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Ventricular tachycardia following head injury
  1. S S Khogali,
  2. J N Townsend,
  3. H Marshal
  1. skhogali{at}

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A 24 year old man was admitted to a neurosurgical intensive care unit in a coma following a severe head injury, and ventilated. The patient was noted to have increased ventricular ectopic activity with occasional couplets and salvoes of ventricular tachycardia (VT) subsequently developing more frequent runs of torsades de pointes. Routine biochemistry was normal. Alcohol was detectable in the blood but the concentration was not particularly high. The patient, who was previously fit with no cardiac history or family history of cardiac disease, had a normal echocardiogram. He subsequently developed malignant and very broad sinusoidal VT (panel A). Following unsuccessful initial treatment with intravenous amiodarone which was discontinued, a bolus of magnesium sulfate was given and intermittent overdrive pacing used to stabilise the rhythm. Serum magnesium and calcium concentrations subsequently revealed pronounced hypomagnesaemia and hypocalcaemia. Magnesium infusion was then administered. Serial ECGs with simultaneous magnesium concentrations illustrate atrial fibrillation with widespread repolarisation abnormalities and prolongation of the QTc (panel B). With normalisation of the magnesium concentration there was a resumption of stable sinus rhythm (panel C).

Our patient had developed malignant VT as a consequence of electrolyte imbalance (low magnesium and calcium concentrations) resulting from his head injury. Head injury patients can develop polyuresis following cerebral trauma even without mannitol. Thus they are at high risk of developing hypomagnesaemia, hypocalcaemia, hypophosphataemia, and hypokalaemia because of increased urinary loss—an important consideration in neurosurgical critical care management. The patient made a complete and uncomplicated recovery.

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