ACS occurs from increased intra-abdominal pressure. Richardson described elevated end-inspiratory pressures and hypoperfusion secondary to a low cardiac output (CO) associated with ACS.¹ Impaired venous return and high peak inspiratory pressure with hypercarbia were present, causing hypoperfusion and severe pulmonary dysfunction. Early surgical decompression is mandatory, and a better outcome is associated with early detection. Release of the restrictive abdominal pressure will result in the correction of organ dysfunction. Oliguria is an early sign of ACS, but the most reliable clinical indicator is progressive failure of ventilation. A typical case of ACS has a peak inspiratory pressure in the range of 85 cm H₂O, with a rise in PaCo₂. A decompressive celiotomy is indicated in the presence of abdominal distention, hypercarbia, and high peak inspiratory pressures. This procedure may be performed either at bedside or in the operating room.

The surgical technique performed for damage control is a continuum that includes primary resuscitation, damage control celiotomy, secondary resuscitation, and delayed reconstruction.² Patients in extremis usually do not tolerate reconstruction. In summary, ACS is a surgical emergency that requires the damage control technique to prevent organ dysfunction. If ACS is recognized late or goes unrecognized, it can lead to multiple organ failure and death.

The boundaries of the intra-abdominal compartment consist of the diaphragm, pelvic floor, retroperitoneum, chest, and abdominal wall. Abdominal compartment compliance decreases with an increase in intra-abdominal pressure, with resultant direct impact upon the contents of the abdominal cavity. The contents of the abdominal compartment consist of the gastrointestinal tract, solid organs (liver, spleen, etc.), nerves, arteries, and veins. The diaphragm has direct impact on the lungs and heart. An increase in the intra-abdominal pressure is associated with increased peak inspiratory pressures, as well as hypercarbia.

The retroperitoneum harbors the kidneys, ureters, and the major abdominal vessels. This area is at risk for major hemorrhage that can result in ACS. Retroperitoneal hemorrhage rarely causes compression of the ureters. Rather, a prerenal state occurs with decreased CO secondary to decreased venous return. The pelvic organs, such as the urinary bladder and the pelvis itself, may also be major sources of blood loss. Monitoring of abdominal compartment pressure is critical. In severe cases of pancreatitis, this organ may be an etiologic factor for ACS.

The abdominal wall provides the ventral covering of the abdominal cavity and allows for limited expansion of the intra-abdominal contents. Hypoperfusion of the abdominal wall due to intra-abdominal hypertension is associated with an increase in wound complications. Ascites may also cause intra-abdominal hypertension when massive amounts of fluid accumulate in the abdomen. The gastrointestinal tract consists of the stomach, the small bowel, and colon. Significant amounts of fluid and/or air can accumulate in these structures, causing intra-abdominal hypertension. Bowel perforation with peritoneal contamination is associated with diffuse peritonitis, another etiologic factor of ACS.

Intra-abdominal pressure is that pressure concealed within the abdominal cavity, which varies with respiration. A normal intra-abdominal pressure is approximately 5 mm Hg, but may be higher with obesity. Intra-abdominal pressure should be expressed in mmHg and measured at end-expiration with the patient in the supine position, without abdominal contractions. The pressure transducer should be zero-referenced to the level of the midaxillary line. Direct intra-abdominal measurement is obtained with direct needle puncture and transduction of the pressure within the abdominal cavity. Indirect intra-abdominal pressure measurement is accomplished through transduction of the pressure within the bladder. Bladder pressure may be measured by injecting 50 to 100 mL of sterile saline into the aspiration port of the Foley drainage tube. The catheter is then clamped distal to the aspiration port, and a 16-gauge needle is used to connect a pressure transducer to the aspiration port of the catheter. The top of the symphysis pubis (or the midaxillary line) is used as the zero point on the supine patient.

For continuous, indirect intra-abdominal pressure measurement, a balloon-tipped catheter in the stomach or a continuous bladder irrigation method is recommended (see Fig. 40.1). The ACS is not seen, as long as the intra-abdominal pressure is normal. The group at Denver Health Medical Center has proposed a grading system based on urinary bladder pressure measurements³ (see Table 40.1). A pressure of 25 mmHg or higher is associated with organ dysfunction and considered clinical intra-abdominal hypertension. At or above this pressure, surgical decompression is justifiable.

Many clinical scenarios may be associated with ACS. Any pathologic process that causes an increase in the intra-abdominal pressure can lead to ACS. Accumulation of fluid in the abdominal cavity may be associated with a marked decrease in the compliance of the abdominal wall, with associated intra-abdominal hypertension. Excessive air in the gastrointestinal tract can increase pressure, but rarely causes ACS unless associated with a primary pathologic process that requires massive fluid resuscitation. Diffuse peritonitis, major hemorrhage, and massive ascites are also associated with ACS.

ACS may be prevented through the early identification of risk factors and diagnosis. A high index of suspicion is necessary for prevention. Liberal use of surgical decompression is strongly recommended when critical intra-abdominal pressure is reached,⁴ or when the clinical scenario is present. High peak inspiratory pressures (>85 cm H₂O), hypercarbia, and oliguria are all clinical signs of ACS.⁵ The change in pressure is a function of the rate of fluid accumulation and the compliance of the abdominal cavity. The pressure-volume curve for the abdominal cavity is nonlinear.⁶

A variety of conditions, both surgical and nonsurgical, increase the risk of developing the ACS. The common
denominator in each of these conditions appears to be the need for large volume resuscitation. For example, patients presenting with acute major abdominal hemorrhage are at very high risk for ACS. Other conditions include “nonmajor” intraperitoneal hemorrhage, intra-abdominal catastrophes, abdominal trauma, hemorrhagic pancreatitis, severe ascites, hepatic transplantation, and ovarian tumors. In the presence of one of the high-risk conditions, the risk of ACS may be heightened by hypothermia, acidosis, and/or coagulopathy due to the volume replacement that may be required for resuscitation. Other factors to be considered include:⁷,⁸,⁹,¹⁰,¹¹,¹²,¹³,¹⁴,¹⁵,¹⁶,¹⁷

ACS may be subdivided into primary, secondary, and tertiary variants:

Respiratory manifestations are related directly to the effect of intra-abdominal hypertension, which elevate the hemidiaphragms, with an associated decrease in intrathoracic volume and compliance. Elevated peak airway pressures and pulmonary vascular resistance will most often be present. In ACS, ventilatory support becomes difficult, and relatively sophisticated strategies of mechanical ventilation are often necessary to stabilize and improve the respiratory mechanics. Respiratory deterioration, if it occurs, may lead to development of severe hypercarbia, worsening acidosis, and hypoxemia.

The changes in cardiovascular parameters are due to increased intrathoracic pressure from intra-abdominal hypertension.¹,¹⁸,¹⁹,²⁰,²¹ Cardiovascular changes include an increase in central venous and pulmonary artery wedge pressures, and systemic vascular resistance. CO decreases progressively with increases in intra-abdominal pressure, and is dependent on the intravascular volume status. Kashtan et al. showed that changes in CO were demonstrable in the setting of ACS. Hypovolemic animals developed a 53% decline in CO, compared with a 17% decline in the euvolemic group and a 50% increase in the hypervolemic group.¹⁹ Patients with ACS may have an increase in CO with intravascular volume replacement, but fluid alone cannot correct the renal dysfunction and decrease in splanchnic blood flow associated with ACS.