Cases reported "Vocal Cord Paralysis"

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1/22. Clinical case seminar: Riedel's thyroiditis: report of a case complicated by spontaneous hypoparathyroidism, recurrent laryngeal nerve injury, and Horner's syndrome.

    A 42-yr-old woman presented with hyperthyroidism and a large, firm, irregular goiter. Within a few weeks she became hypothyroid. Five months later she developed increasingly severe neck pain and compressive symptoms. The goiter had become rock hard. A fine needle aspiration biopsy showed features of chronic thyroiditis and fibrosis. She partially responded to a course of glucocorticoids. tamoxifen was added, with marked improvement in goiter size and pain. Both medications were tapered off. Two months later the patient experienced paresthesias of the fingertips, perioral numbness, and a seizure. She was found to have spontaneous primary hypoparathyroidism. Three months later the patient became hoarse and experienced difficulty in breathing. She was found to have a massively enlarged thyroid with compression of the right internal jugular vein and encasement of the right carotid artery as well as tracheal narrowing. She also had right vocal cord paralysis due to recurrent laryngeal nerve involvement. Because of airway compromise, an emergency isthmusectomy was performed, and the patient was given a postoperative course of glucocorticoids with gradual improvement. Postoperative diagnosis was Riedel's thyroiditis. Two months later she presented with near-syncope and was found to have bradycardia, hypotension, and right Horner's syndrome, presumably due to compression of the right carotid sheath. She was given i.v. glucocorticoids and tamoxifen. Six months later and 18 months after her initial presentation, the patient is doing remarkably well. Her goiter has regressed by more than 50%, and she no longer has any pain or difficulty breathing. She remains a little hoarse and has persistent hypothyroidism and hypoparathyroidism. She is taking prednisone (5 mg, this is being tapered very slowly) and tamoxifen (20 mg) daily. This case illustrates the protean manifestations of Riedel's thyroiditis, a rare but fascinating disease. The epidemiology of this disease, its pathophysiology and complications, and the roles of surgery and medical therapy are reviewed.
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2/22. Bilateral vocal cord dysfunction complicating short-term intubation and the utility of heliox.

    Bilateral vocal cord paralysis is an extremely rare complication of short-term endotracheal intubation. Its etiology following intubation is likely due to recurrent laryngeal nerve injury on intubation. The anterior ramus of the recurrent laryngeal nerve is especially susceptible to pressure injury in intubated patients. Heliox is reported as a successful means of decreasing the work of breathing in upper airway obstruction via decreases in airway resistance. Two cases of bilateral vocal cord dysfunction following short-term intubation are reported. The first case of bilateral vocal cord paresis treated with Heliox is described.
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3/22. syringomyelia and bilateral vocal fold palsy.

    This is a case of a 35-year-old who had complained of noisy breathing for 15 years, and had been on treatment for 'chronic asthma'. She presented to the Accident and Emergency department with an acute episode of difficulty with breathing, and on admission was found to have stridor and bilateral abductor vocal fold palsy. Further workup revealed a syringomyelia with an associated Chiari type 1 malformation. It is important to consider the above diagnosis in the differential of young adults with breathing difficulties. A discussion of syringomyelia, Chiai malformations and bilateral vocal fold palsy follows.
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4/22. Bilateral vocal fold paresis and multiple system atrophy.

    OBJECTIVE: To review a case series of patients with systemic neurodegenerative disease presenting to a laryngologist for workup of dysphonia and found to have bilateral vocal fold paresis. DESIGN: Case series. SETTING: Tertiary care voice center. patients: Series of patients with neurodegenerative disorders examined for dysphonia. MAIN OUTCOME MEASURES: history and physical examination including fiberoptic laryngoscopy were performed on all patients. Some patients underwent polysomnography. RESULTS: Seven patients during a 2-year period were noted to have bilateral abductor vocal fold paresis. Five of 7 (71%) had the diagnosis of multiple system atrophy proposed by the laryngologist. All 7 patients described sleep-disordered breathing with stridor. CONCLUSIONS: patients with systemic neurodegenerative disorders such as parkinson disease should be examined for multiple system atrophy and for evidence of bilateral vocal fold paresis. Workup for stridor should include polysomnography. Treatment of glottic obstruction in these patients includes constant positive airway pressure at night or tracheotomy. The finding of bilateral vocal fold paresis can be life threatening.
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5/22. Obstructive sleep apnea caused by bilateral vocal fold paralysis.

    We describe the case of a woman who had been referred to us with a history of breathing difficulties and snoring and a suspicion of obstructive sleep apnea (OSA). Our investigation revealed that she did indeed have severe OSA in addition to undiagnosed bilateral vocal fold paralysis of unknown origin. Nocturnal polysomnography found that her apnea/hypopnea index was 120 and her minimum arterial oxygen saturation level was 63%. She was treated with laterofixation of the right vocal fold, and her OSA resolved immediately. During 10 years of follow-up with nocturnal polysomnogrpahy, no recurrence of apnea or low oxygen saturation levels was noted. However, she did experience a recurrence of her snoring 4 years postoperatively, along with the onset of progressively worsening daytime fatigue. When these conditions persisted, we performed a repeat laterofixation of the same vocal fold. Following the repeat surgery, subjectively and objectively assessed results were good.
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6/22. life-threatening vocal cord paralysis in a patient with group A xeroderma pigmentosum.

    We report a 19-year-old male with group A xeroderma pigmentosum who presented life-threatening vocal cord paralysis. At 3 months of age, he became sensitive to sunlight, and at the age of 4 years he was diagnosed with group A xeroderma pigmentosum. The neurologic symptoms progressed slowly thereafter. From the age of 18 years, he reported the development of occasional episodic inspiratory stridor and dyspnea, but the cause remained unknown. At the age of 19, he had a common cold and became severely dyspneic and cyanotic. Immediate examination of the glottis upon arrival by an otorhinolaryngologist using a fibroscope indicated complete paralysis of both vocal cords, and tracheal intubation resulted in marked improvement of respiration. tracheostomy was performed thereafter. Inspiratory stridor and dyspnea are the common symptoms in this disease, and some patients with group A xeroderma pigmentosum undergo a tracheostomy, but the pathogenesis remains unknown. To our knowledge, vocal cord paralysis has never been reported in patients with group A xeroderma pigmentosum. This case is presented to illustrate the importance of fibroscopy in the examination of vocal cords in patients with group A xeroderma pigmentosum before the development of life-threatening events.
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7/22. respiratory insufficiency as the primary presenting symptom of multiple-system atrophy.

    BACKGROUND: Respiratory stridor, sleep-disordered breathing, and respiratory insufficiency are part of the clinical spectrum of multiple-system atrophy (MSA). We have encountered cases where these were presenting symptoms, with the diagnosis of MSA being initially unrecognized. OBJECTIVE: To describe cases in which breathing difficulties were the initial and primary manifestation of MSA. DESIGN: database review from January 1, 1996, through October 31, 2005. SETTING: Mayo Clinic, Rochester, Minn. patients: All patients diagnosed as having MSA, cross-referenced for apnea, hypopnea, or hypoventilation. On review, we included only cases in which respiratory dysfunction was the primary initial clinical event in MSA, excluding equivocal cases. INTERVENTIONS: None. MAIN OUTCOME MEASURES: Characteristics and clinical course of patients. RESULTS: Six cases were identified in which substantial respiratory insufficiency occurred as an early, presenting symptom of MSA. Three patients had been examined emergently for acute respiratory distress before the ultimate diagnosis of MSA; the other 3 patients were diagnosed as having obstructive sleep apnea unresponsive to therapy, with bilateral vocal cord paralysis found on ear, nose, and throat examination. Stridor was noted early in the course in all. All patients required tracheostomy, and all eventually developed features consistent with probable MSA. CONCLUSIONS: Multiple-system atrophy may occasionally present as primary respiratory failure or dysfunction, with initially mild motor and autonomic symptoms. Otherwise unexplained central respiratory failure, bilateral vocal cord paralysis, stridor, or refractory central sleep apnea should prompt consideration of MSA.
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8/22. sleep apnea and vocal cord paralysis secondary to type I Chiari malformation.

    A previously healthy 13-year-old boy without myelodysplasia who had mild scoliosis was seen with complaints of nasal congestion, noisy nighttime breathing, and difficulty sleeping. Flattening of the inspiratory loop on the flow-volume curve was found on pulmonary function testing, suggesting a variable extrathoracic obstruction due to a laryngeal lesion. Bilateral abductor vocal cord paralysis and sleep apnea developed precipitously following general anesthesia. Further workup demonstrated a type-I Chiari malformation with syringomyelia. Brainstem abnormalities such as Chiari malformation with secondary tenth cranial nerve deficits should be considered in previously healthy children and adolescents with signs and symptoms of upper airway obstruction and apnea.
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9/22. Respiratory complications in patients with myelodysplasia and arnold-chiari malformation.

    Respiratory complications in four patients with myelodysplasia and the arnold-chiari malformation included abnormal control of breathing, upper-airway dysfunction, aspiration pneumonia, and cor pulmonale. Early and prolonged ventilatory support resulted in a favorable outcome in three of four patients.
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10/22. Chronic stenosis of the larynx in children.

    Severe laryngeal stenosis in children can be corrected successfully with surgery. Re-canalization of the larynx allows for nasal respiration, reduces the danger of respiratory infections, contributes to improved tissue oxygenation, and stimulates the child's psychosomatic development. Contrary to prior otolarngeal approaches to laryngeal stenosis in children, it has been shown that surgery does not hinder the growth of the larynx, but rather stimulates the normalization of laryngeal function; and this function itself stimulates laryngeal skeleton. It is important that surgery be performed as soon as possible in order to avoid an erroneous functional mechanism which is difficult to correct later. This can also lead to chronic irreversible atrophic and fibrotic processes in the laryngeal mucosa.
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