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Many hemorrhagic disorders in children are caused by genetic defects, but there are also a number of important acquired conditions that can lead to abnormal coagulation and subsequently bleeding complications. These conditions occur in disparate clinical situations ranging from otherwise healthy-appearing neonates to critically ill children with multiorgan failure. The most important of these conditions are vitamin K deficiency bleeding, coagulopathy of liver failure, and disseminated intravascular coagulation (a condition that can lead to both bleeding and thrombosis). Other conditions include acquired platelet dysfunction (see Chapter 439) and acquired inhibitors to specific coagulation proteins.

In 1894, Charles Townsend described 50 newborns who developed severe bleeding complications shortly after birth and coined the term hemorrhagic disease of the newborn” (HDN).1 In 1936, Henrik Dam discovered a fat soluble “koagulation factor” (using the German spelling), which he named vitamin K and which was found to be deficient in neonates suffering from HDN.2 Thus the term hemorrhagic disease of the newborn has been replaced by vitamin K deficiency bleeding, as this term is more specific and descriptive. This discovery led to the use of prophylactic vitamin K, which has become routine in the immediate perinatal period and is very effective at preventing HDN.


Vitamin K deficiency bleeding (VKDB) is classified as early, classical, or late (see Table 437-1). Early onset occurs in the first 24 hours of life and is due to the cross-placental transfer of compounds that interfere with vitamin K metabolism or function, including some anticonvulsant drugs, antibiotics, antituberculous agents, and vitamin K antagonists. Classical VKDB as described by Townsend occurs in the first week of life and is due to a physiological deficiency in vitamin K at birth combined with a lack of vitamin K in breast milk or inadequate feeding. Vitamin K prophylaxis has its biggest impact in preventing this type of VKDB. Late onset VKDB can occur at any age, although it is classically described as occurring between 2 weeks and 6 months of age. In infants, it is again due to inadequate vitamin K content in breast milk and is thus found almost universally in those exclusively breast-fed. In older children (though often in infants as well), additional factors are necessary, which have in common reduced vitamin K intake and absorption. Some examples of conditions that lead to late-onset vitamin K deficiency are liver or pancreatic disease, both leading to an inability to absorb fat-soluble vitamins; gastrointestinal disorders that affect intestinal flora, because a secondary source of vitamin K is production by intestinal microorganisms; prolonged antibiotic use due to an alteration of intestinal flora; and ingestion (accidental or otherwise) of vitamin K antagonists that, while perhaps not technically causing vitamin K deficiency, can be overcome with vitamin K therapy (Table 437-1).

Table 437-1. Classification of Vitamin K Deficiency Bleeding

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