SUN-073 Arginine Vasopressin Deficiency Following Myoclonic Status Epilepticus

Abstract E. Makarova: None. A. Jamil: None. A.S. Siddiqui: None. Background: Arginine vasopressin deficiency (AVPD), formerly known as central diabetes insipidus, is a syndrome characterized by abnormal production of large volumes of dilute urine secondary to decreased release of antidiuretic hormone (ADH). One of the documented but lesser-known etiologies of AVPD is status epilepticus. Clinical Case: We present a case of a 36-year-old female with a medical history of traumatic brain injury following a motor vehicle accident three years prior to presentation with subsequent quadriplegia, aphasia, and neurogenic bladder, who developed AVPD secondary to status epilepticus. She initially presented with pyelonephritis and obstructive uropathy secondary to a ureteral stone, but these resolved following urologic intervention. Her clinical course was complicated by acute encephalopathy, which was thought to be secondary to hypernatremia. Laboratory evaluation showed serum sodium 149 mEq/L (reference range 136-145 mEq/L), serum osmolality 315 mOsm/kg (275-295 mOsm/kg), urine sodium 62 (10-30 mEq/L), urine osmolality 268 (100-1000 mOsm/kg). Clinically, she had polyuria with urine output greater than four liters in 24 hours, for two consecutive days. Given her clinical presentation and laboratory evaluation, this was consistent with AVPD. She was treated with desmopressin resulting in appropriate concentration of urine. However, despite resolution of hypernatremia, she continued to be encephalopathic. Further evaluation with an electroencephalogram revealed generalized polyspikes consistent with status epilepticus. Her anti-epileptic drug regimen was adjusted, which led to resolution of both encephalopathy as well as AVPD. Desmopressin was able to be discontinued after her anti-epileptic regimen was modified. Conclusion: Clinicians should be aware that a rare cause of transient AVPD is status epilepticus, and treatment of status epilepticus can resolve AVPD, mitigating the need for prolonged desmopressin treatment. Furthermore, being aware of this etiology is pertinent to consider in conditions where the thirst mechanism may be impaired or where the communication of thirst as a hallmark symptom may be impaired, such as pediatric patients, patients with intellectual disability, cerebrovascular accident, traumatic brain injury, etc. Sunday, June 2, 2024

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Journal
Journal of the Endocrine Society
Published
2024-10-01
DOI
https://doi.org/10.1210/jendso/bvae163.2404
Primary Topic
Electrolyte and hormonal disorders
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article
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article

SUN-073 Arginine Vasopressin Deficiency Following Myoclonic Status Epilepticus

Elizaveta Makarova, Abid Jamil, Ayesha Siddiqui
Journal of the Endocrine Society
Electrolyte and hormonal disorders
article

SUN-073 Arginine Vasopressin Deficiency Following Myoclonic Status Epilepticus

Elizaveta Makarova, Abid Jamil, Ayesha Siddiqui
article en

Abstract

Abstract E. Makarova: None. A. Jamil: None. A.S. Siddiqui: None. Background: Arginine vasopressin deficiency (AVPD), formerly known as central diabetes insipidus, is a syndrome characterized by abnormal production of large volumes of dilute urine secondary to decreased release of antidiuretic hormone (ADH). One of the documented but lesser-known etiologies of AVPD is status epilepticus. Clinical Case: We present a case of a 36-year-old female with a medical history of traumatic brain injury following a motor vehicle accident three years prior to presentation with subsequent quadriplegia, aphasia, and neurogenic bladder, who developed AVPD secondary to status epilepticus. She initially presented with pyelonephritis and obstructive uropathy secondary to a ureteral stone, but these resolved following urologic intervention. Her clinical course was complicated by acute encephalopathy, which was thought to be secondary to hypernatremia. Laboratory evaluation showed serum sodium 149 mEq/L (reference range 136-145 mEq/L), serum osmolality 315 mOsm/kg (275-295 mOsm/kg), urine sodium 62 (10-30 mEq/L), urine osmolality 268 (100-1000 mOsm/kg). Clinically, she had polyuria with urine output greater than four liters in 24 hours, for two consecutive days. Given her clinical presentation and laboratory evaluation, this was consistent with AVPD. She was treated with desmopressin resulting in appropriate concentration of urine. However, despite resolution of hypernatremia, she continued to be encephalopathic. Further evaluation with an electroencephalogram revealed generalized polyspikes consistent with status epilepticus. Her anti-epileptic drug regimen was adjusted, which led to resolution of both encephalopathy as well as AVPD. Desmopressin was able to be discontinued after her anti-epileptic regimen was modified. Conclusion: Clinicians should be aware that a rare cause of transient AVPD is status epilepticus, and treatment of status epilepticus can resolve AVPD, mitigating the need for prolonged desmopressin treatment. Furthermore, being aware of this etiology is pertinent to consider in conditions where the thirst mechanism may be impaired or where the communication of thirst as a hallmark symptom may be impaired, such as pediatric patients, patients with intellectual disability, cerebrovascular accident, traumatic brain injury, etc. Sunday, June 2, 2024

Journal of the Endocrine SocietyVol. 8(Supplement_1)
Penn State Milton S. Hershey Medical Center (US)
Openalex Percentile: Top 54%
Electrolyte and hormonal disorders
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