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首页> 外文期刊>Journal of toxicology-Clinical toxicology >Dural sinus thrombosis with severe hypernatremia developing in a patient on long-term lithium therapy.
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Dural sinus thrombosis with severe hypernatremia developing in a patient on long-term lithium therapy.

机译:长期接受锂治疗的患者发生硬脑膜窦血栓形成伴严重高钠血症。

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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.
机译:锂诱导的肾病性尿崩症导致的高钠血症患者中尚未描述硬脑膜窦血栓形成。一名因精神分裂症而接受长期锂疗法治疗的63岁男子因精神病加重而在精神病医院的一个房间里隔离了3周后因脱水和中枢神经系统功能障碍的症状被转移到急诊科。他拒绝吃。实验室检查发现高渗性高血钠血症(渗透压,359 mOsm / kg,Na,171 mEq / L)和低嗅觉(比重,1.010,重量克分子渗透压,249 mOsm / kg),血清内源性加压素浓度(2.3 pg / mL)。血清锂浓度在治疗范围内(0.94 mEq / L)。颅骨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。尽管用消炎痛治疗(每隔8小时口服25毫克吲哚美辛)在恢复肾脏浓缩能力方面有些有效,但他在住院的第六天死于大规模出血性脑梗死,可能继发于硬脑膜窦血栓形成。死后检查证实了临床诊断。医师应警惕由锂诱导的肾病性尿崩症引起的硬脑膜窦血栓形成作为高钠血症并发症的可能性。

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