Cough (London, England)最新文献

Background: Obstructive sleep apnoea (OSA) has recently been identified as a possible aetiology for chronic cough. The aim of this study was to compare the incidence of chronic cough between patients with and without OSA and the impact of continuous positive airway pressure (CPAP) treatment in resolving chronic cough.

Methods: Patients referred to the sleep laboratory from January 2012 to June 2012 were retrospectively enrolled. Clinical data, treatment course and resolution of chronic cough were analysed. Specifically, gastro-oesophageal reflux (GERD), upper airway cough syndrome, asthma, apnoea-hypopnoea index and the impact of CPAP treatment on chronic cough were assessed.

Results: A total of 131 patients were reviewed. The incidence of chronic cough in the OSA group was significantly higher than the non-OSA group (39/99 (39.4%) vs. 4/32 (12.5%), p = 0.005). Both GERD and apnoea-hypopnoea index were significantly associated with chronic cough in univariate analysis. After multivariate logistic regression, GERD was the only independent factor for chronic cough. Moreover, the resolution of chronic cough was more significant in the OSA patients with CPAP treatment compared with those not receiving CPAP treatment (12/18 (66.7%) vs. 2/21 (9.5%), p = 0.010).

Conclusion: The incidence of chronic cough was significantly higher in the OSA patients. In addition, CPAP treatment significantly improved chronic cough. Therefore, OSA may be a contributory factor to chronic cough.

Altitude-related cough is a troublesome condition of uncertain aetiology that affects many visitors to high altitude. The traditionally held belief that it was due solely to the inspiration of cold, dry air was refuted by observations and experiments in long duration hypobaric chamber studies. It is likely that altitude-related cough is a symptom of a number of possible perturbations in the cough reflex arc that may exist independently or together. These include loss of water from the respiratory tract; respiratory tract infections and sub-clinical high altitude pulmonary oedema. The published work on altitude-related cough is reviewed and possible aetiologies for the condition are discussed.

Background: Non-pharmacological options for symptomatic management of cough are desired. Although chest wall mechanical vibration is known to ameliorate cough reflex sensitivity, the effect of mechanical vibrations on perceptions of urge-to-cough has not been studied. Therefore, we investigated the effect of mechanical vibration of cervical trachea, chest wall and femoral muscle on cough reflex sensitivity, perceptions of urge-to-cough as well as dyspnea.

Methods: Twenty-four healthy male never-smokers were investigated for cough reflex sensitivity, perceptions of the urge-to-cough and dyspnea with or without mechanical vibration. Cough reflex sensitivity and urge-to-cough were evaluated by the inhalation of citric acid. The perception of dyspnea was evaluated by Borg scores during applications of external inspiratory resistive loads. Mechanical vibration was applied by placing a vibrating tuning fork on the skin surface of cervical trachea, chest wall and femoral muscle.

Results: Cervical trachea vibration significantly increased cough reflex threshold, as expressed by the lowest concentration of citric acid that elicited five or more coughs (C5), and urge-to-cough threshold, as expressed by the lowest concentration of citric acid that elicited urge-to-cough (Cu), but did not significantly affect dypnea sensation during inspiratory resistive loading. On the other hand, the chest wall vibration not only significantly increased C5 and Cu but also significantly ameliorated the load-response curve of dyspnea sensation.

Conclusions: Both cervical and trachea vibrations significantly inhibited cough reflex sensitivity and perception of urge-to-cough. These vibration techniques might be options for symptomatic cough management.

Various diseases often result in decompensation requiring resuscitation. In infants moderate hypoxia evokes a compensatory augmented breath - sigh and more severe hypoxia results in a solitary gasp. Progressive asphyxia provokes gasping respiration saving the healthy infant - autoresuscitation by gasping. A neonate with sudden infant death syndrome, however, usually will not survive. Our systematic research in animals indicated that airway reflexes have similar resuscitation potential as gasping respiration. Nasopharyngeal stimulation in cats and most mammals evokes the aspiration reflex, characterized by spasmodic inspiration followed by passive expiration. On the contrary, expiration reflex from the larynx, or cough reflex from the pharynx and lower airways manifest by a forced expiration, which in cough is preceded by deep inspiration. These reflexes of distinct character activate the brainstem rhythm generators for inspiration and expiration strongly, but differently. They secondarily modulate the control mechanisms of various vital functions of the organism. During severe asphyxia the progressive respiratory insufficiency may induce a life-threatening cardio-respiratory failure. The sniff- and gasp-like aspiration reflex and similar spasmodic inspirations, accompanied by strong sympatho-adrenergic activation, can interrupt a severe asphyxia and reverse the developing dangerous cardiovascular and vasomotor dysfunctions, threatening with imminent loss of consciousness and death. During progressive asphyxia the reversal of gradually developing bradycardia and excessive hypotension by airway reflexes starts with reflex tachycardia and vasoconstriction, resulting in prompt hypertensive reaction, followed by renewal of cortical activity and gradual normalization of breathing. A combination of the aspiration reflex supporting venous return and the expiration or cough reflex increasing the cerebral perfusion by strong expirations, provides a powerful resuscitation and autoresuscitation potential, proved in animal experiments. They represent a simple but unique model tested in animal experiments.

Objective: Fentanyl-induced cough is usually mild and transitory, but it can be undesirable in patients with increased intracranial pressure, open wounds of the eye, dissecting aortic aneurism, pneumothorax, and reactive airway disease. The aim of this study is to evaluate the efficacy of lidocaine in suppressing fentanyl-induced cough in children during induction in general anesthesia.

Methods: One hundred and eighty-six children of both sexes, aged between 4-10 years, ASA physical status I and II, and scheduled for elective surgery, were recruited for the study. Patients with a history of bronchial asthma, obstructive pulmonary disease, or infections of the respiratory tract were excluded. Patients were randomly allocated to three equal groups (n = 62) to receive 1.0 mg/kg lidocaine (Group I), 0.5 mg/kg lidocaine (Group II), or placebo (equal volume of 0.9% saline; Group III). Each was administered over 5 s one minute before intravenous (IV) administration of fentanyl 2-3 μg/kg during induction in general anesthesia. The severity of coughing was graded by counting the number of episodes of cough: mild (1-2), moderate (3-4) or severe (5 or more).

Results: Demographic information was comparable between groups. The most frequent coughing was observed in the placebo group (Group III; 43.5%), of whom 4.8% (three patients) were graded with severe cough. In Group II, 22.6% patients had cough, of which 1.6% (one patient) was graded as severe. In Group I, 16.1% patients had cough, none of whom were graded as severe.

Conclusion: Our results demonstrate that IV lidocaine can markedly suppress fentanyl-induced cough in children, even in doses as low as 0.5 mg/kg.

Background: Chronic cough patients are rendered therapies for gastro-esophageal reflux (GERD), upper airway cough syndrome (UACS) and cough-variant asthma (CVA) with varying benefit. Idiopathic or unexplained cough has emerged as an important clinical entity in both primary care and subspecialty clinics. Recent evidence points to a link between chronic cough and untreated obstructive sleep apnea (OSA).

Methods: A prospective observational study was done to evaluate the effect of OSA therapy in patients with chronic cough. Patients enrolled into the study underwent questionnaires to evaluate for GERD, UACS and CVA along with screening questionnaires for OSA and daytime sleepiness. The Leicester cough questionnaire (LCQ) was done at baseline and during serial visits to evaluate cough intensity and was used as the primary outcome measure of the effect of CPAP therapy on chronic cough.

Results: Out of 37 patients enrolled into the study, only 28 patients had follow up LCQ scores available and therefore underwent analysis. 22/28 patients were suspected to have OSA based on abnormal STOP-BANG screening questionnaire scores and overnight oximetry abnormalities. Of these 19/28 patients had overnight attended polysomnography with definitive diagnosis of OSA yielding a 68% prevalence of OSA in our chronic cough population. Chronic cough patients treated for OSA tended to be older with a significantly higher BMI than chronic cough patients without OSA. Significant improvement of LCQ scores occurred with CPAP therapy for OSA in chronic cough patients.

Conclusion: OSA is significantly prevalent in chronic cough patients. Subjects with chronic cough and OSA tend to be older and obese. Treatment of OSA in chronic cough patients yields significant improvement in their health status.

Cough is one of the most common complaints for which patients seek medical attention. Misdiagnosis and mistreatment of cough exist commonly in China. The prevalence of acute cough caused by upper airway infection fluctuates between 9% and 64% in the community, for chronic cough, the prevalence >10% in most surveys, ranging from 7.2%-33%. The common causes of chronic cough are upper airway cough syndrome (previously called as post nasal drip syndrome [PNDS]), cough variant asthma (CVA), gastroesophageal reflux related cough (GERD) and eosinophilic bronchitis (EB). There is a regional discrepancy regarding the prevalence of common causes of cough and distribution of gender among China, UK, USA, the most common cause of chronic cough in China are CVA, followed by UACS, EB and atopic cough (AC), the male is almost equal to female in numbers in China. The risk factors for cough includes cold air, smoking, environmental pollutants, noxious substances and allergens, and unreasonable diet habits.

Over the last 40 years the assessment and treatment of chronic obstructive pulmonary disease has focused primarily on airflow obstruction with little significance given to the problem of cough. The reasons for this include a view that cough arises simply from the direct irritant and inflammatory effect of cigarette smoke or the presence of excess mucus in the airways. Doubt that cough is of any consequence to patients or responsive to current therapies has reinforced this opinion. At odds with this is the emerging evidence that cough impacts adversely on patients' health status and forms an important component of recently validated quality of life instruments. This article presents the arguments why the assessment and treatment of cough should have a more prominent place in the clinical management of COPD.

About 40% of the population will experience chronic cough at some point during their lives and it tends to be more common in women (Thorax 58:901-7, 2003). Post-nasal drip (or upper airway cough syndrome), gastro-esophageal reflux disease and asthma are considered the most common causes. Yet only a small percentage of patients with these common conditions experience chronic cough. Also there is no agreed measure of post-nasal drip and controversy exists about the diagnosis of reflux above the upper esophageal sphincter (laryngopharyngeal reflux) based on observable changes to the larynx. The approach of the otolaryngologist is to consider the upper and lower airways as a continuum and that a common pathology can have an impact on all these anatomical sites.A multidisciplinary approach is advocated, utilising the skills of the respiratory physician, otolaryngologist, gastroenterologist and speech pathologist.

Background: Many patients with chronic cough respond to treatment with inhaled corticosteroids but it is difficult to predict which patients are likely to respond. The primary aim of the present study was to define the capability of hypertonic saline cough provocation test to predict the responsiveness to inhaled corticosteroids in chronic cough. The secondary aim was to assess the ability of the saline test to monitor the healing of cough during corticosteroid treatment.

Methods: Forty-three patients with chronic cough were recruited. Before therapy, spirometry, ambulatory peak flow monitoring, nitric oxide measurement, histamine airway challenge, and saline test were performed. Those responding to the first saline test repeated it and the nitric oxide measurement during the subsequent visits. The patients used inhaled budesonide, 400 ug twice daily, for twelve weeks. The treatment response was assessed by Leicester Cough Questionnaire at baseline, and at one, four, and twelve weeks.

Results: Seventy-seven % of the patients demonstrated the minimal important difference in the Leicester Cough Questionnaire indicating a symptomatic response. Neither the response magnitude nor the speed was predicted by the saline test. Histamine challenge showed the strongest predictive ability: The maximal improvement in Leicester Cough Questionnaire total score was 5.08 (3.76 - 6.40) points in the histamine positive and 2.78 (1.55 - 4.01) points in the histamine negative subjects (p = 0.006). Baseline nitric oxide level also associated with the improvement in Leicester Cough Questionnaire total score (p = 0.02). During the treatment, the cough sensitivity to saline gradually decreased among the budesonide responders but not in the non-responders. Nitric oxide levels decreased very rapidly among the responders.

Conclusions: Saline test cannot predict the responsiveness to inhaled corticosteroids in chronic cough but it may be utilized to monitor the effect of this treatment.

Trial registration: The study was registered in ClinicalTrials.gov database (KUH5801112). ClinicalTrials.gov Identifier: NCT00859274.