Snorers and apnea patients show upper airway sensory impairment
Canadian investigators found that snorers and individuals with obstructive sleep apnea (OSA) demonstrated upper airway sensory impairment, revealing a problem which could predispose them to upper airway obstruction during sleep. The researchers tested 37 patients with OSA, 12 non-apneic snorers, and 15 control patients using a two-point probe and a vibratory threshold test on the lip, hand, and margin of the soft palate of each person. The sensory values for the two- point probe and vibratory sensation test were essentially the same for the OSA patients, the snorers, and the control patients. However, the levels for the soft palate test showed significantly reduced sensory ability in the upper airways of the OSA patients and snorers. The investigators concluded that their findings demonstrated the presence of selective impairment in the upper airway mucosa sensory function in patients who either have OSA or who are snorers. Interference with sensory function in the mucous membrane increases the tendency toward airway collapse, causing obstructive breathing episodes such as apneas. The researchers also found evidence of partial reversibility of the sensory changes after OSA patients were treated with continuous positive airway pressure. This approach utilizes a mask worn by the OSA sufferers during sleep that delivers a mixture of air and oxygen through the nose. The study appears in the second of two July issues of the American Thoracic Society’s peer-reviewed American Journal of Respiratory and Critical Care Medicine.
Editoral by expert claims motor neuron lesions could cause airway collapse
In an editorial in the second issue for July of the American Thoracic Society’s peer-reviewed American Journal of Respiratory and Critical Care Medicine, an expert postulates that the sensory dysfunction found in the airways of the OSA patients studied by the Canadian investigators could be caused by motor neuron lesions. Such lesions could produce partial paralysis of the dilating muscles of the upper airway. She believes that vibrations from heavy snoring night after night could cause neuronal lesions in the upper airway. These lesions, in turn, could produce a gradual collapse of the airway due to muscular weakness and/or impaired reflex mechanisms. When an individual breathes in, the patency--or openness--of the upper airway is maintained by dilating muscles. These are activated by a reflex mechanism resulting from negative intrapharyngeal pressure in the airway. She believes additional studies support the hypothesis that upper airway lesions are present in some snorers and in most patients with OSA. She adds that the Canadian investigators have shown the patient’s neuronal dysfunction can be partially reversed by treatment with continuous positive airway pressure. She would like to see these studies replicated in habitual snorers or persons with mild sleep apnea. Since these types of cases usually develop full-blown OSA later, further positive results might serve as an argument for early preventive therapy.
Low-tidal volume mechanical ventilation produces benefits to all acute respiratory distress syndrome clinical subgroups
Since low-tidal volume ventilation has been shown to reduce mortality by 22 percent in critically ill patients when compared with regular mechanical ventilation, a second study examining the data reveals that it works equally well across all risk factor subgroups associated with acute respiratory distress syndrome (ARDS) and acute lung injury (ALI). The risk factor subgroups included patients who had pneumonia, sepsis, aspiration pneumonitis, trauma, and other clinical problems including those associated with drug overdose, multiple transfusion, and cardiopulmonary bypass. (ARDS, a serious medical emergency usually requiring critical care, results from many disorders that cause pulmonary edema or fluid in the lungs.) Research found no evidence in 473 critically ill patients that the efficacy of low tidal volume ventilation differed among the clinical risk factor subgroups. The clinical benefits occurred in spite of the fact that substantial variation in mortality risk existed in the groups, with sepsis associated with the greatest risk of death (43 percent) and trauma the least (11 percent). There was no evidence that the efficacy of this ventilation strategy varied by clinical risk group for mortality, proportion of patients achieving unassisted breathing, ventilation-free days, or incidence of nonpulmonary organ failure, according to the authors. The article appears in the second issue for July of the American Thoracic Society’s peer-reviewed American Journal of Respiratory and Critical Care Medicine.
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Journal
American Journal of Respiratory and Critical Care Medicine