Obesity in anaesthesia and intensive care
2000; Elsevier BV; Volume: 85; Issue: 1 Linguagem: Inglês
10.1093/bja/85.1.91
ISSN1471-6771
Autores Tópico(s)Bariatric Surgery and Outcomes
ResumoBr J Anaesth 2000; 85: 91–108 The prevalence of significant obesity continues to rise in both developed and developing countries, and is associated with an increased incidence of a wide spectrum of medical and surgical pathologies35Björntorp P Obesity.Lancet. 1997; 350: 423-426Abstract Full Text Full Text PDF PubMed Scopus (276) Google Scholar (Table 1). As a result, the anaesthetist can expect to be presented frequently with obese patients in the operating theatre, intensive care unit or resuscitation room. These patients may provide the anaesthetist with a considerable challenge. A thorough understanding of the pathophysiology and specific complications associated with the condition should allow more effective and safer treatment for this unique group of patients.Table 1Medical and surgical conditions associated with obesityCategoryExamplesCardiovascular diseaseSudden (cardiac) death; obesity cardiomyopathy; hypertension; ischaemic heart disease; hyperlipidaemia; cor pulmonale; cerebrovascular disease; peripheral vascular disease; varicose veins; deep-vein thrombosis and pulmonary embolismRespiratory diseaseRestrictive lung disease; obstructive sleep apnoea; obesity hypoventilation syndromeEndocrine diseaseDiabetes mellitus; Cushing's disease; hypothyroidism; infertilityGastrointestinal diseaseHiatus hernia; gallstones; inguinal herniaGenitourinaryMenstrual abnormalities; female urinary incontinence; renal calculiMalignancyBreast, prostate, colorectal, cervical and endometrial cancerMusculoskeletalOsteoarthritis of weight-bearing joints, back pain Open table in a new tab Obesity is a condition of excessive body fat. The name is derived from the Latin word obesus, which means fattened by eating.69Fisher A Waterhouse TD Adams AP Obesity: its relation to anaesthesia.Anaesthesia. 1975; 30: 633-647Crossref PubMed Google Scholar The difference between normality and obesity is arbitrary, but an individual must be considered obese when the amount of fat tissue is increased to such an extent that physical and mental health are affected and life expectancy reduced.122National Institutes of Health Consensus Development Conference Statement Health implications of obesity.Ann Int Med. 1985; 103: 147-151Crossref PubMed Google Scholar Examples of body fat contents in adults from Western societies are 20–30% for the average female, 18–25% for the average male, 10–12% for a professional soccer player and 7% for a marathon runner.121Murphy PG Obesity.in: Hemmings Jr, HC Hopkins PM Foundations of Anaesthesia. Basic and Clinical Sciences. Mosby, London2000: 703-711Google Scholar Accurate measurement of body fat content is difficult and requires sophisticated techniques such as computed tomography (CT) scanning or magnetic resonance imaging. Useful estimates, however, can be obtained by evaluating weight for a given height and then comparing that figure with an ideal weight. The concept of ideal body weight (IBW) originates from life insurance studies which describe the weight associated with the lowest mortality rate for a given height and gender; for general clinical purposes, IBW can be estimated from the formula IBW (in kg) = height (in cm) – x, where x is 100 for adult males and 105 for adult females. The body mass index (BMI) is a more robust measure of the relationship between height and weight, and is widely used in clinical and epidemiological studies. It is calculated as follows: BMI = body weight (in kg)/height2 (in metres) A BMI of 30, >35 and >55 kg m−2 are considered obese, morbidly obese and super-morbidly obese, respectively.39Bray GA Pathophysiology of obesity.Am J Clin Nutr. 1992; 55: 488S-494SPubMed Google Scholar Morbidity and mortality rise sharply when the BMI is >30 kg m−2.76Garrison RJ Castelli WP Weight and thirty-year mortality of men in the Framingham study.Ann Int Med. 1985; 103: 1006-1009Crossref PubMed Google Scholar Although it is a very robust and practical assessment of obesity, the BMI does have its limitations. For instance, heavily muscled individuals would be classified as overweight. It is now thought that other factors, such as young age and the pattern of adipose tissue distribution, may be better predictors of health risk. There is overwhelming evidence that the prevalence of obesity is increasing worldwide. In 1997, an International Obesity Task Force summarized information on the epidemiology of obesity.35Björntorp P Obesity.Lancet. 1997; 350: 423-426Abstract Full Text Full Text PDF PubMed Scopus (276) Google Scholar Defining obesity as a BMI of >30 kg m−2, they concluded that the prevalence of obesity was 15–20% in Europe with wide regional variations. In the UK over the period 1980–1991 the prevalence of obesity had increased from 6% to 13% in men and from 8% to 15% in women, meaning that the average UK body weight had risen by approximately 1 kg over that 10 yr period. The picture was better for Scandinavia and the Netherlands (10%) but worse for Eastern Europe (up to 50% among women in some countries). The health and economic implications are considerable, since countries such as France, Germany and the UK will each have approximately 10 million obese inhabitants.35Björntorp P Obesity.Lancet. 1997; 350: 423-426Abstract Full Text Full Text PDF PubMed Scopus (276) Google Scholar The situation in the USA is even worse, with the prevalence of a BMI of >25 kg m−2 being 59.4% for men, 50.7% for women and 54.9% for adults overall.70Flegal KM Carroll MD Kuczmarski RJ Johnson CL Overweight and obesity in the United States: prevalence and trends, 1960–1994.Int J Obes Relat Metab Disord. 1998; 22: 39-47Crossref PubMed Google Scholar Furthermore, for the period 1960–1994, the prevalence of obesity (BMI of >30 kg m−2) has increased markedly from 12.8% to 22.5%. The prevalence of obesity varies with socioeconomic status. In developed countries, poverty is associated with a greater prevalence of obesity whereas in developing areas it is affluence that carries the higher risk.147Sobal J Stunkard A Socioeconomic status of obesity: a review of the literature.Psychol Bull. 1989; 105: 260-275Crossref PubMed Google Scholar There is little evidence to suggest that being moderately overweight (actual body weight 110–120% of IBW) carries much excess risk in young adults,143Sjöström LV Mortality of severely obese subjects.Am J Clin Nutr. 1992; 55: 516S-523SPubMed Google Scholar but morbidity and mortality rise sharply when BMI is >30 kg m−2, particularly with concomitant cigarette smoking. The risk of premature death doubles in individuals with a BMI of >35 kg m−2.76Garrison RJ Castelli WP Weight and thirty-year mortality of men in the Framingham study.Ann Int Med. 1985; 103: 1006-1009Crossref PubMed Google Scholar Sudden unexplained death is 13 times more likely in morbidly obese women than in their non-obese counterparts.63Duflou J Virmani R Rabin I Burke A Farb A Smialek J Sudden death as a result of heart disease in morbid obesity.Am Heart J. 1995; 130: 306-313Abstract Full Text PDF PubMed Scopus (129) Google Scholar 106Kral G Morbid obesity and related health risks (a review).Ann Int Med. 1985; 103: 1043-1047Crossref PubMed Google Scholar Overweight men participating in the Framingham study82Harris T Cook F Garrison R Higgins M Kannel W Goldman L Body mass index and mortality among non-smoking older persons: the Framingham Heart Study.J Am Med Assoc. 1988; 259: 1520-1524Crossref PubMed Google Scholar had a mortality rate 3.9 times greater than the normal weight group. Morbidly obese individuals are at a much greater risk of mortality from diabetes, cardiorespiratory62Drenick EJ Fisler JS Sudden cardiac arrest in morbidly obese surgical patients unexplained after autopsy.Am J Surg. 1988; 155: 720-726Abstract Full Text PDF PubMed Scopus (76) Google Scholar and cerebrovascular disorders, and certain forms of cancer,75Garfinkel L Overweight and cancer.Ann Int Med. 1985; 103: 1034-1036Crossref PubMed Google Scholar as well as a host of other diseases99Kannel WB Brand N Skinner JJ Dawber TR McNamara PM The relation of adiposity to blood pressure and the development of hypertension: The Framingham study.Ann Int Med. 1867; 67: 48-59Crossref Google Scholar 100Kannel WB LeBauer JE Dawber JR McNamara PM Relation of body weight to development of coronary heart disease: the Framingham study.Circulation. 1967; 35: 734-744Crossref PubMed Google Scholar (Table 1). These risks are proportional to the duration of obesity;121Murphy PG Obesity.in: Hemmings Jr, HC Hopkins PM Foundations of Anaesthesia. Basic and Clinical Sciences. Mosby, London2000: 703-711Google Scholar it appears that continued weight gain constitutes a higher risk than for obese individuals whose weight is constant. For a given level of obesity, men are at a higher risk than women,107Kushner RF Body weight and mortality.Nutr Rev. 1993; 51: 127-136Crossref PubMed Google Scholar but for both groups weight loss reduces the risk associated with previous obesity. Despite this, weight reduction immediately before surgery has not been shown to reduce perioperative morbidity and mortality.67Fasol R Schindler M Schumacher B et al.The influence of obesity on perioperative morbidity: retrospective study of 502 aortocoronary bypass operations.Thorac Cardiovasc Surg. 1992; 40: 126-129Crossref PubMed Google Scholar 142Shenkman Z Shir Y Brodsky JB Perioperative management of the obese patient.Br J Anaesth. 1993; 70: 349-359Crossref PubMed Scopus (0) Google Scholar Obesity is a complex and multifactorial disease150Stunkard AJ Current views on obesity.Am J Med. 1996; 100: 230-235Abstract Full Text PDF PubMed Scopus (167) Google Scholar but, in simple terms, occurs when net energy intake exceeds net energy expenditure over a prolonged period of time. However, it is not always easy to identify a single explanation as to why this occurs in some individuals and not others. The following observations provide some clues: Obesity tends to be familial, with children of two obese parents having about a 70% chance of becoming obese themselves as compared with a 20% risk for children of non-obese parents. This can, in part, be explained by influences such as diet and lifestyle, but studies of adopted children show weight patterns similar to those of their natural parents, suggesting that a genetic component does exist. Animal studies have confirmed that there is a genetic contribution to obesity. In 1994 the ob gene was identified in mice and was shown to control the production of the protein leptin.21Auwerx J Staels B Leptin.Lancet. 1998; 351: 737-742Abstract Full Text Full Text PDF PubMed Scopus (478) Google Scholar 171Zhang Y Proenca R Maffei M Barone M Leopold L Friedman JM Positional cloning of the mouse obese gene and its human homologue.Nature. 1994; 372: 425-432Crossref PubMed Scopus (9884) Google Scholar Genetically obese ob/ob mice produce insufficient leptin and tend to overeat, leading to obesity. Exogenous leptin reverses hyperphagia and induces weight loss. Clinical studies, however, suggest that only very rarely can such simple genetic defects in leptin production account for significant obesity.48Carlsson B Lindell K Gabrielsson B et al.Obese (ob) gene defects are rare in human obesity.Obes Res. 1997; 5: 30-35Crossref PubMed Google Scholar In fact, most obese individuals have elevated leptin concentrations, probably a consequence of increased amounts of the source tissue, fat. Furthermore, the rapid increase in the prevalence of obesity over the last 30 years and the fact that the gene pool has remained relatively constant suggest that environmental issues are much more important determinants. In the USA there are marked differences in the prevalence of obesity in the different ethnic populations, with African and Mexican Americans being at much higher risk than white Americans. Asian immigrants to the UK have a more central distribution of fat than native Caucasians; this is associated with an increased risk of diabetes and coronary heart disease.35Björntorp P Obesity.Lancet. 1997; 350: 423-426Abstract Full Text Full Text PDF PubMed Scopus (276) Google Scholar In the UK there is an inverse relationship between socioeconomic status and the prevalence of obesity, with women of social class I having a 10% risk as compared with 25% in social class V. Of women who move to a higher social class on marriage, only 12% were overweight as compared with 22% who moved to a lower social class. Endocrine abnormalities such as Cushing's disease or hypothyroidism predispose to obesity. Patients with such diseases are usually identified quickly from symptoms other than obesity, and appropriate medical therapy normally corrects the problem. In the same way, certain drugs—such as corticosteroids, antidepressants and antihistamines—may also lead to weight gain. The total number of calories consumed and, particularly, the dietary fat content, is the prime determinant of obesity (the proportion of fat in the UK diet has increased from 20% to 40% over the last 50 years). Alcohol appears to play a key role too, and may influence the site of fat deposition, encouraging central fat to be laid down. Contrary to popular belief, obese people have a greater energy expenditure than thin people as it takes more energy to maintain their increased body size. Inactivity is usually the result, but not necessarily the cause, of the obesity. However, it has been shown that individuals who remain active in their adult life do best at maintaining healthy weight levels. While an imbalance between energy intake and energy expenditure is typical of obesity, the daily net calorie excess may be quite modest. For instance, a typical weight gain of 20 kg over 10 years implies an initial daily energy excess of 30–40 kcal, the equivalent of less than half a sandwich.35Björntorp P Obesity.Lancet. 1997; 350: 423-426Abstract Full Text Full Text PDF PubMed Scopus (276) Google Scholar It is now becoming clear that it is not only the amount of fat that is important in determining risk, but also its anatomical distribution.34Björntop P Visceral obesity: a “civilization syndrome”.Obes Res. 1993; 1: 206-222Crossref PubMed Scopus (388) Google Scholar 88Hsieh SD Yoshinaga H Abdominal fat distribution and coronary heart disease risk factors in men—waist/height ratio as a simple and useful predictor.Int J Obes Relat Metab Disord. 1995; 19: 585-589PubMed Google Scholar 131Perry AC Applegate EB Allison MD Jackson ML Miller PC Clinical predictability of the waist-to-hip ratio in assessment of cardiovascular disease risk factors in overweight, pre-menopausal women.Am J Clin Nutr. 1998; 68: 1022-1027PubMed Google Scholar In the central or android type of distribution, which is more common in males, fat is predominantly distributed in the upper body and may be associated with increased deposits of intra-abdominal or visceral fat. In the peripheral or gynaecoid type, fat is more typically distributed around the hips, buttocks or thighs; this is the more usual female pattern of distribution.20Ashwell M Chinn S Stalley S Garrow JS Female fat distribution—a simple classification based on two circumference measurements.Int J Obes. 1982; 6: 143-152PubMed Google Scholar Central adipose tissue is metabolically more active than fat in the peripheral distribution and is associated with more metabolic complications such as dyslipidaemias, glucose intolerance and diabetes mellitus, and a higher incidence of mortality from ischaemic heart disease.22Azevedo A Ramos E von Hafe P Barros H Upper-body adiposity and risk of myocardial infarction.J Cardiovasc Risk. 1999; 6: 321-325Crossref PubMed Scopus (0) Google Scholar 40Brodksy JB Anesthetic management of the morbidly obese patient.Int Anesthesiol Clin. 1986; 24: 93-103Google Scholar 131Perry AC Applegate EB Allison MD Jackson ML Miller PC Clinical predictability of the waist-to-hip ratio in assessment of cardiovascular disease risk factors in overweight, pre-menopausal women.Am J Clin Nutr. 1998; 68: 1022-1027PubMed Google Scholar Morbidly obese patients with a high proportion of visceral fat are also at a greater risk from cardiovascular disease, left ventricular dysfunction and stroke.136Reeder BA Senthilselvan A Despres JP et al.The association of cardiovascular disease risk factors with abdominal obesity in Canada. Canadian Heart Health Surveys Research Group.Can Med Assoc J. 1997; 157: S39-S45PubMed Google Scholar The mechanism for this increased risk with intra-abdominal fat is not known, but one widely held theory implicates the products of the breakdown of visceral fat being delivered directly into the portal circulation and thereby inducing a significant secondary metabolic imbalance.121Murphy PG Obesity.in: Hemmings Jr, HC Hopkins PM Foundations of Anaesthesia. Basic and Clinical Sciences. Mosby, London2000: 703-711Google Scholar Although the practical assessment of fat distribution requires sophisticated imaging techniques, the ratio of waist to hip circumference is a useful clinical measure. In European descendants a waist:hip ratio of >1.0 in men and >0.85 in women would tend to suggest a higher proportion of more centrally distributed fat.34Björntop P Visceral obesity: a “civilization syndrome”.Obes Res. 1993; 1: 206-222Crossref PubMed Scopus (388) Google Scholar Approximately 5% of morbidly obese patients will have obstructive sleep apnoea OSA, which is characterized by the following features:10Alpert MA Hashimi MW Obesity and the heart.Am J Med Sci. 1993; 306: 117-123Crossref PubMed Google Scholar 95Jennum P Sjol A Epidemiology of snoring and obstructive sleep apnoea in a Danish population age 30–60.J Sleep Res. 1992; 1: 240-244Crossref PubMed Google Scholar 121Murphy PG Obesity.in: Hemmings Jr, HC Hopkins PM Foundations of Anaesthesia. Basic and Clinical Sciences. Mosby, London2000: 703-711Google Scholar 169Young T Palta M Dempsey J Skatrud J Webber S Bader S The occurrence of sleep-disordered breathing among middle-aged adults.New Engl J Med. 1993; 328: 1230-1235Crossref PubMed Google Scholar (i) Frequent episodes of apnoea or hypopnoea during sleep.161Vgontzas AN Tan TL Bixler EO et al.Sleep apnea and sleep disruption in obese patients.Arch Int Med. 1994; 154: 1705-1711Crossref PubMed Google Scholar An obstructive apnoeic episode is defined as 10 s or more of total cessation of airflow despite continuous respiratory effort against a closed airway. Hypopnoea is defined as 50% reduction in airflow or a reduction sufficient to lead to a 4% decrease in arterial oxygen saturation.61Douglas N Polo O Pathogenesis of obstructive sleep apnoea/hypopnoea syndrome.Lancet. 1994; 344: 653-655Abstract PubMed Scopus (103) Google Scholar 121Murphy PG Obesity.in: Hemmings Jr, HC Hopkins PM Foundations of Anaesthesia. Basic and Clinical Sciences. Mosby, London2000: 703-711Google Scholar The number of episodes thought to be clinically significant is often quoted as five or more per hour or >30 per night. The exact numbers are rather arbitrary and it is obviously the clinical sequelae, such as hypoxia, hypercapnia, systemic and pulmonary hypertension and cardiac arrhythmias, that are more important. (ii) Snoring. This usually gets louder as the airway obstructs, followed by silence, as airflow ceases, and then gasping or choking, as the person rouses and airway patency is restored. (iii) Daytime symptoms: repeated episodes of fragmented sleep throughout the night causes daytime sleepiness, which is associated with impaired concentration, memory problems and road traffic accidents.124Partinen M Guilleminault C Daytime sleepiness and vascular morbidity at seven-year follow-up in obstructive sleep apnea patients.Chest. 1990; 97: 27-32Abstract Full Text Full Text PDF PubMed Google Scholar The patient may also complain of morning headaches caused by nocturnal carbon dioxide retention and cerebral vasodilation. (iv) Physiological changes. Recurrent apnoea leads to hypoxaemia, hypercapnia and pulmonary and systemic vasoconstriction. Recurrent hypoxaemia leads to secondary polycythaemia and is associated with an increased risk of ischaemic heart disease and cerebrovascular disease, while hypoxic pulmonary vasoconstriction leads to right ventricular failure.101Kessler R Chaouat A Weitzenblum E et al.Pulmonary hypertension in the obstructive sleep apnea syndrome: prevalence, cause and therapeutic consequences.Eur Respir J. 1996; 9: 787-794Crossref PubMed Scopus (0) Google Scholar 109Laks L Krieger J Podszus T Pulmonary hypertension in obstructive sleep apnea: multicenter study.Am Rev Respir Dis. 1992; 145: 865Google Scholar Apnoea occurs when the pharyngeal airway collapses during sleep. Pharyngeal patency depends on the action of dilator muscles which prevent upper airway closure. This muscle tone is lost during sleep and, in many individuals, this leads to significant narrowing of the airway, causing turbulent airflow and snoring.61Douglas N Polo O Pathogenesis of obstructive sleep apnoea/hypopnoea syndrome.Lancet. 1994; 344: 653-655Abstract PubMed Scopus (103) Google Scholar Increased inspiratory effort and the response to hypoxia and hypercapnia lead to arousal which, in turn, restores upper airway tone.51Connolly LA Anesthetic management of obstructive sleep apnea patients.J Clin Anesth. 1991; 3: 461-469Abstract Full Text PDF PubMed Scopus (0) Google Scholar 101Kessler R Chaouat A Weitzenblum E et al.Pulmonary hypertension in the obstructive sleep apnea syndrome: prevalence, cause and therapeutic consequences.Eur Respir J. 1996; 9: 787-794Crossref PubMed Scopus (0) Google Scholar The patient then gasps, takes a few breaths and falls asleep again; the cycle then restarts. Total occlusion can occur if the airway is narrowed further, such as by enlarged pharyngeal soft tissues or by a further reduction in muscle tone by drugs or alcohol.120Millman RP Meyer TJ Eveloff SE Sleep apnea in the morbidly obese.Rhode Island Med. 1992; 75: 483-486PubMed Google Scholar The main predisposing factors are male gender, middle age and obesity, with other factors such as evening alcohol or night sedation compounding the problem.61Douglas N Polo O Pathogenesis of obstructive sleep apnoea/hypopnoea syndrome.Lancet. 1994; 344: 653-655Abstract PubMed Scopus (103) Google Scholar Other features that help to identify significant OSA are a BMI of >30 kg m−2, hypertension, observed episodes of apnoea during sleep, collar size >16.5, polycythaemia, hypoxaemia/hypercapnia and right ventricular hypertrophy or impairment on electrocardiography and echocardiography.121Murphy PG Obesity.in: Hemmings Jr, HC Hopkins PM Foundations of Anaesthesia. Basic and Clinical Sciences. Mosby, London2000: 703-711Google Scholar Definitive diagnosis is made by polysomnography in a sleep laboratory. The acid–base disturbance of OSA, i.e. respiratory acidosis, is initially limited to sleep, with a return to homeostasis during the day. However, a long-term consequence of OSA is an alteration in the control of breathing, the characteristic feature of which is central apnoeic events, that is, episodes of apnoea without respiratory effort. Such episodes, which are associated with a progressive desensitization of the respiratory centres to (nocturnal) hypercapnia, are initially limited to sleep, but eventually lead to type II respiratory failure with an increasing reliance on hypoxic drive for ventilation.121Murphy PG Obesity.in: Hemmings Jr, HC Hopkins PM Foundations of Anaesthesia. Basic and Clinical Sciences. Mosby, London2000: 703-711Google Scholar At its worst, such obesity hypoventilation culminates in Pickwickian syndrome, which is characterized by obesity, hypersomnolence, hypoxia, hypercapnia, right ventricular failure and polycythaemia.47Burwell CS Robin ED Whaley RD Bickelman AG External obesity associated with alveolar hypoventilation—a Pickwickian syndrome.Am J Med. 1956; 25: 815-820Google Scholar A careful and detailed assessment of the morbidly obese patient's upper airway is required before they are anaesthetized. Difficulties with mask ventilation and tracheal intubation may be considerable,87Hood DD Dewan DM Anesthetic and obstetric outcome in morbidly obese parturients.Anesthesiology. 1993; 79: 1210-1218Crossref PubMed Google Scholar 112Lee JJ Larson RH Buckley JJ Roberts RB Airway maintenance in the morbidly obese.Anesth Rev. 1980; 7: 33-36Google Scholar with the incidence of difficult intubation being quoted at around 13%.44Buckley FP Robinson NB Simonowitz DA Dellinger EP Anaesthesia in the morbidly obese. A comparison of anaesthetic and analgesic regimens for upper abdominal surgery.Anaesthesia. 1983; 38: 840-851Crossref PubMed Google Scholar These problems are caused by features such as fat face and cheeks, large breasts, short neck, large tongue, excessive palatal and pharyngeal soft tissue, high and anterior larynx, restricted mouth opening and limitation of cervical spine and atlanto-occipital flexion and extension.40Brodksy JB Anesthetic management of the morbidly obese patient.Int Anesthesiol Clin. 1986; 24: 93-103Google Scholar 43Buckley FP Anesthesia and obesity and gastrointestinal disorders.in: Barash PG Cullen BF Stoelting RK Clincal Anesthesia. J. B. Lippincott, Philadelphia1992: 1169-1183Google Scholar Preoperative evaluation of the airway must include: (i) assessment of head and neck flexion, extension and lateral rotation; (ii) assessment of jaw mobility and mouth opening; (iii) inspection of oropharnyx and dentition; (iv) checking the patency of the nostrils; (v) inspection of previous anaesthetic charts and questioning the patient about previous difficulties, especially any episodes of upper airway obstruction associated with anaesthesia or surgery (one should always bear in mind that previous records of uneventful anaesthetics may no longer be relevant and new changes, such as further weight gain, pregnancy, head and neck radiotherapy or development of signs and symptoms of upper airway obstruction, must be sought); (vi) a systemic enquiry into features suggestive of obstructive sleep apnoea syndrome, such as excessive snoring with or without episodes of apnoea and daytime hypersomnolence. These imply potential airway obstruction once the patient has been rendered unconscious. These patients are particularly likely to present considerable airway difficulties. Further imaging of the airway with soft tissue X-rays and CT scans along with consultation with an otolaryngologist for direct or indirect laryngoscopy may provide useful information about the airway if time is available preoperatively. If difficult intubation is envisaged, then an awake fibreoptic intubation should be considered and discussed with the patient. Mass loading of the thoracic and abdominal components of the chest wall in supine, awake obese subjects causes abnormalities of both lung volumes and gas exchange. The well recognized harmful effects of anaesthesia add significantly to the derangement of gas exchange, thereby explaining the problem in gas exchange commonly encountered when anaesthetizing obese patients. Morbid obesity is associated with reductions in functional residual capacity (FRC), expiratory reserve volume (ERV) and total lung capacity,32Biring MS Lewis MI Liu JI Mohsenifar Z Pulmonary physiologic changes of morbid obesity.Am J Med Sci. 1999; 318: 293-297Crossref PubMed Google Scholar 135Ray C Sue D Bray G Hansen JE Wasserman K Effects of obesity on respiratory function.Am Rev Respir Dis. 1983; 128: 501-506Crossref PubMed Google Scholar with FRC declining exponentially with increasing BMI.32Biring MS Lewis MI Liu JI Mohsenifar Z Pulmonary physiologic changes of morbid obesity.Am J Med Sci. 1999; 318: 293-297Crossref PubMed Google Scholar These changes have been attributed to mass loading and splinting of the diaphragm. FRC may be reduced in the upright obese patient to the extent that it falls within the range of the closing capacity with subsequent small airway closure,83Hedenstierna G Gas exchange during anaesthesia.Br J Anaesth. 1990; 64: 507-514Crossref PubMed Google Scholar ventilation– perfusion mismatch, right-to-left shunting and arterial hypoxaemia.18Andersen J Rasmussen JP Eriksen J Pulmonary function in obese patients scheduled for jejuno-ileostomy.Acta Anaesthesiol Scand. 1977; 21: 346-351Crossref PubMed Scopus (5) Google Scholar 86Holley HS Milic-Emili J Becklake MR Bates DV Regional distribution of pulmonary ventilation and perfusion in obesity.J Clin Invest. 1967; 46: 475-481Crossref PubMed Google Scholar 135Ray C Sue D Bray G Hansen JE Wasserman K Effects of obesity on respiratory function.Am Rev Respir Dis. 1983; 128: 501-506Crossref PubMed Google Scholar 158Vaughan RW Wise L Intraoperative arterial oxygenation in obese patients.Ann Surg. 1976; 184: 35-42Crossref PubMed Google Scholar Anaesthesia compounds these problems, such that a 50% reduction in observed FRC occurs in the obese anaesthetized patient, as compared with a 20% fall in anaesthetized non-obese subjects54Damia G Mascheroni D Croci M Tarenzi L Perioperative changes in functional residual capacity in morbidly obese patients.Br J Anaesth. 1988; 60: 574-578Crossref PubMed Google Scholar (Fig.1). Söderberg and colleagues148Söderberg M Thomson D White T Respiration, circulation and anaesthetic management in obesity. Investigation before and after jejunoileal bypass.Acta Anaesthesiol Scand. 1977; 21: 55-61Crossref PubMed Google Scholar found an intrapulmonary shunt of 10–25% in anaesthetized obese subjects and 2–5% in lean individuals. FRC can be increased by ventilating with large tidal volumes (e.g. 15–20 ml kg−1) although this has been shown to improve arterial oxygen tensi
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