AL is a 14-year-old male patient with cerebral palsy. He presented with a 3-day history of cough and haematemesis; the volume quantified was ~125 mL. He was previously treated at a primary healthcare centre for pulmonary tuberculosis (TB). The TB diagnosis was based on prolonged coughing and suggestive radiological changes, but it was not confirmed microbiologically (Gene Xpert or culture confirmation). The chest radiograph from the peripheral hospital was unavailable. 
 Clinically he was apyrexial and haemodynamically stable. He was not pale, had no clubbing and his chest examination was normal, with only epigastric tenderness noted. He was treated with omeprazole for acute gastritis, with a non-urgent gastroscopy planned for the future. The chest radiograph demonstrated an irregular right-sided hilar opacity. 
 At the time of discharge, he had a further significant episode of haemoptysis with vomiting. Approximately 500 mL of blood was noted. He remained haemodynamically stable, but his haemoglobin dropped from 9.1 g/dL to 8 g/dL. Coagulation parameters, including platelets, were normal. A repeat chest radiograph was unchanged from the initial one. Repeated sputum analyses for Gene Xpert and TB culture were negative. 
 A gastroscopy demonstrated a dilated and abnormal oesophagus with an ulcer and an oesophageal biopsy was in keeping with mild oesophagitis. On bronchoscopy, the airway anatomy was normal; a fistula opening was not seen. There was also no evidence of pulmonary haemorrhage or any endobronchial lesions, but purulent secretions were noted to arise from the right lower lobe segments. 
 A computed tomography (CT) scan of the chest showed an irregular contrast-enhancing inflammatory mass, with cavities located in the superior segment of the right lower lobe (Fig. 1).
Two large arteries originating from the right lateral aspect of the descending aorta were noted to supply this mass, with another arterial supply by the  bronchial artery (Fig. 2).
 The upper (more cranial) artery divided: one branch supplied the mass and the second ran superior and posterior and was thought to represent the artery of Adamkiewicz (also known as the great anterior segmental medullary artery). 
 An upper gastrointestinal contrast study confirmed the presence of a fistulous tract between the oesophagus and the cavities within the mass and the right lower main bronchial segments. There was also severe gastro-oesophageal reflux. Given this configuration, the diagnosis of a complex hybrid congenital pulmonary airway malformation with a broncho-oesophageal fistula (BOF) was considered. In view of the complexity of the vascular supply, surgery was deemed unsafe. As the child had ongoing bleeding, he was referred to the Cardiology department for embolisation of the systemic arteries supplying the lesion. One Amplatzer vascular plug (type II) was deployed into each artery, with obliteration of the blood supply to the lesion. Care was taken to not occlude flow to the (possible) artery of Adamkiewicz, as that could result in an anterior spinal artery syndrome. Oral feeds were suspended and a Nissen fundoplication and percutaneous endoscopic gastrostomy was performed to reduce reflux and gastropulmonary aspiration and allow inflammation to subside. 
 At follow-up 5 months after discharge, AL was doing well. He had no further episodes of haemoptysis or vomiting. A chest radiograph showed a considerable reduction in mass size. 
 His barium swallow showed a marked reduction in the fistula size and volume of contrast entering the lesion. There was no evidence suggesting any spinal vascular compromise after occlusion of the arteries feeding the mass. The long-term plan is to continue conservative management and allow the fistula to heal spontaneously. Failure of spontaneous closure will require surgery to excise the mass and remove the fistula.