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未经治疗的低钠血症导致的致命性中枢性糖尿病和尿崩症:一种新综合征。

Fatal central diabetes mellitus and insipidus resulting from untreated hyponatremia: a new syndrome.

作者信息

Fraser C L, Arieff A I

机构信息

Veterans Affairs Medical Center, University of California, San Francisco.

出版信息

Ann Intern Med. 1990 Jan 15;112(2):113-9. doi: 10.7326/0003-4819-112-2-113.

Abstract

After elective hospitalization, eleven healthy young women developed symptomatic hyponatremia that was rapidly followed by polyuria, hypernatremia, hyperglycemia, and death. The patients were 30 +/- 2 years old (+/- SE) with initial serum sodium of 140 +/- 1 mmol/L. They all awoke from analgesia but, 32 hours after completion of the procedure, they went from alertness to respiratory arrest in less than 1 hour. At this time, serum sodium was 116 +/- 2 mmol/L and blood glucose was 6.7 +/- 0.7 mmol/L. Without treatment for the hyponatremia, urine output spontaneously increased from 38 to 689 mL/h and urine osmolality fell from 546 to 83 mmol/kg body weight. Over the next 51 hours, blood glucose rose to a high of 24.1 +/- 2.5 mmol/L while serum sodium rose to a high of 167 +/- 2 mmol/L. None of the patients regained consciousness. At autopsy, all patients had cerebral edema with herniation along with hypoxic brain damage. The pituitary showed infarction of both anterior and posterior lobes in 7 of 7 patients examined, while 8 of 11 had necrosis of the medulla and 8 of 8 patients examined had hypothalamic necrosis. All had normal pancreas and kidneys at autopsy. Soon after respiratory arrest, all of the patients developed fixed, dilated pupils that often led to the diagnosis of brain death. Autopsy showed compression of the third cranial nerve (oculomotor) because of cerebral herniation. Thus, all of the patients were diagnosed as being brain dead when some may have been saved. These data suggest that in otherwise healthy young women, untreated symptomatic hyponatremia may lead to brain edema, cerebral herniation, and infarction of pituitary and hypothalamus, resulting in central diabetes insipidus and mellitus.

摘要

在择期住院后,11名健康年轻女性出现症状性低钠血症,随后迅速出现多尿、高钠血症、高血糖并死亡。这些患者年龄为30±2岁(±标准误),初始血清钠为140±1 mmol/L。她们均从镇痛中苏醒,但在手术结束32小时后,在不到1小时内从清醒状态发展为呼吸骤停。此时,血清钠为116±2 mmol/L,血糖为6.7±0.7 mmol/L。未对低钠血症进行治疗,尿量自发地从38 mL/h增加到689 mL/h,尿渗透压从546 mmol/kg体重降至83 mmol/kg体重。在接下来的51小时内,血糖升至24.1±2.5 mmol/L的高位,而血清钠升至167±2 mmol/L的高位。所有患者均未恢复意识。尸检时,所有患者均有脑水肿伴脑疝形成以及缺氧性脑损伤。在接受检查的7名患者中,7人垂体前后叶均有梗死,而11人中有8人延髓坏死,在接受检查的8名患者中有8人下丘脑坏死。尸检时所有患者的胰腺和肾脏均正常。呼吸骤停后不久,所有患者均出现固定、散大的瞳孔,这常常导致脑死亡的诊断。尸检显示由于脑疝导致动眼神经受压。因此,所有患者均被诊断为脑死亡,而其中一些患者可能本可挽救。这些数据表明,在其他方面健康的年轻女性中,未经治疗的症状性低钠血症可能导致脑水肿、脑疝形成以及垂体和下丘脑梗死,从而导致中枢性尿崩症和糖尿病。

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