Cardiovascular Journal of Africa: Vol 26 No 3 (May/June 2015)

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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 26, No 3, May/June 2015 AFRICA e7
Case Report
An unusual cause of a large fibrinous pericardial
effusion
Noleen Chengetai Tembani-Munyandu, Rudo Makunike-Mutasa, Leolin Katsidzira, Andrew Chinogureyi
Abstract
The commonest cause of a large fibrinous pericardial effusion
in sub-Saharan Africa is tuberculosis. There are, however,
limited resources available for making a definitive diagnosis
of tuberculous pericarditis. The diagnosis is largely based
on clinical criteria. There is a risk of misdiagnosing less-
common causes of large fibrinous pericardial effusions. We
present a patient who had a pericardial angiosarcoma that
was initially thought to be a tuberculous pericardial effusion,
and discuss the challenges in making a definitive diagnosis of
tuberculosis.
Keywords: fibrinous pericardial effusion, tuberculosis (TB),
angiosarcoma
Submitted 3/7/14, accepted 1/12/14
Cardiovasc J Afr 2015; 26: e7–e10
DOI: 10.5830/CVJA-2014-075
The majority of fibrinous pericardial effusions in sub-Saharan
Africa are caused by tuberculosis (TB), which accounts for such
effusions in more than 80% of HIV-positive patients, and 50
to 70% of HIV-negative patients in the region.1-4 Consequently,
it is a common clinical practice to commence patients on TB
treatment on the basis of a fibrinous pericardial effusion seen on
echocardiogram.
While this strategy may have merit, there is the risk that
patients with less-common causes of a fibrinous effusion may
have their diagnosis and treatment unduly delayed. We present a
patient who had a large fibrinous pericardial effusion, which was
managed as tuberculosis, but this turned out not to be the case.
Case report
A 24-year-old male was referred from a peripheral hospital
complaining of two months’ history of shortness of breath on
exertion, left-sided pleuritic chest pain, a non-productive cough
and significant weight loss. He had lost 17 kg over two months
and had drenching night sweats.
He had drunk at least 40 units of alcohol per week and
smoked two packs of cigarettes per week for a year. He had no
significant medical history and had tested HIV negative a month
prior to presentation.
On examination he was wasted, had no significant
lymphadenopathy and had a temperature of 37.2°C. His blood
pressure was 96/50 mmHg and he had a low-volume tachycardia
of 116 beats per minute. The jugular venous pressure was 7 cm
and the apex beat could not be localised. The heart sounds were
muffled and he had a tender hepatomegaly 4 cm below the costal
margin.
The chest X-ray showed a large globular heart shadow but no
pulmonary congestion. The electrocardiogram showed a sinus
tachycardia and echocardiography revealed a large fibrinous
pericardial effusion about 5 cm in maximum depth. There was
early right ventricular diastolic collapse and the inferior vena
cava was 2.5 cm and not collapsing with inspiration.
The full blood count showed a white cell count of 6.4 × 103
cells/μl, haemoglobin 14.6 g/dl and platelet count 275 × 103 cells/
μl. Urea and electrolytes were sodium 126 mmol/l, potassium 3.4
mmol/l, urea 9.1 mmol/l and creatinine 88 μmol/l. Serum albumin
was 28 g/l, total protein was 81 g/l and serum globulin was 53 g/l.
A probable diagnosis of TB pericardial effusion was made on
the basis of a Tygerberg score5 of 8: night sweats = 1, weight loss
= 1, fever > 37.8°C = 0, white cell count < 10 cells/μl = 3, serum
globulin > 40 g/l = 3, total score = 8.
The patient underwent urgent pericardiocentesis and 1 000
ml of haemorrhagic pericardial effusion were drained. The
fluid microscopy showed a negative Ziehl Nielsen stain, a
few leucoytes, many red blood cells, protein of 55 g/l, lactate
dehydrogenase was 1 456 U/l and adenine deaminase was 24
U/l. He was commenced on TB therapy (isoniazid, rifampicin,
pyrazinamide and ethambutol).
Despite treatment, he continued to have severe chest pain
and progressive loss of weight. On review at six weeks, there was
echocardiographic evidence of re-accumulation of the fluid and
he was experiencing severe pain in the thoracic spine.
A computed tomography scan was requested and it showed
a tumour in the pericardium compressing the cardiac chambers
and extending posteriorly into the thoracic spine and upper
lumbar spine (Fig. 1).
Department of Medicine, College of Health Sciences,
University of Zimbabwe, Harare, Zimbabwe
Noleen Chengetai Tembani-Munyandu, MB ChB, MMed Medicine,
Leolin Katsidzira, MB ChB, MMed Medicine
Department of Histopathology, College of Health Sciences,
University of Zimbabwe, Harare, Zimbabwe
Rudo Makunike-Mutasa, MB ChB, MMedSci, FRCPath
Department of Radiology, College of Health Sciences,
University of Zimbabwe, Harare, Zimbabwe
Andrew Chinogureyi MB ChB, FCRad, FRCR