Vitamin K Deficiency Bleeding in Infancy

Abstract

Vitamin K is essential for the synthesis of few coagulation factors. Infants can easily develop vitamin K deficiency owing to poor placental transfer, low vitamin K content in breast milk, and poor intestinal absorption due to immature gut flora and malabsorption. Vitamin K deficiency bleeding (VKDB) in infancy is classified according to the time of presentation: early (within 24 h), classic (within 1 week after birth), and late (between 2 week and 6 months of age). VKDB in infancy, particularly late-onset VKDB, can be life-threatening. Therefore, all infants, including newborn infants, should receive vitamin K prophylaxis. Exclusive breastfeeding and cholestasis are closely associated with this deficiency and result in late-onset VKDB. Intramuscular prophylactic injections reduce the incidence of early-onset, classic, and late-onset VKDB. However, the prophylaxis strategy has recently been inclined toward oral administration because it is easier, safer, and cheaper to administer than intramuscular injection. Several epidemiological studies have shown that vitamin K oral administration is effective in the prevention of VKDB in infancy; however, the success of oral prophylaxis depends on the protocol regimen and parent compliance. Further national surveillance and studies are warranted to reveal the optimal prophylaxis regimen in term and preterm infants.

Keywords: PIVKA; intracranial hemorrhage; intramuscular injection; prophylaxis.

Figure 1

(A) Vitamin K (K₁, or phylloquinone and menaquinone (MK)) content in the liver tissue in adults (closed circles) and neonates (open circles) without definite liver dysfunction. (B) Menaquinone-4 2, 3-epoxide/menaquinone-4 (Epo./MK-4) ratio after vitamin K (MK-4) loading in normal adults and 1-month-old infants.