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

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. 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. 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.