© 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
Summary
Summary
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 [6].
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 [1].
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 [5].
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.
Tube motion causes abrasion and trauma to the mucosa. This can be minimized by securing the tube carefully and by adequate sedation of the intubated patient.
Repeated or traumatic intubations can also lead to mucosal injury.
Subglottic stenosis may present with failure of extubation, tracheotomy dependency or stridor. Children requiring prolonged intubation frequently have other coexistent conditions, such as chromosomal or congenital anomalies.
Clinical symptoms of acquired laryngeal stenosis may begin immediately after removal of the endotracheal tube or may be delayed for as long as 90 days. Initial symptoms may be mild and include various degrees of hoarseness, aphonia or dyspnoea. Sometimes the onset of difficulty is dramatic, with severe respiratory stridor leading rapidly to asphyxiation. The stridor is typically biphasic (inspiratory and expiratory components) due to turbulent airflow through the partially obstructed airway [1, 2].
Laryngeal stenosis is conveniently classified according to the anatomical subdivisions of the larynx. The three basic types of laryngeal stenosis are supraglottic, glottic and subglottic. Most cases of laryngeal stenosis in children are subglottic. Laryngeal stenosis of the supraglottic type usually follows external trauma or in children following the accidental ingestion of a caustic substance.
The gold standard for diagnosis of subglottic stenosis remains rigid endoscopic evaluation under general anaesthesia.
There is still no universally accepted staging system for subglottic stenosis. The most commonly used system was developed by Cotton. The percentage of obstruction and anatomic location of the lesion were determined endoscopically and assigned a grade I-IV based on perceived percentage of obstruction. Grade I – <50% obstruction, grade II – 51-70% obstruction, grade III – 71-99% obstruction, grade IV – no detectable lumen [3].
Management of subglottic stenosis begins with prevention. Control of risk factors is essential.
The management of subglottic stenosis is dependent on the severity or grade of stenosis. The surgical correction of subglottic stenosis may be endoscopic for mild stenosis, or open. Open reconstruction may be resection surgery (cricotracheal resection), anterior cricoid split, and laryngotracheal reconstruction using cartilage grafting. Mild stenosis (grades I and II) can usually be treated with endoscopic techniques. Factors associated with failure of these endoscopic techniques include: previous attempts at endoscopic repair, circumferential scaring, loss of cartilaginous support, exposure of cartilage during excision leading to chondritis, severe bacterial infection, posterior inlet scarring with arytenoids fixation, combined laryngeal or tracheal stenosis.
Grade III or IV stenoses usually require some form of open surgical procedure [2, 3, 4].
The goal of management of subglottic stenosis is decannulation.
Piśmiennictwo
1. Bryce D.P.: "Subglottic stenosis" Laryngoscope 89: 320, 1979. 2.Cotton R.T.: "The management and prevention of subglottic stenosis in infants and children". Adv. Otolaryngol. Head. Neck. Surg., 1987; 1:241-60. 3.Myer C.M., et al.: "Proposed grading system for subglottic stenoses based on endotracheal tube size". Ann. Otol. Rhinol. Laryngol., 1994; 103: 319-23. 4.Pashley M.R.: "Anterior cricoidotomy for congenital and acquired subglottic stenosis in infants and children". J. Otolaryngol., 1984; 13: 187-90. 5.Ratner I., Whitfield J.: "Acquired subglottic stenosis in the very-low-birth-weight infant". Am. J. Dis. Child., 1983; 137: 40-3. 6.Stolovitzky J.P., et al.: "Autoimmune hypothesis of acquired subglottic stenosis: lack of support at time of surgical repair in children". Inter. J. of Ped. Otorhin., 1997; 38: 255-261. 7.Chmielik M.: (red.): Otorynolaryngologia Dziecięca,W-wa PZWL 2001.
