Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Swallow and cough are complex motor patterns elicited by rapid and intense electrical stimulation of the internal branch of the superior laryngeal nerve (ISLN). The laryngeal adductor response (LAR) includes only a laryngeal response, is elicited by single stimuli to the ISLN, and is thought to represent the brain stem pathway involved in laryngospasm. To identify which regions in the medulla are activated during elicitation of the LAR alone, single electrical stimuli were presented once every 2 s to the ISLN. Two groups of five cats each were studied; an experimental group with unilateral ISLN stimulation at 0.5 Hz and a surgical control group. Three additional cats were studied to evaluate whether other oral, pharyngeal, or respiratory muscles were activated during ISLN stimulation eliciting LAR. We quantified < or = 22 sections for each of 14 structures in the medulla to determine if regions had increased Fos-like immunoreactive neurons in the experimental group. Significant increases (P < 0.0033) occurred with unilateral ISLN stimulation in the interstitial subnucleus, the ventrolateral subnucleus, the commissural subnucleus of the nucleus tractus solitarius, the lateral tegmental field of the reticular formation, the area postrema, and the nucleus ambiguus. Neither the dorsal motor nucleus of the vagus, usually active for swallow, nor the nucleus retroambiguus, retrofacial nucleus, and the lateral reticular nucleus, usually active for cough, were active with elicitation of the laryngeal adductor response alone. The results demonstrate that the laryngeal adductor pathway is contained within the broader pathways for cough and swallow in the medulla.
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PMID:Neuronal activation in the medulla oblongata during selective elicitation of the laryngeal adductor response. 1521 23

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

The past decade has witnessed increasing interest in the supraesophageal (ear, nose, and throat (ENT)) symptoms potentially caused by gastroesophageal reflux disease (GERD). Hoarseness, halitosis, problems with vocal presentations, excessive phlegm, frequent throat clearing, globus sensation, sore throat, cough, aspiration, laryngospasm, and laryngeal carcinoma are some, but not all of the ENT symptoms that have been attributed to GERD (1). The availability of highly effective medical and surgical therapies allows for control of these symptoms in many patients adding to the importance of accurately diagnosing GERD.
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PMID:Should upper gastrointestinal endoscopy be part of the evaluation for supraesophageal symptoms of GERD? 1530 53

Stimulation of laryngeal receptors is the natural starting point of defensive airway reflexes including the cough reflex, expiration reflex, spasmodic panting, and apnoea with laryngospasm. Although several different types of laryngeal receptors have been reported, the laryngeal irritant receptors are considered to play the most essential role in elicitation of defensive airway reflexes. Based on the knowledge that the laryngeal irritant receptors are stimulated by water solutions lacking chloride anions, we have developed an experimental method to elicit defensive airway reflexes with a direct instillation of distilled water onto the laryngeal mucosa in humans. Using this experimental method, we studied the characteristics of defensive airway reflexes in lightly anaesthetized patients with multiple system atrophy (MSA). The reflex responses to water stimulation observed in these patients were characterized by apnoea with laryngospasm while the cough reflex was never elicited. Endoscopic images of the larynx in these patients were also characterized by laryngeal oedema. Considering the pathological changes occurring in the central nervous system and the laryngeal mucosa, it is possible that the defensive airway reflexes may be modified by central and/or peripheral mechanisms in patients with MSA.
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PMID:Laryngeal inputs in defensive airway reflexes in humans. 1556 79

Chronic cough is often attributed to reflux, postnasal drip, or asthma. We present 28 patients who had chronic cough or throat-clearing as a manifestation of sensory neuropathy involving the superior or recurrent laryngeal nerve. They had been identified as having sudden-onset cough, laryngospasm, or throat-clearing after viral illness, surgery, or an unknown trigger. Cough and laryngospasm were the most common complaints. Seventy-one percent of the patients had concomitant superior laryngeal nerve or recurrent laryngeal nerve motor neuropathy documented by laryngeal electromyography or videostroboscopy. After a negative workup for reflux, asthma, or postnasal drip, these patients were treated with gabapentin at 100 to 900 mg/d. Symptomatic relief was achieved in 68% of the patients. Sensory neuropathy of the recurrent laryngeal nerve or superior laryngeal nerve should be considered in the workup for chronic cough or larynx irritability. Symptomatic management of patients with cough and laryngospasm due to a suspected sensory neuropathy may include the use of antiseizure medications such as gabapentin.
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PMID:Chronic cough as a sign of laryngeal sensory neuropathy: diagnosis and treatment. 1716 72

When alkalinized lidocaine instead of air is used to fill the endotracheal tube (ETT) cuff, coughing, and bucking are decreased during extubation when ventilation is controlled with N2O. However, sodium bicarbonate (NaHCO3) used to transform lidocaine hydrochloride (L-HCl) to lidocaine base induces a pH increase that could be irritating for mucosa in the case of cuff rupture. Therefore, we determined, in a randomized controlled study with controlled patient ventilation without N2O, whether the smallest concentrations of NaHCO3 (1.4% versus 8.4%) reduced diffusion (in vitro evaluation) and other secondary clinical benefits. After pH determination of different solutions (2 mL of 2% L-HCl and 2 to 6 mL of 8.4%, or 1.4% NaHCO3), an in vitro lidocaine diffusion through the ETT cuffs was evaluated (2 mL of 2% L-HCl and 3 mL of 8.4% or 1.4% NaHCO3). Then, adult patients scheduled for total thyroidectomy surgery were consecutively enrolled (n = 20 for each group). The ETT cuff was filled with air (group air) or with alkalinized lidocaine (2 mL of 2% L-HCl) using 8.4% (group large dose) or 1.4% (group small dose) of NaHCO3. After tracheal extubation, sore throat was evaluated by visual analog scale as the main end-point of the study. Hoarseness, bucking, dysphonia, dysphagia, cough, restlessness, and postoperative nausea and vomiting were also evaluated. There was a slight tendency toward a slower release when a small concentration of NaHCO3 was used (i.e., 1.4%). Compared with group air, the alkalinized-lidocaine groups had a significant reduction in sore throat during the 24-h postoperative period (P < 0.0001). The difference was not significant between the two alkalinized lidocaine groups. This increase in ETT tolerance was confirmed by the analysis of secondary end-points. No laryngospasm, rupture of ETT cuff, or depression of the swallowing reflex were recorded. A decrease in sore throat during the postoperative period was recorded when the cuff was inflated with a small dose of alkalinized lidocaine (i.e., 40 mg of L-HCl and 1.4% of NaHCO3) rather than with air when ventilation was controlled without N2O.
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PMID:Alkalinization of intracuff lidocaine: efficacy and safety. 1624 28

To investigate how sevoflurane modifies airway protective reflexes in anesthetized children, we recruited patients younger than 12-yr-old for our study. Anesthesia was induced with inhaled sevoflurane in oxygen. The airway was managed with a laryngeal mask airway and the patient breathing spontaneously. Depending on the depth of anesthesia, the subjects were divided into two groups: Group 1 and Group 2 (1% and 2% of end-tidal sevoflurane concentration, respectively). Behaviors of the larynx were assessed mainly by the fiberscopic images of the larynx as well as respiratory flow and esophageal pressure. A small dose, 0.02 mL/kg of distilled water (minimum 0.2 mL) was instilled to the larynx through a channel of the scope to evoke an airway protective reflex from the larynx. The responses were categorized into passive (laryngeal closure, laryngospasm, and apnea) and active (cough, expiration reflex, and swallowing reflex) responses. Ten subjects were included in each group. In both groups, the primary responses were passive; however, in Group 1, active reflexes were also observed in 8 of 10 subjects; no subjects in Group 2 had active reflexes (P < 0.01). We concluded that, in children, the depth of general anesthesia with sevoflurane modified airway protective reflexes.
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PMID:Airway protective reflexes evoked by laryngeal instillation of distilled water under sevoflurane general anesthesia in children. 1630 Dec 29

We determine the feasibility of using the intubating laryngeal mask airway Fastrach (ILM) as a ventilatory device during emergence from anesthesia after use as an airway intubator in patients undergoing carotid endarterectomy. Thirty-five patients (ASA 2-3, 53-84 yr) were studied. Induction was with midazolam/fentanyl/etomidate and maintenance was with sevoflurane 1-2% in O2 33-50% and N2O. Neuromuscular blockade was with cisatracurium. Tracheal intubation was with a flexible lightwand via the ILM. After successful intubation, the ILM remained in the pharynx, but with the cuff deflated. After surgery, but before anesthesia was discontinued, baseline cardiovascular variables were recorded. The ILM cuff was then reinflated, the tracheal tube removed, the anesthesia breathing system connected to the ILM and anesthesia discontinued. Any changes in the cardiovascular variables greater than +/- 20% baseline values were noted from cuff reinflation to 1 minute after ILM removal. Any adverse respiratory (laryngospasm, coughing, gagging, stridor, SpO2 <94%, end-tidal carbon dioxide >45 mmHg, regurgitation/aspiration) or electrocardiographic (ST segment or rhythm changes) events were also noted. Patients were questioned about postoperative sore throat at 2 and 24 hr. ILM insertion and intubation through the ILM were successful in all patients. Adequate ventilation was achieved in all patients before intubation and after extubation. The mean (range) time taken from cuff reinflation to ILM removal was 9 (5-21) min. The rate pressure product remained within +/- 20% baseline values in all patients. There were no adverse respiratory or electrocardiographic events. There were no adverse neurological events. The surgical field was satisfactory. Postoperative sore throat occurred in 14% at 2 hr and 0% at 24 hr. We conclude that the ILM can be used as a ventilatory device for emergence from anesthesia after use as an airway intubator for carotid endarterectomy.
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PMID:The intubating laryngeal mask airway Fastrach for emergence after carotid endarterectomy. 1638 Dec 61

Trials of the King LT trade mark (LT, King Systems, Noblesville, IN) in controlled ventilation of the lungs have shown that it is an effective supraglottic airway device. We designed this study to evaluate the King LT regarding ease of insertion, position within the airway, and anatomic sealing properties during spontaneous ventilation in 50 ASA physical status I-III, Mallampati I-III, adult patients undergoing routine general anesthesia. Anesthesia was induced with up to 2 microg/kg fentanyl and 1.5-2 mg/kg propofol and maintained with 70% N2O/30%O2 and isoflurane. Insertion time, oropharyngeal leak pressures, fiberoptic position, and spirometry and hemodynamic data were recorded. Any complications were noted. Insertion was determined to be easy and a patent airway was achieved in all patients. First, second, and third attempt insertion rates were 86%, 12%, and 2%, respectively. Time to place the King LT trade mark was <5 s in 90% of cases. Baseline leak pressures were 31 +/- 8.8 cm H2O (17-50 cm H2O). Complications included laryngospasm (1) and coughing (3) on extubation. The incidence of sore throat at 1 h and 24 h postoperatively was 22% and 15%, respectively. The King LT trade mark is a simple and reliable supraglottic airway device for airway management during spontaneous ventilation.
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PMID:An evaluation of the insertion and function of a new supraglottic airway device, the King LT, during spontaneous ventilation. 1642 73

Laryngospasm is a clinical symptom characterized by involuntary spasms of the laryngeal muscles, which leads to paroxysms of coughing, inspiratory stridor, and sometimes to episodes of complete upper-airway occlusion. Although laryngospasm is a symptom mainly seen in otolaryngeal diseases and in the context of anesthesiological complications, it also occurs in neurological disorders. In this review of the occurrence of laryngospasms in neurological diseases, the clinical symptomatology, additional circumstances, possible underlying causes, and therapeutic options are presented.
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PMID:Laryngospasm in neurological diseases. 1662 8


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