Vitamin K deficiency-related bleeding (VKDB) in neonates

Vitamin K is an important clotting factor synthesized by intestinal bacteria. Universally all newborns are deficient in vitamin K because of absence of gut flora, low ability of fetal liver to store vitamin K and insufficient transfer of vitamin K through breast milk. 

Vitamin K deficiency-related bleeding (VKDB) is defined as a bleeding disorder in which the coagulation is rapidly corrected by vitamin K supplementation. The diagnosis is suggested by an international normalised ratio =4 or a prothrombin time =4 times the control value in the presence of a normal platelet count and normal fibrinogen level, though many times PT/INR or APTT do not corelate well in neonates. 

Confirmation of the diagnosis requires measurement of the specific vitamin K-dependent factors (II, VII, IX, X) whose levels are rapidly corrected by the parenteral administration of 1 mg vitamin K.

Early VKDB presents within 24 hours of birth and is almost exclusively seen in infants of mothers taking drugs which inhibit vitamin K. These drugs include anticonvulsants (carbamazepine, phenytoin and barbiturates), antituberculosis drugs (isoniazid, rifampicin), some antibiotics (cephalosporins) and vitamin K antagonists (coumarin, warfarin). The clinical presentation is often severe with cephalic haematoma and intracranial and intra-abdominal haemorrhages. 

Classical VKDB occurs between 24 hours and 7 days of life and is associated with delayed or insufficient feeding. The clinical presentation is often mild, with bruises, gastrointestinal blood loss or bleeding from the umbilicus and puncture sites.

Late VKDB is associated with exclusive breast-feeding. It occurs between the ages of 2 and 12 weeks. The clinical presentation is severe, with a mortality rate of 20% and intracranial haemorrhage occurring in 50%. In fully breast-fed infants who did not receive vitamin K at birth, the incidence is between 1/15,000 and 1/20,000. Babies with cholestasis or malabsorption syndromes are at greater risk.

To prevent VKBD , Vitamin K1(phylloquinone, phytomenadione or phytonadione) prophylaxis should be given right after birth to all neonates( 0.5mg in less than 1000 grams and 1mg  in more than 1000 grams). In the present scenario it should be given as intramuscular injection using 26G (1/2 inch needle). Its available in market in 0.5 ml(1mg) strength. 

G6PD deficient red blood cells are not at any increased risk of oxidative damage from vitamin K1, so it can be safely given irrespective of G6PD deficiency status of the child.

Currently, not enough information is available regarding effectiveness of oral vitamin K to recommend its routine use.

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