Undiagnosed Thyrotoxicosis Masquerading as Heart Failure

Introduction

Hyperthyroidism or thyrotoxicosis is a clinical condition characterized by toxic manifestations of either central nervous system, or cardiovascular system (occasionally both) resulting in severe tremors, irritability, restlessness, attention deficits, hyperthermia, severe tachycardia, hypertension, arrhythmias, and cardiac failure. Heart failure is considered among the less common manifestations of hyperthyroidism with an incidence ranging from 6% to 19 %.¹ Atrial fibrillation (AF) is the commonest rhythm abnormality seen in these patients and occurs in about 10-21% of patients.². Hyperthyroidism is usually due to an overactive thyroid gland, resulting in increased circulating thyroid hormones. Thyrotoxicosis is described as either primary when the disease develops de novo or as secondary when a pre-existing benign thyroid condition turns toxic as in the case of toxic multinodular goitre. In this case report we discuss an interesting case of undiagnosed hyperthyroidism that presented as severe cardiac failure and atrial fibrillation. 

Case History

A 50 year old lady, known diabetic on oral hypoglycaemic agents presented with a history of shortness of breath for 24 hours duration, associated with fever. She was a known hypertensive on calcium channel blockers. No history of chest pain, palpitations or other cardiorespiratory symptoms were reported. She was not a known case of ischemic heart disease. She was febrile with severe tachycardia and tachypnoea. On evaluation, she was diagnosed with congestive cardiac failure with accelerated hypertension. Routine investigations were done, complete blood counts revealed neutrophilic leucocytosis, cardiac enzymes were normal.Electrocardiogram (ECG) showed sinus tachycardia with few atrial ectopics, chest radiograph showed pulmonary edema (Image 1). Computed tomography (CT) chest showed multiple ground glass opacities predominantly perihilar in distribution. Echocardiogram showed good left ventricular function with 60% ejection fraction, good valvular function, and no regional motion wall abnormalities. Renal function tests were normal.

She was initiated on noninvasive ventilation (NIV) and started on a prophylactic renal failure regimen including diuretics, carvedilol (α+β blocker) and heparin. She was also started on antibiotics after observing raised leucocyte counts and a history of fever. There was initial symptomatic response to the above treatment and shortness of breath decreased. However atrial fibrillation (Image-2) with fast ventricular rate of >180beats/ min developed subsequently. Patient was initiated on amiodarone infusion and other supportive measures were continued. Cardiac rhythm reverted back to sinus rhythm but tachycardia persisted.

Serial cardiac enzymes were normal. Screening for thyroid stimulating hormone (TSH) levels was done. Patient remained breathless and was on NIV. She was afebrile for 48 hours. AF resurfaced and was refractory to medications. In view of grossly decreased TSH suggestive of hyperthyroidism, free T4 and T3 levels were tested. Thyroid profile reports were strongly suggestive of severe thyrotoxicosis (TSH <0.0005, free T4:15.01ug/dl, free T3:2.34ng/dl). ultrasonogram neck showed a diffuse goitre. Grossly elevated antithyroid peroxidise antibodies were seen (1300U/ml; normal range <60U/ml). A diagnosis of primary hyperthyroidism (probable autoimmune etiology) with atrial fibrillation and failure was made. She was started on propranolol (20mg), twice daily and carbimazole (10mg), thrice daily. Hydrcortisone (100 mg), intravenous was started and continued for 48 hours. Diuretics, antiarrhythmic drugs, and rest of the supportive medications were continued.

Patient showed good improvement after initiation of nonselective beta blockers, antithyroid drugs and steroids. Heart rate was under control and sinus rhythm achieved. No recurrence of AF or heart failure was observed. She was discharged on day-8, symptom free with beta blockers and antithyroid drugs. When reviewed 1-week after discharge, she remains asymptomatic and has been advised to undergo radioiodine therapy during subsequent follow up.

Discussion

Very often patients with undiagnosed hyperthyroidism present with severe arrhythmias most commonly AF. Occasionally they also present with heart failure. Untreated AF especially those with fast ventricular response rate (FVR) often progress to severe congestive cardiac failure complicating the clinical picture, resulting in refractory failure. Occasionally, this can even lead to development of catastrophic events such as ventricular fibrillation/shock or cerebral embolic events, resulting in mortality.³ IN some cases. patients present with only congestive cardiac failure (CCF), also known as high output failure. The mechanism of congestive cardiac failure in thyrotoxicosis is said to be due to tachycardia-mediated mechanisms leading to an increased level of cytosolic calcium during diastole with reduced ventricular contractility and diastolic dysfunction.4 Clinically heart failure due to thyrotoxicosis can easily be differentiated from cardiac failure due to other causes by observing for clinical signs such as hypertension with wide pulse pressure, increased myocardial contractility, among others as presented in Table 1. 

The mainstay of treatment in thyrotoxicosis are antithyroid drugs. Most commonly used drugs are propylthiouracil (PTU) and carbimazole. In this case we started the patient on carbimazole with a dose of 10mg, twice daily. Usually, antithyroid drugs take upto 2 weeks for full beneficial therapeutic action. They act at multiple levels of thyroid hormone synthesis by preventing organification of iodide, inhibiting coupling of iodothyronines and blocking iodine uptake. In addition, PTU also inhibits peripheral conversion of T4 to T3. The serum half-life of methimazole is 6–8 hours, whereas the half-life of PTU is 1–2 hours. Carbimazole is administered once daily or at most twice daily, whereas PTU has to be given three to four times a day. Compliance with frequent dosing of PTU is generally lower and methimazole has a better safety profile with lesser side effects compared to PTU, such as lesser incidence of acute liver injury, vasculitis and hypersensitivity.⁵

Patient was also started on nonselective beta blocker (propranolol) at a dose of 20mg, twice daily, orally. Beta blockers have traditionally been the cornerstone of management, for acute manifestations as well as for long term treatment of central nervous system and cardiovascular system symptoms such as tremors, anxiety, sweating, blackouts and palpitations.

Beta blockers mainly act by decreasing AV conduction. In addition, propranolol also helps in inhibiting peripheral conversion of T4 to T3. Beta blockers further stabilize the myocardium, prevents tachyarrhythmias and helps in reversing failure.

Usually some stressful situations such as pregnancy⁶ , bacterial infections including chest infections, urinary tract infections, acute gastroenteritis or any elective surgeries can precipitate congestive cardiac failure in patients with untreated or partially treated thyrotoxicosis. Occasionally, they can progress to a thyroid storm which can become very difficult to treat resulting in high mortality. In this case, severe chest infection seems to have precipitated the crisis resulting in failure. Further, not so apparent or minimal thyroid swelling might have been missed during earlier clinical visits.

Aggressive management of any apparent or hidden infections is very important in preventing further recurrence of crisis.

Definitive treatment of primary thyrotoxicosis is radioiodine therapy, considering its advantages over surgical removal including sparing of parathyroid glands, avoiding risks associated with major surgery, anaesthesia and its associated complications.

Conclusions

Undiagnosed hyperthyroidism often poses significant challenge to the treating clinician, especially when presenting predominantly with cardiovascular manifestations such as severe arrhythmias and CCF.

Routine evaluation with thyroid function test and careful clinical examination should aid diagnosis, however small diffuse thyroid swelling may be difficult to appreciate with only clinical examination, especially in short necked or obese individuals presenting with breathlessness and failure. Use of ultrasound will help in identifying toxic goitre and go a long way in early identification and prompt corrective treatment, thereby reducing mortality and morbidity.

Conflict of interests

Authors declare that there is no conflict of interest