Journal of Postgraduate Medicine
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CASE REPORT
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Year : 2013  |  Volume : 59  |  Issue : 3  |  Page : 229-231  

Thyroid storm presenting as congestive heart failure and protein-S deficiency-induced biventricular and internal jugular venous thrombii

S Kumar1, N Moorthy1, S Yadav2, A Kapoor1, DC Dale2,  
1 Department of Cardiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
2 Department of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Correspondence Address:
S Kumar
Department of Cardiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh
India

Abstract

The thyroid storm is a medical emergency characterized by decompensation of one or more organ systems. Associated cardiac involvement carries poor prognosis. Early recognition and appropriate management of life-threatening thyrotoxicosis is vital to prevent the high morbidity and mortality that may accompany this disorder. We report a young lady presenting with thyroid storm presenting as acute heart failure with biventricular and bilateral internal jugular venous thrombi. In addition, she also had thyrotoxicosis-induced transient protein-S deficiency which recovered following remission.



How to cite this article:
Kumar S, Moorthy N, Yadav S, Kapoor A, Dale D C. Thyroid storm presenting as congestive heart failure and protein-S deficiency-induced biventricular and internal jugular venous thrombii.J Postgrad Med 2013;59:229-231


How to cite this URL:
Kumar S, Moorthy N, Yadav S, Kapoor A, Dale D C. Thyroid storm presenting as congestive heart failure and protein-S deficiency-induced biventricular and internal jugular venous thrombii. J Postgrad Med [serial online] 2013 [cited 2021 Oct 25 ];59:229-231
Available from: https://www.jpgmonline.com/text.asp?2013/59/3/229/118047


Full Text

 Introduction



Thyrotoxic crisis is an endocrinal emergency which requires early recognition, and appropriate management of life-threatening thyrotoxicosis is vital to prevent the high morbidity and mortality associated with this disorder. [1] Congestive heart failure is one of the recognized cardiovascular complications of thyroid storm. Although hyperthyroidism is known to predispose hypercoagulable state simultaneous, the occurrence of arterial and intravenous thrombi are rare. [2]

 Case Report



A 38-year-old female was admitted with history of fever and rapidly progressive dyspnea of 1 week duration. She also gave history of palpitation, dyspnea, orthopnea, and bilateral pedal edema. Past medical history was unremarkable. On examination she was in NYHA class IV and pulse rate was 126/min and blood pressure was 100/56 mmHg. Jugular venous pressure was elevated. Thyroid was normally palpable and there was no bruit. Cardiovascular system examination revealed left ventricular gallop. She also had bilateral basal crackles.

Hemogram showed mild normocytic normochromic anemia. Total leukocyte count and erythrocyte sedimentation rate (ESR) were within normal limit. Liver and renal function was mildly deranged. Electrocardiography showed sinus tachycardia with a heart rate of 126/min. Chest radiograph showed cardiomegaly with a cardiothoracic ratio of 0.60 [Figure 1]a with pulmonary venous hypertension. Transthoracic echocardiography showed cardiomegaly and global left ventricular ejection fraction was 30%. The right ventricle (RV) was also dilated and there was severe RV dysfunction. There was mild mitral and tricuspid regurgitation. A pedunculated soft apical clot [Figure 2] measuring 12 × 15 mm was noted at the left ventricular apex. Another soft clot measuring 15 × 10 mm was observed in the right ventricular apex. Doppler ultrasonography showed total thrombotic occlusion [Figure 3]a of left internal jugular vein and partial occlusion of right internal jugular vein [Figure 3]b.{Figure 1}{Figure 2}{Figure 3}

Coagulation profile showed normal prothrombin time (PT), activated partial thromboplastin time (aPTT), and bleeding and clotting times. The protein-C level was 77% (normal range: 70-130) and the protein-S level was 44% (normal range: 65-140). Immunological work up did not reveal any evidence of connective tissue disorder. Ig-G, Ig-M anticardiolipid antibodies, and anti ds-DNA and anti-nuclear antibody (ANA) were negative. Serology for hepatitis C, hepatitis B, and HIV infection were negative. Blood and urine culture were sterile.

The clinical scenario and laboratory evidences were suggestive acute myocarditis with severe biventricular dysfunction with biventricular thrombi with hypercoagulable state secondary to protein-S deficiency. As a part of work-up of acute heart failure, the thyroid profile was done which showed T3: 3.26 nmol/L, T4: 271.2 nmol/L and TSH: <0.005 μIU/L thus confirming thyrotoxic crisis. Ultrasonography of thyroid gland showed diffusely enlarged thyroid gland with a heterogeneous hypoechoic appearance with increased vascularity. Tc-99m-pertechnetate radionuclide thyroid scan showed diffuse toxic goiter.

She was managed with intravenous diuretics, carvedilol, enalapril, and neomercazole. She also received intravenous unfractionated heparin followed by oral anticoagulation. With conservative management there was dramatic improvement in her symptoms. The repeat echocardiography after 2 weeks showed reduction in left ventricular size with disappearance of biventricular thrombi. Fortunately she did not develop systemic or pulmonary embolism. Later she received successful radioiodine ablation. At 3 month follow-up, there was regression in the cardiac size on chest radiograph [Figure 1]b and repeat echocardiography showed normal left ventricular dimension with normal ejection fraction. The carvedilol, enalapril, and diuretic were gradually tapered off and stopped at 1 year and she was advised to continue thyroid supplementation with periodic monitoring.

 Discussion



Thyroid storm is one of the rare endocrinal emergencies accounting for less than 10% of patients hospitalized for thyrotoxicosis; however, the mortality rate due to thyroid storm ranges from 20% to 30%. [3] Thyroid storm represents extreme manifestation of thyrotoxicosis and virtually involves every organ resulting in decompensation of one or more organs.

The distinction between severe thyrotoxicosis and life-threatening thyrotoxicosis, or thyroid storm, is a matter of clinical judgment. [1] The most common etiologies for thyroid storm include Graves' disease, hypersecretory thyroid carcinoma, thyrotropin-secreting pituitary adenoma, etc. Thyroid storm can be precipitated by systemic insults such as surgery, trauma, myocardial infarction, pulmonary thromboembolism, diabetic ketoacidosis, parturition, discontinuation of antithyroid drugs, excessive ingestion or intravenous administration of iodine (e.g. radiocontrast dyes, amiodarone), or severe infection. [4],[5] However, in our patient, obvious precipitating factor could not be found out.

The cardiovascular manifestations of thyrotoxic crisis include tachycardia, atrial fibrillation, accelerated hypertension, cardiomyopathy, pulmonary edema, etc. Even though cardiovascular effects are typically due to "high-output" heart failure, cases of "low-output" heart failure have also been observed. Congestive heart failure is observed in 6% of patients with thyrotoxicosis. [6] A majority of patients either have underlying heart disease or develop it as a consequence of atrial fibrillation or prolonged marked sinus tachycardia which resolves when the ventricular rate is slowed or sinus rhythm is restored.

The proposed mechanisms of heart failure include tachycardia- mediated cardiomyopathy, thyrotoxic cardiomyopathy, activation of the sympathetic nervous system and renin-angiotensin-aldosterone axis, increased serum vasopressin concentration and volume overload resulting in ventricular enlargement, remodeling, impaired chronotropic, and contractile reserve of heart muscle and myocarditis. [7],[8]

Our patient developed rapidly worsening heart failure secondary to biventricular dysfunction. However, with the early diagnosis and initiation of antithyroid medications as well as decongestive therapy there was dramatic improvement in her symptoms.

Hyperthyroidism can result in hypercoagulability due to increase in the levels of procoagulant factors like factor II, VII, IX, X, fibrinogen, PAI, VWF and decrease in protein-C, protein-S and plasminogen levels. [9],[10] Recent systematic review of literature documented an increased risk of acute venous thrombosis complications in patients with overt hyperthyroidism, especially at cerebral sites. [11] However, there are no reports of intracardiac thrombii and internal jugular vein thrombosis in the literature. Probably in our patient, the hypercoagulable state was precipitated by transient protein-S deficiency induced by thyrotoxic crisis. With the improvement of thyrotoxic crisis ventricular function improved dramatically along with disappearance of intracadiac thrombii. During follow-up at 3 months, the protein-C level reached normal range and the left ventricular function was normal and she was asymptomatic.

 Conclusion



Thyroid storm is a medical emergency and can result in rapidly worsening heart failure. Thyrotoxic status can precipitate hypercoagulable state secondary to transient protein-S deficiency resulting in thrombosis in multiple locations. Thyroid storm should be considered in the differential diagnosis of rapidly worsening heart failure with thrombi at multiple locations. High index of suspicion and early diagnosis and appropriate treatment will lead to prompt recovery.

References

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