Abdominal Compartment Syndrome
Abdominal compartment syndrome results from intra-abdominal hypertension with organ dysfunction after major abdominal trauma and surgery (primary syndrome), although other patients may develop the syndrome without surgery, for example, during massive fluid resuscitation following major trauma or burns (secondary syndrome). The syndrome results from massive edema of abdominal organs produced by shock-induced inflammatory mediators, excessive fluid resuscitation, surgical manipulation, and closure of the abdominal fascia. The significant cardiac, pulmonary, renal, gastrointestinal, hepatic, and CNS dysfunctions caused by this syndrome result in a high mortality rate.
Figure: Physiologic effects of abdominal compartment syndrome. Image in the
center is a patient whose abdomen was left open but covered with nonadhesive
dressing. Cdyn, dynamic pulmonary compliance; CO, cardiac output; CPP, cerebral
perfusion pressure; CVP, central venous pressure; GFR, glomerular filtration rate; ICP,
intracranial pressure; PAOP, pulmonary artery occlusion pressure; Paw, mean airway
pressure; pHi, intramucosal pH; PIP, peak inspiratory pressure; Qsp/Qt, intrapulmonary
shunt; SMA, superior mesenteric artery; SVR, systemic vascular resistance; Vd/Vt, dead
space ventilation. (Adapted from Cheatham ML. Intra-abdominal hypertension and
abdominal compartment syndrome. N Horizons. 1999;7:96.)
Clinically, a tense severely distended abdomen, raised peak airway pressure, CO2 retention, and oliguria should direct the clinician to measure the intravesical pressure, which reflects the intra-abdominal pressure, via a Foley catheter. Values above 20 to 25 mmHg may indicate inadequate organ perfusion and necessitate abdominal decompression, which, if delayed, may result in progression to multiorgan failure and death. Almost all of these patients require mechanical ventilation. If a PAC is in place, attributing a relatively high PCWP to the ventilator and continuing high-volume fluid infusion may further increase intra-abdominal edema and increase mortality. Interestingly, patients who will develop abdominal compartment syndrome often do not respond to fluid administration with elevated cardiac output, despite an increasing PCWP.
It should be emphasized that recent advances in the management of acute trauma and critical care, such as limiting crystalloid infusion, hemostatic resuscitation, damage control, and open abdomen strategies, have substantially decreased the incidence of postinjury abdominal compartment syndrome. Postinjury intra-abdominal hypertension still occurs commonly in severely injured high-risk patients, but it is not associated with multiorgan failure in most instances. In other words, unlike in the past, intra-abdominal hypertension is seldom a harbinger of abdominal compartment syndrome or multiorgan failure. It is believed that limiting crystalloid infusion is the most important factor in this salutary evolution.
LEVON M. CAPAN • SANFORD M. MILLER • COREY SCHER
