Excessive dynamic airway collapse and wheeze: Reasons for contemplation.

Sir,

I read with interest the article by Sindhwani et al.[1] and would like to make the following comments:

The authors have evaluated the existence of excessive dynamic airway collapse (EDAC)/tracheobronchomalacia (TBM) in chronic obstructive pulmonary disease (COPD) patients with the hypothesis that EDAC/TBM could be a cause of persistent wheeze in such patients. In their study, the authors have observed collapse in the tracheal lumen only and implicated the same in the genesis of wheeze in their group of patients. This hypothesis itself seems untenable.

As defined by American Thoracic Society, wheeze is defined as high-pitched continuous musical sound with frequency more than 400 Hz and lasting more than 250 ms. According to the most acceptable mechanism of production of wheeze as described by Forgacs[2] (and later further elucidated by Gavriely et al.[3]) in the flutter theory, the walls of the collapsible airways must touch repetitively to produce the musical sound of wheeze. Hence, according to this theory if EDAC/TBM is thought to be the cause of wheeze the obstruction has to be complete at least momentarily, i.e., the collapse <100% will not be explain the production of wheeze in the subjects. Now wheeze is said to arise from the first five or seven generations of the airway. However, fluttering of the trachea itself has been described very rarely as a cause for wheeze production. It would have more logical if the authors had looked for EDAC in the cartilaginous bronchial airways as well as a cause for wheeze in their cohort. EDAC/TBM has, usually been evaluated in both trachea and cartilaginous bronchi in the previous studies.[4]

The authors have included patients with persistent wheeze on auscultation (? during quiet respiration) in this study and had noted that around 40% had TBM/EDAC – a bronchoscopic/radiological finding elicited during forcible expiration. Hence, it can be reasoned that significant airway collapse of the trachea during quiet expiration would have been noticed in lesser than 40% patients. Hence, what was responsible for the wheeze in the remaining group of patients (more than 60% patients)? It appears that the dynamic airflow obstruction causing obstruction in airways smaller than the trachea was responsible for the wheezes in these patients. Now, even in the group of patients in whom EDAC was observed was it possible to rule out the simultaneous existence of obstruction of more distal airways leading to the causation of wheeze? The diffuse involvement of the airways also has implication in deciding the treatment modality of the patient as modalities like stenting/tracheoplasty will be helpful primarily in focal disease and not in diffuse diseases where the airway collapse is present at multiple points.

The degree of collapse which qualifies as abnormal also differs from one source to other. While some authorities take 50% as the cutoff, others have taken cutoff as high as 70% to define EDAC as up to 78% of normal persons might show airway collapsibility of 50% or more.[56] In the absence of physiological parameters reflecting the effect of the tracheal collapse, it will seem that the different cutoffs are but arbitrary. This makes the diagnosis of EDAC problematic due to the different cutoffs employed. The lower cutoff employed by the authors might account for the higher proportion of patients in this study who had EDAC/TBM.

The authors have evaluated bronchoscopically and radiologically the presence of EDAC but have not elaborated on the exact method to evaluate the degree of collapse during bronchoscopy – since ascertaining a certain degree of collapse would require morphometric/quantitative analysis, i.e., accurate calculation of the change in airway diameter during the phases of respiration. Loring et al.[7] had used a complex method of estimating the shape index to estimate the change in the tracheal luminal area during the phases of respiration observed during bronchoscopy. It would be interesting to know the method adopted by the authors to evaluate exactly the degree of collapse during bronchoscopy.

The authors had treated the group of patients with EDAC with continuous positive airway pressure (CPAP) titrated to the disappearance of auscultatory wheeze. Now CPAP is used for pneumatic splinting in patients with EDAC in the setting of acute illnesses (acute exacerbation of obstructive airway disease) to tide over the crisis.[8] However, its use in the setting as used by authors, in stable COPD patients with persistent wheeze seems difficult to rationalize as it brings forth the question-how long CPAP is to be continued (both in terms of duration of daily therapy and a number of days of use). As the patients were on maximal medical therapy, the wheeze would recur soon after CPAP is withdrawn. Treatment of EDAC has been conventionally done on the basis of presence or absence of symptoms and not on the presence of auscultatory findings like a wheeze. Even in the present group of patients, it appears that emphasis on airway clearance technique as well as pursed lip breathing in addition to continued medical therapy would be more beneficial on the long run to inhibit occurrences of EDAC/TBM.

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