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Pediatric Tracheomalacia Clinical Presentation

  • Author: Emily Concepcion, DO; Chief Editor: Michael R Bye, MD  more...
 
Updated: Oct 25, 2015
 

History

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  • The history of a patient with tracheomalacia typically includes a wheeze that usually begins when the individual is aged 4-8 weeks. Although the congenital lesion is present before this time, airflow is apparently insufficient during the first few weeks of life to generate abnormal sounds. The wheeze generally increases with activity and colds and decreases during quiet periods.
  • At first, wheezing may be mistaken for a sign of bronchiolitis, especially during respiratory syncytial virus season. As wheezing continues, it may be mistaken for that of asthma or cystic fibrosis. If bronchodilator therapy has been attempted, the history usually indicates no improvement; however, in some infants, tracheomalacia worsens with bronchodilator therapy.
  • Unlike most infants with asthma or cystic fibrosis, infants with tracheomalacia are described as "happy wheezers" (ie, they maintain normal oxygenation and disposition and grow and develop normally, despite the chronic airway noises).
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Physical

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  • The physical findings suggest the diagnosis.
  • The baby looks well and happy despite the chronic wheeze.
  • Vital signs, including the patient's respiratory rate and oxygen saturation, are normal.
  • Lungs have good air entry. The typical abnormality is of a wheeze throughout exhalation that sounds the same in all lung fields. It is a coarse monophonic exhalatory sound, which has been described as exhalatory stridor. No asymmetry to the breath sounds is present. On occasion, the lesion is intrathoracic, and the airway sounds occur in inspiration.
  • The patient's voice and cry are normal, unless gastroesophageal reflux is present.
  • Because some children have concomitant laryngomalacia, abnormal sounds may be heard on inspiration.
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Causes

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  • As far as tracheomalacia is understood, most cases are isolated and idiopathic. A recent study proposed a possible neurologic etiology for tracheomalacia. This group was caring for a child with increased intracranial pressure. When the pressure was elevated, the child developed tracheomalacia. When the pressure was relieved, the tracheomalacia remitted. This scenario recurred, although the etiology for increased intracranial pressure causing tracheomalacia is unknow.[2]
  • Transient defects in tracheal cartilage development are assumed to be the cause of this condition. This is sometimes referred to as type 1 tracheomalacia.
  • Autopsy data are lacking, and no animal model is noted.
  • Some children with tracheomalacia have the lesion because of vascular anomalies or other causes of compression of the airway. This is referred to as type 2 tracheomalacia.
  • Tracheomalacia is a common finding after repair of a tracheoesophageal fistula.
  • Tracheomalacia may occur with and complicate other disorders, including gastroesophageal reflux disease, other forms of recurrent aspiration, and bronchopulmonary dysplasia (chronic lung disease of infancy).
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Contributor Information and Disclosures
Author

Emily Concepcion, DO Fellow, Department of Pediatric Pulmonology, State University of New York Downstate Medical Center

Disclosure: Nothing to disclose.

Coauthor(s)

Michael R Bye, MD Professor of Clinical Pediatrics, State University of New York at Buffalo School of Medicine; Attending Physician, Pediatric Pulmonary Division, Women's and Children's Hospital of Buffalo

Michael R Bye, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Chief Editor

Michael R Bye, MD Professor of Clinical Pediatrics, State University of New York at Buffalo School of Medicine; Attending Physician, Pediatric Pulmonary Division, Women's and Children's Hospital of Buffalo

Michael R Bye, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Additional Contributors

Susanna A McColley, MD Professor of Pediatrics, Northwestern University, The Feinberg School of Medicine; Director of Cystic Fibrosis Center, Head, Division of Pulmonary Medicine, Children's Memorial Medical Center of Chicago

Susanna A McColley, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Sleep Disorders Association, American Thoracic Society

Disclosure: Received honoraria from Genentech for speaking and teaching; Received honoraria from Genentech for consulting; Partner received consulting fee from Boston Scientific for consulting; Received honoraria from Gilead for speaking and teaching; Received consulting fee from Caremark for consulting; Received honoraria from Vertex Pharmaceuticals for speaking and teaching.

Acknowledgements

Heidi Connolly, MD Associate Professor of Pediatrics and Psychiatry, University of Rochester School of Medicine and Dentistry; Director, Pediatric Sleep Medicine Services, Strong Sleep Disorders Center

Heidi Connolly, MD is a member of the following medical societies: American Academy of Pediatrics, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

References
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This shows the trachea during inspiration and expiration. Tracheal collapse of more than 50% during expiration is diagnostic of tracheomalacia.
 
 
 
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