Health Consequences of OSA
For those patients with significant OSA, going to sleep can pose a significant health risk. Obstructive apneas produce profound haemodynamic changes. Each obstructive event is associated with cyclical increases in systemic and pulmonary artery pressure. The apnea related hypoxemia can cause O2 saturation to drop, sometimes dramatically.
Cardiac arrhythmias during sleep are often associated with OSA. Usually bradyarrythmias are observed, although ventricular tachycardia is noted occasionally in cases of severe hypoxemia. There are several reports suggesting increased risk of myocardial infarction and stroke and death with OSA .
Long term physiological effects also include an increased risk for the development of hypertension,. as well as increased risk under anesthesia, and during recovery. Children with OSA (usually caused by tonsillar hypertrophy) can suffer from impaired growth, weight loss, poor concentration and other behavior problems. Recent reports suggest a causal role of pediatric OSA in attention deficit hyperactivity disorder.
Impairment of daytime functioning in OSA patients ranges from mild to severe. Although excessive daytime sleepiness (EDS) may be the primary effect of chronic sleep disturbance and hypoxemia, some patients may not even be aware of (or deny) their sleepiness. More subtle but just as important are other manifestations of EDS such as symptoms of tiredness, fatigue, depression, memory and judgment problems, irritability, difficulty concentrating, and personality changes.
Victims of OSA are more likely to fall asleep at inappropriate times and have a higher rate of automobile crashes and work- related accidents. The National Highway Traffic Safety Administration estimates that approximately 56,000 police- reported crashes per year result from drivers who were asleep at the wheel.
To detect the possible presence of OSA, the physician should incorporate sleep related questions into the history- taking process, and be aware of signs of the disease during the physical exam.
The three main symptoms of obstructive sleep apnea are the following:
1. Chronic, loud snoring.
Sleep apnea is unlikely if it can be confirmed that the patient does not snore. Since very few people are aware that they snore or stop breathing in sleep unless they are told, it is often important to obtain a history from the bed partner or other family members.
2. Gasping or choking episodes during sleep.
Again, reports from bed partners or family members will likely be needed to obtain accurate information about snoring and apneic events.
3. Excessive daytime sleepiness (EDS).
The predictive power of these key symptoms is subject to controversy. When combined with hypertension, body mass index, and age they form a sensitive predictor of OSA without much specificity. EDS is often ignored by the patient and again may only come to light when complained about by family, friends or workmates, or, worse, when it causes an automobile or work related accident.
Other symptoms of OSA include:
- Morning headache –
- Cognitive difficulties. – poor memory/concentration
- Personality changes – depression
- Gastro-esophageal reflux
- Frequent nocturnal urination
- Morning sore throat
- Dry mouth in the morning
- Chest and limb pain
Signs of possible presence of obstructive sleep apnea are:
Most OSA patients are overweight (when defined as greater than 120 percent of ideal body weight). However, the relationship between weight and sleep apnea is not simple. It is well recognized and recently reported that certain groups have increased incidence of OSA in the absence of obesity, (probably related to skull and pharynx anatomy) . Central fat distribution is clearly associated with OSA. In fact, waist circumference has been found to be a better predictor of OSA than neck circumference.
Abdominal obesity may reduce lung volumes when supine, which may in turn reduce respiratory muscle force and reflexively influence upper airway dimensions. Obesity has also been linked quite strongly to changes in upper airway muscle function. Chronic snoring (pneumatic battering) may produce damage to the motor nerves of the tongue and pharynx.
2. A thick neck
Large neck girth in both male and female snorers is a good predictor of OSA. In general, men with a neck circumference of 17 inches or greater and women with a neck circumference of 16 inches or greater are at a higher risk for sleep apnea.
3. Nasopharyngeal narrowing
Nasophryngeal obstruction is the most common cause of OSA. (Is there data to support this: I didn’t think this was true. Or did you mean nasophayngeal obstruction? Drb) It is also an important cause in children after pharyngeal flap repair for cleft palate. Nasopharyngeal signs include:
- Reddened and thickened pharyngeal mucosa
- Long soft palate and uvula
- Decreased pharyngeal cross-sectional area
- Mandible length (small mandibles reduce posterior airway space)
4. Systemic hypertension and other cardiovascular consequences
In a review of 8 studies (461 patients), an average of 55% of patients with coronary artery disease were found to have OSA. In a similar review of 4 studies (166 patients), an average of 27% of patients with hypertension were found to have OSA. Unexplained pulmonary hypertension may be a sign (but rarely).
5. Cranio-facial abnormalities
The risk of having OSA increases with increasing numbers of affected relatives, independently of age, obesity, and alcohol consumption, and may be the result of facial similarity and underlying facial abnormalities.
Treatment for sleep apnea
If sleep apnea is suspected after evaluating a patient, some form of sleep study is indicated to establish a diagnosis. Currently,an overnight in laboratory sleep study ( polysomnography) is a commonly used test for diagnosing sleep apnea. It requires an overnight stay in a sleep laboratory and includes evaluation of sleep staging, airflow and ventilatory effort, arterial oxygen saturation, electrocardiogram, body position, and periodic limb movements.
Polysomnography, however, is often not readily available, is uncomfortable for the patient, and is generally expensive (usually over $1000 per test), often requiring extensive time by patient and physician office in obtaining insurance authorization.. In addition, the results of polysomnographic sleep studies can vary significantly, due to the subjective nature of interpretaion).
Pulse oximetry alone has also been used for diagnosis. Unfortunately studies have shown that as a stand-alone test, oximetry only provides moderate sensitivity and specificity. A review of 12 studies (1784 patients) of oximetry alone found an average sensitivity of 87% and average specificity of only 65%.
Attempts have been made to monitor sleep at home, ranging from reduced channel PSG administered by technician, to self-contained devices which the patients administer themselves. Technician-administered home studies are usually reserved for patients who are unable to travel to a sleep facility and are complex and expensive to administer. Some self-administered devices have proven difficult to use and costly to maintain. Simpler devices have not been validated and/or do not meet third party reimbursement qualifications.
However, a new approach to at-home monitoring for the diagnosis of sleep apnea has recently been cleared by the FDA. This unique service, based on the NovaSom QSG™ at-home diagnostic system, will be offered by Sleep Solutions, Inc.
The results of a sleep study will show both the type of sleep apnea, and provide a number of measures of its severity. The Apnea Index (AI) is the number of apneas per hour. Hypopnea is defined as a decrease in airflow of 50% or more (without complete cessation) for more than ten seconds accompanied by a drop in oxygen saturation of 2-4 percent, and the Hypopnea Index (HI) is the number of hypopneas per hour. Finally, the Apnea/Hypopnea Index (AHI) is the sum of AI and HI. The exact definition of sleep apnea in terms of the AHI has recently been proposed by an international committee and published in the journal Sleep. (ref ?) Normal is AHI 0-5, mild 5-15, moderate 15-30, and severe 30+.
The degree and frequency of oxygen desaturations may also be an important parameter, particulary in patients with cardiovascular compromise. In general, most clinicians use a subjective mild/moderate/severe classification if referring to oxygen desaturations.
In very mild cases conservative measures alone may lead to a satisfactory improvement. These include behavioral techniques and oral – dental appliances. They are not effective in all patients and in most cases form an adjunct to more aggressive therapy. Nasal CPAP and surgery remain the most accepted alternatives in the treatment of OSA.
Non Surgical OSA treatments
1. Behavioral Techniques and Oral / Dental Appliances
Appropriate behavioral treatment should be implemented for all patients, even those requiring additional interventions. These measures include weight loss, reduction of alcohol consumption, sleeping laterally, and cessation of smoking. Patients treated with behavioral techniques should be reevaluated periodically after initiation of treatment. If they show improvement with these simple techniques, then continued support and positive reinforcement is extremely helpful. Other therapies are warranted for those patients who continue to experience symptoms.
In addition, oral or dental appliances may be an option for patients with mild sleep apnea. Appliances have also been used for patients who snore but do not have sleep apnea. There are various devices that displace the tongue forward or move the mandible to an anterior and forward position to open the airway. Reported side effects of the devices include excessive salivation and temporomandibular joint discomfort. A dentist or orthodontist experienced in the use of these devices should fit the patient, and a sleep study should be done after the device is fitted to evaluate its effectiveness.
2. Continuous Positive Airway Pressure (CPAP)
CPAP machines became commercially available in 1981, and is now the most common initial therapy for moderate and severe OSA. This treatment is usually prescribed after a sleep study has been performed, and a further study (CPAP titration) has determined the therapeutic level of CPAP pressure required to reduce or eliminate sleep apnea.
The patient must wear a sealed mask over the nose (in some cases, nose and mouth) during sleep. The mask is connected to a blower forcing air through the nasal passages. CPAP acts as a pneumatic splint by increasing the pressure and opening the upper airway.
While there is no doubt about its efficacy, compliance is variable and is usually quoted to be 50-70% but tends to be higher in patients with severe symptoms.
The most common reasons for discontinuing CPAP are intolerance of the mask, nasal- related complaints, and the inconvenience of being connected to a machine. Common side effects include nasal stuffiness, rhinitis, facial skin discomfort, and discomfort with the pressure.
Humidifiers, nasal steroids or decongestants, intranasal anticholinergics, or different CPAP masks may relieve side effects. Variations in pressure application can offer patients options for improving comfort. Assisting patients to focus on symptom reversal and working with home care companies to ensure proper- fitting and effective equipment is essential. Ongoing improvements in mask and machine technology are likely to continue to improve compliance.
CPAP is effective in reversing daytime somnolence and eliminating cardiopulmonary sequelae. CPAP, used properly, produces rhythmic breathing, resulting in the patient feeling dramatically better and being able to function more efficiently (awkward). Compared with no treatment or other treatment modalities, patients treated with CPAP have a lower mortality rate.
Follow-up after the first month of CPAP treatment should include checking the status of equipment, assessing patient symptoms and adherence, and assessing the status of coexisting conditions such as hypertension. In patients who have achieved significant weight loss, the CPAP pressure may need to be adjusted.