Children with cyanotic congenital heart disease frequently have deficiencies in liver-synthesized coagulation factors due to hypoxia and hyperviscosity, which do not respond to parenteral vitamin K.
Vitamin K unlikely to correct coagulopathy in cyanotic CHD; supports hypoxia and hyperviscosity as primary drivers, warranting prospective studies.
An investigation of defects of the haemostatic mechanism in 41 children with cyanotic congenital heart disease concluded that such abnormalities were common and normally involved factors synthesised in the liver, that is the vitamin K dependent factors (rothrombin, factors VII and IX) and factor V. No evidence was found of activation of the coagulation or fibrinolytic systems. The defects can be explained by deficient synthesis resulting from systemic hypoxia as well as from sluggishness of the local microcirculation caused by high blood viscosity. Vitamin K parenterally had no demonstrable effect. Replacement of these factors, possibly combined with measures to improve the microcirculation, therefore, appears to be the appropriate treatment.
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Henriksson et al. (1979) studied this question.
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