James Vinson, Nimkoff Laura
Pediatrics Department, Good Samaritan University hospital, West Islip, NY, 11795, USA.
BMC Pediatr. 2025 Jul 29;25(1):578. doi: 10.1186/s12887-025-05862-8.
This review article discusses a case of sodium imbalance and fluid dysregulation in a patient with traumatic brain injury (TBI), progressing through phases including mannitol-induced osmotic diuresis, arginine vasopressin deficiency (central diabetes insipidus), and syndrome of inappropriate antidiuresis (SIAD), before eventual resolution with euvolemia. The timeline of clinical interventions, laboratory trends, and diagnostic insights highlights the complexity of managing sodium and fluid balance in TBI patients.
To illustrate the diagnostic and management challenges of a pediatric TBI case complicated by the sequential development of osmotic diuresis, arginine vasopressin deficiency, syndrome of inappropriate antidiuretic hormone secretion (SIAD), and subsequent stabilization.
We present a detailed case report of a child with severe TBI who experienced multiple phases of sodium and fluid dysregulation, necessitating vigilant monitoring and dynamic management adjustments.
The patient initially developed profound polyuria due to mannitol-induced osmotic diuresis, which obscured the emerging arginine vasopressin deficiency. The transition to SIAD further complicated management, requiring careful fluid and sodium correction. This case underscores the importance of close monitoring in post-TBI patients to detect evolving endocrine disturbances that necessitate timely interventions.
The sequential manifestation of osmotic diuresis, arginine vasopressin deficiency, SIAD, and eventual stabilization in a single patient is a rare and complex occurrence. This case emphasizes the need for dynamic fluid and electrolyte management, with ongoing assessment to tailor interventions appropriately. Our findings highlight the critical role of multidisciplinary teams in optimizing patient outcomes in pediatric TBI cases.
这篇综述文章讨论了一例创伤性脑损伤（TBI）患者的钠失衡和液体调节异常情况，该患者经历了多个阶段，包括甘露醇诱导的渗透性利尿、精氨酸加压素缺乏（中枢性尿崩症）和抗利尿激素分泌不当综合征（SIAD），最终恢复至血容量正常状态。临床干预的时间线、实验室指标变化趋势以及诊断要点凸显了TBI患者钠和液体平衡管理的复杂性。
阐述一例小儿TBI病例在并发渗透性利尿、精氨酸加压素缺乏、抗利尿激素分泌不当综合征（SIAD）并随后病情稳定过程中的诊断和管理挑战。
我们呈现了一例重度TBI患儿的详细病例报告，该患儿经历了多个钠和液体调节异常阶段，需要进行密切监测并动态调整管理措施。
患者最初因甘露醇诱导的渗透性利尿出现严重多尿，这掩盖了逐渐出现的精氨酸加压素缺乏。向SIAD的转变使管理进一步复杂化，需要谨慎进行液体和钠的纠正。该病例强调了对TBI后患者进行密切监测以发现需要及时干预的内分泌紊乱进展情况的重要性。
同一患者先后出现渗透性利尿、精氨酸加压素缺乏、SIAD并最终病情稳定是一种罕见且复杂的情况。该病例强调了动态液体和电解质管理的必要性，以及持续评估以适当调整干预措施的重要性。我们的研究结果凸显了多学科团队在优化小儿TBI病例患者预后方面的关键作用。
