Vitamin K Deficiency

The normal full-term infant is born with levels of factors II, VII, IX, and X that are low by adult standards (Table 11-3). The coagulation factors fall even lower over the first few days of life, reaching their nadir on about the third day. This is due to the low body stores of vitamin K at birth. As little as 25 |g vitamin K can prevent this fall in activity of the vitamin K-dependent clotting factors. The vitamin K content of

Prothrombin Time

PTT, activitated partial thromboplastin time PT, prothrombin time TT, thrombin time

Fig. 11-6. Coagulation tests and interpretation.

PTT, activitated partial thromboplastin time PT, prothrombin time TT, thrombin time

Fig. 11-6. Coagulation tests and interpretation.

cow's milk is about 6 |g/dL and that of breast milk 1.5 |g/dL. It is a combination of low initial stores and subsequent poor intake of vitamin K that occasionally produces an aggravation of the coagulation defect causing primary hemorrhagic disease of the newborn. Vitamin K deficiency results in hemorrhagic disease between the second and fourth days of life and is manifested by gastrointestinal hemorrhage, hemorrhage from the umbilicus, or internal hemorrhage. Bleeding attributable to this cause is responsive to parenteral vitamin K therapy; for this reason, parenteral vitamin K is routinely administered to newborns.

In premature infants of low birth weight, both the vitamin K stores and the level of coagulation factors are even lower than in term infants. The response to vitamin K is slow and inconstant, suggesting that the immature liver has reduced synthetic capability.

Maternal ingestion of certain drugs may result in neonatal hypoprothrombinemia and reduction in factors VII, IX, and X. These drugs include oral anticoagulants and anticonvulsants (phenytoin, primidone, and phenobarbital).

Table 11-5 lists the conditions associated with deficiency of vitamin K-dependent factors in the newborn and in the older child, and Table 11-6 lists the laboratory findings in vitamin K deficiency in relationship to the findings in liver disease and disseminated intravascular disease (DIC).

Hepatic Dysfunction

Any transient inability of the newborn's liver to synthesize necessary coagulation factors, even in the presence of vitamin K, can result in hemorrhagic disease that is nonresponsive to vitamin K therapy. Hepatic dysfunction as a result of immaturity, infection, hypoxia, or underperfusion of the liver can all result in transient inability

Table 11-5. Conditions Associated with Deficiency of Vitamin K-Dependent Factors

Normal newborn (normal by 3 months of age), prematurity Vitamin K responsive

Vitamin K nonresponsive (caused by immaturity, infection, hypoxia, hepatic underperfusion) Dietary

Cow's milk: 6 |rg/L Human milk: 1.5 |rg/L Altered bacterial colonization Vomiting

Severe diarrhea malabsorption syndromes Celiac disease Cystic fibrosis Biliary atresia

Obstruction of gastrointestinal tract Antibiotics (including antibiotics in breast milk) Hepatocellular disease Acute

Reye syndrome Acute hepatitis Chronic Cirrhosis Wilson disease Drugs

Coumarins

Table 11-6. Laboratory Findings in Vitamin K Deficiency, Liver Disease, and Disseminated Intravascular Coagulation

Component

Vitamin K deficiency

Liver disease

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