ECE2022 Eposter Presentations Late Breaking (59 abstracts)
Permanent central diabetes insipidus after traumatic brain injury
Ludmila Astafyeva 1 , Yuliya Sidneva 1 , Inna Badmaeva 1 , Pavel Kalinin 1 , Svetlana Valiullina 2 & Andrey Marshintsev 2
1Burdenko Neurosurgery Center, Moscow, Russian Federation; 2Clinical and Research Institute of Emergency Pediatric Surgery and Trauma (CRIEPST), Moscow, Russian Federation
The article presents a case of permanent central diabetes insipidus (CDI) in a patient after severe traumatic brain injury (TBI) in traffic accident. A 16-year-old boy entered to a medical facility in the coma (6 points of Glasgow Coma scale (GCS)). Diagnosis: acute TBI; severe cerebral contusion; subarachnoid hemorrhage; depressed comminuted cranial vault fracture; basilar skull fracture; visceral contusion. CDI diagnosed three days after injury when polyuria and hypernatremia (155 mmol/l) developed. Desmopressin therapy started through a feeding tube. Thirst was appeared when patient out of coma on day 21 while desmopressin therapy was continuing. Because of persistent thirst and polyuria desmopressin therapy continued in the spray form. Against this backdrop polyuria reduced to 3-3.5 liters per day while nasal desmopressin therapy was continuing. The symptoms of CDI persisted in the long-term period two years after TBI while the intact adenohypophysis function. This case demonstrates a rare development of permanent diabetes insipidus in a boy after TBI. CDI manifested only as polyuria and hypernatremia in a coma. Thirst joined at rising levels of consciousness. The probable causes of CDI were neurohypophysis and his tract injury as a result of extended basilar skull fracture and/or irreversible secondary hypothalamus injury because of brain diffuse axonal damage after head trauma.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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