JMIR Publications

Vitamin K is an essential fat-soluble micronutrient which is needed for a unique posttranslational chemical modification in a small group of proteins with calcium-binding properties, collectively known as vitamin K – dependent proteins or Gla-proteins. Thus far, the only unequivocal role of vitamin K in health is in the maintenance of normal coagulation. The vitamin K – dependent coagulation proteins are synthesised in the liver and comprise factors II, VII, IX, and X, which have a haemostatic role (i.e., they are procoagulants that arrest and prevent bleeding), and proteins C and S, which have an anticoagulant role (i.e., they inhibit the clotting process). Deficiency of vitamin K leads to inadequate activity of these factors, resulting in bleeding. As opposed to adults, neonates have reduced stores of vitamin K at birth owing to insufficient placental transfer. This is compounded by deficient vitamin K content in breast milk resulting in higher levels of proteins induced in the absence of vitamin K in breastfed neonates. Vitamin K deficiency bleeding (VKDB) is usually categorized into three major groups based on the age of onset: early (first 24 h of life), classical (second to seventh day) and late (2 to 12 weeks of life). Although early VKDB is due to placental transfer of maternal drugs that inhibit vitamin K activity, the classical form occurs because of the low intake via breast milk. Late VKDB is often linked to malabsorption secondary to liver disease and poor intake of vitamin K. Intracranial bleeding (30 to 60%) is the predominant manifestation of late onset VKDB, whereas bleeding from the gastrointestinal tract and/or umbilicus is the usual presenting feature in classical disease.