![]() ![]() Ironically, Apixaban was reintroduced 6 days later as the patient had a suspected pulmonary embolism (PE) based on clinical signs (chest pains and breathlessness). The patient remained under medical supervision for 2 days and was then transferred to the psychiatric. Three measurements were performed during hospitalization, at 16.8, 39.7 and 70.8 h after the intake leading to plasma concentrations, estimated using the anti‐Xa activity, of 2703, 570 and 109 μg l −1, respectively. As Apixaban exposure is closely correlated to the anti‐Xa activity, the drug measurement of Apixaban is not performed 24 h/24 h in our laboratory. Indeed, it has been shown that activated charcoal administered between 2 to 6 h after intake reduces the area under the curve and half‐life at therapeutic doses 2, 3. Activated charcoal was not used because more than 6 h had passed since the drug intake. N‐acetylcysteine was initiated to prevent hepatic injury while no other medication was initiated. The first toxicological tests, carried out on admission, revealed an undetectable alcohol blood concentration and an acetaminophen plasma concentration at 86.3 mg l −1 (therapeutic trough concentrations between 5 and 25 mg l −1). The clinical examination did not show any organ dysfunctions or haemorrhagic signs, and the patient's life was not in danger. Upon admission, the patient explained that 5 h earlier, he had taken 60 tablets of Apixaban, 16 g of Acetaminophen, approximatively 10 tablets of Oxazepam and a few other drugs (not specified). ![]() His medical history included a heart attack and high blood pressure treated by beta‐blockers (bisoprolol), anticoagulant (Apixaban), antianginal drugs (Nitroglycerin and Nicorandil), diuretic (Furosemide) and statins, diabetes treated by insulin and a severe depression treated by antidepressants (Vortioxetine) and anxiolytic benzodiazepine (Oxazepam). Re-dosing of recombinant factor VIIa could be considered and titrated depending on improvement of bleeding.ĭepending on local availability, a consultation of a coagulation expert should be considered in case of major bleedings.A 67‐year‐old man with a medical history of depression was admitted to the emergency department after deliberate self‐poisoning. However, there is currently no experience with the use of recombinant factor VIIa in individuals receiving apixaban. If life-threatening bleeding cannot be controlled by the above measures, administration of recombinant factor VIIa may be considered. Thus, administration of activated charcoal may be useful in the management of apixaban overdose or accidental ingestion. Mean half-life of apixaban decreased from 13.4 hours when apixaban was administered alone to 5.3 hours and 4.9 hours, respectively, when activated charcoal was administered 2 and 6 hours after apixaban. In healthy subjects, administration of activated charcoal 2 and 6 hours after ingestion of a 20-mg dose of apixaban reduced mean apixaban AUC by 50% and 27%, respectively, and had no impact on C max. In controlled clinical trials, orally-administered apixaban in healthy subjects at doses up to 50 mg daily for 3 to 7 days (25 mg BID for 7 days or 50 mg QD for 3 days) had no clinically relevant adverse effects.Ī preclinical study in dogs demonstrated that oral administration of activated charcoal up to 3 hours after apixaban administration reduced apixaban exposure therefore, activated charcoal may be considered in the management of apixaban overdose. The initiation of appropriate treatment, e.g., surgical haemostasis or the transfusion of fresh frozen plasma should be considered. In the event of haemorrhagic complications, treatment must be discontinued and the source of bleeding investigated. Overdose of ELIQUIS may result in a higher risk of bleeding.
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