Chronic pericarditis characterised by adhesions between the parietal and visceral pericardium is called adhesive pericarditis. In South Africa, tuberculosis is the most common cause of chronic pericarditis. We report a case of adhesive pericarditis that mimicked a tumour.
Tuberculous pericarditis is a common disease among the African and Asian populations because of the high prevalence of tuberculous infections.
A 27-year-old female patient presented with swelling of the abdomen and difficulty in breathing. She had a history of a tuberculous pericardial effusion one year prior to admission and had completed a regimen consisting of six months of anti-tuberculous therapy and steroids.
Clinical examination revealed a patient in respiratory distress, with congested neck veins and massive ascites. She had mild pallor, tachycardia and pedal oedema. The lungs were clear. The full blood count showed a low haemoglobin 9.7 g/dL, a low red cell count 3.30 × 1012/L and a normal white cell count. The renal function tests were grossly normal, and this patient did not have the human immunodeficiency virus (HIV). Electrocardiogram (ECG) showed right axis deviation with inverted T waves in leads II, III, aVF, V1–V6. The patient had features of constrictive pericarditis.
The echocardiography report was unresolved and confusing with a conclusion of a suspected tumour or thrombus in the right ventricle. Cardiac catheterisation study showed that the right ventricular (RV) and left ventricular (LV) pressures were consistent with constrictive pericarditis. The patient was then referred for magnetic resonance imaging (MRI) to further evaluate for the suspected tumour and ventricular function.
Magnetic resonance imaging was performed on a Philips Multiva 1.5 Tesla scanner. Images were acquired in the para septal long axis, short axis and four-chamber views. Intravenous contrast was administered to further evaluate the mass lesion. The findings confirmed a large 6 cm × 4 cm × 8 cm mass compressing the right ventricle. The short axis post contrast T1 spectral presaturation inversion recovery black blood (T1_SPIR_BB) sequence image in
Short axis post contrast T1 spectral presaturation inversion recovery black blood sequence showing a high signal mass lesion (black arrow) with an associated nodular pericardium (black arrowhead) and massive ascites (white arrow).
The lesion (black arrow) remains hyperintense on the T2 weighted short axis series.
Proton density (4-chamber view) shows a predominantly hyperintense lesion with mass effect, as indicated by the white arrow.
The patient subsequently underwent total pericardial stripping with excision of the mass. Histology showed fibrous pericardium with chronic inflammatory aggregates, including predominant lymphocytes with granulation tissue formation as seen in
Haematoxylin and eosin (H&E) photomicrograph at 20× magnification of the fibrous pericardium showing organising fibrin deposition.
Haematoxylin and eosin (H&E) photomicrograph at higher magnification (40×) of the organising fibrin deposition showing an amorphous coagulum of acellular fibrin.
Pericarditis is defined as inflammation of the pericardium, and this has a number of causative agents like infection, neoplastic conditions, systemic conditions including collagen vascular diseases, trauma and others.
Tuberculosis is a multisystem disease, which is uncommon in developed countries, with an incidence reported at 4%.
Tuberculosis pericarditis, caused by
In tuberculous pericarditis, granulomas may not be histologically apparent if the patient is treated. In this case, polymerase chain reaction (PCR) may be useful to establish the diagnosis.
Cardiac MRI demonstrates the morphologically thickened pericardium
This patient presented with an unusual form of constrictive tuberculous pericarditis, which was due to a pericardial adhesion that presented as a compressive mass. This resulted in a focal mass-like adhesion causing compression of the right ventricle and RV dysfunction. Surgical treatment in the form of pericardiectomy was performed, and the postoperative period was uneventful. The diagnosis of pericarditis was confirmed at histology. The patient was clinically well at follow-up, 12 months after surgery.
The diagnosis of pericardial adhesions should be included in the differential diagnosis of patients with pericardial effusions who suddenly present with a pericardial mass.
The authors would like to thank Dr M.J. Chokoe-Maluleke who worked closely with Prof. Bida on the histology slides. She could not be contacted at the time of this publication.
The authors declare that they have no financial or personal relationships which may have inappropriately influenced them in writing this article.
M.E.K. was responsible for the conception, design and drafting of the article, acquiring and reporting the MRI images, revising critically for intellectual content and approval of the final version to be published. N.M.B. was responsible for acquiring and reporting the pathology slides, design and revising critically for intellectual content and approval of the final version to be published. P.M. was responsible for the clinical notes and approval of final version for publication. P.S.R. was responsible for the surgical notes and approval of the final version to be published.