Anaesthesia, 1975, Volume 30, pages 633-647 REVIEW ARTICLE

Obesity: its relation to anaesthesia

A. F I S H E R , T . D . W A T E R H O U S E

AND

A . P. A D A M S

‘He’sfat, and scant of breath’ Hamlet, Act V, Sc. I1 In spite of the aesthetic appeal and physical advantages of slimness, obesity remains the commonest nutritional disorder in civilised countries today. Although the Registrar General’s statistical review of England and Wales, for 1971, listed obesity as the cause of death in only 170 patients,‘ the risks imposed on health and life by this disorder are not readily measured. The gross dangers, revealed by the Society of Actuaries’ data, show that people who are 20% overweight increase their chances of dying from heart disease by 40% and from cerebro-vascular disease by 50%.’ It has been suggested that being 10 Ib (4.5 kg) overweight carries a greater risk to health than smoking 25 cigarettes a day.3 Yet, in spite of an increasing indictment against obesity, the full implications of its adverse physiological effects are still incompletely investigated ; not least of all the response of obese people to anaesthesia and surgery. Obesity means excessive adiposity being derived from the Latin ‘obesus’ meaning ‘fattened by eating’. The implication of the word ‘obesity’ itself is that ‘the flesh has been eaten away’ by the f a t 4 A strict definition is difficult as the point at which normality ends and obesity begins is arbitarily selected and varies with taste and fashion. The most widely quoted current definition is an actuarial concept relating lifeexpectancy to weight; this is based on pooled American life assurance statistics which indicate a person to be obese if he or she exceeds the expected or ideal weight, corrected for age and sex, by more than lo%.’ More simply it has been defined as ‘an excessive accumulation of triglyceride fat in the adipose tissue depots of the body’;5 but what is excessive? Objective measurements must be applied and direct cadaver analysis suggests that a fat content of more than 25% in the male and 30% in the female is excessive.6 Many elaborate methods such as densitometry, ultrasonoscopy, total water or body potassium measurements, dilution of fat-soluble gases such as helium, cyclopropane and krypton can be used, but mainly for research In order to overcome the tendency for fat people to be short and lean people to be tall, the A. Fisher, MB, BCh, FFARCS, Consultant Anaesthetist, Radcliffe Infirmary, Oxford and Clinical Lecturer, University of Oxford, T. D. Waterhouse, MB, ChB, DRCOG, FFARCS, DA, Consultant Anaesthetist, Musgrove Park Hospital, Taunton, Somerset, and A. P. Adams, PhD, MB, BS, MRCS, LRCP, FFA, RCS, DA, Consultant Anaesthetist, Radcliffe Infirmary, Oxford and Clinical Lecturer, University of Oxford.

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Ponderal or Somatic Index (height in cm divided by the cube root of weight in lb) has been devised, thereby expressing fatness more independently of height. l1 More recently the use of spring-loaded skinfold calipers which exert a constant pressure at all ranges of thickness over a standard area, has provided a more simple instrument of measurement; good correlation has been demonstrated between the triceps skinfold thickness in the female, or the subscapular skinfold thickness in the male, and some of the more complex methods mentioned above.”

Aetiology

The aetiology of obesity has been reviewed by M ~ C r a c k e n . ’A ~ positive caloric balance in the food intake produces what is termed ‘exogenous’ obesity, there being little evidence that some individuals can receive excess calories without weight increase thereby refuting the oft-repeated doctrine of early German writers known as L u x u s k o n s ~ m p t i o n . ~ The ~ ~ triglyceride which accumulates in fat cells is synthesised (lipogenesis) from an alpha glycerol phosphate molecule plus three fatty acid molecules, the latter being either synthesised from, for example, glucose or derived from circulating fatty acids of dietary origin. Fat can be mobilised and split (lipolysis) into free fatty acids and glycerol, and obesity can, therefore, result from increased lipogenesis or decreased lipolysis or both. The natural history of fat cells has been reviewed16 and studies have shown that in obese adults with an increased number of fat cells the obesity started in childhood, particularly in the first year.” A further period of fat cell multiplication has more recently been demonstrated to occur at puberty.” Although the ultimate cause of obesity is a positive caloric balance, there are other contributing factors.

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Cultural factors In underdeveloped countries the ruling classes tend to be obese, but in economically advanced areas it is, paradoxically, the lower social classes who tend to get fat, due probably to their less discriminating acceptance of advertising and to the relative cheapness of predominately carbohydrate f 0 0 d . l ~

Genetic factors Although it is known that the incidence of obesity in children in overweight parents is increased,” and genetically transmitted ‘metabolic’ obesity has been firmly established in rodents,’l the body of evidence suggests that environmental factors are more important than genetic factors in the aetiology of obesity.22

Psychological factors Food is said to satisfy such hidden needs as security, reassurance, sex, adventure, pleasure, parental pride, individuality, group acceptance and prestige.23,24 The possibility of hidden anxiety should be remembered when the anaesthetist makes his pre-operative visit.”

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Neurological factors Appetite is controlled by the ventrimedial and lateral hypothalmic areas of the brain in response to incompletely understood metabolic and environmental stimuli, and occasionally infective or traumatic damage to these areas can result in excessive food intake and obesity.z6

Metabolic .factors The endocrinological5 and metabolicz7 aspects of obesity have recently been discussed. Obesity can emerge as one feature of endocrine dysfunction, for example, Cushing’s Syndrome, hypothyroidism, hypogonadism and hypopituitarism. Hypokalaemia and elevations of blood lactic acid dehydrogenase, creatinine phosphokinase and fasting blood sugar have been reported.’* Children suffering from hypotonia may develop obesity and diabetes m e l l i t u ~ . ~ ~ Respiratory function

Important structural changes take place related to the duration of obesity: the heavy enlarged abdomen tends to produce a thoracic kyphosis and lumbar lordosis, thereby raising the lower portion of the sternum, limiting rib movement and producing a relative fixation of the thorax in a position of inspiration. The layers of fat on the chest wall and abdomen further reduce the bellows action of the thoracic cage, the diaphragm is elevated and the total work of breathing is increased: ventilation becomes diaphragmatic and very prone to postural deterioration. Although there is no direct linear relationship between the work of respiration and the degree of ~ b e s i t y , ~ ’ the oxygen cost of breathing is increased particularly a t larger minute volume^.^^-^^

Lung volumes Total lung capacity is reduced but excluding otherwise fit young adults,34 and those with associated lumbar lordosis, this is poorly correlated with the degree of weight in~rease.~’ The most consistent changes are considerable reductions in inspiratory capacity (IC) and expiratory reserve volume (ERV),35 which in the sitting position may be reduced to less than 20% of its predicted value,36 and which may be obliterated in the head-down position. Although the vital capacity is reduced the residual volume remains unchanged or slightly increased and there is a decreased functional residual capacity (FRC), that is, the resting end-expiratory position of the chest is lower than normal. Closing volume (CV) has also been found to be increased37 and this together with the decreased ERV implies underventilation of dependent lung regions during resting tidal breathing especially in the supine position, the inspired air being distributed to the upper or non-dependent lung zones3’ Lung function tests may not reveal the severity of physiological disturbances which may occur during anae~thesia;~’ pre-operative blood-gas analysis is important?’ It has been shown that hypoxaemia without hypercapnia is related to overperfusion of the underventilated areas or to perfusion of completely unventilated areas of the lung and an increase in anatomical shunt may also occur.41’4 2 The resulting mis-match between airfiow and blood flow in the lungs results in an increased venous admixture, a decreased arterial oxygen tension and an increase in physiological deadspace.

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Farebrother and colleagues37 showed a good correlation between Pao, and the extent of airway closure and found there was no improvement in gas exchange unless subjects reduced their weight to within 30% of ideal weight as calculated from height, age and sex. Following the induction of anaesthesia there is a further fall in FRC with airway closure, gas trapping and a shift of ventilation to the non-dependent lung zones.43’44 Controlled ventilation with large tidal volumes may reverse this process by moving tidal ventilation above closing volume.

Compliance The chest wall compliance has been shown4’ to differ from a mean value of 224 ml/cm H,O in normal subjects to a mean value of 77 ml/cm H,O in the obese, a figure further reduced by r e c ~ m b e n c yweight ; ~ ~ loss may not lead to an improvement in the chest wall ~ o m p l i a n c eLung . ~ ~ compliance may remain ~ n a l t e r e d , ~or’ may be reduced by 25% in simple obesity and 40% in cases with associated h y p ~ v e n t i l a t i o n . ~ ~ ‘Mass loading’ experiments of the lower thorax and abdomen of normal weight anaesthetised women by means of 22.5 kg sandbags, produced a reduction in the chest wall compliance to values observed in obese anaesthetised women ; furthermore at any respiratory volume the compliance of the obese women was about half that of the normal women. It was concluded that the low chest wall compliance in obesity results from weight only46 but this view has recently been ~ h a l l e n g e d . ~ ~ Although the Pao, is lower than normal in uncomplicated obesity,42 hypoventilation characterised by a raised arterial carbon dioxide tension rarely O C C U ~ S . ~This ~ - ~ ~ is because those parts of the lung which remain relatively well ventilated and well perfused can clear increased amounts of carbon dioxide due to its natural high diffusibility and the favourable characteristics of its dissociation curve. The response of the respiratory centre to inhalation of 5% carbon dioxide is essentially normal in obese patients with normal lungs.30, Thus, in the upright obese person, provided that there is no intrinsic lung disease, no fatty infiltration of muscle5’ and the respiratory centre is unaffected by drugs or disease, hypoventilation does ,not occur. The balance is, however, delicately poised and can be disturbed by simply adopting the head-down position.

Pickwickian syndrome In obese patients with normal lungs the increase in resting ventilation is generally appropriate to the increase in oxygen consumption and carbon dioxide production. This is in contrast to the disproportionate increase in alveolar ventilation found in some other conditions, for example, pulmonary thromboembolic disease and also in contrast to the reduction found in the Pickwickian syndrome.” This syndrome is an association of obesity, episodic somnolence and hypoventilation with twitching, cyanosis, periodic respiration, secondary polycythaemia, right ventricular hypertrophy and right ventricular failure. Although it has been quoted as occurring in 10% of obese this may well be an overestimate.” The word ‘Pickwickian’, originating from the book ‘Pickwick Papers’ by Charles Dickens, published in 1837, relates to the fat messenger-boy Joe who kept falling asleep. Although Fothergill described two similar cases in the 18th century,53,5 4 Burwell and his colleagues introduced ‘Pickwickian’ into the literature and described in detail one extreme case of a 91 kg business

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executive who was accustomed to playing poker once a week; on a crucial occasion he was dealt a hand of three aces and two kings, commonly called a ‘full house’ but because of his somnolence he failed to take advantage of his opportunity and this event led him to seek hospital admission.55

Circulatory function Following a careful prospective investigation of more than 5000 patients over a 12year period, the Framingham heart study concluded that there was a strong positive association between weight gain after the age of 25 years and angina and sudden death, but not, however, of myocardial i n f a r ~ t i o n .Raised ~~ arterial pressures and plasma cholesterol levels were not essential for this correlation, suggesting that obesity imposed a further work load on a heart with an already compromised circulation in an individual with increased basal metabolism and a limited exercise tolerance.57* 5 8

Arterial pressure The measurement of arterial pressure using a conventional sphygmomanometer with a standard adult arm cuff may be subject to i n a c c ~ r a c y ,6o ~ ~usually , an overestimate, but nevertheless, the positive correlation between increased arterial pressure and an increase in body weight first suggested 20 years ago61 has been found too often to leave room for doubt.62,6 3 The degree of hypertension is indicated by two large series: Bare and c o - w o r k e r ~in , ~a~ survey of nearly 17,000 subjects found a 10 kg gain in weight increased the systolic and diastolic pressures by a mean of 3 mmHg and a mean of 2 mmHg respectively. Whyte6’ found that a mean increase of 12.7 kg in weight increased the systolic and diastolic pressures by a mean of 10 mmHg and 7 mmHg respectively. The cause is presumably an increased cardiac output forced into an unaltered peripheral resistance. Normotensive obese individuals must, therefore, have a reduced peripheral vascular resistance-the reverse of essential hypertension.

Cardiac output Alexander66 showed that a gain of 100 kg in body weight increased a normal cardiac output to 10 litres per minute. It has been estimated that 13.5 kg of fat contains 25 miles of blood vessels and, therefore, it is not surprising that both cardiac output and total blood volume are increased.67 The increase in blood flow is due to an increased stroke volume since the resting heart rate remains normal or low. Cerebral, renal and splanchnic blood flow are essentially normal, and assuming unaltered muscle blood flow, the increase is attributed to the adipose tissue.68

Cardiac disease Cardiomegaly can be demonstrated radiologically in both normotensive and hypertensive obese individuals, the cardiac diameter increasing 1 mm for every 1.32 kg excess weight until 91 kg of excess weight is r e a ~ h e d ; ~left ’ ventricular end-diastolic pressure is raised in some obese patients.33 It has been suggested that obesity predisposes to abnormalities in the electro~ardiogram.~~ An earlier view,” that fatty

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infiltration was responsible for the increase in heart size has recently been refuted by evidence from post-mortem examinations which demonstrated consistent left ventricular enlargement with or without right ventricular enlargement, due to muscle hypertrophy and not fatty infiltrati~n.~’Clinically, a loud pulmonary second heart sound can often be heard7’ and pulmonary hypertension is not uncommon,48 with pulmonary arterial pressures reaching 105/25 mmHg.49 The causes include hypoxia, increased venous return, cephalad movement of the diaphragm and diminished vascular distensibility.

Vascular disease Generalised atherosclerosis has been estimated to be 2-3 times more severe in obese people,73 and whilst some studies have shown74,7s a positive association between coronary artery disease and obesity the relationship is not 7 6 * 7 7 The uncertainty is supported by the finding that whereas angina and sudden death occur more frequently, myocardial infarction does not.56 A degeneration of the cerebral vasculature in obesity has been noted,7 this being particularly significant in females.

Other associated disorders

The association between diabetes mellitus and obesity is difficult to define. Certainly it has been known for many years that adult diabetics are often obese and an improved glucose tolerance follows weight reduction.80-82 Continued production of excess insulin in the obese leads to pancreatic exhaustion in patients who are genetically predisposeds3 and thus obesity may unmask genetic diabetes, allowing it to present at an earlier age.84 Abnormal liver function tests have been r e p ~ r t e d , ~and ’ fatty infiltration of the liver is said to occur86although this has not been substantiated in a post-mortem study correlating thickness of subcutaneous fat with the incidence of fatty change in the liver.87 There is no evidence that these patients are more susceptible to drug-induced liver disease, but hepatic complications can follow certain types of surgery in the obese.88 Other obesity-related disorders include gallstones, hiatus hernia, and varicose veins. Females who are overweight at the commencement of pregnancy are more prone to develop toxaemia and hypertensions6 and fibroids of the uterus are more frequently found in overweight subjects.89 From the mechanical aspect, excessive body weight leads to a higher incidence of osteoarthritis, flat feet, and diaphragmatic hernia;” it also predisposes to accidents, fractures and prolapsed intervertebral discs.

Complications of obesity during anaesthesia and surgery

The prospect of anaesthesia in the obese is rarely awaited with eager anticipation by the anaesthetist, for although the mortality associated with surgery is quoted by various authorities as being up to 6%,91*92 these figures refer to elective surgery undertaken for gut by-pass procedure^.^^ Higher figures may be expected for other surgical procedures and there are reports of deaths occurring without adequate e ~ p l a n a t i o n .94 ~ ~The . associated diseases and changes in physiological functions

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require a careful pre-operative assessment with appropriate adjustment of premedication. Problems may present themselves prior to induction when transporting the patient the anaesthetic room and thence to a narrow operating table; the simultaneous use of two operating tables side-by side may be required.”

Induction of anaesthesia The intravenous induction of anaesthesia is technically difficult because of the lack of suitable veins in the limbs and there is a particular risk both of extravascular injection and inadvertent intra-arterial injection. An inhalational induction is no easier due to intermittent upper airway obstr~ction.’~ Too often it is an inelegant procedure punctuated by bucking, salivation, breath-holding and cyanosis. High pressures are often required to inflate the lungs, and when a face-mask is used this may render the cardio-oesophageal sphincter incompetent with consequent risk of the inhalation of gastric contents; the extra likelihood of the presence of a hiatus hernia in the obese is also relevant. Furthermore, laryngoscopy is technically difficult because of supra- and ante-sternal pads of fat and trauma to the mouth and oropharynx can easily occur. Fat people require larger amounts of drugs than is usual, but in fact require much less on a body weight basis. It is often difficult to predict how much is needed so the consequences should be considered ; for example, more suxamethonium may be required for tracheal intubation but less curare for maintenance.”

Maintenance of anaesthesia The uptake and recovery time for inhalation anaesthesia is altered in the obese. Because of the low FRC the mixing time within the lungs is short so permitting a potentially rapid increase in the alveolar tension of relatively insoluble gases such as nitrous oxide and cyclopropane. The uptake and storage of fat-soluble agents into large fat depots during prolonged surgery is significant and will retard recovery. Although the technical difficulties are familiar to the anaesthetist, the adverse physiological changes during the maintenance of anaesthesia in the obese are less well documented. The extent of changes in respiratory function in particular of the FRC and alveolar-arterial Po, gradient during halothane anaesthesia with spontaneous respiration in non-obese patients has produced conflicting results.98-’0’ There is little evidence of progressive atelectasis, and recent work suggests that a reduction in FRC and changes in cardiac output following the induction of anaesthesia are likely causes of decreased arterial oxygenation.lo2It has been predicted that FRC would be reduced following anaesthesia in obese patients” and this has been confirmed recently, the possible causes being a loss of lung elastic recoil with premature airway closure.103 During spontaneous breathing under halothane anaesthesia, non-obese patients with untreated or inadequately treated hypertension have been shown to be prone to hypotension associated with myocardial ischaemia.lo4 In normotensive younger patients this is less common but IPPV producing hypocapnia reduces the cardiac output thereby lowering arterial pressure. l o 5 It seems likely, therefore, that obese patients having compromised respiratory and cardiovascular functions before operation may well react erratically to anaesthesia, but this aspect has not been specifically investigated.

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Technical management Case reports of the anaesthetic management of severely obese patients (weighing 287 kg, 214 kg and 125 kg) have recently been described.28, 9 5 s ' 0 6 The recommended techniques include a trial of artificial ventilation before operation, performing tracheal intubation using local analgesia before unconsciousness is produced'" and not attempting to reverse the action of muscle relaxants at the conclusion of surgery, but to continue mechanical ventilation electively into the post-operative period. Substitution of the volatile anaesthetic agents, which would be expected to delay recovery, by droperidol and fentanyl has been suggested,95 but fentanyl is believed to decrease FRC and thus impair arterial oxygenation so should be avoided unless ventilation is controlled.'08 The prone and Trendelenburg positions should be avoided whenever p ~ s s i b l e . ~ Obstruction of the inferior vena cava may easily occur during surgical retraction."' Positive pressure ventilation of the lungs in severe obesity may further decrease pulmonary blood flow and increase pulmonary vascular resistance and so excessive inflating pressures should be avoided. However, correction of hypoxia and any hypercarbia by controlled ventilation would be expected to offset these effects. Spinal and epidural anaesthesia has been recommended in the obese,'", ''I and a patient weighing over 227 kg has been managed using a continuous spinal technique.' However, conduction analgesia is not recommended particularly for upper abdominal surgery : positioning, palpation of landmarks and needle location are difficult. Falls in cardiac output may occur while levels of anaesthesia conducive to good operating conditions further embarrass respiration and pulmonary gas exchange. ' I 3 Anaesthetic levels following epidural or spinal anaesthesia may be unpredictable for unknown reason^;^' it is possible that distended epidural veins or the presence of fat may reduce the volume of the epidural and subarachnoid spaces. A combined regionalinhalational anaesthetic approach in which the benefits of abdominal relaxation and analgesia normally offered by the regional technique with airway control by use of tracheal anaesthesia has been advocated."

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Fluid balance The presence of excess fat may reduce the body water from 65% to 40% of the body weight which will have a significant effect on the distribution of drugs. Fluid balance can also pose problems : although the total circulating volume is increased in the obese, it is less than normal on a weight basis as fat itself contains relatively little water, 6%lo"/,.' l4 Dehydration and hypovolaemia are difficult to detect clinically while rapid infusion can prove dangerous to an already compromised circulation. The technical difficulties of surgery both prolong the operation and enhance blood loss. Although it is stated that a common finding in obesity is an increased corticosteroid produccortisol levels may be reduced in the obese thereby impairing t i ~ n ,'15~ ~plasma ' the adrenocorticotrophic response to stress. ''

Monitoring Monitoring techniques include intra-arterial blood pressure measurement, respirometry and blood-gas analysis. The use of a thigh blood pressure cuff on the arm has

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also been found useful giving readings of about 20-30 mmHg higher than those recorded intra-arterially.28 Whatever type of anaesthesia is selected, it is important that adequate monitoring of as many parameters as the situation demands is available, and this should be continued into the post-operative period.lo6

Post-operative complications Morbidity and mortality

It is generally assumed that the dangers of obesity are prolonged into the post-operative period, but in terms of mortality the evidence is conflicting. Similar mortality rates have been shown in groups of obese and non-obese patients undergoing hysterectomy'17 and cholecystectomy.'" However, the New York Metropolitan Life Assurance company's statistics show a 2-3-fold increase in mortality figures for appendicitis and gallstones in the obese patients, and more recently the results of duodenal surgery in 2,819 patients have been analysed showing an increase in mortality from 2.7% in the non-obese to 6.6% in the obese patients."' The morbidity following surgery and anaesthesia will depend on the pre-operative condition of the patients, and the type, duration and site of operation. Pulmonary complications

Pulmonary complications are frequent'20-' 22 and respiratory function has been shown to deteriorate particularly after abdominal surgery'233124 with precipitous falls in lung ~ a p a c i t y . " ~Post-operative hypoxaemia has consistently been demonstrated126. 127 persisting up to the 15th day and enhanced by bowel distention, pneumoperitoneum, spasm of abdominal muscles and associated with a reduced FRC and alveolarcollapse.'28-130Although the post-operative work of breathingcomputed from pressure and flow measurements shows an increase in minute work,13' the effect of obesity on post-operative deterioration in pulmonary function has not been fully investigated. The degree of post-operative hypoxaemia has not been related to obesity, but lung function tests do not recover to their pre-operative value for at least 5 days following surgery thus increasing the likelihood of pulmonary complications.'lg' 1 2 5 Because of the low chest wall compliance and the surgical demands for access within the abdomen, large doses of muscle relaxants may be required; these in turn present problems in antagonism and the resulting residual paralysis and inefficient lung ventilation due to a painful wound often necessitate prolonged post-operative mechanical lung ventilation. Other complications

The potential dangers of obesity in the post-operative period are not confined to the respiratory system. Wound infection is more than twice as common"' possibly because of longer incisions, the protracted time of operation, the trauma due to excessive retraction, the difficulty in obliterating the tissue dead space and the inability of adipose tissue to resist infection. It has long been assumed'32. 1 3 3 that obesity is an important aetiological factor in the development of post-operative deep vein thrombosis, and a two-fold increase in the incidence of post-operative pulmonary

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embolism has been demonstrated in patients weighing 91 kg or more.132 Earlier reports associating the development of deep vein thrombosis following surgery with obesity were suspect in technique but more recently, ‘34 using radioactive fibrinogen, a positive association has been confirmed, the incidence being 22.9% in the non-obese and 47.9% in the obese. The duration of operation has also been shown to be significant,’ 3 5 the incidence of deep vein thrombosis being less following operations of under 1 hour’s duration. The mechanisms whereby obesity may lead to this increase in post-operative deep vein thrombosis are open to conjecture. Certainly obesity reduces mobility in the aged thereby increasing the risk of venous stasis. Platelet adhesiveness appears essentially normal but there is a decrease in fibrinolytic activity with increased fibrinogen in the obese136 and an increase in the time taken to complete surgery together with trauma to leg veins may well contribute. Conclusions

Obesity is rarely mentioned as a cause of death associated with anaesthesia; the word ‘obesity’ does not merit sufficient importance to qualify as a ‘key word’ in anaesthetic journals.103 Nevertheless, as Greenelo4has pointed out, it is often the key reason for an error of omission or commission which initiates a fatal series of events; the anaesthetic problems of obesity shorten the lives of many surgical patients and also the lives of some of their anaesthetists. References 1. OFFICEOF POPULATION CENSUSES AND SURVEYS (1973) The Registrar General’s Statistical Review of England and Wales for the year 1971. Part I . Tables, medical, p. 136. Her Majesty’s Stationery Office, London. 2. SOCIETY OF ACTUARIES (1959) Build and blood pressure study, Vol. I. Society of Actuaries, Chicago. 3. OFFICEOF HEALTH ECONOMICS (1969) Obesity and disease. Ofice of Health Economics, Current health problems, Paper No, 30. Her Majesty’s Stationery Office, London. 4. MITCHELL-HEGGS, F. (1974) Operating on fat patients. British Journal of Hospital Medicine, 11, 417. 5. ANDERSON, J. (1972) Obesity. British Medical Journal, 1, 560. 6. WIDDOWSON, E.M. (1965) Chemical analysis of the body. Symposia of the society for the study of human biology. Vol. VII. Human Body Composition: Approaches and Applications (Ed. by J. Brozek), p. 31. Pergamon Press, Oxford. 7. SLOAN,A.W. (1967) Estimation of body fat in young men. Journal of Applied Physiology, 23, 311. 8 . WHITTINGHAM, P. D.G.V. (1962) The measurement of tissue thickness by ultrasound. Aerospace Medicine, 33, 1121. 9. ALLEN, T.H., ANDERSON, E.C. & LANGHAM, W.H. (1960) Total body potassium and gross body composition in relation to age. Journal of Gerontology, 15, 348. 10. LESSER,G.T., DEUTSCH, S. & MARKOFSKY, J. (1971) Use of independent measurement of body fat to evaluate overweight and underweight. Metabolism, Clinical and Experimental, 20, 792. 11. SELTZER, C.C. (1966) Some re-evaluation of the Build and bloodpressure study, 1959, as related to ponderal index, somatotype and mortality. New England Journal of Medicine, 274, 254. 12. DURNIN, J.V.G.A. & RAHAMAN, M.M. (1967) The assessment of the amount of fat in the human body from measurement of skinfold thickness. British Journal of Nutrition, 21, 681. 13. MCCRACKEN, B.H. (1962) Etiological aspects of obesity. American Journal of the Medical Sciences, 243, 99. 14. MILLER,D.S., MUMFORD, P. & STOCK,M.J. (1967) Gluttony. 2. Thermogenesis in overeating man. American Journal of Clinical Nutrition, 20, 1223.

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15. NUEMAN, R.O. (1902) Experimentelle Beitrage zur Lehre von dem taglichen Nahrungsbedarf des Menschen unter besonderer Beriicksichtigung der notwendigen Eiweissmenge. Archiuf i r Hygjipne und Bakteriologie, 45, 1 . 16. HIRSCH,J. & KNITTLE, J.L. (1970) Cellularity of obese and non-obese human adipose tissue. Federation Proceedings, 29, 1516. 17. BROOK,C.G.D., LLOYD, J.K. &WOLF,O.H. (1972) Relation between age of onset of obesity and size and number of adipose cells. British Medical Journal, 2, 25. 18. SALANS, L.B., CUSHMAN, S.W. & WEISHMANN, R.E. (1973) Studies of human adipose tissue: adipose cell size and number in nonobese and obese patients. Journal of Clinical Investigation, 52,929. 19. WALKER, A.R.P. (1964) Overweight and hypertension in emerging populations. American Heart Journal, 68,581. 20. SILVER,S. & BAUER, J. (1931) Obesity, constitutional or endocrine? American Journal of the Medical Sciences, 181, 769. 21. BRAY,G.A. & YORK,D.A. (1971) Genetically transmitted obesity in rodents. Physiological Reviews, 51, 598. 22. SHIELDS, J. (1972) Monozygotic twins brought up apart and brought up together. Oxford University Press, London. 23. SILVERSTONE, J.T. & SOLOMON, T. (1965) Psychiatric and somatic factors in the treatment of obesity. Journal of Psychosomatic Research, 9, 249. 24. MCKENZIE, J.C. (1967) Social and economic implications of minority food habits. Proceedings of the Nutrition Society, 26, 197. 25. SCHWARTZ, H. (1955) Problems of obesity in anesthesia. New York State Journal of Medicine, 55, 3277, 26. SPENCE,A.W. (1950) Discussion on obesity. Proceedings of the Royal Society of Medicine, 43, 339. 27. GARROW,J.S. (1973) Metabolic aspects of obesity. British Journal of Hospital Medicine, 10, 24. 28. VAUGHAN, R.W. & ROA,N.L. (1973) A case of morbid obesity. Anesthesiology, 39,107. 29. BRITISHMEDICALJOURNAL (1 967) Leading article : hypotonia and obesity syndrome. British Medical Joicvnal, 3,694. 30. CULLEN, J.H. & FORMEL, P.F. (1962) The respiratory defects in extreme obesity. American Journal of Medicine, 32,525. 3 1 . KAUFMAN, B.J., FERGUSON, M.H. & CHERNIACK, R.M. (1959) Hypoventilation in obesity. Journal of Clinical Investigation, 38,500. R., SIPPLE,J.H. & AUCHINCLOSS, J.H. JR (1961) Respiratory control and work of 32. GILBERT, breathing in obese subjects. Journal of Applied Physiology, 16,21. 33. ROCHESTER, D.F. & ENSON,Y. (1974) Current concepts in the pathogenesis of the obesityhypoventilation syndrome. Mechanical and circulatory factors. American Journal of Medicine, 57, 402. 34. SHUSTER, E. (1912) First results of the Oxford Anthropometric Laboratory. Biometrika, 8,40. 35. ALEXANDER, J.K., GUTHRIE, A.E., SAKAGUCHI, H., CRAWFORD, H.W. & COLE,V.W. (1959) Lung volume changes with extreme obesity. Clinical Research, 7 , 171. 36. SIEKER,H.O., ESTES,E.H. JR, KELSER,G.A. & MCINTOSH, H.D. (1955) A cardiopulmonary syndrome associated with extreme obesity. Journal of Clinical Investigation, 34,916. 37. FAREBROTHER, M.J.B., MCHARDY, G.J.R. & MUNRO, J.F. (1974) Relation between pulmonary gas exchange and closing volume before and after substantial weight loss in obese subjects. British Medical Journal, 3, 391. 38. DOUGLAS, F.G. & CHONG, P.Y. (1972) Influence of obesity on peripheral airways patency. Journal of Applied Physiology, 33,559. 39. MILLER,W.F. & BASHOUR, F.A. (1963) Cardiopulmonary changes in obesity. In: Anesthesia for patients with endocrine disease (Ed. by M. T. Jenkins), p. 128. Clinical Anesthesia Series 196313. Blackwell Scientific Publications, Oxford. 40. SMITH,J.R. (1958) Pulmonary physiology in the obese. Surgical Forum, 9,386. 41. BARRERA, F., REIDENBERG, M.M., WINTERS,W.L. & HUNGSPREUGS, S. (1969) Ventilationperfusion relationships in the obese patient. Journal of Applied Physiology, 26,420. 42. SAID,S.T. (1960) Abnormalities of pulmonary gas exchange in obesity. Annals of Internal Medicine, 53, 1121.

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