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- W2090836174 abstract "The prevalence of diabetes is increasing.1Will new diagnostic criteria for diabetes mellitus change phenotype of patients with diabetes? Reanalysis of European epidemiological data. DECODE Study Group on behalf of the European Diabetes Epidemiology Study Group.Br Med J. 1998; 317: 371-375Crossref PubMed Scopus (408) Google Scholar Over 150 million people world-wide have diabetes mellitus and this is expected to increase to 220 million by the year 2010.2Zimmet P Alberti KG Shaw J Global and societal implications of the diabetes epidemic.Nature. 2001; 414: 782-787Crossref PubMed Scopus (4547) Google Scholar An additional 200 million have impaired glucose tolerance, and 40% of these individuals will progress to diabetes over 5–10 yr. The figures are based on the latest definitions of diabetes and glucose intolerance by the World Health Organization (WHO) and the American Diabetes Association (ADA). The diagnosis of diabetes now depends on either a fasting plasma glucose ≥7 mmol litre–1, or the symptoms of diabetes plus a casual plasma glucose ≥11.1 mmol litre–1. In addition, the WHO definition of diabetes includes people with a 2 h plasma glucose ≥11.1 mmol litre–1 during a standard 75 g oral glucose tolerance test. Impaired fasting glucose is defined as a fasting plasma glucose ≥6.1 mmol litre–1, and an impaired glucose tolerance as a plasma glucose of 7.8–11 mmol litre–1, 2 h after an oral glucose load. The fasting plasma glucose limits for the diagnosis of diabetes mellitus have been lowered in recognition of the development of complications of diabetes at lower plasma glucose concentrations. The plasma glucose threshold for developing diabetic retinopathy is estimated to be as low as 7 mmol litre–1. The risk of diabetes developing in later life is increased by a fasting plasma glucose greater than 6.1 mmol litre–1, and in the Paris prospective study of middle aged men made over 20 yr, coronary heart disease was more common in individuals with a fasting plasma glucose greater than 5.8 mmol litre–1.3Balkau B Bertrais S Ducimetiere P Eschwege E Is there a glycemic threshold for mortality risk?.Diabetes Care. 1999; 22: 696-699Crossref PubMed Scopus (148) Google Scholar The increased prevalence of diabetes is caused by an increase in Type II diabetes, compounded by the increased prevalence of obesity and sedentary habit. Type II diabetes affects all age groups, including children, and may be greatly underestimated in clinical practice. In one recent study, 2030 consecutive admissions to a general hospital in the USA were observed for hyperglycaemia using the WHO criteria of two or more fasting plasma glucose concentrations greater than 7 mmol litre–1, or random plasma glucose concentrations greater than 11.1 mmol litre–1. Thirty-eight per cent of patients had hyperglycaemia. One-third of these patients were not known to be diabetic, and patients with newly diagnosed hyperglycaemia had a higher in-hospital mortality rate (16%) than patients with either known diabetes (3%) or normoglycaemia (1.7%).4Umpierrez GE Isaacs SD Bazargan N You X Thaler LM Kitabchi AE Hyperglycemia: an independent marker of in-hospital mortality in patients with undiagnosed diabetes.J Clin Endocrinol Metab. 2002; 87: 978-982Crossref PubMed Scopus (1579) Google Scholar It is generally accepted that diabetes is associated with an increased risk of morbidity and mortality in the perioperative period. Some of this increase may be related to the organ complications of diabetes mellitus, particularly in terms of myocardial risk,5Fuller JH Stevens LK Wang SL Risk factors for cardiovascular mortality and morbidity: the WHO Multinational Study of Vascular Disease in Diabetes.Diabetologia. 2001; 44: S54-S64Crossref PubMed Google Scholar but many perioperative complications are attributable to infectious complications. Wound infections and nosocomial chest infections are more common in diabetes,6Golden SH Peart-Vigilance C Kao WH Brancati FL Perioperative glycemic control and the risk of infectious complications in a cohort of adults with diabetes.Diabetes Care. 1999; 22: 1408-1414Crossref PubMed Scopus (466) Google Scholar 7Pomposelli JJ Baxter 3rd, JK Babineau TJ et al.Early postoperative glucose control predicts nosocomial infection rate in diabetic patients.J Parenter Enteral Nutr. 1998; 22: 77-81Crossref PubMed Scopus (556) Google Scholar and diabetics are at greater risk of infection and rejection after renal transplantation.8Thomas MC Mathew TH Russ GR Rao MM Moran J Early peri-operative glycaemic control and allograft rejection in patients with diabetes mellitus: a pilot study.Transplantation. 2001; 72: 1321-1324Crossref PubMed Scopus (85) Google Scholar Hyperglycaemia has similarly been found to affect outcome from medical disorders. It is an independent risk factor in the development of renal failure in type II diabetes mellitus,9Colhoun HM Lee ET Bennett PH et al.Risk factors for renal failure: the WHO Multinational Study of Vascular Disease in Diabetes.Diabetologia. 2001; 44: S46-S53Crossref PubMed Google Scholar and in the Diabetes Insulin-Glucose in Acute Myocardial Infarction (DIGAMI) study, patients with a blood glucose ≥6.1 mmol litre–1 on admission had a worse outcome after myocardial infarction. This effect persisted over 3.4 yr of follow-up.10Malmberg K Prospective randomised study of intensive insulin treatment on long term survival after acute myocardial infarction in patients with diabetes mellitus.Br Med J. 1997; 314: 1512-1515Crossref PubMed Scopus (1205) Google Scholar In the Whitehall, Paris, and Helsinki trials, involving follow-up for over 20 yr, longevity was related to a 2 h blood glucose concentration within 80% of the normal distribution.11Balkau B Shipley M Jarrett RJ et al.High blood glucose concentration is a risk factor for mortality in middle-aged nondiabetic men. 20-year follow-up in the Whitehall Study, the Paris Prospective Study, and the Helsinki Policemen Study.Diabetes Care. 1998; 21: 360-367Crossref PubMed Scopus (597) Google Scholar One largely ignored area is the impact of hyperglycaemia on lung function. In 1989, Lange and colleagues12Lange P Groth S Kastrup J et al.Diabetes mellitus, plasma glucose and lung function in a cross-sectional population study.Eur Respir J. 1989; 2: 14-19PubMed Google Scholar measured lung function in 11 763 people, of whom 2.5% had diabetes mellitus and a further 7.1% were glucose intolerant. Plasma glucose was negatively associated with vital capacity and forced expiratory volume in 1 s (FEV1.0). More recent studies have shown that diabetics have an impaired ventilatory response to hypoxia. Patients with diabetes have an increased perception of dyspnoea when hypoxic and make an increased respiratory effort, but changes in tidal volume are decreased, compared with controls.13Scano G Filippelli M Romagnoli I et al.Hypoxic and hypercapnic breathlessness in patients with type I diabetes mellitus.Chest. 2000; 117: 960-967Abstract Full Text Full Text PDF PubMed Scopus (27) Google Scholar Abnormal peripheral airway function is thought to be responsible for the altered response to hypoxia. Population studies have confirmed a decline in pulmonary function associated with diabetes, but as yet have failed to associate the decline directly with hyperglycaemia.14Davis TM Knuiman M Kendall P Vu H Davis WA Reduced pulmonary function and its associations in type 2 diabetes: the Fremantle Diabetes Study.Diabetes Res Clin Pract. 2000; 50: 153-159Abstract Full Text Full Text PDF PubMed Scopus (103) Google Scholar However, in a study of 150 patients with cystic fibrosis, deterioration in lung function has not only been observed to coincide with the onset of glucose intolerance, but the rate of decline was strongly associated with the severity of glucose intolerance over a 4-yr period.15Milla CE Warwick WJ Moran A Trends in pulmonary function in patients with cystic fibrosis correlate with the degree of glucose intolerance at baseline.Am J Respir Crit Care Med. 2000; 162: 891-895Crossref PubMed Scopus (288) Google Scholar For patients with chronic obstructive airways disease (COPD), an association between impairment of ventilatory function, coronary heart disease, and insulin resistance has been observed,16Lazarus R Sparrow D Weiss ST Baseline ventilatory function predicts the development of higher levels of fasting insulin and fasting insulin resistance index: the Normative Aging Study.Eur Respir J. 1998; 12: 641-645Crossref PubMed Scopus (107) Google Scholar and in a Danish study, patients with impaired glucose tolerance were found to be more likely to develop chronic obstructive airways disease.17Engstrom G Janzon L Risk of developing diabetes is inversely related to lung function: a population-based cohort study.Diabetes Med. 2002; 19: 167-170Crossref PubMed Scopus (96) Google Scholar The duration of type II diabetes mellitus has been associated with significant reductions in FEV1.0 and peak expiratory flow rate (PEFR).14Davis TM Knuiman M Kendall P Vu H Davis WA Reduced pulmonary function and its associations in type 2 diabetes: the Fremantle Diabetes Study.Diabetes Res Clin Pract. 2000; 50: 153-159Abstract Full Text Full Text PDF PubMed Scopus (103) Google Scholar The reductions in PEFR have been found to be independently predictive of vascular complications of the lower limbs and even survival in patients with diabetes.18Klein BE Moss SE Klein R Cruickshanks KJ Is peak expiratory flow rate a predictor of complications in diabetes? The Wisconsin Epidemiologic Study of Diabetic Retinopathy.J Diabetes Complications. 2001; 15: 301-306Crossref PubMed Scopus (6) Google Scholar Recently, an association between disordered sleep and glucose intolerance has been observed.19Elmasry A Lindberg E Berne C et al.Sleep-disordered breathing and glucose metabolism in hypertensive men: a population-based study.J Intern Med. 2001; 249: 153-161Crossref PubMed Scopus (212) Google Scholar Diabetics have a significantly greater apnoea– hypopnoea index than non-diabetics matched for body mass index, smoking history, and age.19Elmasry A Lindberg E Berne C et al.Sleep-disordered breathing and glucose metabolism in hypertensive men: a population-based study.J Intern Med. 2001; 249: 153-161Crossref PubMed Scopus (212) Google Scholar Diabetes is an independent risk factor for death from pulmonary tuberculosis,20Oursler KK Moore RD Bishai WR Harrington SM Pope DS Chaisson RE Survival of patients with pulmonary tuberculosis: clinical and molecular epidemiologic factors.Clin Infect Dis. 2002; 34: 752-759Crossref PubMed Scopus (109) Google Scholar and is associated with an increased risk of pulmonary infection by Staphylococcus aureus and Gram-negative organisms. Pulmonary infections by other organisms, for example influenza virus and streptococcus, are associated with increased morbidity and mortality in diabetic patients.21Joshi N Caputo GM Weitekamp MR Karchmer AW Infections in patients with diabetes mellitus.N Engl J Med. 1999; 341: 1906-1912Crossref PubMed Scopus (771) Google Scholar In mice, hyperglycaemia is associated with greatly increased rates of influenza virus replication when compared with non-diabetic mice or normoglycaemic diabetic mice.22Reading PC Allison J Crouch EC Anders EM Increased susceptibility of diabetic mice to influenza virus infection: compromise of collectin-mediated host defense of the lung by glucose?.J Virol. 1998; 72: 6884-6887Crossref PubMed Google Scholar In a recent study, diabetes was found to be an independent disease modifier for pneumonia in young patients, and in older patients was associated with an increase in the severity of COPD.23Zanobetti A Schwartz J Are diabetics more susceptible to the health effects of airborne particles?.Am J Respir Crit Care Med. 2001; 164: 831-833Crossref PubMed Scopus (148) Google Scholar Finally, in a meta-analysis, diabetes was found to be associated with poor outcome from community acquired pneumonia.24Fine MJ Smith MA Carson CA et al.Prognosis and outcomes of patients with community-acquired pneumonia. A meta-analysis.JAMA. 1996; 275: 134-141Crossref PubMed Google Scholar It is postulated that hyperglycaemia affects the lungs by damaging capillaries and by the non-enzymatic glycosylation of collagen.25Bell D Collier A Matthews DM Cooksey EJ McHardy GJ Clarke BF Are reduced lung volumes in IDDM due to defect in connective tissue?.Diabetes. 1988; 37: 829-831Crossref PubMed Scopus (56) Google Scholar In a study of diabetes induced in hamsters, hyperglycaemia to concentrations of 23–25 mmol litre–1 was observed to cause direct lung damage. The capillary endothelium became full of plasmalemmal vesicles, alveoli collapsed, and the lung interstitium enlarged. These changes were observed after only 6 weeks of hyperglycaemia.26Popov D Simionescu M Alterations of lung structure in experimental diabetes, and diabetes associated with hyperlipidaemia in hamsters.Eur Respir J. 1997; 10: 1850-1858Crossref PubMed Scopus (77) Google Scholar Hyperglycaemia appears to cause cellular stress by a number of mechanisms, which could be detrimental to the lung.27Brownlee M Biochemistry and molecular cell biology of diabetic complications.Nature. 2001; 414: 813-820Crossref PubMed Scopus (7030) Google Scholar First, during hyperglycaemia the movement of glucose through the polyol pathway is increased. Normally, very little glucose is metabolized by aldose reductase, but when the polyol pathway is active, sorbitol is produced. Increased sorbitol concentrations may cause osmotic stress to cells and dihydronicotinamide adenine dinucleotide phosphate (NADPH) is consumed, depleting intracellular glutathione. Secondly, hyperglycaemia increases concentrations of advanced glycation end products. These glycosylated proteins are formed by non-enzymatic reactions, and changes in protein structure may alter their cellular functions. Thirdly, glucose activates various isomers of protein kinase C. This in turn affects the expression of nitric oxide, endothelin, nuclear factor kappa B (NF-κB), and plasminogen activator inhibitor, amongst others. Finally, hyperglycaemia increases the flux of glucose through the hexosamine pathway, again affecting inflammatory mediators and insulin resistance. The combined effect of the four mechanisms is a large over-production of mitochondrial superoxides, causing cellular stress and damage.27Brownlee M Biochemistry and molecular cell biology of diabetic complications.Nature. 2001; 414: 813-820Crossref PubMed Scopus (7030) Google Scholar Some of these mechanisms may also explain how hyperglycaemia affects immunity and could increase susceptibility to pulmonary infection. Non-enzymatic glycosylation of immunoglobulins, sufficient to cause impairment of function after only a few hours of hyperglycaemia, has been described in animal models.28Hennessey PJ Black CT Andrassy RJ Nonenzymatic glycosylation of immunoglobulin G impairs complement fixation.J Parenter Enteral Nutr. 1991; 15: 60-64Crossref PubMed Scopus (76) Google Scholar Neutrophil phagocytic activity and chemokinesis are also impaired by hyperglycaemia, an effect attributed to excess consumption of NADPH,29Mazade MA Edwards MS Impairment of type III group B Streptococcus-stimulated superoxide production and opsonophagocytosis by neutrophils in diabetes.Mol Genet Metab. 2001; 73: 259-267Crossref PubMed Scopus (43) Google Scholar and activated protein kinase C.30Oldenborg PA Sehlin J Hyperglycemia in vitro attenuates insulin-stimulated chemokinesis in normal human neutrophils. Role of protein kinase C activation.J Leukoc Biol. 1999; 65: 635-640PubMed Google Scholar Notably, the impairment of function has been shown to be reversible by rigorous control of glucose.31Ihm SH Yoo HJ Park SW Park CJ Effect of tolrestat, an aldose reductase inhibitor, on neutrophil respiratory burst activity in diabetic patients.Metabolism. 1997; 46: 634-638Abstract Full Text PDF PubMed Scopus (15) Google Scholar Hyperglycaemia also reversibly impairs mitogen stimulated proliferation of lymphocytes.32Alexiewicz JM Kumar D Smogorzewski M Massry SG Elevated cytosolic calcium and impaired proliferation of B lymphocytes in type II diabetes mellitus.Am J Kidney Dis. 1997; 30: 98-104Abstract Full Text PDF PubMed Scopus (27) Google Scholar So what are the implications of the effects of hyperglycaemia on the lung for anaesthesia? Should all diabetics have preoperative lung function tests? Probably not, but there should be an increased awareness of the risks of respiratory compromise when assessing diabetic patients, particularly if other risk factors for respiratory failure are present. An area of concern is the postoperative period. Little is known about the incidence of postoperative hypoxia in patients with diabetes and, given the available evidence, it would seem likely that diabetics have an increased likelihood of obstructive sleep apnoea. Add this to the known risks of postoperative obstructed sleep patterns caused by opiate analgesia,33Rahman MQ Kingshott RN Wraith P Adams WH Drummond GB Association of airway obstruction, sleep, and phasic abdominal muscle activity after upper abdominal surgery.Br J Anaesth. 2001; 87: 198-203Abstract Full Text Full Text PDF PubMed Scopus (14) Google Scholar and a reversible cause of perioperative morbidity and mortality may have been overlooked in these patients. This is an area that warrants investigation. In terms of optimizing the perioperative control of blood glucose, the study by van den Berghe and colleagues34van den Berghe G Wouters P Weekers F et al.Intensive insulin therapy in the surgical intensive care unit.N Engl J Med. 2001; 345: 1359-1367Crossref PubMed Scopus (8161) Google Scholar must be considered. Over 1500 patients (70% cardiothoracic) admitted to a surgical intensive care unit were randomized to receive either standard control of blood glucose (aiming for a blood glucose <11.1 mmol litre–1), or intensive insulin therapy to achieve a blood glucose between 4.4 and 6.1 mmol litre–1. Maintaining normoglycaemia was associated with a 40% reduction in mortality, a staggering result made all the more impressive as the study included non-diabetic as well as diabetic patients. Before this study, surveys of anaesthetists showed that many were content with maintaining a perioperative blood glucose between 7 and 10 mmol litre–1, a compromise between the risks of hyperglycaemia and the dangers of undetected hypoglycaemia.35Eldridge AJ Sear JW Peri-operative management of diabetic patients. Any changes for the better since 1985?.Anaesthesia. 1996; 51: 45-51Crossref PubMed Scopus (28) Google Scholar However, the reduction in mortality in the study by van den Berghe and colleagues,34van den Berghe G Wouters P Weekers F et al.Intensive insulin therapy in the surgical intensive care unit.N Engl J Med. 2001; 345: 1359-1367Crossref PubMed Scopus (8161) Google Scholar was almost entirely through a decrease in serious infections. Stricter control of the blood glucose concentration may therefore be very important in the perioperative period. The risks of unobserved hypoglycaemia under anaesthesia may be increased but can be minimized by close monitoring. The required technology is readily available in every UK hospital for hourly blood sugar measurements to be done with minimal effort. Indeed, it is possible that this should be done for all patients, not only known diabetics. The wider implications of glycaemic control will depend on how many patients have temporary stress-induced hyperglycaemia, and whether it can be shown directly that hyperglycaemia is contributing to the risks of infectious complications of surgery." @default.
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- W2090836174 title "Editorial III" @default.
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- W2090836174 cites W1993692590 @default.
- W2090836174 cites W2016037514 @default.
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- W2090836174 cites W2024976786 @default.
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- W2090836174 cites W2046589550 @default.
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- W2090836174 cites W2088624742 @default.
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