Mike Cannon, age 57, is admitted to the intensive care unit (ICU) with septic shock from pyelonephritis and undergoes aggressive early sepsis resuscitation. After 6 hours, he has received 10 L of I.V. fluid. He’s also receiving a norepinephrine drip to maintain adequate blood pressure. His mean arterial pressure (MAP) is 55 mm Hg; pulse, 126 beats/minute; respiratory rate, 14 breaths/minute with a ventilator; central venous pressure, 24 mm Hg; and temperature, 101° F (38.4° C). Urine output for the last 6 hours is 35 mL. His chest X-ray shows bilateral diaphragm elevation, atelectasis, and massively distended air-filled bowel loops.
Based on these findings, Mr. Cannon’s nurse recognizes that abdominal compartment syndrome (ACS) may be developing and measures his intra-abdominal pressure at 31 mm Hg—a dangerously high reading. What should this nurse do next?
Defining ACS and IAH
To answer that question, let’s first review what ACS is. As you know, compartment syndrome results when the pressure in a closed anatomic space becomes so elevated that blood flow is compromised and tissue ischemia develops. Usually, we think of compartment syndrome as developing in the arms or legs as a complication of orthopedic trauma—a condition that requires urgent surgical fasciotomy. But compartment syndrome can develop in any closed anatomic space, such as the skull, thorax, or abdomen.
ACS develops when a massive, systemic inflammatory response and aggressive fluid resuscitation cause tissue edema in the abdominal compartment. As fluid accumulates, the abdominal wall and fascia are slowly stretched, making them less compliant and increasing pressure in the abdominal cavity. As intra-abdominal pressure (IAP) rises, blood flow to the heart, kidneys, and gut decreases, causing progressive organ dysfunction and failure. (See How intra-abdominal hypertension causes organ dysfunction by clicking on the download now button below.)
Pressure greater than 12 mm Hg is called intra-abdominal hypertension (IAH); the spectrum of organ dysfunctions that results from IAH is called ACS.
Any patient who develops a significant systemic inflammatory response and a resulting increase in capillary permeability is at risk for IAH/ACS. Several epidemiologic studies show that IAH/ACS is common in all ICU populations, including pediatric, medical, cardiothoracic, surgical, and neurologic. (See Risk factors for intra-abdominal hypertension by clicking on the download now button below.)
Your role in detecting rising pressure
Usually, an abdominal examination won’t detect elevated IAP, but a nurse will. A nurse may note subtle changes that suggest IAH—such as a rise in peak inspiratory pressure, a drop in urine output, and mild trends toward higher central venous pressure and lower MAP. By being aware of a patient’s risk factors for IAH/ACS and monitoring the patient closely, you can detect the developing problem early on.
Because more than 30% of ICU patients develop IAH, international consensus guidelines recommend that all patients at risk have frequent intra-abdominal pressure measurements taken via the bladder. Bladder pressure accurately reflects intra-abdominal pressure, and it’s easy to measure using a urinary catheter.
Every ICU should have written nursing guidelines for measuring bladder pressure. Results that are inaccurate or difficult to reproduce can lead to delays in care or inappropriate procedures, causing harm to the patient. The guidelines should include patient assessment and education sections and a checklist of the steps needed to obtain accurate data. The guidelines should also specify a reliable monitoring device that allows frequent IAP measurements to detect IAH before ACS develops. Devices that allow noninvasive, rapid, reliable IAP monitoring with little nursing effort include the AbViser (www.wolfetory.com), the FoleyManometer (www.holtech-medical.com), the IAP-Monitor (www.spiegelberg.de), and the CiMON (www.pulsion.com). (See Measuring intra-abdominal pressure by clicking on the download now button below.)
Managing pressure, improving outcomes
Because IAH/ACS occurs in many critically ill populations, therapy must be tailored to a patient’s specific needs. Still, the same principles apply to all patient groups:
• Use serial IAP monitoring to detect rising pressures early.
• Optimize tissue perfusion and organ function with adequate fluid and pressor support.
• Intervene to lower IAP before organ dysfunction is overt.
• Use prompt surgical decompression for refractory IAH.
Using these principles can prevent ACS and improve outcomes. IAH and ACS substantially increase morbidity (renal insufficiency and failure, delayed ventilator weaning, ventilator-induced lung injury, and mesenteric ischemia) and mortality. Plus, these conditions nearly double both ICU and hospital lengths of stay. Increasing data show that aggressive IAP monitoring and protocol-driven interventions improve patient survival and result in fewer organ failures, more rapid recoveries, and shorter lengths of stay. (See Addressing intra-abdominal hypertension by clicking on the download now button below).
Today, temporary abdominal closure to prevent ACS is a standard surgical technique that improves outcomes in high-risk trauma, pancreatitis, and vascular-surgery patients. Certain nonsurgical interventions have also improved outcomes. Renal replacement therapy and paracentesis can effectively treat severe pancreatitis with IAH before organ failure can develop. Two prospective trials note that these interventions reduce mortality from the 20%-to-30% range to the 6%-to-10% range and reduce ICU lengths of stay.
Another study indicates that protocol-driven interventions combining early medical therapy with aggressive surgical intervention dramatically improve outcomes and reduce cost. This study shows a mortality decrease from 49% to 29% and a decrease in hospital length of stay from 29 days to 18 days. The authors conclude that evidence-based strategies for IAH/ACS lead to significant improvements in survival and faster returns to normal function. You can find the recommended protocol at www.wsacs.org.
Mr. Cannon’s outcome
Now, let’s return to Mr. Cannon and the question of what to do after detecting a dangerously high IAP. The nurse caring for this patient immediately consults a surgeon, who schedules a decompressive laparotomy. Before surgery, several interventions are implemented simultaneously.
After being placed in the supine position to expand his abdominal space, the patient receives a sedative and cisatracurium (Nimbex), a neuromuscular blocker. He also has nasogastric and rectal tubes inserted and placed on suction.
An hour later, Mr. Cannon’s MAP is 84 mm Hg; his IAP is 12 mm Hg; he produces 210 mL of urine; and his norepinephrine drip is discontinued. Thus, he doesn’t need surgery. On day 3, he’s extubated and transferred from the ICU. Clearly, he benefited from having an alert nurse who recognized subtle signs and symptoms early, measured his IAP, and consulted a surgeon stat.
Like Mr. Cannon, all high-risk patients need IAP monitoring to ensure early detection and intervention. Waiting for ACS to cause multiple organ failure is no longer accepted critical-care practice. Today, the goal is to prevent ACS-induced organ failure, using early monitoring, early interventions, and, if needed, early surgical decompression.
Brush KA. Abdominal compartment syndrome: the pressure is on. Nursing. 2007;37(7):36-41.
Cheatham ML, Malbrain ML, Kirkpatrick A, et al. Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. II. Recommendations. Intensive Care Med. 2007;33(6):951-962.
Kimball EJ, Mone MC, Wolfe TR, Baraghoshi GK, Alder SC. Reproducibility of bladder pressure measurements in critically ill patients. Intensive Care Med. 2007;33(7):1195-1198.
Malbrain ML, Chiumello D, Pelosi P, et al. Incidence and prognosis of intraabdominal hypertension in a mixed population of critically ill patients: a multiple-center epidemiological study. Crit Care Med. 2005;33(2):315-322.
Wolfe TR, Gallagher J. Intra-abdominal hypertension: pitfalls, prevalence and treatment options. AACN News. 2006;23(10):1-8.
Timothy R. Wolfe is an Adjunct Associate Professor in the Department of Surgery at the University of Utah School of Medicine in Salt Lake City.