Cardiac tamponade in a patient with primary hypothyroidism.

Pericardial effusion is frequently found in patients with hypothyroidism, but it is rarely associated with cardiac tamponade. Hypothyroidism complicated by cardiac tamponade is rarely referenced in the medical literature. Here we report an unusual case of a 45-year-old female, who presented with breathlessness and was found to have hypothyroidism with large pericardial effusion with cardiac tamponade. Treatment included an emergency pericardiocentesis followed by thyroxine hormone replacement.

INTRODUCTION

The occurrence of pericardial effusion in hypothyroidism appears to be dependent on the severity of the disease. Pericardial effusion (PE) may be a frequent manifestation in myxedema, an advanced severe stage, as previously found, but is rarely associated with mild hypothyroidism.[1] The recent studies, concluded that PE is extremely infrequent in hypothyroidism, with an incidence of 3% to 6%. To our knowledge, about 20 cases of hypothyroid with cardiac tamponade have been reported in the literature.Cardiac tamponade is usually a consequence of increased pericardial pressure with accumulation of pericardial effusion. Pericardial effusion may be caused by acute pericarditis, tumor, uremia, hypothyroidism, trauma, cardiac surgery, or other inflammatory/noninflammatory conditions.[2] A small pericardial effusion can cause clinically significant cardiac tamponade when it accumulates rapidly. It is important to suspect cardiac tamponade when patients have hemodynamic compromise regardless of the amount of pericardial effusion.[3] Here we report an uncommon case of hypothyroidism with cardiac tamponade.

CASE REPORT

A 45-year-old female was brought by her relative to emergency department (ED) with history of shortness of breath for 2 days. Patient was apparently asymptomatic 2 months back; when she gradually started noting malaise, lethargy, slow speech, edema of the face and extremities, and progressive weight gain. There was no history of medical illness and drug history in the past. Vital signs on admission were recorded (temperature, 36°C; blood pressure, 90/52 mmHg; heart rate, regular at 74 beats/min). Body mass index (BMI) was 32.6 kg/m2(obese). Patient was hypothermic with pulsus paradoxus (inspiratory fall in systolic blood pressure >10 mmHg). Physical examination found facial edema, coarse hair, dry skin, an engorged jugular vein, mild pallor, and non-pitting edema of the extremities. Oxygen saturation (SpO2) was 84%. The cardiac apical impulse was not visible. The apex beat was not felt. The heart sounds were soft and distant with bilateral basal rales in both lung fields. On per abdomen examination, there was mild hepatomegaly. Her deep reflexes showed delayed relaxation.

Chest radiogram showed cardiomegaly with globular enlargement of the cardiac silhouette with “water bottle” configuration [Figure 1]. Electrocardiogram showed heart rate of 74/min with low voltage pattern with electrical alternans. Bedside echocardiogram demonstrated small heart size with massive pericardial effusion and signs of early diastolic right ventricular (RV) collapse. There was swinging motion of heart within large effusion, prominent respiratory alteration of RV dimension with right atrial (RA) and RV collapse during diastole. Pericardial effusion was all around and all cardiac chambers were of small size with predominant diastolic heart failure [Figure 2]. Right ventricular diastolic collapse was echocardiographic hallmark of cardiac tamponade. Considering echocardiographic findings and clinical scenario, diagnosis of large pericardial effusion with cardiac tamponade was made.

Figure 1

Chest radiogram showing cardiomegaly with globular enlargement of the cardiac silhouette with “water bottle” configuration

Figure 2

Two-dimensional transthoracic echocardiogram showing large, all around pericardial effusion with right ventricular collapse in diastole, a subtle sign of cardiac tamponade

Immediately, we shifted the patient to intensive care unit for pericardial fluid tapping procedure (pericardiocentesis). Written and informed consent was taken for pericardiocentesis. Pericardial tapping was done under all aseptic precautions. We tapped about 450 ml of pericardial fluid through standard xiphisternal route under cardiac monitoring. Evacuative pericardiocentesis was carried out using a spinal needle connected to an ECG line. Fluid was yellowish golden in color which was sent for cytological and biochemical investigation.

Immediately after pericardial fluid tapping, the patient showed significant improvement in the cardiopulmonary status. Tachycardia and tachypnea was significantly reduced. Oxygen saturation was increased to 94% from 84% without oxygen supplementation. After pericardiocentesis, chest radiogram showed significant reduction of cardiomegaly. Post pericardiocentesis, two-dimensional echocardiogram revealed minimal pericardial effusion with no evidence of tamponade.

Considering her history and findings, we did thyroid function test for this patient, which was suggestive of primary hypothyroidism with high thyroid-stimulating hormone (TSH) and very low T3 and T4 levels. The patient was treated with thyroxine 100 μg daily which was later increased gradually to 200 μg daily. The patient's condition improved and she was discharged in a good general condition after 2 weeks. Follow-up echocardiogram after a period of 3 months showed near total resolution of pericardial effusion. Within a few weeks, all her symptoms and signs disappeared and she became normal.

Investigations

Hemoglobin (Hb), 11.5 g%; erythrocyte sedimentation rate (ESR), 24 at the end of 1 hour; total leukocyte count, 9850 mm3; platelet count, 2.1 lac; blood urea level (BUL), 24 mg%; serum creatinine level, 1.1 mg%; liver function test (LFT), within normal limits. Thyroid function test: serum TSH, 84 mU/ml (normal 0.35–5.5 mU/ml); T3, 26.2 ng/dl (normal 90–190 ng/dl); and T4, 0.56 μg/dl (normal 5–12 μg/dl). Lipid profile: total cholesterol, 317 mg/dl; high-density lipoprotein cholesterol (HDL-C), 52 mg/dl; triglyceride, 214 mg/dl. Serum sodium was 136 mEq/l and serum potassium was 4.2 mEq/l. HIV and HbSAg were negative.

Chest radiogram PA view

Cardiomegaly with globular enlargement of the cardiac silhouette with “water bottle” configuration Figure 1 was seen.

Electrocardiogram

Electrocardiogram showed heart rate of 74/min with low voltage pattern with electrical alternans (alternating size of QRS complex due to swinging of heart).

Two-dimensional trasthoracic echocardiography

There was massive pericardial effusion (about 600–700 ml) and signs of early diastolic RV collapse. There was swinging motion (apical-4-chamber view) of heart within large effusion; prominent respiratory alteration of RV dimension with RA and RV collapse during diastole (parasternal long axis view) was seen. Pericardial effusion was all around and all cardiac chambers were of small size with predominant diastolic heart failure. Right ventricular diastolic collapse was an echocardiographic hallmark of cardiac tamponade. Left ventricular (LV) systolic function was normal with an overall LV ejection fraction of 60% [Figure 2]. Pericardial fluid analysis: appearance, golden yellow in color (“Gold Paint” effusion); lymphocytes, 8–10/mm3; proteins, 4.7 g%; sugar, 80 mg% and cholesterol, 192 mg%; no organisms were grown on culture.

DISCUSSION

The pathophysiologic derangements responsible for the collection of fluid in the serous cavities of hypothyroid patients are probably increased systemic capillary permeability and disturbances in electrolyte metabolism.[4] Alexander first used the term “Gold Paint Effusion” to describe the golden brown appearance of the pericardial fluid due to the shimmering satin cholesterol crystals. The high cholesterol content of the fluid has been attributed to disturbances in lipid metabolism; possibly, a churning action of the heart plays a role in the precipitation of cholesterol from pericardial fluid or the poor absorptive capacity of the pericardium may be a major factor.[3-5]

Thyroid replacement alone is sufficient for resolution of these effusions, although it may take many months. Pericardiocentesis is indicated only if cardiac tamponade develops. This rare but significant condition should be considered, especially when it occurs after acute cold exposure. Pericardial effusion, lipid metabolic abnormality and abnormal liver function can be easily reversed with thyroid replacement.[67]

Cardiac tamponade is life-threatening, slow or rapid compression of the heart due to the pericardial accumulation of fluid, pus, blood, clots, or gas, as a result of effusion, trauma, or rupture of the heart. Tamponade is more common in patients with malignant pericarditis. Less common causes include tuberculosis, acute myocardial infarction (MI), pericarditis, radiation damage, bacterial infection, cardiomyopathy, lupus, dissecting aortic aneurysm, etc.[89] Retnam et al.,[3] Chou et al.,[4] Chatterji et al.,[6] LIN et al.,[7] Al-Mahroos et al.,[8] and Usalan et al.[5] have reported cases of cardiac tamponade with hypothyroidism, similar to the present case.

CONCLUSION

To conclude, hypothyroidism with cardiac tamponade is a rare condition. Cardiac tamponade is one of the life-threatening conditions that clinicians should have high degree of suspect in relevant clinical scenario. Bedside echocardiography is one of the gold standard investigations to diagnose pericardial effusion with cardiac tamponade. Hypothyroidism presenting with massive pericardial effusion with cardiac tamponade is an uncommon presentation as in the present case report. How rapidly pericardial fluid gets accumulated is more important as per as cardiac hemodynamics is concerned rather than the volume of effusion. Mild pericardial effusion does respond to thyroxine supplementation over a long period and pericardiocentesis is necessary only when tamponade develops.