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Reactions 1131 - 9 Dec 2006 S Desmopressin Hyponatraemic seizures leading to fatal head injury: case report A 27-year-old man developed hyponatraemic seizures that led to a fatal head injury during desmopressin therapy for enuresis. The man, who had been receiving desmopressin nasal spray [dosage not stated] for 8 years and who had a history of two previous hospitalisations in the previous 3 years for hyponatraemic seizures, experienced seizures which caused him to fall off his chair and injure his head [time to adverse reaction onset not stated]. He continued to have seizures and, on admission, he was still fitting and was deeply comatose; his Glasgow Coma Score was 4. The man received IV diazepam and phenytoin, and his trachea was intubated. A brain CT scan revealed a small subdural haematoma, and a left frontotemporal contusion with mass effect. His serum sodium level was 116 mmol/L and he had a calculated serum osmolality of 254 mosm/kg. He was transferred to the neurosurgical ICU where an intracranial pressure (ICP) monitor was inserted in order to maintain an ICP of < 20mm Hg and a cerebral perfusion pressure of > 60mm Hg. Laboratory investigation showed hypotonic hyponatraemia. Clinical examination revealed that he was euvolaemic and it was felt that his hyponatraemia was caused by a combination of excess fluid intake and desmopressin therapy. He received hypertonic saline and his fluids were restricted; over 24 hours, his sodium level increased from 116 mmol/L to 130 mmol/L. He required a craniotomy and partial left frontal lobectomy due to severe cerebral oedema and increased ICP. His condition deteriorated postoperatively, his ICP continued to increase and, 4 days after hospitalisation, he died from his head injury. Author comment: "Although the patient’s demise was not directly due to the presence of desmopressin-induced hyponatraemia, it played a pivotal role leading to seizure activity and a subsequent fall resulting in a traumatic brain injury. The cerebral oedema which resulted was further exacerbated by the presence of hyponatraemia and ultimately proved fatal." Larney V, et al. Hyponatraemic convulsions and fatal head injury secondary to desmopressin treatment for enuresis. European Journal of Anaesthesiology 23: 895-897, No. 10, Oct 2006 - Ireland 801051230 1 Reactions 9 Dec 2006 No. 1131 0114-9954/10/1131-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved

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Reactions 1131 - 9 Dec 2006

SDesmopressin

Hyponatraemic seizures leading to fatal head injury:case report

A 27-year-old man developed hyponatraemic seizures thatled to a fatal head injury during desmopressin therapy forenuresis.

The man, who had been receiving desmopressin nasal spray[dosage not stated] for 8 years and who had a history of twoprevious hospitalisations in the previous 3 years forhyponatraemic seizures, experienced seizures which causedhim to fall off his chair and injure his head [time to adversereaction onset not stated]. He continued to have seizures and,on admission, he was still fitting and was deeply comatose; hisGlasgow Coma Score was 4.

The man received IV diazepam and phenytoin, and histrachea was intubated. A brain CT scan revealed a smallsubdural haematoma, and a left frontotemporal contusion withmass effect. His serum sodium level was 116 mmol/L and hehad a calculated serum osmolality of 254 mosm/kg. He wastransferred to the neurosurgical ICU where an intracranialpressure (ICP) monitor was inserted in order to maintain anICP of < 20mm Hg and a cerebral perfusion pressure of> 60mm Hg. Laboratory investigation showed hypotonichyponatraemia. Clinical examination revealed that he waseuvolaemic and it was felt that his hyponatraemia was causedby a combination of excess fluid intake and desmopressintherapy. He received hypertonic saline and his fluids wererestricted; over 24 hours, his sodium level increased from116 mmol/L to 130 mmol/L. He required a craniotomy andpartial left frontal lobectomy due to severe cerebral oedemaand increased ICP. His condition deteriorated postoperatively,his ICP continued to increase and, 4 days after hospitalisation,he died from his head injury.

Author comment: "Although the patient’s demise was notdirectly due to the presence of desmopressin-inducedhyponatraemia, it played a pivotal role leading to seizureactivity and a subsequent fall resulting in a traumatic braininjury. The cerebral oedema which resulted was furtherexacerbated by the presence of hyponatraemia and ultimatelyproved fatal."Larney V, et al. Hyponatraemic convulsions and fatal head injury secondary todesmopressin treatment for enuresis. European Journal of Anaesthesiology 23:895-897, No. 10, Oct 2006 - Ireland 801051230

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Reactions 9 Dec 2006 No. 11310114-9954/10/1131-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved