Article, Endocrinology

Thyroid storm and arrhythmic storm: a potentially fatal combination

Unlabelled imageThyroid storm and arrhythmic storm: a po”>American Journal of Emergency Medicine 31 (2013) 1418.e3-1418.e5

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Case Report

Thyroid storm and arrhythmic storm: a potentially Fatal combination

Abstract

Thyroid storm is a rare clinical emergency with a mortality rate between 20% and 30%. Cardiac arrhythmias associated with thyrotox- icosis are usually supraventricular. Ventricular arrhythmias are rarely associated with this entity and tend to occur in patients with intrinsic cardiac disease. We present a 35-year-old woman with Graves disease and a thyroid storm manifested with multiple malignant dysrhythmic episodes, without underlying cardiac disease. The mechanism for ventricular arrhythmia is not clear but seems to be due to the increased myocardial excitability directly caused by the thyroid hormones. The presence of myocarditis lesions may constitute an arrhythmogenic substratum and contribute further to this manifestation. This case emphasizes the importance of cardiac monitoring in patients with thyroid storm.

A 35-year-old woman was admitted to the emergency department complaining of coriza-like symptoms, fever, and palpitations for 1 week; weight loss; and heat intolerance during recent months. Medical and familiar histories were unremarkable, and no medication was taken. Physical examination revealed mild agitation, proptosis, goiter, blood pressure of 101/84 mm Hg, and regular pulse with 111 beats per minute. The electrocardiogram revealed sinus tachycardia, normal QRS complex, and QTc. Troponin and Serum electrolytes levels were normal. Thyroid study showed elevated free triiodothyronine

32.6 pg/mL (2.0-4.4 pg/mL), free thyroxin 7.8 ng/dL (0.93-1.7 ng/dL), and suppressed thyrotropin (TSH) 0.02 uIU/L (0.27-4.2 uIU/L) (Table). A highly suggestive score of thyroid storm (by the Burch and Wartofsky score, 50/140 points; and Japan Thyroid Association criteria) [1,2] was obtained, and methimazole and glucocorticoids were started. She was admitted to the endocrine ward, and Lugol’s

solution was added 8 hours after.

Thirty-four hours after admission, the patient was found unconscious after a probable seizure. Cardiac monitoring revealed monomorphic ventricular tachycardia with cardiac arrest, and standard cardiopulmonary resuscitation was initiated. Five episodes of ventricular fibrillation and 1 of asystole occurred. After 40 minutes, sinus rhythm was restored, and she was transferred to the intensive care unit (ICU) assisted by ventilation. Minimal anterior neck manipulation was made to minimize the risk of worsening thyrotoxicosis [3,4]. Upon arrival at the ICU, the electrocardiogram revealed sinus tachycardia, and the echocardio- gram showed global hypokinesia with mildly depressed systolic left ventricular function. A low likelihood of underlying coronary disease was assumed, and cardiac catheterization was not performed. Thyroid storm treatment was changed to propylthiour- acil 200 mg every 4 hours, hydrocortisone 100 mg and Lugol’s solution 10 drops every 8 hours, and cholestyramine 4 g every 6

hours. Despite the bolus and perfusion (100 ug/kg/min) of esmolol, the patient presented Recurrent episodes of hemodynamically stable sustained monomorphic ventricular tachycardia (Fig), which remained refractory to other parenteral antiarrhythmic medications. Graves disease was confirmed based on hyperfunc- tioning goiter revealed by thyroid scintigraphy and positive TSH- receptor antibodies (8.6 IU/L; positive if >1.5 IU/L). She was extubated on the third day, and on the fifth, her thyroid function was finally controlled. However, malignant dysrhythmic episodes continued. Suspecting Wolff-Chaikoff effect escape, total thyroid- ectomy was performed on the seventh day. A progressive reduction in arrhythmic events occurred allowing the transference at day 9 to the cardiology department under metoprolol 100 mg every 12 hours. She remained stable, with rare episodes of asymptomatic nonsustained ventricular tachycardia, and the echo- cardiogram showed systolic function recovery. As she was discharged against medical advice, the electrophysiological study was performed 3 months later. Ventricular and supraventricular arrhythmias were not induced by programmed stimulation. During

15 months’ follow-up, the patient presents rare episodes of palpitations with only isolated and coupled ventricular extrasys- toles registered in the autotriggered loop recorder.

Only 1% to 2% of the hospitalized thyrotoxic patients present criteria for thyroid storm [5]. It is a life-threatening exacerbation of thyrotoxicosis with a mortality rate between 20% and 30% [6]. Thyroid storm is usually precipitated by a stressful event [7]. In this case, an upper respiratory viral infection may have been the trigger. Arrhythmias in hyperthyroidism are common and usually supraven- tricular. Ventricular arrhythmias are rare in thyrotoxicosis and, when present, tend to reflect underlying cardiac disease [8].

In this case, the thyroid storm evolved with an arrhythmic storm in a patient without underlying structural and electrical heart abnor- malities nor serum electrolyte disturbances [9].

Table

Summary of the laboratory data

Admission

ICU admission

Day 5

Discharge

TSH (uIU/L)

0.02

Free T3 (pg/mL)

32.6

23.1

3.9

1.4

Free T4 (ng/dL)

7.8

7.8

5.5

1.2

K (mmol/L)

4.04

4.27

3.26

4.29

Mg (mmol/L)

0.72

Ca (mmol/L)

2.45

Abbreviations: Free T3, free triiodothyronine; Free T4, free thyroxin; K, potassium; Mg, magnesium; Ca, calcium.

Referencevalues:TSH, 0.27 to4.2uIU/L;freetriiodothyronine, 2.0to4.4pg/mL;freethyroxin,

0.93 to 1.7 ng/dL; K, 3.50 to 5.00 mmol/L; Mg, 0.60 to 1.10 mmol/L; Ca, 2.09 to 2.42 mmol/L.

0735-6757/$ – see front matter (C) 2013

1418.e4 D. Anjo et al. / American Journal of Emergency Medicine 31 (2013) 1418.e31418.e5

Fig. Electrocardiogram obtained during a ventricular tachycardia episode in the ICU.

Very few reports of ventricular tachycardia and fibrillation in this context are described [4,10-15], and their mechanism is not clear. Triiodothyronine can change the cardiac plasma membrane ion channels’ characteristics, modifying the electrochemical responses of the cell and altering the myocardial depolarization/repolarization properties [16]. In addition, triiodothyronine modifies the response to sympathetic stimulation by modulating the adrenergic receptor function and/or density [17]. These seem to be the main mechanisms responsible for a higher myocardial excitability. Another arrhythmo- genic factor that may be involved is the possible existence of autoimmune myocarditis lesions, similar to the typical autoimmune extraocular muscles involvement [18].

This case emphasizes the need of cardiac monitoring in patients with thyroid storm to identify and treat these challenging and Malignant arrhythmias appropriately.

Diana Anjo MD

Cardiology Department, Hospital Santo Antonio Centro Hospitalar do Porto

Porto, Portugal E-mail address: [email protected]

Jose Maia MD

Intensive Care Unit, Hospital Santo Antonio Centro Hospitalar do Porto

Porto, Portugal

Andre Couto Carvalho MD

Division of Endocrinology, Diabetes and Metabolism Hospital Santo Antonio – Centro Hospitalar do Porto, Porto, Portugal

Heloisa Castro MD Irene Aragao MD

Intensive Care Unit, Hospital Santo Antonio Centro Hospitalar do Porto

Porto, Portugal

Antonio Pinheiro Vieira MD Antonio Hipolito Reis MD Cardiology Department, Hospital Santo Antonio Centro Hospitalar do Porto

Porto, Portugal

Fatima Borges MD

Division of Endocrinology, Diabetes and Metabolism Hospital Santo Antonio – Centro Hospitalar do Porto, Porto, Portugal

Severo Torres MD

Cardiology Department, Hospital Santo Antonio Centro Hospitalar do Porto

Porto, Portugal

http://dx.doi.org/10.1016/j.ajem.2013.04.026

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