Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040586 (tracheobronchitis)
 449 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this investigation was to study the effect of an angiotensin converting enzyme inhibitor (enalaprilat) on the morphologic manifestations of experimentally induced necrotizing tracheobronchitis (NTB). Twenty piglets were anesthetized before saline lung lavage. High frequency flow interrupter (HFFI) ventilation was used with a strategy known to produce NTB. Animals were randomly assigned to receive IV enalaprilat 0.1 mg/kg (ENP-Hi), enalaprilat 0.01 mg/kg (ENP-Lo), or saline (C). After 8 hours of ventilation, the piglets were sacrificed. Total airway injury scores (mean +/- S.D.) were 1.2 +/- 0.7 for ENP-Hi, 0.2 +/- 0.2 for ENP-Lo, and 21.3 +/- 16 for group C. Enalaprilat minimizes NTB lesions in neonatal piglets exposed to high frequency oscillatory ventilation. Although the origin of NTB is multifactorial, airway mucosa ischemia may play an important role. Enalaprilat may compensate for the reduction of mucosal blood flow by limiting formation of angiotensin II and/or preventing degradation of bradykinin.
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PMID:Necrotizing tracheobronchitis (NTB) following high frequency ventilation: role of an angiotensin converting enzyme inhibitor. 184 39

Neonates with necrotizing tracheobronchitis present a diverse clinical spectrum from asymptomatic disease to severe airway obstruction. A retrospective clinicopathologic study of 206 neonatal autopsy reports spanning a three-year period yielded 122 cases of necrotizing tracheobronchitis with an incidence of 59%. All study patients received treatment prior to the development of high-frequency ventilator jet, oscillator, or interruption. The site and submucosal depth of airway involvement was variable. The most commonly affected anatomic site was the middle or thoracic trachea (56%). The common cause identified was severe ischemia to the airway mucosa and submucosa, occurring with profound birth asphyxia and/or shock. The presence of ischemia supports the concept that decreased tracheoperfusion may be an important factor in the development of tracheobronchial abnormalities.
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PMID:Necrotizing tracheobronchitis. An ischemic lesion. 281 48

Intubation in the child presenting with severe viral tracheobronchitis or prior subglottic injury can be detrimental to the child and the subglottis. Intubation may lead to further mucosal ischemia, scar, subglottic stenosis, or failed extubation requiring a tracheotomy. Heliox is a combination of helium and oxygen that produces less-dense gas exchange. Its use leads to a decrease in turbulent airflow, which may obviate the need for intubation. Here we report our experience using heliox as initial therapy in 14 consecutive children presenting with severe airway distress and the need for intubation. (Five had viral tracheobronchitis, 5 had inflammatory exacerbation of subglottic stenosis, and 4 had acute iatrogenic subglottic injury.) In 10 of the 14 children, intubation, which can lead to mucosal injury and scarring, was avoided by the use of heliox therapy. Of the 4 children in whom heliox therapy failed, 3 had a prior history of subglottic stenosis. Heliox is a relatively safe and reliable alternative to intubation of children with severe subglottic edema or injury. Heliox should be considered before intubation for selected children with subglottic inflammation and severe airway distress.
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PMID:Avoiding intubation in the injured subglottis: the role of heliox therapy. 1151 Jul 26