Approach

ACS is most frequently seen in critically ill ICU patients. The diagnosis of ACS can be divided into 3 components: identification of patients at risk; recognition of clinical signs associated with the transition from intra-abdominal hypertension to ACS; and proactive measurements to confirm the suspected diagnosis.

Identifying risk factors enables earlier detection of intra-abdominal hypertension and ACS.[18] The classic clinical findings are of increased airway pressure, decreased urine output, and a tense abdomen on physical exam. However, these findings are nonspecific and often only clinically apparent once severe ACS is present. It is recommended that early and protocolized intra-abdominal pressure (IAP) monitoring be done in all those who present with two or more risk factors for intra-abdominal hypertension (IAH) or ACS.[1] Continuous IAP monitoring should be initiated as soon as intra-abdominal hypertension or ACS diagnosis is suspected. Factors involved in determining the frequency of IAP monitoring include the baseline pressure measurement, the ability to alter etiologic and risk factors, and the evolution of the clinical course.

History and examination

The key to diagnosis is to start monitoring IAP early in patients who are at risk. The main aim of the history is to identify these patients. Risk factors include excessive fluid resuscitation (>3 L in 24 hours), massive blood transfusion (>10 units in 24 hours), recent intra-abdominal infection/inflammation (especially peritonitis and pancreatitis), hemoperitoneum, ileus, pneumoperitoneum, loss of abdominal domain, diminished abdominal compliance, and a history of cirrhosis. The term "loss of abdominal domain" refers to a situation in which more of the viscera are located outside the abdominal cavity than inside because the abdominal cavity is unable to accommodate all of the abdominal contents within its fascial boundaries.

The main clinical sign is a tense, distended abdomen. Patients also have difficulty maintaining minute ventilation and oxygenation due to transmission of pressure to the torso. Later signs include oliguria progressing to anuria, hypotension, and an increase in peak airway pressure.

Monitoring of IAP

Protocolized monitoring of IAP is the only way to establish a diagnosis and should be done in all patients with two or more risk factors for IAH or clinical signs of ACS.[1] If baseline IAP is elevated, serial IAP measurements are performed.[1] The pressure should be monitored at least every 3 to 4 hours, but more frequent measurements are required if the pressure is elevated or the clinical condition is rapidly changing. This gives clinicians the opportunity to intervene early to prevent disease progression.

The abdominal perfusion pressure is the difference between the mean arterial BP and the IAP. It must be 60 mmHg or greater for organ perfusion to be adequately maintained. The diagnosis is established as follows:[1]

  • IAP greater than 12 mmHg indicates intra-abdominal hypertension, which is graded by severity: grade I (12 to 15 mmHg), grade II (16 to 20 mmHg), grade III (21 to 25 mmHg), and grade IV (>25 mmHg).

  • IAP greater than 20 mmHg (grade III or IV), with or without an abdominal perfusion pressure below 60 mmHg, with new-onset organ failure or dysfunction indicates ACS.

  • In pediatric patients, the exact IAP that signals the transition from intra-abdominal hypertension to ACS is not currently known, but an IAP greater than 10 mmHg with new-onset organ dysfunction has been proposed for children.[8] However, further research is needed to fully establish a threshold.

IAP is measured using a pressure transducer positioned in the bladder.[19][20][21] The bladder is catheterized and 25 mL of sterile saline is instilled into the bladder. The catheter tubing is clamped, and a needle is inserted via the specimen collection port proximal to the clamp or via a needleless side port and attached to a calibrated pressure transducer (zeroed at the level of the midaxillary line). An increase in the measured pressure with gentle palpation of the abdomen confirms a good fidelity of pressure transduction. To ensure accuracy and reproducibility, the pressure should be measured at end-expiration with the patient completely supine, as slight changes in the elevation of the head of the bed can significantly increase IAP measurements.[2][22][23] Abdominal muscle contractions should be absent, which can be achieved with the use of sedatives and, in rare instances, pharmacological paralysis. Also, the utilization of positive end expiratory pressure does not seem to affect measured IAP.[24]

Modifications of this system allow continuous measurement.[25][26][27] Devices are now commercially available that allow for measurement of transvesicular pressure without the use of a needle puncture and the associated risks of needle sticks.[28] IAP can be assessed via other intra-abdominal vantage points including the inferior vena cava, the rectum, or the abdominal cavity itself.[29][25] However, these methods are not routinely recommended.

Monitoring of organ function

Patients develop impaired organ function, which must be monitored. It is important to monitor the adequacy of perfusion, alterations in acid-base status, and organ function. Unexplained or worsening acidosis, impaired pulmonary function, and alterations in renal function are the most common manifestations of organ dysfunction seen with ACS. The following investigations are required:

  • Serum electrolytes, BUN, and creatinine are required to monitor renal function and associated electrolyte balance.

  • Arterial blood gas measurements are required to monitor acid-base disturbances. Acidosis is common, which is usually metabolic or mixed metabolic and respiratory.

  • BP should be monitored regularly; invasive monitoring may be required. It should be noted that an increase in IAP can lead to unreliability of measurements of central venous pressure or pulmonary artery occlusion pressure.

  • Oxygen saturation should be monitored in all patients.

  • Direct measurement of peak airway pressure is possible in mechanically ventilated patients; increased peak airway pressure is a late sign.

Radiologic investigations

Abdominal CT scan

  • This is frequently used to identify underlying intra-abdominal pathologic conditions. It is not used to assess a rise in IAP. However, a careful interpretation of the CT study can reveal associated signs of elevated IAP. The key sign is "circularization" of the transverse abdominal contour, as defined by increased ratio of the antero-posterior:transverse diameter, due to the increased pressure. If this sign is found, measurement and monitoring of IAP should be considered to provide a definitive diagnosis.[30][31][32][33]

Abdominal ultrasound

  • This is used to identify underlying intra-abdominal pathologic conditions and, increasingly in the ICU setting, to assess intravascular volume. If the ultrasound shows the presence of intra-abdominal fluid, renal vein compression, or inferior vena cava compression, measurement and monitoring of IAP should be considered to exclude intra-abdominal hypertension and ACS.[34]

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