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Over recent years, new oral anticoagulant agents (NOAC) have been commercialized as a new treatment in order to prevent or treat thromboembolic events. Although the use of NOACs is easier than for vitamin K antagonists (VKA), their risk-benefit balance still raises concerns, especially in the elderly. To evaluate bleeding complications with anticoagulants agents (NOAC and VKA) among a geriatric population. A retrospective study performed in the four units of the acute geriatric department of CHU Charleroi (116 beds). All the patients who received at least one dose of oral anticoagulant (NOAC or VKA) during their hospitalization between January 1st 2013 and May 31th 2014 were enrolled. Medical files of 242 patients were analyzed, and the type and severity of bleeding were recorded. Mean age was 84 ± 5.4 years old. Seventy-three percent were prescribed VKA. Rivaroxaban was the most prescribed NOAC among this population. Atrial fibrillation was the primary indication of oral anticoagulation in 73% with VKA and 94% with NOAC. Fourty-six patients presented a bleeding (38 patients (22% of patients with VKA) with VKA and 8 patients with NOAC (12% of patients with NOAC)). We found 13 major bleedings with VKA and only one with NOAC. The results of this study are encouraging concerning the utilization of NOACs in the geriatric population. However, larger studies are needed to confirm this.

Background: Hyponatremia occurring as a result of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a common and potentially lethal complication in critically ill patients. Urea, by inducing renal water excretion and promoting sodium (Na) retention, has been well described as a treatment for chronic SIADH. However, there are limited data on its use for the treatment of SIADH as encountered in patients admitted to the intensive care unit (ICU). We assessed the effects of urea administration for treatment of SIADH in ICU patients. Methods: Data from ICU patients treated with urea for SIADH between January 2000 and August 2010 were reviewed. The time courses of Na and urea concentrations were analyzed by variance analysis (ANOVA). Results: Records from 24 patients were analyzed. The most common etiology of SIADH was neurological (18 patients). Before urea administration, the mean serum Na concentration was 124.8 ± 5.9 mEq/l. There was a significant increase in serum Na from the second day of treatment (131.4 ± 3.5 mEq/l, p < 0.001) and a normalization of mean serum Na by the fourth day (136.2 ± 4.1 mEq/l, p < 0.001). The mean serum urea concentration also increased (from 29.8 ± 11.1 mg/dl before urea to 57.6 ± 24.0 mg/dl on the first day of treatment, p < 0.001). Conclusions: Urea administration appears useful for the treatment of SIADH-associated hyponatremia in critically ill patients. Prospective randomized controlled studies are needed to confirm these results.

Dear Editor, Low-molecular-weight heparin (LMWH) is extensively used in intensive care unit (ICU) patients for prevention of thrombosis, with few adverse effects [1]. We report three cases of severe hyperkalemia induced by prophylactic doses of enoxaparin. A 71-year-old diabetic man was admitted for sepsis, with creatinine and serum potassium concentrations of 1.5 mg/dL and 2.0 mEq/L. Potassium increased to 4.7 mEq/L with 60 mEq/day supplement. On day 4, potassium supplement was stopped and enoxaparin started [40 mg subcutaneously (SC) once daily (o.d.)]. By day 6, potassium had increased to 6.1 mEq/L and was resistant to insulin/dextrose and sodium polystyrene sulfonate (SPS) treatments. Enoxaparin was discontinued, and potassium decreased in 4 days. A few days later, enoxaparin (20 mg o.d.) was reintroduced and potassium increased to 5.2 mEq/L. The patient was treated with SPS and discharged without thrombosis prophylaxis (Fig. 1a). A 63-year-old diabetic woman was admitted with cardiogenic shock. Creatinine was 0.7 mg/dL. Enoxaparin 20 mg o.d. was started and increased to 40 mg o.d. after 4 days. Serum potassium increased to 6.1 mEq/L within 3 days. The hyperkalemia was resistant to SPS treatment, and enoxaparin was withdrawn, following which there was a decrease in the potassium level. A few days later, enoxaparin was reintroduced and potassium increased again to 5.3 mEq/L rapidly. Enoxaparin was switched to fondaparinux (2.5 mg o.d.), and the potassium returned to normal values (Fig. 1b). A 71-year-old woman, treated for arterial hypertension, was admitted for spinal cord injury. Her creatinine concentration was 0.4 mg/dL. Five days after surgery, enoxaparin (40 mg o.d.) was started. Potassium rapidly increased, needing treatment with SPS. Enoxaparin was switched to fondaparinux (2.5 mg o.d.), resulting in a decrease in potassium to 4.6 mEq/L. A few days later