Morbidly obese patients require smaller UFH infusion rates per kilogram actual body weight compared to patients with lower body mass indices. UFH dosing recommendations should be modified to reflect body mass index classification.
Our purpose was to describe anti-Xa levels, dosage requirements, and complications associated with enoxaparin treatment doses in patients with morbid obesity. Inpatients with a BMI >40 kg/m(2) at an academic medical center prescribed therapeutic enoxaparin from 2004 to 2010 who also had an associated anti-Xa level were included in this retrospective evaluation. Twenty-six patients were identified having median weight of 162 kg (range 106-243), median BMI of 49.5 kg/m(2) (range 40.1-98.1), and median enoxaparin duration of 4 days (range 1-32). Venous thromboembolism was the most common reason for anticoagulation (n = 19, 73%). The median starting dose was 0.8 mg/kg actual body weight (range 0.51-1; absolute dose 80-150 mg) every 12 h. Twelve patients (46%) achieved a goal anti-Xa level, 10 (38%) were above goal and 4 (15%) were uninterpretable. Among the 10 patients with anti-Xa levels above goal, the median initial dose was 0.85 mg/kg (range 0.75-1) versus 0.74 mg/kg (range 0.51-1) for patients at goal with similar median peak serum creatinine (PSCr) values between these two groups (P > 0.05). No bleeding events occurred in patients achieving goal anticoagulation versus 4/10 (40%) with high anti-Xa levels (P = 0.033) with similar median PSCr between these groups. No thrombotic events occurred while on therapy. The majority in this cohort with morbid obesity achieved anti-Xa levels at or above goal at doses less than the recommended 1 mg/kg every 12 h. Bleeding events were more frequent among patients with anti-Xa levels above goal, despite similar PSCr values.
Results suggest that dosing enoxaparin in morbidly obese patients (up to 175 kg in weight) with doses capped at 150 mg was not associated with increased bleeding incidence.
Background: Delays in time to therapeutic activated partial thromboplastin time (aPTT) have been associated with poor outcomes in patients with acute pulmonary embolism (PE). Objective: To investigate the relationship between time to therapeutic anticoagulation and in-hospital mortality in critically ill, obese patients with acute PE. Methods: This study examined 204 critically ill patients with a body mass index (BMI) ≥30 kg/m2 receiving unfractionated heparin (UFH) for PE treatment. Patients achieving therapeutic anticoagulation within 24 hours of UFH initiation (early) were compared to those in >24 hours (delayed). Additional end points included 30-day mortality, median time to therapeutic aPTT, proportion of therapeutic and supratherapeutic aPTT values, hemodynamic deterioration, thrombolytic therapy after UFH initiation, length of stay, and bleeding. Results: No difference in in-hospital or 30-day all-cause mortality was seen (odds ratio [OR]: 1.33, confidence interval [CI]: 0.647-2.72; OR: 1.003, CI: 0.514-1.96). Patients in the early group had a greater proportion of therapeutic aPTT values (66.7% vs 50%, P < .001) and higher percentage of supratherapeutic aPTT values (20.9% vs 11.3%, P < .001); however, no increase in clinically significant bleeding was evident (15.2% vs 10.9%, P = .366). Conclusion: In this population, a shorter time to therapeutic aPTT was not associated with improved survival.
Use of dronedarone should be limited to patients with paroxysmal or persistent AF and should not be used in patients with heart failure or with permanent AF. Newer antithrombotic agents appear to be promising alternatives for the prevention of stroke in patients with AF; however, more data are needed to understand their role.
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