Dysregulated Macrophages Are Present in Bleomycin-Induced Murine Laryngotracheal Stenosis.

OBJECTIVE: To define the inflammatory cell infiltrate preceding fibrosis in a laryngotracheal stenosis (LTS) murine model. STUDY DESIGN: Prospective controlled murine study. SETTING: Laboratory. SUBJECTS AND METHODS: Chemomechanical injury mice (n = 44) sustained bleomycin-coated wire-brush injury to the laryngotracheal complex while mechanical injury controls (n = 42) underwent phosphate-buffered saline (PBS)-coated wire-brush injury. Mock surgery controls (n = 34) underwent anterior transcervical tracheal exposure only. Inflammatory and fibrosis protein and gene expression were assessed in each condition. Immunohistochemistry served as a secondary outcome. RESULTS: In chemomechanical injury mice, there was an upregulation of collagen I (P < .0001, P < .0001), Tgf-ß (P = .0023, P = .0008), and elastin (P < .0001, P < .0001) on day 7; acute inflammatory gene Il1ß (P = .0027, P = .0008) on day 1; and macrophage gene CD11b (P = .0026, P = .0033) on day 1 vs mechanical and mock controls, respectively. M1 marker inducible nitric oxide synthase (iNOS) expression decreased (P = .0014) while M2 marker Arg1 (P = .0002) increased on day 7 compared with mechanical controls. Flow cytometry demonstrated increased macrophages (P = .0058, day 4) and M1 macrophages (P = .0148, day 4; P = .0343, day 7; P = .0229, day 10) compared to mock controls. There were similarities between chemomechanical and mechanical injury mice with an increase in M2 macrophages at day 10 (P = .0196). CONCLUSIONS: The bleomycin-induced LTS mouse model demonstrated increased macrophages involved with the development of fibrosis. Macrophage immunophenotype suggested that dysregulated M2 macrophages have a role in abnormal laryngotracheal wound healing. These data delineate inflammatory cells and signaling pathways in LTS that may potentially be modulated to lessen fibroblast proliferation and collagen deposition.

Pediatric dyspnea caused by supraglottic stenosis: a rare complication of alkali corrosive injury.

Acquired supraglottic stenosis is a rare, but potential late sequela of corrosive injury, usually occurring 1 to 2 months after the initial trauma. The presentation may be delayed in children and is potentially lethal. We describe two pediatric patients, aged 31 and 16 months, who developed progressive inspiratory stridor and hoarseness about 2 months after accidental alkali ingestion. Fiberoptic laryngoscopy showed supraglottic stenosis. Intubation was achieved with a very small endotracheal tube under fiberoptic laryngobronchoscopic guidance prior to general anesthesia. Both patients successfully underwent CO(2) laser treatment under direct laryngoscopic guidance. There has been no case of recurrence reported after 1 year of follow-up other than a thin membranous scar in one case at the 3rd month of follow-up, which was easily dealt with by bronchoscopy dilatation. For such patients, monthly laryngoscopic examinations are advisable after alkaline corrosive injury for a minimum of 6 months. Prompt diagnosis and early airway intervention can reduce the need for tracheostomy and decrease the mortality rate.

[Pharyngeal scars stenosis in children]. / Rybtsovye stenozy glotki u detei.

The treatment and follow-up data are available for 18 children (12 boys and 6 girls) with persistent scarry pharyngostenosis. The disease was first diagnosed at the age of 1 year 8 months to 12 years. Pharyngostenosis has resulted from burn induced by KMnO4 crystals. After treatment (laser destruction in 13 patients and bourginage in 4 patients) 15 patients resumed free breathing. 2 patients continue the treatment.

Upper airway compromise after inhalation injury. Complex strictures of the larynx and trachea and their management.

OBJECTIVE: Strictures of the upper airway caused by burns have features distinct from other benign stenoses. The authors reviewed their experience with burn-related stenoses to define the principles of treatment. SUMMARY BACKGROUND DATA: The combined effects of inhaled gases and heat in burn victims produce an intense, often transmural, inflammation of the airway, further complicated by intubation. The incidence of laryngotracheal strictures in survivors of inhalation injury is high, but the reported experience with their treatment is limited and often unduly separated into injuries of larynx and trachea. METHODS: Presentation, treatment, and long-term follow-up are reviewed in 9 women and 9 men age 9 to 63 years, who were evaluated over a 22 year period for chronic airway compromise after inhalation injury. There were 18 tracheal stenoses, 14 subglottic strictures, and 2 main bronchial stenoses. Laryngotracheal strictures stenosis. T-tubes were placed in 15 patients, in low subglottic or tracheal stenosis below the vocal cords, in high subglottic stenosis through the vocal cords, and as a stent after resection of subglottic stenosis. RESULTS: There were two deaths during follow-up, one from respiratory failure and one from an unrelated cause. Two patients underwent evaluation only. Early in this series, one tracheal and one laryngotracheal resection resulted in prompt restenosis. Of the remaining 14 patients, 9 are without airway support from 2 to 20 years later. Four have permanent tracheal tubes. One patient required tracheostomy 8 years after successful subglottic reconstruction. CONCLUSIONS: Strictures of the upper airway related to inhalation injury are associated with prolonged inflammation and involve larynx and trachea in a majority of patients. These complex injuries respond to prolonged tracheal stenting (mean, 28 months) and resection or stenting of subglottic stenoses with recovery of a functional airway and voice in most patients. Early tracheal resection should be avoided.

Pharyngoesophageal bypass using a free jejunal graft for corrosive stricture--a case report.

The management of corrosive strictures of the esophagus involving the pharynx and/or larynx continues to be a challenge to surgeons. This paper presents a case of a corrosive stricture extending from the hypopharynx to the cervical esophagus associated with complete obstruction of the larynx, which was successfully treated by pharyngoesophageal bypass using a free jejunal graft. Postoperative recovery was smooth without any complications, and swallowing was restored. Three months after the bypass operation, the patient underwent laryngoplasty. Although aspiration occurred immediately after the laryngoplasty, six months later she was again able to tolerate the oral intake of semisolid food without any need for supplementary nutritional support. Reconstruction of a short segment of the pharyngoesophageal stricture by a free jejunal graft restores almost normal swallowing provided that dilatation of the lower esophagus is achieved.

Chronic stenosis of the larynx in children.

Severe laryngeal stenosis in children can be corrected successfully with surgery. Re-canalization of the larynx allows for nasal respiration, reduces the danger of respiratory infections, contributes to improved tissue oxygenation, and stimulates the child's psychosomatic development. Contrary to prior otolarngeal approaches to laryngeal stenosis in children, it has been shown that surgery does not hinder the growth of the larynx, but rather stimulates the normalization of laryngeal function; and this function itself stimulates laryngeal skeleton. It is important that surgery be performed as soon as possible in order to avoid an erroneous functional mechanism which is difficult to correct later. This can also lead to chronic irreversible atrophic and fibrotic processes in the laryngeal mucosa.

Act of swallowing in the fixed larynx.

In a 16-year-old female, complete stenosis of the larynx and hypopharynx developed as a consequence of the ingestion of lye cristals. Supraglotic laryngectomy, plastic surgery of the hypopharynx and antethoracic oesophagus were performed and the upper aero-digestive tract reconstructed. The dilated larynx remained fixed by the surrounding fibrous tissue, but the sphincteric action of the mobile vocal cords was partly salvaged. In that condition, the act of swallowing could be reestablished. The pathophysiology of this new mechanism of swallowing is discussed.