SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Congenital stridor in children is a major sign of airway obstruction which occasionally may be alarming. The relevant embryology is discussed and the developmental, acquired or combined causes of airway obstruction producing congenital stridor are described. The need for careful assessment of chronic stridor in childhood is emphasized and the pros and cons of direct laryngoscopy under general anaesthesia in assessment are mentioned.
Stridor, when present since birth, should alert the physician of the possibility of a major cause of airway obstruction. In some cases, it can be life-threatening if timely and adequate intervention is not performed. In this report we discuss an infant who presented with stridor since birth. It's clinical picture, diagnostic approach and management are reviewed. The use of fiberoptic bronchoscopy as the most important diagnostic tool in the evaluation of stridor is emphasized and prompt referral for proper evaluation is recommended.
Stridor in the neonate is usually congenital in etiology, the most common cause being laryngomalacia. Emergency airway management is always the first priority. The history is highly suggestive of the diagnosis in the majority of cases, but endoscopy is required for confirmation. The possibility of synchronous lesions must not be overlooked. Laryngomalacia presents with stridor usually within the first few weeks of life. The stridor is inspiratory in nature and varies with position and activity level. Anatomic, histologic, and neurologic factors have been proposed as the cause of laryngomalacia. Patients typically have a benign form of the disease, which they outgrow by age two. A small percentage of patients will have a severe form of the disease requiring surgical intervention.
To identify which clinical findings serve to differentiate acute epiglottitis from laryngotracheitis and also to evaluate the role of direct inspection of the epiglottis in the evaluation of children initially thought to have laryngotracheitis, we prospectively evaluated 155 children presenting to the emergency room with acute stridor. Three of the findings on physical examination were associated with epiglottitis: absence of spontaneous cough, drooling, and agitation. The diagnosis assigned prior to inspection of the epiglottis was incorrect in two of six patients with epiglottitis and in three of 149 patients with laryngotracheitis. The diagnosis made after inspection was correct in all 155 patients. Minor complications of inspection were seen in seven patients with laryngotracheitis. No complications were seen in the children with epiglottitis. We conclude that drooling, agitation, and absence of cough are predictors of epiglottitis, but clinical findings alone cannot exclude epiglottitis in every child who appears to have laryngotracheitis. When laryngotracheitis is the suspected diagnosis, inspection of the epiglottis by a pediatrician in a hospital emergency room is an effective aid to the evaluation of the child with acute stridor.
Bronchogenic cysts are congenital anomalies that represent aberrant development of the foregut. Bronchogenic cysts in the mediastinum have been documented in both children and adults, but only one case of tracheal bronchogenic cyst in an infant was found in the literature. We report on a case of an infant with wheeze, stridor, and retractions, caused by a midtracheal bronchogenic cyst. This entity, with its unusual location, should be considered in the differential diagnosis of respiratory distress, cyanotic spells, wheezing, and stridor in infants.
We evaluated 4 patients who developed severe, symptomatic stridor during maximal cardiopulmonary exercise testing, all referred due to exercise-related dyspnea. All underwent resting, unsedated transnasal fiberoptic laryngoscopy and had normal findings. Four patients performed repeat maximal exercise testing with fiberoptic laryngoscopy, and they form the basis of this report. They had normal vocal cord motion during exercise, but developed abnormal anterior motion of the arytenoid and aryepiglottic folds only at peak exercise, leading to partial airway obstruction and severe stridor. This report details the workup and characterizes patients at risk for this unusual phenomenon.
To demonstrate that airway obstruction may be the first manifestation of a congenital fistula, a female newborn is reported who presented with increasing stridor during her first 23 months of life. Magnetic resonance imaging and Doppler echocardiography revealed an enlarged innominate artery with turbulent flow. Angiography demonstrated an arteriovenous fistula between the right subclavian artery and right subclavian vein and an abnormal origin of the right internal thoracic artery. Bronchoscopy showed a pulsating compression of the middle section of the trachea. Closure and division of the fistula and aortotruncopexy were performed. The stridor disappeared, and there was marked relief of the tracheal obstruction, confirmed by bronchoscopy. It is concluded that, a search for enlarged vessels is necessary in cases of airway obstruction.
Esophageal inflammatory disease is an unusual cause of stridor in infants and children. Pediatric patients with upper respiratory tract obstructive symptoms secondary to foreign body esophagitis and esophageal moniliasis are presented. The importance of esophageal abnormalities as a potential cause of stridor is emphasized.
Invasive laryngeal candidiasis is an uncommon cause of epiglottitis, seen most often in immunocompromised or antibiotic-treated patients. We present the clinical and radiographic findings in an HIV-infected infant who developed significant stridor due to candidal epiglottitis. Stridor or hoarseness of unknown cause in an immunocompromised patient should lead to prompt evaluation for opportunistic laryngeal infection.
The review compares five methods that utilise electronic/computer acoustic processing techniques for the analysis of infantile stridor sounds. The first method uses traditional spectrographic techniques to produce time/frequency/intensity three-dimensional representation of the waveform. The second method is computer-based and uses the fast Fourier transformation (FFT) to show the frequency composition of the waveform. The third uses linear prediction coefficients (LPCs) to produce a power spectrum and inverse filtering to estimate the cross-sectional area of the human upper airway. The fourth technique employs a proprietary digital filterbank to analyse normal infant vocalisations, which may be used as a control by subsequent researchers. In the fifth method, a physiologically based digital filterbank, designed to closely model the human ear response, is proposed. It is envisaged that this approach will offer the flexibility of all the previous techniques and also closely model the analysis procedure carried out using subjective auscultation. It is concluded that none of the above techniques are sufficiently robust to provide unambiguous diagnosis of stridor type and that a reappraisal is required in terms of feature extraction so that relevant features can be identified. To this end, the authors propose that a physiologically based model of the human airway, including the vocal cords, be developed as an aid to the assessment of acoustic features.
Congenital stridor is one of the rare presentations of respiratory distress at birth. The commonest cause of congenital stridor is laryngomalacia, which accounts for 60% of the causes. The other common causes are congenital subglottic stenosis and vocal cord palsy (VCP). VCP is usually unilateral and most often linked with birth trauma, and is temporary. Bilateral palsy can be associated with other congenital anomalies. The current report describes a case of congenital bilateral VCP, not related to birth trauma and severe enough to require tracheostomy.
Coarctation of the aorta is a relatively common congenital condition. Most infantile presentations of aortic coarctation are related to the associated congenital cardiac abnormalities leading to congestive heart failure or systemic hypoperfusion. We describe a 4-month-old infant who presented with stridor as the sole manifestation of coarctation. Radiologic studies revealed enlarged innominate artery due to the aortic coarctation that resulted in tracheal compression. After surgical correction, respiratory signs and symptoms completely resolved. This case report describes a unique cause of stridor in newborn infants and discusses the potential for vascular anomalies to result in tracheal narrowing.
This report describes a rare case of acute life-threatening stridor due to membranous tracheitis that occurred as a complication of endotracheal intubation, performed for video-assisted thoracotomy. An obstructive fibrin clot was found in the subglottic region by bronchofiberscopy, and removal provided complete relief of the airway obstruction. The mechanism of the development of this fibrin membrane may have interacted with local tracheal trauma from the endotracheal tube. Membranous tracheitis should be considered in the differential diagnosis of stridor and airway obstruction after endotracheal intubation because it is a life-threatening complication of this procedure.
Fibreoptic laryngoscopy in 6 patients with laryngeal stridor showed immobile vocal cords in a paramedian position but no other local cause. Thus a diagnosis of Gerhardt's syndrome, usually ascribed to paralysis of vocal-cord abductor muscles, was made in 3 patients who had no other signs or symptoms of dystonia, and in 3 patients who had multifocal dystonia. Electromyography (EMG) showed evidence of overactivity of vocal-cord adductors, with no evidence of denervation in the abductor muscles. Botulinum toxin injection of the overactive thyroarytenoid muscles abolished stridor. These clinical and EMG findings indicate that Gerhardt's syndrome is not caused by paralysis of vocal-cord abductors, but represents a focal laryngeal dystonia which may be treatable by botulinum toxin injections of vocal-cord adductor muscles rather than by arytenoidopexy or tracheostomy.
Two cases of congenital stridor caused by merely unusual redundancy of the mucosa covering the arytenoids are reported in this paper. The stridor was noted only when the patients were awake, and was not affected by postural changes of patients. The patients who did not reach their full mental and physical development had congenital abnormalities: cleft palate in one case, and hypertrichiosis, short palpebral fissures of camptodactyly in the other. No abnormalities were revealed in the patients on examinations of chromosomes, thyroid hormones and brains using the techniques of computerized axial tomographic scanning and electroencephalography. The diagnosis of these cases should be confirmed by a direct laryngoscopy or a laryngofiberscopy. Although the etiology of redundant arytenoid mucosa is not known, it may be suggested that this condition is incidental to other congenital abnormalities.
Bronchogenic cyst of the mediastinum, a cause of stridor in the neonate, is one of a group of congenital lesions of the mediastinum that results from abnormal budding of the ventral segment of the primitive foregut. A review of our treatment of 15 patients over 10 years at Le Bonheur Children's Medical Center is highlighted by a case report of a newborn with stridor and severe respiratory distress caused by a mediastinal bronchogenic cyst. We assess the literature on these rare but life-threatening lesions, and discuss the embryology, diagnostic work-up, and treatment, emphasizing the roles of different radiologic modalities in evaluating patients.
A 40-year-old woman was seen with stridor and mediastinal widening secondary to tuberculous mediastinal lymphadenopathy mimicking neoplasm. Initially, stridor could only be controlled with high-dose corticosteroids, but following initiation of antituberculous chemotherapy corticosteroids were withdrawn successfully and the mediastinal lymphadenopathy resolved.
We prospectively studied the sleep patterns and laryngeal function of 20 patients with multiple system atrophy and found sleep disturbances in all subjects and vocal cord abduction dysfunction in 14 (70%). In three patients with nocturnal stridor and complete vocal cord abductor dysfunction, continuous positive airways pressure eliminated laryngeal stridor, obstructive apnoea, and haemoglobin desaturation.