However, one likely mechanism involves an endotracheal tube catching in a fold of membrane and tearing it as it is advanced downward through the airway. When an endotracheal tube tears the trachea, it typically does so at the posterior (back) membranous wall. Unlike TBI that results from blunt trauma, most iatrogenic injuries to the airway involve longitudinal tears to the back of the trachea or tears on the side that pull the membranous part of the trachea away from the cartilage. Excessive pressure from the cuff of an endotracheal tube can reduce blood supply to the tissues of the trachea, leading to ischemia and potentially causing it to become ulcerated, infected, and, later, narrowed.The mucosal lining of the trachea may also be injured by inhalation of hot gases or harmful fumes such as chlorine gas. This can lead to edema (swelling), necrosis (death of the tissue), scar formation, and ultimately stenosis. However, TBI due to inhalation, foreign body aspiration, and medical procedures is uncommon. Mechanism
The structures in the tracheobronchial tree are well protected, so it normally takes a large amount of force to injure them. In blunt trauma, TBI is usually the result of violent compression of the chest. Rapid hyperextension of the neck, usually resulting from vehicle crashes, can also injure the trachea, and trauma to the neck can crush the trachea against the vertebrae.
Fibrochondrogenesis is a rare autosomal recessive form of osteochondrodysplasia, causing abnormal fibrous development of cartilage and related tissues.It is a lethal rhizomelic (malformations which result in short, underdeveloped limbs) form of dwarfism, exhibiting both skeletal dysplasia (malformations of bone) and fibroblastic dysplasia (abnormal development of fibroblasts, specialized cells that make up fibrous connective tissue, which plays a role in the formation of cellular structure and promotes healing of damaged tissues). Death caused by complications of fibrochondrogenesis occurs in infancy. Presentation
Fibrochondrogenesis is a congenital disorder presenting several features and radiological findings, some which distinguish it from other osteochondrodysplasias. These include: fibroblastic dysplasia and fibrosis of chondrocytes (cells which form cartilage); and flared, widened
long bone metaphyses (the portion of bone that grows during childhood).Other prominent features include dwarfism, shortened ribs that have a concave appearance, micrognathism (severely underdeveloped jaw), macrocephaly (enlarged head), thoracic hypoplasia (underdeveloped chest), enlarged stomach, platyspondyly (flattened spine), and the somewhat uncommon deformity of bifid tongue (in which the tongue appears split, resembling that of a reptile). Cause
The cause of platyspondyly in fibrochondrogenesis can be attributed in part to odd malformations and structural flaws found in the vertebral bodies of the spinal column in affected infants.Fibrochondrogenesis alters the normal function of chondrocytes, fibroblasts, metaphyseal cells and others associated with cartilage, bone and connective tissues. Overwhelming
disorganization of cellular processes involved in the formation of cartilage and bone (ossification), in combination with fibroblastic degeneration of these cells, developmental errors and systemic skeletal malformations describes the severity of this lethal osteochondrodysplasia.