It is difficult to determine the incidence of TBI: in as many as 30–80% of cases, death occurs before the person reaches a hospital, and these people may not be included in studies. On the other hand, some TBI are so small that they do not cause significant symptoms and are therefore never noticed. In addition, the injury sometimes is not associated with symptoms until complications develop later, further hindering estimation of the true incidence. However, autopsy studies have revealed TBI in 2.5–3.2% of people who died after trauma. Of all neck and chest traumas, including people that died immediately, TBI is estimated to occur in 0.5–2%. An estimated 0.5% of polytrauma patients treated in trauma centers have TBI. The incidence is estimated at 2% in blunt chest and neck trauma and 1–2% in penetrating chest trauma. Laryngotracheal injuries occur in 8% of patients with penetrating injury to the neck, and TBI occurs in 2.8% of blunt chest trauma deaths. In people with blunt trauma who do reach a hospital alive, reports have found incidences of 2.1% and 5.3%. Another study of blunt chest trauma revealed an incidence of only 0.3%, but a mortality rate of 67% (possibly due in part to associated injuries). The incidence of iatrogenic TBI (that caused by medical procedures) is rising, and the risk may be higher for women and the elderly.
Areas near the cricoid cartilage and carina are fixed to the thyroid cartilage and the pericardium respectively; thus if the airways move, they can tear at these points of fixation.The third mechanism occurs when the chest is compressed from front to back, causing it to widen from side to side. The lungs adhere to the chest wall because of the negative pressure between them and the pleural membranes lining the inside of the chest cavity; thus when the chest widens, they are pulled apart. This creates tension at the carina; the airway tears if this tensile force exceeds its elasticity. This mechanism may be the cause of injury when the chest is crushed. Most TBI are probably due to a combination of these three mechanisms.When airways are damaged, air can escape from them and be trapped in the surrounding tissues in the neck (subcutaneous emphysema) and mediastinum (pneumomediastinum); if it builds up to high enough pressures there, it can compress the airways. Massive air leaks from a ruptured airway can also compromise the circulation by preventing blood from returning to the heart from the head and lower body; this causes a potentially deadly reduction in the amount of blood the heart is able to pump out. Blood and other fluids can build up in the airways, and the injury can interfere with the patency of the airway and interfere with its continuity.