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Stridor: intracranial pathology causing postextubation vocal cord paralysis
F C Chaten1, S E Lucking, E S Young
1Division of Pediatric Critical Care Medicine, Children's Medical Center, Medical College of Virginia, Richmond.
Insights
Pediatric vocal cord paralysis, often causing stridor after extubation, can result from nerve injury or intracranial pressure. Early laryngeal evaluation is crucial for affected children.
Area of Science:
- Pediatric critical care medicine
- Otolaryngology
- Pediatric neurology
Background:
- Vocal cord paralysis is a serious complication in pediatric intensive care.
- Stridor upon extubation can indicate vocal cord dysfunction.
Purpose of the Study:
- To identify the incidence and causes of vocal cord paralysis in pediatric intensive care patients.
- To evaluate the outcomes of vocal cord paralysis in this population.
Main Methods:
- Flexible bronchoscopy was used to diagnose vocal cord paralysis in nine pediatric patients over 18 months.
- Patient data including age, paralysis type, cause, and treatment outcomes were collected.
Main Results:
- Nine pediatric patients (17 days to 5.5 years) presented with vocal cord paralysis and stridor post-extubation.
- Bilateral abductor paralysis (7 patients) frequently required tracheostomy (6/7), while unilateral paralysis (2 patients) did not.
- Neurologic disorders with increased intracranial pressure were the likely cause in most cases (7/9).
- Recovery of cord mobility occurred in 4/7 bilateral cases within 4 months; unilateral cases resolved within 1 year.
Conclusions:
- Increased intracranial pressure may cause vagal nerve compression leading to vocal cord paralysis.
- Early laryngeal visualization is recommended for extubated children with stridor, particularly those with a history of thoracic procedures or neurological conditions associated with intracranial hypertension.
Abstract:
During an 18-month period in a pediatric intensive care unit, nine patients with vocal cord paralysis were identified using flexible bronchoscopy. When tracheally extubated, each child was found to have stridor. The children ranged in age from 17 days to 5 1/2 years. Two patients had unilateral paralysis, but neither required tracheostomy. Seven patients displayed bilateral abductor vocal cord paralysis. Of these, six patients required tracheostomy. Surgical injury to the recurrent laryngeal nerve was the probable cause in two patients. The other seven patients had neurologic disorders with documented or suspected increases of intracranial pressure. Four of the seven patients with bilateral abductor vocal cord paralysis regained cord mobility within 4 months. Both children with unilateral cord paralysis have no stridor and vocalize well 1 year later. Cord paralysis in the setting of intracranial hypertension probably results from compression or ischemia of the vagus nerve before it exits the skull. Early visualization of the larynx should be done in patients who become stridulous when extubated, especially those with prior thoracic procedures or with neurologic disorders associated with intracranial hypertension.