Intra-abdominal hypertension monitoring

Our columnist outlines the dangers of intra-abdominal hypertension and its sequela, abdominal compartment syndrome.


Many hospitalists have never heard of intra-abdominal hypertension (IAH), or its life-threatening sequela, abdominal compartment syndrome (ACS). Most hospitalists are internists, and IAH and ACS are commonly thought of as surgical issues. But any patient with large volume resuscitation (>5 liters) or a major intra-abdominal inflammatory process like severe pancreatitis is at risk of undergoing this process.

Consider a patient with severe pancreatitis who has a massive inflammatory stimulus in his retroperitoneum. This can trigger the development of systemic inflammatory response syndrome, with systemic pro-inflammatory cytokines causing capillary leak within the bowel and mesentery, as well as lungs and soft tissues. Concomitant ileus and increased bowel luminal contents contribute to mass effect.

Despite its large volume capacity, the abdominal compartment space is not unlimited. Intra-abdominal pressure is normally 0-5 mm Hg. Once the pressure rises over 10 mm Hg, mesenteric venous flow becomes compromised, leading to bowel congestion and further edema. As pressure rises further, abdominal compartment syndrome develops, with compromised venous and arterial flow to intra- and retroperitoneal organs, bowel ischemia, infarct, perforations, necrosis, and multiple organ system failure possible. Acute renal failure may occur. Aggressive volume resuscitation contributes to mesenteric edema. The high intra-abdominal pressure compromises diaphragmatic compliance, resulting in high airway pressures, and inability to adequately ventilate and oxygenate the patient. Depressed cardiac venous return causes poor cardiac output, hypotension, and further inadequate systemic tissue perfusion, completing the vicious cycle. Shock, metabolic and respiratory acidosis, refractory hypoxia, anuria and death may all occur within hours of onset of IAH.

Even experienced surgeons have difficulty accurately diagnosing IAH. The process is clinically silent until organ failure manifests, when potentially irreversible damage has already occurred. Many of us believe we can poke on an abdomen and decide if it feels too hard, but venous congestion can be happening long before that point. We can also be fooled by the central venous pressure (CVP) or pulmonary capillary wedge pressure (PCWP), as these may be artificially elevated by IAH and ACS. We must maintain a high level of suspicion for IAH and/or ACS in patients with certain conditions who have unexplained organ dysfunction. These conditions include: severe pancreatitis; massive volume resuscitation in shock state; multiple trauma, with or without abdominal trauma; ruptured aortic abdominal aneurysm; abdominal hemorrhage: intraperitoneal or retroperitoneal; massive ascites; peritoneal dialysis; abdominal mass; severe ileus or bowel obstruction; severe colitis; vasopressors to maintain organ perfusion; and laparotomy with fascial closure.

Better yet, we should already be monitoring these patients' abdominal pressures to avoid unexplained organ dysfunction.

The World Society of the Abdominal Compartment Syndrome has an algorithm of recommended nonoperative management available on its Web site. Medical management consists of five interventions:

  • Evacuate intraluminal contents
  • Evacuate extraluminal contents
  • Improve abdominal wall compliance
  • Optimize fluid administration
  • Optimize tissue perfusion

Surgical decompression is indicated if IAH or ACS is refractory to medical management.

Bladder pressure has been shown to be an accurate form of intra-abdominal pressure measurement. Commercially available kits can provide standardized equipment and improve accuracy. Bladder-pressure monitoring using a closed system does not increase the risk of urinary tract infection.

However, many ICUs use homemade systems. These systems vary with the institution, but can consist of clamping the existing Foley drain port, connecting the sampling port to a transducer through a stopcock, injecting saline through the Foley sampling port to fill the bladder, and then measuring the bladder pressure. There are many problems with this approach. The necessity of gathering multiple pieces of equipment may delay or inhibit the implementation of bladder pressure monitoring, thus causing IAH to go unrecognized. There is no standard or quality control for this method, and trending data is not possible. An under- or overfilled bladder may result in incorrect readings, as can inter-user variability. ICU managers and directors using homemade systems should undertake quality control measures to ensure accuracy, or consider using commercially available kits already tested for accuracy and safety.

In addition to equipment and user-related errors, several patient-related issues require attention. Thoracic and abdominal wall muscular activity may cause erroneous readings. Respiratory effort that is asynchronous with the ventilator, coughing or patient movement may affect readings. Abdominal binders or muscular guarding may falsely elevate IAP. Variations in patient position such as Trendelenburg, reverse Trendelenburg, or elevated head of bed may affect results as well. In some cases, heavy sedation or even temporary neuromuscular blockade may be necessary for accurate readings.