Nocturnal GER is relatively common. One population survey reported that approximately 10% of all responders reported troublesome symptoms of nighttime reflux (39). A Gallup poll reported that 79% of all people with heartburn had symptoms at night, and approximately 75% of these felt that heartburn impaired their sleep (40). Despite medical therapy, only half of all heartburn patients felt they had adequate control of night-time symptoms. Finally, in an analysis of 15,314 subjects surveyed as part of the Sleep Heart Health Study, 24.9% reported heartburn during sleep (41).
Sleep is associated with physiologic changes that can affect GER. The lower esophageal sphincter (LES) is the main barrier against GER. The LES appropriately relaxes during normal swallowing, but transient LES relaxation can also occur without swallowing, which accounts for the vast majority of GER episodes. Transient LES relaxations typically occur at night during wakefulness and after brief arousals from sleep. Sleep produces other physiologic changes that may enhance the impact of GER. For example, swallowed saliva neutralizes acid, but production of saliva normally ceases during sleep. Swallowing itself is also markedly reduced, if not absent, during continuous sleep, and swallowing episodes typically occur only after arousal from sleep. These physiologic changes impair esophageal acid clearance. More prolonged episodes of GER during the night also promote acid migration to more proximal regions of the esophagus.
Symptoms of nocturnal GER include disrupted sleep, chest discomfort, subster-nal burning, heartburn, and indigestion. With more proximal migration of esophageal acid, patients are more likely to awaken with a sour taste, coughing, and even choking. Nocturnal GER is best diagnosed via esophageal pH monitoring, with an esophageal pH probe positioned in the distal esophagus approximately 5 cm above the LES. Episodes of GER can thereby be defined by decreases in esophageal pH to less than four. Such studies are typically performed in the ambulatory setting, allowing 18 to 24 hours of continuous esophageal pH monitoring. Esophageal pH probes can also be utilized during standard polysomnography, allowing for the assessment of GER in relation to sleep disruption and obstructive apneas/hypopneas.
Nocturnal GER has been associated with other respiratory disorders at night, including OSA and asthma. OSA causes physiologic changes during sleep that promote GER, including frequent arousals and awakenings from sleep, plus increasingly negative intrathoracic pressure during discreet obstructive apneas/hypop-neas. In addition, obesity is a common condition that is associated with both GER and OSA. Green et al. (42) prospectively evaluated 331 patients with diagnosed OSA. Significant nocturnal GER was detected in 62% of all patients at baseline. Subsequent CPAP therapy reduced nocturnal GER symptoms by 48% in CPAP adherent patients, but no change in GER symptoms occurred in CPAP nonadherent patients. This suggests that nocturnal GER is common in OSA patients, and that effective therapy with CPAP can reduce the frequency and severity of nocturnal GER episodes. The potential importance of diagnosing and treating GER in OSA patients is underscored by observations in 29 OSA patients that laryngeal inflammation correlated strongly with OSA severity (43).
There has also been extensive interest in the potential relationship between nocturnal GER and nocturnal worsening of asthma. Jack et al. (44) monitored both tracheal and esophageal pH in four asthmatic patients with a history of recurrent nocturnal worsening and GER symptoms. Thirty-seven episodes of GER were identified, of which five were also associated with a fall in tracheal pH, suggesting aspiration. The episodes of tracheal acidity were associated with more prolonged GER episodes, awakenings from sleep, and indications of bronchospasm.
Although aspiration of acidic reflux is clearly a potent trigger of bronchocon-striction, GER may not have to result in aspiration to trigger increased bronchomotor tone. Afferent vagal fibers are located in the distal esophagus, where they can be stimulated by exposure to acid reflux, leading to a reflex-induced increase in bron-chomotor tone. Cuttitta et al. (45) monitored esophageal pH and lower respiratory resistance in seven asthmatics with a history of recurrent GER. They observed that GER episodes were associated with increased lower respiratory resistance, and that duration of esophageal acid exposure was an important predictor of an increase in lower respiratory resistance. However, Tan et al. (46) utilized virtually identical techniques, but were unable to demonstrate increases in lower respiratory resistance in response to either spontaneous episodes of GER or esophageal perfusion with acid.
In view of these discrepancies, there remains some uncertainty as to whether effective treatment of nocturnal GER can improve asthma severity. Several uncontrolled studies have demonstrated improvement in asthma after aggressive GER therapy. However, a systematic review of previous studies addressing this issue concluded that there is insufficient evidence that treatment of GER improves asthma in the general asthmatic population (47). It remains common practice to assess the clinical benefit from a three-month therapeutic trial with antireflux agents for individual patients with symptoms of both nocturnal GER and nocturnal worsening of asthma.
Both behavioral and pharmacologic interventions are typically employed to treat nocturnal GER. Patients should avoid eating at least two hours before bedtime, and should avoid high-fat content foods, caffeine, alcohol, chocolate, mint, citrus fruits, and caffeinated sodas, all of which may promote GER. Nicotine may decrease LES pressure, and patients should obviously be counseled to stop smoking. Obesity is associated with increased risk for GER, and obese patients should always be encouraged to lose weight via a combination of diet and exercise. Patients can be advised to sleep with the head of their bed elevated at least six inches, which can be achieved by placing blocks under the head of the bed. Evaluation of each patient's medical regimen is warranted, as many medications promote GER, including theophylline, calcium channel blockers, prostaglandins, and bisphosphonates.
Pharmacologic management of nocturnal GER typically includes antacids for immediate symptom relief, histamine H2 receptor antagonists, proton pump inhibitors, and esophageal motility agents. Once the mainstay of GER therapy, H2 receptor antagonists still provide symptomatic relief for 60% of treated patients, and can be dosed once daily at bedtime. However, proton pump inhibitors appear to provide superior suppression of gastric acid (48). GER therapy now commonly includes the bedtime administration of a proton pump inhibitor, such as omeprazole.
Esophageal motility agents, such as metoclopramide, may be considered in patients who remain refractory to H2 receptor antagonists and proton pump inhibitors. However, these agents have a high risk for side effects, limiting their utility. In those patients who remain refractory to all medical management, esophageal fundoplication surgery can be performed using laparoscopic methods. This procedure is often quite successful, yielding GER symptom control in 80% to 90% of treated patients.
Was this article helpful?