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A patient is described with idiopathic Parkinson's disease and severe laryngeal stridor. Other than urinary frequency and urgency, not uncommon in this condition, and postoperative levodopa-sensitive postural hypotension, there were no features of generalized autonomic failure. The laryngeal stridor responded to levodopa therapy, and we are not aware that this has been reported previously.
The case is described of a 72 year old woman who presented with a two year history of exertional stridor in whom the diagnosis of myasthenia gravis was delayed. Although an uncommon cause, myasthenia gravis should be included in the differential diagnosis of stridor.
We describe two adolescent patients in whom a disorder of the vocal cords associated with emotional factors resulted in acute episodes of stridor. Adduction of the vocal cords on inspiration and abduction on expiration was found on indirect laryngoscopy. The problem responded to either placebo treatment or psychotherapy. The similarity between vocal cord dysfunction presenting as stridor and that presenting as asthma is discussed. The importance of diagnosing these functional problems in children is emphasized in order to avoid unnecessary diagnostic procedures and hazardous treatment.
The reliability of parameters used to assess pediatric postextubation upper respiratory distress is unknown. We prospectively studied the interobserver reliability of six parameters commonly used to assess respiratory distress in children. Eligible patients were less than 15 years old and hospitalized for traumatic injuries at Harborview Medical Center between March and September 1989. At extubation, patients were examined independently by a physician, a nurse, and a respiratory therapist, each of whom evaluated respiratory rate (RR), stridor, air movement, flaring/retractions (F/R), level of consciousness (LOC), and oxygen saturation (O2 sat). Reliability was measured by percentage agreement and weighted kappa (Kw). The 25 children (27 extubations) had a median age of 7 years, and eight of the 27 required treatment for upper airway obstruction. Percentage agreement ranged from 82% (for air movement) to 96% (for O2 sat). Weighted kappas were excellent for RR and F/R (Kw greater than .6); moderate for LOC, stridor, and O2 sat (0.4 less than Kw less than .06); and poor for air movement (Kw less than .4). Further improvements in interobserver agreement are required to provide more consistent upper airway management in critically ill children.
Electromyography (EMG) was performed in 10 patients with multiple system atrophy, laryngeal or pharyngeal symptoms, or both. In patients with stridor, EMG during quiet breathing revealed persistent tonic activity in both abductor and adductor vocal cord muscles. In patients with dysphagia, the cricopharyngeal muscle showed persistent EMG activity throughout all phases of swallowing. Botulinum toxin injection into the adductor muscle determined subjective improvement and reduced tonic EMG activity. Therefore, the cause of stridor in multiple system atrophy is dystonia of the vocal cords.
Functional laryngeal dyskinesia is a disorder that presents with stridor. Failure to recognize its features can result in inappropriate investigation and treatment for a condition that has a psychogenic origin. The key feature in diagnosis is paradoxical vocal fold adduction on inspiration, as seen on fibre-optic nasendoscopy. This phenomenon together with the associated stridor may disappear after distraction techniques or when the patient is asleep. We present five such cases which presented to hospitals in south west London over a 12 month period.
Use of rigid direct larygnoscopy (RDL) in the investigation of stridor in children is well recognized. This study presents awake flexible fibre-optic laryngoscopy (FFL) as the first line in investigation of children, under six months of age, who present with stridor without any associated respiratory distress. Using the per oral approach the procedures were conducted either in the out-patient department or in the ward. No anaesthesia, local or general, nor sedation was used. Of the 20 cases included in the study, in 16 (80 per cent) cases a working diagnosis was reached on awake FFL. Eleven had laryngomalacia, two subglottic stenosis, one glottic web and two were normal. Only four (20 per cent) cases needed RDL to reach a definitive diagnosis. There were no problems with the maintenance of the airway during the procedure. It is particularly useful in the diagnosis of functional abnormalities of the larynx, such as laryngomalacia and vocal fold palsies. Awake FFL using the per oral approach is a safe and reliable technique for reaching a working diagnosis in approximately 80 per cent of cases.
Achalasia is a motility disorder of the oesophagus that typically presents with dysphagia, regurgitation and chest pain. A rare presenting symptom is stridor. A case of previously treated achalasia re-presenting with stridor is described and associated imaging presented.
Paradoxical vocal cord motion (PVCM) is an important cause of laryngeal stridor and dysphonia; however, only two previous cases have been reported. We report three additional cases, one of which was tracheotomized on two occasions before the diagnosis was made. These patients, typically young females who have had a recent upper respiratory infection, present with stridor. They can phonate weakly, but they cannot cough. Indirect laryngoscopy reveals smooth, symmetric vocal cord adduction on inspiration and abduction on expiration. Laboratory values are normal. PVCM appears to be self-limited (up to 72 hours), and patients respond to supportive care and sedation. Tracheotomy appears to be unnecessary. The etiology is obscure and may be functional; however, a case is discussed in which PVCM was seen in association with chronic aspiration in a patient with organic brain syndrome. An awareness of this entity and a high index of suspicion can prevent unnecessary tracheotomy.
Stridor in children is usually acute. This paper represents a chart review and telephone survey of 60 patients with chronic pediatric stridor. The most common etiology was laryngomalacia, which required airway intervention in 22% of the patients. The symptoms persisted beyond 18 months of age in 17% of the patients. Twelve percent of the patients had multiple lesions; 65% of the second lesions were below the vocal cords. It appears that the presence of cyanosis should increase physician suspicion of multiple lesions. There was not a higher risk of recurrent upper respiratory infections with any of the diagnoses.
The authors present the case of an infant with laryngeal stridor, apneic spells, and an open lumbar myelomeningocele; granulomatous vernix caseosa meningitis was found at autopsy. The suggest that chemical meningitis which also involved the cranial nerves might be held partly responsible for the laryngeal stridor.
A number of respiratory tract illnesses may produce acute wheezing and stridor in children, and treatment may vary, depending on the specific illness. These illnesses, however, may be difficult to differentiate solely on clinical grounds. A uniform therapeutic approach for children with acute wheezing or stridor independent of the specific etiology can be employed. In this prospective study, 246 children received aerosolized albuterol and cromolyn sulfate. Children who remain in distress after aerosolized medications should be admitted to the hospital. Those with partial improvement may be treated with home aerosol treatments after intramuscular injection of dexamethasone.
A six-week-old child with tracheal duplication presenting with congenital stridor is being reported. To the best of our knowledge, a tracheal web or tracheal duplication (as the present condition may be named) has not been described as a causative factor of infantile stridor.
A case is presented of a 48 year-old woman with symptoms of severe rhoncopathy and obstructive sleep apnea, followed by middle inspiratory stridor and dyspnea to any phisial effort. Redundant hyperplasia of the arytenoid mucosa was discovered during exploration, with vibration during inspiration and closure of the lumen as it goes closer to the epiglottis. Also, severe septal deviation, hypertrophy of the pharyngeal tonsil, soft palate and uvula, and macroglossia, were diagnosed. Neither CPAP/BIAP or triple anti-reflux therapy were effective, and laser endoscopic excision resolved the laryngeal obstruction. Currently the stridor has disappeared, whereas rhoncopathy is improved with low pressure CPAP. Pathogenesis of the giant hyperplasia of the arytenoid mucosa of unknown origin is discussed, as literature search revealed only three cases reported worldwide.
Endotracheal intubation is an important airway procedure in the management of neonates and infants. Prolonged intubation may result in severe laryngeal injury which may lead to chronic laryngeal disability. The nature and causes of post-extubation airway obstruction were evaluated with videoendoscopy. From June 1998 to September 2000, detailed videoendoscopic examination of pediatric airway was performed in 30 children who had persistent stridor after endotracheal extubation or failure of elective extubation. Common locations of post-extubation lesion are the posterior glottis and subglottis. Retrospective analysis of the causes of stridor included: (1) isolated intubation laryngotracheitis (n = 19); (2) intubation laryngotracheitis with neuromuscular dysfunction which resulted in tongue drop, laryngotracheal incoordination, saliva pooling over the larynx or poor cough reflex(n = 5); and (3) specific airway problems such as laryngomalacia, subglottic stenosis or vocal paralysis(n = 6). We favored the term of "intubation laryngotracheitis" instead of "intubation injury" or 'intubation trauma". Although most cases of intubation laryngotracheitis heal, leaving a normal or near-normal larynx, some of them still suffer from airway obstruction after endotracheal extubation. Specific airway problems such as severe laryngomalacia or vocal cords paralysis and neurogenic defects should also be taken into consideration.
BACKGROUND: Patients with heart failure or elevated intracranial pressure are at risk of developing lung oedema when anaesthesized. Lung oedema may develop in patients with airway obstructions as well. MATERIAL AND RESULTS: We refer to a four-year-old boy anaesthesized for elective adenotomia and paracentesis. After being extubated, he developed a moderate inspiratory stridor lasting for hours. Clinically he normalized in two hours on a therapy with oxygen in a mask with continuous positive airway pressure (CPAP) and finally bronchodilator therapy with epinephrine and salbutamol. Successive lung X-rays showed lung oedema almost normalizing in 48 hours. INTERPRETATION: The triggering mechanism of lung oedema in airway obstruction is the negative intrathoracal pressure generated because of forced inspiratory effort. This pressure is transformed to a negative interstitial hydrostatic pressure that according to Starling's hypothesis on capillary filtration may generate a lung oedema. We conclude that our patient with nasal polyps had a lowered threshold for developing lung oedema faced with postextubatory complications causing inspiratory stridor. Pathogenic mechanisms are discussed.
The spectrum of degenerative ataxia includes the symptomatic degenerative ataxias and the primary degenerative ataxias. The later may be sporadic and idiopathic or hereditary, being genetically determined. When an individual ataxic patient presents with an adult-onset degenerative ataxia and has a negative family history, the physician is faced with a diagnosis of pure idiopathic sporadic degenerative ataxia or one of the hereditary ataxias. The clinical spectrum of olivopontocerebellar atrophy (OPCA) usually consists of pancerebellar signs with pyramidal and abnormal eye movements. Although Stridor is more commonly found in multisystem atrophy, it is rarely seen in OPCA. We, here report a case of third decade onset of ataxia presenting with stridor.
Three cases of adolescents with respiratory stridor of psychiatric etiology are described. All three fulfilled DSM-III-R criteria for diagnoses of somatoform disorders and showed characteristics of repressive defense style. Such patients are likely to undergo extensive medical investigation and treatment if the psychiatric nature of their disorder is not recognized, but few data describing their psychological characteristics or treatment exist. Repressors are typically unaware of emotional arousal and do not recognize the negative affects which lead to their somatic symptoms. They therefore respond poorly to confrontational psychotherapy and are at risk of discontinuing treatment and repeating their maladaptive symptom cycle. Identification of repressive defense style in patients with stridor which has no obvious organic cause may be useful both as a possible "marker" of psychiatric disorder and as a guide to treatment.