Abstract
Cardiac involvement in tuberculosis is relatively rare when compared to other organs and often involves the pericardium leading to constrictive pericarditis. Myocardial tuberculoma is exceedingly rare and only seldom cases have yet been reported. Our report is of a case diagnosed on fine-needle aspiration cytology.
Case report
An 8-year-old boy presented to our paediatrics outpatient department with complaints of fever, cough and reduced appetite for the previous 2 months, associated with breathlessness for the last 3 days. Fever was intermittent in nature, devoid of chills or rigours. Initially, the rise in temperature was noted twice or thrice a week, which gradually progressed to four times a day. In course of time, evening rise of temperature was also noted. Fever was also associated with shortness of breath on exertion. There was no history of rashes, coryza or abdominal pain. At a local hospital, the boy underwent chest radiography, which showed perihilar and left upper zone air space opacities suggesting consolidation. Mild cardiomegaly was also present.
On physical examination, the child was pale, febrile (38.5°C), tachycardic (140 beats/ min) and normotensive (118/72 mmHg), with normal oxygen saturation (SpO2 96%) on room air and with breath sounds reduced on the left side. No palpable lymph nodes were found.
On bronchoscopy, the left upper lobe segmental bronchi were dilated, although no significant secretions or endobronchial obstruction was noted. Echocardiography showed abnormal thickening of right ventricular free wall along with mild tricuspid and pulmonary regurgitation. An infiltrating mass was also observed outside the heart, anterior to the right ventricle and around the great vessels. Chest computed tomography (CT) scanning displayed mass lesions that were multiple, well-defined, homogeneously enhancing and infiltrating the right atria, right ventricle and left ventricular wall (Figure 1(a) to (c)). The cardiac masses involved the cardiac myocardium and showed an intraluminal projection. The lesion in the right ventricular wall was also seen infiltrating the pulmonary infundibulum leading to narrowing of the main pulmonary artery. Infiltrating soft tissue lesion of similar attenuation measuring 2.1 × 2.4 × 4.1 cm was seen in the left upper lobe and along the pericardium, abutting the cardiac masses in the pre-vascular space of the anterior mediastinum. A few foci of calcification with few air bronchograms were noted in the infiltrating soft tissue mass. Based on these radiological findings, a provisional diagnosis of lymphoma was made.
(a–c) Contrast-enhanced computed tomography of chest showing multiple well-defined homogeneously enhancing mass lesions infiltrating the right atria, right ventricle and left ventricle wall, Infiltrating soft tissue lesion of similar attenuation was seen in the apico-posterior segment of left upper lobe and along the pericardium, abutting the cardiac masses in the pre-vascular space of anterior mediastinum.
Laboratory investigations revealed moderate anemia (Hb 70 g/l). Liver, renal function tests and serum electrolytes were unremarkable. Serum complement levels (C3, C4) were within normal limits. Viral serology markers (anti-HIV-1 and 2 antibody, Hepatitis B surface antigen and anti-HCV antibody) were negative. Absolute neutrophil and total leucocyte counts were within normal limits. Blood cultures were sterile.
In view of persisting fever and tachycardia, empirical injectable antibiotics were commenced. (Inj. Ceftriaxone 100 mg/kg/day in two divided doses and tab. Faropenem 30 mg/kg/day three times a day for 1 week) Although there was a slight reduction in temperature, the tachycardia did not subside. An ultrasound-guided fine-needle aspiration of the right ventricular pericardial thickening was performed. The smears prepared were of adequate cellularity and showed multiple epithelioid cell granulomata composed of epithelioid histiocytes with multinucleated Langhans giant cells (Figure 2(a) to (d)). Focal areas showed amorphous, granular debris suggestive of caseous necrosis (Figure 2(e)). No Reed–Sternberg or any atypical cells were seen. Occasional acid-fast bacilli were seen on Ziehl–Neelsen staining (Figure 2(f)). A diagnosis of cardiac tuberculosis was finally recorded. Anti-tubercular therapy produced signs of improvement on a 6-month follow-up. Repeat CT scanning showed resolution of the cardiac and lung lesions. Serial echocardiography on follow-ups showed normal ejection fraction.
(a) Granulomatous inflammation showing multiple epithelioid cell granulomas (Wright-Giemsa stain 40x). (b) Well-defined granuloma composed epithelioid histiocytes in a caseous background (Wright-Giemsa 40x). (c and d) Aggregates of epithelioid histocytes with Langhans giant cells in a necrotic background (Wright-Giemsa 400x). (e) Caseous necrosis with degenerated inflammatory cells (Wright-Giemsa 40x). (f) Ziehl–Neelsen stain showing acid-fast bacillus in a necrotic background (ZN stain 1000x).
Discussion
Tuberculosis (TB), a global public health disease and tenacious challenge, remains poorly controlled and unrestrained in many low-income countries. It may rarely manifest as an isolated cardiac disease, especially in immune-compromised patients, usually involving the pericardium, thus leading to constrictive pericarditis and accounts for a sizeable proportion of the cases in endemic countries. 1 In contrast tubercular involvement of the endocardium, myocardium, valves and great vessels is extremely rare.2–5 Thus optimal diagnostic assay and the correct treatment protocol have not been well defined. The myocardium has been reported to be involved in 0.24–0.28% of TB infections on autopsy. 6 Although involvement of the myocardium can occur through the bloodstream, the most likely mechanism of myocardial involvement is due to an extension from a pericardial focus or a direct retrograde spread from contiguous mediastinal lymph nodes. TB has an anatomical predisposition for right-sided mediastinal lymph nodes; thus, the right side of heart is most vulnerable for contiguous spread. 7
Cardiovascular tuberculosis portends an unfavourable prognosis. Acute clinical manifestations of tuberculous myocarditis may become apparent as disturbances of the conduction system, causing prolonged QT syndrome, ventricular fibrillation, or cardiac arrest. On the other hand, chronic myocardial involvement may manifest with symptoms of gradual heart failure or even as asymptomatic patient who is diagnosed on postmortem examination. 5
Tuberculomas are often sharply demarcated, well-defined, circumscribed lesions distinct from the adjacent normal parenchyma. They exist as single or multiple lesions in the right heart chambers and can possibly arise from active TB elsewhere or an associated finding with miliary tuberculosis.
Diagnosis of cardiac tuberculosis has been considerably amplified by the evolution of non-invasive imaging modalities, such as 2D echocardiography, magnetic resonance imaging and computerised tomography. These technological advances in the field of imaging are particularly helpful in the confirmation of mass lesions. An echocardiogram is the first step in diagnosing cardiovascular involvement. For tubercular effusions, adenosine deaminase levels, gamma interferon or polymerase chain reaction, each test having a high diagnostic sensitivity could aid in diagnosis. Diagnosing cardiac tuberculosis is challenging as obtaining a tissue diagnosis is difficult. Fine-needle aspiration cytology is one solution.2,3,8
Appropriate treatment of tuberculous myocardial lesions in patients with cardiac arrhythmias may result in resolution of both the lesion and the cardiac arrhythmias. 9 Surgical management is indicated in patients with refractory malignant arrhythmias, significant haemodynamic obstruction, inadequate response to anti-tubercular therapy or risk of thromboembolism.
Footnotes
Declaration of conflicting interests
The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding
The author(s) received no financial support for the research, authorship, and/or publication of this article.
Guarantor of submission
The corresponding author is the guarantor of submission.
Declaration of patient consent
The authors certify that they have obtained the appropriate consent from the patient. The patient has given his consent for the images and other clinical information to be reported in the journal. The patient understands that the name and initials will not be published, and due efforts have been made to conceal the same.
