: The Surgical Patient

CHAPTER Abdominal Compartment although a case has been made to instead approximate the mean IAP
by accounting for the impact of ventilation. Erroneous values can
10
114 Syndrome be obtained in the presence of abdominal muscle contraction, active
expiration (common in ventilated patients, especially those with airflow
11
Adam Schlichting obstruction), bladder pathology, or if the bladder contains more than
Gregory A. Schmidt its unstressed volume. With careful attention to methodology, interrater
reliability is quite good. Methods for measuring IAP continuously have
12
been described, relying on specialized bladder or gastric devices. 13
KEY POINTS Normally, IAP is roughly 0 mm Hg; however, pressures may be
slightly higher in the obese. During critical illness, IAP is often
14
• Abdominal compartment syndrome (ACS) is caused by an acute mildly increased to 5 to 7 mm Hg due to volume resuscitation, posi-
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increase in intra-abdominal pressure resulting from a number of tive pressure ventilation, fluid redistribution, or recent abdominal
medical and surgical conditions. surgery. IAH is defined as sustained or repeated elevations of IAP of
3
• Abdominal compartment syndrome and intra-abdominal hyper- at least 12 mm Hg and graded by severity: Grade I (IAP 12-15 mm Hg),
tension are often unrecognized causes of organ dysfunction in Grade II (IAP 16-20 mm Hg), Grade III (IAP 21-25 mm Hg), and Grade IV
critically ill patients. (IAP >25 mm Hg). Grade III or IV IAH with concurrent organ dysfunc-
• The reference standard for measurement of intra-abdominal tion defines ACS, which is classified as primary (when due to injuries
pressure is via bladder catheter using a standardized protocol. or disease in the abdomen or pelvis such as acute pancreatitis, retroperi-
• Primary ACS results from direct, abdominopelvic pathology, toneal hemorrhage, or abdominal trauma) and secondary, when associ-
whereas secondary ACS does not. ated with systemic inflammation from a nonabdominal cause, such as
sepsis. A single, isolated measure of IAP greater than 20 mm Hg is not
• By elevating the diaphragm and decreasing respiratory system necessarily diagnostic of ACS, and serial measurements demonstrat-
compliance, ACS causes a restrictive respiratory defect. However, ing sustained or repeated elevations are required for the diagnosis.
3,15
ACS affects a number of other organs, especially the kidneys, and Recurrent IAH or ACS describes the redevelopment of IAH or ACS after
may cause multiorgan system failure. treatment of the initial primary or secondary episode of IAH or ACS.
• Diagnosis relies on maintaining a high degree of clinical sus-
picion, measurement of intra-abdominal bladder pressure, and PATHOPHYSIOLOGY
identification of organ dysfunction.
• The abdomen should be decompressed before critical organ In health, the volume of abdominal contents is less than the unstressed
dysfunction develops. volume of the abdominal cavity, so that IAP merely reflects atmospheric
• Failure to recognize and treat ACS portends a poor prognosis. 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 relation-
ship to the abdominal compliance. Conditions that increase compliance
of the abdominal wall such as obesity, prior pregnancy, and cirrhosis
DEFINITION AND DIAGNOSIS appear to protect against ACS, whereas inflexible scars or burns increase
Compartment syndrome occurs when tissue pressure within a the risk. 16,17 IAP can also be raised by extra-abdominal factors, such as
confined compartment threatens perfusion within and through retroperitoneal or pelvic hemorrhage, prone position, 18-20 and the effects
the compartment. Compartment syndrome can be seen in upper and of ventilation and positive end-expiratory pressure (PEEP), 21,22 which all
lower extremities, where there are multiple fascial compartments, as reduce the unstressed volume of the abdomen.
well as the abdomen. Abdominal compartment syndrome (ACS) was Rising abdominal pressure has effects within and beyond the perito-
first described in 1863 by the French surgeon Etienne-Jules Marey, who neal contents. Since the driving pressure for visceral blood flow is the dif-
described the relationship between respiratory function and intra-abdominal ference between arterial pressure and IAP, organ function is threatened
pressure. The abdominal compartment is delineated by the pelvis, lum- as IAP rises. 23-27 This effect is amplified by decreased cardiac output,
1
28
bar spine, abdominal musculature and soft tissues, diaphragm, and ribs. hemorrhage, and hypovolemia. Thus, the abdominal perfusion pressure
As described further below, ACS is defined by the World Congress on (APP; mean arterial pressure minus IAP) has been proposed as a superior
29
Abdominal Compartment Syndrome as sustained intra-abdominal hyper- measure of visceral perfusion, with a goal APP of 60 mm Hg, but this
tension (above 20 mm Hg; IAH) with attendant organ dysfunction. 2,3 has not yet been widely adopted. With IAH, gut mucosal blood flow is
The diagnosis of ACS should be considered in any patient with a impaired as a function of both pressure and duration. When pressure is
tense or distended abdomen who also has hemodynamic instability, a sufficiently high, intestinal permeability increases, translocation is facili-
falling urine output, mental status changes, progressive organ failure, or tated, mitochondria are damaged, and the mucosa becomes necrotic. 30,31
lactic acidosis. Development of ACS during ICU stay is an independent A vicious cycle ensues in which IAH produces gut dysfunction, leading
predictor of mortality, with high mortality in established ACS. Failure to more edema and inflammation, causing IAP to rise further. Direct
4
to recognize that IAH can occur without abdominal distension, or that compression of mesenteric veins increases venous pressure, promoting
multiorgan failure is a manifestation of ACS, is a potentially lethal error. visceral edema and further increases in IAP that decrease gut perfusion. 32
Paramount to defining IAH or ACS is how intra-abdominal pressure ■
(IAP) is measured. Clinical examination has been shown to be inac- RENAL EFFECTS
curate at indicating increased IAP. Although there are clues to IAH on One of the hallmarks, and often the earliest sign, of ACS is oliguric
5,6
abdominal CT, definitive diagnosis requires estimation of IAP. Several acute kidney injury. IAH directly compresses the renal veins, increasing
7
techniques have been described, but the most widely adopted method venous resistance and lowering glomerular filtration rate. 27,33,34 Direct
8,9
is to transduce the bladder pressure, a simple, safe, and inexpensive pressure on the renal parenchyma may also play a role, as may ureteral
procedure. The patient should be supine and the bladder catheter compression at the renal pelvis. Further, because ACS depresses cardiac
3,9
connected to a pressure transducer zeroed at the level of the superior output, global and renal perfusion fall. Activation of the sympathetic
iliac crest in the midaxillary line. The catheter is instilled with 25 mL nervous system and renin-angiotensin may compound the impact on
2
of sterile saline and the detrusor muscle is allowed to relax for 30 to the kidneys. Finally, the rise in central venous pressure (CVP) typi-
60 seconds. IAP is estimated as the bladder pressure at end expiration, cally seen in ACS causes back pressure and reduced renal perfusion in

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