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Primary Hypothyroidism Leading to Massive Pericardial Effusion and Diastolic Right Ventricular Compression: a Case Report

  • Saeide Bahrani
  • Sayed Ali EmamiEmail author
  • Mehrbod Vakhshoori
  • Mansour Siavash
  • Keivan Kiani
  • Farhad Mahmoudi
Medicine
  • 54 Downloads
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  1. Topical Collection on Medicine

Abstract

Although hypothyroidism with primary etiology could cause small pericardial effusion, massive one leading to cardiac tamponade and ventricular diastolic compression is rare and less reported in the literature. Here we described a patient with severe primary hypothyroidism leading to pericardial effusion and right ventricular compression. A 56-year-old diabetic man referred to the emergency department complaining of dyspnea worsening over the prior month. Further evaluations including electrocardiography, chest X-ray, and echocardiography plus laboratory data were requested. Para-clinic data revealed massive pericardial effusion in the presence of primary hypothyroidism. Pericardiocentesis was performed due to his severe symptoms which symptoms improvement were considerably achieved. Despite its rareness, hypothyroidism should be kept in mind whenever evaluating patients with massive pericardial effusion, especially after exclusion of other more common etiologies.

Keywords

Hypothyroidism Pericardial effusion Levothyroxine Pericardiocentesis 

Introduction

Although cardiac manifestations of hypothyroidism, including bradycardia and pericardial effusion (PE) are common, massive pericardial effusion or pericardial tamponade is rarely reported [1]. Hypothyroidism is infrequently presented primarily by pericardial effusion, but the most common cardiac manifestation which could happen in patients suffering from severe hypothyroidism would be bradycardia and pericardial effusion [2]. Cardiac tamponade leading to right ventricular (RV) and right atrial (RA) compression happens extremely rare [1]. Here, in this paper, we described a patient with right ventricular (RV) collapse as the first presentation of severe primary hypothyroidism.

Case Presentations

A 56-year-old Iranian male presented to our emergency department with worsening of dyspnea associated with weakness, fatigue, slow speech, and periorbital edema since last month before his admission. He also complained of orthopnea. His medical history was unremarkable except for smoking one packet of cigarette daily for 10 years (10 packs/year) and type two diabetes mellitus diagnosed 10 years earlier.

On physical examination, he was stable without any signs and symptoms of respiratory difficulty. Blood pressure was 100/70 mmHg, pulse, and respiratory rate were 74 and 20 per minute, respectively. Head and neck examinations revealed a raised jugular venous pressure (JVP), periorbital puffiness, and dry and cold skin. The only positive finding on heart auscultation was the presence of muffled heart sounds. Pulsus paradoxus was not detected. Other examinations did not reveal any positive findings except decreased deep tendon reflexes and severe non-pitting pretibial edema. Requested CXR and ECG showed huge cardiomegaly (increased cardio-thoracic ratio) with globular pattern and low-voltage QRS complexes, respectively (Fig. 1a, b). In transthoracic echocardiography (TTE), severe PE with RA collapse during diastole was reported (Fig. 2). Left ventricular and RV systolic function were normal, and there was evidence of tamponade. Due to the persistence of his symptoms, pericardiocentesis was performed, and about 400 ml of serous fluid was drained and sent for laboratory and culture analysis. Concurrently, his blood sample was taken, and positive findings were in agreement with the diagnosis of primary hypothyroidism (thyroid stimulating hormone 100 mIU/ml, free T4:0.870 mg/dl, and T3 < 3 nmol/L). The pericardial fluid analysis was unremarkable for the presence of any malignancies or infections. After fluid drainage, patient’s symptoms were relieved and para-clinic examinations returned approximately back to normal ranges. Thyroxin replacement therapy (25 mcg/day of levothyroxine) was initiated. The patient was discharged in a healthy physical condition; and on the next follow-up, within 6 months after the attack, all laboratory parameters had been normalized, and no PE was detected on TTE.
Fig. 1

a CXR, cardiomegaly with a globular pattern. b low-voltage ECG

Fig. 2

Echocardiography of apical four chamber views showing pericardial effusion of thickness by 296 mm

Discussion

Here, we presented a patient suffering from massive pericardial effusion leading to cardiac tamponade due to severe primary hypothyroidism confirmed by clinical and laboratory findings.

The prevalence of this condition in patients with severe and mild hypothyroidism was estimated to be 20–30% and 3–6%, respectively [2]. PE and cardiac tamponade are among two of the rarest manifestations of hypothyroidism [3]. Parving et al. believed that it is caused by a combination of albumin extravasation and slow lymphatic drainage [4]. In another study, the molecular mechanism of the effect of triiodothyronine (T3) in cardiac cells was responsible. After binding T3 to its nuclear receptors, expression of some genes including alpha-myosin heavy chain, beta-1 adrenergic receptor, voltage-gated potassium channels, and sarcoplasmic reticulum calcium ATPase would be changed. Many cardiac manifestations are considered to be related to those gene expression alterations [5]. Diagnosis of cardiac tamponade in hypothyroidism is difficult and almost mistaken for heart failure because of several nonspecific symptoms including tachypnea, lower limb edema, and increased venous pressure [6]. Beck’s triad components, including increased jugular venous pressure, hypotension, and diminished heart sounds, define cardiac tamponade. From non-invasive para-clinic tools, the gold standard way to confirm the diagnosis is TTE, which is optimal for assessing the severity of effusion and compressive effects on the heart chamber [7]. ECG findings include low-voltage QRS complexes, ST segment deviation, PR segment depression, and T wave changes [8]. In patients suffering uremia or hypothyroidism, bradycardia may be the only cardiac manifestation [9]. Even if the definite diagnosis of hypothyroidism was made, other etiologies must be kept in mind because this relationship is commonly rare and other pathophysiological mechanisms need more aggressive and different management strategies [10].

While some scientists prefer immediate surgical approaches to make pericardial window initially to prevent symptom recurrence, others believe in the individualization of therapy. For instance, in case of mild hemodynamic alteration, conservative management including close monitoring, performing serial ECGs and avoidance of volume depletion should have been done. In patients with pulsus paradoxus or recurrent PE, pericardiocentesis or pericardial window, respectively, would be the right management strategies [11].

The base of hypothyroidism treatment is thyroxin replacement therapy. It is usually started with low dose thyroxin (25 mcg/day), especially in older people to prevent complications like atrial fibrillation and worsening coronary heart diseases and will gradually increase to higher dosages [12]. After initiation of therapy, pericardial effusion will resolve gradually, and as patients gain euthyroid level, effusion would be entirely resolved. Our patient, because of poor compliance with drug usage, returned to the hospital with massive pericardial effusion within few months [2].

In conclusion, it is reasonable that on a routine evaluation of massive pericardial effusion after excluding common causes such as malignancies, infections, and connective tissue disorders, hypothyroidism should be kept in mind and appropriate diagnostic and therapeutic management must have been performed.

Notes

Compliance with Ethical Standards

Conflict of Interest

The authors declare that they have no conflict of interest.

Ethical Approval

All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.

Informed Consent

Written informed consent was obtained from the patient for publication of this case report and accompanying images.

References

  1. 1.
    Spodick DH. Acute pericarditis: current concepts and practice. Jama. 2003;289(9):1150–3.CrossRefGoogle Scholar
  2. 2.
    Kabadi UM, Kumar SP. Pericardial effusion in primary hypothyroidism. Am Heart J. 1990;120(6):1393–5.CrossRefGoogle Scholar
  3. 3.
    Manolis AS, Varriale P, Ostrowski RM. Hypothyroid cardiac tamponade. Arch Intern Med. 1987;147(6):1167–9.CrossRefGoogle Scholar
  4. 4.
    Parving H-H, 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(9):460–5.CrossRefGoogle Scholar
  5. 5.
    Danzi S, Klein I. Thyroid hormone and the cardiovascular system. Minerva Endocrinol. 2004;29(3):139–50.Google Scholar
  6. 6.
    Dattilo G, Crosca S, Tavella S, Marte F, Patanè S. Pericardial effusion associated with subclinical hypothyroidism. Int J Cardiol. 2011;153(3):e47–50.CrossRefGoogle Scholar
  7. 7.
    Zimmerman J, Yahalom J, Bar-On H. Clinical spectrum of pericardial effusion as the presenting feature of hypothyroidism. Am Heart J. 1983;106(4 Pt 1):770–1.CrossRefGoogle Scholar
  8. 8.
    Meyers DG, Bagin RG, Levene JF. Electrocardiographic changes in pericardial effusion. Chest. 1993;104(5):1422–6.CrossRefGoogle Scholar
  9. 9.
    Spodick DH. Acute cardiac tamponade. N Engl J Med. 2003;349(7):684–90.CrossRefGoogle Scholar
  10. 10.
    Sainz AJ, Encinar JCB, Torregrosa IQ, de Teresa Parreño L. Taponamiento pericárdico como forma inicial de presentación de hipotiroidismo primario. Rev Esp Cardiol. 2000;53(1):145–6.CrossRefGoogle Scholar
  11. 11.
    Sagristà-Sauleda J, Mercé J, Permanyer-Miralda G, Soler-Soler J. Clinical clues to the causes of large pericardial effusions. Am J Med. 2000;109(2):95–101.CrossRefGoogle Scholar
  12. 12.
    Rachid A, Caum LC, Trentini AP, Fischer CA, Antonelli DA, Hagemann RP. Pericardial effusion with cardiac tamponade as a form of presentation of primary hypothyroidism. Arq Bras Cardiol. 2002;78(6):583–5.CrossRefGoogle Scholar

Copyright information

© Springer Nature Switzerland AG 2019

Authors and Affiliations

  • Saeide Bahrani
    • 1
  • Sayed Ali Emami
    • 1
    • 2
    Email author
  • Mehrbod Vakhshoori
    • 3
  • Mansour Siavash
    • 4
  • Keivan Kiani
    • 4
  • Farhad Mahmoudi
    • 1
  1. 1.Cardiac Rehabilitation Center, Isfahan Cardiovascular Research InstituteIsfahan University of Medical SciencesIsfahanIran
  2. 2.School of medicineIsfahan University of Medical SciencesIsfahanIran
  3. 3.Heart Failure Research Center, Isfahan Cardiovascular Research InstituteIsfahan University of Medical SciencesIsfahanIran
  4. 4.Isfahan University of Medical SciencesIsfahanIran

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