A 40-year-old man is evaluated in the hospital after being admitted for acute alcohol-induced pancreatitis 24 hours ago. He has been receiving aggressive intravenous hydration and pain control. Over the past 2 hours, the patient has become increasingly restless and now reports difficulty breathing and abdominal distension. Blood pressure is 80/60 mm Hg, pulse is 122/min, and respirations are 28/min. Heart and lung sounds are normal. The abdomen is significantly distended and tense. Bowel sounds are decreased. Bilateral lower extremity and flank edema are present. Chest x-ray reveals basilar atelectasis but no other infiltrates. His urine output has markedly decreased over the past 2 hours. Which of the following pathophysiologic changes are most likely present in this patient at this time compared to a few hours earlier?
Abdominal compartment syndrome | |
Etiology |
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Clinical manifestations |
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Management |
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CVP = central venous pressure; NG = nasogastric. | |
This patient has been receiving aggressive fluid resuscitation in the setting of acute pancreatitis, an inflammatory condition that can cause abdominal swelling from visceral edema, intraabdominal third spacing of fluids, and ileus (evidenced by decreased bowel sounds). Now, he has a tensely distended abdomen and clinical signs concerning for abdominal compartment syndrome (ACS), including difficulty breathing and basilar atelectasis (from diaphragmatic elevation causing lung compression) and decreased urine output (from increased intraabdominal pressure reducing renal perfusion).
ACS occurs when a rise in intraabdominal pressure (IAP) reduces abdominal organ perfusion to the point of causing organ dysfunction. Because elevated IAP is transmitted to the thoracic cavity through the diaphragm, ACS also has significant cardiovascular consequences:
Increased intraabdominal and intrathoracic pressure cause extrinsic venous compression, resulting in elevated central venous pressure (CVP) (Choice B).
The compression restricts vena cava blood flow and decreases venous return to the heart (ie, cardiac preload). Although reduced cardiac preload is typically reflected in a low CVP, the two are uncoupled in ACS, where CVP is increased (despite reduced preload) due to external compression rather than increased intravenous volume.
Diaphragmatic elevation compresses the heart and decreases ventricular filling.
Decreased cardiac preload and ventricular filling lead to decreased cardiac output, hypotension, and compensatory tachycardia (Choice E).
(Choice C) Increased IAP from ACS causes increased compression of the intraabdominal venous drainage, including the inferior vena cava and iliac veins; back pressure to the lower extremities results in increased (vs decreased) venous hydrostatic pressure and, often, peripheral edema.
(Choice D) Abdominal wall compliance cannot increase in the acute setting; therefore, a relatively small volume of rapidly accumulating intraabdominal fluid can markedly increase IAP and cause ACS. In contrast, progressive abdominal wall stretching over time (eg, weeks) may greatly increase abdominal wall compliance, allowing large fluid volumes (eg, >15 liters) to be accommodated without causing ACS.
Educational objective:
The increased intraabdominal and intrathoracic pressure seen in abdominal compartment syndrome can cause significant cardiovascular consequences, including venous compression with increased central venous pressure, decreased venous return to the heart (decreased cardiac preload), and decreased cardiac output.