Kamijo Yoshito, Soma Kazui, Hamanaka Satoko, Nagai Tomonori, Kurihara Katsuyoshi
Department of Emergency and Critical Care Medicine, Kitasato University School of Medicine, Sagamihara Kanagawa, Japan.
J Toxicol Clin Toxicol. 2003;41(4):359-62. doi: 10.1081/clt-120022003.
Dural sinus thrombosis has not been described in a patient with hypernatremia resulting from lithium-induced nephrogenic diabetes insipidus. A 63-year-old man on chronic lithium therapy for schizoaffective disorder was transferred to the Emergency Department with dehydration and signs of central nervous system dysfunction after a 3-week isolation in a room in a psychiatric hospital due to exacerbation of psychiatric disorder, during which he refused to eat. Laboratory examination revealed hypertonic hypernatremia (osmolality, 359 mOsm/kg and Na, 171 mEq/L) and hyposthenuria (specific gravity, 1.010 and osmolality, 249 mOsm/kg), with normal serum endogenous vasopressin concentration (2.3 pg/mL). The serum lithium concentration was within the therapeutic range (0.94 mEq/L). Cranial computed tomography demonstrated subarachnoid hemorrhage and suggested dural sinus thrombosis. Although treatment with indomethacin (25 mg parenterally at 8-hour intervals) was somewhat effective in restoring renal concentrating capacity, he died of massive hemorrhagic infarction on the sixth hospital day, probably secondary to dural sinus thrombosis. The clinical diagnosis was confirmed by postmortem examination. Physicians should be alert for the possibility of dural sinus thrombosis as a complication of hypernatremia resulting from lithium-induced nephrogenic diabetes insipidus.
锂诱导的肾性尿崩症导致高钠血症的患者中尚未有硬脑膜窦血栓形成的报道。一名63岁患有分裂情感性障碍并接受慢性锂治疗的男性,因精神障碍加重在精神病院一间病房隔离3周后,出现脱水和中枢神经系统功能障碍体征,被转至急诊科,在此期间他拒绝进食。实验室检查显示高渗性高钠血症(渗透压,359 mOsm/kg;钠,171 mEq/L)和低比重尿(比重,1.010;渗透压,249 mOsm/kg),血清内源性血管加压素浓度正常(2.3 pg/mL)。血清锂浓度在治疗范围内(0.94 mEq/L)。头颅计算机断层扫描显示蛛网膜下腔出血并提示硬脑膜窦血栓形成。尽管使用吲哚美辛(每8小时静脉注射25 mg)治疗在恢复肾脏浓缩能力方面有一定效果,但他在住院第6天死于大面积出血性梗死,可能继发于硬脑膜窦血栓形成。尸检证实了临床诊断。医生应警惕锂诱导的肾性尿崩症导致高钠血症时硬脑膜窦血栓形成作为并发症的可能性。