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Authors' reply

The Editor—Sir,

We thank Dr Jackson and colleagues for their interest in our report and their thoughtful and well reasoned letter. Following their suggestion that the vascular anomaly we identified as a rare congenital arteriovenous malformation might be bronchopulmonary sequestration, we examined our finding once again.

Our report described the CT and digital subtraction angiography (DSA) findings of a rare vascular anomaly arising from the posterior mediastinal aorta and presenting as catastrophic haemorrhage. On CT, there was a large mediastinal haematoma and bilateral haemothoraces. The left lower lobe was collapsed, with no cystic or solid lung mass or lung hypervascularity being seen (Figure 1). DSA demonstrated that the abnormal vessels with systemic arterial supply and venous drainage were confined to the posterior mediastinum. There was no enlarged vessel in the left lower lobe. There was no characteristic radiological sign permitting a presumptive diagnosis of intralobar bronchopulmonary sequestration. On macroscopic examination, there were torturous anomalous vessels with aneurysmal dilatation (Figure 2) that were distinctive and suggestive of vascular anomaly. The vessels were rather bizarre and did not supply any definite mass or named anatomy. One of them had been ruptured, with adjacent tan coloured tissue and surrounding blood clots. Microscopically, the specimens showed hyalined fibrous tissue, smooth muscle and myxoid degeneration. There was no bronchial epithelium or pleural sac to indicate intralobar or extralobar sequestration.

View larger version (141K): [in this window] [in a new window]   Figure 1. CT shows no evidence of soft tissue mass or lung hypervascularity but there are bilateral haemothoraces and a large posterior mediastinal haematoma.

View larger version (141K): [in this window] [in a new window]   Figure 2. Gross specimens show aberrant torturous vessels with aneurysmal dilatation.

We regret our oversight in using the incorrect term of malformation when describing various congenital and acquired causes of arteriovenous communication in our article.

Yours etc.,

A S C Ching and Y L Chan

Department of Diagnostic Radiology and Organ Imaging, Prince of Wales Hospital, Shatin, NT, Hong Kong SAR, China

Acknowledgments

We are grateful to Dr P C L Choi, FRCPath (Department of Cellular and Anatomical Pathology, Prince of Wales Hospital) for reviewing the pathology of this case.

Footnotes

See the original letter on page 565

Received for publication March 12, 2001. Accepted for publication April 17, 2001.

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