Treatment arms of subcutaneous vitamin K (3, n = 58 31% 95% CI, 7%-55%) and placebo/observation (2, n = 27 20% 95% CI, 0%-47%) were less likely to achieve target INR at 24 hours. Among oral vitamin K treatment arms (4, n = 75), the proportion with a target INR at 24 hours was 82% (95% confidence interval, 70%-93%), which was similar to intravenous vitamin K treatment arms (6, n = 69 target INR, 77% 95% CI, 60%-95%). Results Twenty-one studies (10 randomized and 11 prospective trials) were included. Summary estimates were calculated using a random effects model. The primary outcome was achievement of the target INR (1.8-4.0) at 24 hours after vitamin K administration. Randomized controlled trials or prospective, nonrandomized trials that used vitamin K to treat patients without major hemorrhage with an INR greater than 4.0 due to oral anticoagulant use were included. Methods The MEDLINE, EMBASE, and Cochrane Library databases were searched (without language restrictions) for articles published between January 1985 and September 2004. We performed a meta-analysis to determine the effectiveness of phytonadione (vitamin K) in treating excessive anticoagulation. Shared Decision Making and Communicationīackground Patients taking oral anticoagulants with an international normalized ratio (INR) greater than 4.0 are at increased risk for bleeding.Scientific Discovery and the Future of Medicine.Health Care Economics, Insurance, Payment.Clinical Implications of Basic Neuroscience.Challenges in Clinical Electrocardiography.Preadministration of FFP does not alter INR values at 48 hours or more after vitamin K administration. INR reduction is similar for intravenous vitamin K doses of 2 mg or greater. Vitamin K dose, route, and initial INR influence subsequent INR values. Although longer anticoagulation bridge therapy seemed to be associated with higher vitamin K doses, the incidence (p = 0.63) and duration (p = 0.61) were not significant. FFP did not influence INR values at 48 hours. Home warfarin dose did not affect INR responses to intravenous (p = 0.27) or oral vitamin K (p = 0.98). The INR reduction was similar for intravenous vitamin K doses 2 mg or greater. The dose of vitamin K (p < 0.001), route of administration (p < 0.001), and baseline INR (p < 0.001) influenced subsequent INR values. Intravenous vitamin K reduced INR more rapidly than oral vitamin K (5.09, 1.91, 1.54, and 1.41 vs 5.67, 2.90, 2.14, and 1.58) at baseline, 12, 24, and 48 hours, respectively. Data collected included international normalized ratios (INRs) 12 hours, 24 hours, and 48 hours prior to vitamin K administration intravenous or oral vitamin K dose and whether or not fresh frozen plasma (FFP) was administered. This was a chart review of 400 patients who received vitamin K for reversal of warfarin effects between February 2008 and November 2010. To determine factors influencing the extent and rate of INR reversal with vitamin K in the acute/critical care setting. However, the optimal dose and route of vitamin K that does not increase the duration of bridging therapy is unknown. Vitamin K is commonly used for reversal of anticoagulation of warfarin.
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