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a The National Service for Severe Tracheal Disease in Children, The Great Ormond Street Hospital for Children NHS Trust, London, United Kingdom
b McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania
Accepted for publication December 30, 2011.
* Address correspondence to Dr Speggiorin, The Tracheal Service, The Great Ormond Street Hospital for Children NHS Trust, Great Ormond St, London WC1N 3JH, United Kingdom (Email: simone.speggiorin{at}gmail.com).
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Abstract |
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 Top Abstract IntroductionPatients and MethodsResultsCommentReferences |
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Methods: This was a retrospective study. In follow-up bronchography performed 1, 6, 12, 18, and 24 months after slide tracheoplasty, we measured the cross-sectional areas of the midtrachea and distal trachea at each investigation and correlated the measurements with the anthropomorphic factors (body weight, height, and body surface).
Results: Fourteen patients were enrolled in this study. The midtracheal and distal tracheal cross-sectional areas significantly increased with time (p 
0.0001). The average rates of midtracheal growth were 21.0 mm2year in the first 6 months and 8.0 mm2/year in the first 2 years, and the distal trachea grew 18.5 mm2/year and 8.4 mm2/year, respectively. Regression analysis showed that both the midtrachea and the distal trachea increase significantly with weight (r
2 = 0.257, p 0.0001), height (r
2 = 0.376, p 0.0001), and body surface area (r
2 = 0.315, p 0.0001). Balloon dilation did not significantly alter the tracheal growth in the first 2 years after slide tracheoplasty.
Conclusions: Slide tracheoplasty does not inhibit tracheal growth. The reconstructed trachea grows faster in the first 6 months and slows in the following 18 months. There is a positive correlation between tracheal cross-sectional area and weight, height, and body surface area.
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Introduction |
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TopAbstractIntroductionPatients and MethodsResultsCommentReferences |
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There was initial reluctance to perform STP because of questions regarding the ability of this reconstructed trachea to experience somatic growth [4, 5]. It is now generally accepted that the trachea does grow after STP, but it is not clear whether the rate of growth is normal. Therefore, the objective of the present study was to evaluate tracheal growth in children who underwent STP at our institution for CTS between February 1995 and November 2009. The rate of tracheal growth in patients with STP was compared with previously published data describing its rate in the normal population.
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Patients and Methods |
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TopAbstractIntroductionPatients and MethodsResultsCommentReferences |
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Our routine technique for surveillance after STP is to perform flexible bronchoscopy with the patient under general anesthesia, breathing spontaneously, usually through a laryngeal mask airway, in a biplane angiography suite.
After the bronchoscopy, small aliquots of iohexol (Omnipaque 240, GE Healthcare Ireland, Cork, Ireland) are injected into the airway through the working channel, and posteroanterior and laterolateral bronchographic images are obtained. The total amount of contrast medium usually used is approximately 1 mL.
Measurements were performed by a single operator (S.S.) on posteroanterior and laterolateral views of the trachea retrieved from bronchogram images obtained 1, 6, 12, 18, and 24 months after STP by using Horizon Cardiology software version 12.2 (McKesson Corporation, UK). The measurements were taken at the end of inspiration, when the diameter was maximal, and no positive pressure was applied to the airways.
For standardization, tracheal diameters were measured at the entry of the trachea into the chest between the medial end of the clavicles (midtrachea) and 1 cm above the carina (distal trachea). The cross-sectional area (CSA) was assumed to be an ellipse and was calculated as follows:
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| (1) |
Differences among groups for continuous variables were analyzed with unpaired t test. One-way analysis of variance (ANOVA) (repeated measures) with Bonferroni's correction was used to analyze the effect of time on the tracheal CSA, and two-way ANOVA was used to study the effect of dilation on tracheal growth after STP. All statistical analyses were performed with a commercial software package (Graphpad Prism, GraphPad Software, Inc., La Jolla, CA).
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Results |
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TopAbstractIntroductionPatients and MethodsResultsCommentReferences |
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The midtracheal and distal tracheal CSAs significantly increased with time (p 0.0001) as shown in Figure 1
. Regression analysis showed that the midtracheal CSA increased significantly with weight (r
2 = 0.257, p 0.0001), height (r
2 = 0.376, p 0.0001), and BSA (r
2 = 0.315, p 0.0001). The distal trachea grew significantly with the weight, height, and BSA but at a lower rate (Fig 2). The average rates of midtracheal growth were 21.0 mm2/year during the first 6 months after operation and 8.0 mm2/year during the 2 years of evaluation. For the distal trachea, the average growth rate during the first 6 months of follow-up was 18.5 mm2/year, with a 2-year growth rate of 8.4 mm2/year.
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Comment |
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TopAbstractIntroductionPatients and MethodsResultsCommentReferences |
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The present study demonstrated that the trachea does grow significantly after STP in children. The median CSAs of both the midtrachea and the distal trachea increased significantly with the time, almost doubling in 2 years, as was confirmed by linear regression between the weight, height, BSA, and CSA (Fig 2). The fastest growth was observed in the first 6 months after STP, after which the rate of growth slowed but continued. This initial relative increment of the tracheal size may be due either to the physiologic growth of young children or to the effect of the STP on a preexisting mismatch between airway and body size. We think that it is more likely to be due to the scarring effect that lowers the elasticity of the new trachea, hence reducing the rate of growth. The rates of growth did not appear to be different when the midtrachea and the distal trachea were compared. Even when balloon dilation was medically necessary, growth was still observed despite the predictably smaller size.
There are few normative data with which to compare tracheal growth rates in children. However, two previous studies have proved useful. Butz [9] performed a cadaveric study in 1968 and reported the size of 24 tracheas from children ranging in age from premature to 14 years of age. The growth rate was found to be generally linear, with a slope of 5.1 mm2/year, which is comparable with the growth rates observed in the present study beyond 6 months after operation. In a recent study, Masters and associates [10] measured the CSA of the large airways in children 10 years old or younger using videobronchoscopy, and they defined the factors that influence airway size in children. Although the growth rate calculated from this study (0.5 mm2/year) was much less than that in the present study or the study by Butz, Masters and associates [10] showed the luminal areas to be quite comparable with the CSA measured in the present study after 24 months, particularly for patients who did not require balloon dilation. Masters and associates concluded that anthropomorphic factors such as weight and height were significantly related to the airway size, but with weak predictive influence. Chen and colleagues [11] measured tracheal size using computed tomography in children with congenital heart disease. Their results suggested that height is the most effective measurement in predicting the transverse intrathoracic tracheal diameter. In our study, we also found patients' height to correlate well with both midtracheal and distal tracheal sizes.
In our series, half the patients needed balloon dilation for recurrent stenosis. This treatment did not reduce growth rates in affected children. However, the tracheal growth curves in Figure 3 show that patients who underwent a dilation procedure had constantly smaller sizes of the trachea compared with those in the other group. Tracheas that require dilation are going to be smaller in diameter, so it is likely that this smaller size represents selection bias rather than an effect of dilation. It is not clear whether recurrent stenoses are the effect of the physiologic scarring process after STP or are triggered by the wall stretching caused by balloon dilations. Nevertheless, we think that airway dilation should not be avoided, because it improves patients' symptoms and, according to the results we report, does not hamper tracheal growth.
We routinely examine patients who have undergone STP, using flexible bronchoscopy in an angiography suite. This allows us to obtain bronchography by injecting a small quantity of nonionic water-soluble radiographic contrast medium through the working channel of the bronchoscope [12]. Assessing luminal diameter with a bronchoscope is always difficult, but biplane bronchography allows accurate measurements to be made at reproducible positions in the airway. Various authors have expressed concerns about the safety of bronchography, but we have seen no complications attributable to the contrast medium in more than 1600 procedures.
There are several limitations to this present study. First, the number of patients who met the inclusion criteria was small, mainly because of the rarity of the disease and the scarcity of patients who undergo STP. Second, it was not possible to identify a control group whose tracheal size was measured by similar methods, given the obvious radiologic constraints. Even the literature that was available to assess normal tracheal growth was based on cross-sectional individual measurements in a group of patients, rather than longitudinal tracking of the tracheal size over time.
Even though bronchography allows us to obtain good airway measurements, we believe that a volumetric three-dimensional reconstruction of the airway with magnetic resonance imaging or computed tomography has the potential to give a more accurate and precise estimation of tracheal growth in patients after STP in comparison with the normal population.
Finally, longer-term longitudinal growth beyond 24 months will be necessary to enable us to definitely determine the progression of growth in patients after STP.
In conclusion, STP does not inhibit tracheal growth. The trachea experiences rapid growth by 6 months after operation, and, although growth slows, it continues until at least 24 months after operation. There is a positive correlation between tracheal CSA and weight, height, and BSA, likely caused by the increased somatic growth rates of patients shortly after STP. The present study should reduce any remaining concern about the potential for growth after STP.
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