Risk factors for ACS include the following:[4]
Diminished abdominal wall compliance in patients who undergo abdominal surgery, have major trauma or burns, or have a high body mass index with central obesity
Patients on mechanical ventilation
Increased intraluminal content secondary to gastroparesis, ileus, colonic pseudo-obstruction, or intra-abdominal or retroperitoneal tumors
Increased abdominal contents in hemoperitoneum, pneumoperitoneum, or ascites
Capillary leak and fluid resuscitation in acidosis or hypotension
Massive transfusion (>10 units in 24 hours)
Massive fluid resuscitation (>5 L/24 hours)
Damage control laparotomy
Several case reports have been published on enoxaparin-associated retroperitoneal bleeding and ACS.[5,6]
Patients with two or more risk factors or with new or progressive organ failure should be screened for ACS. Investigations for ACS should include abdominal radiography to look for free air or bowel obstruction and an abdominal CT scan to look for the "round-belly" sign (abdominal distention with an increased anteroposterior-to-transverse abdominal diameter (ratio >0.80), collapse of the vena cava, or bowel wall thickening.
In addition, an IAP measurement should be performed. Bladder pressure can be monitored fairly easily by connecting a transurethral Foley catheter to a pressure transducer. Changes in intraperitoneal pressure are reflected by parallel change in intraluminal bladder pressure.[1] IAPs have the following usual ranges based on the patient's condition:
Healthy adults: 0-5 mm Hg
Critically ill adults: 5-7 mm Hg
Post-laparotomy patients: 10-15 mm Hg
Patients with septic shock: 15-25 mm Hg
Patients with an acute surgical abdomen: 25-40 mm Hg
Burch and associates classified patients into the following categories on the basis of IAP measurement via bladder catheterization[7]:
Grade I: 10-15 cm H2O
Grade II: 15-25 cm H2O
Grade III: 25-35 cm H2O
Grade IV: >35 cm H2O
A multicenter, prospective, epidemiologic study reported that the mean IAP in all intensive care unit admissions was 10 ± 4.8 mm Hg. A total of 67.9% of patients had a normal IAP (<12 mm Hg), 32.1% had IAH >12 mm Hg, and 4.2% had ACS. The prevalence of ACS in patients with IAH was 12.9%. The mortality rate was significantly higher in the group with IAH compared with the non-IAH group.[8]
The hemodynamic consequences of IAH include a fall in cardiac output and stroke volume; a decrease in celiac, superior mesenteric, and renal artery blood flow; an increase in oxygen consumption; and a decrease in pH and arterial partial pressure of oxygen. The reduction in cardiac output is probably explained by compression of the inferior vena cava leading to a reduction in venous return (as seen in this case). Additionally, an increase in afterload may contribute to systemic hypotension.[9]
Increased IAP impairs pulmonary function through mechanical effects. As IAP increases, the diaphragm is forced higher into the chest and decreases lung and chest wall compliance. Adequate ventilation with a mechanical ventilator then requires increased airway pressures.[4] IAH decreases renal plasma flow and the glomerular filtration rate. The pathophysiology of these IAH effects is uncertain but does not necessarily reflect the decreased cardiac output. Shunting of blood away from the renal cortex into the medulla, reduced renal blood flow, direct compression of the kidneys or renal veins, and high levels of antidiuretic hormone may explain renal impairment.[2] Abdominal perfusion pressure (APP) is used to assess the severity and adequacy of abdominal blood flow. It can be calculated by subtracting the IAP from the mean arterial pressure. APP should be kept above 50-60 mm Hg. APP is superior to IAP, arterial pH, base deficit, and arterial lactate in predicting organ failure and patient outcome.
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Cite this: Abdominal Pain, Anemia, and Oliguria in a Distressed Woman - Medscape - Apr 30, 2021.
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