Tracheal Collapse versus Tracheobronchomalacia: Normal Function versus Disease

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AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE VOL 174 2006

comprehensive review of the literature, Pope and Dockery (2) present concentration–response relationships from various studies of long-term exposure. They found that in both the Harvard Six Cities study and in the American Cancer Society cohort there were no significant deviations from linearity. Conflict of Interest Statement : None of the authors has a financial relationship with a commercial entity that has an interest in the subject of this manuscript.

Francine Laden Joel Schwartz Frank E. Speizer Douglas W. Dockery Harvard School of Public Health and Channing Laboratory Brigham and Women’s Hospital and Harvard Medical School Boston, Massachusetts References 1. Laden F, Schwartz J, Speizer FE, Dockery DW. Reduction in fine particulate air pollution and mortality. Am J Respir Crit Care Med 2006;173: 667–672. 2. Pope CA, Dockery DW. Health effects of fine particulate air pollution: lines that connect. J Air Waste Manage Assoc 2006;56:709–742.

Tracheal Collapse versus Tracheobronchomalacia: Normal Function versus Disease To 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. Conflict of Interest Statement : Neither author has a financial relationship with a commercial entity that has an interest in the subject of this manuscript.

Daniel Baram Gerald Smaldone Stony Brook University Stony Brook, New York References 1. Ghanei M, Moqadam FA, Mohammad MM, Aslani J. Tracheobronchomalacia and air trapping after mustard gas exposure. Am J Respir Crit Care Med 2006;173:304–309. 2. Pride NB, Permutt S, Riley RL, Bromberger-Barnea B. Determinants of maximal expiratory flow from the lungs. J Appl Physiol 1967;23:646–662. 3. Smaldone GC, Smith PL. Location of flow-limiting segments via airway catheters near residual volume in humans. J Appl Physiol 1985;59:502– 508. 4. Takishima T, Grimby G, Graham W, Knudson R, Macklem PT, Mead J. Flow-volume curves during quiet breathing, maximum voluntary ventilation, and forced vital capacities in patients with obstructive lung disease. Scand J Respir Dis 1967;48:384–393. 5. Miyazawa T, Miyazu Y, Iwamoto Y, Ishida A, Kanoh K, Sumiyoshi H, Doi M, Kurimoto N. Stenting at the flow-limiting segment in tracheobronchial stenosis due to lung cancer. Am J Respir Crit Care Med 2004; 169:1096–1102.

From the Authors:

We appreciate the comments by Drs. Baram and Smaldone regarding our article on the correlation of air trapping and tracheobronchomalacia (TBM) as long-term sequelae of bronchiolitis obliterans in mustard gas–exposed patients (1). Since we did not aim to explain tracheal anatomical abnormalities in our study, they were not mentioned in the manuscript. Nevertheless, some evidence shows that our finding was not just normal tracheal collapse. Normal and abnormal tracheal collapse have been described for years (2). In our study, TBM was considered to be present if the airway diameter decreased by more than 30% during expiration (3). The high degree of collapse presented in our study is not expected to occur in a functionally normal trachea and is more than a normal collapse. We agree with Drs. Baram and Smaldone that flow limitation is not due to tracheal collapse, and tracheal collapsibility does not have to impede flow. In our study, flow limitation was located at the level of the lobar bronchi, and it led to air trapping visible on chest high-resolution computerized tomography. There is a strong relationship between severity and frequency of air trapping and the presence of TBM (4). Although patients with chronic obstructive pulmonary disease, symptomatic asthma, and obesity are often flow-limited, most of our subjects had approximately normal results in FEV1 and FVC; only a minimal increase in residual volume was seen in most patients. Considering the age (mean age, 42 years) and the mild obstruction found in our series, tracheal collapse as a normal variation is not reasonable according to the Starling resistor model. We hypothesize that, in bronchiolitis obliterans, both air trapping and TBM are caused by a single underlying process affecting both lobar bronchi and large airways (i.e., weakness of the airway walls and supporting cartilages). It can be explained independently of

Correspondence

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pulmonary function testing results. We believe that detection of significant air trapping is suggestive of the presence of TBM, and when both air trapping and TBM exist, bronchiolitis obliterans should be considered. Conflict of Interest Statement : Neither author has a financial relationship with a commercial entity that has an interest in the subject of this manuscript.

Mostafa Ghanei Ali Amini Harandi Baqiyatallah University of Medical Sciences Tehran, Iran

References 1. Ghanei M, Moqadam FA, Mohammad MM, Aslani J. Tracheobronchomalacia and air trapping after mustard gas exposure. Am J Respir Crit Care Med 2006;173:304–309. 2. Gamsu G, Webb WR. Computed tomography of the trachea: normal and abnormal. AJR Am J Roentgenol 1982;139:321–326. 3. Aquino SL, Shepard JA, Jinns LC, Moore RH, Halpern E, Grillo HC, McLoud TC. Acquired tracheomalacia: detection by expiratory CT scan. J Comput Assist Tomogr 2001;25:394–399. 4. Zhang J, Hasegawa I, Hatabu H, Feller-Kopman D, Boiselle PM. Frequency and severity of air trapping at dynamic expiratory CT in patients with tracheobronchomalacia. AJR Am J Roentgenol 2004;182:81–85.