A 65-year-old Malay female with underlying hypertension, type 2 diabetes mellitus, chronic kidney disease stage 3A, history of ischaemic stroke 4 years ago and was semi-dependent for activities of daily living. She presented with complaints of dyspnoea of 1 year duration. Otherwise, she had no chest pain, no palpitation, no constipation, no weight gain. There was no history of pulmonary tuberculosis contact and no family history of malignancy. On physical examination, she had coarse, dry skin with slow mentation and obvious delayed relaxation of deep tendon reflexes. She was hemodynamically stable with blood pressure of 139/86 mmHg, absence of pulsus paradoxus or bradycardia (pulse rate 84 bpm). On auscultation, heart sounds were muffled. Respiratory examination was unremarkable. There was a 3 cm firm and mobile submandibular swelling with no goitre or surgical scar in the neck. Fine needle aspiration cytology of the submandibular swelling was performed and reported to have features of sialadenosis. Gynaecological assessment did not reveal any gynaecology pathology.
Blood investigation showed severe hypothyroidism with FT4 3.4 pmol/L (11.5-22.7 pmol/L) and TSH 114.47 mIU/L (0.55-4.78 mIU/L). Her initial electrocardiogram showed low voltage complexes with electrical alternans. Chest radiograph showed massive cardiomegaly (Figure 4). Echocardiogram revealed large global pericardial effusion ranging from 1.2-3.9 cm but no collapse of right ventricular free wall in diastole with left ejection fraction of 65 % (Figure 5). A provisional diagnosis of primary hypothyroidism with massive pericardial effusion was made. She was commenced immediately on a single high dose 400 mcg levothyroxine followed by lower daily dose of 100 mcg (1.6 mcg/kg/dose) together with liothyronine of 10 mcg thrice daily. Her TSH decreased by half to 49.92 mIU/L (0.55-4.78 mIU/L), with FT4 of 8.3 pmol/L (11.5-22.7 pmol/L) after two days of combination therapy of levothyroxine and liothyronine, which subsequently normalized after one week of treatment, with TSH 4.65 mIU/L, FT4 of 10 pmol/L (Figure 1). Oral liothyronine was given for 10 days.
Repeat echocardiogram did not show improvement in pericardial effusion and it was decided to proceed with pericardial tapping for diagnostic purpose. One litre of pericardial fluid was drained. Echocardiogram reassessment post tapping showed more than 50% reduction of pericardial effusion, ranging from 5-9 mm, no right ventricular chamber collapse during diastole, with ejection fraction of 69% (Figure 5). Pericardial fluid analysis was reported to be acellular with absence of organisms on gram stain and Ziehl-Neelsen stain for acid fast bacilli (AFB). Fluid biochemistry analysis showed normal total protein of 58 g/L (57-82 g/L) and lactate dehydrogenase of 128 U/L (120-246 U/L). There was no growth on bacterial and tuberculosis culture media of the pericardial fluid. Her electrocardiogram showed normal voltage complexes.
Subsequently, the patient was discharged well with levothyroxine 100 mcg OD (1.6 mcg/kg/dose). During clinic review, she appeared well with no complaints of dyspnoea. Her thyroid function improved further and normalized at the second clinic visit with minimal pericardial effusion on echocardiogram reassessment.