Abdominal compartment syndrome: Diagnosis
Critical Care, Physics, Monitoring, & Devices, Advanced
Patient Population: Occurs predominately in patients in profound shock, in patients requiring large amounts of vasopressors, resuscitation fluids and blood (more than 6 L of crystalloid or 6 units of packed red blood cells over a 6-hour period – Ref 1), in patients who require abdominal packing for abbreviated/staged laparotomy, and in those with major visceral or vascular abdominal injuries.
- Sudden increase in intra-abdominal pressure
- Increased peak inspiratory pressure
- Decreased urinary output despite adequate CO
- The 3 H’s (Hypoxia secondary to increased airway pressures, Hypercapnia, and Hypotension secondary to decreased venous return to the heart.)
Diagnosis : Confirmed by measuring bladder pressure, which ultimately represents intra-abdominal pressure. The level of IAP at which ACS occurs is patient specific, and thus the diagnosis (and treatment) is based on the patient’s physiologic response to increased IAP. Most patients with IAP between 25 and 35 mm Hg (grade III) ultimately require decompression. All patients with IAP greater than 35 mm Hg (grade IV) require immediate decompression because this group of patients may deteriorate to cardiac arrest at any time.
Treatment : Rapid decompression of the elevated intra-abdominal pressure by opening the abdominal wound and performing a temporary closure of the abdominal wall with mesh or a plastic bag (Bogota bag).
Physiologic consequences of persistent elevated intra-abdominal pressure:
- Cardiac output
- Central venous return
- Visceral blood flow
- Renal blood flow
- Glomerular filtration
- Cardiac rate
- Pulmonary capillary wedge pressure
- Peak inspiratory pressure
- Central venous pressure
- Intrapleural pressure
- Systemic vascular resistance