© Borgis - New Medicine 3/2006, s. 56-57
Lidia Zawadzka-Głos, Mieczysław Chmielik
Acquired laryngotracheal stenosis in children
Department of Paediatric Otorhinolaryngology, Medical University, Warsaw, Poland
Head of Department: Prof. Mieczysław Chmielik, MD, PhD
Laryngotracheal stenosis is a congenital or acquired narrowing of the subglottic airway. Subglottic stenosis can present as a life-threatening airway emergency. Endotracheal intubation may result in significant injury to the larynx and trachea. Subglottic stenosis is the most dangerous consequence of this injury in the paediatric age.
Congenital anomalies and acquired diseases of the larynx manifest themselves by disturbing laryngeal function. The airway may be obstructed and produce stridor or the voice may change. Acquired subglottic stenosis in children is a more severe problem than is congenital subgottic stenosis. Causes of acquired subglottic stenosis include endotracheal intubation, external trauma, infection or inflammation, thermal or caustic injuries. But the most common cause of acquired subglottic stenosis is endotracheal intubation. Because advances in neonatology have resulted in the survival of very premature infants, the number of infants requiring prolonged periods of endotracheal intubation has increased. As a result, the incidence of acquired subglottic stenosis has also increased.
The pathogenesis of acquired subglottic stenosis is not completely understood. There are several theories. One of them includes mucosal compression by the endotracheal tube leading to mucosal oedema, ischemia and ulceration. This ulceration leads to perichondritis which extends into the cartilage leading to chondritis. The cartilage may necrose and collapse. Healing is by secondary intention with granulation tissue proliferation and deposition of fibrous tissue. This results in a weak cartilage framework and firm scar narrowing the subglottic airway.
The autoimmune hypothesis for acquired subglottic stenosis arises from an understanding of the immune system´s response to cartilage trauma. Subglottic stenosis begins with erosion of the respiratory epithelium by the endotracheal tube. The erosion, friction or infection, alone or in combination, may extend through the soft tissues into the cricoid cartilage itself. During the phase of trauma to the cricoid cartilage, presumably there is early loss of the proteoglycans of the extracellular matrix. The autoimmune hypothesis of acquired subglottic stenosis is that otherwise-sequestered antigens of the cartilage framework are exposed to the immune system, evoking additional inflammation with resultant scarring that is identified clinically as acquired subglottis stenosis .
The mechanism of a baby acquiring subglottis is still poorly understood. There is no good explanation as to why the large majority of babies with similar predisposing factors do not manifest the problem .
Risk factors for development of acquired subglottic stenosis in neonates include prolonged endotracheal intubation, size of the endotracheal tube, increased motion of the endotracheal tube, repeated or traumatic intubations, birth weight less than 1,500 g, infection, compromised immune status, presence of nasogastric tubes and the presence of gastroesophageal or laryngotracheal reflux .
The most important risk factor for the development of acquired subglottic stenosis is the length of intubation. There is no safe period of intubation. Premature infants tolerate prolonged intubation better than adults.
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Adres do korespondencji:
Department of Paediatric Otorhinolaryngology, Medical University in Warsaw
00-576 Warszawa, ul. Marszałkowska 24
tel./fax +48 22 628 05 84
e-mail: firstname.lastname@example.orgNew Medicine 3/2006
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