Extreme correction of hyponatremia in a patient treated with intravenous conivaptan.
ABSTRACT Intravenous administration of conivaptan, an arginine vasopressin (AVP) receptor antagonist, has been demonstrated to be a safe and effective therapy for euvolemic and hypervolemic hyponatremia. In this case report, we report an extremely rapid correction of serum sodium with a typical dosing regimen of conivaptan. The patient was a 24 year woman who presented with nausea and vomiting, and was found on imaging to have two intracranial tumors, one of which was a large pituitary macroadenoma. Her serum sodium declined to 121mmol/L and intravenous conivaptan therapy was started. After approximately 25mg of conivaptan, her sodium increased 16mmol/L over 8.5hours. Fortunately, in this case, this correction was well tolerated, and the patient experienced no adverse effects of such a dramatic correction of serum sodium. Despite the good clinical result in this case, it should serve as a warning regarding the use of conivaptan, that although a gradual steady improvement in serum sodium can be expected in the majority of patients, more extreme corrections can be inadvertently achieved with even moderate doses. Thus, the exact clinical situation should be taken into consideration, especially in cases of subacute to chronic hyponatremia, where such an extreme correction could lead to neurologic devastation.
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ABSTRACT: Hyponatremia frequently complicates acute brain injury and may precipitate neurological worsening by promoting cerebral edema. An increase in brain water may be better managed through water excretion than with fluid restriction or hypertonic fluids. Vasopressin-receptor antagonists such as conivaptan, which promote free water excretion, may be ideal agents to treat this common and potentially serious disorder. The efficacy of intermittent bolus doses of conivaptan to correct hyponatremia was examined in a consecutive series of patients treated in our neurointensive care unit. Patients were excluded if baseline sodium was over 135 mEq/l or if another conivaptan dose was given within 12 h. We assessed the proportion responding with a 4 or 6 mEq/l rise in sodium by 12 h, the change in sodium from baseline, and, in those not receiving another dose for at least 72 h, the long-term ability of a single dose to maintain sodium at least 4 mEq/l above baseline. We also recorded the effects of conivaptan on urine output and specific gravity, and noted any adverse events. A total of 25 doses given to 19 patients were included (out of 44 total doses administered in the study period). Sodium rose by 5.8 +/- 3.2 mEq/l within 12 h, with 71% rising by at least 4 mEq/l and 52% manifesting at least a 6 mEq/l increase. In those receiving only a single dose, 69% maintained at least a 4 mEq/l rise up to 72 h. Conivaptan also consistently led to increased urine output and a significant drop in urine specific gravity (i.e., aquaresis). No cases of phlebitis were observed despite administration of conivaptan through peripheral IVs. Intermittent dosing of conivaptan was effective in increasing free water excretion and correcting hyponatremia in neurologically ill patients. This supports its further evaluation for managing hyponatremia in this population.Neurocritical Care 02/2009; 11(1):14-9. · 2.60 Impact Factor
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ABSTRACT: Hyponatremia is the most common electrolyte abnormality encountered in clinical practice. The reported frequency of the disorder is determined by a number of factors, including the definition of hyponatremia, the frequency of testing, the healthcare setting, and the patient population. This review focuses on the incidence and prevalence of hyponatremia. In acute hospital care, particular attention is given to admission versus hospital-acquired hyponatremia. Although less well studied, the epidemiology of hyponatremia in the ambulatory-based setting and the geriatric/nursing home population is also summarized. Finally, the frequency of hyponatremia occurring in special clinical conditions--including congestive heart failure, cirrhosis, pneumonia, and acquired immunodeficiency syndrome--as well as in marathon runners will be reviewed. Substantial additional work is still required to determine the true occurrence of hyponatremia in the various clinical settings. Beyond the phenomenologic value, advances in the epidemiology of hyponatremia should also provide insights in the prognostic implications as well as the preventive and management strategies of the disorder in various clinical settings.The American journal of medicine 08/2006; 119(7 Suppl 1):S30-5. · 5.30 Impact Factor
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ABSTRACT: Hyponatremia [serum sodium concentration ([Na(+)]), <135 mEq/liter] is the most common fluid and electrolyte abnormality among hospitalized patients. It is frequently caused by the inappropriate release of arginine vasopressin. The objective of this study was to evaluate the efficacy and safety of oral conivaptan, a vasopressin V(1A)/V(2) receptor antagonist, in patients with euvolemic or hypervolemic hyponatremia. The study design was a 5-d placebo-controlled, randomized, double-blind study. The study was performed at a hospital. Intervention: Oral conivaptan (40 or 80 mg/d) or placebo was given in two divided doses. Seventy-four patients (average baseline serum [Na(+)], 115 to <130 mEq/liter) were studied. The main outcome measure was the change from baseline in serum [Na(+)] area under the curve. The least-squares mean change from baseline in the serum [Na(+)] area under the curve with conivaptan (40 and 80 mg/d) was 2.0-fold (P = 0.03) and 2.5-fold (P < 0.001) greater, respectively, than that with placebo. The median time to achieve a confirmed increase in serum [Na(+)] of 4 mEq/liter or more from baseline was 71.7 h for placebo, 27.5 h for 40 mg/d conivaptan (P = 0.044), and 12.1 h for 80 mg/d conivaptan (P = 0.002). The mean total times during which patients had a serum [Na(+)] level of 4 mEq/liter or more above baseline were 46.5, 69.8, and 88.8 h (P = 0.001), respectively. The least-squares mean change in serum [Na(+)] from baseline to end of treatment was 3.4 mEq/liter for placebo, 6.4 mEq/liter for 40 mg/d conivaptan, and 8.2 mEq/liter for 80 mg/d conivaptan (P = 0.002). A confirmed normal serum [Na(+)] (>/=135 mEq/liter) or increase of 6 mEq/liter or more was observed in 48% of patients given placebo, 71% given 40 mg/d conivaptan, and 82% given 80 mg/d conivaptan (P = 0.014). Headache, hypotension, nausea, constipation, and postural hypotension were the most common adverse events. Oral conivaptan (40 and 80 mg/d) was well tolerated and efficacious in correcting serum [Na(+)] in hyponatremia.Journal of Clinical Endocrinology & Metabolism 06/2006; 91(6):2145-52. · 6.31 Impact Factor