Abstract
BACKGROUND: Tracheomalacia (TM) is a condition of excessive tracheal collapse during exhalation. Both acquired and congenital forms of TM are believed to result from morphological changes in cartilaginous, fibrous and/or smooth muscle tissues reducing airway mechanical properties to a degree that precipitates collapse. However, neither the specific amount of mechanical property reduction nor the malacic segment lengths leading to life threatening airway collapse in TM are known. Furthermore, the specific mechanism of collapse is still debated. METHODS: Computational nonlinear finite element models were developed to determine the effect of malacic segment length, tracheal diameter, and reduction in tissue nonlinear elastic properties on the risk for and mechanism of airway collapse. Cartilage, fibrous tissue, and smooth muscle nonlinear elastic properties were fit to experimental data from preterm lambs from the literature. These elastic properties were systematically reduced in the model to simulate TM. RESULTS: An intriguing finding was that sudden mechanical instability leading to complete airway collapse occurred in airways when even a 1 cm segment of cartilage and fibrous tissue properties had a critical reduction in material properties. In general, increased tracheal diameter, increased malacic segment length coupled with decreased nonlinear anterior cartilage/fibrous tissue nonlinear mechanical properties increased the risk of sudden airway collapse from snap through instability. CONCLUSION: Modeling results support snap through instability as the mechanism for life threatening tracheomalacia specifically when cartilage ring nonlinear properties are reduced to a range between fibrous tissue nonlinear elastic properties (for larger diameter airways > 10 mm) to mucosa properties (for smaller diameter airways < 6 mm). Although reducing posterior tracheal smooth muscle properties to mucosa properties decreased exhalation area, no sudden instability leading to collapse was seen in these models.