An 8-year-old child presented to Pediatric cardiology outpatient services with complaints of bluish discoloration of nails and lips with poor growth since early childhood. On evaluation, child had low weight- and height-for-age with central cyanosis and grade-2 pan-digital clubbing. Oxygen saturation was 68% at room air. Cardiovascular examination revealed single second sound without any murmur. Chest radiograph revealed pulmonary oligemia with left lower zone cavitary lesion (Fig. 1a). There was no history of cough, hemoptysis or tuberculosis contact, and evaluation of respiratory system was normal.

(a)	(b)
Fig. 1 (a) Chest radiograph PA view showing left lower zone cavitary lesion; (b) Angiographic projection AP view showing a large tortuous aorto-pulmonary collateral arising from celiac trunk and curving in left lower zone masquerading as cavity on chest radiograph.

On echocardiography, the diagnosis confirmed was tricuspid atresia and pulmonary atresia. Patient was planned for cardiac catheterization to determine the source of pulmonary blood flow. Upon catheterization, single large aorto-pulmonary collateral arising from celiac trunk was noted, which was the sole source of pulmonary blood flow (Fig. 1b). The tortuosity of collateral in left lower zone of lung appeared like a cavity on chest radiograph.

Incidence of tuberculosis in congenital heart disease is almost 2.5 times that of the normal population [1]. In children with increased pulmonary blood flow, it is because of chronically wet lungs, and in those with reduced pulmonary blood flow, it happens because of ventilation-perfusion mismatch. Recognizing and treating tuberculosis is important before cardiac surgery. In cyanotic congenital heart disease with reduced pulmonary blood flow, radiological features mimicking tuberculosis include apical caps and pseudo fibrotic lesions [2,3]. Collaterals give lacy reticular pattern with non-homogenous pulmonary vascularity as collateral flow is non-uniform [4]. Aortopulmonary collaterals in our patient radiologically suggested pulmonary parenchymal pathology, sometimes they manifest with hemoptysis as well, making the differentiation further difficult. Awareness of this possibly may help the clinician to suspect and appropriately manage these children.

Acknowledgement: Dr SS Kothari, Professor, Department of Cardiology, AIIMS, Delhi, for help in critically reviewing the manuscript.

1. van der Merwe PL, Kalis N, Schaaf HS, Nel EH, Gie RP. Risk of pulmonary tuberculosis in children with congenital heart disease. Pediatr Cardiol. 1995;16: 172-5.

2. Mcloud TC, Isler RJ, Novelline RA, Putman CE, Simeone J, Stark P. The apical cap. Am J Radiol. 1981;137:299-306.

3. Haroutunian LM, Neill CA, Dorst JP. Pulmonary pseudofibrosis in cyanotic heart disease: A clinical syndrome mimicking tuberculosis in patients with extreme pulmonic stenosis. Chest. 1972;62:587-92.