Murphy Theresa, Dhar Rajat, Diringer Michael
Department of Pharmacy, Neurology/Neurosurgery Intensive Care Unit, Barnes-Jewish Hospital, Washington University School of Medicine, 216 S. Kingshighway Blvd, Saint Louis, MO 63110, USA.
Neurocrit Care. 2009;11(1):14-9. doi: 10.1007/s12028-008-9179-3. Epub 2009 Jan 4.
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.
低钠血症常使急性脑损伤病情复杂化,并可能通过加重脑水肿促使神经功能恶化。相较于液体限制或高渗液体,通过排水来更好地处理脑内水分增加的情况或许更为有效。血管加压素受体拮抗剂,如促进自由水排泄的考尼伐坦,可能是治疗这种常见且潜在严重病症的理想药物。
在我们神经重症监护病房接受治疗的一系列连续患者中,研究了间歇性推注考尼伐坦纠正低钠血症的疗效。若基线血钠超过135 mEq/l或在12小时内已给予过另一剂考尼伐坦,则将患者排除。我们评估了在12小时内血钠升高4或6 mEq/l的患者比例、血钠相对于基线的变化,以及在至少72小时内未接受另一剂药物的患者中,单剂量考尼伐坦使血钠维持在高于基线至少4 mEq/l的长期能力。我们还记录了考尼伐坦对尿量和尿比重的影响,并记录了任何不良事件。
共纳入了给予19例患者的25剂药物(研究期间共给药44剂)。血钠在12小时内升高了5.8±3.2 mEq/l,71%的患者血钠升高至少4 mEq/l,52%的患者血钠升高至少6 mEq/l。在仅接受单剂量药物的患者中,69%的患者在长达72小时内血钠维持升高至少4 mEq/l。考尼伐坦还始终导致尿量增加和尿比重显著下降(即排水利尿)。尽管通过外周静脉给予考尼伐坦,但未观察到静脉炎病例。
间歇性给予考尼伐坦可有效增加自由水排泄并纠正神经疾病患者的低钠血症。这支持对其在该人群中管理低钠血症进行进一步评估。