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Severe hyponatremia complicated by seizure following 3,4‐methylenedioxymethamphetamine ingestion

Melanie C Armitage, R. Bryant, C. Page

Emergency Medicine Australasia August 14, 2018 DOI: 10.1111/1742-6723.13159 (opens in new tab)

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Study at a glance

AI-extracted from the abstract
Characteristics Case report Peer reviewed
Sample size 1
Population An 18-year-old woman presenting to the emergency department after alcohol and presumed MDMA ingestion
Dose 1 L 0.9% sodium chloride; 250 mL 3% sodium chloride boluses (three further 250 mL boluses); diazepam 5 mg; droperidol 10 mg (two doses)
Duration 30-hour admission
Measures Glasgow Coma Score (GCS), serum sodium, serum osmolality, urine drug screen, computed tomography head scan
Topics MDMA
Key findings The authors report that an 18-year-old woman who took tablets she believed were MDMA developed severe hyponatremia (sodium 121 mmol/L) with encephalopathy and a generalized tonic-clonic seizure. They attribute the presentation to MDMA-induced hyponatremia and note that most reported cases occur in young women aged 15-30, possibly related to estrogen effects and CYP2D6 metabolism.

Abstract

Dear Editor, An 18 year old woman with an altered level of consciousness presented with friends at 03:00 to the ED having consumed alcohol throughout the evening and ingesting two tablets at midnight that she presumed to be 3,4-methylenedioxy methamphetamine (MDMA). She had no past medical history and was not on any regular medications. On arrival, she was haemodynamically normal (heart rate 81 and blood pressure 146/72) and afebrile. There were no clinical signs of the neuromuscular effects commonly seen in MDMA toxicity. Bedside monitoring was commenced and blood tests including full blood count and electrolytes were requested. Her Glasgow Coma Score (GCS) was initially calculated at seven (E1V2M4); however, this improved within 40 min to a GCS 13 (E3V4M6). Shortly afterwards, she self-discharged and while in the waiting room approximately 2 h after presentation, she suffered a generalised tonic–clonic seizure that resolved with intravenous (IV) diazepam 5 mg. Blood results prior to the seizure revealed a sodium of 121 mmol/L and a serum osmolality of 252 mmol/L. Her renal function was normal. The patient was initially treated with IV 1 L 0.9% sodium chloride with repeat sodium showing an improvement to 125 mmol/L. A bolus of 250 mL 3% sodium chloride was then administered with repeat sodium of 127 mmol/L (Fig. 1). A urine drug screen was positive for cocaine and amphetaminerelated substances and a computed tomography head scan was normal. The patient was then admitted to the ED short stay ward where she became agitated and required chemical sedation with two doses of IV droperidol 10 mg. Serial sodium measurements were then repeated over the course of the day, which showed a trending decline down to a serum sodium of 124 mmol/L (Fig. 1). Given her ongoing altered level of consciousness and hyponatremia, the patient was treated with two further boluses of IV 3% sodium chloride 250 mL (Fig. 1), after which her sodium increased to 134 mmol/L. The patient’s level of consciousness slowly improved and she was discharged the following morning after a 30 h admission. Repeat sodium on discharge was 135 mmol/L. The patient’s clinical presentation is most likely consistent with MDMAinduced hyponatremia causing encephalopathy and seizures. Hyponatremia from MDMA toxicity is an uncommon but life threatening complication from its use. First described in 1993, its pathophysiology is multifactorial with contributing causes from sodium loss from excessive diaphoresis, water intoxication and the syndrome of inappropriate antidiuretic hormone. The majority of cases (>85%) occur in young (15–30 years) women. Oestrogen’s inhibitory effect on Na-KATPase, an important compensatory response for cerebral oedema in the setting of hyponatremia, may explain this female predominance. In addition MDMA is metabolised by the liver cytochrome P450 isoenzyme CYP2D6 to 4-hydroxy-3-methoxymethamphetamine (HMMA). HMMA is a more potent stimulator of antidiuretic hormone secretion than MDMA and so genetic variance of this enzyme may play a role in MDMA-induced hyponatremia. Symptomatic hyponatremia is a medical emergency necessitating prompt recognition and management, often including the use of hypertonic

Comparable studies

Other case reports and case series on MDMA, most cited first.

Study Year Design Participants
'Eve' and 'Ecstasy'. A report of five deaths associated with the use of MDEA and MDMA Individuals whose deaths were associated with MDMA or MDEA use 1987 Case series n = 5
Pathology of deaths associated with "ecstasy" and "eve" misuse. Young white men aged 20 to 25 who died after using ring-substituted amphetamines (MDMA... 1996 Case series n = 7
'Eve' and 'Ecstasy' Individuals who died after using MDMA or MDEA 1987 Case series n = 5
A Method of Conducting Therapeutic Sessions with MDMA Clients with clear therapeutic purpose, excluding those with serious functional... 1998 Case study n = 2
Diversity of Psychopathology Associated with use of 3,4-Methylenedioxymethamphetamine (‘Ecstasy’) Psychiatric patients presenting between 1990 and 1992 whose symptoms developed in the... 1994 Case series n = 13

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