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CFA with preserved lung volumes
  1. NICOLA STRICKLAND,
  2. J M B HUGHES
  1. Department of Imaging
  2. Hammersmith Hospital
  3. DuCane Road
  4. London W12 0HS, UK
  1. M J DOHERTY,
  2. P M A CALVERLEY
  1. Aintree Chest Clinic
  2. Fazakerley Hospital
  3. Liverpool, UK

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Doherty et al 1 seem confident of their ability to distinguish emphysematous spaces from large cystic spaces of honeycomb lung on the basis of a wall thickness on HRCT scanning of greater or less than 1 mm. In cryptogenic fibrosing alveolitis (CFA) we think this is difficult unless an assessment of function (with V/Q scanning or expiratory CT scans) is made at the same time.2 The situation is complicated by the ability of fibrosis in mixed emphysematous-fibrotic areas to support the airways and mitigate the expected gas trapping.

“Emphysematous” changes were seen in only six of 21 patients with CFA and preserved lung volumes (only seven of whom had HRCT scans). Were expiratory CT scans performed? We note the normal RV/TLC and FEV1/VC ratios. In the absence of functional data for these spaces, we reserve judgement about the pathology.

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authors’ reply We thank Dr Strickland and Professor Hughes for their helpful comments on the differentiation of emphysema from large cystic changes in CFA. We have tried to stress the limitations of our data in the discussion section of our paper and have tried to emphasise that emphysema was found on CT scans in only six of 21 patients with preserved lung volumes, though this included six of the seven patients who had a comparable CT scan appearance. We also commented on the findings of the normal RV/TLC and FEV1/FVC ratios.

The CT criteria used in our paper to diagnose emphysema were rather more specific than indicated in their letter in that they included the presence of areas of low attenuation or bullae (air spaces with a 1 cm diameter with a wall frequency of less than 1 mm). The former description of unmarginated areas could not be mistaken for the cystic changes of CFA. The subjects with preserved lung volumes did not show more extensive fibrosis which might otherwise have caused pathological enlargement of the air spaces. All this supports our view that their changes were due to emphysema; neither do we believe that the effects of cigarette smoking on the airways are necessarily confined to pathological alveolar destruction. Co-existing small airways disease provides an alternative and plausible explanation of the physiological findings we noted in our patients with preserved lung volumes. Clearly, this is related to their significant cigarette exposure.

Neither expiratory CT scans nor V/Q scanning were performed in these subjects. This reflects the retrospective nature of the data, many of the subjects having been investigated before the publication of the paper by Strickland and Hughes.

Prospective studies utilising their technique would be helpful in providing further information to support our view that the changes seen in patients with CFA with this pattern of physiological abnormality are indeed due to smoking related obstructive lung disease.

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