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 Table of Contents  
CASE REPORT
Year : 2022  |  Volume : 24  |  Issue : 3  |  Page : 125-128

Cardiac tamponade as first manifestation of primary hypothyroidism


1 Department of Endocrinology, Command Hospital (NC), Udhampur, Jammu and Kashmir, India
2 Department of Cardiology, Command Hospital (NC), Udhampur, Jammu and Kashmir, India
3 Commandant, Command Hospital (NC), Udhampur, Jammu and Kashmir, India

Date of Submission17-Jan-2021
Date of Decision16-Mar-2021
Date of Acceptance13-Apr-2021
Date of Web Publication21-Jan-2022

Correspondence Address:
Col (Dr) Nitin Bajaj
Department of Cardiology, Command Hospital (NC), Udhampur, Jammu and Kashmir - 182 101
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jmms.jmms_11_21

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  Abstract 


Pericardial effusion is commonly present in patients with moderate-to-severe hypothyroidism. However, large pericardial effusion causing cardiac tamponade (CT) is extremely rare. We report an atypical presentation of primary hypothyroidism (PH) where a young male presented with CT as the first manifestation of PH. The patient was treated with an immediate pericardiocentesis followed by levothyroxine replacement and showed complete resolution of pericardial effusion on follow-up. Hypothyroidism should be suspected as a possible etiology of massive pericardial effusion/CT in patients who have associated signs and symptoms of hypothyroidism and have bradycardia in the setting of CT.

Keywords: Cardiac tamponade, pericardiocentesis, primary hypothyroidism


How to cite this article:
Shekhawat VS, Bajaj N, Gupta RM. Cardiac tamponade as first manifestation of primary hypothyroidism. J Mar Med Soc 2022;24, Suppl S1:125-8

How to cite this URL:
Shekhawat VS, Bajaj N, Gupta RM. Cardiac tamponade as first manifestation of primary hypothyroidism. J Mar Med Soc [serial online] 2022 [cited 2022 Aug 18];24, Suppl S1:125-8. Available from: https://www.marinemedicalsociety.in/text.asp?2022/24/3/125/336181




  Introduction Top


Primary hypothyroidism (PH) is the second most common endocrine disorder after diabetes mellitus. An overwhelming majority of the patients with hypothyroidism have mild and nonspecific symptoms. Very rarely, they may present as a life-threatening emergency. While mild pericardial effusion is common in PH, large pericardial effusion leading to cardiac tamponade (CT) is extremely rare. The diagnosis can be made by the characteristic physical appearance of a hypothyroid patient who has cardiomegaly, characteristic echocardiographic findings of CT in combination with low T3/T4 with raised thyroid-stimulating hormone (TSH). We describe a young male who presented with CT as the first manifestation of PH.


  Case Report Top


A 39-year-old male, presented with complaints of insidious onset, progressively worsening breathlessness of 3 months' duration. He denied any history of fever, cough, hemoptysis, chest pain, palpitation, syncope, orthopnea or paroxysmal nocturnal dyspnea. On asking further, he gave a history of cold intolerance, progressive weight gain despite poor appetite, easy fatigue ability, and hair loss of 6 months' duration. He denied any family history of thyroid illness. Clinical examination revealed puffy face [Figure 1], pulse rate 52/min, blood pressure 106/50 mm Hg, jugular venous pressure (JVP) was raised, paradoxical pulse of 18 mm Hg, and bilateral nonpitting edema below the knees. His skin was cold and dry, he had puffy hands and feet, diffuse alopecia and spoke in a slow and hoarse voice. Thyroid gland was not palpable. The heart sounds were distant, and no murmurs or pericardial rub could be heard. Chest examination was essentially normal. His deep-tendon reflexes were symmetrical with delayed relaxation.
Figure 1: Clinical photographs of the patient showing the change in the facial appearance before and after levothyroxine therapy. (a) At presentation, coarse facial features with periorbital edema. (b) 3 months after levothyroxine therapy

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Electrocardiogram (ECG) showed sinus bradycardia, low voltage complexes with T-inversion in leads V2 – V6 [Figure 2]. Chest X-ray revealed marked cardiomegaly with “water bottle sign” suggestive of pericardial effusion [Figure 3]. Two-dimensional ECHO showed large circumferential pericardial effusion measuring 39 mm lateral to the left ventricle (LV), 22 mm posterior to LV and 16 mm anterior to the right ventricle with features suggestive of CT in the form of swinging motion of the heart, early right ventricle diastolic collapse, and late right atrial diastolic collapse [Figure 4]. Pericardiocentesis was performed through the subcostal route under echocardiographic and fluoroscopic guidance and 700 ml of “golden paint colored” fluid was aspirated. A 6 Fr pig tail catheter was placed in the pericardial cavity for intermittent drainage of fluid. Intermittent drainage was done through the pig tail catheter, and it was removed after 48 h when no significant fluid was present on echocardiography.
Figure 2: Electrocardiogram of the patient. (a) At presentation showing sinus bradycardia, low voltage complexes with T-inversion in leads V2-V6. (b) After 3 months of levothyroxine therapy showing a normal electrocardiogram with normal sinus rhythm

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Figure 3: Chest X-ray of the patient. (a) At presentation showing cardiomegaly with “water bottle sign” suggestive of massive pericardial effusion. (b) After 3 months of levothyroxine therapy showing complete resolution of pericardial effusion

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Figure 4: Two-dimensional echocardiography of the patient at presentation. (a) PLAX view showing large circumferential pericardial effusion with RV collapse (white arrow). (b) 4 chamber view showing circumferential pericardial effusion max 39 mm

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Hematological and biochemical parameters revealed hypoalbuminemia (albumin 3.3 gm/dl) and deranged lipid profile (total cholesterol/triglycerides/high-density lipoprotein – 279/348/30 mg/dl). Thyroid function test revealed FT3 0.3 pg/ml (2.2 – 3.99 pg/ml), FT4) 0.2 ng/dl (0.75-1.5 ng/dl), TSH 286.5 μIU/ml (0.30-4.5 μIU/ml), and anti TPO 1424 IU/ml (< 20 IU/ml). USG of the thyroid revealed a small atrophic and hypoechoic thyroid gland. Pericardial fluid analysis revealed an exudative fluid (protein 7.2 gm/dl) with few lymphocytes and no malignant cells.

A diagnosis of PH (Hashimoto's thyroiditis) was made based on his clinical and biochemical profile. Following urgent pericardiocentesis, he was started on levothyroxine therapy with relief of his symptoms, gradual normalization of his thyroid profile, and complete resolution of pericardial effusion with no recurrence on follow-up.


  Discussion Top


PH is a common endocrine disorder with an incidence of 4 in 1000 females and 1 in 1000 males.[1] Symptoms related to hypothyroidism are insidious in onset, nonspecific, and often go unnoticed for long. The patient may be harboring the disorder for long before the diagnosis is finally made. Very rarely, they present in emergency with associated life-threatening condition such as CT. While mild pericardial effusion is commonly present in patients of PH, moderate to severe pericardial effusion is rare and pericardial effusion leading to pericardial tamponade is extremely rare.[2] Prompt early recognition and appropriate replacement therapy with levothyroxine are essential for effective treatment.

The systemic manifestations of hypothyroidism vary considerably and depend on factors like the cause, duration, and degree of thyroid hormone deficiency. Virtually, every organ system is affected. The cardiovascular system is invariably affected. The thyroid hormone status chiefly affects the heart rate, cardiac output, and systemic vascular resistance.[3] Hypothyroidism is usually associated with bradycardia, diastolic hypertension, narrow pulse pressure, and decreased activity of the pericardium. Ventricular arrhythmias are common. Heart failure is rare as the low cardiac output in hypothyroidism is usually sufficient to meet the reduced oxygen demand.[4]

The incidence of pericardial effusion in hypothyroidism varies widely and is chiefly related to both the degree and duration of the disease. The incidence varies from 3% in patients with mild hypothyroidism to 80% in those with myxoedema.[5] The pericardial effusion in hypothyroidism results from extravasation of plasma proteins into pericardial space due to increased capillary permeability, decreased lymphatic clearance, and increased retention of salt and water due to increased vasopressin sensitivity.[6]

CT is an uncommon and extremely rare complication of PH. Hypothyroidism leading to CT is invariably present if the thyroid hormone deficiency is long standing and severe. In most cases the patient usually seeks medical assistance long before he develops CT. Very rarely, like in the index case, does hypothyroidism presents with CT as an initial presentation of PH. The inherent elasticity of the pericardial layers and gradual accumulation of pericardial fluid in hypothyroidism allows significant pericardial fluid to accumulate without hemodynamic compromise. However, once it develops, CT is usually unmissable on clinical examination. It presents with clinical triad known as Beck's triad which includes hypotension, distant heart sounds, and raised JVP and the diagnosis is confirmed by the characteristic echocardiographic findings. Massive pericardial effusion causing tamponade is usually caused by infection, malignancy, tuberculosis, idiopathic pericarditis, connective tissue disease, following cardiac surgery, and trauma. Hypothyroidism is a rare cause of massive pericardial effusion/tamponade, and only a handful of cases are reported in the literature.[7],[8],[9],[10] Certain clinical pointers such as presence of signs/symptoms of hypothyroidism and bradycardia in face of CT, like in our patient, should make one suspect hypothyroidism.

The ECG can both aid in the diagnosis of CT and as in our case also suggest possible aetiology. ECG abnormalities commonly seen in hypothyroidism include sinus bradycardia, prolonged QTc interval, low voltage complexes, and very rarely atrioventricular block. The most common ECG abnormalities associated with CT include sinus tachycardia, electrical alterans (EA), and low-voltage QRS complexes. These ECG abnormalities have low sensitivity when present alone; however, all three of them present together strongly suggests CT. Sinus tachycardia occurs as a compensatory mechanism in patients with CT and is invariably present in all patients with CT. However, the presence of bradycardia in CT, as in our patient, strongly suggests hypothyroidism as the possible etiology of pericardial effusion. EA, defined as an alternating QRS amplitude in any or all ECG leads is an insensitive but specific abnormality seen in CT. It results from the oscillating heart changing its position relative to the ECG electrodes in the pericardial sac distended by the fluid. EA is present in only 10%–20% of patients with CT as its appearance is not dependant solely on the presence of large pericardial effusion. Other factors determining the presence of EA in patients of CT include heart rate, pericardial sac pressure and compliance and the volume, viscosity and rate of build-up of the pericardial fluid. Our patient did not had EA.

Characteristic ECHO findings in CT include massive pericardial effusion, systolic collapse of the right atrium, and diastolic collapse of the right ventricle. The pericardial fluid accumulation due to hypothyroidism is characteristically golden colored due to the presence of α/β globulins, exudative with high protein content and is lymphocyte predominant. Exudative pericardial fluid in hypothyroidism results from extravasation of albumin due to increased capillary permeability and inadequate drainage of the lymphatic fluid. The presence of CT along with pulsus paradoxus necessitates emergency pericardiocentesis. These patients respond well to levothyroxine replacement and the pericardial effusion gradually resolves completely over 3–6 months.


  Conclusion Top


The degree of pericardial effusion in hypothyroidism correlates with disease severity and duration. PH presenting with CT is extremely rare. Patients of hypothyroidism presenting with tamponade invariably have signs and symptoms of hypothyroidism. Bradycardia in patients with CT may suggest hypothyroidism as a possible etiology. These patients respond well to levothyroxine therapy.

Learning points

  1. Cardiac tamponade is an extremely rare presentation of primary hypothyroidism.
  2. Cardiac tamponade with bradycardia should raise a suspicion of hypothyroidism.
  3. These patients respond well to levothyroxine therapy.


Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Vanderpump MP, Tunbridge WM, French JM, Appleton D, Bates D, Clark F, et al. The incidence of thyroid disorders in the community: A twenty-year follow-up of the Whickham Survey. Clin Endocrinol (Oxf) 1995;43:55-68.  Back to cited text no. 1
    
2.
Chahine J, Ala CK, Gentry JL, Pantalone KM, Klein AL. Pericardial diseases in patients with hypothyroidism. Heart 2019;105:1027-33.  Back to cited text no. 2
    
3.
Kahaly GJ, Dillmann WH. Thyroid hormone action in the heart. Endocr Rev 2005;26:704-28.  Back to cited text no. 3
    
4.
Klein I, Ojamaa K. Thyroid hormone and the cardiovascular system. N Engl J Med 2001;344:501-9.  Back to cited text no. 4
    
5.
Lin CT, Liu CJ, Lin TK, Chen CW, Chen BC, Lin CL. Myxedema associated with cardiac tamponade. Jpn Heart J 2003;44:447-50.  Back to cited text no. 5
    
6.
Parving HH, Hansen JM, Nielsen SL, Rossing N, Munck O, Lassen NA. Mechanisms of edema formation in myxedema – Increased protein extravasation and relatively slow lymphatic drainage. N Engl J Med 1979;301:460-5.  Back to cited text no. 6
    
7.
Coetzee A, Kyriakakis C, Greyling C, Ascott-Evans BH. Cardiac tamponade due to hypothyroidism: a case cluster report. J of Endocrinology, Metabolism and Diabetes of South Africa 2016;21:16-19.  Back to cited text no. 7
    
8.
Maddali VR, Miryala S, Bellamkonda YS, Nagula P. Cardiac tamponade due to primary hypothyroidism: Acute management and approach to prevent recurrence – A case report. Eur Heart J Case Rep 2020;4:1-5.  Back to cited text no. 8
    
9.
Apaydin M, Beysel S, Demirci T, Caliskan M, Kizilgul M, Ozcelik O, et al. A case of primary hypothyroidism initially presenting with massive pericardial effusion. Case Reports. J Clin Transl Endocrinol 2016;2:1-2.  Back to cited text no. 9
    
10.
Bahrani S, Emami SA, Vakhshoori M, Siavash M, Kiani K, Mahmoudi F, et al, Primary hypothyroidism leading to massive pericardial effusion and diastolic right ventricular compression: A case report. SN Compr Clin Med 2019;1:924-7.  Back to cited text no. 10
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]



 

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