| | Sleep-disordered breathing and anaesthesia in the morbidly obeseSummary Clinically significant Sleep-Disordered Breathing (SDB) is commonly found in the morbidly obese population. The obesity epidemic has resulted in ever larger numbers of morbidly obese patients presenting for surgery, both for bariatric and other procedures. It is essential that anaesthetists are aware of these conditions, and the associated risks. This article will focus on the common types of sleep-disordered breathing and investigation of these patients. It will discuss the issues around anaesthetising patients with these conditions, and suggest solutions to the problems that these patients present. 1. Introduction  SDB encompasses a spectrum of abnormality, which ranges from uncomplicated snoring, through obstructive sleep apnoea to frank nocturnal hypoventilation. The prevalence of SDB rises sharply with body mass index (BMI) and with some 25% of the UK adult population now obese, anaesthetists will see ever-increasing numbers of patients with these conditions. Whilst the morbidly obese, especially males, have the highest incidence of severe SDB, body weight and clinical assessment alone are poor predictors of severe hypoventilation. This chapter will focus on the syndromes of sleep apnoea and obesity hypoventilation, with reference to the role of Sleep Study in their assessment. It will also consider the effects of obesity on breathing, and the progression of such patients to respiratory failure, including the role of respiratory support in intervention. The guidelines of the American Society of Anaesthesiology1 are referred to, with particular regard to those undergoing bariatric surgery. The obese may be broadly categorised. The ‘fit fat’ are typically young, prior to the development of significant co-morbidity (ASA 1 and 2). Of intermediate risk are those with early metabolic syndrome and mild co-morbidities related to hypertension and diabetes, typically of ASA grade 2–3. At the other end of the scale are the cardio-respiratory cripples of ASA 4 status, with profoundly limited exercise tolerance. In between is the real danger group; those ‘ASA 3+’ patients, not obviously crippled but potentially harbouring severe occult cardio-respiratory disease. It is the identification of significant co-morbidity, and minimising peri-operative adverse events in this group of patients that is the key challenge. 2. Obstructive sleep apnoea syndrome 2.1. Definition The obstructive sleep apnoea/hypopnoea syndrome (OSAHS) refers to the development of symptoms secondary to repetitive upper airway occlusion during sleep. During transient airway occlusion, airflow either stops (apnoea) or is reduced (hypopnoea), often but not necessarily associated with a drop in oxygen saturation. Such occlusive episodes are terminated by an arousal, by which control of airway musculature is regained. Though these arousals may occasionally result in awakening from sleep, often with a choking or gasping sensation, the vast majority of such arousals are to a lighter plane of sleep, visible during polysomnography. Thus sufferers usually have no recollection of these arousals in the morning, though they may have experienced hundreds of such episodes overnight. By far the most common clinical manifestation is daytime somnolence, secondary to the fragmentation of deep sleep these arousals cause. However, it is known from population screening studies that somnolence is by no means an invariable association of repetitive nocturnal airway closure. Indeed studies indicate that between 5 and 15% of the population may have an abnormal sleep study, by contrast to a symptomatic population of 1–4%. Hence the diagnosis of the “Obstructive Sleep Apnoea/Hypopnoea Syndrome” is used only for those with symptoms arising from sleep-disordered breathing. 2.2. Incidence In the classical Wisconsin Sleep Study, a population was examined using polysomnography to measure the apnoea/hypopnoea index (AHI), being the number of such events per hour of sleep.2 Taking a threshold AHI of 5, the investigators found that 2% of women and 4% of men had both daytime somnolence and SDB compatible with diagnosis of OSAHS. Notably, 9% of women and 24% of men had an AHI of 5 or greater without daytime somnolence. Obesity is an important risk factor. Thus the prevalence of OSAHS has been reported at 30% in those with a BMI of >30 and 40% in those with a BMI of >40.3 There is a particular association between OSAHS and a visceral pattern of obesity, classically seen in men who are prone to deposition of fat within the neck, abdominal wall and viscera (“apples”). By contrast, the classically female subcutaneous deposition of fat, often localised around the hips (“pears”) appears to confer risk to sleep-disordered breathing. Neck circumference is probably an even better predictor of the presence of OSA. Men with a neck circumference of greater than 43 cm and women greater than 41cm are very likely to have OSAHS.4 2.3. Pathophysiology The precise cause of airway collapse is contentious, but certainly the physical space in the oro-pharynx plays a very substantial role. Excessive tissue volumes, i.e. large tonsils or deposition of fat in the tongue5, 6 or pharyngeal wall, combined with a smaller bony channel, i.e. receding chin, narrow mandible and short neck, are the typical anatomical pre-dispositions. These are also the pre-disposing factors to difficult intubation, so it is no surprise to find a strong association between higher grades of both Mallampati score and of difficult laryngoscopy with sleep apnoea severity.7 During sleep tone in the upper airway musculature reduces, resulting in further narrowing of the airway channel, to the point that the negative intra-luminal pressure during inspiration results in apposition of the pharyngeal walls. The symptoms of the condition do not correspond closely to the severity of the disease, but are all markers of poor quality sleep. Daytime somnolence, in its worst form associated with uncontrollable falling asleep (such as at the wheel of a lorry), is the cardinal symptom, although a host of more subtle behavioural changes and intellectual deterioration can also mark the condition. In advanced disease, and particularly as hypoventilation becomes more significant and hypercapnia persist into the daytime, cerebral vasodilation and early morning headaches settling after some 30min or so may be a feature. At this advanced stage there tend to be signs of right heart failure, including peripheral oedema, and these signs suggest patients are progressing towards decompensation and acute respiratory failure (Fig. 1, Fig. 2). 2.4. Symptoms of OSAHS Daytime somnolence is the most common manifestation of sleep-disordered breathing, and a common reason for seeking medical attention. However, its onset is insidious, frequently over years or decades and sufferers grow into the self-image of a habitual “sleepyhead”, often with little insight. Thus there is a large clinical iceberg of untreated sleep apnoeics, who may present for anaesthesia undiagnosed. The question “do you ever fall asleep during the day, particularly when not busy” is a sensitive screening enquiry8 though lacks specificity. A positive reply should be tempered by a brief assessment of adequacy of night-time sleep; less than 7h of consolidated sleep may account for daytime somnolence. Furthermore, night-time sleep is often poor in the obese. Indeed the fascinating concept of a U-shaped relationship between sleep duration and obesity has recently gained currency.9 Patients with OSAHS may present in a number of other ways, including accounts of apnoeas witnessed by their partners, nocturia, waking with choking episodes or polycythaemia. A history from a partner of prolonged apnoeas, terminated by a prod with the elbow, is common and highly specific, although the duration may be inaccurate. Awareness of nocturnal choking attacks may be terrifying to the point that the sufferer sleeps in the sitting position, or paradoxically attempts to avoid sleep altogether. Snoring is invariably a feature of OSAHS, giving its absence (if confirmed) good negative predictive value. 2.5. Epworth score The Epworth sleepiness scale was designed to measure the impact of sleep apnoea on daily life. It is self-scored by asking a subject to complete a questionnaire which describes eight scenarios, each of which are graded for their propensity to induce asleep. The scenarios range in their level of stimulation, from sitting quietly after lunch to stopped in a car at traffic lights. Each scores between 0 and 3, from never dozing to high chance of dozing, giving a possible total score of 0–24. In a normal Sleep clinic population, a score of greater than 10 has a 93% sensitivity and 100% specificity for distinguishing pathological somnolence from normal sleepiness.10 However, the utility of this tool in predicting sleep-disordered breathing, particularly in the bariatric surgical population is very limited. Whilst a high Epworth score usually predicts a very significantly elevated Apnoea/Hypopnoea Index, a low score does not exclude the presence of very significant obstructive sleep apnoea.11 2.6. Physical examination The patient will classically have a thickset, short neck, but this is not invariable. Limited space in the oropharynx, with obvious tonsils and bulky tongue are commonly found, but again not an inevitable association. The correlation of higher Mallampati scores with the incidence of higher levels OSA is common, but again not highly specific. Physical examination has a limited role in identifying sleep-disordered breathing. 2.7. Treatment of OSA In the short term, CPAP offers effective treatment for obstructive apnoea, and its benefit has been proven in a number of trials which were controlled by comparison of a treatment group to a “sham CPAP” group, where CPAP was used at sub-therapeutic pressure.12 Application of pressure through a nasal mask is preferred, as the mask is less prone to displacement by movement of the jaw, allows for speech and sips of fluid and is better tolerated by those with any tendency to claustrophobia. Numerous technological refinements are available, including bilevel pressure capability, automatic titration of pressure to critical value required to prevent airway occlusion and relaxation of pressure during expiration.13 None have any proven advantage over conventional fixed pressure CPAP. Airway humidification, especially if heated, is of benefit in subjects who experience excessive drying of mucosal membranes. Mandibular advancement devices (MADs) are worn within the mouth, supported by teeth and work by advancing the mandible to increase the retroglossal space. Their role is considered to be either alternative first-line treatment for mild OSA,14 or a second line treatment for those who do not tolerate CPAP.15 Paradoxically, a MAD may exacerbate OSA in a minority of subjects, so that a repeat sleep study using this treatment is recommended. In the longer term, weight loss, though difficult to achieve, restores normality in a high proportion of cases where adiposity is significant.16 Even modest weight loss (of the order of 20–30kg) can produce marked improvement in the morbidly obese, and when there is the incentive of proceeding to a definitive, i.e. surgical option, patients can often achieve these weight losses prior to anaesthesia and surgery. Palatal surgery is often touted as a cure for OSA, despite absence of demonstrable benefit in numerous meta-analyses.17 Tonsillar hypertrophy is an indication for surgery in children, in whom a normal AHI is restored in 87%,18 though the procedure has been less successful in adults. Removal of nasal polyps reduces the CPAP pressure required to treat OSAHS, but may not bring about cure. Mandibular advancement is a significant undertaking but has a role in selected cases with significant retrognathia. 3. Obesity hypoventilation syndrome At the more extreme end of the sleep-disordered breathing spectrum, obesity hypoventilation exists when nocturnal hypoventilation leads to a state of daytime hypercapnia and hypoxia, in those with a BMI of greater than 30.19 It is synonymous with the Dickensian “Pickwickian syndrome”. By contrast, daytime hypercapnia does not occur in uncomplicated OSAHS. Although the prevalence of obesity hypoventilation syndrome (OHS) in the community is not known, its incidence amongst those with OSAHS has been estimated at between 10 and 20%, depending upon the prevalence of obesity, with which it is strongly associated. A mixed picture of hypoventilation and obstruction is seen in the majority. 3.1. Pathogenesis of obesity hypoventilation Chest wall adiposity applies a significant additional load to the respiratory system, reducing chest wall compliance. However, only one-quarter of those with a BMI of greater than 40 develop OHS, implicating factors other than body mass. Pulmonary physiology in the obese population shows wide variation, even between those with similar body mass, and probably plays an important role. Compliance is a fundamental property of the respiratory system, which in turn determines resting lung volume, itself an important factor in airway resistance. Patients with OHS have lower respiratory compliance then the eucapnic morbidly obese.20 Obese hypoventilators have been found to have higher upper airway resistance than in equally obese patients with lesser degrees of sleep-disordered breathing.21 An analysis of a number of studies which examined lung function in the obese, collated a range of mean vital capacities from 57 to 102% predicted. A moderate restrictive defect is typical, caused by loss of expiratory reserve volume. Other determinants of hypoventilation include a blunted central responsiveness to hypercapnia and hypoxia and a state of leptin resistance (a satiety protein that increases ventilation). In approximately 90% of cases, sleep studies show obstructive sleep apnoea, usually of severe degree. In the remaining 10% of cases, discreet apnoeas and hypopnoeas are not seen. Sleep studies in such cases show more extended periods of hypoventilation, typically of 20min duration or more. There may be profound oxygen desaturation during such episodes, to levels below 40% (see Fig. 3). Severe desaturations of this kind are prone to occur during REM sleep22 during which the diaphragm is unaided by the intercostal and accessory musculature, which are under the atonic conditions that characterise the REM state. The development of REM-related hypoventilation is likely to be key, as a progression has been demonstrated from here through non-REM hypoventilation to daytime hypercapnia, the sequence seen in other chest wall diseases.23 The fundamental difference between OHS and OSA lies in the ability of the respiratory system to clear the CO2 in the intervals of “normal breathing” which intersperse apnoea/hypopnoea. Whereas the uncomplicated sleep apnoeic inevitably accrues CO2 during periods of apnoea (typically 30s duration), it is presumably cleared by the brief periods of compensatory hyperventilation which intersperse these events. By contrast, the obese hypoventilator cannot keep pace, and accumulates CO2 steadily throughout the night. A model which incorporates the severity of OSA bicarbonate buffering has been proposed to predict this progression.24 3.2. Clinical features Although some patients with OHS may be identified in Respiratory or Sleep clinics, many will escape detection until presentation with decompensated ventilatory failure. This may ultimately be precipitated by trivial intercurrent illness, such as viral infection, or indeed as a gradual decline without any specific precipitant. Morning headache is a symptom strongly associated with nocturnal CO2 retention, presumably by its vasodilatatory effect upon cerebral vasculature. Somnolence is a little more severe than in uncomplicated OSA, but may be extreme, to the extent of falling asleep standing or mid-sentence. Cor pulmonale, evidenced by peripheral oedema, is also correlated with CO2 retention,25 and may reach extraordinary levels, necessitating gradual diuresis of more than 40l of fluid when severe. Low daytime oxygen saturation gives a clue to the presence of daytime hypercapnia. Other clues are a raised venous bicarbonate (>32mmol/l is seen in 50% of cases) or desaturation to less than 80% on the sleep study, which was found to be uncommon in uncomplicated OSA, but occurred during 13% of the total sleep time in those with OHS.26 Daytime hypercapnia is the defining feature, and should be measured when OHS is suspected on the basis of the above. Even then, hypercapnia is often misdiagnosed as COPD by the unwary. 3.3. Treatment In the extreme situation, patients presenting acutely with decompensated ventilatory failure require ventilatory support, preferably by non-invasive means. By contrast to OSA, a mask covering both nose and mouth is usually required for acute non-invasive ventilation (NIV). Such patients require high levels of nursing care, which is best-provided in a higher dependency setting, particularly when there is decompensated acidosis. In the severely obtunded, endotracheal intubation may be required to provide airway protection and a period of mechanical ventilation. In those without significant precipitating illness, weaning is best managed by early extubation onto non-invasive ventilation. Attempting to wean to total ventilator independence places an unnecessary loop in the pathway, as most such patients will then need to be established on long-term domiciliary ventilatory support. Once stabilised on NIV, many such patients may be managed in the longer term by CPAP, rather than NIV, despite the fundamental hypoventilatory nature of the condition. In the pre-operative setting following sleep study, many patients will receive CPAP only, not least in part to the difficulties and considerable expense of providing domestic NIV at short notice. 3.4. Natural history of hypoventilation Given the positive experience of treating obese hypoventilators with NIV, it is unsurprising that there are few clinical data describing the natural history of the untreated condition. Retrospective analysis of experience from a Spanish centre showed that of eight patients who presented with chronic OHS, but rejected treatment, three died within the period of study (mean 50months). There was a similar mortality rate amongst those who presented acutely but rejected treatment with NIV.27 4. Sleep-disordered breathing and anaesthesia The first, and sometimes most difficult part of dealing with sleep disorders in the peri-operative period is identification of the high-risk patient. In those patients who come with previous symptoms and following formal testing, and a diagnosis of OSA or OHS, one can optimise the patient pre-operatively, adjust the anaesthetic technique, then utilise a high dependency or critical care area to watch for delayed respiratory compromise. Patients with a diagnosis and who are on established CPAP (and compliant) are a group who rarely cause problems. Unfortunately the majority of patients do not have these diagnostic labels and the screening tests to identify these conditions are imperfect. 4.1. Who should undergo formal sleep study? The incidence of sleep disorders in the general population is high and rising. To study all patients pre-operatively is clearly not practical, yet using the signs and symptoms associated with OSA is neither very specific, nor sensitive as a screening test to identify these patients.28 As previously discussed, the Epworth Sleep scale is a poor predictor of the severity of apnoeic episodes. The reason why most patients are referred to sleep physicians is to improve quality of life by improving daytime somnolence. In dealing with patients who are to undergo surgery, the rationale is to reduce peri-operative risk of death. The vast majority of sleep literature and research focuses on symptom control, and there is a paucity of data on the effects of treating sleep-disordered breathing with the intention of reducing peri-operative risk. However, there is little doubt that a number of patients with developing cardiac compromise and reduced exercise tolerance see a marked improvement in function once commenced on treatment. This is particularly obvious in those patients progressing to right heart failure with significant fluid retention, and there is a fairly extensive literature demonstrating that both right and left ventricular function improve, albeit not to a huge degree, by the use of ventilatory support, especially BIPAP. Patients who demonstrate clear signs and symptoms of sleep disorders should be referred for formal sleep study then treatment if indicated. This is one of the primary purposes of outpatient pre-operative assessment. Unfortunately, many patients are seen by the anaesthetist only shortly before operation, even in those centre running true multi-disciplinary assessment clinics. This leaves the anaesthetist with the difficult dilemma of proceeding with caution or deferring. Patients with signs and symptoms of sleep disorders, but with no other co-morbidities and excellent exercise tolerance probably have a low peri-operative risk. In this group it is usually reasonable to proceed. 4.2. Who should undergo formal lung function testing? The presence of near-normal forced vital capacity makes the presence of significant hypoventilation very unlikely. Few centres routinely perform formal measurement of forced vital capacity. In the absence of formal pulmonary function testing, a simple measure easily performed during the pre-oxygenation phase of anaesthetic induction, is to ask the patient to take a full breath in and out whilst holding the face mask firmly to the patient's face. Holding a standard 2l reservoir bag within sight of the patient and asking them to breathe in and out hard, whilst using modest fresh gas (oxygen) flows, one can see what proportion of the 2l the patient is able to inspire. Those patients who can empty the bag are unlikely to have post-op respiratory problems. Those who struggle to half-empty the bag need to be handled cautiously, both in terms of ensuring full reversal and in obtaining optimal positioning prior to extubation, in order to avoid immediate post-operative respiratory insufficiency; these patients mark themselves out as more likely to retain Carbon Dioxide post-operatively. Patients who are to undergo more major surgery, especially open procedures, and particularly those who will receive either intravenous opioids (i.e. PCA morphine) or epidural analgesia with opioids, are at much greater risk of respiratory depression. In this patient group identification and assessment of the degree of sleep disorder is much more important, if necessary entailing postponement of the procedure. 4.3. If Anaesthesia is unavoidable Pre-operative investigation and optimisation is always the ideal, but in the acute setting may not be possible. If emergency surgery and anaesthesia are required, certain measures will reduce the risk of those respiratory problems that may necessitate post-operative ventilation. The first issue is to suspect the presence of a sleep disorder, and the default position in the morbidly obese is that these patients will have a significant degree of opioid sensitivity and a high likelihood of post-operative respiratory complications. Specifically there is a high likelihood of CO2 retention and narcosis, so it is expected that there are long periods of reduced conscious level during the emergence phase, even when the measured MAC level is less than 0.1 – on occasion this recovery to extubation phase may take in excess of 30min. Clearly the use of ultra-short acting agents, which are rapidly cleared is ideal, and although there is much discussion as to the added benefit of desflurane over sevoflurane, the vast majority of bariatric anaesthetists worldwide use this agent. Studies in smaller patients (BMI of 30–35) show a marginally quicker wake-up when using Desflurane, but in the super-obese (BMI>50) the benefit is likely to be much greater. Although residual volatile is undoubtedly a component, the key factor is to minimise the use of longer acting opioids, especially morphine, usually achieved by giving large doses of simple analgesics. Loading the patient with high dose intravenous paracetamol per-operatively, together with the use of regular post-operative non-steroidal agents, has been shown to significantly reduce both PCA morphine requirements (by over a third), and more importantly significantly reduce arterial PaCO2 levels over the critical first 24h. Where appropriate skills and experience allow, regional anaesthesia and/or per-operative infusions of Remifentanil have a useful role. There is no doubt a great deal of variability in the sensitivity of individuals to opioids in general, and a variable sensitivity to different opioids is also seen. Many anaesthetists, if concerned that patients may be overly sensitive, will give a small dose of morphine or fentanyl pre-induction, and observe the degree of desaturation that ensues over the next 5min. This opioid challenge allows a more logical customisation of dosing and helps guide the levels of both post-op opioid dosing, and levels of observation required. In terms of maximising the chance of successful extubation at the end of the surgical case, it is important to ensure that muscle weakness, i.e. residual paralysis is absolutely minimal. The theoretical advantage of using Cyclodextrans to chelate amino-steroid muscle relaxants (i.e. Sugammadex for Rocuronium) is very appealing and many would advocate this. In the absence of Cyclodextrans some would suggest the use of Atracurium as the offset is more reliable than rocuronium, and the chance of residual curarisation smaller. Others would cite the need to minimise relaxant usage as the grounds to use remifentanil infusions or epidural analgesia. The practical point is to minimise the usage of relaxants towards the end of the case, to avoid residual weakness, and to ensure positioning of the patient in order to optimise mechanical advantage prior to extubation. These practices should be standard in all morbidly obese patients, but in those with obtunded CO2 responsiveness, the risk of failed extubation is significantly elevated At extubation, sitting the patient upright is key, and this is best managed using special bariatric beds, usually electrically powered. Some form of pressure support ventilation and monitoring end-tidal CO2 levels in the immediate pre-extubation phase is helpful. Extubation must be delayed until the patient has a very good respiratory effort and is opening eyes and awake; and although there is no good evidence to support this, some bariatric anaesthetists would advocate the use of a small dose of a respiratory stimulant, e.g. doxapram, immediately following the extubation, to minimise the chance of failure. 5. Post-operative care of the patient with sleep-disordered breathing Post-operative care of patients with proven or suspected OHS/OSA should follow the management guidelines of the American Society of Anaesthesiology Task Force guidelines.1 Most would advocate the admission of these patients to a high dependency area or at least a closely observed area of a specialised surgical ward. Analgesia should be with minimal amounts of opioid, and as much non-steroidal or paracetamol as can be tolerated. The role of Dexmedetomidine is unclear but many consider this a useful opioid-sparing agent. If used, PCA morphine doses will typically be set with half the bolus dose and sometimes twice the lockout time to minimise the risks of overdosage. Regional analgesia is discussed elsewhere, the important point is that epidural opioids are not demonstrably safer than systemic opioids. Patients who undergo laparoscopic procedures will frequently have lower pain scores and a lesser requirement for analgesia, and with the generous use of paracetamol and non-steroidals will often avoid post-operative opioids altogether. Those patients who are using CPAP should be advised to bring their own mask and ventilatory equipment, but in those who are compliant this is infrequently required on the first post-operative night, and indeed this is not part of the recommendations of the task force. Some surgeons are reluctant to allow the use of CPAP because of the hypothetical risk of aerophagia and distension of the pouch, but this rarely seems to occur. Supplemental oxygen will be given initially, but once patients are maintaining normal oxygen saturations on air it is usually only given by nasal specula at a low flow rate. Close monitoring for respiratory insufficiency is the main driver for the admission of these high-risk patients to a level 2 (high dependency) unit. Many advocate the placement of arterial lines to allow overnight sampling of arterial CO2 levels, and regular and frequent blood gas analysis allows the identification of upward trends and hence CO2 retention before levels become dangerous. Opioid administration can then be stopped and BiPAP instituted to prevent the patient progressing to hypercapnic narcosis and respiratory arrest. In the most extreme situations, Naloxone and Doxapram can used to stimulate respiration, but prevention is invariably better than cure. 6. Dilemmas When faced with an asymptomatic patient with severe OHS/OSA: at what point is treatment indicated? The only evidence-base comes from the neuromuscular literature. In this context there is a consensus opinion that desaturation to less than 88% for 5 consecutive minutes should indicate NIV. A study of patients with neuromuscular disease found that trans-cutaneous CO2 was greater than 6.5kPa for more than 70% of the night in those who subsequently developed decompensated ventilator failure.29 However, the difference between neuromuscular patients and obesity patients is that the former are invariably in progressive decline, whereas someone with obesity may actually be stable if their body weight is stable. Therefore, the neuromuscular criteria may be over-aggressive for bariatric patients. The quoted AHI is not of much help, and can be deeply misleading in obesity hypoventilation. Because it counts events per hour, it does not take stock of the length of events. In the extreme case, a patient may have one profound and prolonged desaturation per hour, but therefore only score one. This index is only really valid for OSA, where the desaturations are short and frequent. Consensus seems to suggest that arterial oxygen saturations continuously below 80 for more than a couple of minutes probably indicate introduction of treatment. Daytime hypercapnia would be another indication. Given the progressive reduction in vital capacity en route to respiratory failure, a significantly reduced vital capacity associated with the preceding factors should be taken into account if known. When faced with an asymptomatic patient with markedly limited exercise tolerance, at what point is treatment indicated? There is no good evidence in the literature that demonstrates objectively an increased exercise capacity in patients commenced on CPAP or BiPAP for SDB. However it is intuitive that by resolving the factors leading to hypertension and right heart strain, these processes should resolve. Certainly, the experience of many has been of patients who report markedly improved walking distances following four to six weeks of support. This is an area that needs further study. 7. Summary Sleep-disordered breathing is present in the majority of morbidly obese patients. Possible post-operative implications are myriad. Large numbers of patients with asymptomatic and probably low grades of Obstructive Sleep Apnoea undergo anaesthesia without complication Obesity hypoventilation is less common, but a much more serious problem because of the blunted CO2 sensitivity. There is a high risk of difficult weaning following general anaesthesia; these patients are the group requiring the shortest-acting anaesthetic agents and the use of opioid-sparing techniques, in order to minimise risk of post-operative hypercapnic respiratory failure developing. They should be managed in a high-dependency area with invasive arterial monitoring and regular blood gas analysis to identify developing CO2 retention, and frequently will require post-op BiPAP Untreated obesity hypoventilation syndrome will progress to acute on chronic respiratory failure and is ultimately lethal. In the event of post-operative respiratory failure, the essential goal is to oxygenate, whilst positioning the patient to optimise ventilation. If opioids have been given recently, then Naloxone is indicated. In the short term respiratory drive can be increased by the use of doxapram; and if this is inadequate then assisted ventilation is required, either by non-invasive means or through re-intubation. Conflict of interest None. References 1. 1Gross JB, Bachenberg KL, Benumof JL, Caplan RA, Connis RT, Cote CJ, et al. 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a Dept of Respiratory Medicine, Queen Alexandra Hospital, Portsmouth, United Kingdom b Dept of Anaesthesia, St Richard's Hospital, Spitalfield Lane, Chichester, West Sussex PO19 6SE, United Kingdom  Corresponding author. Tel./fax: +44 7811 333 613.
PII: S0953-7112(09)00127-6 doi:10.1016/j.cacc.2009.10.008 © 2009 Elsevier Ltd. All rights reserved. | |
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