2. Case history
An eight-year-old boy presented to our emergency department in June, 2011 with complains of intermittent fever for last seven days associated with cough, breathlessness, and chest pain. There was no important family, traumatic or surgical history. His psychomotor development was normal. On physical examination, he was conscious but irritable, febrile (temperature: 39 °C) having tachypnea (respiratory rate: 32/min), tachycardia (heart rate: 108/min), narrow pulses, blood pressure: 108/80 mmHg, and raised jugular venous pressure. The cardiovascular examination revealed poorly localized cardiac apex, distant, muffled heart sounds and absence of murmur. He had normal facies and skin. Examination of other systems including ankle jerks was normal.
Chest X-ray showed marked cardiomegaly with normal lung field. Urgent echocardiogram was arranged that revealed large PE without tamponade (Fig. 1). Sub-xiphoid pericardiocentesis was performed and 250 ml of sero-sanguinous fluid was aspirated. Initial blood investigations like complete hemogram, serum electrolytes, renal and liver function test were within normal limit except serum albumin which was 2.7 g/dl (range: 3.5–5 g/dl). Blood and urine culture were negative. Examination of sputum and Mantoux test were negative. Cytological, microbiological and biochemical examination of the aspirated fluid were inconclusive other than increased protein content (5 g/dl) and a predominance of mononuclear cells in the differential count. Smear examination of pericardial fluid by Gram stain and Ziehl–Neelsen stain failed to demonstrate the presence of bacteria or tubercle bacilli. Cultures of the pericardial fluid were negative for both bacteria as well as Mycobacterium tuberculosis and the activity of adenosine deaminase (ADA) was not elevated.
Following an initial improvement of several days’ duration, symptoms recurred. Repeat echocardiography revealed moderate collection of serous clear pericardial fluid. Child was subjected for further investigations. Serology for selected viral pathogens like human immunodeficiency virus, Epstein–Barr virus, cytomegalovirus and herpes virus were all negative. Serologic markers for autoimmune diseases and streptococcal infection were negative. Considering exudative nature of the pericardial fluid and definite positive history of contact to tuberculosis, tubercular pericarditis was suspected and anti-tubercular drugs and oral prednisolone were added empirically. General condition of the patient became improved within few days following initiation of anti-tubercular therapy. The patient was discharged home with the advice to attend follow-up clinic.
Following four months of anti-tubercular treatment, in the beginning of November 2011, symptoms recurred and got hospitalized. Urgent chest X-ray showed cardiomegaly and echocardiogram revealed massive PE with impending cardiac tamponade (Fig. 2). Evidence of constrictive pericarditis was detected neither on echocardiographic finding nor in chest computed tomography scan. Patients became hemodynamically stable following aspiration of 350 ml of straw color fluid but developed unexplained bradycardia (pulse rate: 52/min). General examination revealed mild puffiness of face and non-pitting pedal edema. His deep tendon reflexes showed delayed relaxation. Analysis of pericardial fluid again was inclusive other than exudative character due to high protein content (6 g/dl).
Considering recurrent PE and clinical features, thyroid function was ordered. The result showed low free thyroxine (FT4): 0.28 ng/dl [range: 0.9–2.6 ng/dl], free tri-iodothyronine (FT3): 180 pg/dl [range: 240–560 pg/dl] and thyroid stimulating hormone (TSH): 22.51 mIU/l [range: 1.7–9.1 mIU/l]. Ultrasound of thyroid gland was performed showing normally located gland. Both anti-thyroid peroxidase antibodies and anti-thyroglobulin antibody test results were negative. Child was diagnosed as primary hypothyroidism and levo-thyroxine replacement therapy was started at a dose of 5 μg/kg/day. On follow-up visit at six week, repeat thyroid function showed FT4: 2.3 ng/dl and TSH: 3.5 mIU/l. Follow-up echocardiography revealed minimal PE. Till date, child is on levo-thyroxine replacement, maintaining euthyroid state without further recurrence of PE. It was concluded that primary hypothyroidism was the etiology of initial massive PE which was not suspected due to absence of common clinical findings.