Fatal outcome during anaesthesia induction in a patient with amiodarone-induced thyrotoxicosis

EDITOR:

Amiodarone is a class III anti-arrhythmic drug which has been used in Europe since 1967 to treat angina and refractory arrhythmias of supraventricular, junctional and ventricular origin [1]. It is an iodinated benzofuran derivative with a molecular structure that is similar to thyroxine and triiodothyronine [2]. It has a high iodine content (37% per weight). A significant amount of iodine is liberated during drug metabolism [3]. The large iodine load has been implicated as the main factor in the pathogenesis of amiodarone-induced thyroid dysfunction, such as amiodarone-induced thyrotoxicosis [2,3]. We report a case of amiodarone-induced thyrotoxicosis after a single dose of amiodarone for the treatment of atrial fibrillation and the impact on induction of anaesthesia for thyroidectomy.

A 53-yr-old female with a medical history of a dilatated cardiomyopathy was admitted to the medical ICU with congestive heart failure and first time occurrence of atrial fibrillation. The patient had hyperthyroidism (free thyroxine: 4.1 ng dL⁻¹, thyroid-stimulating hormone <0.01 mU L⁻¹). She had been treated with potassium perchlorate and thiamazol for 5 days before the actual hospital admission. After thrombus exclusion by echocardiography, the patient was electrically cardioverted but sinus rhythm could not be established. A single dose of 600 mg amiodarone intravenous (i.v.) was administered, again followed by electrical cardioversion. Sinus rhythm was achieved and the patient rapidly recovered from congestive heart failure. However, 1 day later thyrotoxicosis with tachyarrhythmia, haemodynamic instability, sweating and severe neuromuscular weakness developed. Despite additional treatment with carbimazole and corticosteroids, the symptoms of thyrotoxicosis worsened. Finally, the patient was scheduled for thyroidectomy 13 days after the development of amiodarone-induced thyrotoxicosis. On arrival in the operating room, the patient had a heart rate of about 140 beats per minute with atrial fibrillation and a bifascicular block. An arterial line was placed in the left radial artery. Mean arterial pressure was 80 mmHg. Oxygen was applied by a mask until oxygen saturation reached 100%. Induction of anaesthesia was with sufentanil 0.3 μg kg⁻¹, etomidate 0.25 mg kg⁻¹ and rocuronium bromide 0.6 mg kg⁻¹. Immediately after induction, mean arterial pressure decreased to 40 mmHg and norepinephrine infusion was started (0.1 μg kg⁻¹ min⁻¹). The patient was intubated and ventilated with 100% oxygen. At this time, ventricular tachycardia developed and this rapidly progressed to ventricular fibrillation. Resuscitation in accordance with The International Liaison Committee on Resuscitation (ILCOR) guidelines was initiated. Transoesophageal echocardiography did not reveal any treatable cause, e.g. thrombus formation or pericardial fluid. The unsuccessful resuscitation attempts were ceased after 90 min.

Amiodarone-induced thyrotoxicosis is a life-threatening disease with a mortality of up to 50% in patients who are refractory to medical treatment [4]. However, mortality is reduced to 0–13% when operative thyroidectomy is performed [1,4]. Here, we report the fatal outcome of a patient with amiodarone-induced thyrotoxicosis refractory to medical, mechanical and electrical treatment during induction of anaesthesia for thyroidectomy. In previous reports, amiodarone-induced thyrotoxicosis developed in patients with long-term oral amiodarone treatment [2,3,5,6]. In our case, a single dose of amiodarone 600 mg i.v. was administered. The patient had a goitre and manifest hyperthyroidism at the time of amiodarone administration. The high iodine load of the amiodarone molecule was responsible for excessive thyroid hormone synthesis. Therefore, excessive hormonal synthesis was blocked by thionamides. Additionally, potassium chlorate (KClO₄) was administered for the depletion of intrathyroidal iodine stores. Finally, i.v. glucocorticoid therapy was initiated to treat a possible amiodarone- or iodine-induced destructive thyroiditis [5]. The pharmacological properties of amiodarone make the medical management of this situation difficult. Amiodarone accumulates in the thyroid gland and produces a large increase in iodine stores. It also has high lipid solubility with an elimination half-life of up to 107 days. [2]. When medical treatment is not successful, plasmapheresis and peritoneal dialysis have been applied for transient improvement [1]. These patients have been successfully treated with thyroidectomy [1–4], but patients with manifest hyperthyroidism have a high anaesthesia-related risk for morbidity and mortality due to haemodynamic instability and cardiac arrhythmias.

There is no specific recommendation for the management of anaesthesia induction in these patients. In one report, drugs similar to those in our case were used with success [1]. Thyroidectomy could have alternatively been performed after the infiltration of local anaesthetic. However, surgical management is more complex under these circumstances and endogenous catecholamine release could have contributed to a further deterioration of haemodynamic dysfunction and tachyarhythmia. Our patient had refused surgery with local infiltration. The use of dantrolene has been reported to stabilize the haemodynamics in a patient with thyroid crisis. Dantrolene might inhibit the effect of circulating thyroid hormones on calcium flux across the sarcoplasmatic reticulum [5]. This treatment is experimental and therefore dantrolene was not administered in our case.