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Recognition and Treatment of Abdominal Compartment Syndrome Following Ruptured Abdominal Aortic Aneurysm Repair


Abdominal compartment syndrome (ACS) and intraabdominal hypertension (IAH) caused by elevated intraabdominal pressure (IAP) are commonly encountered in patients with ruptured abdominal aortic aneurysms (AAAs) and carry a high morbidity and mortality risk ( Table 1 ). However, IAH/ACS are still overlooked by many physicians and therefore timely diagnosis is not made and treatment is often inadequate.

TABLE 1
Incidence and Mortality of Abdominal Compartment Syndrome in Patients with Ruptured Abdominal Aortic Aneurysm and Relation to Type of Repair
Author Year Treatment No. of Patients ACS MORTALITY
No. % ACS − ACS +
Metha 2013 EVAR 136 32 24 18 59
Djavani 2011 OR 108 20 19 — —
Djavani 2011 EVAR 29 3 10 10% 33%
Starnes 2009 OR 24 6 25 44% 83%
Starnes 2009 EVAR 27 2 7 16% 50%
Mayer 2009 EVAR 102 27 22 9% 26%
Mehta 2005 EVAR 30 6 20 13% 57%
Papavassiliou 2003 OR 22 6 27 25% 100%
Foy 2003 OR 21 4 20 — 5×
Rasmussen 2002 OR 135 45 33 9% 56%
Oehlschlager 1997 OR 38 8 21 50% 73%
Fietsam 1989 OR 100 4 4 First description
ACS (+/-), Abdominal compartment syndrome (yes/no); EVAR , endovascular aneurysm repair; OR , open repair.

Detection

The World Society of the Abdominal Compartment Syndrome (WSACS) has first brought order into the chaos of differing definitions of IAH and ACS by publishing part one of the WSACS Consensus Definitions and Recommendations in 2006. In this document, state-of-the-art definitions for IAH and ACS are proposed based upon current medical evidence as well as expert opinion. In 2013, these consensus definitions and recommendationshave been revised and resulted in updated consensus definitions and clinical practice guidelines ( Box 1 ).

BOX 1
World Society of the Abdominal Compartment Syndrome Consensus Definitions

  • Definition 1: IAP is the pressure concealed within the abdominal cavity.

  • Definition 2: APP = MAP – IAP

  • Definition 3: Filtration gradient = GFP – PTP = MAP – 2 × IAP

  • Definition 4: IAP should be expressed in millimeters of mercury and measured at end expiration in the complete supine position after ensuring that abdominal muscle contractions are absent and with the transducer zeroed at the level of the midaxillary line.

  • Definition 5: The reference standard for intermittent IAP measurement is via the bladder, with a maximum instillation volume of 25 mL of sterile isotonic saline.

  • Definition 6: Normal IAP is approximately 5–7 mm Hg in critically ill adults.

  • Definition 7: IAH is defined by sustained or repeated pathologic elevation of IAP ≥12 mm Hg.

  • Definition 8: IAH is graded as follows:

    • Grade I: IAP 12–15 mm Hg

    • Grade II: IAP 16–20 mm Hg

    • Grade III: IAP 21–25 mm Hg

    • Grade IV: IAP >26 mm Hg

  • Definition 9: ACS is defined as a sustained IAP >20 mm Hg (with or without an APP <60 mm Hg) that is associated with new organ dysfunction or failure

  • Definition 10: Primary ACS is a condition associated with injury or disease in the abdominopelvic region that often requires early surgical or interventional radiologic intervention.

  • Definition 11: Secondary ACS refers to conditions that do not originate from the abdominopelvic region.

  • Definition 12: Recurrent ACS refers to the condition in which ACS redevelops following previous surgical or medical treatment of primary or secondary ACS.

ACS, Abdominal compartment syndrome; APP, abdominal perfusion pressure; GFP, glomerular filtration pressure; IAH, intraabdominal hypertension; IAP, intraabdominal pressure; MAP, mean arterial pressure; PTP, proximal tubular pressure.

Routine surveillance for IAH and ACS should be implemented in patients treated for ruptured AAA in every intensive care unit, and a steady education program should be provided for all staff involved in managing those patients. Clinical examination alone has been shown to be inaccurate in estimating IAP. Hence, a variety of methods have been published regarding how to best measure or monitor abdominal pressure. Extensive research has shown that IAP can reliably be measured via the transvesical route by measuring either continuous or intermittent bladder pressure. One quick and simple way to assess IAP is to use an existing three-way Foley catheter (FoleyManometer, Holtech Medical, Charlottenlund, Denmark) connected to the patient’s urine catheter, using the patient’s own urine as a pressure medium (zero established at the iliac crest in the midaxillary line level). A higher incidence of urinary tract infections accompanying these instrumentations has not been proved.

The WSACS website ( www.wsacs.org ) provides several links to educational movies showing various techniques of measuring bladder pressure with different industrially assembled IAP measurement kits (see Education, IAP techniques [requires password]). It is generally regarded as less important which method is used for IAP measurement so long as IAP is routinely measured. IAP values should always be expressed as mm Hg (1 mm Hg = 1.36 cm H 2 O).

Unresolved issues remain, such as how much fluid should be instilled into the bladder to measure IAP, in which position IAP should be measured, and what the confounders would be for adequate IAP measurement. To date, a maximal instillation volume of 25 mL sterile saline in the adult is recommended. It is generally advised to carry out the IAP measurement in the supine position. However, a significant number of patients with ruptured AAA need the head of the bed elevated in the intensive care unit, and recent clinical trials have demonstrated that in this position IAP measurements increase significantly. The true impact of this unresolved issue is unclear, and to date, measurement in the supine position remains the standard. Bladder compliance alterations have been shown to be a confounder for IAP measurement. This fact underlines the WSACS recommendation to instill a maximum of 25 mL of saline before measurement.

When transvesical IAP measurement is contraindicated, intragastric IAP measurement is a valuable alternative to the standard bladder pressure measurement.

It is important to realize that detection of ACS should not be reduced to IAP measurement. Abdominal perfusion pressure (APP) should always be monitored and maintained at more than 50 to 60 mm Hg. Certain patients, formally not qualifying for the diagnosis of ACS (e.g., IAP of 18 mm Hg), can nonetheless suffer from ACS when the mean arterial pressure (MAP) drops below a certain critical value (e.g., owing to sepsis). Furthermore, absolute IAP values must be weighed against the clinical condition of the patient. Individual patients with an IAP greater than 20 mm Hg might not experience organ dysfunction and demonstrate adequate APP as a result of a high MAP.

Pathophysiology

Significant physiologic derangements occur as a result of IAH and affect not only the intraabdominal organs but also every organ system in the body (polycompartment syndrome). All of these pathophysiologic derangements are potentially reversible if IAH is recognized and rapidly treated before significant organ dysfunction has developed. If these derangements are prolonged or untreated, subsequent organ failure occurs at variable pressure thresholds (specific for each organ system) owing to inappropriate tissue perfusion ( Figure 1 ). Preexisting comorbidities, such as chronic kidney failure, pulmonary disease, or cardiovascular disease can further reduce the threshold of IAH that causes the clinical manifestations of ACS.

FIGURE 1, Basic pathophysiology and consequences of intraabdominal hypertension and abdominal compartment syndrome. RAAA, Ruptured abdominal aortic aneurysm; MOF, multiple organ failure.

Cardiovascular Derangements

Venous return is significantly reduced by the increased intrathoracic pressure through cephalad deviation of the diaphragm, resulting in reduced cardiac output at an IAP of only 10 mm Hg. Hypovolemia as encountered in patients with ruptured AAA can further lower the threshold for organ dysfunction. Increased intrathoracic pressure can cause direct cardiac, vascular, and pulmonary compression, further reducing cardiac output owing to an increased afterload. Furthermore, cardiac preload is reduced by the reduction of venous return from the lower extremities.

Pulmonary Derangements

Compression of the pulmonary parenchyma through direct IAP transmission and cranial deviation of the diaphragm leads to pulmonary dysfunction at an IAP of 16 to 30 mm Hg. Patients with shock or hypotension are particularly affected. Furthermore, parenchymal compression reduces pulmonary capillary blood flow, leading to decreased carbon dioxide excretion and an increased alveolar dead space. The intrapulmonary shunt fraction increases owing to decreased oxygen transport across the pulmonary capillary membrane. Peak inspiratory and mean airway pressures are significantly increased, potentially leading to alveolar barotrauma. In combination, these effects eventually result in arterial hypoxemia and hypercarbia.

Renal Derangements

IAH reduces renal blood flow, resulting in oliguria at an IAP of 15 mm Hg and anuria at an IAP of 30 mm Hg. Compression of the renal vein induces a significant elevation of renal vein pressure and renal vascular resistance, shunting blood away from the renal cortex and leading to impaired glomerular and tubular function. Reduced cardiac output further exacerbates the renal dysfunction.

Gastrointestinal Derangements

The bowel reacts most sensitively of all the organ systems to elevations in IAP. Reductions in mesenteric blood flow can appear with an IAP as low as 10 mm Hg. Venous hypertension caused by compressed thin-walled mesenteric veins and the resulting intestinal edema further increase IAH. The intestinal mucosal perfusion deficit can result in the loss of the mucosal barrier and subsequent development of bacterial translocation, sepsis, and multisystem organ failure (see Figure 1 ). Hypovolemia or hemorrhage aggravates the negative effects of IAH on mesenteric perfusion.

Hepatic Derangements

IAH reduces hepatic function at IAP levels of only 10 mm Hg, even in the presence of both normal cardiac output and mean arterial blood pressure. Decreased cardiac output directly affects hepatic artery flow. Compression of the liver and anatomic narrowing of the hepatic veins as they pass through the diaphragm result in decreased hepatic and portal venous flow. The impaired hepatic microcirculatory blood flow leads to hepatic mitochondrial dysfunction, decreasing the production of energy substrates as well as lactic acid clearance.

Central Nervous System Derangements

IAH directly affects cerebral perfusion and function. Additionally, intracranial pressure may be directly affected by elevations in intraabdominal and intrathoracic pressure and can result in significant reductions in cerebral perfusion pressure. Intrathoracic pressure impairs venous return from the cranium and decreases cerebral venous blood flow, leading to intracerebral venous pooling. Hypovolemia can further worsen already marginal cerebral perfusion.

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