Obstructive Sleep Apnea Case File

Obstructive Sleep Apnea Case File

Eugene C. Toy MD, Donald Briscoe, MD, FA  AFP, Bruce Britton, MD, Joel J. Heidelbaugh, MD, FA  AFP, FACG

Case 57

A 55-year-old white man presents to your office after an accident. He reports rear ending another vehicle with his truck. He complains of some neck soreness, but no other injuries. Later, he admits to having fallen asleep at the wheel right before the accident occurred, and is somewhat amnestic of what happened prior to impact. He admits that he has frequently gotten sleepy while driving in the past, and even dozed off for a few seconds, but has never had a previous accident. He sleeps 7 to 8 hours per night but doesn't feel rested in the morning. His wife reports that he snores loudly and several times per night almost stops breathing. He smokes a pack of cigarettes daily and drinks a few beers on the weekends. On examination, he is an obese man with a short, wide neck. His body mass index (BMI) is 36 kg/m2, blood pressure (BP) is 147/96 mm Hg, pulse rate is 88 beats/min, and respiratory rate is 16 breaths/min. On head, ears, eyes, nose, throat (HEENT) examination, you can only see his hard palate when he opens his mouth and says "ahhh:' His cardiac and pulmonary examinations are unremarkable. On examination of his neck, he has mild paraspinal muscle tenderness, but no midline cervical tenderness and he has full range of motion.

⯈ What condition is most likely to be responsible for his sleepiness?

⯈ What should be the first step in his evaluation?

⯈ What would be the most effective initial management?

ANSWER TO CASE 57:

Obstructive Sleep Apnea

Summary: A 55-year-old man with snoring and excessive daytime sleepiness (EDS), resulting in a motor vehicle accident, presents to the office. On examination, he is an obese and hypertensive male with a short, wide neck.

• Condition responsible for his sleepiness: Obstructive sleep apnea (OSA)
• Next step in his evaluation: Comprehensive sleep evaluation including Epworth Sleepiness Scale and polysomnogram (PSG ). If the PSG is positive, then continuous positive airway pressure (CPAP ) titration is indicated.
• Most effective initial therapy: CPAP for nighttime use and lifestyle modifications including weight reduction, control of hypertension, and smoking cessation.

ANALYSIS

Objectives

1. Identify patients at risk for OSA, the common signs and symptoms of OSA, and indications for conducting a comprehensive sleep evaluation.
2. Understand the pathophysiology and differential diagnosis of OSA.
3. Understand the diagnosis and management of OSA and the importance of patient support and education.
4. Identify comorbid conditions associated with OSA.

Considerations

The patient in this case presents with a history and examination that suggest a diagnosis of OSA. The first step in his management is advising him not to drive, for the safety of himself and others, until further evaluation occurs and a treatment plan has been developed. A comprehensive sleep evaluation, including a sleep history, medical history, and physical examination, should be performed. Confirmation of the diagnosis of OSA is then obtained by overnight polysomnography. The initial treatment approach should include patient education, weight reduction, smoking cessation, and CPAP with close follow-up.

Approach To:

Obstructive Sleep Apnea

DEFINITIONS

APNEA: Defined in adults as breathing pauses lasting at least 10 seconds accompanied by a 90% or more drop in airflow

HYPOPNEA: A 50% reduction in airflow lasting at least 10 seconds with a 3% drop in oxygen saturation, or a 30% reduction in airflow lasting at least 10 seconds with a 4% drop in oxygen saturation

APNEA HYPOPNEA INDEX (AHI): Number of apnea and hypopnea episodes per hour of sleep

RESPIRATORY DIS TURBANCE INDEX (RDI): Number of apnea, hypopnea, and respiratory effort-related arousal (RERA) episodes per hour of sleep

RERA: Respiratory effort-related arousals

CLINICAL APPROACH

OSA is a chronic disease that affects 2% to 9% of adults and 2% to 5% of children. Its prevalence has increased dramatically in the last few decades with a direct correlation to obesity rates. It causes significant morbidity including EDS, cognitive impairment, increased risk of motor vehicle accidents, and impaired relationships, and has been associated with several metabolic and cardiovascular conditions (Table 57-1).

People with OSA experience repetitive collapse of the upper airway during sleep leading to hypopnea, apnea, and RERA episodes. The upper airway is comprised of flexible muscles, including the soft palate, that allow for the processes of speech, respiration, and eating. They lack rigid support and during normal sleep, this muscle tone decreases. In OSA, collapse of the flexible musculature of the upper airway during sleep leads to reduced or absent airflow despite continued respiratory effort. This phenomenon is demonstrated on the PSG by abdominal and chest wall movement during an obstructive event. In contrast, during a central apnea there is no respiratory effort, evidenced by absence of chest wall or abdominal wall movement on PSG. The collapse of the upper airway musculature results in occlusion and apnea (often preceded by snoring), which leads to hypoxia and hypercapnia. This results in arousal, wakefulness, and increased sympathetic activity in an attempt to restore airway patency, leading to fragmented sleep. Pathophysiologic factors associated with OSA are listed in Table 57-2.

Evaluation

The diagnosis of OSA is based on a comprehensive sleep evaluation, which includes a sleep-related history and physical examination. If OSA is suggested by the history

and physical, a PSG with CPAP titration must be performed to confirm the diagnosis and to determine the severity of OSA, which will help guide treatment. A differential diagnosis for OSA is included in Table 57-3.

A comprehensive sleep history includes asking the patient and their bed partner about snoring, daytime sleepiness not explained by other causes, witnessed apneas, choking or gasping during sleep, sleep amount, nocturia, decreased libido, morning headache, insomnia, frequent awakenings, concentration and memory, alertness, and history of falling asleep at the wheel. Often a patient's partner will be able to provide important information. It is important to ask about other medical conditions that could be related to OSA.

Several standardized scales are available to assess fatigue and sleepiness. The most widely used, the Epworth Sleepiness Scale, is a useful tool to help determine the extent of sleepiness, although a low score does not rule out sleep apnea. Other available tools include the Stanford Sleepiness Scale and the Fatigue Severity Scale.

The physical examination should include evaluation for features suggestive of the presence of OSA. They include BMI greater than 30 kg/m2, hypertension, retrognathia, obesity, thick neck (likely correlated to a Mallampati class 3 or 4 score), macroglossia (large tongue), acromegaly, thyroid enlargement, large tonsils, enlarged uvula, enlarged nasal turbinates or polyps, and narrow or high-arched palate. The appearance of the oropharynx may be assessed using the Mallampati score (Table 57-4).

Diagnosis

According to the American Academy of Sleep Medicine (AASM), in-lab (PSG) and home testing with portable monitors are acceptable objective tests for OSA.

PSG includes the following physiologic assessments: electroencephalogram (EEG), electrocardiogram (ECG) or heart rate, electrooculogram (EOG), chin electromyogram (EMG), airflow, and oxygen saturation. Additionally, anterior tibialis EMG can help assess for periodic limb movements which can coexist with sleep-related breathing disorders. According to the AASM, the diagnosis of OSA in adults is confirmed by the following:

• AHI or ROI greater than or equal to 15, defined by at least 15 obstructive events (apneas, hypopneas, RERAs) per hour on polysomnogram with or without symptoms

Or

• AHI or ROI greater than or equal to 5, defined by five or more obstructive respiratory events per hour on polysomnogram in a patient who has symptoms of the following:

• Daytime sleepiness

• Unrefreshing sleep

• Fatigue

• Insomnia

• Nighttime awakenings associated with gasping, choking, or breath holding, or witnessed loud snoring and/ or breathing interruptions

Severe OSA is defined as having more than 30 RDI per hour; moderate OSA is defined as 15 and 30 RDI per hour; and mild OSA is defined as 5 to 15 RDI per hour.

TREATMENT

The medical, behavioral, and surgical therapies for OSA and treatment should involve a multidisciplinary approach. It is always important to include the patient in the decision-making process when deciding on treatment options. Positive airway pressure (PAP) is the treatment of choice for OSA of all severities, although alternative therapies may be indicated based on the patient's anatomy and severity of OSA.

All patients should be educated on behavioral changes. These include weight loss, smoking cessations, avoidance of alcohol and sedating medications, modifying risk factors, and driving precautions. There is a direct correlation between smoking and the development of sleep apnea, placing these patients at an increased risk of sudden cardiac death. Some individuals have elevated AHI or RDI in the supine, but not in other positions and may benefit from sleep-position measures to prevent sleeping in the supine position. One technique is to sew a tennis ball to the back of the sleepwear to prevent supine sleeping. After significant weight loss, the need for continued therapy or for PAP adjustment should be evaluated.

PAP acts as support to maintain patency of the upper airway and reduces the AHI The level of PAP is determined by an in-lab attended overnight PSG and sometimes by a split-night diagnostic and titration study. A split-night study may occur if a patient has AHI greater than or equal to 40 during 2 hours of a diagnostic study; in this case, PAP may be applied and titrated in the same night.

Different modes of PAP delivery include continuous (CPAP), bilevel (BiPAP ), and automatic titrating (APAP). PAP can be applied using a full face mask, oral mask, nasal mask, or nasal pillows. Heated humidification can assist in patient comfort. Adverse effects include nasal congestion and dryness, nosebleeds claustrophobia, inconvenience, air swallowing, skin rash, or minor trauma from the mask. Close follow-up with the health-care team is imperative, especially within the first few weeks after initiation.

Oral appliances work by enlarging the upper airway and preventing upper airway collapse. Examples include mandibular repositioning appliances (MRA) and tongue retaining devices (TRD). They are not as effective as PAP, but are indicated for people with mild-to-moderate OSA who have contraindications to the use of PAP, cannot tolerate PAP, or in whom PAP and behavioral therapy are ineffective. Patients should have a thorough dental examination prior to consideration of use. A repeat sleep study should be performed with the oral appliance in place in order to assess the treatment outcome. Regular follow-up with a dental specialist trained in sleep medicine should occur.

Surgical therapy may be considered as primary therapy if the OSA is mild, resistant to PAP, and when there is an anatomic cause of major airway obstruction that can be reversed. Surgery can be considered as secondary therapy after a trial of PAP or an oral appliance if treatment response is inadequate, or if the patient does not tolerate them. Surgery, specifically an uvulopalatopharyngoplasty (UPPP) may also be used as an adjunct to other therapies. Bariatric surgery may be a helpful adjunct to other OSA treatments in patients who have failed to lose weight through lifestyle modifications. Tracheostomy is curative and can be considered in extremely advanced cases refractory to treatment. There is no pharmacologic therapy for OSA aside from treating underlying diseases such as acromegaly or hypothyroidism that are causative etiologies. All patients with OSA require individualized care and regular follow-up to assess symptoms, treatment response, side effects, and to treat medical conditions associated with OSA.

CASE CORRELATION

• See Cases 2 (Dyspnea), 19 (Upper Respiratory Infection), 24 (Pneumonia), and 56 (Wheezing and Asthma).

COMPREHENSION QUESTIONS

57.1 A 47-year-old obese woman presents to your office complaining of excessive daytime sleepiness, snoring, and frequent awakenings from sleep. She is having difficulty concentrating and her sleepiness is affecting personal and professional relationships. She smokes three-fourths of a pack of cigarettes per day, averages two glasses of wine per night, and has hypertension and hyperlipidemia. You perform a comprehensive sleep history and physical examination and determine that she is at increased risk for OSA. Which of the following physical examination findings is most suggestive of OSA?

A. Mallampati score of 2

B. Obesity

C. Acanthosis nigricans

D. Peripheral edema

E. Elevated blood pressure

57.2 You decide to perform an overnight PSG to confirm the diagnosis for the patient in question 57.1. The study is converted into a split-night study because her AHI was found to be over 40 in the first 2 hours of the study. 

What is the most likely diagnosis?

A. Mild OSA

B. Moderate OSA

C. Severe OSA

D. Positional OSA

E. Central apnea

57.3 What is the next step in management of this patient?

A. Dobutamine stress echocardiogram

B. Treatment with PAP

C. Referral for UPPP

D. Pulmonary function testing

E. Dental evaluation for oral appliance

57.4 A 54-year-old man comes to your clinic for a follow-up on OSA. He has been using PAP with a nasal mask for the last 3 years since he was diagnosed. He has recently purchased a CPAP machine and tells you he has been unable to use it because of facial discomfort. You check the machine and all the parts are in good condition. What is the next most appropriate step in management?

A. Decrease the pressure

B. Refer to surgery

C. Refer for an oral appliance

D. Change the mask

E. Add heated humidification

ANSWERS

57.1 B. Obesity is the physical examination finding most suggestive of the presence of OSA. People who are obese are considered to be at high risk for OSA. A Mallampati score of 3 or more suggests increased risk for OSA. Acanthosis nigricans is suggestive of insulin resistance. Peripheral edema has a broad differential diagnosis and further evaluation is warranted. Elevated blood pressure, in contrast to resistant hypertension, is not a risk factor for OSA.

57.2 C. This patient has severe OSA based on a RDI over 30 per hour.

57.4 B. PAP is the treatment of choice for OSA and, as this patient had an AHI over 40 for 2 hours of the study, it was converted into a split-night study, meaning PAP was applied and titrated in the same night. Surgery and oral appliances are alternative treatment options, but for this patient the initial treatment should be PAP. Pulmonary function testing and cardiac stress testing are not indicated.

57.4 E. Heated humidification is indicated to improve patient comfort while using PAP. If the patient remains uncomfortable despite this addition, other measures should be taken such as a trial of a different type of mask ( eg, nasal pillows), or pressure relief. If all modifications and patient comfort interventions fail, then an alternative treatment may be necessary.

CLINICAL PEARLS

⯈ OSA is a chronic treatable disease that, if left untreated, is associated with increased risk of several cardiovascular disorders .

⯈ A diagnosis of OSA should be considered in people with high-risk medical conditions, or features on history or physical examination that may suggest the presence of this disease .

⯈ Polysomnography is required to confirm the diagnosis of OSA and determine the severity, which will help to guide treatment.

REFERENCES

Eckert DJ, Malhotra A. Pathophysiology of adult obstructive sleep apnea. Proc Am Thorac Soc. 2008:5(2):144-153. 

Epstein LJ, Kristo D, Strollo PJ, et al. Clinical guideline for evaluation, management and long-term care of obstructive sleep apnea in adults.] Clin Sleep Med. 2009:5(3):263-276. 

Greenstone M, Hack M. Obstructive sleep apnoea. BM]. 2014;348:g3745. 

Krishnan V, Dixon-Williams S, Thornton JD. Where there is smoke ... there is sleep apnea: exploring the relationship between smoking and sleep apnea. Chest. 2014;146(6):1673-1680. 

Myers KA, Mrkobrada M, Sime! DL. Does this patient have obstructive sleep apnea? The Rational Clinical Examination systematic review.JAMA. 2013;310(7):731-741. 

Ramar K, Olson EJ. Management of common sleep disorders. Am Fam Physician. 2013;88( 4):231-238. 

Wellman A, Redline S. Sleep apnea. In: Kasper D, Fauci A, Hauser S, et al., eds. Harrison's Principles of Internal Medicine. 19th ed. New York, NY : McGraw -Hill Education; 2015. Available at: http:// accessmedicine.mhmedical.com. Accessed May 25, 2015.

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