In 2010, a tissue‐engineered trachea was transplanted into a 10‐year‐old child using a decellularized deceased donor trachea repopulated with the recipient's respiratory epithelium and mesenchymal stromal cells. We report the child's clinical progress, tracheal epithelialization and costs over the 4 years. A chronology of events was derived from clinical notes and costs determined using reference costs per procedure. Serial tracheoscopy images, lung function tests and anti‐HLA blood samples were compared. Epithelial morphology and T cell, Ki67 and cleaved caspase 3 activity were examined. Computational fluid dynamic simulations determined flow, velocity and airway pressure drops. After the first year following transplantation, the number of interventions fell and the child is currently clinically well and continues in education. Endoscopy demonstrated a complete mucosal lining at 15 months, despite retention of a stent. Histocytology indicates a differentiated respiratory layer and no abnormal immune activity. Computational fluid dynamic analysis demonstrated increased velocity and pressure drops around a distal tracheal narrowing. Cross‐sectional area analysis showed restriction of growth within an area of in‐stent stenosis. This report demonstrates the long‐term viability of a decellularized tissue‐engineered trachea within a child. Further research is needed to develop bioengineered pediatric tracheal replacements with lower morbidity, better biomechanics and lower costs.

A multidisciplinary care model significantly expedited the decannulation process and reduced the overall time that a tracheostomy was in situ. The intervention was associated with a reduction in clinical incidents and shorter intensive care unit admissions, which can be associated with significant monetary savings.

During a rapid inhalation, such as a sniff, the flow in the airways accelerates and decays quickly. The consequences for flow development and convective transport of an inhaled gas were investigated in a subject geometry extending from the nose to the bronchi. The progress of flow transition and the advance of an inhaled non-absorbed gas were determined using highly resolved simulations of a sniff 0.5 s long, 1 l s−1 peak flow, 364 ml inhaled volume. In the nose, the distribution of airflow evolved through three phases: (i) an initial transient of about 50 ms, roughly the filling time for a nasal volume, (ii) quasi-equilibrium over the majority of the inhalation, and (iii) a terminating phase. Flow transition commenced in the supraglottic region within 20 ms, resulting in large-amplitude fluctuations persisting throughout the inhalation; in the nose, fluctuations that arose nearer peak flow were of much reduced intensity and diminished in the flow decay phase. Measures of gas concentration showed non-uniform build-up and wash-out of the inhaled gas in the nose. At the carina, the form of the temporal concentration profile reflected both shear dispersion and airway filling defects owing to recirculation regions.

This paper considers factors that play a significant role in determining inspiratory pressure and energy losses in the human trachea. Previous characterisations of pathological geometry changes have focussed on relating airway constriction and subsequent pressure loss, however many pathologies that affect the trachea cause deviation, increased curvature, constriction or a combination of these. This study investigates the effects of these measures on tracheal flow mechanics, using the compressive goitre (a thyroid gland enlargement) as an example. Computational fluid dynamics simulations were performed in airways affected by goitres (with differing geometric consequences) and a normal geometry for comparison. Realistic airways, derived from medical images, were used because idealised geometries often oversimplify the complex anatomy of the larynx and its effects on the flow. Two mechanisms, distinct from stenosis, were found to strongly affect airflow energy dissipation in the pathological tracheas. The jet emanating from the glottis displayed different impingement and breakdown patterns in pathological geometries and increased loss was associated with curvature.

The effort required to inhale a breath of air is a critically important measure in assessing airway function. Although the contribution of the trachea to the total flow resistance of the airways is generally modest, pathological alterations in tracheal geometry can have a significant negative effect. This study investigates the mechanisms of flow energy loss in a healthy trachea and in four geometries affected by retrosternal goitre which can cause significant distortions of tracheal geometry including constriction and deviation with abnormal curvature. By separating out the component of energy loss related to the wall shear (frictional loss), striking differences are found between the patterns of energy dissipation in the normal and pathological tracheas. Furthermore the ratio of frictional to total loss is dramatically reduced in the pathological geometries.

Quality-of-life data are an important measure when deciding on a specific clinical intervention. In the short term, quality-of-life measures have been shown to improve after adenotonsillectomy for obstructive sleep apnoea. Our study demonstrates that the benefits of surgery are still persistent and the children continue to improve in the long term.

Nasal decongestant reduces blood flow to the nasal turbinates, reducing tissue volume and increasing nasal airway patency. This study maps the changes in nasal anatomy and measures how these changes affect nasal resistance, flow partitioning between superior and inferior cavity, flow patterns and wall shear stress. High-resolution MRI was applied to capture nasal anatomy in 10 healthy subjects before and after application of a topical decongestant. Computational fluid dynamics simulated nasal airflow at steady inspiratory flow rates of 15 L.min$$^{-1}$$ - 1 and 30 L.min$$^{-1}$$ - 1 . The results show decongestion mainly increases the cross-sectional area in the turbinate region and SAVR is reduced (median approximately 40$$\%$$ % reduction) in middle and lower parts of the cavity. Decongestion reduces nasal resistance by 50$$\%$$ % on average, while in the posterior cavity, nasal resistance decreases by a median factor of approximately 3 after decongestion. We also find decongestant regularises nasal airflow and alters the partitioning of flow, significantly decreasing flow through the superior portions of the nasal cavity. By comparing nasal anatomies and airflow in their normal state with that when pharmacologically decongested, this study provides data for a broad range of anatomy and airflow conditions, which may help characterize the extent of nasal variability.

Computational Fluid Dynamics (CFD) is fast becoming a useful tool to aid clinicians in pre-surgical planning through the ability to provide information that could otherwise be extremely difficult if not impossible to obtain. However, in order to provide clinically relevant metrics, the accuracy of the computational method must be sufficiently high. There are many alternative methods employed in the process of performing CFD simulations within the airways, including different segmentation and meshing strategies, as well as alternative approaches to solving the Navier–Stokes equations. However, as in vivo validation of the simulated flow patterns within the airways is not possible, little exists in the way of validation of the various simulation techniques. The data presented here consists of very highly resolved flow data. The degree of resolution is compared to the highest necessary resolutions of the Kolmogorov length and time scales. Therefore this data is ideally suited to act as a benchmark case to which cheaper computational methods may be compared. A dataset and solution setup for one such more efficient method, large eddy simulation (LES), is also presented.