© 2006 American Thoracic Society
Tracheal Collapse versus Tracheobronchomalacia: Normal Function versus DiseaseTo the Editor:We read the recent article regarding tracheobronchomalacia (TBM) and bronchiolitis obliterans by Ghanei and colleagues (1) and would like to offer an alternate explanation for the tracheal collapse seen on computerized tomography (CT) of patients with bronchiolitis after exposure to mustard gas. Tidal flow limitation in patients with small airway obstruction can lead to expiratory collapse of a normal trachea. There are no data in the article proving an anatomic or functional tracheal abnormality. Dynamic intrathoracic tracheal compression during expiration has been understood for years (2). During flow-limited breathing, the trachea becomes compressed and can be almost completely collapsed during forced expiration and cough. The Starling resistor model shows that the pressure drop occurs across a very short length of airway and that proximal airway (downstream) resistance should not affect flow. Pressure catheters demonstrate this flow-limiting choke point and the lack of any further pressure drop in airways between the mouth and flow-limiting segment (3). As the choke point in adult humans is often located at the level of the lobar bronchi, tracheal collapsibility should not impede flow. The model predicts that replacing the trachea with a fully collapsible Penrose drain should not affect the expiratory flow–volume curve of a lung. Flow limitation during tidal breathing is not uncommon; patients with chronic obstructive pulmonary disease, symptomatic asthma, and obesity are often flow-limited (4). Bronchoscopic or radiologic detection of expiratory tracheal compression should trigger a search for causes of airflow obstruction within the lung, not the trachea. Stenting of the large airways in these patients will not improve airflow, as there is no demonstrable pressure drop along their course (5). There appears to be a piqued interest in TBM, likely due to increased use of CT scanning and increased availability of tracheal stenting. Numerous studies published recently have used radiographic evidence of tracheal compression as proof of tracheal disease without supporting physiologic data. Visualizing weakness or collapse of tracheal cartilage during expiration is not normal, but even this does not prove functional significance. Tracheal disease manifests as functional obstruction only when there is a stenotic component; diseases that purely increase collapsibility should not limit flow. Studies reporting "abnormal" tracheobronchial collapse need careful assessment for flow limitation, as normal tracheas collapse in conditions that cause flow limitation during tidal breathing.
Stony Brook University, Stony Brook, New York FOOTNOTES Conflict of Interest Statement: Neither author has a financial relationship with a commercial entity that has an interest in the subject of this manuscript. REFERENCES
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