Abdominal Compartment Syndrome
Organ dysfunction due to increased abdominal pressure which compromises perfusion to vital organs
Can be thought of similarly as Cerebral Perfusion Pressure in that while normally, perfusion to organs within the abdominal compartment is MAP-RAP, when abdominal compartment pressure increases, perfusion pressure becomes MAP-Abdominal pressure
Normal intraabdominal pressure in adults is about 5 mmHg
Intraabdominal Hypertension in adults is >12 mmHg
Abdominal Compartment Syndrome in adults is defined as an intraabdominal pressure of >20 mmHg with evidence of organ dysfunction. In reality, a more relevant definition may be an elevated intraabdominal pressure with evidence of organ dysfunction. There are no clear values for intraabdominal hypertension or compartment syndrome in children.
Increased abdominal wall compliance that develops over time (ie chronic cirrhosis with ascites) may be protective against abdominal compartment syndrom
Intraabdominal pressure rises due to ascites, bowel wall edema, organomegaly, intraabdominal bleeding, or some combination thereof
As intraabdominal pressure rises, it impairs perfusion pressure to vital organs (defined as MAP-Intraabdominal Pressure). In adults, a target of a abdominal perfusion pressure of 60 mmHg is generally quoted.
Cardiac: impairs venous return (functionally obstructs IVC flow), pushes the diaphragm cephalad which can also cause cardiac compression
Pulmonary: Due to abdominal competition and pushing of the diaphragm cephalad, higher peak inspiratory and airway pressures, reduced chest wall compliance and lower tidal volumes. Pulmonary infection also more common with IAH
Renal: Renal vein compression increases venous resistance and impairs renal perfusion (major mechanism). The renin-angiotensin system is also upregulated due to low cardiac volume, leading to renal artery vasoconstriction. Hence, patients develop acute kidney injury and reduced urine output
Gastrointenstinal: Mesenteric blood flow and intestinal mucosal perfusion is decreased. Mesenteric veins are also compressed, impairing venous return and leading to intestinal edema, which further increases abdominal compartment pressures, inducing a vicious cycle
Hepatic: Hepatic clearance of lactic acid is reduced by increased intraabdominal pressure
CNS: ICP can also be elevated as a result of increased IA pressure
Tense, distended abdomen (not a very reliable physical exam finding for IAH)
Worsening oliguria and ventilatory requirements
Jugular venous distension
Imaging not always helpful
Measurement of IAP is key
1) Drainage catheter of Foley is clamped.
2) Sterile saline (1 cc/kg up to 25 cc) is instilled into the bladder via the aspiration port and the catheter also is filled with fluid
3) 18 gauge needle attached to pressure transducer is inserted into the aspiration port (or via the same set up as an arterial line transducer)
4) Pressure is measured at end expiration in the supine position after ensuring no abdominal muscle contractions are present
5) Zeroed at level of mid-axillary line
May not be accurate if there are intraperitoneal adhesions, a neurogenic bladder, or pelvic fractures/hematomas
Supportive care including gastric and rectal decompression
Percutaneous drainage of ascites or intraperitoneal hematomas
Percutaneous catheter placement (we tend to place acute peritoneal dialysis catheters at the level of the linea alba (non vascular) below the umbilicus)
Sedation and chemical paralysis to relax the abdominal musculature
Ventilatory suppot as needed
Hemodynamic support as needed
Surgical decompression and usually maintenance of an open abdomen via a temporary abdominal wall closure is the definitive treatment
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