Hospital Medicine

Obstructive sleep apnea

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I. What every physician needs to know.

Obstructive Sleep Apnea (OSA) is a mechanical closure/obstruction of the upper airway during sleep. The obstruction results from the collapse of soft tissue structures in the airway secondary to relaxation and may be highly position sensitive. The relaxation of the tissues occurs with sleep, decreased level of consciousness for any reason, and may be particularly problematic post anesthesia or under the influence of narcotics, alcohol or other sedating substances.

Prominent risk factors for OSA include obesity, particularly individuals with thick necks, advanced age, and of course, patients with oropharngeal distortion, such as patients with craniofacial abnormalities, either congenital or acquired. Characteristics of the syndrome were identified by Dickens in the novel,Pickwick Papers, in the character of "Joe, the fat boy." William Osler coined the term "Pickwickian" for people who exhibited these classic features, namely, a portly fellow who snores and is beset by daytime sleepiness; these are common features of OSA, because of the lack of uninterrupted nighttime sleep. Another term sometimes used synonomously with OSA is Sleep Disordered Breathing (SDB), however, SDB may include other sleep disturbances in addition to OSA.

The basic pathology involves collapse of the soft tissue of the airway while sleeping, resulting in apneic episodes and significant associated hypoxia. When the hypoxia is severe enough, the patient awakens to breathe or sometimes startles awake taking several gasps of air. Some patients become fully awake with these episodes, but others dose back to sleep hardly recognizing the event. In either case, sleep is interrupted and sleep quality and architecture are diminished, rendering the patient sleep deprived.

The old admonition, "blood pressure begets blood pressure," seems to hold true for OSA also, called a "loop gain" phenomenon. With the collapsed airway and subsequent arousal with "air hunger" the patient hyperventilates and indeed, over compensates for the hypoxic event. On returning to sleep, the low CO2 from hyperventilation decreases the respiratory drive further, and thus, sets the patient up for the next apneic event.

Repetitive episodes of nocturnal hypoxia and hypercarbia are felt to be the etiology of many of the comorbidities associated with sleep apnea. Both bradycardia and ventricular tachycardias are commonly identified during hypoxic episodes. Hypertension has an excellent correlation with OSA and frequently improves when the sleep apnea is treated. Associated illnesses include LVH, pulmonary hypertension, stroke and ischemic heart disease.

Significantly, patients with this disorder are capable of self arousal when the oxygen saturation falls, but may not be able to wake up when hypoxic if they are under the influence of sedating medications, such as post-operative narcotics or sleeping medications. Many, if not most hospitalized patients are at risk of hypoventilation when treated with sedating medications.

II. Diagnostic Confirmation: Are you sure your patient has Obstructive Sleep Apnea?

Firm diagnostic confirmation requires polysomnographic study. This data is obtained in a sleep laboratory where episodes of hypoventilation and apneas are measured and recorded under direct observation. Hypoventilation is documented by recording decreased respirations with associated lowered oxygen saturation levels, confirming the diagnosis. Sometimes these episodes are highly positional - most often when lying supine - and may be prevented by simply rolling to one side or even elevation of the head of the bed. Although definitions of apnea are somewhat variable, most will accept the definition of cessation of breathing/airflow for 10 seconds.

It is in this setting that a positive pressure breathing apparatus, such as CPAP or BIPAP, may be fitted to the patient and titrated to proper settings to prevent hypoventilation while sleeping. In the laboratory, it is possible to confirm that the appropriately applied positive pressure apparatus prevents apnea during sleep. Mouth-breathing patients may not have success with nasal CPAP and may require a full face mask. The decisions for the type of positive pressure breathing device and the appropriate mask type are made by the sleep laboratory professionals.

The apnea hypopnea index (AHI) is the number of apneas and hypopneas, defined as 10 second events, identified per hour of sleep. Apnea is the complete cessation of breathing and hypopnea is slow or shallow breathing that results in a significant drop in blood oxygen. Mild OSA may have five episodes per hour while severe disease may have more than 30 episodes per hour. Although in most labs the diagnosis is made by the number of apneic events, most clinicians feel that the degree of hypoxia generated per event should also drive the need for intervention.

Restless Legs Syndrome, a not infrequent comorbidity with OSA, may be observed and diagnosed during the polysomnographic study also. Most sleep laboratories monitor not only oxygen saturation, but also motor activity and several other parameters.

Family members who report observing long apneic spells while the patient is sleeping provides a reasonably reliable history for OSA, and these patients should be assumed to have the clinical diagnosis pending confirmation with a formal sleep study. Although snoring is a feature of OSA, many snorers have nasal obstruction and do not have apneas. Patients that describe both loud snoring and symptoms of daytime sleepiness have a high pre-test probability of having sleep apnea; the converse - patients that deny these symptoms - are at lower risk, but may still have obstructive sleep apnea. The key feature in clinical diagnosis is the observation of apneas and the definitive diagnosis is with polysomnography.

A. History Part I: Pattern Recognition:

"Mr. Smith, a mildly obese, plethoric man with significant face and neck fullness, was dosing - and snoring - in the examination room chair when I entered the room."

Classical history of OSA is the patient that complains of loud snoring, daytime sleepiness and gasping awakenings in the night. The history may be better described by the patient's partner, who often is the one complaining of the loud snoring and may also be able to describe apneas, followed by a gasping resumption of breathing. Daytime sleepiness may be associated with increased incidence of motor vehicle accidents. Additionally, OSA has a slight male gender predominance.

In addition to daytime sleepiness, patients with OSA often complain of impaired cognitive function and mood disorders. They may also report chronic morning headaches.

Obese patients have a high incidence of OSA. Bariatric patients are at very high risk and are usually assumed to have OSA unless they have had a sleep study that confirms they do not. Any patient with a history of respiratory arrest when taking sedating medication or post operative hypoventilation or desaturations in the past, particularly if the event required intubation or transfer to the ICU, should be considered at risk for OSA. Patients with sleep apnea and hypoventilation syndromes may have a plethoric appearance as a result of hypoxemia induced polycythemia. Patients that report a history of stroke, hypertension, nocturnal angina and atrial fibrillation should be screened for OSA, since all of these comorbidities are associated with moderate to severe apneas and hypoxemia.

There are several useful surveys to quantitate a patient's clinical risk of having OSA. Anesthesiologists have developed a series of validated screening questions. Another document, the Berlin questionnaire, is, in my opinion, a cumbersome survey. For clinical practice and screening purposes, the validated STOP-BANG survey is easy to use and provides an easy way to access a patient's risk of hypoventilation.

The following questions are asked:

S Snore: Do you snore loud enough to be heard through the door?........Yes=1

T--Tired: Do you frequently note daytime sleepiness or fatigue?..............Yes=1

O--Observed: Has anyone observed you stop breathing while asleep?.....Yes=1

P--Pressure: Do you have high blood pressure?...................................Yes=1

B--BMI: Is the patient's BMI > 35 kg/M2?.............................................Yes=1

A--Age greater than 50 years?.............................................................Yes=1

N--Neck: Neck circumference > 15.75 inches or 40cm?.........................Yes=1

G--Gender male?................................................................................Yes=1

SCORE......3 or more: high risk

2 or less: low risk

This screening tool was validated by using the above scoring system, however, in my clinical practice, I have found a cut off point of greater than 3 to be more reliable.

The Epworth Scale is another screening tool to help quantitate the degree of daytime sleepiness and can be used repetitively over time to document interval change. This questionnaire asks the patient to estimate the probablility they would fall asleep in eight different situations, rendering a score between 0-24. A score of 0-9 is considered normal and a score >9 is abnormal. Generally, the Epworth Scale can be administered as follows:

Scale Rating

0= No inclination to fall asleep

1= Slight to moderate inclination to doze off

2= Moderate inclination to fall asleep

3= High inclination to fall asleep

In the following circumstances:

A. Sitting or reading

B. Watching TV

C. Sitting in a public place

D. Sitting in a car for 1 hour

E. Lying down in the afternoon

F. Sitting and talking to people

G. Sitting alone after lunch

H. In a car at a traffic light

Scoring: Total points less than or equal to 9 is within normal limits. Total score >9 is abnormal.

Prolonged and untreated OSA may result in pulmonary hypertension and subsequent heart failure. OSA is associated with systemic hypertension, CHF and atrial fibrillation. OSA may worsen existing ischemic heart disease and may present with nocturnal angina secondary to low nighttime oxygen saturations.

B. History Part 2: Prevalence:

OSA should be considered in all obese patients, particularly those with adiposity of the face and neck. The American Society of Anesthesiologists identified a BMI > 35 as an independent risk factor for OSA. Seventy percent of patients presenting for bariatric surgery were diagnosed with sleep disordered breathing.

The usual definition for OSA is documented 5 or more apnea/hypopnea episodes per hour of sleep. The number of apneas per hour of sleep is called the "apnea-hypopnea index" or AHI. Some investigators define OSA as AHI >5 plus symptoms of daytime sleepiness or cognitive dysfunction. Since the number of patients who report identified symptoms is significantly less than the number of patients with documented apneas, there is wide discrepancy noted in the published date on incidence and prevalence of disease.

If defined as an AHI >5, about 20% of the adult population in the United States has OSA, but AHI=5 is somewhat of a low threshold, especially if not combined with the co-condition of daytime sleepiness. Some prefer using a higher threshold AHI of 10-15. Naturally, the higher threshold makes the testing more specific and a bit less sensitive. Prevalence of OSA, as well as other abnormalities in sleep habits and sleep architecture, increases with age, particularly over the age of 60 years.

Several studies on patients with ESRD on hemodialysis or peritoneal dialysis revealed over 60% testing positive for sleep apnea. With this information, ESRD patients should be viewed as high risk for hypoventilation.

Identified risk factors for OSA include obesity, male gender (between 18 and 65 years of age), heredity, craniofacial/oral abnormalities, smoking and nasal obstruction. African Americans are at increased risk for OSA, even when corrected for age and BMI.

Patients, especially elderly patients, who are noted to be "overly sensitive to narcotics," may actually have sleep apnea. It is common in the general population and very common in a hospital population.

C. History Part 3: Competing diagnoses that can mimic Obstructive Sleep Apnea.

The differential diagnosis may include narcolepsy, drug or alcohol addiction, neuromuscular disease and Cheyne-Stokes breathing, sometimes referred to as central sleep apnea. Various sleep disorders increase in frequency in the geriatric population.

Other diagnostic considerations include a long list of other disorders that may present with daytime fatigue and sleepiness due to poor sleep quality. Some of these disorders include insomnia, poor sleep hygiene, restless legs syndrome and hypersomnias.

Polysomnography can usually confirm the diagnosis of sleep apnea and rule out the other sleep disorders.

D. Physical Examination Findings.

Although obesity is a risk factor for OSA, thin patients may also have sleep apnea, so do not assume that a thin patient is immune. Physical examination should always start with vital signs and pulse oximetry, height and weight. The BMI should be calculated. Hypertension noted on examination is another risk factor. Unusual or abnormal face size and shape can be at increased risk. Small oral cavity, micrognathia, macroglossia, small mandible and crowded oropharynx (fullness in the soft palate) are risk factors for OSA. Neck thickness is a risk factor and the neck should always be measured when screening a patient for OSA. A neck circumference of 15.75 inches (40 cm) is another risk factor.

Usually, there are no specific lung findings. Although there are no pathognomonic heart findings, cardiac arrhythmias -particularly atrial fibrillation - are commonly associated. Patients with OSA are at increased risk of ischemic heart disease, hypertension, pulmonary hypertension, congestive heart failure, and signs and symptoms of these illnesses should be sought during the examination.

Patients with hypothyroidism are at increased risk of OSA, physical exam findings such as slow pulse, slow refexes, weight gain and deepening voice should be noted. Likewise, acromegaly, with the enlarged jaw and tongue is a risk for OSA also. If clinical signs of acromegaly are present, the appropriate would up should be pursued.

E. What diagnostic tests should be performed?

If the suspicion for OSA has been raised by history or physical examination, the next recommended step is using one of the validated questionnaires to objectively assess risk. Several validated questionnaires are available to evaluate patients at risk for OSA. They include the Berlin Questionnaire, STOP-BANG questionnaire, and ASA (American Society of Anethesiology) checklist. The STOP-BANG questionnaire (see section "A" above) has been validated and is simple to implement. Three or more positive responses on the questionnaire corresponds to a high risk of having OSA and less than 3 positve responses corresponds to a low risk for OSA.

Associated illnesses that raise the index of suspicion include a history of hypertension, ischemic heart disease, stroke, and a history of otherwise unexplained pulmonary hypertension.

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

The most definitive test is Polysomnography performed overnight in a sleep laboratory. The sleep study generates data on the number of apneas and hypopneas that occur per hour of sleep, and the associated hypoxia related to the hypoventilation events. The definition for the level of severity of OSA is not well standarized in the discipline, leading to confusion in the definition of disease.

Polysomnography is performed as an overnight study in well-controlled, laboratory conditions. The patient is monitored with a breathing monitor, oxygen saturation pulse oximeter, EEG, EKG, EMG and EOG (electrooculargram) and then asked to sleep normally! Although most patients find it difficult to sleep under these circumstances, they usually are able to monitor enough sleep time to make a diagnosis.

The Centers for Medicare and Medicaid Services definition is apnea hypopnea index (AHI) of greater than or equal to 15 or, 5 to 15 events associated with clinical endpoints such as mood disorders, heart disease or daytime sleepiness. Other researchers in the field feel that the AHI (number of events per hour) should be used in conjunction with information on the length and severity of the oxygen desaturation per event.

Questions have been raised about whether patients with jobs in which alertness is critical, such as airplane pilots, physicians, bus drivers, etc, should have a lower threshold for treatment. The Federal Motor Carrier Safety Administration Expert Panel Report January 14th, 2008, included data that moderate and severe OSA had a documented increased risk of motor vehicle accidents and the panel recommended that patients with an AHI of more than 20 should not be certified to drive.

Interpretation of Polysomnography testing may depend, in part, on the institution or guidelines being used. Some groups use the following scale:

Mild: AHI of 5-15 with mild symptoms of daytime sleepiness.

Moderate: AHI 15-30 usually complain of daytime sleepiness and are at risk of complications from OSA.

Severe: AHI >30 with prolonged nighttime oxygen desaturations. Most likely present with sequelae of OSA.

Another Interpretation of Polysomnography is the following:

Mild: AHI = 5-15

Mod: AHI =15-30, or, AHI=10-14 plus daytime sleepiness, plus any ONE of the following symptoms or illnesses: insomnia, ischemic heart disease, Epworth scale>9, mood disorder or cognitive impairment, stroke, HTN

Severe: AHI >30

Other testing options:

A portable device available for home use, called a Remmer Sleep Recorder, is advertised and sold commercially to measure the pulse, air flow, respiratory effort, number of apneas and to estimate the efficacy of positive pressure breathing. This device is purported to replace the need for overnight polysomnography in a laboratory. Although this may have some utility as a screening tool, available data does not support the efficacy of this modality for diagnosis and treatment.

Overnight pulse oximetry is also used as a screening test for sleep apnea. The overnight pulse oximetry generates a desaturation event index (DEI), which may help to risk stratify the patient and determine if polysomnography is indicated.

Patients with severe sleep apnea may have alterations in basic blood work. Elevated pCO2,elevated HCO3,and polycythemia may be lab indicators of sleep apnea. Since hypothyroidism is a possible etiology of OSA, a screening TSH is appropriate if OSA is diagnosed.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

No specific imaging studies are universally indicated.

Neck soft tissue X-rays or other imaging may be needed if structural head/neck abnormality is suspected. Most of the imaging work up will be ordered by the surgical specialist.

If the patient has secondary complications of OSA, such as hypertension or pulmonary hypertension, then studies to evaluate these problems may be indicated.

F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis.

Most patients are managed with positive pressure breathing devices and do not require imaging studies and they should not be ordered routinely.

If it is determined that the patient will need surgery, certain imaging studies will be ordered, but this should be left to the descretion of the attending surgeon.

III. Default Management.

Patients with craniofacial abnormalities may need to be referred to ENT for evaluation and potentially surgical correction, such as a mandibular-maxillary osteotomy (MMO). Similarly, patients with a crowed oropharnyx or a very large uvula, tonsils and soft palate may benefit from ENT evaluation, however, rarely is a uvulaectomy helpful. The more aggressive surgery of uvulopalatopharygoplasty (UPPP) is sometimes helpful in patients who have already failed trials with CPAP. I have seen some patients that still needed CPAP after the surgery, but at least the CPAP was then effective.

Morbidly obese patients who fail positive pressure breathing aparatus management or who have other comorbid conditons may be referred for bariatric surgery consideration.

Extreme and refractory cases may require tracheostomy to protect ventilation.

A. Immediate management.

All patients with a new diagnosis of obstructive sleep apnea require a full explanation of the disorder, methods of managing the problem and an overview of the possible negative consequences of non-treatment. Since the treatment is heavily dependent on patient compliance to the planned regimen, it is essential that the patient understands the goals and purpose of the therapy. Patient education also will encourage adherence to a weight loss program (if that is indicated).

Most patents with polysomnographic confirmation of sleep apnea are evaluated for the use of positive pressure breathing devices. If desaturations persist on CPAP or BiPAP, supplemental O2 may be needed; remember to use caution if the patient has concomitant COPD, as they may also be CO2 retainers. All patients with documented OSA should be cautioned about the use of alcohol and other sedating medications and should be carefully monitored to avoid oversedation. If narcotics are prescribed, they should be used judiciously. When hospitalized, if narcotic medications are prescribed, there should be ready access to Narcan to reverse the sedation, if needed.

Some patients are discovered to have apneic and hypopneic episodes only when they are sleeping in the supine postiion. In this subset of patients, if effective methods can be employed to keep them sleeping continually on their side, they may not require a positve pressure breathing device. Creative options have included sewing tennis balls in the back lining of a snug-fitting sleep shirt, so if the patient rolls to their back during sleep, the discomfort of the tennis balls moves them back to their side. In patients that do not take the shirt off during the night, this method has had some (limited) success.

In some patients a dental appliance may prove successful. These patients usually have mild disease, and a positive pressure breathing apparatus is not required. Use of nasal steroids may be considered as a simple measure that may have benefit in patients with nasal blockage and allergies. Any patient who uses CPAP or BiPAP at home, should always use it if admitted to the hospital. If the patient is being seen in the ED, send a family member home to pick up the device, since hospitalized patients are at even greater risk of hypoventilation (they are sick, elderly, weaker and getting new medications). Avoid in-patient use of PCA pumps in patients with known or suspected OSA.

When a patient with OSA has surgery, extra precautions should be observed perioperatively. Patients with confirmed OSA and using CPAP at home, should bring their positive pressure equipment to the hospital and it should be used at their usual pressure settings as soon as possible after surgery. The positive pressure equipment should be employed almost continuously while the patient is receiving sedating medications and anytime the patient is sleeping while in the hospital. Surgery and post-operative recovery is safer with the use of a specifically fitted positive pressure breathing apparatus, used at the predetermined pressure settings.

If a patient is seen pre-operatively and felt to have risk factors for OSA, some precautions should be taken. If the surgery is elective and there is time to perform polysomnography prior to surgery, this should be done. Frequently, the patient is seen just a few days prior to surgery or even a few hours prior to surgery and confirmation of suspected sleep apnea is not possible.

Recommendations for patients with suspected OSA include use of continuous pulse oximeter post operatively, especially while they are receiving sedating medications. Narcotic analgesics and sedating medications should be used sparingly. Patient controlled anesthesia (PCA pumps) should be avoided when possible. Supplemental oxygen should be continued post operatively until the patient is consistently maintaining oxygen saturations in the pre-hospital range without desaturations. Regional anesthesia is preferred to general anesthesia and is better tolerated. Avoid extubation until the patient is fully awake post procedure. If the surgery is a same-day surgery, the patient should be observed for additional time, usually 2 hours off oxygen and maintaining pre-hospital oxygen saturations, before discharge.

If there is not sufficient time to have outpatient titration of CPAP prior to surgery and the patient develops clinical evidence of hypoventilation/apneas post operatively, a trial of APAP may be useful. APAP has automatic pressure adjustments and has been found to be non-inferior to CPAP by at least one study. If CPAP was used in the hospital in a patient not previously known to have OSA, the patient should be sent for a sleep study at discharge. They also need to be warned about risks of operating hazardous equipment and driving.

Nocturnal CPAP has been shown to improve daytime sleepiness, cognition, and there are many testimonials that it improves quality of life. Despite this, compliance with using positive pressure breathing apparatus is problematic. Patients find the face mask cumbersome. Patients that refuse to use CPAP should be recommended for a mouth appliance trial. Benefits of therapy with positive pressure breathing often results in resolution of the daytime sleepiness and a return to more normal function. Progress and improvement in symptoms may be followed with an Epworth Scale. (Note: Epworth Scale is discussed in Section 1.A.)

B. Physical Examination Tips to Guide Management.

Patients with craniofacial abnormalities should be referred to ENT for evaluation. Edentulous patients are usually not candidates for oral appliances and may be difficult to fit with a full-face mask (nasal mask is not a problem).

After initiation of nocturnal positive pressure breathing, the patient may demonstrate improvement in daytime sleepiness and fatigue. Patients may be noticeably more alert. For patients being monitored in the hospital, one can anticipate fewer alarm reports on the pulse ox monitor. After a few weeks - or occasionally days - of treatment, there is often a blood pressure response, and the patient may actually require less antihypertensive medication than prior to using CPAP or BiPAP. If the patient is on a cardiac monitor, there may be less dysrhythmia noted. Many patients volunteer a report of feeling better and being in a better mood than prior to treatment.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

Once the patient is diagnosed with OSA and successfully started on positive pressure breathing, this treatment is continued indefinitely. Patients that have had a good clinical response to therapy are disinclined to want to stop the treatment.

If a patient has had a significant change in physical status, such as significant weight loss from diet or gastric bypass/banding, then repeat sleep evaluation may be indicated to see if they still require CPAP/BiPAP.

Similarly, patients that have tested negatively for OSA may need repeat testing as they get older or gain weight.

D. Long-term management.

Overall goal is to prevent hypoxia and the long term sequelae, such as hypertension, pulmonary hypertension, congestive heart failure, daytime sleepiness and cognitive impairment. In addition to the well-documented relationship between OSA and heart and lung disease, there are a host of "associated" illnesses, from diabetes to kidney disease. Some of these conditions may be causally related to OSA, but others may more accurately reflect comorbidities with common risk factors.

Positive Pressure breathing apparatus: CPAP, BIPAP (bilevel positive airway pressure), APAP (autotitrating positive airway pressure), used with the appropriate nasal or full face mask as prescribed by the sleep lab professionals. Most common cause of treatment failure is non-compliance to using CPAP or BiPAP. Often, patients refuse treatment because the equipment is too cumbersome or uncomfortable. By working with the patient and trying a variety of devices, usually an acceptable solution will be reached. If the patient absolutely cannot tolerate positive pressure devices, then an oral appliance may be tried. Oral appliances should be used for mild OSA or in patients who refuse CPAP.

If the patient's OSA is felt to be secondary to obesity, then weight loss and appropriate behavior modification shouLd be encouraged. There is good evidence for the effectiveness of weight loss and improvement of symptoms in OSA. All patients with OSA should be instructed to avoid alcohol and medications that are sedating, as this will worsen the hypoventilation.

As previously noted, patients with severe OSA associated with pharyngeal obstruction, massive tonsils or oversized uvula and/or soft palate, may be considered for surgical evaluation. (Some patients have remarkably good results from various surgical interventions.)

Medications have been considered for the treatment of OSA, but none are in popular use. The carbonic anhydrase inhibitor, acetazolamide, that has some benefit in central sleep apnea, has not shown efficacy in obstructive sleep apnea. Carbonic anhydrase inhibitors stimulate respiration by causing a metabolic acidosis, resulting in respiratory compensatory hyperventilation. Although OSA patients may hyperventilate while awake as a result of the medication, it does not improve apneas while sleeping.

E. Common Pitfalls and Side-Effects of Management.

Managing patients with OSA post operatively is a challenging task and presents a significant risk of morbiditiy and even mortality. Post operative hypoventilation as a result of anesthesia and pain medication is a problem in patients without OSA and a major risk for patients with suspected or known disordered breathing.

Any patient with the diagnosis of OSA and using a positive pressure breathing device at home, should bring the device to the hospital when admitted for surgery, or for that matter, any other hospitalization, and it should be used at the home settings immediately post operatively and until the patient no longer requires narcotic analgesics.

Patients with suspicion of OSA, but without a diagnosis, who proceed to surgery are at risk of post operative hypoventilation or respiratory arrest. If there is a high index of suspicion based on anesthesia evaluation or the STOP-BANG questionnaire, the patient should be monitored carefully and should have continuous pulse oximetry post operatively, at least while they are receiving sedating analgesia. If possible avoid the supine position; sometimes the patient may be positioned in the lateral decubitus position with good results. Regional anesthesia is considered preferable to general anesthesia.

Avoid sedating medications including benzodiazepines, barbiturates, opiates, alcohol, and antihistimines.

*A caveat: If a sedated patient is repeatedly hypoxic while wearing CPAP, reposition the head and try to achieve extension of the neck. If hypoxia persists, remove the CPAP and check the equipment for any type of obstruction or malfunction. If oxygen sats come up while off CPAP, call respiratory therapy to bring another machine.

Suggested Orders for patients suspected to have OSA:

1. Continuous pulse oximeter with an alarm for O2 saturation <90% (or below their baseline).

2. May use supplemental oxygen for O2 low saturations. Saturation goal depends on comorbidities.

3. Elevate HOB 30%.

4. Avoid oversedation. Hold sedating medications for somnolence.

5. Early ambulation if possible.

6. Any patient with prescribed CPAP, the equipment should be used while in bed continuously (except when eating) and should be continued at the predetermined pressure settings, or the pressure settings recommended by respiratory therapy.

IV. Management with Co-Morbidities.

Oversedation is a major problem in patients with OSA. Any co-morbid condition that decreases level of consciousness or increases the blood level of sedating medication can be a problem. Monitor patients with liver or kidney disease who are receiving sedating medications that are metabolized by these organs. Also consider drug interactions that may cause an increase in drug bioavailability. Since end stage renal disease is frequently associated with sleep apnea, this relationship should be kept in mind when prescribing sedating medications to patients with renal function impairment.

A. Renal Insufficiency.

Sleep apnea is common in patients with chronic renal failure and patients with OSA have increased sensitivity to sedating medications. Any sedating or analgesic medications that are excreted by the kidney may result in higher blood levels in patients with renal insufficiency and therefore, have an increased effect.

As noted earlier, patients with ESRD have a very high incidence of OSA, so this is a common problem.

B. Liver Insufficiency.

Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) have an increased incidence in patients with OSA. Incidence rate of OSA in patients with biopsy proven NAFLD or NASH was 46%, even when corrected for BMI, diabetes, triglyceride levels and cholesterol.

Patients with OSA have increased sensitivity to sedating medications. Any sedating or analgesic medications that are metabolized by the liver may result in higher blood levels in patients with hepatic insufficiency and therefore, have an increased effect. Additionally, if the patient has hepatic encephalopathy, OSA with daytime cognitive impairment may complicate the mental status examination.

C. Systolic and Diastolic Heart Failure.

Obstructive Sleep Apnea increases the risk of hypertension, left ventricular hypertrophy and likewise, diastolic dysfunction. A prospective study of 81 ambulatory men with CHF found 51% positive for >15 hypopneas per hour (AHI=15). In systolic heart failure, patients may demonstrate both obstructive sleep apnea and central sleep apnea simultaneously. Consequently, patients with heart failure, systolic or diastolic, have a high incidence of OSA and should be monitored carefully for this condition, even if not previously recognized. Furthermore, the severity of nocturnal apneas may be severe, since the patient may also have concomitant central sleep apnea. Nocturnal increase in dysrhythmia on the heart monitor may be a clue that the patient is hypoxic during sleep.

D. Coronary Artery Disease or Peripheral Vascular Disease.

Studies confirm that patients with ischemic heart disease suffer ST depressions and evidence of worsening ischemia during nocturnal hypopneas, particularly in the rebreathing phase when the heart rate increases concomitantly with low oxygen saturations. These effects were ameliorated by the use of CPAP. OSA is felt to be etiologic in the development of ischemic heart disease and also worsening of symptoms of previously diagnosed coronary artery disease.

E. Diabetes or other Endocrine issues.

Sleep apnea has been proposed as an independent risk factor for insulin resistance, independent of obesity.

Patients with significant hypoglycemia and concomitant decreased level of consciousness are at increased risk of prolonged apneas with OSA.

Hypothyroid patients may hypoventilate secondary to their disease and many features of hypothyroidism - increased weight, enlarged tongue, fatigue and lethargy - predispose to OSA. Untreated hypothyroidism is a risk for sleep apnea.

Cushinoid patients, from endogenous or exogenous steroids, who develop trunkal and neck adiposity are at increased risk of obstructive hypoventilation and should be monitored for this problem.

F. Malignancy.

Patients with cancer or other chronic pain syndromes who are maintained on sedating pain medication should be monitored for symptoms of OSA. Frailty and weakness that may accompany cancer also increases the risk of hypoventilation.

Treatment for head and neck cancers with chemotherapy or radiation, may result in swelling that may, in turn, predispose to develop obstructive sleep apnea.

There is an increased incidence of oral cancer in patients diagnosed with OSA. No causality of this relationship has been found.

G. Immunosuppression (HIV, chronic steroids, etc).

OSA is a relatively common diagnosis among HIV patients, most commonly as a result of adenotonsilar hypertrophy. One case resport describes a patient with antiretroviral induced lipodystrophy with severe OSA. This patient's BMI was only 26.1, but his neck circumference was 53 cm.

H. Primary Lung Disease (COPD, Asthma, ILD).

In patients with COPD and baseline hypoxic lung disease, OSA exacerbates the nighttime hypoxia. Similar issues prevail with other lung disorders, since the hypoxia is additive. Concomitant lung disease complicates the management of OSA. Each disease needs to be managed independently.

I. Gastrointestinal or Nutrition Issues.

There is a relationship between OSA and gastroesophageal reflux disease. OSA is more common in patients with GERD. Interestingly, treating GERD can improve sleep apnea and likewise, treating sleep apnea can improve the symptoms of GERD. It is not known if this is a causal relationship or not, but most seem to favor the idea that both diseases have common risk factors and therefore, tend to occur in the same population.

J. Hematologic or Coagulation Issues.

Head and neck lymphadenopathy may predispose patients to obstructive hypoventilation. Pharyngeal and soft palate swelling may result in obstructive apnea. Patients with OSA have some hypercoagulable predisposition which may be increased by hemotologic problems that are at increased risk of clotting, such as thrombocytosis, polycythemia and malignancy.

Significant underlying anemia may exacerbate the tissue hypoxia associated with the nocturnal hypoventilation.

K. Dementia or Psychiatric Illness/Treatment.

Sedating psychiatric meds may worsen the frequency of apneas and severity of hypoxia. Weight gain associated with psychiatric medication may predispose to OSA.

Depression is a frequent comorbid condition with OSA, and may improve with treatment.

V. Transitions of Care.

A. Sign-out considerations While Hospitalized.

Note:

-Avoid oversedation; avoid PCA. Use sleeping medications with care.

-Mention positional apnea, if appropriate.

-If patient is using CPAP while sleeping, mention that in the cross cover note.

-If the patient is having nocturnal symptoms or dysrhythmia, discuss management plan.

B. Anticipated Length of Stay.

Many hospitalized patients have this disorder, but it is rarely the reason for admission.

C. When is the Patient Ready for Discharge.

For patients that were not on home oxygen prior to admission, the patient should be able to maintain pre-hospital O2 saturations for 1-2 hours without supplemental oxygen prior to discharge. If they were on home oxygen, the same rule applies, that is, they should be back to their prior baseline.

If the patient was previously known to have OSA, they should be sent home on their usual CPAP or BiPAP with the prescribed settings. If the patient was started on positive pressure therapy in the hospital, they must be fully back to pre-hospital baseline at discharge and should also be referred for polysomnography as soon as possible.

D. Arranging for Clinic Follow-up.

Making an appointment for a formal sleep study prior to the follow up primary care appointment, may save time for the work up. Sometimes patients refuse a sleep study appointment until they have an appointment to discuss the issue with their primary doctor. It is a good practice to make sure they soon have a follow up appointment with the PCP and to discuss the issues, by phone or email with the PCP.

1. When should clinic follow up be arranged and with whom.

Under most circumstances, the patient may be referred back to the primary care physician for work up and management of sleep apnea. Many community hospitals do not have access to formal sleep study laboratories for in-patients; these studies are usually done as out-patients. Frequently, the diagnosis of sleep apnea is entertained because of patient risk factors and sometimes, evidence of hypoventilation, usually in the context of oxygen desaturations, noted while the patient is receiving sedating medications. If the patient is not discharged on sedating medications and their breathing status is back to pre-hospital state, then referring the patient back to the primary doctor to set up the sleep study is an option.

No specific guidelines have been published for acceptable time frame for follow up, so the urgency of follow up is determined by the severity of the hypoxia and the subsequent risk to the patient. Severe hypoxic events that occur in the hospital are often associated with PCA pumps or episodes of severe pain that requires multiple injections of pain medication to achieve control. If the patient had a severe apneic event or respiratory arrest as a result of sedating medication and presumed sleep apnea during the hospitalization, then it would be appropriate to make an appointment for a sleep study in a week or two of discharge and prior to the follow up visit with the primary care doctor.

Suspicion of OSA, particularly severe episodes of hypoventilation, should be discussed with the PCP who will be assuming care in follow up. This recommendation assumes the patient achieved a reasonable baseline. We recently had a patient admitted with such persistent hypoxia that achieving adequate CPAP was requisite for discharge.

2. What tests should be conducted prior to discharge to enable best clinic first visit.

The continuous pulse oximetry reading, documenting desaturations is valuable to the primary care physician's on going management. If an echocardiogram was performed in the hospital, this can also provide evidence for sequelae of long standing hypertension (such as LVH) or evidence of pulmonary hypertension, and should be made available to the primary care doctor.

3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit.

If a hospitalized patient is suspected or confirmed to have sleep apnea, it is important to schedule a formal overnight sleep study prior to the return visit to their primary care physician. The formal study will quantitatively evaluate the severity of hypoventilation and look for concomitant other related diagnoses.

E. Placement Considerations.

Rarely would a patient require placement for sleep apnea unless the disorder was so severe that patient required constant monitoring. On the other hand, many, if not most patients being referred for placement will have sleep apnea, risk factors for sleep apnea or other sleep disordered breathing. If the patient uses a positive pressure breathing device, it should accompany them to the long term facility.

F. Prognosis and Patient Counseling.

With good patient compliance on appropriate therapy, most patients experience significant improvement in quality of life and in symptoms of secondary disease. Counseling is key, since the treatment program requires patient participation for implementation. Weight loss alone may result in resolution of the disorder in some patients.

VI. Patient Safety and Quality Measures.

A. Core Indicator Standards and Documentation.

Outcomes assessment is based on level of daytime sleepiness or an objective evaluation of maintenance of wakefulness. The assessment also addresses adherence to treatment plan, quality of life issues and weight loss objectives.

B. Appropriate Prophylaxis and Other Measures to Prevent Readmission.

Good patient education and patient compliance with the planned management program is essential. This is facilitated by good communication with the primary physician. The patient should be instructed not to drive or operate dangerous equipment if the AHI is greater than 20, until sleep analysis outcome assessment has documented improvement on therapy.

VII. What's the evidence?

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Hauri, PJ. The International Classification of Sleep Disorders. 2005.

http://www.guidelines.gov/content.aspx?id=15298.

"Obstructive Sleep Apnea and Commercial Motor Vehicle Driver Safety presented to : Federal Motor Carrier Safety Administration". 2008.

Gupta, RM, Parvizi, J, Hanssen, AD, Gay, PC. "Postoperative complications in patients with OSA syndrome undergoing hip or knee replacement: a case-control study". Mayo Clin Proc. vol. 76. 2001. pp. 897.

Gross, JB. "Practice Guidelines for the Perioperative management of patients with OSA: A report by the Am Soc Anesthesiology Task Force on Perioperative Management of Patients with OSA". Anesthesiology. vol. 104. 2006. pp. 1081-93.

Adesanya, AO, Lee, W, Greilish, ND, Joshi, GP. Chest. vol. 138. 2010. pp. 1489-98.

Peled, Nir, Abinader, E, Giora, P. "Nocturnal ischemic events in patients with obstructive heart disease". JACC. vol. 34. 1999. pp. 1744-1749.

Vasu, TS, Doghramjik, Cavallazzi, R. "Obstructive Sleep Apnea Syndrome and Post Operative Complications: Clinical Eval of the STOP-BANG Questionnaire". Arch Otolaryngol Head and Neck Surgery. vol. 136. 2010. pp. 1020-4.

Chung, F. Anesthesiology. vol. 108. 2008. pp. 812-821.

Chung, F. Anesthesiology. vol. 110. 2009. pp. 194.

Jobin, V, Mayer, P, Bellemare, F. "Predictive Value of Automated Oxygen Saturation anaysis for the diagnosis and treatment of OSA in a home-based setting". Thorax. vol. 62. 2007. pp. 422-427.

Greenburg, DL. "Effects of surgical weight loss on measures of OSA: a meta-analysis". AmJ Med. vol. 122. 2009. pp. 535.

Eur Respir, J. vol. 9. 1996. pp. 634-635.

Stepanski, E, Faber, M, Zorick, F, Basner, R, Roth, T. "Sleep Disorders in patients on CAPD". J Am Soc Nephrol. vol. 6. 1995. pp. 192-7.

Kimmel, PL, Miller, G, Mendelson, WB. "Sleep apnea syndrome in Chronic Renal Disease". Am J Med. vol. 86. 1989. pp. 308-14.

Sharp, JT, Druz, WS, Souza, VD, Diamond, E. "Effect of Metabolic Acidosis upon sleep apnea". Chest. vol. 87. 1996. pp. 619-24.

McNeil, Jane. "Screen Sleep Disorder patients for GI reflux.". 2007. pp. 39. www.internalmedicinenews.com,.

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