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首页> 外文期刊>Journal of Clinical Medicine Research >Severe Hyponatremia Due to Valproic Acid Toxicity
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Severe Hyponatremia Due to Valproic Acid Toxicity

机译：丙戊酸毒性引起的严重低钠血症

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Hyponatremia is a very commonly encountered clinical entity with potentially dangerous effects and for which many precipitating factors have been identified. We present a case of valproic acid (VPA) overdose causing profound hyponatremia, with one of the lowest serum sodium levels ever documented in literature. A 54-year-old woman with hypothyroidism, hypertension and bipolar disorder presented with somnolence after intentionally ingesting 7,500 mg VPA. She was drowsy but easily arousable with no hemodynamic compromise and an unremarkable physical exam. There was no clinical suspicion for organic neurological or pulmonary disease, adrenal insufficiency or volume depletion. She was found to have a serum sodium of 99 mEq/L, low plasma osmolality (211 mOsm/kg H2O), and high urine osmolality (115 mOsm/kg H2O). Her urine sodium was 18 mEq/L. She was euthyroid (TSH: 3.06 mIU/L) and compliant with thyroxine replacement. She was admitted to the intensive care unit for close monitoring and VPA was withheld. Over 36 hours her VPA level fell from 59.3 mg/L to 22.8 mg/L, serum sodium steadily rose to 125 mEq/L and there was concomitant improvement in her mental status. At 72 hours, she was transferred for an inpatient psychiatric evaluation and her sodium level was 135 mEq/L. She luckily did not experience any seizures or decline in neurological function. The clinical presentation in this patient is consistent with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) leading to a dramatic fall in sodium to a level of 99 mEq/L. Chronic VPA use has been associated with SIADH and chronic hyponatremia. Review of records in this patient from 1 year prior revealed that her last measured sodium level was 127 mEq/L. It is therefore most likely that our case is one of acute on chronic hyponatremia provoked by VPA overdose in the setting of chronic VPA use. Whilst our patient’s course was relatively benign, this case illustrates a rare consequence of VPA toxicity, which if unnoticed in another patient may be tragic.J Clin Med Res. 2015;7(9):717-719doi: http://dx.doi.org/10.14740/jocmr2219w
机译：低钠血症是一种非常常见的临床实体，具有潜在的危险作用，并且已经鉴定出许多促发因素。我们提出一例丙戊酸（VPA）过量引起严重的低钠血症，这是文献中记载的最低的钠水平之一。一名54岁的甲状腺功能低下，高血压和躁郁症患者，故意摄入7500 mg VPA后表现出嗜睡感。她昏昏欲睡，但容易被唤醒，没有血流动力学损害，体格检查也不明显。没有针对器质性神经系统疾病或肺部疾病，肾上腺功能不全或体质消耗的临床怀疑。发现她的血钠含量为99 mEq / L，血浆渗透压低（211 mOsm / kg H2O），尿液渗透压高（115 mOsm / kg H2O）。她的尿钠含量为18 mEq / L。她甲状腺功能正常（TSH：3.06 mIU / L），甲状腺素替代治疗符合要求。她被送进重症监护病房进行密切监测，并保留了VPA。在超过36个小时的时间内，她的VPA水平从59.3 mg / L降至22.8 mg / L，血清钠稳定地上升至125 mEq / L，并且精神状态随之改善。在72小时时，她被转送住院进行精神病学评估，其钠水平为135 mEq / L。幸运的是，她没有任何癫痫发作或神经功能下降。该患者的临床表现与抗利尿激素分泌不当（SIADH）综合征相一致，导致钠水平急剧下降至99 mEq / L。长期使用VPA与SIADH和慢性低钠血症有关。对该患者1年前的记录进行的回顾显示，她最后一次测得的钠水平为127 mEq / L。因此，在长期使用VPA的情况下，我们的病例很可能是由VPA过量引起的慢性低钠血症的急性病例之一。尽管我们患者的病程相对较温和，但此例说明了VPA毒性的罕见后果，如果在另一名患者中不注意，可能会造成悲剧。JClin Med Res。 2015; 7（9）：717-719doi：http://dx.doi.org/10.14740/jocmr2219w

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