OBJECTIVE: To investigate the frequency, predisposing factors, clinical presentation, and outcome of abdominal compartment syndrome (ACS) in critically ill pediatric patients. DESIGN: A prospective study over a 5-yr period. SETTING: Pediatric intensive care unit of a tertiary care, university hospital. PATIENTS: All patients admitted to the pediatric intensive care unit were screened for the presence of ACS and were treated with a uniform protocol. ACS was defined as abdominal distention with intra-abdominal pressure (IAP) > 15 mm Hg, accompanied by at least two of the following: oliguria or anuria; respiratory decompensation; hypotension or shock; metabolic acidosis. MEASUREMENTS AND MAIN RESULTS: Of 1762 patients admitted over 5 yrs, ten patients (0.6%) had a total of 15 episodes of ACS. Of 406 trauma cases, three had ACS (0.7%). Three of the ten patients had primary abdominal conditions (mesenteric vein thrombosis, intussusception, enterocolitis), three had abdominal surgery (trauma, Kasai operation, esophageal perforation and peritonitis), three had primary central nervous system involvement, and one had meningococcemia. At laparotomy, bowel ischemia or necrosis was found in four episodes of ACS (27%). Mean IAP at diagnosis of ACS was 23.9 +/- 3.8 (range 17-31) mm Hg. Physiologic parameters were compared during 4 hrs before the development of ACS, during ACS, and after abdominal decompression. Mean arterial pressure, Pao(2), Pao(2)/Fio(2) ratio, and urinary output decreased significantly, whereas Paco(2), peak inspiratory pressures, positive end-expiratory pressures, and base deficit increased significantly after the development of ACS. After decompressive laparotomy, the condition of the patients improved promptly and these variables returned to pre-ACS values. Overall mortality rate in this group was 60%. CONCLUSIONS: Although relatively infrequent compared with adults, ACS occurs in critically ill children. Timely decompression of the abdomen results in uniform improvement, but overall mortality is still high. In contrast with adults, children with ACS have diverse primary diagnoses, with a significant number of primary extra-abdominal-mainly central nervous system-conditions. Ischemia and reperfusion injury appear to be the major mechanisms for development of ACS in children. Clinical presentation is similar to adults, but children may develop ACS at a lower IAP (as low as 16 mm Hg).

FAST is an effective tool in screening pediatric trauma patients for blunt abdominal trauma.

Parenteral but not enteral Omegaven augments and accelerates structural bowel adaptation in a rat model of SBS. Increased cell proliferation and decreased apoptosis reflect increased cell turnover in Omegaven-treated animals.

Despite a significant decrease in PV blood flow, persistent IAP for 2 hours results in few changes in liver histology, and stimulates hepatocyte proliferation and apoptosis in only a few animals, supporting the presence of a recovering mechanism. Treatment with hyperoxia did not significantly change hepatocyte proliferation and apoptosis.

Aim: Recent clinical experience suggests that minimal access portoenterostomy (the Kasai procedure) for biliary atresia leads to transplantation sooner, compared to the traditional open approach. It should be emphasized that elevated intra-abdominal pressure (IAP) may reduce hepatic and portal blood flow and thus may cause histologic liver damage. The aim of the present study was to evaluate the effects of IAP on blood flow in the portal vein (PV), compared to the superior mesenteric artery (SMA), and on the systemic mean arterial blood pressure (MABP). Materials and Methods: Male Sprague-Dawley rats were anesthetized with intraperitoneal ketamine (90 mg per kg) and xylasine (13 mg per kg). Polyethylene catheters (PE-50) were introduced into the right carotid artery for the measurement of MABP. After a midline laparotomy, the SMA and PV were isolated. Ultrasonic bloodflow probes were placed on the vessels for the continuous measurement of regional blood flow. Two large-caliber percutaneous peripheral intravenous catheters were introduced into the peritoneal cavity for inflation of air and for the measurement of IAP. The time course of MABP and SMA and PV flow as well as the relationship between IAP and SMA and PV flow were determined. Results: Although all three hemodynamic parameters decreased with the increase in the IAP, the most significant changes were observed in PV blood flow. IAP at 3 mm Hg resulted in a 26% decrease in PV flow (P Ͻ 0.05), a 19% decrease in SMA flow (P Ͻ 0.05), and an 11% decrease in MABP (P Ͻ 0.05). IAP at 6 mm Hg caused a two-fold decrease in PV flow (P Ͻ 0.05), a 30% decrease in SMA flow (P Ͻ 0.05), and a 19% decrease in MABP (P Ͻ 0.05). There were no changes in the time course of MABP and PV and SMA flow. PV and SMA flow returned to normal values immediately after abdominal deflation. Conclusions: Persistent IAP decreased MABP, SMA, and, especially, PV flow by 50%. We speculate that in biliary atresia patients with already present liver dysfunction, decrease in SMA flow and even a greater decrease in PV flow from increased IAP, which occurs during a laparoscopic Kasai procedure, may further compromise liver function. This may be one of the explanations for the progression to earlier transplantation in infants undergoing a laparoscopic Kasai procedure.