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We experienced a case of bronchospasm during upper gastrointestinal endoscopy under sedation. An 80-year-old man came to our hospital with abdominal distension with pain, nausea and vomiting. He has the history of splenectomy, cholecystectomy for hemolytic anemia and thyroidectomy for thyroid cancer, surgery for bilateral shoulder joints and diabetes. Abdominal X-ray suggested obstruction of the small intestine. On the third hospital day, gastrointestinal endoscopy was scheduled for insertion of a long ileus tube. Under sedation with diazepam 10 mg and local anesthesia of the pharynx with lidocaine spray 24 mg, the endoscope was inserted and when it reached the esophageal-gastrojunction, respiratory rate increased to 30 breaths.min-1 with expiratory stridor. The endoscope was removed immediately. He was oro-tracheally intubated and artificially ventilated. On the fourth hospital day, he was extubated under bronchoscopy. No abnormalities were observed in the trachea, vocal cord, pharynx and larynx. Later, it was revealed that he had a history of hoarseness and dysphasia. His left recurrent nerve and cervical nerve had been resected with thyroid and right cervical nerve anastomosed to the rest of the left recurrent nerve. The insertion of upper gastrointestinal endoscope might have induced bronchospasm stimulating distal esophageal afferent vagal reflex partly by regurgitation of gastric acid under sedation.
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PMID:[Bronchospasm during upper gastrointestinal endoscopy under sedation]. 1264 76

Children who require intubation as a component of their burn management generally need heavy sedation, usually with a combination of opiate and benzodiazepine infusions with a target sensorium of light sleep. When extubation approaches, the need for sedation to prevent uncontrolled extubation can conflict with the desire to lighten sedation enough to ensure that airway protective reflexes are strong. The several hours' half-life of these medications can make this period of weaning challenging. Therefore, the hours preceding extubation are among the most difficult in which to ensure safe adequate sedation. The pharmacokinetics of propofol allow for the rapid emergence of a patient from deep sedation. We have had success with an extubation strategy using short-term propofol infusions in critically ill children. In this work, children were maintained on morphine and midazolam infusions per our unit protocol, escalating doses as required to maintain comfort. Approximately 8 hours before planned extubation, these infusions were decreased by approximately half and propofol infusion added to maintain a state of light sleep. Extubation was planned approximately 8 hours later to allow ample time for the chronically infused opiates and benzodiazepines to be metabolized down to the new steady-state level. Thirty minutes before planned extubation, propofol was stopped while morphine and midazolam infusions were maintained at the reduced level. When the children awakened from the propofol-induced state of light sleep, they were extubated while the reduced infusions of morphine and midazolam were maintained. These were subsequently weaned slowly, depending on the child's need for ongoing pain and anxiety medication, per our unit protocol to minimize the incidence of withdrawal symptoms. Data are shown in the text as mean +/- standard deviation. These 11 children (eight boys and three girls) had an average age of 6.6 +/- 5.6 years (range, 1.2-13 years), average weight of 36.9 +/- 28.7 kg (range, 9.3-95 kg), and burn size of 43 +/- 21.4% (range, 10-85%). Three children had sustained scald burns and eight had flame injuries with associated inhalation injury. They had been intubated for an average of 12.7 +/- 10.9 (range, 2-33 days). Morphine infusions immediately before the initiation of propofol averaged 0.26 +/- 0.31 mg/kg/hour (range, 0.04-1.29 mg/kg/hr) and midazolam averaged 0.15 +/- 0.16 mg/kg/hr (range, 0.06-0.65 mg/kg/hr). Morphine infusions after beginning propofol and at extubation averaged 0.16 +/- 0.16 (range, 0.04-0.65 mg/kg/hr) and midazolam averaged 0.09 +/- 0.08 mg/kg/hr (range, 0.02-0.32 mg/kg/hr). Propofol doses after initial titration during the first hour of infusion averaged 3.6 +/- 2.9 mg/kg/hr (range, 0.4-8.1 mg/kg/hr). Nine of the 11 children (82%) were successfully extubated on the first attempt. Two required reintubation for postextubation stridor 2 to 6 hours after extubation but were successfully extubated the next day after a short course of steroids, again using the same propofol technique. All were awake at extubation and went on to survive. Morphine and midazolam infusions were gradually weaned, and there were no withdrawal symptoms noted. Although prolonged (days) infusions of propofol have been associated with adverse cardiovascular complications in critically ill young children and should probably be avoided, short-term (in hours) use of the drug can facilitate smooth extubation.
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PMID:Short-term propofol infusion as an adjunct to extubation in burned children. 1461 Apr 18

Hydrogen peroxide is an oxidising agent that is used in a number of household products, including general-purpose disinfectants, chlorine-free bleaches, fabric stain removers, contact lens disinfectants and hair dyes, and it is a component of some tooth whitening products. In industry, the principal use of hydrogen peroxide is as a bleaching agent in the manufacture of paper and pulp. Hydrogen peroxide has been employed medicinally for wound irrigation and for the sterilisation of ophthalmic and endoscopic instruments. Hydrogen peroxide causes toxicity via three main mechanisms: corrosive damage, oxygen gas formation and lipid peroxidation. Concentrated hydrogen peroxide is caustic and exposure may result in local tissue damage. Ingestion of concentrated (>35%) hydrogen peroxide can also result in the generation of substantial volumes of oxygen. Where the amount of oxygen evolved exceeds its maximum solubility in blood, venous or arterial gas embolism may occur. The mechanism of CNS damage is thought to be arterial gas embolisation with subsequent brain infarction. Rapid generation of oxygen in closed body cavities can also cause mechanical distension and there is potential for the rupture of the hollow viscus secondary to oxygen liberation. In addition, intravascular foaming following absorption can seriously impede right ventricular output and produce complete loss of cardiac output. Hydrogen peroxide can also exert a direct cytotoxic effect via lipid peroxidation. Ingestion of hydrogen peroxide may cause irritation of the gastrointestinal tract with nausea, vomiting, haematemesis and foaming at the mouth; the foam may obstruct the respiratory tract or result in pulmonary aspiration. Painful gastric distension and belching may be caused by the liberation of large volumes of oxygen in the stomach. Blistering of the mucosae and oropharyngeal burns are common following ingestion of concentrated solutions, and laryngospasm and haemorrhagic gastritis have been reported. Sinus tachycardia, lethargy, confusion, coma, convulsions, stridor, sub-epiglottic narrowing, apnoea, cyanosis and cardiorespiratory arrest may ensue within minutes of ingestion. Oxygen gas embolism may produce multiple cerebral infarctions. Although most inhalational exposures cause little more than coughing and transient dyspnoea, inhalation of highly concentrated solutions of hydrogen peroxide can cause severe irritation and inflammation of mucous membranes, with coughing and dyspnoea. Shock, coma and convulsions may ensue and pulmonary oedema may occur up to 24-72 hours post exposure. Severe toxicity has resulted from the use of hydrogen peroxide solutions to irrigate wounds within closed body cavities or under pressure as oxygen gas embolism has resulted. Inflammation, blistering and severe skin damage may follow dermal contact. Ocular exposure to 3% solutions may cause immediate stinging, irritation, lacrimation and blurred vision, but severe injury is unlikely. Exposure to more concentrated hydrogen peroxide solutions (>10%) may result in ulceration or perforation of the cornea. Gut decontamination is not indicated following ingestion, due to the rapid decomposition of hydrogen peroxide by catalase to oxygen and water. If gastric distension is painful, a gastric tube should be passed to release gas. Early aggressive airway management is critical in patients who have ingested concentrated hydrogen peroxide, as respiratory failure and arrest appear to be the proximate cause of death. Endoscopy should be considered if there is persistent vomiting, haematemesis, significant oral burns, severe abdominal pain, dysphagia or stridor. Corticosteroids in high dosage have been recommended if laryngeal and pulmonary oedema supervene, but their value is unproven. Endotracheal intubation, or rarely, tracheostomy may be required for life-threatening laryngeal oedema. Contaminated skin should be washed with copious amounts of water. Skin lesions should be treated as thermal burns; surgery may be required for deep burns. In the case of eye exposure, the affected eye(s) shod eye(s) should be irrigated immediately and thoroughly with water or 0.9% saline for at least 10-15 minutes. Instillation of a local anaesthetic may reduce discomfort and assist more thorough decontamination.
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PMID:Hydrogen peroxide poisoning. 1529 93

We describe five patients with cervical spondylosis and large anterior osteophytes causing pharyngeal compression. All had dysphagia, two had obstructive sleep apnoea and another two had dyspnoea and stridor on inspiration. One, with perforation of the pharynx, required emergency tracheostomy. Only three had pain in the neck or arm. Compression of the retroglottic space was confirmed in all patients by pharyngoscopy and in all the symptoms were relieved by excision of the osteophytes. Three also underwent intervertebral fusion. One had some persistent sleep apnoea.
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PMID:Retro-pharyngeal obstruction in association with osteophytes of the cervical spine. 1533 24

This manuscript reports on our experience with purulent chondritis of the laryngeal cartilages (PCLC), an entity that has not yet been described. Three patients had a diagnosis of PCLC. The probable causes were relapsing polychondritis, a previous prolonged intubation, and an idiopathic cause. The patients suffered from hoarseness and inspiratory stridor for 1 to 3 months before diagnosis. None complained of pain in the neck. Laryngoscopy showed supraglottic edema. A computed tomography scan revealed abscess formation between the intact inner and outer perichondria of the thyroid cartilage. The treatment included rigid endoscopy, external incision and drainage, and prolonged medical therapy. The culture results were Staphylococcus aureus in the first 2 cases and Aspergillus fumigatus in the third. The second patient (in whom the cricoid cartilage was also affected) required emergency tracheotomy. The other 2 patients did not require airway intervention. The rarity of PCLC and the relatively mild symptoms require a high index of suspicion for its diagnosis.
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PMID:Purulent chondritis of the laryngeal framework cartilages. 1582 72

Dysphagia is a common presenting complaint in otolaryngology practice, and there are many causes. Forestier syndrome is a rare cause of dysphagia. It is also known as diffuse idiopathic skeletal hyperostosis (DISH) syndrome or vertebral ankylosing hyperostosis. Forestier syndrome consists of anterolateral perivertebral ligament calcification. It was first described by Forestier and Rotes-Querol in 1950; diagnosis is primarily radiological and the etiology is unknown. In addition to dysphagia Forestier syndrome has been reported to cause laryngeal stridor, dyspnea, snoring and hoarseness. Other important symptoms associated with Forestier syndrome are stiffness and pain in the back, pain related to tendinitis, myelopathy related to core compression associated with the ossification of the posterior longitudinal ligament, and pain related to vertebral complications such as fracture or subluxation. We report six cases of Forestier syndrome as an etiologic factor in dysphagia and present clinical and radiological findings.
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PMID:Six cases of Forestier syndrome, a rare cause of dysphagia. 1680 20

Cricoarythenoid arthritis can be part of rheumatoid arthritis, which can present with laryngeal symptoms as in other systemic diseases. Bilateral vocal cord paralysis can developed with the progression of cricoarythenoid arthritis and can endanger the patient who suffers from dyspnea and eventually choking. Ankylosis and no mobility of the arythenoids, secondary to chronic inflammatory process in the cricoarythenoid joint, induce in the chronic phase bilateral vocal cord paralysis with symptoms such as stridor, horseness, dyspnea and also pain during speaking and swallowing in the acute phase. The treatment for cricoarythenoid arthritis with bilateral vocal cord paralysis include operations for improvement of breathing and voice. Tracheostomy gives an immediate solution for acute medical condition of dyspnea, resulting from the location of the vocal cords in paramedian or median position, due to their immobility. There are other operations aiming to produce adduction of the vocal cords and widen the glottic inlet and thereby improve the airway condition. The family physician needs to consider the damage and fixation of the vocal cord in patients with advanced arthritis. Patients who have rheumatic arthritis need an otolaryngologic follow-up and periodic laryngoscopic evaluation in order to prevent delayed diagnosis of bilateral vocal cord paralysis which endangers the patient's airway. It is recommended to be examined by an otolaryngologist and also to evaluate the vocal cords as part of the pre-operative evaluation of the anesthesiologist, as performed in the evaluation of the larynx in patients prior to thyroidectomy. This is a case study of a patient who had severe rheumatoid arthritis and developed cricoarythenoid arthritis and bilateral vocal cord paralysis presented with stridor and dyspnea and needed an immediate tracheostomy. Cricoarythenoid arthritis with bilateral vocal cord paralysis including treatments options are discussed.
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PMID:[Bilateral vocal cord paralysis due to rheumatoid arthritis]. 1735 74

Oncocytic cysts of the larynx are rare benign, slow growing lesions that are lined predominantly or exclusively by oncocytes, the cytoplasm of which contains a considerable number of hypertrophied mitochondria, which accounts for their eosinophilia and swollen appearance. The oncocytic change is a phenomenon of metaplasia which occurs frequently in epithelial endocrine cells with high metabolic activity and it is also associated with inflammation, degenerative process or cellular ageing. In the larynx, oncocytic metaplasia is very uncommon, but it is occasionally seen in the lining of laryngeal cysts, which are found most commonly in the ventricles or in the false vocal cords, where seromucinous glands are more abundant. Oncocytic cysts typically occur in the elderly and are usually solitary, with involvement of an isolated site, whereas diffuse involvement with multiple cysts is extremely rare. Hoarseness is the most common presenting symptom, while pain, stridor or laryngeal obstruction are unusual complaints. Management of these lesions is conservative and consists of local excision, endoscopic removal being the treatment of choice. Although oncocytic cysts are benign lesions, follow-up is recommended, as recurrence is possible, especially in the case of patients with multiple involvement, since they may show a tendency to develop new cysts. To date, approximately 150 cases of laryngeal oncocytic cysts have been published. Herein, a very unusual case is presented occurring in a 43-year-old male patient, therefore, "epidemiologically" atypical for developing oncocytic lesions. Causes of oncocytic changes and pathogenesis of laryngeal cysts are discussed.
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PMID:Oncocytic cyst of the larynx: an unusual occurrence. 1795 53

Acupuncture has been used to treat a variety of childhood problems; however, the efficacy and safety of pediatric acupuncture remains unclear. This article reviews the existing empirical literature relating to the use of acupuncture for medical conditions in children. A systematic search of the literature revealed that acupuncture has been used to treat five main conditions in children, including pain, nocturnal enuresis, postoperative nausea/vomiting, laryngospasm/stridor, and neurological disorders. Despite a number of methodological issues, including limited sample sizes, lack of randomization, and inappropriate control groups, it is concluded that acupuncture represents a promising intervention for a variety of pediatric health conditions. To further address the safety, effectiveness, and acceptability of acupuncture in children, large-scale randomized controlled trials are needed.
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PMID:Efficacy of acupuncture for health conditions in children: a review. 1866 Oct 55

The granular cell tumor (GCT) is an uncommon neoplasm, with slow progression, usually benign, that can be found in any organ. The most common region for GCT involvement is in the head and neck. Laryngeal involvement is uncommon and accounts for 6 to 10% of all cases reported. Among the major theories of origin and based on the strongest evidence, the most accepted one is that the tumor stems from neuronal tissue. The GCT has a higher incidence in African-descendent patients, and most commonly in their 4th and 6th decades of life. The posterior larynx is the most common laryngeal site. Pediatric laryngeal GCT is rare, anterior subglottis involvement has been described and extensive glottic involvement may occur. Affected patients typically present with hoarseness, dysphagia, cough, haemoptysis, stridor and pain. The GCT presents as a small, firm nodule, sessile or polypoid, with intact mucosa, well outlined but not encapsulated. Cytoplasm granules are typically seen under light microscopy, and the cells are positive for S100 immunoperoxidase and neuron-specific enolase. Treatment of laryngeal GCT is based on surgical excision. This paper describes a pediatric patient with GCT and its clinical course before and after surgical treatment, stressing the importance of GCT diagnosis in the pediatric population. We review clinical course, pathology characteristics and treatment.
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PMID:Granular cell tumor of the larynx in children: a case report. 1908 63


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