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| #83 |
| "Gastric Reflux" |
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A few papers publications have reported patients with obstructive sleep apnea to often have gastroesophageal reflux (GER)--the irritant flow of acid stomach contents back into the esophagus. In one study, this was present in 5 of 6 OSA patients. Another study found that CPAP treatment reduced this reflux. Like OSA, GER is associated with obesity. GER may cause symptoms similar to OSA--nocturnal choking and arousals. GER may also aggravate OSA by causing inflammation and swelling of the airway. At the same time, OSA may trigger GER, because the increased negative pressures in the chest, generated by the effort to breathe in against obstruction, results in a relatively greater pressure upwards from the abdomen, across the diaphragm. Also, the arousals and decreased sleep efficiency associated with OSA may trigger relaxation of the lower esophageal sphincter muscle that closes off the stomach from the esophagus, promoting reflux in this way as well. The occurrence of GER can be detected by monitoring the pH--degree of acidity--in the esophagus. The studies reported here attempted to determine the prevalence of GER in a group of patients with OSA, compared with a group of matched controls. They also looked at at the relationship in time between GER events, apneic events, and arousals. Furthermore, they undertook two treatment studies to further investigate a possible causal relationship between OSA and GER, by seeing whether treatment of OSA affected GER and vice versa. The authors studied 63 patients with OSA and compared them with 41 control subjects of similar age A(64 vs. 61 years), body mass indices (BMI; 31 vs. 30), waking pulmonary function, and extent of alcohol use. OSA patients had Apnea Hypopnea Indices (AHI) averaging 43/hr, indicating moderately severe sleep apnea, significantly higher than the AHIs of controls (3/hr). Note that they required a minimum AHI of 15/hr to include a subject in the OSA group, whereas controls were required to have AHI les than 5/hr. Even though controls showed a relatively high frequency of GER episodes (over 20/night), predictable on the basis of their age, weight, and alcohol intake, OSA patients had significantly more reflux events (110/night). Also, OSA patients spent more time of the night (about 22%) with an abnormally acidic esophageal pH, and had longer episodes of GER. Half of all reflux episodes showed no relationship in time to episodes of apnea or hypopnea, but 11% occurred within a minute after a respiratory event, 30% preceded respiratory events by a minute or less, and 12% occurred simultaneously with a respiratory event. Conversely, half of respiratory events showed no relationship in time to reflux events, but 28% followed immediately after a reflux, 10% immediately preceded a reflux, and 8% occurred simultaneously with a reflux event. Likewise, half of all arousals proved unrelated to reflux events, but 25% followed immediately after reflux and 13% occurred simultaneously with reflux. Repeat studies, on CPAP, were conducted in 14 patients who had both OSA and GER, while repeat studies also done with CPAP were conducted with 8 controls who had GER without OSA. Among the OSA patients, in whom CPAP effectively reduced AHIs, arousals, and oxygen desaturations, it also reduced all three measures of GER. Among the controls, CPAP also reduced GER. Twelve patients with both GER and OSA then received treatment with either nizatidine (an over-the-counter antihistamine for GER) or inactive placebos for one month. Compared to both pre-treatment measures and the placebo group, nizatidine reduced reflux. Nizatidine also reduced arousals, though it had no effect on AHI or minimum oxygen saturation. Placebo had no effect. The authors concluded that reflux events were related to half of all arousals and all apneas in OSA patients. Since CPAP reduced reflux events in both OSA patients and controls, they concluded that the effect of CPAP on GER was nonspecific, unrelated to its effects on apnea per se, but possibly related to its effect on reducing the pressure differential between thorax and abdomen (transdiaphragmatic pressure). From the beneficial effects of nizatidine on both GER and apnea measures, they suggested that GER may contribute to arousals and therefore excessive daytime sleepiness in patients with OSA, though they acknowledged this finding to be equivocal and in need of confirmation with larger, better-matched groups, and other anti-reflux drugs.
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I found this study eye-opening. Even though the treatment substudies used very small sample sizes, the combined effect of the multiple ways the authors examined the issue impressed me, and helped convince me of the reality of this relationship between OSA, GER, and arousals. Note particularly that this study comes early in the course of research on the subject, citing only three prior publications. Certainly it came as a surprise to me. As I often point out, multiple factors may contribute to sleep disruption, most classically in the frequent co-occurrence of OSA and Periodic Leg Movements of Sleep. However, one can think of many other factors disruptive of sleep that may add to the adverse effects of OSA, and more importantly, prevent complete resolution of symptoms with treatment. In this case, we appear fortunate in that CPAP improves both OSA and GER. I am also impressed with the magnitude of the frequency of GER and its effect on sleep, comparable to that of OSA itself. Also of great interest is the speculation that cause and effect may proceed in both directions, that is, OSA leading to GER, and GER aggravating OSA. I recall that some people have written to me complaining of gastric symptoms, often considered as independent of OSA, but now apparently much more closely related. So it seems that we must add yet another to the myriad of "complications" and "complicating factors" associated with OSA!
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