|Year : 2019 | Volume
| Issue : 3 | Page : 97-99
Cardiac tamponade combined with pleural and peritoneal effusions, as the presenting manifestation of primary hypothyroidism
Muhammad Zahid, Gowri Karuppasamy, Dabia Hamad S H Al-Mohanandi
Department of General Internal Medicine, Hamad General Hospital, Doha, Qatar
|Date of Web Publication||15-Oct-2019|
Dr. Muhammad Zahid
Hamad General Hospital, Doha
Source of Support: None, Conflict of Interest: None
We present a rare case of cardiac tamponade as the initial presentation of primary hypothyroidism. A 38-year-old woman presented with shortness of breath and fatigue for 2 months. She had cardiomegaly on chest X-ray, and transthoracic echocardiogram showed evidence of cardiac tamponade. Urgent pericardiocentesis was performed; the pericardial fluid was exudative with negative cultures and cytology. She was also found to have pleural effusions and ascites. Laboratory tests revealed severe hypothyroidism, and thyroxine replacement therapy was started. The case highlights that the diagnosis of hypothyroidism should not be overlooked during the evaluation of patients with pericardial effusions.
Keywords: Hypothyroidism, pericardial temponade, pericardiocentesis
|How to cite this article:|
Zahid M, Karuppasamy G, H Al-Mohanandi DH. Cardiac tamponade combined with pleural and peritoneal effusions, as the presenting manifestation of primary hypothyroidism. Libyan J Med Sci 2019;3:97-9
|How to cite this URL:|
Zahid M, Karuppasamy G, H Al-Mohanandi DH. Cardiac tamponade combined with pleural and peritoneal effusions, as the presenting manifestation of primary hypothyroidism. Libyan J Med Sci [serial online] 2019 [cited 2020 Jan 21];3:97-9. Available from: http://www.ljmsonline.com/text.asp?2019/3/3/97/269221
| Case Report|| |
A 38-year-old woman, with no known medical history, was admitted to our hospital with the chief complaints of shortness of breath and generalized fatigue for 2 months. Her symptoms worsened 2 weeks before admission. She had loss of appetite but denied chest pain, palpitations, cough, fever, chills, night sweats, or changes in weight. She previously had menorrhagia but had amenorrhea for 2 months before admission. Family and social history was not contributory. On admission, her vital signs were normal, with blood pressure 110/74 mmHg and apical heart rate 62 beats/min, regular. Her physical examination was significant for muffled heart sounds, jugular vein distention (JVP), and bilateral edema over the ankles. Bilateral basal crackles were auscultated. Her abdomen was distended with palpable liver edge 2 cm below the costal margin, and shifting dullness was positive. Her skin was dry and rough. Conjunctival pallor, macroglossia, and loss of lateral third of eyebrows were also noted.
ECG showed sinus bradycardia with low voltage [Figure 1]. Chest X-ray showed enlarged cardiac silhouette [Figure 2]a and [Figure 2]b. She underwent two-dimensional (2D) echocardiogram that showed a large circumferential pericardial effusion, 50–60 mm anterior and posterior to the heart, with heart swinging within the effusion, indicating impending cardiac tamponade. The thickened visceral pericardium was also noted. The early diastolic collapse of the right ventricle (RV) was present. A pulse-wave Doppler showed respiratory variation of RV and left ventricular inflow to be more than 30% and 25%, respectively. Dilated plethoric inferior vena cava with inspiratory collapse <50% was found [Figure 3]. The patient was admitted to the cardiac intensive care unit. She underwent urgent pericardiocentesis with drainage of 1200 ml serous fluid and pericardial drain was placed. The pericardial fluid assay results were total protein 66.5 g/L and lactate dehydrogenase 764 IU/L. Fluid cultures were negative and cytology was also negative for malignant cells. Further, 150 ml was drained over the next 24 h. Postpericardiocentesis, 2D echocardiogram revealed minimal fibrinous pericardial effusion with no evidence of tamponade.
|Figure 2: (a) Chest X-ray showing cardiomegaly. (b) Chest X-ray showing resolution of cardiomegaly after pericardiocentesis|
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|Figure 3: Two-dimensional echocardiogram showing the heart swinging within the effusion, indicating cardiac tamponade|
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A complete laboratory panel was obtained which revealed thyroid-stimulating hormone level of >100 mIU/L (0.3–4.2 mIU/L) and free T4 of <0.5 pmol/L (11.6–21.9 pmol/L). The patient was started on levothyroxine for primary hypothyroidism. Other significant investigations include bicytopenia, hemoglobin of 8.3 g/dL (13–17 g/dL), and white blood cells count of 2.7 × 103/μL (4–10 × 103/μL). Anemia workup was suggestive of iron deficiency anemia, and she was started on iron supplementation. Total serum cholesterol was 6.7 mmol/L; low-density lipoprotein cholesterol was 4.5 mmol/L; creatine kinase (CK) level was 724 U/L; and lactate dehydrogenase level was 1024 U/L (125–220 IU/L). HIV serology, hepatitis serology, and QuantiFERON were all negative. Autoimmune workup, including antinuclear antibody (ANA), Antineutrophil cytoplasmic antibodies (ANCA), anticardiolipin, anti-double stranded DNA (anti-dsDNA), anti-smith, and ribonucleoprotein (RNP) antibodies, was negative. The patient was also found to have bilateral pleural effusion. Thoracentesis revealed hemorrhagic fluid with mixed cellularity and high mesothelial cells. Pleural fluid chemistry was borderline between exudate and transudate as per Light's criteria. Both pericardial and pleural fluids were negative for acid-fast bacilli. Computed tomography of the neck, chest, abdomen, and pelvis did not show any features of lymphadenopathy, malignancy, or infection. Bilateral mammogram was normal as well. Magnetic resonance imaging of the heart was also performed and showed no evidence of infiltrative myocardial disease. Repeat echocardiography after 1 week showed reaccumulation of the moderate volume of pericardial effusion, but there were no signs of tamponade, and the patient remained hemodynamically stable, requiring no further intervention. The cardiac tamponade was attributed to overt primary hypothyroidism, as all other etiologies of tamponade had been excluded. Her symptoms improved over the next 2 weeks, and she was discharged on levothyroxine.
| Discussion|| |
Hypothyroidism is a common condition; the prevalence of overt hypothyroidism is estimated to vary from 0.1% to 2% in the population. Pericardial effusion is one of the well-known manifestations of hypothyroidism. A study by Kabadi andKumar found the incidence of pericardial effusion in hypothyroidism to be 3%–6%, the occurrence of which is dependent on the severity of the disease. However, it is rare for cardiac tamponade to be the first manifestation of hypothyroidism. This is attributed to slow accumulation of the fluid and marked dispensability of the pericardium. Classic signs of cardiac tamponade are raised JVP, hypotension, and muffled heart sounds (Beck's triad). Our patient had muffled heart sounds and raised JVP but did not have hypotension, tachycardia, or pulsus paradoxus. A review by Wang et al. described that usual symptoms of cardiac tamponade may be absent in hypothyroidism. For patients diagnosed with cardiac tamponade without sinus tachycardia, hypothyroidism should be highly suspected. Decreased sympathetic activity despite decrease in cardiac output is the reason for bradycardia seen in hypothyroidism.
Furthermore, our patient was found to have elevated creatine kinase and lactate dehydrogenase levels. A review by Hardisty et al. noted similar findings and also observed that levels were higher in the presence of an effusion. Our patient has a combination of ascites, pleural effusion, and pericardial effusion. The pathogenesis of multiple effusions in hypothyroidism is due to generalized polyserositis, impaired lymphatic drainage, as well as increased leak of plasma proteins, because of abnormal capillary permeability. A review of 128 patients with hypothyroidism and pleural effusions  reported that these effusions were borderline between exudates and transudates, similar to our patient. Thyroxine replacement alone is sufficient for the resolution of these effusions; however, resolution may take about 2–12 months. A previous study investigated patients during thyroxine replacement therapy and reported that effusions did not disappear until thyroid function tests had returned to normal. In pericardial effusions due to hypothyroidism, various authors , have noted recurrence of effusion after needle drainage of pericardial fluid, as was seen in our patient.
| Conclusion|| |
The case demonstrates that hypothyroidism should be considered in all patients, with an unexplained pericardial effusion. The symptoms and signs of hypothyroidism may be subtle, leading to delay in diagnosis. Furthermore, it is important to remember that patients with hypothyroidism may not present with the classic signs of cardiac tamponade. With early diagnosis, thyroxine replacement therapy should be started, leading to clinical improvement.
- Hypothyroidism should be considered in all patients with an unexplained pericardial effusion
- Patients with hypothyroidism may not present with the classic signs and symptoms of cardiac tamponade. Hypothyroidism should be suspected in patients diagnosed with cardiac tamponade without tachycardia
- With early diagnosis, thyroxine replacement therapy should be started, leading to complete reversal and cure of the disorder.
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.
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Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3]