Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Predicting outcome following uvulopalatopharyngoplasty (UPPP) in obstructive sleep apnea is difficult. We hypothesized that UPPP is effective in obstructive sleep apnea patients with severe tonsillar hypertrophy. We examined the relationship between the severity of pre-operative tonsillar hypertrophy and the effect of UPPP in 38 patients with obstructive sleep apnea (oxygen desaturation index (ODI) > or = 20). The patients were classified into three groups according to the Mackenzie Classification of tonsillar hypertrophy. Ten patients were classified as grade 1 (M1) hypertrophy, i.e. tonsils just visible beyond the palatal arch. Five patients had grade 3 (M3) hypertrophy, i.e. tonsils appearing to contact each other at the midline. The remaining 23 patients had grade 2 (M2) hypertrophy, i.e. intermediate enlargement. We measured the apnea index, ODI, DST 90, and DST 85 (%time with SaO2 < or = 90% and < or = 85%, respectively) using a screening device for sleep apnea (Apnomonitor II, CHEST M. I. Co. Tokyo, Japan) before and after UPPP. Following UPPP, the mean ODI decreased significantly in all groups: 59 to 9/hr (p < 0.005) in the M3 group, 53 to 27/hr (p < 0.001) in the M2 group, and 48 to 33/hr (p < 0.05) in the M1 group. Post-UPPP ODI decreased by 83% in M3, 45% in M2, and 28% in M1 patients. Successful UPPP, defined by a post-UPPP ODI of less than 20/hr and a greater than 50% decrease in post-UPPP ODI, occurred in 80% of M3, 43% of M2, and 10% of M1 patients. We conclude that tonsillar hypertrophy can predict a successful response to UPPP in obstructive sleep apnea patients.
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PMID:[Effects of uvulopalatopharyngoplasty on patients with obstructive sleep apnea--the severity of preoperative tonsillar hypertrophy]. 961 74

We investigated the clinical usefulness of continuous nocturnal oxygen saturation monitoring in patients undergoing home oxygen therapy (HOT). The subjects were 11 patients with chronic respiratory disease in the process of healing from acute exacerbation. None were mechanically ventilated. Each subject underwent full overnight oximetry. One patient was excluded from further investigation because of periodic desaturation suggestive of sleep apnea. The remaining 10 subjects included 5 patients with sequelae of pulmonary tuberculosis, 2 with diffuse panbronchiolitis, 1 with chronic pulmonary emphysema, 1 with chronic bronchitis, and 1 with kyphoscoliosis. All underwent full overnight and 30 min daytime oximetry monitoring for 23.7 +/- 7.4 (mean +/- SD) consecutive days. Daytime oximetry was performed when subjects were awake and resting in supine position. Mean nocturnal oxygen saturation (NmSpO2) and mean daytime oxygen saturation (DmSpO2) were calculated from data obtained from 0:00 through 5:00 hrs and from data obtained during a stable 10 min daytime period, respectively. The difference between NmSpO2 and DmSpO2 (delta SpO2), the percentage of total sleep time with SpO2 < or = 90% (DST 90) and nocturnal lowest oxygen saturation (NLSpO2) were calculated once daily for each subject. There were significant (p < 0.05) correlations between NmSpO2 and NLSpO2, between NmSpO2 and DST 90, and between NLSpO2 and DST 90 in all subjects. However, significant (p < 0.05) correlations between NmSpO2 and DmSpO2 were observed in only 6. During acute exacerbation, NmSpO2 was lower than DmSpO2, and delta SpO2 increased. Conversely, with the amelioration of acute symptoms, delta SpO2 decreased and NmSpO2 was higher than DmSpO2. There was a significant (p < 0.05) reverse correlation between NmSpO2 and delta SpO2 in 9 subjects. We concluded that monitoring nocturnal oxygen saturation is clinically useful to assessments of oxygenation status in patients undergoing HOT, and that it may assist the early diagnosis of acute exacerbation of respiratory failure.
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PMID:[Continuous oximetry monitoring in patients undergoing home oxygen therapy for chronic respiratory failure]. 1054 Aug 34

We investigated nocturnal oxygen desaturation (NOD) in 36 patients with stable chronic respiratory disease who were receiving home oxygen, therapy (HOT). Study data included medical history, chest roentgenograms, measurement of daytime arterial blood gases while awake, and spirometry. Each subject underwent full overnight oximetry monitoring. Three patients were excluded from further investigation because of periodic desaturation suggestive of sleep apnea. The remaining 33 subjects were divided into two groups: 21 patients with sequelae of pulmonary tuberculosis (TB-sequela) and 12 patients with chronic obstructive pulmonary disease (COPD). The COPD group was divided into two subgroups according to the Burrows classification (Am Rev Resp Dis. 90: 14-27, 1964): 5 patients with type A (Type A) and 7 patients with type B (Type B) COPD. The percentages of total sleep time with SaO2 < or = 85% (DST 85) and SaO2 < or = 90% (DST 90) were calculated for each subject. NOD was defined as DST 85 > or = 1%. Arterial oxygen partial pressure (PaO2) while awake was > or = 60 Torr in all subjects. No difference was observed in mean awake PaO2 values between the TB-sequela and COPD groups. NOD was detected in 8 TB-sequela patients but in none of the COPD patients. Mean DST 85 and DST 90 values were significantly (p < 0.05) higher for the TB-sequela group than for the COPD group. Of 15 TB-sequela patients who were able to complete spirometry tests, 6 had NOD. All 6 of these patients had hypercapnia while awake (PaCO2 > or = 50 Torr) and reduced vital capacity (< or = 50% predicted). No difference was observed in mean DST 90 or DST 85 values between the TypeA and TypeB COPD subgroups. We conclude that NOD is common in patients with chronic stable respiratory disease treated with HOT despite daytime euoxia. TB-sequela patients with hypercapnia and restrictive ventilatory impairment are at high risk for NOD.
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PMID:[Nocturnal oxygen desaturation during home oxygen therapy in patients with chronic respiratory disease]. 1072 46