Objective To analyze the causes of missed diagnosis of sleep apnea hypopnea syndrome ( SAHS) . Methods 42 missed diagnosed cases with SAHS from May 2009 to May 2011 were retrospectively analyzed and related literatures were reviewed. Results The SAHS patients often visited the doctors for complications of SAHS such as hypertension, diabetes mellitus, metabolic syndrome, etc. Clinical misdiagnosis rate was very high. Lack of specific symptoms during the day, complicated morbidities, and insufficient knowledge of SAHS led to the high misdiagnosis rate and the poor treatment effect of patients with SAHS. Conclusion Strengthening the educational propaganda of SAHS, detail medical history collection, and polysomnography monitoring ( PSG) as early as possible can help diagnose SAHS more accurately and reduce missed diagnosis.
ObjectiveTo investigate the diagnostic value of oximetry in sleep apnea hypopnea syndrome (SAHS). MethodsAdult patients suspected for SAHS were enrolled between May 2010 and May 2013. The patients underwent both polysomnography (PSG) and oximetry for further diagnosis. Apnea hyponea index (AHI) and oxygen desaturation index four (ODI4) were calculated on a single night. The relationship between AHI and ODI4 were analyzed. ResultsA total of 628 adult patients were recruited.ODI4 was linearly correlated with AHI with a regression coefficient of almost 1. The cut-off values of ODI4 for indentifing SAHS and moderate to severe SAHS were 10 events per hour and 20 events per hour, with specificities of 99.9% and 99.3%, and AUCs of 0.931 and 0.934, respectively. Female, lower weight and less severe SAHS patients were easily misdiagnosed. ConclusionsThere is a high agreement between AHI and ODI4. Oximetry is less likely misdiagnose SAHS.
ObjectiveTo investigate the effects of smoking combined with intermittent hypoxia on the pathophysiology of lung tissue and thoracic aorta, and the endothelial injury.MethodsTwenty-four rats (SPF, female, six weeks old) were divided randomly into 4 groups (n=6). The control group was given false smoking and normal oxygen exposure, the smoking-exposed group was exposed in smoking, the intermittent hypoxia group was exposed in intermittent hypoxia environment, and the overlap group was exposed to smoking and intermittent hypoxia. After 8 weeks, body weight, right ventricular hypertrophy index (RVHI), the pathological changes of lung tissue and thoracic aorta were measured, and the level of endothelin-1 (ET-1), endothelial nitric oxide synthase (eNOS), vascular endothelial growth factor (VEGF) and stromal cell-derived factor-1α (SDF-1α) in serum of rats were evaluated.ResultsRVHI of rats in the smoking-exposed group, intermittent hypoxia group, overlap group were higher than that in the control group. In addition, RVHI in the overlap group was higher than that in the smoking-exposed group, intermittent hypoxia group (all P<0.05). The levels of ET-1, VEGF and SDF-1α in the serum of the smoking-exposed group, intermittent hypoxia group and overlap group were higher than those in the control group, while the level of eNOS was lower than that in the control group, (all P<0.05), the most significant difference was between control group and the overlap group. Pathological observation of lung tissue and thoracic aorta showed obvious emphysema in the smoking-exposed group and overlap group, which was more obvious in the overlap group than that in the smoking-exposed group (all P<0.05). Lung interstitial inflammatory infiltration, bronchial wall lymphocyte hyperplasia and pulmonary fibrosis were shown in different degrees in the smoking-exposed group, intermittent hypoxia group and overlap group, and the pulmonary arteriole wall showed thickening, fibrosis and peripheral inflammatory infiltration also were found in these groups. Thoracic aorta in the smoking-exposed group, intermittent hypoxia group and overlap group showed different degrees of endothelial cell injury, middle membrane thickening, and collagen fiber hyperplasia. The pathological features of the overlap group were most obvious compared to the other two groups.ConclusionsSmoking and intermittent hypoxia exposure can lead to different degrees of lung tissue and vascular endothelial injury and decrease of vascular endothelial protective factors in rats, resulting in dysfunction of vascular endothelial cells, which leads to the structural remodeling of pulmonary arterioles and aorta, such as thickening, fibrosis, etc. Combined smoking and intermittent hypoxia exposure can lead to more serious pathological damage.