Regional Anesthesia for Thyroidectomy in Two Patients with Amiodarone-Induced Hyperthyroidism

Amiodarone is a potent antiarrhythmic with a wide spectrum of activity in the treatment of both atrial and ventricular arrythmias. Unfortunately, its antiarrhythmic efficacy is counterbalanced by a variety of serious side effects, including pneumonitis and thyroid disease [1]. Because of its ability to liberate iodine, amiodarone can cause hyperthyroidism, which is often refractory to conventional treatment [2,3]. These patients are frequently intolerant of beta-blockade due to their underlying cardiomyopathies. Continuing life-threatening manifestations of thyroid excess with medical management has led to the performance of surgical thyroidectomy, which provides prompt, effective metabolic control [4]. Little information is available regarding the anesthetic management of these patients. Anesthetic concerns include the medical condition for which amiodarone was originally given, associated side effects of the drug, uncontrolled hyperthyroid state, and any coexisting diseases [1,5]. We report the use of regional anesthesia in two patients with amiodarone-induced hyperthyroidism having surgical thyroidectomy after failed medical management. Case Reports Patient 1 A 64-year-old man presented for subtotal thyroidectomy as treatment for amiodarone-induced hyperthyroidism. The patient had been receiving amiodarone for 2 yr prior to admission for treatment of refractory ventricular tachycardia. Symptoms of tremor, dry skin, insomnia, and anorexia began 6 mo after institution of amiodarone. The patient also reported a 25-kg weight loss over a year and a half. He was initially treated with methimazole, which decreased his free thyroxine (T4) level from 5.2 to 4.9 mg/dL (normal 4.2-12.5 mg/dL), which was considered clinically insignificant. His history included a myocardial infarction complicated by ventricular tachycardia that required placement of a permanent automatic implantable cardiac defibrillator (AICD) 7 yr prior to admission. On the same admission, a left ventricle thrombus had been noted, and coumadin therapy was instituted. The last discharge of his defibrillator was 5 mo prior to surgery. In addition, 3 yr prior to admission, the patient had been admitted with atrial flutter and subsequently underwent placement of a pacemaker. A cardiac catheterization revealed an ejection fraction of 15% and significant coronary artery disease. Other coexisting diseases included a 15 pack-a-year tobacco habit and a 3.5-cm infrarenal abdominal aortic aneurysm with associated 100% left renal artery stenosis. His oral medications included amiodarone 200 mg daily, digoxin 0.25 mg every other day, furosemide 20 mg daily, atenolol 25 mg daily, benezepril 40 mg daily, and coumadin held 2 wk prior to admission. Physical examination revealed a cachectic male, pulse 64 bpm, regular, blood pressure 104/78 mm Hg, respiratory rate 16 breaths/min, oral temperature 36.7 degrees C, weight 56 kg. The patient's neck was supple with an enlarged multinodular thyroid. Chest auscultation revealed clear lung fields and regular cardiac rate and rhythm with no murmurs or S3. Laboratory investigations included prothrombin time 13.5 s, creatinine 1.2 mg/dL, T4 5.2 mg/dL, thyroid-stimulating hormone 0.7 uIU/mL (normal 0.49-5.66 uIU/mL). Electrocardiogram revealed a ventricular paced rhythm at 70 bpm, left axis deviation, and an old anterior wall infarct. The patient was brought to the preoperative holding area where routine noninvasive monitors were placed and peripheral intravenous access was obtained. Transcutaneous defibrillation pads were attached and connected prior to AICD deactivation by a cardiologist. A right radial arterial line was inserted. Oxygen was administered by face mask. After sedation with midazolam 1.5 mg and fentanyl 50 micro g, bilateral superficial cervical plexus blocks were performed. The midpoint of the posterior border of the sternomastoid muscle was identified. From this point, using a 25-gauge 2-inch needle, superficial infiltration 3 cm caudad and 3 cm cephalad was performed using 5 mL of bupivacaine 0.5% with 1:400,000 epinephrine [6]. This dose of epinephrine was chosen to maximize the duration of blockade and to minimize the cardiovascular effects of epinephrine [6]. Adequate cutaneous anesthesia to pinprick occurred in 12 min over the C2-C4 dermatomes. The patient was brought to the operating room, and all monitors and oxygen were reattached. Using a 22-gauge 2-inch needle, a transtracheal injection of 5 mL of lidocaine 2% was performed to decrease airway reactivity during surgical manipulation. The patient was sedated with intermittent doses of fentanyl 25 micro g and midazolam 0.5 mg. Communication was maintained with the patient throughout surgery. Hemodynamics were stable. The patient reported one episode of discomfort described as "deep pressure." This was relieved by readjustment of the surgical retractors and reinjection of transtracheal lidocaine. Surgery time was 3 h. The total dose of sedation was fentanyl 270 micro g and midazolam 4.5 mg. The patient recovered uneventfully and had no complaints of unpleasant intraoperative events. Patient 2 A 71-yr-old man with amiodarone-induced hyperthyroidism was admitted for subtotal thyroidectomy. The patient complained of a 2-mo history of fatigue, tremor, anorexia, scaly skin, dysphonia, and an associated 15-kg weight loss. Three weeks earlier, he had been admitted for right upper lobe pneumonia and diagnosed with thyrotoxicosis. His T4 level was 23 mg/dL. Complicating this presentation was superimposed congestive heart failure. Echocardiogram showed an ejection fraction of 32%, moderate mitral regurgitation, severe tricuspid regurgitation, and global hypokinesis. He received aggressive diuretic therapy, his amiodarone was discontinued, and he was sent home on antibiotics. Sixteen years prior to admission, the patient had an anterior wall myocardial infarction. He did well until 3 yr ago, when he presented with acute onset of atrial fibrillation, which was treated with digoxin and quinidine. The quinidine was subsequently discontinued because of gastrointestinal irritation, and small-dose amiodarone therapy was begun. One year prior to admission, he underwent cardioversion twice, and his amiodarone was increased to 400 mg daily, which resulted in a normal sinus rhythm with a left bundle branch block. Other coexisting diseases included hypertension and chronic renal insufficiency. His oral medications included furosemide 80 mg daily, propylthiouracil 300 mg three times a day, digoxin 0.25 mg every other day, enalapril 20 mg twice a day, and coumadin discontinued 3 wk prior to surgery. Physical examination revealed a thin man in no apparent distress, heart rate 100 bpm, irregular, arterial blood pressure 160/56 mm Hg, respirations 16 breaths/min, oral temperature 36.8 degrees C, weight 81 kg. His neck was remarkable for an enlarged nodular thyroid, chest examination revealed decreased breath sounds at the bases, cardiac auscultation was significant for an irregular rate and rhythm, with normal S1 and S2, II/VI systolic ejection murmur heard greatest at the upper left sternal border, and a I/VI holosystolic murmur radiating to the axilla. Preoperative evaluation also included a white blood cell count 4.1 x 103, prothrombin time 13.4 s, creatinine 1.4 mg/dL. A chest radiogram revealed a right upper lobe opacity with volume loss most consistent with resolving pneumonia with underlying atelectasis. An electrocardiogram revealed atrial fibrillation at 90 bpm, left axis deviation, left ventricular hypertrophy by voltage criteria, and an old anterior wall infarct. The patient was brought to the preoperative holding area where routine noninvasive monitors were applied. Oxygen was administered by face mask. An arterial line was inserted. Using the same technique and drug described for Patient 1, bilateral superficial cervical plexus blocks were performed. Surgical anesthesia ensued within 10 min. The patient was taken to the operating room, and all monitors were reapplied. A transtracheal lidocaine injection was also performed using 5 mL of lidocaine 4%. Intraoperative sedation was provided by intermittent doses of midazolam and fentanyl. Total sedation was midazolam 7 mg and fentanyl 175 micro g. At all times, the patient was able to communicate freely with the staff. He was hemodynamically stable throughout surgery, which was uneventfully and completed after 3 h, after which the patient was transferred to a prearranged intensive care unit bed. His subsequent course was uneventful. Discussion Although effective, general anesthesia in amiodaronetreated patients has been associated with serious arrhythmias, hypotension, and congestive heart failure [1,5,7]. For example, sinus arrest, junctional rhythm, heart block, atropine-resistant bradycardia, persistent hypotension, and a blunted response to phenylephrine have all been reported as complications [1,5]. The approach to general anesthesia in these patients usually involves full invasive monitoring and a narcoticbased anesthetic. The special anesthetic concerns in these two cases were considerable and included atrial and ventricular arrhythmias, ischemia, cardiomyopathies, and peripheral vascular disease. The use of regional anesthesia for thyroid surgery is an alternative anesthetic option [8], which offers several advantages to conventional techniques. Bilateral superficial cervical plexus blockade is easy to perform, and complications are rare [6]. Aspiration of the syringe prior to injection is essential to avoid inadvertent intravascular injection into the external jugular vein, internal jugular vein, or carotid artery [6]. Advantages of the technique are that patients are conscious and able to speak at the end of surgery and to receive good postoperative analgesia. It provides complete sensory anesthesia of the C2-C4 dermatomes with a minimum of local anesthetic [9]. This innervation supplies the skin over the neck from the mandible to the clavicle anteriorly and laterally [9]. The small local anesthetic dose required helps avoid the toxicity and systemic manifestations of absorbed epinephrine. The deep branches of the cervical plexus, which provide motor innervation to the muscles of the neck, and the visceral afferents accompanying the systemic innervation to the thyroid, are not blocked [9]. This is not a problem because the visceral afferents provide minimum sensory innervation to the thyroid, accompanied by gentle retraction of the strap muscles and combined with intravenous narcotic analgesia. Transtracheal lidocaine was injected to help prevent any cough reflex elicited from transmitted pressure on the trachea. The use of two different concentrations of lidocaine in the case reports was due to individual preference. Due to the rapid systemic absorption, this technique provides a very short duration of action. If necessary, the block can be repeated during surgery. Amiodarone, a benzofuran derivative, is 37% iodine by weight and structurally resembles thyroid hormones [3,10]. Amiodarone is a potent antiarrhythmic drug with a wide spectrum of activity against refractory atrial and ventricular arrythmias and has been used for this indication in the United States since 1986 [10]. Trip et al. [11] prospectively examined 58 patients begun on amiodarone for signs of thyroid dysfunction. They reported an overall incidence of 12.1% for amiodarone-induced hyperthyroidism. In contrast to these results, the incidence of amiodarone-induced hyperthyroidism was found to be 2.6% (53 of 2070) in 20 collective American studies and 2.1% (30 of 1448) in a European report [12]. Due to the low incidence of amiodarone-induced hyperthyroidism, routine thyroid hormone testing is not recommended and should only be performed when patients develop symptoms of thyrotoxicosis [11]. Amiodarone-induced hyperthyroidism is often refractory to conventional medical therapy for a variety of reasons, including the systemic release of iodine and the ability of amiodarone to inhibit 5 prime monodeiodinase enzyme, which converts T4 to triiodothyronine (T3) in the periphery [10]. Due to the large iodine load of chronic amiodarone therapy, thioamides are less effective. When combined with potassium perchlorate, iodine uptake may be further inhibited; however, in most cases, amiodarone must be withdrawn to control the thyrotoxicosis [2]. This withdrawal may produce a paradoxical exacerbation of thyrotoxicosis due to an increase in peripheral T3 production and loss of peripheral adrenergic blockade and T3 binding [13]. Radioactive ablation therapy is not an option because of a very low 24-hour iodine (131) uptake [10]. The treatment of choice when amiodarone-induced hyperthyroidism is manifested by life-threatening arrhythmias, when amiodarone therapy cannot be withdrawn, or when the disorder persists after medical therapy is subtotal thyroidectomy [4,14]. Surgical therapy has produced prompt, effective metabolic control when medical therapy has failed. Amiodarone-induced hyperthyroidism presents considerations that are different from the conventional management of thyrotoxicosis. These patients have severe coexisting disease in addition to hyperthyroidism. To our knowledge, there is only one other report regarding this issue in the literature [15]. In that report, although the anesthetic technique and monitoring were not described, a favorable outcome from thyroidectomy under local anesthesia was achieved. This technique provides an alternative method of management that is simple and may offer an improved outcome.