成人正常血压外伤患者抗利尿激素引起的低钠血症1例报告。

Maulik K Lathiya, Emily Pepperl, Daniel Schaefer, Hussam Al-Sharif, Adel Zurob, Susan M Cullinan, Antonios Charokopos
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引用次数: 0

摘要

背景:精氨酸加压素是一种在下丘脑产生并由垂体后叶释放的神经肽。除了维持血浆渗透压,在低血容量或低血压的情况下,它有助于通过肾脏水重吸收维持血浆容量,并增加全身血管张力。它的合成类似物广泛用于重症监护病房作为连续输注,除了作为静脉注射或鼻内剂量的医院地板。有限数量的低钠血症患者与脓毒性或失血性休克已报道了先前的加压素。我们首次报道一个血压正常的病人发展为抗利尿激素引起的低钠血症。病例总结:一名39岁男子从叉车上摔下,颅骨轴向载荷损伤。他之前没有外伤史。除运动和感觉障碍外,检查正常。Imagine试验显示C7终板骨折和C7急性外伤性椎间盘伴皮质退变。他接受了颈椎椎间盘切除术和融合术,椎板切除术和后路内固定融合术。术后入住重症监护病房后,患者在输注苯肾上腺素和加压素维持血压维持后出现121-124 mEq/L的低钠血症。诊断为抗利尿激素分泌不当、甲状腺功能减退、肾上腺诱导或利尿剂诱导的低钠血症。在广泛评估低钠血症的潜在原因后,停用抗利尿激素。患者同时限流,给予外源性去氨加压素,并在水中输注5%葡萄糖,以防止钠矫治过度引起的渗透性脱髓鞘综合征,使其钠水平提高到135 mmol/L。结论:抗利尿激素引起的低钠血症在正常血压患者中并不常见,而这种情况最困难的方面是确定低钠血症的潜在原因。我们的病例说明,考虑到住院患者低钠血症的大量鉴别诊断,医院医生和重症监护医生都应该意识到抗利尿激素治疗的严重并发症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Vasopressin-induced hyponatremia in an adult normotensive trauma patient: A case report.

Background: Arginine vasopressin is a neuropeptide produced in the hypothalamus and released by the posterior pituitary gland. In addition to maintaining plasma osmolarity, under hypovolemic or hypotensive conditions, it helps maintain plasma volume through renal water reabsorption and increases systemic vascular tone. Its synthetic analogues are widely used in the intensive care unit as a continuous infusion, in addition to hospital floors as an intravenous or intranasal dose. A limited number of cases of hyponatremia in patients with septic or hemorrhagic shock have been reported previously with vasopressin. We report for the first time a normotensive patient who developed vasopressin-induced hyponatremia.

Case summary: A 39-year-old man fell off a forklift and sustained an axial load injury to his cranium. He had no history of previous trauma. Examination was normal except for motor and sensory deficits. The Imagine test showed endplate fracture at C7 and acute traumatic disc at C7 with cortical degeneration. He underwent cervical discectomy and fusion, laminectomy, and posterior instrumented fusion. After intensive care unit admission post-surgery, he developed hyponatremia of 121-124 mEq/L post phenylephrine and vasopressin infusion to maintain blood pressure maintenance. He was evaluated for syndrome of inappropriate secretion of antidiuretic hormone, hypothyroid, adrenal-induced, or diuretic-induced hyponatremia. At the end of extensive evaluation for the underlying cause of hyponatremia, vasopressin was discontinued. He was also put on fluid restriction, given exogenous desmopressin, and a dextrose 5% in water infusion to prevent osmotic demyelination syndrome caused by sodium overcorrection which improved his sodium level to 135 mmol/L.

Conclusion: The presentation of vasopressin-induced hyponatremia is uncommon in normotensive patients, and the most difficult aspect of this condition is determining the underlying cause of hyponatremia. Our case illustrates that, considering the vast differential diagnosis of hyponatremia in hospitalized patients, both hospitalists and intensivists should be aware of this serious complication of vasopressin therapy.

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