Mild and severe cases of sleep apnea

EA AARON E. SHER, MD, FACS, PHILLIP R. WESTBROOK, MD, ACP, FRANK J. ZORICK, MD INTRODUCTION: In this section two real case histories are presented along with the response of a panel of three authorities on the subject of obstructive sleep apnea regarding their management. Although these types of cases are not unusual, their management is difficult and at times controversial. The first case is that of a patient with relatively mild obstructive sleep apnea, but with significant subjective complaints and especially loud snoring. The question how to treat this patient is offen being asked, and significant divergence of opinion may exist in that respect among treating physicians. The second case is that of a patient with severe obstructive sleep apnea associated with alveolar hypoventilation syndrome. Management of this patient, particularly in regard to the appropriate selection of treatment modality, is quite problematic.

CASE ONE: WHEN AND HOW TO TREAT THE MILD SLEEP APNEA PATIENT A 36-year-old man with treatmentresistant hypertension was seen in outpatient consultation complaining of fitful sleep, dyspnea on exFrom the Division of OtolaryngologyHead and Neck Surgery, Albany Medical College, and the Capital Region Sleep ' Wake Disorders Center of Albany Medical Center and St. Peter's Hospital, Albany, NY; the Sleep Disorders Center, Cedars-Sinai Medical Center, Los Angeles, CA; and the Sleep Disorders Center, Henry Ford Hospital, Detroit, MI. Address reprint requests to Aaron E. Sher, MD, FACS, 980 Western Ave, Albany, NY 12203. Copyright © 1991 by W.S. Saunders Company 1043·1810/91/0202-0008 $05.00/0

ertion, and daytime sleepiness of 3 years' duration. At night, he fell asleep quickly, but awakened frequently due to nocturia and for other unknown reasons. His wife stated that his snoring was "terrible" and that he "gasped for breath" during the night. His usual bed-time was 11 PM and he arose at 8 AM each morning. He claimed to sleep only 3 hours per night due to the awakenings. No accessory symptoms of narcolepsy were elicited. Medications at the time of the initial consultation were minoxidil 10 mg, ranitidine HC( 150 mg, furosemide 40 mg, verapamil HCI 120 mg, and a clonidine patch. Past medical history showed no previous history of pulmonary disease, alcohol or drug misuse, or cardiac disease. Patient has a history of significant peptic ulcer disease of 1 year's duration and a gunshot wound to the jaw 20 years previous to the consultation. Patient had gained 30 Ibs over the past 2 years. He smoked one pack of cigarettes per day for 20 years. On examination patient is 172 V2 cm tall, weighs 141 kg, is afebrile and has a blood pressure of 160/ 110 mm Hg (supine left arm) . Pulse is 104 and regular. On oral exam there are large tonsils and extremely redundant tissue in the posterior oropharynx; the uvula is of normal size. There are no jugular venous distention, carotid bruits, thyromegaly, or lymphadenopathy. There are decreased breath sounds, but no adventitial sounds on chest examination. Other than obesity. abdominal exam is unremarkable. There is no cyanosis or clubbing, but there is 2 + pedal edema. Chest x-ray. ECG, and arterial blood gases were all within normal limits.

In laboratory studies, the following were found : CPK, 432 lUlL (lab reference range 0 -190); SGOT, 54 lUlL (lab reference value 0 - 33); SGPT. 99 lUlL (lab reference range o- 40). Hemoglobin, glucose and electrolytes were within normal limits. The nocturnal polysomnography values were the following: time in bed, 479.5 minutes; total sleep time , 287.5 minutes; percent stage 1 sleep, 41%; percent stage REM sleep, 3.5%. . Respiration recording showed 28 apneas per hour of sleep, 88% of the apneas were obstructive, and there were an additional 18 hypopneas per hour of sleep. Waking oxygen saturation was 96% and the oxygen saturation fell below 85% 5 times per hour of sleep from 0.6 minutes per hour of sleep below 85%. Loud snoring was noted throughout the recording session. The ECG demonstrated waking tachycardia with mild sinus arrhythmias associated with the apneic events. A daytime multiple sleep latency test (MSLT) showed a mean sleep latency of 15 minutes and no REM sleep is recorded on any of the four nap opportunities.

DR. SHER: The patient's history of "terrible" snoring , nocturnal gasping for breath, frequent nocturnal arousals, and excessive daytime sleepiness (EDS) sug gests the diagnosis of obstructive sleep apnea syndrome (OSAS) . Factors contributing to his pro.pensltyfor OSAS include morbid obesity. Note that his daytime sleepiness has been observed for 3 years, while his weight rapidly increased over most of this period. His large tonsils and extremely re-

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dundant oropharyngeal soft tissue contribute to compromise the oropharyngeal airway despite the normal uvula. . He had a gunshot wound to his mandible many years ago. It is not stated whether this injury resulted in permanent alteration of structure or function of the mand ible or temporomandibular joints. If, indeed. the latter were sequelae of the mandibular injury, then there may be resultant compromise of the hypopharyngeal airway as well. The latter would be a consequence of posterior displacement of the tongue into the hypo pharyngeal airway. The resistance to treatment of the patient's hypertension may result from the OSAS. Similarly, his pedal edema is suggestive of right-sided congestive heart failure. the latter being exacerbated by the OSAS. Polysomnographic evaluation confirms the diagnosis of moderately severe OSAS. Interestingly, the 'mu lt iple sleep latency test (MSLT) does not confirm the subjective complaint of excessive daytime sleepiness. However, one may have an erroneously negat ive MSLT if arousals are so frequent that early sleep onset is, in a sense, camouflaged. With the diagnosis of OSAS thus established, one should initiate a therapeutic trial of nasal continuous positive air pressure (CPAP) with simultaneous polysomnographic evaluation. If effective and accepted by the patient, CPAP should be prescribed . Simultaneously, the patient should commence a medically supervised program of weight reduction. Although he is morbidly obese, his history suggests that his EDS was progressive during a recent period of rapid weight gain. This implies that weight loss even to a level considerably above his ideal body weight might have a significant impact in ameliorating the OSAS. It may be that his threshold for OSAS was crossed at a point far in excess of his ideal body weight. If, on the other hand, CPAP is ineffective or rejected by the patient, the severity of his OSAS and the treatment-resistant hypertension would justify immediate con-

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sideration of surgical options in addition to weight loss. Fiberoptic endoscopy with Muller's maneuver and cephalometric analysis would help to define the focus of oropharyngeal compromise as being "upper," ie, naso- and oropharyngeal, or " lower," le, hypopharyngeal, or a contribution of both . If investigation suggests " upper" compromise, uvulopalatopharyngoplasty (UPPP) is more likely to be effective than if significant "lower" compromise is suspected. On the other hand, if investigation suggests that the patient has significant hypopharyngeal collapse, then UPPP is less likely to provide adequate modification of the airway for resolution of the OSAS. The patient might need a surgical procedure that augments the hypopharyngeal airway, ie, laser midline glossectomy and Iinguoplasty, horizontal inferior sliding mandibular osteotomy and hyoid myotomy and suspension, or mandibular advancement. These procedures may be performed alone or in conjunction with UPPP depending on the observed pattern of airway compromise. Mandibular advancement would be appropriate if cephalometric evaluation documents significant anatomical mandibular deficiency. Permanent tracheostomy remains a universally effective, therapeutic approach for OSAS. Similarly, maxillary and mandibular advancement appears to be as effective as permanent tracheostomy in severe cases. The documentation of the efficacy of this latter procedure is limited. The decision regarding the appropriateness of a permanent tracheostomy or maxillary-mandibular advancement in this patient would depend on the severity of his EDS and the clinical impression of whether his treatment-resistant hypertension is significantly exacerbated by the OSAS. DR. ZORICK: This patient's symptoms are consistent with sleep apnea syndrome. Polysomnographic recording documents sleeprelated respiratory disturbance, associated with little change in ox-

ygen saturation or ECG. Daytime sleepiness is not confirmed by the multiple sleep latency test. My evaluation is mild sleep apnea syndrome. Conservative treatment would be the best start. The patient would be counseled about his sleep habits, alcohol use, weight and the need for better control of his blood pressure through his internist. A referral for behavior treatment and dietary counseling to plan for weight control is suggested . Also, an otolaryngologic consultation to examine the upper airway anatomy and suggest surgical options is requested. The next step is a discussion with the patient of the previous findings and of the treatment possibilities. Continuing conservative treatment is an acceptable alternative with annual polysomnographic re-evaluation. My experience 1 shows that patients with .mild sleep apnea do not worsen over 1 to 2 years unless there is significant weight gain . Most patients who experience moderate (5% to 10%) weight loss will improve. Nevertheless, preparation for active treatment is started early because the patient's course might worsen or the patient may not follow the treatment plan. In that case, the preparation for an intervention is accomplished. Once the degree of sleep apnea is judged more severe, then one must pursue a specific surgical intervention (such as UPPP, tonsillectomy, or nasal surgery), or nasal CPAP. See the discussion on case 2 for the protocol typically followed when active treatment is required . If the patient rejects the conservative .treatment plan, then a surgical intervention is presented as an option. The patient needs to realize that the degree of symptomatic improvement may be modest, even if the respiratory disturbance in sleep is improved significantly by surgery. Polysomnographic follow-up after surgery is necessary to define the objective changes. After successful surgery, the patient must continue to stabilize weight or risk recurrence of the sleep apnea syndrome."

MILD AND SEVERE CASES OF SLEEP APNEA

DR. WESTBROOK: This 36year-old man has very serious hypertension in spite of intensive medical therapy. The observation by his wife would be consistent with obstructive sleep apnea, as would be his complaint of daytime sleepiness, but the frequent awakenings at night are not typical. These may be due, in part, to his medication. An interesting piece of history is the gunshot wound to the jaw in the past. One wonders what this did to his oropharyngeal anatomy. It is not mentioned on examination, which does, however, show very large tonsils with redundant tissue in the posterior oropharynx. He is very obese. Although there is pedal edema, arterial blood gases are reported to be within normal limits, and apparently he does not have cardiomegaly either by chest x-ray or electrocardiogram. Laboratory studies are given that-are difficult to interpret without further information. These are the enzymes that could reflect anything from a recent muscular bruise to some mild hepatitis. They are only mildly elevated, and absent other information, I do not believe they contribute to the understanding of this patient's problem or its therapy. Polysomnography shows a total of 46 respiratory events per hour. Although 88% of the apneas are reported as obstructive, meaning that apparently three were central, the loud snoring indicates that there is significant airway obstruction. Presumably, the 18 hypopneas are also obstructive and do lead to arousal. Thus, 46 events per sleep hour is a clinically important level of disordered breathing events and sleep fragmentation. Interestingly enough, he does not desaturate significantly despite the obesity, and his electrocardiogram shows a normal response to apnea. It is surprising that his multiple sleep latency test shows a normal level of alertness. One would like to know that the mean number is not strongly influenced by a nap in which he did not fall asleep at all, where other naps showed he was SHER ET AL

quite sleepy. This can happen occasionally in hypersomnolence patients, especially with the last nap. Regardless of the multiple sleep latency test, the patient's hypertension, daytime symptoms, and polysomnogram are all reasons for urgent treatment. The longterm goal of treatment will be weight loss because of the hypertension and the sleep apnea, but I think he also should have a trial of nasal continuous positive airway pressure to see if controlling his sleep apnea will help bring his hypertension under better control. The description of this patient's pharyngeal passageway suggests that he is a candidate for uvulopalatopharyngoplasty and tonsillectomy. He should have a very careful examination of his nasopharynx, possibly with Muller's maneuver, to try to determine the site of collapse. Cephalometries might be helpful in assessing his likelihood of response to surgery, although there is no imaging technique reported to date that completely reliably predicts response to surgery. Some of the newer techniques, such as ultrafast CT scanning, show promise in this regard. In summary, this gentleman should have a nasal CPAP trial and treatment, enroll in a weight loss program, and be considered for uvulopalatopharyngoplasty.

REFERENCES 1. Zorick Fl, Roehrs TA, Rosenthal LD, et

al: Natural course of sleep apnea: A preliminary report, in Chase MH, Lydic R, O'Conner C (eds): Sleep Research. Vol. 19. Los Angeles, CA, Brain Information Service, 1990. 2. Conway W, Fujita S, Zorick F, et aI: Uvulopalatopharyngoplasty-one year followup. Chest 88:385-387, 1985.

CASE TWO: HOW TO TREAT THE SEVERE SLEEP APNEA PATIENT WITH ALVEOLAR HYPOVENTILATION SYNDROME

A 37-year-old woman was referred for evaluation with a history of

snoring and fatigue. She has snored loudly for most of her life; however, the intensity has increased in the past year. Her husband reports pauses in her snoring, followed by a gasp. She reports awakenings nearly every 2 hours twice a night, associated with heartburn, or for dyspnea and palpitations (five times per week). The patient frequently has night sweats and has fallen out of bed several times. She has worked nights for 13 years. When working, she goes to bed at 9:30 AM and gets up around 4:30 PM. When not working, she goes to bed at 10:30 PM and gets up with an alarm at 7:30 AM. She generally takes 30 to 60 min utes to fall asleep and does not feel refreshed on awakening. She describes significant sleepiness at work during the past 2 years, unintentionally falling asleep at her 2:00 AM break, even when standing. She esti'mates that once a week she falls asleep drivinq home from work, though denies sleepiness during her commute to work. Five years ago, she had a motor vehicle accident as a result of falling asleep. When not at work, she falls asleep after reading for 10 minutes, watching television, or while sitting on the toilet. The patient usually naps for an hour in the evening before going to work. She reports hypnagogic hallucinations twice a week when falling asleep, but she denies symptoms of cataplexy or sleep paralysis. Past medical history showed she had a tonsillectomy and adenoidectomy in 1956; was hospitalized for pneumonia in 1982, asthma in 1986, and a bleeding ulcer in 1989. Review of systems significant for sleep apnea revealed frequent sinus infections, a chronic dry cough, and dyspnea on walking half a block. Her medications include Zantac 150 mg BID, Vanceril inhaler PRN for shortness of breath. On physical examination she is 5 feet tall and 388 Ibs, with a body mass index of 75.8. Her blood pressure is 116/64 in the right arm, sitting, using a large cuff; pulse at 88 regular. Throat exam showed a large uvula, a long soft palate, with

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a small oropharyngeal introitus. Nasal exam showed a right septal deviation with a small passage on the right and bilateral congestion . There was 2 + bilateral pedal edema of the lower extremities. Rest of the exam was unremarkable. In laboratory studies, her arterial blood gases on room air were pH 7.41, Pc0 2 44, P0 2 68, CO2 32, BE 1.8, Sa0 2 90%. Pulmonary functions test showed mild to moderate restriction; chest x-ray was negative. The polysomnography values were as follows. The patient slept 378 minutes for a sleep efficiency of 68.7% . Sleep latency was 5 minutes and REM latency was 100 minutes. Her sleep architecture was stage 1 sleep at 39.7% REM at 8.9%. Respiratory monitoring showed 284 obstructive apneas, 356 partial upper airway obstructions; there were 101.6 abnormal breathlnq events per hour of sleep. All data were obtained in the supine position. Baseline Sa0 2 ranged from 80% to 90% in non-REM and 70% to 80% in REM sleep. The lowest Sa0 2 was 52%. There were 6 episodes of desaturation below 60%, 30 below 70% , and 202 below 80%. The longest apnea was 38 seconds. ECG showed a sinus arrhythmia with apnea, with a range of 44 to 109 beats per minute. Occasional multifocal PVCs were noted. Tibialis anterior EMG monitoring was unremarkable. MUltiple sleep latency testing showed a mean sleep latency of 4 minutes. Individual sleep latencies for the five subtests were 2.5, 4.5, 4.0, 7.0, and 2.0 minutes. Sleep-onset REM was noted in the fourth subtest. DR. SHER: The patient presents with a complex problem, as at least two sleep-wake disorders contribute to her complaints. Her history and physical findings suggest the diagnosis of obstructive sleep apnea syndrome (OSAS), and this diagnosis was confirmed by polysomnography (PSG). Mean sleep latency (MSL) of 4 minutes corroborates her severe excessive daytime sleepiness (EDS). While severe OSAS might alone account

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for this degree of EDS, her frequently changing sleep-wake schedule is a contributing problem, as it results in disrupted sleep architecture. Her OSAS should be treated with urgency, while she is encouraged to slrnultaneously regularize her irregular sleep/wake cycle. She should have a trial of nasal CPAP while monitored by PSG. If nasal CPAP is effective in eliminating her OSAS, and if she tolerates its use and agrees to regular nightly compliance, CPAP therapy should be initiated along with a formal protocol of medically supervised weight reduction. If CPAP proves to be unsuccessful because her nasal obstruction mandates inordinately high CPAP pressures, a course of decongestant and/or nasal steroid therapy might induce a decrease in nasal resistance and greater CPAP efficacy at lower pressures. If this does not succeed, then nasal septal reconstruction might diminish nasal resistance and permit use of CPAP. A more adequate nasal airway might also have a beneficial effect on her OSAS. The severity of her OSAS would mandate a concomitant temporary tracheostomy to protect her upper airway perioperatively. Assuming that nasal CPAP is effective, then the next consideration relates to the ultimate degree of success of her weight reduction program. If unsuccessful, gastric surgery such as gastroplasty might be considered. When the patient achieves an acceptable weight, repeat PSG should be undertaken. If she still has OSAS, then she has two options: to remain permanently on CPAP or to undergo surgical intervention to her upper airway to eliminate the OSAS. On the other hand, if CPAP proves not to be useful, then tracheostomy is her first line of de-. fense from the outset. In this situation, she should undergo immediate tracheostomy to permit stabilization of her medical status while she proceeds with an attempt at weight reduction and/or evaluation for upper airway corrective surgery.

If the option of upper airway correct ive surgery is contemplated, an attempt should be made to localize the region of the upper airway that is most vulnerable to collapse. Fiberoptic endoscopy with MOiler 's maneuver and lateral cephalometry are both helpful in this regard. Dynamic cephalometry awake and fiberoptic endoscopy and fluoroscopy asleep can yield further information in difficult cases. If her upper pharynx is compromised, uvulopalatopharyngoplasty (UPPP) is indicated. If she still has severe OSAS at the point when UPPP is contemplated, one should perform a concomitant temporary tracheostomy to protect her upper airway during the perioperative period. Alternatively, one may consider using nasal CPAP to maintain patency of her upper airway in the perioperative period . If she has not yet undergone correction of her nasal problem, and medical therapy for it has proven inadequate, nasal surgery should be undertaken. If both nasal surgery and UPPP are contemplated, one should consider staging these procedures to avoid perioperative compromise of the upper airway at two different locations simultaneously (ie, pharyngeal edema as well as nasal 'edema and/or packing), unless a protective temporary tracheostomy is performed. If the pharyngeal region of greatest vulnerability to collapse is determined to be the lower pharynx and hypopharynx, the patient would need a procedure that augments the hypopharyngeal airway, ie, laser midline glossectomy and Iinguoplasty, horizontal inferior sliding mandibular osteotomy with hyoid myotomy and suspension , or mandibular advancement. If cephalometric evaluation documents significant anatomical mandibular deficiency, then mandibular advancement would be indicated. If both the upper and lower pharynx are involved, UPPP may also be required. If all of the above prove unsuccessful, permanent tracheostomy or maxillary and mandibular advancement remain options. Tracheostomy is universally effec-

MILD AND SEVERE CASES OF SLEEP APNEA

tive. Maxillary-mandibular advancement may be as effective as tracheostomy in severe cases that are otherwise resistant to the usual therapeutic approaches outlined above. While aggressively receiving treatment for her OSAS, she must be encouraged to correct her irregular sleep/wake cycle. Assignment to a regular day or evening shift would be to her advantage, as it would permit her to sleep consistently at night in harmony with most of the rest of society. If this cannot be arranged and she must continue to work the night shift and persists in having EDS despite correction of her OSAS, it should be suggested that she maintain the same sleep/wake schedule throughout the week and weekend . Although this may be difficult because of social pressures , elimination of frequent sleep/wake cycle shifts would help to regularize her sleep architecture and diminish her EDS.

DR. WESTBROOK: Polysomnography demonstrates that this 37year-old woman has severe obstructive sleep apnea, at least in the supine position. Unfortunately, no data were obtained with the patient sleeping on her side. However, the history is consistent with severe hypersomnofence secondary to sleep fragmentation, and the multiple sleep latency shows objective evidence of hypersomnolence. So, presumably, she either routinely sleeps on her back, or her obstructive apneas and hypopneas are position-independent. There are a number of caveats about the history and the findings that need to be mentioned before discussing her severe sleep apnea and its treatment. First of all , the patient has a circadian rhythm disorder secondary to her shift work. On weekends, she has the equivalent of crossing a number of time zones, going to bed at 10:30 PM rather than her usual 9:30 AM . Also, on nonworkdays she will sleep 9 hours rather than the 7 hours plus a 1-hour nap she gets on workdays. It is interesting and, SHER ET AL

indeed, almost inexplicable that despite severe hypersomnolence, she " generally" has an initial sleep latency of 30 to 60 minutes. This may reflect the circadian rhythm disorder which, while due to shift work, is more like a time-zone change of some 13 hours. Another problem revealed by her history is awakening frequently with heartburn, suggesting sleeprelated gastroesophageal reflux. This is not surprising in view of her extreme obes ity. On examination, in addition to her extreme obesity, the patient has another risk factor for obstructive sleep apnea, which is her abnormal pharyngeal passageway. Examination shows a large uvula, long soft palate, and small oropharyngeal introitus. In addition, there is some nasal septal deviation with bilateral congestion indicating a possible increase in nasal or upstream resistance. Perhaps the most worrisome finding on examination is the 2 + bilateral pedal edema of the lower extremities, which must have raised the possibility of right heart failure. However, arterial blood gases do not show CO2 retention (a Pco 2 of 44 is at the borderline upper limit given her Po 2 ) . and her awake P0 2 does not show the level of hypoxemia usually associated with pulmonary hypertension and right heart failure. Arterial blood gases are puzzling in that the saturation of 90% does not fit with a P02 of 68 and a pH of 7.41. A P0 2 of 68 would usually be associated with a saturation of between 93% and 94% given a normal oxyhemoglobin dissociation curve. Pulmonary function tests show a pattern presumably consistent with her obesity. As noted, the polysomnography shows extremely severe obstructive sleep apnea. The baseline saturation of 80% to 90% suggests a P0 2 of 58 to 45 and again raises a question about the initial arterial blood gases. Perhaps they were obtained in the seated position while the oximetry monitoring was done with the patient in the supine position. As expected with her massive obesity and the decrease in lung volume that occurs during

REM, saturation falls in that state. Although the electrocardiogram showed the expected bradytachycardia, only occasional multifocal PVCs were noted, which is reassuring . The multiple sleep latency test is consistent with the hypersomnolence expected with this level of sleep fragmentation, but must be interpreted with some caution. Presumably, the multiple sleep latency test was done during the daytime, which is actually her habitual sleep time, and this fact and the fact of the severe sleep fragmentation due to her obstructive apnea make the REM episode on the nap unremarkable. Obstructive sleep apnea of this severity is unusual in premenopausal women which, we presume, at age 37, describes this patient. However, she has overwhelming risk factors of massive obesity and an abnormal nasopha.ryngeaJ passageway. She has lifethreatening symptoms, already having had one motor vehicle accident due to falling asleep. Treatment is urgent, and I think the first thing that should be done is a trial of nasal continuous positive airway pressure. If successful and tolerated, this will provide an immediate relief of the apnea and her symptoms, and allow time for weight loss, which would be the long-term treatment goal. Indeed, weight loss is so important that the first surgical consideration might be gastric reduction surgery rather than upper airway reconfiguration. In my experience, surgical relief of nasal obstruction and uvulopalatopharyngoplasty stand a better chance of success after weight loss. Another reason for weight loss is her position-related gastroesophageal reflux. Weight loss would be the primary treatment modality for this condition. Once her obstructive sleep ap. nea is treated and she is no longer hypersomnolent, the patient should be warned that her circadian rhythm disorder will be uncovered and she might have significant insomnia secondary to this. She should either try to work days or, if she must continue working nights, she should try to

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maintain the same sleep/wake schedule, even on her days off. Appropriate exposure to light may be required in addition to a regular sleep/wake schedule. DR. ZORICK: There are atypical aspects of this case that require mention before a discussion of management. For example, it is unusual to find significant obstructive sleep apnea in younger women. As well, her diurnal symptoms of sleepiness are unusual as typically, patients with frequent respiratory events in sleep are continuously somnolent. It is important to note her very irregular sleep habits and the resulting chronic sleep loss, which plays a role in the degree of sleep apnea.' Similarly, the polysomnographic bedtime and the multiple sleep latency nap times are not stated, and interpretation of values such as sleep efficiency, total sleep time, and sleep latencies, is dependent on this information. Finally, the extreme obesity of the patient is relevant to the severity of the illness and its treatment. Certainly, this is not a typical patient with sleep apnea syndrome, and thus generalization to other cases is limited. Her symptoms of daytime sleepiness, fatigue, loud snoring, and disturbed nocturnal sleep are secondary to obstructive sleep apnea. Her complaints of nocturnal indigestion, nocturnal dyspnea, and tachycardia are also related to the sleep apnea. The severity of the sleep apnea syndrome determines the best management course. As severity increases, medical complications are more Iikely2 and an active treatment is selected . Severity is determined by the polysomnographic mea sures ." Most important is the amount of apneas and associated changes in oxygen saturation and ECG. The degree of objective daytime sleepiness (MSLT) measures the severity of the effects on functioning. The above factors are evaluated in the context of the patient's current medical diagnoses , particularly cardiovascular disease. In her case it is easy to establish severe sleep apnea

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syndrome as the number of respiratory events in sleep and associated physiological effects including sleepiness and the current medical evaluation are consistent with this judgment. The patient is told to avoid alcohol and other central nervous system depressants and to maintain regular sleep habits. Because she is a shift worker, the latter will be difficult to accomplish and may require leave from work or adjustment of her work shift. In discussing the treatment alternatives there are two possibilities, namely nasal continuous positive airway pressure (CPAP) or specific surgery. An otolaryngologic consult is requested to determine the presumed site of upper airway obstruction, to assess nasal patency, and to evaluate surgical options. The patient is then educated about CPAP and evaluated for nasal mask size and fit. These are important steps to assure future compliance with CPAP. The patient returns to the sleep disorders laboratory for CPAP initiation. A determination of the expiratory pressure that eliminates abnormal respiration in sleep in all positions and sleep stages is made. At this juncture, the patient is knowledgeable about treatment options, and an assessment of the most suitable therapy is determined. Several possibilities may emerge. The patient may reject either surgical treatment or CPAP therapy. If so, then the other intervention is used. If the patient rejects CPAP and no specific surgical option is feasible, then tracheostomy is necessary. At this point, once the sleep apnea is managed by CPAP or surgery, then weight management is considered. Significant weight Joss may eventually allow the patient to discontinue CPAP or allow removal of the tracheostomy. The patient is told weight gain w ill diminish improvement with specific treatment. Weight control may be attempted through referral for behavioral treatment and in some cases, a very lowcalorie diet or surgical treatment. Management of CPAP therapy requires ongoing patient contact to observe compliance, to support

the patient, and to solve difficulties that arise. These difficulties often involve nasal symptoms, nasal mask fittings, and equipment failures. In some cases, before initiation of CPAP, nasal surgery for an anatomic obstruction will be necessary. In most circumstances the use of CPAP results in nasal symptoms, most of which resolve with local treatment (eg, humidification, saline spray, nasal decongestants, or air filters) . A re evaluation of sleep and respiration takes place 6 weeks after initiation of treatment to determine the effectiveness of CPAP. Thereafter, the patient is seen in the office about every 6 months to evaluate continuing use, to provide support, and to monitor symptom remission. If CPAP is not the initial therapy, then specific surgery such as uvulopalatopharyngoplasty (UPpp), tons illectomy, or nasal surgery is recommended. A polysomnographic re-evaluation occurs 6 weeks after surgery to assess efficacy. Further treatment is required if the patient has not responded sufficiently, le, apnea index is greater than 20, there is significant oxygen desaturation in sleep , or significant ECG effects associated with sleep apnea. In that case, further surgery or nasal CPAP is suggested. The goal is to reduce the sleep apnea to a mild level, ie, apnea index of 20 or less with mild desaturation and no evidence of significant associated cardiac arrhythmia and remission of the patient's sleepiness. Once this is achieved, follow-up occurs in the office setting, with re evaluation in the sleep laboratory if symptoms significantly change.

REFERENCES 1. Leiter JC, Knuth SL, Bartlett D: The effect of sleep deprivation on activity of the genioglossus muscle. Am Rev Respir Dis 132:1242-1245, 1985 2. Shepard JW: Cardiopulmonary change s in obstructive sleep apnea, in Kryger MH, Roth T, Dement WC (eds): Principles and Practice of Sleep Medicine. Philadelphia, PA, Saunders, 1989, p 537 3. He J, Kryger MH, Zorick FJ, et al: Mortality and apnea index in obstructive sleep apnea. Chest 94:9-14, 1988

MILD AND SEVERE CASES OF SLEEP APNEA