Abdominal compartment syndrome complicating paediatric extracorporeal life support: diagnostic and therapeutic challenges.

We report three paediatric cases, and summarise the reported experience in two others, with cardiorespiratory failure requiring extracorporeal life support for which supportive pump flows could not be maintained due to abdominal compartment syndrome. In two of our patients, the mechanism of abdominal compartment syndrome was massive intra-abdominal fluid extravasation secondary to sepsis, while in the third, the mechanism was post-traumatic intra-abdominal haemorrhage. Although all three children eventually died, decompressive laparotomy and arrest of haemorrhage in the trauma patient restored venous return and enabled technically adequate extracorporeal life support. In two previously reported cases of sepsis with massive fluid resuscitation resulting in abdominal compartment syndrome, one patient died without attempted decompression, while the other patient survived after peritoneal catheter placement restored venous return. Once correctable causes of inadequate venous cannula drainage have been excluded, abdominal compartment syndrome should be considered in any patient on extracorporeal life support with a taut abdomen and reduced venous return. If abdominal compartment syndrome can be proven or is strongly suspected, there may be a role for selective decompressive laparotomy.

Hypoadiponectinemia is associated with impaired endothelium-dependent vasodilation.

Adiponectin may have an antiatherogenic effect by reducing endothelial activation. We hypothesized that plasma adiponectin levels were correlated with endothelial function. Plasma adiponectin level was determined by an in-house RIA assay using a rabbit polyclonal antibody in 73 type 2 diabetic patients and 73 controls. Endothelium-dependent and independent vasodilation of the brachial artery was measured by high-resolution vascular ultrasound. Plasma adiponectin level was lower in diabetic patients than in controls (4.73 +/- 1.96 vs. 7.69 +/- 2.80 microg/ml, respectively; P < 0.001), and they also had impaired endothelium-dependent (5.6 +/- 3.6 vs. 8.6 +/- 4.5%, respectively; P < 0.001) and -independent vasodilation (13.3 +/- 4.9 vs. 16.5 +/- 5.6%, respectively; P < 0.001). Plasma adiponectin correlated with endothelium-dependent vasodilation in controls (P = 0.02) and diabetic patients (P = 0.04). On general linear-model univariate analysis, brachial artery diameter, the presence of diabetes, plasma adiponectin, and high-density lipoprotein were significant independent determinants of endothelium-dependent vasodilation. In vitro experiments showed that endothelial cells expressed adiponectin receptors, and adiponectin increased nitric oxide production in human aortic endothelial cells. In conclusion, low plasma adiponectin level is associated with impaired endothelium-dependent vasodilation, and the association is independent of diabetes mellitus. Adiponectin may act as a link between adipose tissue and the vasculature.