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The effect of vitamin K on prothrombin time in critically ill patients: an observational registry study
Sofia Dahlberg1, Ulf Schött2,3, Thomas Kander2,3
1Division of Anaesthesia and Intensive Care, Department of Clinical Sciences, Lund University, SE-22184, Lund, Sweden. sofia.irma.dahlberg@gmail.com.
Insights
Vitamin K administration in critically ill patients with elevated PT-INR (1.3-1.9) led to a slightly greater reduction in PT-INR compared to controls. Further research is needed to identify patient groups that benefit most from vitamin K.
Area of Science:
- Critical Care Medicine
- Hematology
- Pharmacology
Background:
- Vitamin K deficiency is common in critically ill patients with slightly prolonged PT-INR.
- The effect of vitamin K administration on PT-INR in these patients has not been thoroughly investigated.
Purpose of the Study:
- To evaluate changes in PT-INR in response to vitamin K administration in critically ill patients with PT-INR between 1.3 and 1.9.
Main Methods:
- A registry study matched 129 critically ill patients receiving vitamin K with 129 controls using propensity scores.
- PT-INR was measured before and 12-36 hours after vitamin K administration.
- Exclusion criteria included liver cirrhosis and recent blood transfusions.
Main Results:
- PT-INR decreased in both the vitamin K group and the control group.
- The decrease in PT-INR was slightly more pronounced in patients who received vitamin K (p = 0.01).
Conclusions:
- Vitamin K administration resulted in a slightly larger PT-INR decrease in critically ill patients with PT-INR 1.3-1.9 compared to controls.
- Future studies should identify patient populations benefiting from vitamin K and compare its efficacy to plasma or prothrombin complex concentrate.
Background:
Previous studies have indicated that vitamin K deficiency is common in non-bleeding critically ill patients with slightly prolonged prothrombin time-international normalized ratio (PT-INR). It has never been investigated thoroughly whether the administration of vitamin K to these patients could affect their PT-INR. Therefore, the aim of this registry study was to evaluate changes in PT-INR in response to vitamin K in critically ill patients with PT-INR in the range of 1.3-1.9.
Methods:
Patients admitted to a mixed 9-bed general intensive care unit at a University Hospital, between 2013 and 2019 (n = 4541) with a PT-INR between 1.3 and 1.9 at any time during the stay were identified. Patients who received vitamin K with appropriate sampling times for PT-INR and without exclusion criteria were matched with propensity score to patients from the same cohort who did not receive vitamin K (controls). PT-INR was measured at admission, within 12 h before vitamin K administration and 12-36 h following vitamin K administration. Exclusion criteria included pre-existing liver cirrhosis, any plasma or platelet transfusion, or > 1 unit red blood cell transfusion between PT-INR samplings.
Results:
Propensity score matching resulted in two groups of patients with 129 patients in each group. PT-INR decreased in both groups (1.4 [1.3-1.4] in the vitamin K group and 1.4 [1.3-1.6] in the controls, p < 0.001 and p = 0.004, respectively). The decrease in PT-INR was slightly more pronounced in patients who received vitamin K (delta PT-INR - 0.10 [- 0.30 to - 0.10] in the vitamin K group and - 0.10 [- 0.20 to 0.10] in the controls, p = 0.01).
Conclusion:
In critically ill patients with a PT-INR of 1.3-1.9, the administration of vitamin K resulted in a slightly larger decrease of PT-INR 12-36 h after administration compared to controls. Future studies should focus on identifying which patient populations may benefit most from vitamin K administration as well as whether vitamin K could be a better alternative than plasma or prothrombin complex concentrate to improve PT-INR before non-emergent invasive procedures.
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