Research Article Open Access
Surgery in Refractory Amiodarone-Induced Thyrotoxicosis
Carine Ghassan Richa1,2*, Mohamad Souheil El Rawas1,3
1Department of Endocrinology, Rafic El Hariri University Hospital, Beirut, Lebanon.
2Endocrinology fellow, Lebanese University, Hadath, Lebanon.
3Endocrinologist, Rafic El Hariri University Hospital, Beirut, Lebanon.
*Corresponding author: Carine Ghassan Richa, Department of Endocrinology, Rafic El Hariri University Hospital, Beirut, Lebanon, Tel: +961 70144157;Email: @
Received: June 18, 2018; Accepted: July 02, 2018; Published: July 11, 2018
Citation: Richa CG, Souheil MD Rawas EI (2018) Surgery in Refractory Amiodarone-Induced Thyrotoxicosis J Endocrinol Diab. 5(4): 1-9. DOI: 10.15226/2374-6890/5/4/001110
Background: Thyroidectomy is a challenging treatment for refractory amiodarone induced thyrotoxicosis (AIT).

Objectives: The authors’ aim in this article is to conduct a systematic review of the currently available literature regarding thyroidectomy for the treatment of refractory AIT.

Methods: The authors’ systematic review yielded 14 studies encompassing 39 patients.

Results: All patients in this study developed thyrotoxicosis on amiodarone especially those with cardiac fragility and benefit from thyroidectomy to control all the symptoms of the hyperthyroid state without surgical risk or consequence on the cardiac status.

Conclusion: Thyroidectomy remains the definitive management of refractory AIT and should be instituted sooner rather than later in a patient suffering from this condition.
Amiodarone is a class III anti-arrhythmic drug used to manage different cardiac problems, but its high iodine content and its direct toxic effect may cause thyroid dysfunction. Thyrotoxicosis is a harmful side effect of amiodarone use. Management of AIT is usually resistant to conventional methods and require prompt resolution of thyrotoxicosis-related cardiac decomposition. Definitive treatment can include surgery of the thyroid gland.

So here comes many studies about the safety and utility of thyroidectomy as definitive way to treat AIT and restore thyroid function.

The purpose of the present study was to systematically review the existing recent data regarding total thyroidectomy for the treatment of refractory AIT.
A review of the existing published data on thyroidectomy for the treatment of amiodarone induced thyrotoxicosis performed using PubMed for articles published in English. The terms used included amiodarone, thyrotoxicosis, thyroidectomy, amiodarone induced thyrotoxicosis. The search was not limited to any date range. 38 articles were identified and a total of 14 remained after duplicates were removed. 11 cases, 3 studies of case series reporting total thyroidectomy as definitive treatment for amiodarone induced thyrotoxicosis especially in those refractory to medical management.
A total of 14 studies were included in this review article. All were published between 2002 and 2016 from different countries.

We have in total 39 patients, 23 were males, 16 were females and the age range varies between 32 and 82.

All patients have heart problems and started amiodarone for atrial fibrillation, ventricular tachyarrythmias or dilated ischemic cardiomyopathy with heart failure and all these cardiac conditions were refractory to the usual medical or interventional therapy (drugs, implantable cardiac devices or even radiofrequency ablation).

The usual dose of amiodarone present is 200 mg daily and the duration of amiodarone use extends from 6 months to 4 years and most of patients were admitted for thyrotoxicosis state ranging from recurrent rapid atrial fibrillation, decompensated heart failure to even thyroid storm which is reported in one case.

Laboratory tests in the 11 cases showed an elevated free or total thyroxine and triiodothyronine and suppressed TSH levels. In the 3 case-series, thyroid function tests were not identified. The reasons for intervention were failure of therapy to control thyrotoxicosis, persistence and deterioration of clinical symptoms and appearance of drug’s side effects secondary to high doses used.(Table 1)

The definitive mechanism by which amiodarone has contributed to thyrotoxicosis, whether type 1, type 2 or both, has been identified in most of the patients; in the 11 cases, 7 had type II AIT confirmed by either Doppler ultrasound which showed hypovascularization or by pathological features, 1 patient had type I AIT revealed by thyroid gland hypervascularization in addition to nodular goiter seen macroscopically and in 3 patients the exact mechanism was unknown. In the case –series of, all patients had destructive thyroiditis seen on pathology, in Lorberboym et al, type II AIT was established in the 11 patients and the type of AIT has not been mentioned [10,12,14]. 2 patients out of 39 had toxic MNG with pathology confirming type II AIT (they may have mixed disorder) and 1 patient had nodular goiter with unknown pathology. .(Table 2)
Table 1: Summary of case reports for 11 patients with amiodarone-associated thyrotoxicosis who were treated successfully with total thyroidectomy


Age and Sex

Medical history

Reason for starting amiodarone

Amiodarone dose

Mehta et al. 2008(1)

66 year-old man


CABG complicated by AF

800 mg for one week then 200 mg daily

Cunha et al.2016(2)

52 year-old man


Acute MI, complicated by AF (patient refused radiofrequency ablation).

300 mg daily

Hashimoto et al.2015(3)

40 year-old man


DCMP on amiodarone for 2.5 years


Ishay et al.2013(4)

48 year-old man

Non obstructive HCMP, CHF, CAD, MI, DM, CKD (3A), COPD, recurrent CVA, paroxysmal AF

Persistant episodes of AF treated with amiodarone since 5 years


Kotwal et al.2015(5)

61 year-old Caucasian man

AF, CAD, ischemic CMP, CHF, DM.

AF and CHF


Batori et al.2006(6)

65 year-old woman

CMP (due to moderate-severe aortic regurgitation) complicated by VA and FA. Multiple nodular formations in thyroid lobes (treated with MTZ 5mg/day)

VA and FA

200 mg daily

Calis et al.2010(7)

46 year-old man

Idiopathic DCMP Sustained VT, VF (treated with radio frequency ablation and ICD)

Persistent episodes of VT and VF


Tonnelier et al.2013(8)

62 year-old caucasian man

AF since 4 years AI grade 1-2/4


200 mg daily for 2 years

Gavira et al.2013(9)

51 year-old man

Obstructive HCMP, AF


200 mg daily since 4 years

Marinis et al.2013(10)

52 year-old man

Recurrent AF

Uncontrolled AF (despite cardioversion, propafenone, sotalol and catheter ablation)

200mg daily for 6months

Zhu et al.2016(11)

56 year-old Chinese man



200mg daily for 2 years


Reason for Intervention

lab tests

Ultrasound thyroid+echocardiography

Treatment of      AIT

Mehta et al. 2008(1)

SOB, palpitations, AF with rapid ventricular rate

TSH 0.008

-Thyroid gland enlarged with diffuse heterogeneity, no Doppler evidence of increased vascularity

MTZ 10mg TID later increased to 15mg TID then replaced by PTU  1000mg loading then 250 mg every 4hours dexamethasone 2mg every 6hours

TT3 5.61

TT4 28.4

Cunha et al.2016(2)

-TFT monitoring (after 1   year) - 2months after, recurrent AF

TSH 0.01

-EF 34%, mild atrial dilatation

Bisoprolol 5 mg daily, MTZ 10 mg twice daily and prednisolone 5 mg daily

FT4  4.06

FT3  9.23.

After 2 Months

TSH 0.03

FT4 1.49

FT3 3.22

Hashimoto  et al.2015(3)

symptoms of CHF

TSH <0.05

-Thyroid gland was not swollen, slightly enlarged, with monotonous echogenicity. The Doppler flow was not increased

Inorganic iodine administration (189mg/day), Hydrocortisone 200 mg replaced by prednisolone 40mg, increased to 60 then 80mg, MTZ 15mg

FT4 3.39

FT3 6.61

Ishay et al.2013(4)

symptoms of CHF

TSH <0.03

-EF 50% with grade 2 diastolic dysfunction and enlarged left atrium

MTZ 40mg/day replaced by PTU 800 mg/day, prednisone 40mg/day replaced by dexamethasone

FT4 5.8

FT3 8.39

Kotwal et al.2015(5)

SOB, palpitations, tremor, generalized weakness

TSH 0.02

-Bilaterally heterogeneous, hypovascular and hypoechoic thyroid gland -EF 25%

Prednisone 60mg and methimazole 40mg replaced by PTU 200mg TID, lithium, 8 daily cycles of plasmapheresis, with increasing volumes of plasma exchange

FT4 4.88

FT3 5.4

Batori et al.2006(6)

Symptoms of hyper functioning MNG: Weight and hair loss, insomnia, nervousness

TSH 0.97

-Thyroid gland moderately enlarged with colloidal-cystic nodules, the largest of 1 cm in the isthmus, solid, isoechogenic, with thin rarefaction halo of the echoes -Moderately dilated left ventricular with hypertrophy, EF 35-40%, moderate-severe aortic valvular regurgitation, light-moderate mitral insufficiency and light tricuspidal insufficiency

MTZ 5mg/day replaced by PTU 50mg/day

FT4 1.81

FT3 2.36

Calis et al.2010(7)

Fine tremor and tachycardia.

TSH <0.005

-Left ventricular dilatation, EF 30%, mild mitral regurgitation.

PTU, sodium per chlorate, prednisone, metoprolol

FT4 >7.76

TT3 1.62

Tonnelier et al.2013(8)

Tremor, heat intolerance, excessive sweating, weight loss, palpitations, SOB

TSH < 0.015

-Diffusehypo-echogenic heterogenous gland. Absence of hypervascularity  -Normal EF

Methylprednisolone 32mg/day, MTZ 30mg then 60mg/day, potassium per chlorate 1g/day, sotol 240mg/day, 6 cycles of plasmapheresis

FT4 > 3.1

FT3 19.2

Gavira et al.2013(9)

New episode of AF, decompensated CHF, nervousness, palpitations, weight loss

TSH 0.008

-Generalized hypovascularization in thyroid gland

carbimazole 45 mg/d, prednisone 60 mg/d, propranolol 60 mg/d, Lugol’s solution 5 drops BID, cholestyramine 12 g/d, 10 sessions of plasmapheresis, iopanoic acid 500 mg BID

FT4 7.5

FT3 10.99

Marinis et al.2013(10)

Tachycardia progressively leading to CHF

TSH <0.01

-Slightly enlarged thyroid, with heterogeneous echogenity and increased vascularity -EF 30-35%

carbimazole 40mg TID, prednisolone 16mg daily, propranolol 100mg BID

Zhu et al.2016(11)

Fever (40°C), SOB, rapid AF, hypotension (thyroid storm)

TSH <0.015

-Normal EF

propranolol 20 mg TID replaced by esmolol infusion up to 200 μg/kg/min, hydrocortisone 100 mg every 6 hours, intravenous digoxin 500 μg once, PTU 400 mg, Lugol’s iodine 10 ml, cholestyramine, plasmapheresis

FT4 4.97

FT3 11





Mehta et al. 2008(1)

Despite maximal medical therapy, FT4 and TT3 continued to increase and TSH remained below 0.03

Clinically and biochemically euthyroid 10 days after thyroidectomy

The gland was soft, not hypervascular. The epithelium in many of the follicles was degenerated or partially denuded, with vacuolated cytoplasm and pyknotic nuclei. Aggregates of foamy histiocytes were found within the injured follicles, as well as in the adjacent interstitium. These changes are typical for amiodarone-induced thyroid injury

Cunha et al.2016(2)

Electrical cardio version performed then radiofrequency ablation was proposed for the recurrent AF but the patient refused.

TFT improved gradually in the first week and the patient became asymptomatic. Control echocardiography was normal, with EF of 59%.


Hashimoto et al.2015(3)

Overt thyrotoxicosis was not controlled despite 2.5 months of steroids  and anti-thyroid drugs

After surgery, the patient’s thyrotoxicosis rapidly disappeared, EF ameliorated and TFT normalized with 100 𝜇g of levothyroxine

Findings characterized by scattered follicle disruption, vacuoles in epithelial cells, and macrophage infiltration, compatible with amiodarone toxicity

Ishay et al.2013(4)

Persistant symptoms of decompensated CHF (recurrent pulmonary edema with episodes  of supraventricular and ventricular tachycardia)

Within 2 weeks of thyroidectomy, patient developed hypothyroidism and started on levothyroxine

Macroscopically: small and fibrotic diffuse goiter Microscopically: thyroid follicular cells were degenerated with picnotic nuclei. Infiltration with foamy histiocytes was noted

Kotwal et al.2015(5)

Reccurent symptoms with poor response to medical therapy and increased cardiovascular risk

Within 24 hours, his FT4 and FT3 levels decreased. On follow-up 2 months later, he remained clinically euthyroid on levothyroxine and maintained a stable cardiac status.

Macroscopically: a hard thyroid on both sides with severe fibrosis and adhesions especially over the trachea. Microscopically: intra-follicular histiocytes, patchy fibrosis and involuted follicles, suggestive of destructive thyroiditis

Batori et al.2006(6)

No amelioration depite anti-thyroid drugs, reccurent symptoms of CHF

Amelioration of thyrotoxic state


Calis et al.2010(7)

No improvement in TFT (TT3 and FT4 remained high)

Within several weeks, TFT improved and the patient was started on levothyroxine.


Tonnelier et al.2013(8)

Worsening of symptoms

Rapid improvement of symptomatology after thyroidectomy. Levothyroxine was prescribed at day 28 post-surgery


Gavira et al.2013(9)

Worsening of hyperthyroidism (TSH 0.008, FT4 >7.7 and FT3 15.14), uncontrolled atrial flutter

After 12 months of follow-up on treatment with levothyroxine 125 mcg/day, the patient has experienced no new episodes of tachyarrhythmia.

Normal sized thyroid gland with no nodules, involution of thyroid follicles, and degenerative changes.

Marinis et al.2013(10)

Persistant tachycardia and abnormal TFT

2 weeks after thyroidectomy, the patient experienced better tolerance of physical activity, reduced his β-blocker regimen and demonstrated a higher EF (50%). One month postoperatively, the patient has discontinued his β-blocker and has returned to normal daily activity.

Nodular goiter with follicular hyperplasia

Zhu et al.2016(11)

Refractory tachycardia, therapeutic options were limited by the severe derangement of liver function.

After thyroidectomy, there was a significant drop of FT4, FT3 and heart rate. 12 months after discharge, his TFT were stable on thyroxine replacement.

Microscopically, there was a predominance of colloid containing thyroid follicles. Several features compatible with type II AIT were seen, including foamy histiocytes, vacuolated desquamated epithelial cells and multinucleated giant cells

DM: diabetes mellitus CAD: coronary artery disease CVA: cerebrovascular accident AF: atrial fibrillation
CABG: coronary artery bypass graft MI: myocardial infarction DCMP: dilated cardiomyopathy CHF: congestive heart failure CKD: chronic kidney disease COPD: chronic obstructive pulmonary disease CMP: cardiomyopathy
VA: ventricular arrhythmia MTZ: methimazole VT: ventricular tachycardia VF: ventricular fibrillation AI: aortic insufficiency SOB: shortness of breath TFT: thyroid function test MNG: multinodular goiter NA: not available
TSH (thyroid stimulating hormone) :0.35-5.5 mIU/l
TT4 (total thyroxine) : 4.5-12 mcg/dl
TT3 (total triiodothyronine) : 0.6-1.81 ng/ml
FT4 (free thyroxine) : 0.61-1.12 ng/dl
FT3 (free triiodothyronine) : 2.5-3.9 pg/ml
Table 2: Summary of case-series for 5 patients with amiodarone-associated thyrotoxicosis who were treated successfully with total thyroidectomy


Age +sex

Past medical history

Reason for starting amiodarone

Reason for intervention

Duration of amiodarone use

Treatment of AIT




Gouch et al.2002(12)

82 year-old female

Toxic MNG treated with carbimazole for 20 years



4 months

PTU, prednisone, potassium per chlorate.

Failure of therapy to control thyrotoxicosis

patients recovered rapidly and remain well and euthyroid on thyroxine replacement

Destruction of follicles, and macrophages in the colloid. Marked inflammatory cell infiltration. Fibroblasts creating fibrous tissue.

Gouch et al.2002(12)

39 year-old man

4 operations for tetralogy of Fallot and on waiting list for cardiac transplantation

Recurrent VT

worsening VT due to thyrotoxicosis(requiring automatic implanted cardiac defibrillator)

3 years

carbimazole, prednisone, potassium per chlorate and lithium carbonate

Failure of therapy to control thyrotoxicosis

Same as before

Same as before.

Gouch et al.2002(12)

32 year-old man

Familial DCMP


Thyrotoxicosis for 18 months. CHF : EF 4%

4 years

PTU, potassium per chlorate and lithium carbonate.

Failure of therapy to control thyrotoxicosis

Same as before

Same as before

Gouch et al.2002(12)

61 year-old man

Rheumatic heart disease with aortic valve replacement and congestive cardiac failure

Ventricular tachycardia and fibrillation

Thyrotoxicosisdeveloped two months after amiodarone was discontinued.

two years

propylthiouracil, prednisone and lithium carbonate.

Failure of therapy to control thyrotoxicosis

Same as before

Same as before

Gouch et al.2002(12)

63 year-old man

CABG and cardiac pacemaker.


Thyrotoxicosis developed 3 months after amiodarone was discontinued

2 years

carbimazole and prednisolone

Failure of therapy to control thyrotoxicosis

Same as before

Same as before

Many trials were conducted to control the hyperthyroid state, from anti-thyroidal drugs (high doses of thionamides (60mg/day) and propylthiouracil (1200 mg)) to high doses of corticosteroids, iodine solution, cholestyramine and even plasmapheresis, without any benefit. In all cases, thyrotoxicosis was refractory to these different treatment modalities, unresponsive with worsening of the underlying cardiac conditions in several cases and the only solution remains total thyroidectomy whether they had type I (underlying thyroid pathology) or type II AIT (destructive thyroiditis).(Table 3)

All patients ameliorated after thyroidectomy and restored the euthyroid state with improvement of symptoms and ventricular function. Only one died after surgery but this is secondary to his preexisting comorbid conditions.
Table 3: 2 case-series presenting patients who underwent successful thyroidectomy for the treatment of amiodarone-associated thyrotoxicosis


Number of patients

Age +sex

Reason for intervention

Duration of amiodarone use

Treatment of




Lorberboym  et al.2007(13)

11 patients

Sex:6 men and 5 women

5patients:reccurrence of AF

1 to 12 months(mean:7months)

All patients: High doses of PTU up to 1200 mg/day

4 patients did not respond to medical treatment after 3 months

There was a  rapid correction of thyrotoxicosis. Subsequently, all patients recovered rapidly and remained well and euthyroid on thyroxine after 12 months of follow-up replacement therapy



In all cases thyroid histopathology demonstrated degenerative and destructive follicular lesions with multinuclear cell infiltrate and focal fibrosis.



7patients:beta-receptor antagonist

3 patients were treated with high doses of steroids, one of them with PTU and ipodate without therapeutic effect

5patients:ventricular premature beats and deterioration of clinical condition  under amiodarone treatment

1 patient developed marked impairment of hepatic function. Therapy was stopped and the patient had severe decompensated CHF with tachycardia unresponsive to medical treatment.

Age: 63 to 82 years

5patients: prednisone 60mg/day

1 patient had large toxic MNG treated with MTZ for 20 years. He began amiodarone treatment for AF and developed thyrotoxicosis after 4 months.

1patient:severe CHF

-2 patients chose surgery

3 patients: high doses of steroids, one of them with PTU and ipodate

Drescher et al.2006(14)

12 patients

Sex:3men and 9 women

All patients had underlying cardiac disease(4 CAD, 2 DCMP, 1 valvular heart disease, 3 HTN, 1 arrythmia, 1unkownbut on ICD)

1year to 4 years(mean 2.9 years)

Thionamides,glucocorticosteroids or both administered for 3-10 weeks

Unresponsiveness to medical therapy and worsening of the underlying cardiac conditions in several cases

Euthyroidism was restored quickly in all subjects. Temporary intensive care was required for 3 patients. One died after surgery because of multiple preexisting comorbid conditions, All other were euthyroid after levothyroxine replacement and on stable or improved cardiac condition after at least 1 year


Age:49-81(mean 60)

8 had ICD 1

7 out of 12 had EF of 35% or below (the rest between 45 or 50%)

Amiodarone is a widely used anti-arrhythmic drug treating mainly supraventricular and ventricular tachycardia’s, used safely in patients with atrial fibrillation and heart failure in order to obtain sinus rhythm without affecting ventricular function.

However, like any other drug, its benefit can be out weighted by numerous side effects especially that most individuals administered it on a chronic basis so they will experience definitely at least one side effect among others. The most hazardous one is thyroid dysfunction (hypo or hyperthyroidism) as amiodarone is an iodine rich compound and similar structurally to thyroid hormone.(1)

Some patients on amiodarone remain euthyroid but others develop thyrotoxicosis and have consequently higher adverse cardiovascular events.

Amiodarone-induced thyrotoxicosis (AIT) is a serious complication of long-term amiodarone use. It occurs in patients with already established cardiac dysfunction on amiodarone, who didn’t tolerate the hyperthyroid state. It is classified as iodine-induced thyrotoxicosis (type 1) existing in patients with underlying thyroid disease exacerbated by thyroid autonomous function, mainly in iodine-deficient areas and destructive thyroiditis (type 2) in those with no history of thyroid problems causing direct cytotoxic and inflammatory effects, occurring in iodine-repleted areas. [4] Mixed forms also are present. Those effects are probably due to high iodine content of amiodarone, and its long half-life (107 days).[2]

Changes seen microscopically in type I AIT are consisting of preexisting thyroid disease, usually multinodular goiter or underlying latent Graves disease, in whom iodine exposure triggers the development of clinical disease. This subgroup usually has normal or only slightly elevated serum levels of interleukin-6, while patients with type 2 AIT have randomly distributed disrupted follicules, filled with desquamated vacuolated epithelial cells, foamy macrophages and lymphocytes, involutional changes and fibrosis. They have higher levels of IL-6, rendering it a good marker of the thyroid-destructive processes. [13] Thyroid scan and doppler ultrasound can differentiate also between the 2 types. Absence of tracer uptake in the thyroid bed and Doppler flow demonstrate type 2 AIT.

The exact type of thyrotoxicosis cannot be identified most of the time and treatment for both conditions is given. [2] Mixed cases of amiodarone induced thyrotoxicosis occur in 15 to 27% of cases.[4]

In patients with preexisting cardiac disease, the effect on heart is more worrisome. When established, AIT worsens the underlying arrhythmia and most patients developed decompensated heart failure, recurrent atrial fibrillation or any arrhytmia because of the superimposed hyperthyroid state.[3]

Hyperthyroidism may be mild (free thyroxine (T4) levels 1 to 1.5 times the upper limit of normal), moderate (free T4 levels 1.5 to 2 times the upper limit of normal) or severe (free T4 levels approximately 2 to 3 times the upper limit of normal).

AIT is a challenging problem difficult to manage with substantial morbidity and mortality especially in elderly patients with signs and symptoms of cardiac instability. Thus, resolution of this severe hyperthyroid state is crucial.

Ideally, amiodarone should be discontinued but cessation of this potent drug is impractical in some patients because it is the only anti-arrhythmic capable of controlling tachyarrhythmias, and even if it can be stopped, AIT can take up to nine months to resolve, its effect may last seven years. When stopping amiodarone, a loss of beta blockage may exacerbate thyrotoxicosis which may not improve and lead to comorbid cardiac conditions and major problems.[2]

Many trials of medical therapy with anti-thyroid drugs, steroids, radioactive iodine, plasmapheresis failed due to the high intrathyroidal iodine content that reduces the efficacy of thionamides which also have many side effects and complications, the low suppressed RAI uptake mainly in type II and the refractoriness of AIT to steroids and plasmapheresis.[13]

Thionamides, usually with a short course of potassium per chlorate are beneficial, and if no response we can add steroids but the effect of medical therapy may take as long as 4 months to be efficient.[7]

Major anti-thyroid drugs are able to temporary control symptoms but all are hepatotoxic especially that treatment requires high doses, steroids can reduce the inflammation but have major side effects, plasmpharesis can provide acute relief of type 2 amiodarone induced thyrotoxicosis but its effect is transient, with higher cost and impossibility of long term use. Radioactive iodine is not feasible in all conditions especially in type 2 because of a low uptake.[3]

Clinical manifestations and morbidity of thyrotoxicosis leading even to thyroid storm, can be the reason for choosing thyroidectomy as the only curative solution. Many series have reported the successful surgical management of amiodaroneinduced thyrotoxicosis.[15]

Most studies have shown that total thyroidectomy reduce mortality and morbidity, despite that euthyroidism is difficult to achieve. None of those case series presented here showed a significant complication post thyroidectomy, despite the risk of anesthesia associated with thyrotoxicosis, mainly in patients with heart disease, and the high surgical risk. The anesthetic management should be considered. Patients with mild hyperthyroidism do not require special considerations while those with severe Intraoperative hyperthyroidism (thyrotoxic storm secondary to manipulation of the thyroid gland during thyroidectomy] may require hydration, cooling, and administration of antithyroid drugs, beta-blockers and sodium iodine to prevent any hyperthyroid crisis (storm].[29]. Thus, it is preferable to control hyperthyroid and to restore euthyroidism before thyroidectomy but in most cases, there is a necessity for an urgent treatment before establishing a normal euthyroid state.

When surgery is performed, the postoperative risk of arrhythmias, hemodynamic compromise, and thyroid storm is very minimal.

All patients improved clinically, in addition to amelioration of their cardiac status. Those in whom discontinuing amiodarone is not feasible can be also referred to surgery.[6]
As amiodarone can cause thyroid dysfunction and thyrotoxicosis especially in patients with preexisting heart problems, checking for and treatment of amiodarone induced thyrotoxicosis is important. Total thyroidectomy is an effective method for treatment of amiodarone induced thyrotoxicosis unresponsive to medical therapy, because of severe cardiac morbidity and mortality associated with overt hyperthyroidism.
we sharing our gratitude towards the Novo Nordisk company for their financial support to our Research paper.
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