Vitamin K for the Prevention of Bleeding in Newborns

Marcia L. Buck, PharmD, FCCP

Pediatr Pharm. 2001;7(10) 

In This Article

Classification

VKDB, the term adopted by the Committee of the International Society on Thrombosis and Hemostasis in 1999, is defined as an acquired coagulopathy secondary to reduced levels of vitamin K-dependent coagulation factors II (prothrombin), VII, IX, and X. Vitamin K is necessary in the hepatic post-translational carboxylation of glutamic acid residues on these factors. The conversion of glutamic acid to gamma-carboxyglutamic acid creates functional calcium binding sites on the proteins, allowing them to interact with phospholipid surfaces and rendering them active. Vitamin K is also essential in the synthesis of the anticoagulant proteins C and S.[1,4,5,6]

VKDB can be classified according to patient age at onset: early (within the first day of life), classic (within the first week), and late (from the second week to six months of age). Early VKDB is rare and almost exclusively related to placental transfer of drugs which inhibit vitamin K activity, such as carbamazepine, phenytoin, rifampin, or warfarin. Classic VKDB is the most common form, occurring in 0.25 to 1.5% of newborns without prophylaxis. This form is typically associated with inadequate vitamin K intake, resulting from a delay in feeding or consumption of an inadequate volume of breastmilk or formula. Late VKDB is also rare, occurring in 5 to 7 of every 100,000 live births without prophylaxis. The development of late VKDB suggests long-standing inadequacy of vitamin K intake, malabsorption, or impaired utilization. While rare, late VKDB is a cause of significant morbidity and mortality. Intracranial hemorrhage occurs in up to 60% of affected infants.[1,4,5,6]

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