1 NYC Health and Hospitals/Kings County, New York, NY, USA
2 NYU Langone Medical Center, New York, NY, USA
Background
Definition of disease
ACS is defined as a sustained IAP >20 mmHg that is associated with a new organ dysfunction or failure.
Normal IAP in critically ill patients is 5–7 mmHg and IAH is defined by sustained or repeated elevation of IAP >12 mmHg.
Disease classification
Primary ACS is associated with injury/disease in the abdomino‐pelvic region.
Secondary ACS refers to conditions that do not originate from the abdomino‐pelvic region, such as large volume resuscitation.
Etiology
Primary ACS can result from free ruptured abdominal aortic aneurysms, abdominal trauma, retroperitoneal hemorrhage from pelvic trauma, acute gastric dilation, severe pancreatitis, abdominal packing, repair of gastroschisis or omphalocele, and reduction of large hernias as well as other causes.
Secondary ACS can result from mangled extremities, burns, systemic inflammatory response syndrome (SIRS), or septic shock.
Pathology/pathogenesis
The pathophysiology of ACS is best understood by examining the different systems affected by the ACS.
Cardiovascular dysfunction is revealed as a decrease in cardiac output (CO) as IAP increases. The IAH results in direct compression of the IVC/portal flow causing a decrease in venous return. Intrathoracic displacement of the diaphragm causes an increased thoracic pressure. This increased thoracic cavity pressure results in cardiac compression and decreased cardiac compliance. Coupled with increased systemic afterload seen with IAH, the result is failure of adequate CO.
Pulmonary system dysfunction is caused by increases in IAP that displace the diaphragm leading to reduction in total lung capacity, functional residual capacity, and residual volume. All of these reductions produce ventilation–perfusion abnormalities that ultimately result in hypoxia and hypercarbia.
Renal derangements are expressed clinically as oliguria, which then progresses to anuria and eventually pre‐renal azotemia that does not respond to volume. The failure of volume administration to correct an oliguric state is likely secondary to compression of renal outflow. There is a reduction in renal blood flow (caused by decreased CO and direct compression) with increased renal vascular resistance and subsequent reduced glomerular filtration.
Intestinal dysfunction results from decreases in mesenteric arterial, hepatic arterial, intestinal mucosal, and portal venous blood flow. These impaired flow states seen with increasing IAH all lead to impaired intestinal perfusion which can result in intestinal ischemia and, if untreated, subsequent necrosis.
Predictive/risk factors
Hemorrhage.
Primary closure of abdominal wall.
Reduction of diaphragmatic hernias.
Damage control laparotomy.
Massive fluid resuscitation.
Poly trauma/burn injuries.
Prone positioning.
Intra‐abdominal or retroperitoneal tumors.
Acute pancreatitis.
Gastroparesis/gastric distention/ileus.
Intra‐abdominal sepsis/abscess.
Acute ascitic cirrhosis/liver dysfunction.
Prevention
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