Paper
Life-threatening magnesium toxicity
Published Feb 1, 2000 · S. Fletcher, M. Parr
Intensive Care Medicine
9
Citations
0
Influential Citations
Abstract
Sir: A 29-year-old woman was referred for investigation of an episode of confusion and dysphasia occurring 6 h post-partum. Although this episode was associated with a diastolic blood pressure of 90 mmHg, the preceding pregnancy had been uncomplicated with no hypertension. On arrival her blood pressure was 115/78 and physical examination, laboratory analyses and computed tomographic (CT) scan of the head were all normal. Seventeen hours after delivery she had a generalised tonic-clonic seizure. This was treated by increments of midazolam (total 7 mg). An infusion of magnesium sulphate was prepared with 24.7 g (100 mmol) in a 500 ml bag of 0.9 % saline. A loading dose of 4 g (16 mmol) was commenced by burette. After the seizure the patient had a Glasgow coma score (GCS) of 10 and was transferred to the intensive care unit. Shortly after arrival, she became rapidly comatose (GCS 3) and apnoeic, but remained in sinus rhythm with a pulse rate of 100 and blood pressure of 130/80. Oxygenation was maintained by bag-mask ventilation followed by tracheal intubation. It was noticed that the bag containing the magnesium was empty and biochemical analysis revealed marked hypermagnesaemia (Table 1). Within 30 min of her collapse, the patient's conscious level was improving and after 3 h she was extubated with a normal neurological examination. She made a full recovery with no recollection of the episode. A subsequent MRI revealed a small thalamic infarct (unrelated to the magnesium toxicity) for which she was anticoagulated. The toxic effects of magnesium are well described and predictable, with flushing, nausea and vomiting being early symptoms. At 2.5 to 5 mmol/l there are electrocardiographic changes (PR interval and QRS prolongation); loss of tendon reflexes at 5 mmol/l; respiratory arrest at 7.5 mmol/l and cardiac arrest at 12.5 mmol/l [1]. In the setting of normal renal function, toxicity with therapeutic doses is only seen when administration is rapid [2]. Our patient received 100 mmol over approximately 20 min; it is possible that her peak serum level of magnesium was higher than our measured value of 6.87 mmol/l. The absence of circulatory compromise or arrhythmias in this case was notable; however, if the respiratory arrest had occurred outside the intensive care unit the outcome could have been much worse. Although calcium is used as a magnesium antagonist in cases where magnesium has resulted in cardiovascular instability, our patient did not require specific treatment [3]. We recommend that infusions of magnesium be given by pump with anti-syphon protection. This was specified in our hospital protocol but was not done; a programme of staff education has been undertaken. In the non-critical care environment it may be appropriate to prepare infusions containing doses of magnesium that would not cause toxicity in the event of uncontrolled administration. All staff involved in the administration of magnesium should be fully aware of its toxic effects and personnel skilled in airway management and cardiopulmonary resuscitation should be readily available.
Case ReportMagnesium toxicity can be life-threatening when administered rapidly, especially in the setting of normal renal function.
Full text analysis coming soon...