Chapter 474 Postneonatal Vitamin K Deficiency

Although “late” hemorrhagic disease has been reported in breast-fed children, vitamin K deficiency occurring after the neonatal period is usually secondary to a lack of oral intake of vitamin K, alterations in the gut flora due to the long-term use of broad-spectrum antibiotics, liver disease, or malabsorption of vitamin K. Intestinal malabsorption of fats may accompany cystic fibrosis or biliary atresia and result in a deficiency of fat-soluble dietary vitamins, with reduced synthesis of vitamin K–dependent clotting factors (factors II, VII, IX, and X, and protein C and protein S). Prophylactic administration of water-soluble vitamin K orally is indicated in these cases (2-3 mg/24 hr for children and 5-10 mg/24 hr for adolescents and adults), or vitamin K may be administered at 1-2 mg IV. In patients with advanced cirrhosis, synthesis of many of the clotting factors may be reduced because of hepatocellular damage. In these patients, vitamin K may be ineffective. The anticoagulant properties of warfarin (Coumadin) and related anticoagulants depend on interference with vitamin K, with a concomitant reduction of factors II, VII, IX, and X. Rat poison (superwarfarin) produces a similar deficiency; vitamin K is a specific antidote.