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* From Anesthesia and Critical Care (Dr. Loring), Pulmonary and Critical Care Medicine (Dr. O’Donnell), and Interventional Pulmonology (Drs. Feller-Kopman and Ernst), Beth Israel Deaconess Medical Center, Boston, MA.
Correspondence to: Stephen H. Loring, MD, Beth Israel Deaconess Medical Center, 330 Brookline Ave, DA 717, Boston, MA 02215; e-mail: sloring{at}bidmc.harvard.edu
Abstract
Background: Acquired tracheobronchomalacia (TBM) can cause central airway collapse in patients with COPD and may worsen airflow obstruction and symptoms. It is usually not known whether central airway malacia contributes to airflow obstruction. This study was undertaken to quantify central airway collapsibility and relate it to expiratory flow limitation in patients with TBM.
Methods: Eighty patients evaluated for acquired TBM and 4 healthy control subjects were studied with measurements of central airway narrowing derived from bronchoscopic videotapes and simultaneous pressure measurements in the trachea and esophagus. Tracheal narrowing was assessed by a shape index and plotted against the transtracheal pressure to measure collapsibility. Subsequently, airflow and transpulmonary pressure (PL) were measured to identify expiratory flow limitation during quiet breathing and to determine the critical PL required for maximum expiratory flow.
Results: Tracheal collapsibility varied widely among patients. Some had profound tracheal narrowing during quiet breathing, and others showed substantial collapse only during forced exhalation. Of the patients, 15% were not flow limited during quiet breathing, 53% were flow limited throughout exhalation, and 30% were flow limited only during the latter part of the exhalation. Patients with flow limitation at rest showed greater tracheal narrowing than those without (p = 0.009), but the severity of expiratory flow limitation was not closely related to tracheal collapsibility. Twenty-three patients were flow limited during quiet exhalation at PLs that did not cause central airway collapse.
Conclusions: In TBM, central airway collapse is not closely related to airflow obstruction, and expiratory flow limitation at rest often occurs in peripheral airways without central airway collapse.
Key Words: bronchoscopy • COPD • esophageal balloon • tracheomalacia
Tracheobronchomalacia (TBM) generally results from weakness of the tracheal or mainstem bronchial walls caused by either softening of the supporting cartilaginous rings, redundancy of the connective tissue of the posterior membrane due to a reduction in the size and number of elastic fibers,123 or both. Acquired TBM can be localized, as occurs following prolonged endotracheal intubation or tracheostomy or with vascular anomalies, or more diffuse, as is commonly seen in association with COPD. During exhalation, increasing pleural pressure causes the weakened central airways to narrow (collapse), which may exacerbate obstructive symptoms. Typically, dyspnea is brought on by the hyperpnea of exercise and may be both sudden and severe. Symptoms can masquerade as worsening asthma or COPD,4 and it is not generally known which patients with COPD have TBM contributing to their symptoms. Acquired TBM has been reported in 4.5% of bronchoscopies in one large general series,2 in 12.7% of 4,283 patients undergoing bronchoscopic evaluation for respiratory disease,5 and in up to 44% of patients undergoing bronchoscopy in the setting of chronic bronchitis.6
The diagnosis of TBM has traditionally been made at bronchoscopy or bronchography,7 although noninvasive methods, such as rapid CT scanning, are now available for documenting dynamic tracheal narrowing.8910 Although characteristics of the spirogram can suggest tracheal collapse,711 spirometry alone is not usually adequate to diagnose tracheomalacia or indicate the site of flow limitation.12 Diagnosis by bronchoscopy or CT usually depends on demonstrating an excessive degree of tracheal narrowing during quiet breathing, forced exhalation, or cough. By consensus, excessive narrowing (collapse) is defined as a decrease of at least 50% in tracheal diameter during forced exhalation. We have demonstrated a technique to improve the sensitivity of TBM detection by obtaining the expiratory CT scan during dynamic (forced) exhalation at low lung volume.13
At present, there is no widely used method for quantifying the degree of tracheal collapsibility except by specifying the extent of narrowing, which, in turn, necessarily depends on the pressure difference across the airway wall. For example, Baroni et al13 demonstrated that central airway narrowing is substantially greater when patients are exhaling than when they are holding their breath at a low lung volume, suggesting that the extent of the dynamic decrease in transtracheal pressure during exhalation can affect the diagnosis of TBM. Furthermore, in patients who have both COPD and abnormal degrees of tracheal collapse, it is usually not known whether expiratory flow limitation is caused primarily by narrowing (choking) of the central airways or the more peripheral intrapulmonary airways. Central airway narrowing during exhalation could be the consequence of a forceful expiratory effort, such as a cough, causing very high pleural pressures that collapse a central airway with a relatively normal pressure-area characteristic (compliance). Alternatively, an extremely compliant central airway could collapse even during exhalations with relatively low pleural pressures. Such pathologic central airway collapse could occur in patients with or without diffuse obstructive pulmonary disease.
In this study, we describe tracheal and central airway mechanics in unselected patients undergoing bronchoscopy for suspected acquired TBM. By relating airway narrowing to the pressure differences measured across the central airway wall during graded expiratory efforts, we characterized airway pressure-area characteristics. We also related central airway narrowing to flow limitation during quiet breathing, and we measured the pressures required to achieve maximum expiratory flow. Our hypothesis was that in many patients with suspected TBM, peripheral airflow obstruction limits expiratory flow independent of tracheal collapse. In this situation, the expiratory pressures required to cause central airway collapse could be substantially greater than those required to achieve maximum expiratory flow. In such patients, we would not expect expiratory flow limitation at rest to be improved by stenting or tracheoplasty that stiffen the central airways.
Materials and Methods
Subjects included 34 men and 46 women (age range, 29 to 94 years; mean ± SD, 63 ± 12 years) who had been referred for diagnostic bronchoscopy for suspected or previously diagnosed TBM. To provide examples of normal central airway mechanics, we also studied four healthy subjects without lung disease (two men and two women; age range, 33 to 47 years) during bronchoscopy done as part of an unrelated investigation. None of the patients had a systemic disease or localized condition known to cause localized TBM, although 40% carried a diagnosis of COPD, 30% had gastroesophageal reflux disease or Barrett esophagus, and 24% had asthma. Other comorbidities included obstructive sleep apnea (16%), bronchiectasis (9%), and history of pulmonary infections (18%) that may have been a cause or a result of TBM. All subjects gave written informed consent for the study, which was approved by our Committee on Clinical Investigations. Patients were sedated with midazolam and fentanyl and topically anesthetized with lidocaine for diagnostic bronchoscopy, and were studied in the supine position, whereas control subjects had only topical anesthesia for BAL and were studied while seated and reclining slightly. As part of their evaluation, 72 of the patients underwent standard spirometry in a clinical pulmonary function laboratory to determine FEV1.
In each patient, we first assessed central airway mechanics during bronchoscopy. To quantify airway narrowing, we made bronchoscopic videotape recordings of the trachea and mainstem bronchi during tidal breathing and during graded forced exhalation (push) in the volume range of tidal breathing. Because respiratory movements cause the bronchoscope to move relative to the airway, the recorded image of the airway cross-section appears to change size during breathing. To compensate for this artifact, we manually traced the perimeter of the airway cross-section, and calculated a shape index (SI), defined as the cross-sectional area divided by the area of a circle with the same perimeter, assuming that the airway perimeter remains constant as the airway narrows (Fig 1 ). For large degrees of airway narrowing (low values of SI), parts of the perimeter were obscured by apposition of the airway walls; in this case, we traced the perimeter to include a conservative estimate of the length of hidden sections. We found that, on average, tracheal narrowing that resulted in an SI of 0.5 appeared on bronchoscopy to be a 50% reduction in tracheal cross-sectional area; but with greater degrees of collapse, the SI tended to underestimate the fractional narrowing estimated by the bronchoscopist. In this report, we will use the term collapse to denote SI < 0.5.
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To assess the presence or absence of expiratory flow limitation during quiet breathing, we displayed flow vs volume during quiet breathing and graded forced exhalations in the tidal breathing range. We determined expiratory flow to be limited during quiet breathing if the expiratory flow rates equaled or exceeded the maximum expiratory flow-volume envelope (Fig 3 ). Subjects were identified as exhibiting expiratory flow limitation throughout exhalation, during only part of exhalation, or not at all during quiet breathing.
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Results
Figure 1 shows the trachea of a healthy control subject and a patient with TBM during inhalation (left panels), exhalation (center panels), and push (right panels). The trachea of the control subject is relatively round during inhalation, shows no appreciable narrowing during exhalation, and only slight narrowing during a push, with an SI that ranges from 0.95 to 0.87. By contrast, the trachea of a patient with TBM in Figure 1 is nearly round during inhalation (SI = 0.92) but becomes markedly narrowed by invagination of a wide posterior membranous portion during exhalation (SI = 0.65), and is nearly occluded during a forced exhalation (SI = 0.14). All patients had a wide posterior membranous portion that invaginated to cause tracheal narrowing, and in no patient did tracheal collapse appear to be due to softening of the cartilaginous rings. One patient was noted to have a saber sheath trachea.15
Summary plots of tracheal SI vs the negative of Ptm for these two subjects are shown in Figure 2, with the characteristic Pcrit for flow limitation indicated. The control subject’s SI stays in the range of 0.8 to 1.0 despite forced exhalations that cause highly negative Ptm, whereas the patient’s trachea narrows substantially during quiet exhalation at modest collapsing pressures.
Of the 80 patients evaluated for TBM, 42 were flow limited during the entire exhalation, 24 were flow limited during the latter part of the exhalation, and 12 patients were not flow limited during quiet breathing; in 2 subjects, neither flow limitation nor Pcrit could be determined. Figure 4 shows how Pcrit was related to the PL values during exhalation in subjects with various degrees of flow limitation. Because of differences in the baseline Pes and because many subjects with severe obstruction exhaled forcefully during quiet breathing, we plotted the decrease in PL from inhalation to Pcrit normalized by the decrease in PL from inhalation to exhalation; ratios > 1 indicate that PL during exhalation was less negative than the Pcrit sufficient to cause maximum expiratory flow. In patients who were not flow limited during quiet breathing, this ratio was more often > 1; whereas in most patients with flow limitation, Pcrit was between PL values during inhalation and exhalation. There were 23 patients with flow limitation during quiet breathing in whom the tracheal SI was > 0.5 during quiet exhalation, suggesting that flow limitation was not due to tracheal collapse, and tracheal SI was < 0.5 during forced exhalation, indicating TBM. In these subjects, tracheal collapse apparently occurred at PL values more negative than those required for maximum expiratory flow.
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Right and left mainstem bronchial characteristics were evaluated in 61 patients. The SI values of bronchi during exhalation and push had a distribution similar to those of the trachea, and bronchial SI values were weakly correlated with those of the trachea (R2 = < 0.25 for both left and right mainstem bronchi).
Figure 6 shows tracheal SI during exhalation plotted against FEV1 percentage of predicted. There was no correlation between tracheal collapse during quiet breathing and airflow obstruction.
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Tracheal and mainstem bronchial narrowing varied widely among patients with suspected TBM during both quiet exhalation and forceful expiratory efforts. We had presumed that most patients with suspected TBM would exhibit severe airflow obstruction. However, central airway collapse was not correlated with the degree of obstruction as assessed by FEV1, and central airway collapse could be found irrespective of the degree of expiratory flow limitation during quiet breathing. We conclude that significant central airway narrowing, especially during quiet exhalation, cannot be assumed in patients with obstructive airways disease, and that symptomatic central airway narrowing may exist without significant airflow obstruction.
The etiology of acquired TBM in many patients is not obvious. TBM is often seen in association with COPD in patients with a smoking history, leading to the inference that chronic inflammation and smoking are important contributing factors,172 although the authoritative text "Diagnosis of Diseases of the Chest"15 does not list COPD or cigarette smoking as etiologies of TBM. Nevertheless, little is known of the mechanism of the association between COPD and TBM, and tracheomalacia is not related to severity of obstruction. In 10 patients with tracheobronchial collapse, Samad et al18 found no relationship between the severity of the obstructive disease and the degree of tracheobronchial collapse during cough, a lack of association confirmed in our cohort. We speculate that repeated mechanical stress from coughing or the high expiratory pleural pressures during exercise in patients with airflow obstruction might, over a period of years, cause stretching and degeneration of the posterior membranous portion of the trachea and mainstem bronchi.
For definitive therapy, most cases of severe and symptomatic TBM are treated surgically, either with insertion of a stent that maintains the patency of the central airways (usually the trachea, mainstem bronchi, or both), or with procedures such as tracheoplasty19 that stiffen the trachea. When airflow obstruction is due to localized central airway disease, stenting is a highly effective treatment. For example, in 64 patients with localized stenosis due to lung cancer, FEV1 was significantly improved after stent placement.20 However, few investigations have systematically explored the effects of stenting on expiratory flow rates in more diffuse acquired TBM. Instead, the success of stenting is usually judged by relief of symptoms such as cough and dyspnea, reduced frequency of infection, and the bronchoscopic demonstration that the trachea no longer collapses.4 Ashiku et al21 recently described the results of plication and reinforcement of the membranous part of the central airways in patients with the more diffuse acquired TBM often seen in patients with COPD, reporting reductions in intractable cough and dyspnea, improved clearance of secretions, and reduced incidence of bronchitis and pneumonia.
Our study has limitations that deserve comment. First, the transtracheal Ptm we measured may have been affected by several factors, including the presence of the bronchoscope through the vocal cords (which could affect intratracheal pressures), small amounts of local anesthetic solution remaining in the working channel of the bronchoscope, and known elevation of baseline Pes in the supine position due to compression of the esophagus by the heart.22 To minimize the effects of positional change on Pes, all measurements within a subject were made within 30 min and without changing esophageal balloon placement or the subject’s position. Thus, pressures during airway collapse could be compared with those at the onset of expiratory flow limitation. In most patients who were flow limited during quiet breathing, Pcrit values were between the PL values during inhalation and exhalation. However, in four subjects who were flow limited, Pcrit values were more negative than PL values seen on exhalation; conversely, in four subjects who were not obviously flow limited, Pcrit was less negative than PL during exhalation. In these eight subjects, Pcrit values were inconsistent with our determination of flow limitation during quiet breathing, suggesting that Pcrit may have been inaccurately determined or flow limitation may have been intermittent, perhaps because of changes in breathing pattern after the bronchoscopy. Second, our method of assessing airway narrowing with SI, the ratio of airway area to perimeter, probably overestimates airway size and underestimates airway narrowing when much of the airway perimeter is invisible during marked airway narrowing. In addition, the airway perimeter may actually decrease during airway narrowing, which would similarly reduce estimates of airway narrowing. Finally, improvements in airflow and FEV1 may not be the most important predictors of clinical improvement after central airway stabilization in patients with acquired TBM. Further research is necessary to identify other physiologic variables that may better identify patients who are symptomatic from their TBM, as opposed to those whose airway collapse is an epiphenomenon of peripheral flow limitation.
We initially hypothesized that in some patients with severe airflow obstruction, central airway collapse would occur at values of PL more negative than those required to achieve maximum expiratory flow (Pcrit). We found 23 such patients with flow limitation during quiet exhalation in whom the tracheal SI was > 0.5 during quiet exhalation and decreased to < 0.5 only during forced exhalation, suggesting that tracheal collapse was not responsible for limiting maximum expiratory flow. We would predict that in such patients, expiratory flow limitation at rest, presumably due to obstruction in peripheral intrapulmonary airways, might not be improved by stenting or tracheoplasty that stiffen the central airways. However, some patients with severe TBM derive symptomatic and functional benefit from such procedures without showing improvement in expiratory flow rates.21 We hope to explore the possibility that quantitative characterization of central airway mechanics and physiology in patients with acquired TBM can help predict which patients would benefit symptomatically and functionally from central airway stabilization.
Acknowledgements
The authors thank Michael Hervey, Dana Williams, Heidi Matus, Elizabeth Tegins, Amy Lawrason, Christine Edmonds, Lauren Marquis, Dang Nguyen, and Negin Behazin for analyzing the data, and Emil Millet for developing software to acquire the data.
Footnotes
Abbreviations: Pcrit = critical transpulmonary pressure; Pes = esophageal pressure; PL = transpulmonary pressure; Ptm = transmural pressure; SI = shape index; TBM = tracheobronchomalacia
This work was conducted at Beth Israel Deaconess Medical Center, Boston, MA.
This work was supported by grant HL-52586 from the National Institutes of Health.
The authors have no actual or potential financial conflict of interest in the subject matter presented.
Received for publication October 20, 2006. Accepted for publication December 5, 2006.
References
This article has been cited by other articles:
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  A. Ernst, A. Majid, D. Feller-Kopman, J. Guerrero, P. Boiselle, S. H. Loring, C. O'Donnell, M. DeCamp, F. J. F. Herth, S. Gangadharan, et al. Airway Stabilization With Silicone Stents for Treating Adult Tracheobronchomalacia: A Prospective Observational Study Chest, August 1, 2007; 132(2): 609 - 616. [Abstract] [Full Text] [PDF]
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