Abdominal compartment syndrome (ACS) is defined by the presence of organ dysfunction that can be attributed to elevated intra-abdominal pressure (IAP). ACS is the end result of a cumulative increase in IAP above the upper limit of normal (normal 5 to 11 mm Hg) to values defining intra-abdominal hypertension (IAH). IAH is defined as the sustained or repetitive pathologic elevation of IAP to 12 mm Hg or more and is graded and classified according to a four-tiered continuum articulated by consensus by the World Society of Abdominal Compartment Syndrome (WSACS; www.wsacs.org ; Table 75-1 ). To understand how best to prevent, identify, and treat IAH and ACS, one needs to understand the pathophysiology, monitoring, categorization, and management techniques before and after ACS is diagnosed.
| Grade | IAP (mm Hg) |
|---|---|
| I | 12-15 |
| II | 16-20 |
| III | 21-25 |
| IV | >25 |
Pathophysiology and Mechanism of Action
The pathophysiology of ACS is complex. Rising IAP provides a clue that changes in arterial inflow, venous outflow, and the space occupied by viscera and intra-abdominal fluid have created disequilibrium in the normal pressure-volume relationship. Typical adult IAP ranges from 0 to 5 mm Hg; however, obesity, pregnancy, and advanced age may elevate the baseline. A recent study showed that IAP increased between 0.14 and 0.23 mm Hg for each increase in body mass index unit and 0.20 mm Hg/year for advancing age. Open abdominal surgery also may elevate the measured IAP.
ACS may be further classified as primary, secondary, or recurrent. Primary ACS develops as a direct result of an abdominal injury or other surgical abdominal emergency (i.e., intestinal perforation or ischemia). Secondary ACS reflects a response to a condition that is not of primary abdominal origin (e.g., visceral edema and/or the acute accumulation of ascites secondary to massive volume resuscitation). Lastly, recurrent ACS develops after successful medical or surgical therapy for primary or secondary ACS. The classic example is IAP secondary to application of a temporary closure device used to secure an open abdomen after initial successful surgical decompression. Blood, ascites, or visceral edema (or any combination of the three) may increase the IAP and recreate the ACS. Likewise, external compression from an excessively tight binder may also dangerously elevate IAP. Regardless of cause, ACS affects every organ system in a deleterious fashion. Risk factors for the development of ACS are detailed in Table 75-2 .
| Acidosis (pH < 7.2) |
| Hypothermia (core temperature <33° C) |
| Massive transfusion (>10 U of packed red blood cells) or resuscitation (>5 L of colloid or crystalloid per 24 hours) |
| Coagulopathy (platelets <55,000 or activated partial thromboplastin >2 times normal or international normalized ratio >1.5) |
| Severe sepsis/septic shock (AECC definitions) regardless of source |
| Bacteremia |
| Intra-abdominal infection and/or abscess |
| Hepatic dysfunction or cirrhosis with ascites |
| Mechanical ventilation |
| Elevated PEEP or the presence of auto-PEEP |
| Abdominal surgery (especially with tight fascial closures or massive incisional hernia repair) |
| Disordered intestinal motility |
| Intestinal volvulus or intestinal obstruction (mechanical or functional) |
| Peritoneal or retroperitoneal space occupying lesions |
| Major burn injury |
| Major traumatic injury |
| Body mass index >30 kg/m 2 |
| Prone patient positioning |
| Acute pancreatitis |
| Damage control laparotomy |
| Laparoscopy with excessive inflation pressures |
| Peritoneal dialysis |
Diagnosis
Physical examination performs poorly as a diagnostic aid in IAH with a sensitivity of 60%.
Pressure-Volume Metrics
Pressure-volume metrics that aid in monitoring abdominal pressure include the following:
- 1.
Bladder pressures: IAP can be measured with an indwelling bladder catheter and the use of a protocolized transbladder technique that has been approved by the WSACS. Problematic measurements may result when the patient is agitated or not supine and when the transducer is not zeroed at the mid-axillary line.
- 2.
Abdominal perfusion pressure (APP), defined as
where a normal value is greater than 50 mm Hg.
Trending the APP may be a useful parameter to follow progression of IAH, but the absolute number does not define ACS. At this time, the WSACS makes “no recommendation” regarding APP as an endpoint of resuscitation or management.
Adjunctive Measurements
- 1.
A decreased urine output (UOP) may identify incipient acute kidney injury (AKI) secondary to rising IAP but is equally likely to reflect other problems (e.g., septic AKI, chronic kidney disease [stage III or greater]). UOP is not useful in anuric or dialysis-dependent patients.
- 2.
Elevated airway pressure may aid in identification of dynamic changes in abdominal pressure–volume relationships. When on volume-cycled ventilation, where the tidal volume (V T ) is fixed, increased abdominal pressure will increase peak airway pressures. In pressure controlled ventilation, in which the peak pressure is fixed, rising IAP will lead to a decreased V T . Escalating abdominal pressures will decrease the release volume on airway pressure release ventilation.
- 3.
Various other more sophisticated measures may track changes in pulmonary compliance, pulmonary elastance, and chest wall compliance but appear to provide less fidelity in presaging ACS than the measures noted above. Although ultrasound measurement of IVC diameter has proven useful in identifying hypovolemia, close correlation with IAP has not been noted.
Systemic Impact of ACS
Increased IAP results in dysfunction of the respiratory, cardiovascular, and renal systems. Elevated ICP and depressed cerebral perfusion pressure (CPP) also may result from increased IAP and ACS.
Cardiovascular System
Increases in IAP elevate intravascular and intrapleural pressures in a manner similar to progressively increased positive end-expiratory pressure (PEEP). Flow per unit time and the stroke volume per cardiac cycle are typically reduced, despite elevated intrathoracic pressures.
Cardiac output (CO) decreases progressively as the IAP increases, principally as a result of decreased venous return (VR), diminished pulmonary flow, and impairment of left ventricular filling. The magnitude of the decline in CO may depend on the patient’s intravascular volume. One animal study demonstrated a 53% decrease in CO in hypovolemia but only a 17% decrease in euvolemia. CO increased in hypervolemic animals. Thus hypovolemia exacerbates the cardiovascular effects of IAH and ACS.
Respiratory System
Progressive increases in IAP displace the hemidiaphragms cephalad, limiting alveolar filling and creating basilar and posterior alveolar collapse. As a result, adaptive hypoxic pulmonary vasoconstriction is activated and shunt increases. The decrease in pulmonary artery cross-sectional area creates a relative increase in pulmonary artery pressure, impairing right ventricular ejection. This sequence further decreases net pulmonary flow, exacerbating impaired oxygen (O 2 ) uptake and carbon dioxide (CO 2 ) off-loading. Complicating these untoward effects is progressive compression of the inferior vena cava (IVC), decreasing VR, further increasing IAP. Increasing PEEP to improve oxygenation and compliance may further impede VR. Plasma volume expansion may improve VR but can also increase extravascular lung water. It is clear that the management priority is to relieve the excessive IAH and to restore homeostasis. Alveolar recruitment should be an integral aspect of the management strategy and may help guide ventilation.
Renal System
The renal system is most readily evaluated by following UOP and laboratory data such as serum creatinine concentration. In patients with normal renal function, oliguria (UOP < 0.5 mL/kg/hr) is the most commonly identified initial abnormality of IAH. Although changes in creatinine as little as 0.3 mg/dL when accompanied by oliguria for 6 hours or more, meet criteria for AKI, an increase in the creatinine concentration is a late marker of impending AKI; thus, it is a poor index. Various more sensitive biomarkers (e.g., N -galactosamine) are gaining acceptance, but most have not been universally accepted. It is important to recall that AKI may also reflect distorted flow or nephrotoxins and that septic AKI is the most common cause of AKI in the critically ill. In animal models of ACS, decompression failed to restore normal biochemistry despite clearly restoring a normal IAP.
Although hypovolemic oliguria responds to volume expansion, the response in the presence of IAH and ACS is at best transient. Progressive compression of the IVC and renal veins is exacerbated by decreased flow secondary to compromised CO. These derangements compromise renal blood flow and glomerular filtration rate. Consequently, an inadequate renal filtration gradient and renal perfusion pressure may importantly affect the development of IAH-induced AKI. The filtration gradient is the pressure-driven mechanical force across the glomerulus and is determined by the difference between the glomerular filtration pressure (GFP) and the proximal tubular pressure (PTP). GFP is estimated by the difference between MAP and IAP, where GFP = MAP − 2(IAP). In the presence of IAH or ACS, PTP is assumed to be equal to the IAP. Consequently, changes in IAP are more likely to exert a greater effect on renal function than changes in MAP. Although IAP and renal vein compression recreate the findings of ACS in a laboratory model, extrinsic renal parenchymal compression does not. Interestingly, one model of Gerota fascia incision in the setting of visceral edema also helped reverse some abnormalities.
Nonrenal Viscera
As IAH progresses to ACS, increasing IAP can compromise splanchnic blood flow. Animal studies indicate that ileal and gastric mucosal blood flow are specifically effected. Hepatic arterial, portal venous, and hepatic microcirculatory blood flow decrease as IAH progresses and may impair hepatic energy production and small bowel tissue oxygen delivery and utilization. Unrelieved IAH creates physiology similar to nonocclusive mesenteric ischemia and may lead to intestinal infarction and the need for resection.
Central Nervous System
Because central nervous system activity is dependent on cerebral blood flow, IAP increases that decrease CO and elevate central venous pressure (CVP) may compromise CPP (MAP—either CVP or intracranial pressure [ICP], whichever is higher). Although under normal conditions CVP exceeds ICP, the common association of abdominal injury and traumatic brain injury may make ICP clinically relevant. Indeed, animal studies indicate that elevated IAP increased ICP and decreased CPP, an effect reversed by decompression.
Ocular System
The ACS has been associated with the rupture of retinal capillaries, resulting in the sudden onset of decreased central vision (Valsalva retinopathy). The mechanism behind this clinical entity is likely related to the venous hypertension stemming from increased intrathoracic pressure and impeded central VR. Retinal hemorrhage usually resolves within days to months, and no specific treatment is necessary. This diagnosis should be considered in any patient with ACS who develops visual changes.
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