The effect of torso elevation on minimum effective continuous positive airway pressure for treatment of obstructive sleep apnea.

BACKGROUND: Continuous positive airway pressure (CPAP) is considered the gold standard treatment of obstructive sleep apnea (OSA). However, it can be a challenge in some patients to find an effective CPAP setting that is well tolerated. A lower CPAP setting may improve patient tolerance of the treatment. The objective of this study was to evaluate the effect of approximately 30° torso elevation on minimum effective CPAP for the treatment of OSA. METHODS: A retrospective chart review was performed to determine the effective CPAP setting required to treat OSA in patients who underwent CPAP titration with torso elevation using a wedge cushion, after having failed during the same titration study to achieve therapeutic results at CPAP of 20 cm H2O without torso elevation. RESULTS: Thirty-nine patients who underwent CPAP titration with and without torso elevation utilizing a wedge cushion had statistically significant lowering of the minimum effective CPAP setting with torso elevation, with a mean CPAP reduction of 4.7 (p < 0.001) compared to ineffective treatment at CPAP of 20 cm H2O without torso elevation. Apnea hypopnea index (AHI), respiratory disturbance index (RDI), and lowest oxygen saturation (SpO2) were all improved with torso elevation, with a mean AHI difference of 4.4 (p = 0.03), mean RDI difference of 14.2 (p = 0.001), and mean SpO2 difference of 5.9% (p = 0.002). Age and BMI were inversely correlated, and gender had no correlation with therapeutic CPAP settings with use of torso elevation. CONCLUSION: Torso elevation of approximately 30° resulted in effective CPAP treatment at settings significantly lower than 20 cm H2O in all reviewed OSA patients, who had been ineffectively treated without torso elevation at the maximum tested setting of 20 cm H2O. This intervention may be a useful adjunct during in-lab titration studies for patients who are not effectively treated at or cannot tolerate high CPAP settings.

Personalized feedback to improve CPAP adherence in obstructive sleep apnea.

Obstructive sleep apnea (OSA) is effectively treated with continuous positive airway pressure (CPAP). Low rates of CPAP adherence led to the development of a personalized feedback intervention requiring minimal provider burden. In a comparison of the intervention to standard information, group differences failed to reach significance. Explanations for the findings include low power, that machines were not provided, and an atypical sample. Effect sizes were medium to large at 2 weeks, suggesting that sufficiently powered studies may be warranted.

Approach to the patient with sleep complaints.

Sleep disorders are both common and consequential, but too often remain undiagnosed. The insidious, chronic course of most sleep disorders and lack of patient awareness of signs and symptoms during sleep can complicate the clinical evaluation. Typical chief complaints include snoring, excessive daytime sleepiness, insomnia, and behaviors during sleep. Sleep disorders can be primary or secondary to medical, neurologic, or psychiatric conditions, so a multidisciplinary approach is often desirable. Family members can be a critical source of information as they may have observed nocturnal or daytime symptoms unrecognized by the patient. Objective testing plays an important role in assessment for obstructive sleep apnea, parasomnias, and other specific sleep disorders, and can be used most effectively in combination with a thorough clinical evaluation. Nonsleep specialists should consider obtaining assistance from sleep clinicians for more challenging presentations or management of sleep disorders unfamiliar to them.

Sleep-related laryngospasm caused by gastroesophageal reflux.

Gastroesophageal reflux is a suspected cause of sleep-related laryngospasm [Thurnheer R, Henz A, Knoblauch A. Sleep-related laryngospasm. Eur Respir J 1997;10:2084-6], but the relationship has not been directly documented by polysomnography (PSG). We report the case of an eight-year-old girl with asthma who was referred for evaluation of awakenings with respiratory distress. The description of her events included stridorous breathing suggestive of laryngospasm. A PSG was performed with esophageal pH monitoring, and during the recording pH dropped below four on nine occasions. Following two of the pH drops, acute respiratory distress with stridor was documented in video and audio recording, supporting a causal relationship between sleep-related gastroesophageal reflux and laryngospasm.

Posttraumatic stress disorder in the spouse of a patient with sleep terrors.

A 27-year-old woman who developed posttraumatic stress disorder (PTSD) as a consequence of her husband's severe sleep terror episode is reported. A 29-year-old man suddenly aroused from sleep and jumped through the closed second-story window of the room he shared with his wife, sustaining major lacerations to his arms. He hung onto the roof as his wife screamed at him from the window, and eventually climbed back inside. He was evaluated with polysomnography and was given the diagnosis of sleep terrors, which was effectively treated with behavioral and pharmacologic interventions. During a routine follow-up visit with the patient, his wife's PTSD symptoms came to clinical attention and she was referred for treatment. She demonstrated marked improvement in her condition after an 8 week course of cognitive-behavioral therapy. We conclude that family members of patients with sleep disorders manifesting as violent behaviors during sleep can suffer psychological trauma even if they are not physically injured.

Change in periodic limb movement index during treatment of obstructive sleep apnea with continuous positive airway pressure.

STUDY OBJECTIVES: The following hypotheses were investigated: 1) severe obstructive sleep apnea (OSA) can mask concurrent periodic limb movement (PLM) disorder (PLMD), which becomes evident or worsens after treatment with continuous positive airway pressure (CPAP); 2) in patients with mild OSA, PLMs are not masked but may be triggered by subclinical hypopneas or respiratory effort-related arousals and improve after CPAP. DESIGN: Retrospective analysis was performed on 2 polysomnographic studies per patient--1 baseline, the second with CPAP titration. The apnea-hypopnea index (AHI) and PLM index (PLMI) under the 2 conditions were statistically analyzed. SETTING: University hospital sleep disorders center. PATIENTS: Patients were selected if they had a baseline AHI of 5 or greater and CPAP titration resulted in reduced AHI. Also, each needed to have either a PLMI of 5 or greater on baseline PSG or during CPAP titration. Patients who started or discontinued a medication that could affect PLMs after the baseline PSG were excluded. INTERVENTIONS: As clinically indicated, CPAP for OSA. MEASUREMENTS AND RESULTS: Eighty-six patients qualified and were divided into 3 groups based on OSA severity. Significant correlations (P < 0.05) were found between AHI and PLMI on the baseline PSG (-0.50), between AHI on baseline PSG and PLMI on CPAP titration (0.49), and between PLMI on baseline PSG and on CPAP titration (-0.21). The increase in PLMI during CPAP titration in patients with severe OSA was statistically significant (P < 0.001). The PLMI decreased with CPAP in 20 of 86 patients, mostly in the mild OSA subgroup. Regression of post-CPAP reduction of AHI and change in PLMI yielded a significant logarithmic relationship (R2 = 0.3042). CONCLUSIONS: Severity of OSA may determine the effect of CPAP on PLMs. The PLMs may increase in moderate to severe OSA due mainly to "unmasking" of underlying PLMD. The PLMs may decrease in mild OSA post-CPAP due to resolution of PLMs associated with respiratory effort-related arousals. This suggests that PLMs may have more than 1 etiology and may be categorized as spontaneous (as in PLMD) and induced (when secondary to respiratory effort-related arousals).

A review of common sleep disorders.

What should clinicians know about sleep disorders? This article briefly introduces the reader to sleep medicine and succinctly reviews common sleep disorders. First, the authors describe the diagnostic tools unique to sleep medicine: the over-night polysomnogram and the multiple sleep latency test. Next, the authors review essential features of a subset of the sleep, described in the International Classification of Sleep Disorders-Revised, that sleep disorder specialists commonly evaluate, diagnose, and treat. The disorders reviewed include the intrinsic and circadian rhythm subsets of the dyssomnias group and the parasomnia group of sleep disorders. The authors identify the core signs and symptoms, polysomnogram findings, multiple sleep latency test findings, and treatment of these disorders.

Obstructive sleep apnea and depression.

Is there an association between obstructive sleep apnea (OSA) and depression? OSA is a common breathing-related sleep disorder. There have been reports that depressive symptoms can be associated with this sleep disorder. A number of investigations have addressed this issue. Although some have found no correlation, most studies have concluded that there is an association between OSA and depressive symptoms. Other investigations have shown that depressive symptoms improve with treatment of OSA, and that untreated OSA may contribute to treatment resistance in some cases of mood disorders. Within the framework of current psychiatric diagnostic criteria, the depressive symptoms associated with OSA can be viewed as a combination of a mood disorder secondary to a primary medical condition and an adjustment disorder with depressed mood. The question of whether OSA causes depressive symptoms can perhaps be best answered by viewing OSA and depression as having certain symptoms that are common to both disorders.

Sleep apnea and hypertension: pathophysiologic mechanisms.

This article reviews the pathophysiology of hypertension (HTN) in obstructive sleep apnea (OSA). The article is divided into 3 sections. The first section describes epidemiologic studies of the relationship of sleep-related breathing disorders, including OSA, to HTN and argues that OSA contributes to the genesis of HTN. The second section describes the known immediate physiologic consequences of 3 components of OSA that may contribute to the genesis of persistent systemic HTN. The 3 components are (1) the large negative intrathoracic pressure changes associated with OSA, (2) intermittent hypoxemia, and (3) arousal from sleep. The last section reviews current physiologic models of essential HTN genesis and attempts to integrate them with the suspected HTN-generating aspects of OSA. In its summary, the authors conclude that OSA contributes to the genesis of HTN and advise physicians not to ignore the contribution of frequently comorbid non-OSA factors, such as obesity, to the genesis of OSA-related HTN.