Cardiac Tamponade Secondary to Massive Pericardial Effusion in Severe Primary Hypothyroidism: A Case Report

Background: Pericardial effusion is a recognized manifestation of overt hypothyroidism, but progression to cardiac tamponade is rare. In tuberculosis-endemic settings, diagnostic focus often favors tuberculous pericarditis, risking delayed recognition of reversible endocrine causes. Case Presentation: A 65-year-old Black African woman from Northern Uganda presented with five months of progressive dyspnea, orthopnea, and generalized edema, followed by acute pleuritic chest pain. She had a history of hypertension and type 2 diabetes mellitus. No prior thyroid disease, tuberculosis, malignancy, or rheumatologic condition was identified. Examination revealed marked sinus bradycardia (42 beats/min), elevated jugular venous pressure, muffled heart sounds, pulsus paradoxus, and Woltman’s sign. The thyroid gland was diffusely enlarged without palpable nodules or cervical lymphadenopathy. Electrocardiography showed low-voltage QRS complexes. Transthoracic echocardiography demonstrated a large circumferential pericardial effusion (maximal posterior separation 3.2 cm) with right ventricular diastolic collapse and Doppler evidence of tamponade physiology, and a mildly reduced left ventricular ejection fraction of approximately 40%, with diffuse hypokinesis and no regional wall motion abnormalities, making ischemic cardiomyopathy less likely. Urgent pericardiocentesis drained 520 mL of clear, straw-colored fluid. Pericardial fluid analysis showed elevated total protein (4.2 g/dL; serum protein 7.0 g/dL; fluid-to-serum ratio 0.6), moderately elevated lactate dehydrogenase (below 1000 U/L), low adenosine deaminase (< 5 U/L), and negative mycobacterial studies, making tuberculous pericarditis unlikely. Thyroid function tests confirmed severe primary hypothyroidism (thyroid-stimulating hormone 88.08 mIU/L; free thyroxine 4.0 pmol/L) with positive anti-thyroid peroxidase antibodies, consistent with autoimmune thyroiditis. Low-dose levothyroxine was initiated with gradual titration. Hemodynamic status improved immediately after pericardiocentesis. Follow-up echocardiography showed complete resolution of the effusion, and the patient achieved biochemical euthyroid within three months. Conclusion: Severe primary hypothyroidism should be routinely considered in patients with unexplained pericardial effusion, even in tuberculosis-endemic settings. Paradoxical bradycardia in tamponade, Woltman’s sign, low-voltage electrocardiography, and a protein-rich pericardial effusion with low adenosine deaminase are important diagnostic clues. Prompt pericardiocentesis treats hemodynamic compromise, while cautious levothyroxine replacement prevents recurrence.