Abstract
Patients with advanced liver disease who are not taking vitamin K antagonists often have an elevated international normalized ratio, potentially due to vitamin K deficiency and the decreased synthesis of clotting factors by the liver. It is possible that vitamin K deficiency is due to dietary deficiency, impaired absorption in the small intestine, or both. This has led to the practice of the administration of phytonadione to limit the risks of bleeding in these patients. However, phytonadione is available in different formulations with varying pharmacokinetics and there is a paucity of data in the literature to guide optimal management. The routine use of phytonadione to correct INR in cirrhotic patients not taking warfarin should be avoided due to the lack of proven benefits. However, intravenous phytonadione may be considered in actively bleeding or critically ill patients with vitamin K deficiency. Oral formulation is unlikely to be absorbed in cirrhotic patients and should be avoided.
Highlights
Liver plays a crucial role in hemostasis, and advanced cirrhosis causes several pathophysiological changes that may appear as coagulopathic imbalances [1]
Patients with end stage liver disease (ESLD) commonly present with a prolonged prothrombin time (PT) and an elevated international normalized ratio (INR). This is concerning because the incidence of bleeding and its associated mortality is high in patients with advanced cirrhosis [2,3,4], but the majority of clinically significant bleeding episodes in cirrhotic patients seem to be due to increased portal venous pressure rather than altered hemostasis [5,6]
Vitamin K 10 mg IV for up to three days was reported as adequate to correct vitamin K deficiency [38] and this is often seen in clinical practice; significant reductions in INR were only observed after the first dose in a study by Sulaiman et al [39]
Summary
Deficiency is a portion of the proposed mechanism of elevated INR in cirrhotic patients through dietary deficiency (common in alcohol-induced liver disease or chronic illness) and reduced absorption in the small intestine, likely due to decreased bile flow, impaired vitamin K cycle, and increased use of antibiotics, which reduce the vitamin K produced by normal gastrointestinal flora [14,27,28]. It is important to note that while bile production and vitamin K absorption may be decreased in patients with cirrhosis, not all cirrhotic patients with increased INR have a vitamin K deficiency.
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