Salonvaara M, Riikonen P, Kekomäki R, Heinonen K. Clinically symptomatic central venous catheter‐related deep venous thrombosis in newborns. Acta Pædiatr 1999; 88: 642‐6. Stockholm. ISSN 0803‐5253The objective of this study was to evaluate the incidence of clinically symptomatic central venous catheter (CVC)‐related deep venous thrombosis (DVT) in newborns and small infants and to try to identify clinical and genetic risk factors for catheter‐related DVT among children with thrombotic complications. CVC was inserted in 44 consecutive infants (age range 0‐90 d) during the period January 1990 to December 1995 in the neonatal intensive care unit (NICU) of Kuopio University Hospital in Kuopio. The symptoms of DVT were: syndrome of superior vena cava in 2, swelling at the CVC puncture site in 6 and repeated CVC obstructions in 2. The formation of DVT was verified by venography. Children with DVT (n= 10) had 26 (10‐365, in total 623) catheter days compared with 9 d (1‐155, in total 591) in patients without DVT (n = 26) (p < 0.005). The median (range) number of days from catheter insertion to diagnosis of DVT was 19 (7‐210). CVC had to be removed from 11 (25%) children due to various complications. There was no DVT‐related mortality. A positive family history with thromboembolic episodes at a young age was found in 3 of 10 families with a child suffering CVC‐related DVT. The levels of coagulation inhibitors were evaluated at the age of 9‐69 mo in all 10 (23%) children with CVC‐related DVT. We detected no deficiencies in protein S, protein C or antithrombin III. One child was heterozygous for the point mutation (R506Q) in the factor V gene known to cause activated protein C resistance (APCR). We conclude that newborns with CVC are at great risk of DVT and that the aetiology of DVT can rarely be identified via measurements of coagulation inhibitors. □Antithrombin III, central venous catheter, children, factor Vgene mutation, protein C, protein S, thrombosis
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