a b s t r a c t

Seizures can be difficult to distinguish from other causes of transient cerebral hypoxia in the emergency depart- ment. We present a case of Seizure activity in a woman in whom EKG led to a diagnosis of intermittent monomor- phic and Polymorphic ventricular tachycardia (Torsades de pointes), highlighting the need for careful consideration of alternative causes of seizures, even in patients with known epilepsy.

(C) 2016

A 41-year-old woman presented to the emergency department with concern for seizure. Family had witnessed at least five episodes of unre- sponsiveness with tensing of the entire body and shaking or tremor of the upper extremities, without gaze deviation. Each episode lasted ap- proximately 30 s, resolved on its own, and was followed only by mild confusion. She had a history of alcohol-related cirrhosis, ongoing daily alcohol use, and history of alcohol withdrawal. Her chronic medications included methadone 82 mg daily, furosemide 100 mg daily, and spironolactone 200 mg daily. Physical exam was remarkable only for mild postural tremor.

Electrocardiogram obtained in the emergency department during one of these episodes is shown in Fig. 1

The EKG shows monomorphic ventricular tachycardia. Monitor leads during subsequent events demonstrated polymorphic ventricular tachycardia (torsades de pointes). The patient spontaneously converted to normal sinus rhythm after approximately 30 s during these initial and subsequent events, but continued to have several brief runs of mono- morphic and polymorphic ventricular tachycardia (torsades de pointes) with associated clinical Seizure-like activity. intravenous magnesium followed by lidocaine bolus and drip were initiated, and the patient remained in sinus rhythm with decreasing ectopy. Repeat EKG is shown in Fig. 2.

Repeat EKG showed sinus rhythm with markedly prolonged QT in- terval, calculated at 789 ms. Blood obtained prior to any intervention re- vealed serum magnesium of 0.6 mg/dL and serum potassium of

2.3 mEq/L. The patient was admitted to the cardiac intensive care unit for monitoring.

* Corresponding author at: Division of Emergency Medicine, University of Washington, 325 9^th Ave Seattle, WA 98104, United States.

E-mail address: [email protected] (S.C. Morris).

Many cardiac events can cause loss of consciousness with associated seizure-like movements on clinical exam. Video analysis of patients in whom syncope is induced has shown that nearly 90% of patients exhibit transient multifocal arrhythmic movements with superimposed myoc- lonus, head turning, or other automatisms [1]. These movements are thought to result from transient cerebral hypoxia. These events can be interpreted as seizures by laypersons and medical providers, especially when the episodes are self-limited or recurrent.

As many as 20% of patients carrying a diagnosis of epilepsy may be misdiagnosed, and Cardiovascular causes including syncope are most commonly missed [2,3]. This highlights the difficulty in using clinical exam to rule out transient cerebral hypoxic events. EKG is recommend- ed for otherwise unprovoked First-time seizure evaluation to monitor for cardiovascular syncope, including long QT syndrome or arrhythmia [4]. In patients with potential alternative causes or risk factors for pro- voked seizures (as in our patient), a high index of suspicion is required [5].

Several prior case reports have described cases of long QT syndrome associated ventricular tachycardia causing transient cerebral hypoxia and clinical presentation as Epileptic seizures [6,7,8]. Physiologically, long QT syndrome is characterized by slowing of the outward potassium current or slowing of the inactivation of the inward sodium current dur- ing the third phase of the cardiac action potential. Changes in ion flow across the cardiac membrane lead to a longer action potential and prolonged QT interval. The acquired form of long QT syndrome is most common, and is typically caused by medications, drugs of abuse, or elec- trolyte abnormalities (hypomagnesemia, hypokalemia, and hypocalce- mia) which affect those same cardiac ion channels [9]. Methadone is one of several medications shown in vitro to block the hERG (human ether-a-go-go-related-gene) cardiac potassium channel; this is clinical- ly associated with QT interval prolongation [10]. Patients with

http://dx.doi.org/10.1016/j.ajem.2016.11.051 0735-6757/(C) 2016

804.e6 M. Wentlandt et al. / American Journal of Emergency Medicine 35 (2017) 804.e5–804.e6

Fig. 1. Monomorphic Ventricular Tachycardia.

Fig. 2. Sinus ryth with prolongued QT interval.

prolonged QT intervals are at risk for episodes of polymorphic ventricu- lar tachycardia; these arrhythmias are usually self-limited, but can lead to ventricular fibrillation [11]. Clinically, these arrhythmias most com- monly present as syncope.

Our patient’s risk factors for long QT syndrome included methadone use, electrolyte abnormalities, ongoing daily use of high sugar content alcoholic drinks, and chronic high dose diuretic therapy [9].

The present case highlights the need for careful consideration of al- ternative causes of seizures, including cardiac disturbances. It is clinical- ly difficult to differentiate between seizures and other causes of transient cerebral hypoxia. Rapid recognition of long QT syndrome and cardiac arrhythmias can lead to intervention on underlying risk fac- tors and avoid an inappropriate diagnosis of epilepsy.

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