Newall et al. (2003) retrospectively collected cases of HIT in a tertiary pediatric hospital. During the 2-yr study, 116 patients received UFH over a 7-day period (25 reexposures). HIT was suspected in four patients who received therapeutic-dose UFH and developed a platelet count fall of more than 85% of the pre-heparin value. Three of the patients were tested for HIT antibodies, with one positive result (incidence 1/116 = 0.9%).

Etches et al. (2003) conducted a prospective pilot study to determine the incidence of HIT in a pediatric intensive care population. Patients received UFH during cardiopulmonary bypass (CPB) and continuous intravenous (i.v.), intraarterial infusion, and/or subcutaneous injection. During a 41-mo study period, 233 patients with a median age of 2.3 yr were enrolled. Three of 233 study patients had a positive HIT assay (by platelet lumi-aggregometry), giving a seroconversion incidence of 1.3%. All three patients were post-cardiovascular surgery. None of the HIT assay-positive patients showed a 50% or greater decrease in platelet count, and none had clinically evident thrombosis.

In a randomized, double-blind, placebo-controlled trial in neonatal ICU patients receiving either i.v. UFH or saline to prolong patency of peripheral venous catheters (Klenner et al., 2003b), of 108 neonates receiving UFH (0.5 IU/mL) and 105 receiving saline for at least 5 days, none developed HIT or anti-PF4/heparin antibodies (assessed by EIA). This suggests that the incidence of HIT is lower in neonatal ICU patients than previously reported. However, no neonates following cardiac surgery were enrolled. The results of this study were confirmed by a smaller trial (Kumar et al., 2004). None of 42 newborns receiving UFH for prolonging patency of a central venous access line developed heparin-dependent antibodies, either in the anti-PF4/heparin EIA or in a functional (platelet activation) assay. Although 57% of the newborns developed thrombocytopenia, none had clinical suspicion of thrombosis.

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