Vitamin K deficiency bleeding (VKDB) is a coagulopathy that develops in infants who do not have sufficient vitamin K stores to support production of clotting factors. In adults, vitamin K is absorbed from food and from vitamin K synthesized by gut bacteria. However, placental transfer in humans is limited; cord blood and infant liver reserve levels of vitamin K are substantially below adult levels. As a result, infants are predisposed to develop VKDB, which is classified as early, classic, and late, according to when it presents. In the United States, administration of intramuscular vitamin K at birth to prevent all forms of VKDB has been standard practice since first recommended by the American Academy of Pediatrics in 1961. Without this prophylaxis, incidence of early and classical VKDB ranges from 0.25% to 1.7% of births; incidence of late VKDB ranges from 4.4 to 7.2 per 100,000 infants. The relative risk for developing late VKDB has been estimated at 81 times greater among infants who do not receive intramuscular vitamin K than in infants who do receive it.