Numerical simulation of blunt thoracic trauma followed by aortic rupture

Blunt thoracic trauma followed by aortic rupture (BTAR), is a unique injury to the aorta (which is the main output of blood from the heart). BTAR could be explained as a compression of the rib cage, (produced by a trauma to the chest), which affects the internal organs and injure the aorta in a specific spot. This thesis work will analyze the mechanism of this injury. A hypothesis has been developed to explain the mechanism of BTAR, if the mechanism is known an external device could be designed to prevent it. In this thesis, numerical simulations will be performed as a way to recreate BTAR and prove that the mechanism is not due to only one assumption, instead of being a complex trauma, it triggers different mechanisms. The study starts with an explanation of the trauma and a rough rationale for the mechanisms proposed in this work. Literature has been reviewed marking the starting point for this research. This first chapter concludes with the methodology that will take place and how will be studied throughout the chapters. A validation of the mechanical properties and material model is performed on the first simulation of the second chapter. Once the mechanical properties and material model have been validated, a simulation to prove the first mechanism proposed is performed. A scar at the inner aspect of the aortic isthmus will generate a concentration of stress, if the tissue is subjected to an increment of pressure. A simulation of a bubble inflation test with the insertion of a patch, which varies in diameter and stiffness is performed on this second chapter, finding an intensity factor of 1.53, 1.43 and 1.66 in diameters of 1 mm, 2 mm and 3 mm respectively, these values represents a concentration of stress and strain at the border of the patch and the aorta. This is shown in the second chapter which validates the mechanism that a scar at the aortic isthmus, due to the closure of the Ductus Arteriosus, will weaken the aortic wall. The third chapter compares two ways of geometry generation. With an increment of internal pressure first in a high pressure range having the highest error before 150 kPa, hence a normal physiological pressure range was simulated and a dramatic increase of errors started at 18.7 kPa, the outermost layer of the aorta shows the highest values. To achieve these a 10 mm specimen from the descending aorta was generated by two methods; a geometric approximated model designed with a Computational Assisted Design software, and a segmented model, which was designed by segmenting 3D medical images. The simulation of the third chapter demonstrates that the aorta changes its cross section when it is subjected to hypertension values, therefore the fourth chapter tests the architecture of the thoracic aorta when is subjected to a pressure range which includes the different levels of hypertension. For this analysis the aorta is divided into four different sections, ascending aorta, descending aorta, external aortic isthmus and internal aortic isthmus. The internal part of the aortic isthmus, at the innermost layer, shows higher stress values with less displacement. On the displacement analysis, the descending aorta shows a value at 18.7 kPa of 0.6 x 10^-3 m and the internal part of the aortic isthmus of 0.2 x 10^-3 m, for the stress values the descending aorta shows a value of 0.4 MPa and the internal part of the aortic isthmus of 0.35 MPa. The last chapter employs the finite element method with a fluid solid interaction, and a smooth particle hydrodynamics formulation for the blood. This simulation uses a geometric approximation of the chest including the sternum and spine, heart and a three layered aorta. This model is subjected to different values of speed, introduced at the sternum, which will compress the heart recreating a blunt thoracic trauma. For this analysis, the aorta is also divided into the same zones as in the fourth chapter. It is shown that at a velocity of 20 m x s^-1 values of pressure higher than 270 kPa (rupture pressure validated on the second chapter) and stress values higher than 1819.2 kPa experimental minimum ultimate stress [Pearson et. al., 2008] (tested and validated on the second chapter) are located at the inner aspect of the aortic isthmus of the intima layer. When the four results chapters are analysed together, it can be seen that the architecture of the aorta changes during hypertension values, and the concentration of stress and strain changes from the adventitia layer to the Intima layer, due to the change of the cross section geometry. This thesis concludes that a mechanism of a BTAR is too complex to explain only by one mechanism, therefore a conjunction of numerical simulations test and validate a multivariate hypothesis proposed. The limitations of this thesis are also explored in the final chapter, with a proposal of a future work, to keep track with the research, and could design an external device to prevent people from dying in car crashes due to BTAR