Authors

• Petra Grubić Rotkvić — Klinička bolnica “Sveti Duh”, Zagreb, Hrvatska — ORCID: 0000-0002-2587-1932
• Petar Pekić — Klinička bolnica “Sveti Duh”, Zagreb, Hrvatska — ORCID: 0000-0003-0084-3465
• Dario Gulin — Klinička bolnica “Sveti Duh”, Zagreb, Hrvatska — ORCID: 0000-0001-8502-7816
• Jozica Šikić — Klinička bolnica “Sveti Duh”, Zagreb, Hrvatska — ORCID: 0000-0003-4488-0559
• Tea Friščić — Klinička bolnica “Sveti Duh”, Zagreb, Hrvatska — ORCID: 0000-0003-3189-8661
• Gordana Sičaja — Klinička bolnica “Sveti Duh”, Zagreb, Hrvatska — ORCID: 0000-0002-0184-8949
• Hrvoje Budinčević — Klinička bolnica “Sveti Duh”, Zagreb, Hrvatska — ORCID: 0000-0002-5666-7934

Abstract

**Introduction**: Acquired QT prolongation can be caused by drug therapy and electrolyte abnormalities but can also occur as a result of raised intracranial pressure (ICP). QT prolongation is associated with torsades de pointes (TdP), a life-threatening form of polymorphic ventricular tachycardia. **Case report**: 36-year-old man with a known opioid addiction and receiving methadone maintenance therapy (100 mg/day), came to emergency room after an epileptic seizure. On the admission day he took additional unknown dose of methadone. An expansive intracranial process with cerebral edema was found on CT scan. The ECG showed sinus bradycardia and prolonged QT interval, he had recurrent episodes of TdP, some requiring defibrillation (**Figure 1** and **Figure 2**). Intravenous magnesium was immediately applied. Serum potassium and calcium were mildly decreased and therefore adequately corrected. Antiedematous therapy with glucocorticoids was also initiated. Methadone could not be discontinued because of abstinence syndrome, but the dose was reduced. Acute coronary syndrome was excluded, and no structural heart disease was found. Despite the medicamentous therapy, he continued to have TdP so a transjugular temporary pacemaker was placed and the patient was paced at a rate of 90 bpm with successful resolution of ectopy and TdP. Subsequently the patient was transferred to neurosurgical clinic. FIGURE 1. ECG on admission showing QT prolongation and sinus bradycardia. FIGURE 2. Telemetry strip demonstrating polymorphic ventricular tachycardia consistent with torsades de pointes. **Conclusion**: ECG abnormalities can occur in a variety of central nervous system lesions and are related to ICP fluctuation (1). Methadone is a synthetic opioid and QT prolongation is its side effect. Higher doses of methadone (>100 mg/day) are a strong risk factor of inducing QT prolongation, but the lowest dose at which it occurs, has not been clearly established (2). The above-mentioned causes combined with electrolyte abnormalities could contribute to QT prolongation and TdP in our patient. Even though we couldn’t completely discontinue methadone because the patient was opioid addicted, and we couldn’t control ICP until neurosurgical intervention, pacing was a reasonable and effective approach since it shortens QT interval, prevents TdP recurrence and it is especially useful in cases refractory to magnesium or when TdP is precipitated by bradycardia (3).

Keywords

methadone, intracranial pressure, torsades de pointes

DOI

Literature

1. Jachuck SJ, Ramani PS, Clark F, Kalbag RM. Electrocardiographic abnormalities associated with raised intracranial pressure. BMJ. 1975 Feb 1;1(5952):242–4. https://doi.org/10.1136/bmj.1.5952.242
2. Gheshlaghi F, Izadi-Mood N, Mardani A, Piri-Ardekani MR. Dose-Dependent Effects of Methadone on QT interval in Patients under Methadone Maintenance Treatment. Asia Pac J Med Toxicol. 2013;2(1):6–9. https://doi.org/10.22038/apjmt.2013.509
3. Gupta A, Lawrence AT, Krishnan K, Kavinsky CJ, Trohman RG. Current concepts in the mechanisms and management of drug-induced QT prolongation and torsade de pointes. Am Heart J. 2007;153(6):891–9. https://doi.org/10.1016/j.ahj.2007.01.040