Intravenous vitamin K1 prior to orthotopic heart transplantation: effects in vivo and in vitro

Barnette, Rodger E.; Wendling, Woodrow W.; Schweiger, John W.; Brister, Neil W.; Schartel, Scott A.; Chen, D.; Shuman, C. A.; McClurken, James B.; Jeevanandam, Valluvan

doi:10.1111/j.1399-6576.1997.tb04616.x

Cited by 3 publications

(3 citation statements)

References 13 publications

(11 reference statements)

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“…The current dominant management strategy of warfarin cessation, FFP transfusion and vitamin K administration may not be an effective way of reversing warfarin coagulopathy in a medical emergency such as oral anticoagulant therapy-related intracranial haemorrhage. Vitamin K administration entails a small risk of anaphylaxis, may induce modest haemodynamic changes in patients with cardiac dysfunction 10 , which is a common co-existing medical problem in patients on warfarin, and should not be used as monotherapy because it generally takes more than 12 to 24 hours to completely normalise the INR. The use of FFP, at the recommended dose of 15 to 20 ml/kg, implies the infusion of large volumes of plasma, which not only takes several hours to complete, but can also lead to volume overload and heart failure, especially in those with cardiac impairment.…”

Section: Discussionmentioning

confidence: 99%

Rapid Reversal of Coagulopathy in Warfarin-Related Intracranial Haemorrhages with Prothrombin Complex Concentrates

Chong

Lew

Kuperan

et al. 2010

Anaesth Intensive Care

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We report our initial experience using Profilnine SD, a 3-Factor prothrombin complex concentrate (PCC) in combination with fresh frozen plasma and vitamin K in seven patients admitted to our neurointensive care unit with oral anticoagulation therapy-related intracranial haemorrhage over a six-month period, to achieve rapid normalisation of the international normalised ratio (INR) and allow surgical evacuation when indicated. Four patients presented with subdural haematomas while three had intracerebral haematomas. Six of seven patients had admission INR in the appropriate therapeutic range for oral anticoagulation therapy. The median dose of PCC administered was 28.5 IU/kg body weight (interquartile range 21.3 to 38.5 IU/kg). All four patients with subdural haematoma underwent surgical evacuation once INR was less than 1.5. Median time from computed tomography diagnosis to surgery was 275 minutes (range 102 to 420 minutes). The median time to INR normalisation post-PCC administration was shorter, at 85 minutes (range 50 to 420 minutes) for the four patients who survived, versus 10 hours (range 9 to 44 hours) in the three patients who died. Two of the three patients who died had haematoma increase, worsening midline shift and subfalcine herniation, leading to withdrawal of therapy. Prothrombin complex concentrates should be considered for use in the urgent reversal of INR in oral anticoagulation therapy-related intracranial haemorrhage, potentially halting haematoma expansion and expediting urgent neurosurgical intervention, although data from randomised controlled trials is still lacking. The literature supporting the use of PCC is reviewed and a protocolised emergent treatment algorithm is proposed, which may help achieve earlier consistent normalisation of the INR.

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Section: Discussionmentioning

confidence: 99%

Rapid Reversal of Coagulopathy in Warfarin-Related Intracranial Haemorrhages with Prothrombin Complex Concentrates

Chong

Lew

Kuperan

et al. 2010

Anaesth Intensive Care

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“…31 Since that report, several in vivo and in vitro studies have been conducted to better elucidate the mechanism behind the cardiovascular effects of vitamin K1. [37][38][39] Barnette et al found that IV vitamin K1-induced hemodynamic changes were consistent with dilation of the arterial system and possibly the venous system through a humoral inflammatory or allergic response. 37 In contrast, Tirapelli et al determined that the dose-dependent decrease in mean arterial pressure seen with IV vitamin K1 most likely involves activation of the nitric oxide pathway and vasodilator release.…”

mentioning

confidence: 99%

“…[37][38][39] Barnette et al found that IV vitamin K1-induced hemodynamic changes were consistent with dilation of the arterial system and possibly the venous system through a humoral inflammatory or allergic response. 37 In contrast, Tirapelli et al determined that the dose-dependent decrease in mean arterial pressure seen with IV vitamin K1 most likely involves activation of the nitric oxide pathway and vasodilator release. 38 Drolet et al reported that IV vitamin K1 exerted a direct effect of on cardiac action potential through blocking major ionic currents, warranting caution in patients sensitive to small changes in action potential (eg, QT interval prolongation [QT] prolongation).…”

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confidence: 99%

Characterizing the Severe Reactions of Parenteral Vitamin K1

Britt

Brown

2016

Clin Appl Thromb Hemost

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Parenteral vitamin K1 (phytonadione) is used for anticoagulant reversal, and a boxed warning exists with intravenous and intramuscular administration due to the possibility of severe reactions, including fatalities. These reactions resemble hypersensitivity or anaphylaxis, including anaphylactoid reaction, and have led to shock and cardiac and/or respiratory arrest. The objective of this review is to summarize the available literature detailing the anaphylactic/anaphylactoid reactions with parenteral vitamin K1 in order to better characterize the reaction and provide a more in-depth understanding of its importance. A comprehensive literature search of MEDLINE (1946 to June 2016) and EMBASE (1947 to June 2016) was conducted using the terms vitamin K1, phytonadione, phytomenadione, vitamin K group, anaphylaxis, polyoxyethylated castor oil, and cremophor. A total of 2 retrospective surveillance studies, 2 retrospective cohort studies, and 17 case reports were identified for inclusion and assessment. Based on a review of the literature, use of parenteral vitamin K1 may result in severe hypotension, bradycardia or tachycardia, dyspnea, bronchospasm, cardiac arrest, and death. These reactions are most consistent with a nonimmune-mediated anaphylactoid mechanism. It appears that intravenous administration is more frequently associated with these reactions and occurs at an incidence of 3 per 10 000 doses of intravenous vitamin K1. The solubilizer may also increase the risk of adverse reactions, which occurred in patients with and without previous exposure to vitamin K1. Although there are known factors that increase the risk of an adverse drug event occurring, reactions have been reported despite all precautions being properly followed.

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