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of the newborn has been replaced by vitamin K deficiency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
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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