Incidence of vein thrombosis in peripheral intravenous nutrition: effect of fat emulsions.

The relative risk of thrombophlebitis induced by either Long-chain Triglycerides (LCTs) or Medium-chain Triglycerides (MCTs) during peripheral i.v. nutrition (PIN) was evaluated. A total of 76 patients were randomly assigned into group A (n=40) and group B (n=36). The nutritional requirements in both groups were covered by a standardized regime of osmolality 1130 mOsm and pH 5.2, which provided 14 kg/day(-1) nitrogen, 600 kcal/day(-1) of carbohydrates and 1000 kcal/day(-1) of lipids. Group A received the lipids as pure LCTs while group B received a mixture of LCTs/MCTs at a ratio 1:1. The infused nutritional volume was 2000 ml and was delivered via a suitable vein in a proximal forearm, using a fine bore polyurethane 22G catheter. The two standardized regimes were evaluated over a 10 day period regarding the incidence of thrombophlebitis. The cumulative risk of thrombophlebitis was documented to be significantly lower in group A compared to group B (17.5% versus 44.4%, P < 0.05). LCTs appear to prolong peripheral vein feeding by lessening the reaction of venous endothelium to the irritating nutritional infusate.

Plasma level of the creatine phosphokinase BB isoenzyme during experimental intestinal ischemia.

Changes in the serum of CPK-BB isoenzyme were investigated in dogs with intestinal ischemia in order to determine their use as an enzymatic diagnostic test for bowel infarction. The study consisted of 12 mongrel dogs. Group I (n = 6) was assigned as a control and was subjected to lumen obstruction of a jejunal segment 50-60 cm in length. Group II (n = 6) had an intestinal infarction created by ligation of the arteries of a jejunal segment 50-60 cm in length. A catheter was placed into the right atrium through the left jugular vein for blood sampling and monitoring. Blood samples were withdrawn every three hours for biochemical assays. CPK-BB measurements were performed by electrophoresis in agarose gel. CPK-BB remained unchanged in Group I during the course of the study (median range 17 to 20 IU) showing no significant difference from normal levels. Significant elevation of CPK-BB occurred three hours after establishing the ischemia in Group II (median 50 IU) as compared to Group I (p less than 0.05). The highest levels were determined to be 96 and 80 IU at the sixth and ninth hour, respectively. From hour 15 until completion of the experiment, no significant difference was detected between Groups I and II. We conclude that CPK-BB elevation in serum signifies its release from the smooth muscles of the bowel due to ischemic cellular damage.