 \200 \200 Immediate consequences of OSAS Once signi \201 cant upper airway obstruction occurs there will be increased inspiratory effort to overcome it. At a speci \201 c level of pleural pr essure (usually about \210\22215 cmH2O in non-sleep deprived subjects, but down to \210 \22280 cmH2O in OSAS) patients tend to arouse from sleep. The recurrent arousals result in two major consequences: sleep fragmentation, which leads to excessive daytime sleepi- ness, and autonomic changes including elevation of arterial blood pressure. Treatment success is de \201 ned as a normal ESS (Epworth Sleepiness Score <10) and eviden ce of adequate nasal CPAP usage (minimum usage of at least 3 hours per night, every night, veri \201 ed by downloaded machine data). Cardiovascular complications Severe sleep apnoea syndrome (affecting about 1 \200\2232% of the male population) is associated with a high cardiovascu- lar risk. Over 10 years, 14% of this group are predicted (by Framingham-index) to experience a stroke and 23% a myocardial infarction \200\223 a 37% combined risk. There are several potential mechanisms of vascul ar dam- age operating in sleep apnoea. During each apnoea cycle there are stereotypic rises in blood pressure, usually >30mmHg, and not uncommonly >100mmHg. These rises will induce s hear stresses in blood vessel walls \200\223 forces that are thought to cause vascular wal l damage and initiation of atherosclerosis. Each apnoea is also associated with hypox- aemi a and re-oxygenation, which may be disadvantageous through repeated \200\230ischaemia re-p erfusion injury \200\231. Sleep apnoea patients show evidence of increased production of re active oxygen species, increased systemic catecholamine production, abnormal vascular react ivity, reduced baro- receptor sensitivity and possibly impaired insulin resistance. Further more, circulating vascular risk factors (e.g. choles- terol, CRP) have been shown to be ele vated in OSA. Thus many features of the sleep apnoea syndrome may poten- tially contribute to vascular damage. It is dif \201 cult to esti- mate the risk reduction that correcting t hese factors might produce, because it has not been accurately de \201 ned from long-term randomized, controlled clinical trials. Cor pulmonale can result from severe untreated OSAS which probably constituted the original \200\230Pickwickian syndrome \200\231. It occurs if a patient has daytime hypoxaemia, Fig. 15.1.5 Blood pressure swings in OSAS. Arterial tracing during sleep (3 mins, Finapre s device) showing instant return of large systemic BP surges, with each of three apnoea ter minations, following removal of affective CPAP in a man with obstructive sleep apnoea. Long-term consequences of OSAS OSAS may be associated with various complications, including the following: \200 \200 \200 \200 \200 \200 \200 Accidents. Arterial hypertension. Arrhythmias. Myocardial infarction and stroke. Cor pulmon ale. Ventilatory failure. Insulin resistance. CHAPTER 15.1 Obstructive sleep apnoea 363 The most common complaint of patients with OSAS is excessive daytime sleepiness. This \201 nding shows a consid- erable inter-subject variability and the de \201 nition of abno r- mality can be dif \201 cult. The most widely used score to assess daytime sleepiness is the Epworth sleepiness scale (ESS) which asks patients to rate their tendency to fall asle ep in eight different situations of varying stimulation. most often resulting from co-existing COPD. Chronic hypoxaemia results in pulmonary hyperte nsion and \202 uid retention, producing the picture of cor pulmonale. Epidemiology There are a large number of studies on the prevalence of OSAS in the general p opulation, but the frequency of this disorder is still open to debate, mainly because of co ntrover- sies concerning clinical diagnostic approaches and the lack of a uniform de \201 nition of OSA(S). As a consequence, the reported prevalence of OSA differs considerably bet ween the various population based studies with a range from as low as 0.3% to as high as 26 % in middle-aged people. Broadly it is believed that up to approximately 2 \200\2234% of th e popula- tion in Western countries suffer from clinically signi \201 cant OSAS. The highe st frequencies are found in countries with a high prevalence of obesity as there is evidenc e for a strong correlation between BMI and OSA. The prevalence of OSA has been reported to be >20% in a community sample of middle-aged men with a mean BMI of 30.5kg/m2. Ethnic origi n seems to in \202 uence the prevalence of OSA, since a higher proportion of individuals w ith African or Oriental origin seem to have OSA compared to whites and Asians. An inherited basis for OSA is suggested by reports of fam- ilies with multiple affected members and gen etic epidemio- logic studies; the genetic basis for upper airway narrowing during sleep has not been de \201 ned yet. However, risk of OSA among relatives of patients with the disor der is almost twice that among neighborhood control subjects. Potential pathogenetic explan ations for these \201 ndings are provided by familial studies which have demonstrated tha t craniofacial abnormalities, structural features of the upper airway, and the propensity t o develop obesity are at least partially inherited. There is a strong predominance of OSA i n men, 2 \200\2233 times more men are affected than pre-menopausal women. Why men are at hi gher risk for the development of OSA is still unclear, however, hormonal in \202 uences on breathing during sleep and fat distribution cannot fully explain this differ- ence. The pr evalence in females probably increases after menopause, shifting the male-to-female ratio t o 2:1, possi- bly because body fat is redistributed to the upper body. OSA occurs in all ag es, although the prevalence in children and the elderly has been investigated less thorough ly. Several large population-based studies suggest that the mean age of patients with OSAS at presentation lies between 40 and 50 years. The prevalence of OSA and OSAS seems to rise continually with age and to level off after the age of 65 years. Of note, healthy elderly i ndividu- als commonly have a higher frequency of apnoeas/ hypopnoeas, which makes the de \201 nition of a clinically sig- ni \201 cant cut-off level of apnoeas even more dif \201 cult. Epworth Sleepiness Scale How likely are you to doze off or fall asleep in the situations described in the box below, in contrast to feeling just tired? This refers to your usual way of life in recent times. Even if you haven \200\231t done som e of these things recently try to work out how they would have affected you. Use the following scale to choose the most appropriate number for each situation: 0 = would never doze 2 = Moderate chance of dozing 1 = Slight chance of dozing 3 = High chance of dozing Situation Chance of dozing Sitting and reading Watching TV Sitting, inactive in a public place (e.g. a theater or a meeting) As a passenger in a car for an hour without a break Lying down to rest in the afternoon when circumstances permit Sitting and talking to someone Sitting quietly after a lunch without alcohol In a car, while stopped for a few minutes in the traffic Fig. 15.1.6 Epworth sleepiness scale. An ESS score of \211 10 is generally regarded as abn ormally sleepy and requires further investigations to \201 nd the underlying cause. Of no te, there is no good correlation between ESS and the severity of OSA which might be explain ed by perception problems of patients with OSA regarding their sleepiness. Furthermore, the re are many other possible reasons for excessive daytime sleepiness which are discussed els ewhere in this book. The bed-partner \200\231s account provides important informa- tion about what happens durin g a night, thus a complete medical history includes the patient \200\231s partner. The foll ow- ing symptoms are frequently observed by the bed-partner during the night: \200 \200 \200 \200 Snoring. Apnoeas. Restless sleep. Choking episodes. Diagnosis To date there is no sufficiently precise test in awake patients which diagnoses O SAS. However, there are some typical clinical features that should raise the clinical suspi - cion of OSAS: \200 \200 \200 \200 \200 \200 A physical examination of all patients with suspected OSAS is advised as it is important to detect possible causes and complications of OSA. The examination should include assessment s of: \200 \200 \200 \200 \200 Sleepiness rather than tiredness. Unrefreshing sleep. Dif \201 culty concentrating. Noctur nal choking. Nocturia. Witnessed apnoea. Weight and height (BMI). Neck circumference (distribution of fat). Craniofacial appearance (e.g. retrognathia, prognathia). Oral cavity and pharynx (e.g. size of tongue and tonsils). Nasal patency. M KOHLER & J STRADLING 364 \200 \200 Cardiovascular system (blood pressure, ankle oedema). Diabetes mellitus. Respiratory system (e.g. lower airway obstruction, chest wall disease, respiratory failure). Neurological sys tem (Neuromuscular diseases). Signs of predisposing diseases (e.g. hypothyroidism, acromega ly). \200 The majority of patients with OSAS are male with a ten- dency to have upper body obesity (n eck circumference >17in/>43cm), a retrognathic appearance of the mandible and a history of excessive daytime sleepiness. Fig. 15.1.8 Overnight oximetry. Eight hours of overnight oximetry in a patient with severe OSA. Note the many dips >4% in SaO2 with typical saw-tooth appearance. Sleep studies The sleep study is the crucial investigation in the process of making the dia gnosis of OSAS. There is a wide choice of equipment available for monitoring sleep, some ca n be used in an ambulatory setting (home sleep studies) others are only available in specia lized hospital centers. Principally, there are three major types of sleep studies: \200 \200 It is not possible to tell if the patient is awake or asleep, consequently a home sleep stu dy might be falsely negative, although this is rarely an issue if the patient says he slept . Other diagnoses than OSAS might be missed (e.g. periodic limb movements syndrome). Overnight oximetry alone. Respiratory polygraphy (RP), which normally includes assessments of snoring, body and leg movement, heart rate, oronasal air \202 ow, excursion of the ches t and abdo- men in addition to oximetry. Full polysomnography (PSG) with EEG, EOG, and EMG, to stage sleep electrophysiologically, in addition to the channels of respiratory polygrap hy. Limited sleep studies (RP) have become the usual routine investigation in most sleep center s as full polysomnography (PSG) is not needed to make the diagnosis of OSA. In fact, there is evidence that most cases that are eligible for CPAP treatment can be identi \201 ed by oximetry alone. However, false positive oximetry occurs with Cheyne \200\223Stokes breath- ing (e.g. in heart failure), and when there is a low baseline SaO2 (e.g. COPD) SaO2 oscilla tes considerably. False nega- tives can occur in thin young patients who hardly desatu- rat e during apnoeas. Equipment for oximetry and RP is suitable for home sleep studies, whereas full PSG usually requires a sleep labora- tory and a technician to set up and supervise the sleep study duri ng the night. Overnight sleep studies at home allow patients to sleep in their own environm ent which may re \202 ect normal condi- tions better than a sleep laboratory. Furthermore, most of the available equipment can be set up by the patient with- out any help from techn ical staff, thus home sleep studies may be cheaper than in-hospital studies. There may be s ome limitations in interpretating the results from home sleep studies: \200 Home sleep monitoring systems sometimes use sensors which have a different sensitivity and reliability compared to those used in RP or full PSG systems. Fig. 15.1.9 Visilab sleep recording (RP device). Recordings obtained from a patient with se vere OSA. Oxygen desaturations are associated with cyclic alterations in heart rate, and ar ousals indicated by movements in the channel. The microphone records periodic snoring, inte rrupted by apnoeas. Alterations in pulse transit time (similar to oesophageal pressure) sho ws increases in ventilatory effort during the apnoeas, indicating that the cause of the apn oeas is upper airway obstruction. In the authors \200\231 view, the expertise in interpreting a sleep study is more important than the particular sleep study equipment used. However, any system used should at least a llow assessment, directly or inirectly, of the degree of sleep fragmentation and the degree of upper airway narrowing. Fig. 15.1.7 Respiratory polygraphy. Recordings obtained from a patient with OSA. Progressiv e oesophageal pressure swings and paradoxical signals from rib cage and abdominal sensors ( arrows) indicate that the apnoeas are obstructive. They are associated with oxygen desatura tions, and cyclic alterations in heart rate. (Adapted from Kohler M, Bloch KE 2003). Treatment Patients should not be treated unless the diagnosis of OSA has been established b y a sleep study. This is because there are other casues of sleepiness, it is potentially a lifetime CHAPTER 15.1 Obstructive sleep apnoea 365 diagnosis, and there are driving and DVLA implications. It is also important to state that not all patients need treatment as the current evidence from randomized controlled trials i ndicates that signi \201 cant treatment bene \201 ts are mainly found in symptomatic pati ents. Improvement in daytime sleepiness and alertness are the major bene \201 ts of treat- ment, whether it also decreases the risk of cardiovascular events (e.g. myocardial infarct ion, stroke) or results in improved mortality remains to be proven in appropriately powered randomized controlled studies. However, many experts in the \201 eld apply a lower thres hold for treatment in patients with additional severe cardiovascular disease, poorly contro lled hypertension or heart failure. There are some key questions which might help in making a treatment decision, these include the following: \200 which maintains a constant supra-atmospheric pressure (about 10 cmH2O) within the tubing, m ask and the upper airways. A leak valve built into a tightly fitting nasal mask allows CO2 washout via a continuous leak. The gen- erated positive air \202 ow pressure splints open the pharynx thereby preventing apnoeas, hypopnoeas, snoring and sleep fragmentation. How sleepy is the patient, do the symptoms affect his quality of life? Do the symptoms in \202 uence the patient \200\231s ability to drive or work? Is the patient motivated to do a nything about it? Has the patient underestimated the impact of his sleepi- ness, or misled the doctor because of concerns over driving issues? Is there any underlying cause which can be treated speci \201 cally (e.g. hypothyroidism, tonsillar hypertrophy)? Is there suppor t from the patients \200\231 partner and/or family? \200 Fig. 15.1.10 The principle of CPAP. CPAP has been shown in randomized placebo-controlled trials to be an effective therapy in p atients with OSAS; it improves excessive daytime sleepiness, quality of life, vigilance, co gnitive and driving simulator performance, and daytime blood pressure. Furthermore, blood p ressure variations associated with obstructive apnoeas and exces- sive sympathetic tone are also improved. Compliance with CPAP therapy is strongly in \202 uenced by the severity of the patients \200\231 symptoms, the benefit they perceive by the treatment, the support an d informa- tion given by doctors and other health care workers spe- cialised in sleep medic ine. Therefore, most sleep centers in the UK employ a dedicated CPAP nurse or technician, a nd many centers provide special patient education pro- grammes, including video presentatio ns, informative lea \202 ets and telephone help lines. The compliance with CPAP shows a co nsiderable inter-individual variability which tends to be better in patients with severe OS AS than in mild \200\223moderate OSAS. In addition to the severity of symptoms other factor s can predict CPAP use, including whether the patient self-initiated the referral to the sl eep center, the patients \200\231 age and co-morbidities. Certain patients refuse to use CP AP because of the initial inconvenience, possible side effects, and for psychological reaso ns. General approaches The underlying mechanisms and the clinical signi \201 cance of the diso rder should be explained to all patients with OSAS and their partners. It is crucial that t hey understand why the treatment is important because in most cases it will be a life-long commitment to treatment. Simple approaches to improve OSA severity and symptoms may include the following: \200 \200 \200 \200 \200 Weight loss. Reduction of alcohol consumption in the evening. Avoid sleeping tablets or sed atives. Try to sleep in decubitus rather than in supine position. Treat underlying conditio ns such as hypothyroidism, acromegaly, tonsillar or adenoid hypertrophy, chronic nasal obst ruction. Speci \201 c approaches In addition to the above mentioned general measures the appropriat e treatment largely depends on the severity and symptoms of OSA. For snorers and mild OSA \200 Nasal CPAP is a highly effective therapy for moderate to severe OSAS, with complete resolut ion of sleepiness and large gains in quality of life. To achieve maximal bene \201 ts from CPAP a careful induction program is required. Mandibular advancement devices. For signi \201 cant OSA \200 \200 Nasal CPAP. Bariatric surgery (e.g. gastroplasty or gastric bypass operations). Mandibular/ maxillary advancement surgery in highly selected cases. Tracheostomy (only if all other tre atment options are not effective and the patient is severely compromised by the symptoms). It is a matter of debate how to derive the required mask pressure, and many different appro aches appear to work. Conventionally, after the diagnosis of OSAS has been established by h istory and a sleep study, the therapeutic pressure is determined during an overnight titrat ion study with a sleep technician present; CPAP pressures are set by manual adjustment in o rder to abolish apnoeas and mini- mise arousals. In most cases this is a successful approac h but obviously expensive as it requires overnight staf \201 ng. Alternatively, \200\230i ntelligent \200\231, but more expensive, CPAP machines, which automatically adjust the CPAP pressure in Nasal CPAP Nocturnal application of CPAP via a nasal mask is the standard therapy for OSAS. Continuous positive pressure is generated by an airflow turbine pump M KOHLER & J STRADLING 366 Alternative treatment options Mandibular advancement devices For patients with mild \200 \223moderate sleep apnoea and patients who cannot tolerate CPAP, \201 tting a removable m andibular advancement device that is snapped onto the teeth during sleep is a valuable alte rnative treatment option. Such devices are designed to advance the mandible (usually by 5 t o 10mm), thereby enlarging the upper airway caliber. They need to be customized to match th e patient \200\231s dentition, which usually requires the services of a dentist. Several ra ndomized trials have documented effectiveness of this therapy in improve- ment of mild to m oderate OSA, daytime symptoms and qual- ity of life. However, there are some potential limi tations: \200 response to apnoeas, inspiratory flow limitation, and snoring, can be used to determine wha t pressure of CPAP is needed, generating similar pressures to manual titrations. As an even less labor intensive alternative, an algorithm (a predictive model which takes into accoun t the dip rate and neck size of a patient) can be used to set an initial CPAP pres- sure, a n approach shown to be as effective as the conven- tional approach using a titration night, but much less costly. Patients require subsequent life-long follow-up to maintain their CP AP equipment and solve possible problems. Fortunately, CPAP is a safe therapy and serious s ide effects are extremely rare. The most common problems encoun- tered include: \200 Mouth leakage leads to increased air \202 ow through the nose and out of the mouth, with c onsequent excessive drying of the mucosa, sore throat, nasal congestion, nasal stuf \201 n ess, and rhinitis. This problem is recognized in up to 60% of all patients on CPAP. Pain an d skin ulceration; most commonly over the nasal bridge. Claustrophobia Abdominal bloating, usually a minor problem Side effects include tooth and jaw ache, which often lessen with time. Effects on teeth and temporo-mandibular joints have to be carefully evaluated as long-term use may be associate d with movement of the teeth and alterations to the bite. The initial cost (often over 30 0) is similar to that of a CPAP machine ( 250) but mandibular advancement devices usually only last about a year. \200 AUTHOR \200\231S TIPS \200 The most effective way to deal with mouth leaks is to either use a chin support to close th e mouth or use a full-face mask. Initial steps of dealing with nasal congestion are adding humidi \201 ed air and correcting potential leakage from the nasal mask. Nasal congestion can be treated with topical intranasal steroids (e.g. \202 uticasone) in addition to avoi dance of any relevant allergens. Topical decongestant nasal sprays (e.g. oxymetazoline) can also reduce nasal congestion, but treatment duration is limited as therapy lasting more th an 5 days can lead to rebound nasal congestion. Patients who have obvious nasal polyps, sev ere tur- binate hypertrophy or a distinctive abnormality of the nasal anatomy should be ref erred to an ENT-specialist for surgical therapy. Pain and skin ulceration can be addressed by trying dif- ferent types of masks (e.g. nasal cushion masks) or patient interfaces (e.g. oracle, an oral CPAP interface). Claustrophobia usually settles but it may be worth trying a different patient interface. Fig. 15.1.12 Mandibular advancement device. (Adapted from Kohler M, Bloch KE 2003.) Surgical treatment With the exception of adeno-tonsillectomy in children and adults with si gni \201 cantly enlarged adenoids and tonsils, surgical treatment is rarely indicated as t herapy for OSAS. Although sometimes performed for snoring and OSAS, uvulopalatopharyngoplas ty (UPPP), and other surgical techniques such as radiofrequency tissue ablation, and laser- assisted uvulopalatoplasty have not been proven to be effective treatments for OSAS in the few randomized controlled trials performed. Even for snoring the evidence for ef \201 cacy is poor. Pharmacological treatment To date there is no speci \201 c pharmacological treatment avail able for OSAS. Alerting drugs (such as moda \201 nil) have no place in the routine managem ent of sleepiness in OSAS as it is unclear if these agents help. They are rarely used as an adjunct in selected patients with OSAS in whom excessive sleepiness persists despite optim al adaptation of CPAP therapy. Further reading Douglas NJ. Clinicians \200\231 guide to sleep medicine. London: Arnold 200 2. Jordan A, White D, Fogel R. Recent advances in understanding the pathogenesis of obstruc tive sleep apnea. Curr Opin Pulm Med 2003; 9: 459 \200\223464. Fig. 15.1.11 Oracle device \200\223 delivery of CPAP via the mouth rather than via the nos e. CHAPTER 15.1 Obstructive sleep apnoea 367 Polotsky VY, O \200\231Donnell CP. Genomics of sleep-disordered breath- Kohler M, Bloch KE. Sleep-related breathing disorders. Swiss Arch ing. Proc Am Thorac Soc 2007; 4: 121 \200\223126. Neurol Psychiatr 2003; 154: 302 \200\223309. Pepperell JC, Ramdassingh-Dow S, Crosthwaite N, et al. Ambula- tory blood pressure after th erapeutic and subtherapeutic nasal continuous positive airway pressure for obstructive slee p apnoea: a randomized parallel trial. Lancet 2002; 359: 204 \200\223210. Kohler M, Bloch KE, Stradling JR. The role of the nose in the pathogenesis of sleep apnoea and snoring. Eur Respir J 2007; 30: 1205 \200\2231215. Management of obstructive sleep apnoea/hypopnoea syndrome in adults. A national clinical gu ideline. Scottish Intercollegiate Guidelines Network, 2003, Edinburgh, UK. Schwab RJ. Upper airway imaging. Clinics in Chest Medicine 1998; 19(1). Smith PL, Wise RA, Gold AR, Schwartz AR, Permutt S. Upper airway pressure- \202 ow relatio nships in obstructive sleep apnea. J Appl Physiol 1988; 64: 789 \200\223795. Marin JM, Carrizo SJ, Vicente E, et al. Long-term cardiovascular out- comes in men with obs tructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway p ressure: an observational study. Lancet 2005; 365: 1046 \200\2231053. Young T, Palta M, Dempsey J, et al. The occurrence of sleep disor- dered breathing among mi ddle aged adults. N Engl J Med 1993; 328: 1230 \200\2231235. Stradling JR, Davies RJO. Obstructive Sleep Apnoea, de \201 nitions, epidemiology and natural history. Thorax 2004; 59: 73 \200\22378. NICE technology appraisal of CPAP for OSA, 2008: http://www. nice.org/guidance/index.jsp?ac tion=byID&o=11944 Young T, Skatrud J, Peppard P. Risk factors for obstructive sleep apnea in adults. JAMA 2004; 291: 2013 \200\2232016. M HACK 368 15.2 Driving Driving is a task involving a variety of sensory inputs includ- ing visual, auditory and sp atial awareness which are proc- essed and result in a coordinated motor output. Vigilance a nd cognitive processing are required to accurately place the vehicle on the road, drive at an appropriate speed and react to external factors. The ability to drive may be impaired in a range of respira- tory and sleep disorders. Examples include confusion caused by hypoxia or carbon dioxide retention, reduced vigilance due to medications causing sedation, or sle epiness resulting from nocturnal dyspnoea or sleep disorders. Other sections of the guidelines include advice on cogni- tive impairment, blackouts and im paired consciousness which could be relevant to a sleepy patient. Other sleep disorders are not speci \201 cally mentioned. Clinical approach: key points Doctors in training should be assisted by a senior colleague in establishing the presence of symptoms of excessive sleepiness, the diagnosis of a sleep disorder, the appropri- ate therapy and advice regarding driving. Some patients describe fe w symptoms of sleepiness and it can be helpful to obtain information from a partner or rela tive. Sleepiness Symptoms of excessive sleepiness that lead to impairment of driving performance can result in accidents. In the UK approximately 25 percent of all motor vehicle accidents (MVAs) are due to sleepiness. There are many causes of sleepiness including lack of sleep, poor quality sleep due to shift work and sleep disorders. History \200 Symptoms of sleepiness, extent of sleepiness and exam- ples of situations, involvement in M VAs or near misses, presence of cognitive impairment. Driving and type of license held. Occ upational history, e.g. driving, operating machinery, shift work. Medication causing sedati on, alcohol consumption. Symptoms of sleep disorders and sleep pattern. \200 \200 Sleep disorders There are over 80 sleep disorders recognized in the International Classi \201 cation of Sleep Disorders. In the UK most patients with sleep and breathing disorders including OSAS are investigated and managed by respiratory con- sultants. Untreated OSAS pa tients have an increased risk of being involved in a MVA of up to 6 times that of a nor- ma l individual. Patients with other sleep disorders such as narcolepsy are also often referre d to specialist respiratory sleep clinics. Advice regarding the \201 tness to drive is an important part of the care of any patient with a sleep disorder. Examination \200 \200 Speci \201 c to detect enlarged tonsils, thyroid disease. General to detect respiratory, c ardiology or neurologi- cal conditions. Investigation To establish a diagnosis \200 Sleep investigation/study as evidence of the presence of OSAS, e.g. oximetry, multi-channel respiratory record- ing, polysomnography. Sleepiness score to estimate the presence of exc essive sleepiness e.g. Epworth Sleepiness Score (ESS) Guidelines In the UK the body responsible for issuing driving licenses is the Driver and Ve hicle Licensing Agency (DVLA). Group 1 licenses include drivers of motorcars and motorcycle s, Group 2 licenses include drivers of large lorries and busses. The DVLA issue written gui delines for medical practition- ers on the current \200\230Medical Standards of Fitness to Drive \200\231. There is a section on respiratory and sleep disorders including OSAS causi ng excessive daytime/awake time sleepiness. Group 1 license entitlement requires that if ex cessive sleepiness is present driving must cease until satis- factory control of symptoms h as been attained, con \201 rmed by medical opinion. Group 2 license entitlement requires t hat if excessive sleepiness is present driving must cease until satisfactory control of sym ptoms has been attained, with ongoing compliance with treatment, con \201 rmed by consulta nt/ specialist opinion. Regular, normally annual, licensing review required. The guidelines include a section on neurological disorders which applies to narcolepsy and cataplexy. Gro up 1 license entitlement requires an individual to cease driving on diag- nosis. Driving wi ll usually be permitted if symptoms are satisfactorily controlled when a license will be gr anted for a period of 1, 2 or 3 years with regular medical review. Until the age of 70 a li cense will be restored after at least seven years of satisfactory control. A patient is gen erally considered permanently un \201 t for a Group 2 license, but if a long period of con trol has been established licensing may be considered on an individual basis. To obtain an objective measurement of sleepiness \200 Maintenance of Wakefulness Test (MWT) or the behav- ioural version (MWTosler) thought to pr ovide a meas- urement of the ability of the individual to stay awake. Multiple Sleep Latenc y Test (MSLT) thought to provide a measurement of ability of the individual to fall asleep. Simulation studies are sometimes performed but the relevance to driving on the real road i s not clear. Fitness to drive in the UK is not assessed by objective measurements of wakefulness/sleepin ess, unlike some other countries. Debate continues about how these objec- tive tests should be interpreted as an indication of \201 tness to drive. Treatment CPAP therapy is the treatment of choice for moderate to severe OSAS. Compliance w ith therapy can be estimated as most devices have a clock to measure running time. CPAP the rapy improves steering simulator performance and reduces the risk of accidents in patients with OSAS to that of the normal population. Patients with OSAS who drive for a living may r equire a facility for rapid set up with CPAP therapy. Advice This includes an explanation of the results of the investiga- tions, the diagnosis a nd appropriate treatment. CHAPTER 15.2 Driving 369 \200 Written information should be provided to the patient and general practitioner on the advic e given. Copies of documentation should be kept. Every attempt should be made to resolve th e issues whilst maintaining patient con- \201 dentiality. It may be useful to offer refer ral for a second opinion. If a patient continues to drive against medical advice or fails t o notify the DVLA, a senior doctor may have to consider notifying the DVLA by contacting a medical advisor. Verbal and written warnings of the intention to do so should be given to t he patient where possible. An explanation of the effect of the disorder on driving. Advice not to drive when the indiv idual is sleepy or advice that driving must cease if excessive sleepiness is present. This may have implications on work which may have to cease prior to treatment. Explanation of th erapy available. If possible, have a family member, partner or a friend present for informa tion and to hear advice. Keep clear documentation. Recommend provision of written advice to the patient. \200 \200 Noti \201 cation to DVLA In the UK it is the doctor \200\231s responsibility to advise the patient to notify the DVLA on diagnosis of a sleep disorder that may affect the ability to drive. It is the responsibility of the patient who holds a license to notify the DVLA by t elephone or letter. The DVLA will then send forms both to the patient and doctor requesting information about diagnosis, treatment and satisfactory control of symptoms. The written c onsent of the patient is usually forwarded by the DVLA with the form. The doc- tor should e nsure this is obtained before providing any information. The DVLA considers the information provided and will then continue or revoke the driving license. It is advis- able to follow -up drivers to ensure adequate control of symptoms and compliance with therapy. Further reading American Academy of Sleep Medicine (2005). The International Classi \201 c ation of Sleep Disorders 2nd edn. Diagnostic and Coding Manual, Westchester: USA. Driver and Vehicle Licensing Agency drivers medical group (2008) Guide to current medical s tandards of \201 tness to drive. www. dvla.gov.uk George CF. Reduction of motor vehicle collisions following treat- ment of sleep apnea with nasal CPAP. Thorax 2001; 56: 508 \200\223512. George CF, Findley LJ, Hack MA. Across countr y viewpoints on sleepiness during driving. Am J Resp Crit Care Med 2002; 165(6): 74 746 \200\223749. National Institute of Clinical Excellence Technology Appraisal (2008). Sleep Apnoea- Contin uous Positive Airway Pressure (CPAP) TA139. www.nice.org.uk/guidelines/TA/ published Insurance The patient should be advised to notify the insurers of the diagnosis of a sleep disorder. Dif \201 cult situations If a symptomatic patient with a sleep disorder continues to drive against medical advice it is important to involve other people in discussions including ge neral practitioners, nurses, family and friends. G VAN RENSBURG & J CATTERALL 370 15.3 The overlap syndrome Introductions The overlap syndrome was \201 rst used to describe the coex- istence of OSA S and COPD. Patients are prone to severe hypoxemia during sleep, especially rapid eye movem ent (REM) sleep, in addition to the hypoxaemic episodes from obstructive sleep apnoea. This is due to worsening of alve- olar hypoventilation during sleep. The most marked falls in n octurnal arterial oxygen saturation occur in COPD patients who are hypoxic and hypercapnic when awake. In recent years, the term has come to be used more widely and to include obesit y-related hypoventilation. Obesity is not only associated with obstructive sleep apnoea but it is an increasingly common cause of hypoventilation. Daytime hypoxia and hypercapnia are increased in patients with a BMI >40. Most authors now regard the overlap syndrome as any combination of two or more of these three conditions (Fig. 15.3.1). The syndrome is being d iagnosed with increas- ing frequency, and as obesity levels continue to rise, it is set to become more prevalent in the future. resistive load in contributing to alveolar hypoventilation is illustrated by the ability of CPAP alone to reverse hyper- capnia and hypoxia in some patients with the overlap syndrome . However, in other patients CPAP alone is insuf \201 cient to restore ventilation to adeq uate levels. In these patients, the other factors which contribute to non-apnoeic hypoventi - lation are presumably of more importance. These factors include decreased functional resi dual capacity, reduced ventilatory response to hypercapnia and hypoxia, decreased chest com pliance in morbid obesity and generalized airway resistance in COPD. The reduced ventilator y drive is of particular interest for there is evidence that it is not \201 xed. Some pat ients who do not respond well to CPAP at \201 rst can be established on CPAP after a peri od of non-invasive ventilation. The short- term ventilatory support improves arterial gas t ensions and results in the ventilatory drive being re-set. After this, relatively normal ox ygen and carbon dioxide levels can be maintained with CPAP alone. Clinical aproach General The overlap syndrome should be suspected when COPD or morbid obesi ty is associated with sleep disruption and daytime sleepiness, especially if there is dayti me hypoxia and hypercapnia. It should also be considered when patients already receiving CP AP treatment for OSAS have persistent symptoms of sleep disruption or carbon dioxide retent ion (especially if they are morbidly obese and/or have COPD). History: key points \200 \200 \200 \200 Obesity hypo- ventilation OSA COPD Daytime sleepiness and/or poor sleep quality. Known COPD or signi \201 cant smoking histor y. Morning headaches due to hypercapnia in a few patients. Inadequate or incomplete respons e to CPAP (in patients already on CPAP for OSA). Fig. 15.3.1 The overlap syndrome. Pathogenesis and implications for treatment In pure obstructive sleep apnoea, the arterial oxygen satu- ration usually returns to baseline after each episode of hypoxaemia, and the a rterial blood gas tensions when awake are usually normal. In contrast, in the overlap syn- drome, the arterial oxygen saturation usually remains low between episodes of obstructive s leep apnoea, and these patients are usually hypoxaemic and hypercapnic when awake. Alveolar ventilation is reduced. Ventilation falls normally during non-REM sleep and drops further during periods of REM sleep. In healthy individuals, the resulting falls in arterial oxygen tension cause little change in arterial oxygen saturation because they lie on the flat par t of the oxyhaemoglobin dissociation curve. However, patients with severe COPD or obesity h ypoventi- lation syndrome often have marked falls in arterial oxygen saturation during REM sleep. This is partly because they lie on a steeper part of the oxyhaemoglobin dissociation curve and partly because they hypoventilate more than healthy individuals, both when awake and during sleep. When obstructive sleep apnoea coexists with severe COPD or obesity-relat ed hypoventilation the level of ven- tilation tends to fall further because of the episodes of upper airway obstruction. The importance of this extra Examination: key points \200 Morbid obesity \200\223 usually BMI >40 unless COPD also present. Physical signs of pulmon ary hypertension and right ven- tricular failure. Investigations Overnight oximetry \200 The baseline arterial oxygen saturation during sleep is usually lower and less stable than in pure obstructive sleep apnoea. In a typical study, gradual falls in arterial oxygen satu ra- tion caused by hypoventilation are combined with more rapid ( \200\230saw-tooth \200 \231) \202 uctuations caused by obstructive sleep apnoea. However, note that, at low SaO2 , sharp falls in arterial oxygen saturation can also result from hypoventilation alone, bec ause of the shape of the oxyhaemoglobin dissociation curve. Arterial blood gas measurements Daytime hypercapnia is common. Measure arterial blood gas t ensions if the daytime oxygen saturation is low and/or symptoms of hypercapnia are present. CHAPTER 15.3 The overlap syndrome 371 Transcutaneous CO2 This is a useful adjunct if available. It can be used to help titrate th e level of ventilation.