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Anaesthesia in the obese patient
ENDOCRINOLOGY
Anaesthesia in the obese patient
Learning objectives After reading this article you should be able to: C list five risk factors in predicting a difficult airway in obese patients C describe eight specific physiological consequences of prolonged obesity C calculate lean body weight and understand the rational for drug dosing in obese patients
Claire E Moore Mark Forrest
Abstract The aim of this article is to give a brief but comprehensive overview of the current management of the patient undergoing obesity surgery. This article will present important aspects related to pathophysiology and pharmacology.
(OSA) and a high Mallampati score are all considered major airway risk factors.
Keywords Anaesthesia; obesity; pathophysiology; pharmacology Respiratory system Obese individuals have a greater energy expenditure daily than the general population due, in part, to the work needed to support and move their increased body mass. Large fat stores also constitute a large metabolically active organ. Oxygen consumption and carbon dioxide production are both increased. Adipose tissue around the chest and abdomen increases the work of breathing and reduces the compliance of the chest wall. Furthermore this tissue mass acts mechanically to reduce functional residual capacity (FRC), expiratory reserve volume (ERV) and total lung capacity (TLC). About 40e70% of morbidly obese patients will have some degree of OSA and increasing BMI makes OSA more likely. The increased incidence of conditions such as OSA and OHS, along with reduced lung capacities, all contribute to abnormalities in gas exchange that are often apparent in the awake morbidly obese subject. These abnormalities may manifest themselves as dyspnoea, hypoxia and hypercarbia and all may become significantly worse in the supine position with further exacerbation following induction of anaesthesia.
Introduction A body mass index (BMI) of over 30 kg/m2 defines obesity, whilst a BMI of over 35 kg/m2 and over 55 kg/m2 describes those that are ‘morbidly obese’ and ‘super morbidly obese’ respectively. The incidence of obesity in adults in the UK is greater than 25%. In addition the incidence in childhood is also around 20%. There is clear evidence that an increased BMI can significantly reduce life expectancy, more so in men than women. With the continuing increase in the frequency of obesity, and earlier onset, all anaesthetists will find themselves encountering more obese patients more frequently. It is important to realize that complications of obesity increase with both degree and duration. Pathophysiological findings and co-morbidities associated with morbid obesity are outlined in Table 1.
Cardiovascular system Total circulating blood volume is increased to serve the extra adipose tissue although the total volume in ml/kg is reduced from the normal of around 75 ml/kg to 50 ml/kg. Cardiac output is increased, mainly through an increase in stroke volume. The left ventricle is subject to both pressure and volume overload, consequently it becomes dilated and hypertrophied. Left ventricular (LV) muscle mass increases and the left atrium also dilates. It was thought that systolic left ventricular function was maintained, but more recent studies have shown this to be incorrect. Left ventricular contraction has a radial component (Figure 1) that is preserved until later in the disease progression, and a longitudinal component that has been shown to be reduced significantly in the morbidly obese. Longitudinal function decreases with both increasing BMI and duration of obesity and has been seen in childhood obesity. Diastolic function is also affected. Relaxation of the left ventricle, an active process, is impaired. As a consequence left atrial volume and eventually pressure will increase and there will be left atrial dilatation. All this means that the super-obese have less reserve to increase stroke volume or ejection fraction. They also have increased systemic vascular resistance and often suffer from
Pathophysiology Airway Difficulties with the obese airway are well recognized and occur through fat deposition around the face, soft tissues of the palate and pharynx, with secondary anterior displacement of the larynx and enlargement of the tongue. The reported incidence of difficult intubation has been revised down however as more surgery in obese patients has been performed. It is estimated that around 1% of the morbidly obese population may be difficult to intubate, with around 10% being difficult to manually ventilate. Male sex, large neck circumference, presence of obesity hypoventilation syndrome (OHS)/obstructive sleep apnoea
Claire E Moore MBChB FRCA is a Specialist Registrar in Anaesthesia in the North Western Deanery, UK. Conflicts of interest: none declared. Mark Forrest MBChB, FRCA is a Consultant in Anaesthesia at Central Manchester Foundation Trust, UK. Conflicts of interest: none declared.
ANAESTHESIA AND INTENSIVE CARE MEDICINE 12:7
277
Ó 2011 Elsevier Ltd. All rights reserved.
ENDOCRINOLOGY
hypertension. Diabetes and ischaemic heart disease which are common will tend to exacerbate these problems. The respiratory effects of obesity can lead to increased pulmonary vascular resistance and right heart failure. In reality, whilst it can be seen in those with severe OHS, it is quite rare.
Conditions associated with, and pathophysiology of, obesity Airway
Respiratory system
Cardiovascular
Others
Increased adipose tissue pharyngeal wall. Increased incidence of difficulty in bag valve mask ventilation Lung compliance decreased due to increased pulmonary blood flow Decreased chest wall compliance due to adipose tissue Decreased FRC (around 1 litre when BMI>40), closing volume can reach FRC during normal respiration, thus V/Q mismatch, leading to possible hypoxia at rest, worse when supine OSA OHS Increased blood volume and CO Obesity cardiomyopathy Hypertension Increased O2 consumption and CO2 production Ischaemic heart disease Pulmonary hypertension (secondary to OSA/OHS) Thromboembolic disease Increased risk of gastric aspiration secondary to reflux hiatus hernia Altered drug kinetics Diabetes Fatty liver disease Dyslipidaemia Metabolic syndrome Osteoarthritis
Miscellaneous Development of type 2 diabetes is common in obesity through tissue resistance to insulin and accumulation of fat around the islet cells of the pancreas. This insulin resistance as well as leading to dysregulation of glucose metabolism will also cause problems in regulating fat metabolism. Excessive delivery of fat to the liver results in hepatic steatosis, which in turn can precipitate an inflammatory response known as nonalcoholic steatohepatitis. Although reversible through weight loss in its early stages it will progress to cirrhosis in up to 25% of patients. The combination of hypertension, dyslipidaemia, insulin resistance and central obesity is termed metabolic syndrome and these patients appear to be at increased risk of morbidity and mortality through accelerated atherosclerosis. Gastro-oesophageal reflux disease and a higher incidence of hiatus hernia in the obese all increase the risk of aspiration during induction of anaesthesia. Importantly those patients who have had previous bariatric procedures and subsequent weight loss have been found to be at increased risk of aspiration when they present for further surgery.
Pharmacology for obese patients Several factors are important in determining how pharmacodynamics and pharmacokinetics are affected by morbid obesity. They include increased cardiac output, increase in lean body weight (LBW), increased fat mass and increased extracellular fluid volume. These factors affect drug distribution and elimination. There are several possible dosing scalars available based around total body weight (TBW), LBW, or ideal body weight (IBW).
BMI, body mass index; FRC, functional residual capacity; OHS, obesity hypoventilation syndrome; OSA, obstructive sleep apnoea.
Table 1
Figure 1 The image on the left shows a cross-section of the ventricle and contraction in this plane (radial) is often preserved. The image on the right shows a longitudinal section. Here contraction is reduced earlier in the disease process. This image also shows left atrial and right ventricular enlargement characteristic of obesity induced cardiac changes.
ANAESTHESIA AND INTENSIVE CARE MEDICINE 12:7
278
Ó 2011 Elsevier Ltd. All rights reserved.
ENDOCRINOLOGY
IBW ¼ height (cm) x where x ¼ 100 for men and 105 for women Male LBW ¼ 1.1(weight) 128(weight/height)2 Female LBW ¼ 1.07(weight) 148(weight/height)2 Recent evidence suggests that dosing scalars based on cardiac output and lean body weight are less likely to be associated with undesirable side effects.
Inhalational agents There is no evidence that uptake of inhalational anaesthetic agents is affected by obesity. There is, however, evidence that offset of anaesthesia is more rapid in this population with desflurane than with other agents. It has been demonstrated that airway reflexes return earlier and oxygen saturations in recovery are higher in patients following desflurane rather than isoflurane or sevoflurane based anaesthesia. This article has provided an overview of the pathophysiology and pharmacology associated with morbid obesity. A subsequent article will look at the anaesthetic management of patients presenting for weight loss surgery. A
Intravenous agents Dosing propofol and thiopentone according to TBW is likely to lead to marked hypotension. As a result of the increased cardiac output associated with morbid obesity peak arterial concentrations of intravenous agents are lower than in lean patients for a given dose. This suggests that propofol and thiopentone should be dosed according to LBW as it is closely related to cardiac output. It should be noted that emergence from a single dose will be more rapid in this population. Evidence regarding propofol and thiopentone infusions is scanty, but does suggest that at steady state there is a much greater volume of distribution and therefore offset time.
FURTHER READING Adams JP, Murphy PG. Obesity in anaesthesia and intensive care. Br J Anaesth 2000; 85: 91e108. Gallagher MJ, Frankin BA, Ehrman JK, et al. Comparative impact of morbid obesity vs heart failure on Cardio respiratory fitness. Chest 2005; 127: 2197e203. Lemmens HJM. Perioperative pharmacology in morbid obesity. Curr Opin Anaesthesiol 2010; 23: 485e91. Mackay RE, Malhotra A, Cakmakkaya OS, et al. Effect of increased body mass index and anaesthetic duration on recovery of protective airway reflexes after sevoflurane vs desflurane. Br J Anaesth 2010; 104: 175e82. McCullough PA, Gallagher MJ, DeJong AT, et al. Cardio respiratory fitness and short-term complications after bariatric surgery. Chest 2006; 130: 517e25. Mullen JT, Moorman DW, Davenport JL. The obesity paradox: body mass index and outcomes in patients undergoing nonbariatric general surgery. Ann Surg 2009 Jul; 250: 166e72. Poirier P, Alpert M, Fleisher L, et al. Cardiovascular evaluation and management of severely obese patients undergoing surgery (A science advisory from the AHA). Circulation 2009; 120: 86e95.
Opioids As for induction agents, peak concentrations of opioids appear to relate to cardiac output and as such, most intravenous opioids should be dosed according to LBW. The morbidly obese are, however, sensitive to the respiratory effects of opioids so they should always be used with caution. Muscle relaxants All muscle relaxants are polar molecules and as such lipid insoluble. Peak concentrations will be related to extracellular fluid volumes which may be increased in the morbidly obese. Most evidence suggests that muscle relaxants should be dosed according to IBW. Dosing based on TBW is likely to lead to profound block with prolonged duration of action. The exception is suxamethonium, a depolarizing agent, which should be dosed according to TBW in order to achieve satisfactory intubating conditions.
ANAESTHESIA AND INTENSIVE CARE MEDICINE 12:7
279
Ó 2011 Elsevier Ltd. All rights reserved.
Anaesthesia in the obese patient
Learning objectives After reading this article you should be able to: C list five risk factors in predicting a difficult airway in obese patients C describe eight specific physiological consequences of prolonged obesity C calculate lean body weight and understand the rational for drug dosing in obese patients
Claire E Moore Mark Forrest
Abstract The aim of this article is to give a brief but comprehensive overview of the current management of the patient undergoing obesity surgery. This article will present important aspects related to pathophysiology and pharmacology.
(OSA) and a high Mallampati score are all considered major airway risk factors.
Keywords Anaesthesia; obesity; pathophysiology; pharmacology Respiratory system Obese individuals have a greater energy expenditure daily than the general population due, in part, to the work needed to support and move their increased body mass. Large fat stores also constitute a large metabolically active organ. Oxygen consumption and carbon dioxide production are both increased. Adipose tissue around the chest and abdomen increases the work of breathing and reduces the compliance of the chest wall. Furthermore this tissue mass acts mechanically to reduce functional residual capacity (FRC), expiratory reserve volume (ERV) and total lung capacity (TLC). About 40e70% of morbidly obese patients will have some degree of OSA and increasing BMI makes OSA more likely. The increased incidence of conditions such as OSA and OHS, along with reduced lung capacities, all contribute to abnormalities in gas exchange that are often apparent in the awake morbidly obese subject. These abnormalities may manifest themselves as dyspnoea, hypoxia and hypercarbia and all may become significantly worse in the supine position with further exacerbation following induction of anaesthesia.
Introduction A body mass index (BMI) of over 30 kg/m2 defines obesity, whilst a BMI of over 35 kg/m2 and over 55 kg/m2 describes those that are ‘morbidly obese’ and ‘super morbidly obese’ respectively. The incidence of obesity in adults in the UK is greater than 25%. In addition the incidence in childhood is also around 20%. There is clear evidence that an increased BMI can significantly reduce life expectancy, more so in men than women. With the continuing increase in the frequency of obesity, and earlier onset, all anaesthetists will find themselves encountering more obese patients more frequently. It is important to realize that complications of obesity increase with both degree and duration. Pathophysiological findings and co-morbidities associated with morbid obesity are outlined in Table 1.
Cardiovascular system Total circulating blood volume is increased to serve the extra adipose tissue although the total volume in ml/kg is reduced from the normal of around 75 ml/kg to 50 ml/kg. Cardiac output is increased, mainly through an increase in stroke volume. The left ventricle is subject to both pressure and volume overload, consequently it becomes dilated and hypertrophied. Left ventricular (LV) muscle mass increases and the left atrium also dilates. It was thought that systolic left ventricular function was maintained, but more recent studies have shown this to be incorrect. Left ventricular contraction has a radial component (Figure 1) that is preserved until later in the disease progression, and a longitudinal component that has been shown to be reduced significantly in the morbidly obese. Longitudinal function decreases with both increasing BMI and duration of obesity and has been seen in childhood obesity. Diastolic function is also affected. Relaxation of the left ventricle, an active process, is impaired. As a consequence left atrial volume and eventually pressure will increase and there will be left atrial dilatation. All this means that the super-obese have less reserve to increase stroke volume or ejection fraction. They also have increased systemic vascular resistance and often suffer from
Pathophysiology Airway Difficulties with the obese airway are well recognized and occur through fat deposition around the face, soft tissues of the palate and pharynx, with secondary anterior displacement of the larynx and enlargement of the tongue. The reported incidence of difficult intubation has been revised down however as more surgery in obese patients has been performed. It is estimated that around 1% of the morbidly obese population may be difficult to intubate, with around 10% being difficult to manually ventilate. Male sex, large neck circumference, presence of obesity hypoventilation syndrome (OHS)/obstructive sleep apnoea
Claire E Moore MBChB FRCA is a Specialist Registrar in Anaesthesia in the North Western Deanery, UK. Conflicts of interest: none declared. Mark Forrest MBChB, FRCA is a Consultant in Anaesthesia at Central Manchester Foundation Trust, UK. Conflicts of interest: none declared.
ANAESTHESIA AND INTENSIVE CARE MEDICINE 12:7
277
Ó 2011 Elsevier Ltd. All rights reserved.
ENDOCRINOLOGY
hypertension. Diabetes and ischaemic heart disease which are common will tend to exacerbate these problems. The respiratory effects of obesity can lead to increased pulmonary vascular resistance and right heart failure. In reality, whilst it can be seen in those with severe OHS, it is quite rare.
Conditions associated with, and pathophysiology of, obesity Airway
Respiratory system
Cardiovascular
Others
Increased adipose tissue pharyngeal wall. Increased incidence of difficulty in bag valve mask ventilation Lung compliance decreased due to increased pulmonary blood flow Decreased chest wall compliance due to adipose tissue Decreased FRC (around 1 litre when BMI>40), closing volume can reach FRC during normal respiration, thus V/Q mismatch, leading to possible hypoxia at rest, worse when supine OSA OHS Increased blood volume and CO Obesity cardiomyopathy Hypertension Increased O2 consumption and CO2 production Ischaemic heart disease Pulmonary hypertension (secondary to OSA/OHS) Thromboembolic disease Increased risk of gastric aspiration secondary to reflux hiatus hernia Altered drug kinetics Diabetes Fatty liver disease Dyslipidaemia Metabolic syndrome Osteoarthritis
Miscellaneous Development of type 2 diabetes is common in obesity through tissue resistance to insulin and accumulation of fat around the islet cells of the pancreas. This insulin resistance as well as leading to dysregulation of glucose metabolism will also cause problems in regulating fat metabolism. Excessive delivery of fat to the liver results in hepatic steatosis, which in turn can precipitate an inflammatory response known as nonalcoholic steatohepatitis. Although reversible through weight loss in its early stages it will progress to cirrhosis in up to 25% of patients. The combination of hypertension, dyslipidaemia, insulin resistance and central obesity is termed metabolic syndrome and these patients appear to be at increased risk of morbidity and mortality through accelerated atherosclerosis. Gastro-oesophageal reflux disease and a higher incidence of hiatus hernia in the obese all increase the risk of aspiration during induction of anaesthesia. Importantly those patients who have had previous bariatric procedures and subsequent weight loss have been found to be at increased risk of aspiration when they present for further surgery.
Pharmacology for obese patients Several factors are important in determining how pharmacodynamics and pharmacokinetics are affected by morbid obesity. They include increased cardiac output, increase in lean body weight (LBW), increased fat mass and increased extracellular fluid volume. These factors affect drug distribution and elimination. There are several possible dosing scalars available based around total body weight (TBW), LBW, or ideal body weight (IBW).
BMI, body mass index; FRC, functional residual capacity; OHS, obesity hypoventilation syndrome; OSA, obstructive sleep apnoea.
Table 1
Figure 1 The image on the left shows a cross-section of the ventricle and contraction in this plane (radial) is often preserved. The image on the right shows a longitudinal section. Here contraction is reduced earlier in the disease process. This image also shows left atrial and right ventricular enlargement characteristic of obesity induced cardiac changes.
ANAESTHESIA AND INTENSIVE CARE MEDICINE 12:7
278
Ó 2011 Elsevier Ltd. All rights reserved.
ENDOCRINOLOGY
IBW ¼ height (cm) x where x ¼ 100 for men and 105 for women Male LBW ¼ 1.1(weight) 128(weight/height)2 Female LBW ¼ 1.07(weight) 148(weight/height)2 Recent evidence suggests that dosing scalars based on cardiac output and lean body weight are less likely to be associated with undesirable side effects.
Inhalational agents There is no evidence that uptake of inhalational anaesthetic agents is affected by obesity. There is, however, evidence that offset of anaesthesia is more rapid in this population with desflurane than with other agents. It has been demonstrated that airway reflexes return earlier and oxygen saturations in recovery are higher in patients following desflurane rather than isoflurane or sevoflurane based anaesthesia. This article has provided an overview of the pathophysiology and pharmacology associated with morbid obesity. A subsequent article will look at the anaesthetic management of patients presenting for weight loss surgery. A
Intravenous agents Dosing propofol and thiopentone according to TBW is likely to lead to marked hypotension. As a result of the increased cardiac output associated with morbid obesity peak arterial concentrations of intravenous agents are lower than in lean patients for a given dose. This suggests that propofol and thiopentone should be dosed according to LBW as it is closely related to cardiac output. It should be noted that emergence from a single dose will be more rapid in this population. Evidence regarding propofol and thiopentone infusions is scanty, but does suggest that at steady state there is a much greater volume of distribution and therefore offset time.
FURTHER READING Adams JP, Murphy PG. Obesity in anaesthesia and intensive care. Br J Anaesth 2000; 85: 91e108. Gallagher MJ, Frankin BA, Ehrman JK, et al. Comparative impact of morbid obesity vs heart failure on Cardio respiratory fitness. Chest 2005; 127: 2197e203. Lemmens HJM. Perioperative pharmacology in morbid obesity. Curr Opin Anaesthesiol 2010; 23: 485e91. Mackay RE, Malhotra A, Cakmakkaya OS, et al. Effect of increased body mass index and anaesthetic duration on recovery of protective airway reflexes after sevoflurane vs desflurane. Br J Anaesth 2010; 104: 175e82. McCullough PA, Gallagher MJ, DeJong AT, et al. Cardio respiratory fitness and short-term complications after bariatric surgery. Chest 2006; 130: 517e25. Mullen JT, Moorman DW, Davenport JL. The obesity paradox: body mass index and outcomes in patients undergoing nonbariatric general surgery. Ann Surg 2009 Jul; 250: 166e72. Poirier P, Alpert M, Fleisher L, et al. Cardiovascular evaluation and management of severely obese patients undergoing surgery (A science advisory from the AHA). Circulation 2009; 120: 86e95.
Opioids As for induction agents, peak concentrations of opioids appear to relate to cardiac output and as such, most intravenous opioids should be dosed according to LBW. The morbidly obese are, however, sensitive to the respiratory effects of opioids so they should always be used with caution. Muscle relaxants All muscle relaxants are polar molecules and as such lipid insoluble. Peak concentrations will be related to extracellular fluid volumes which may be increased in the morbidly obese. Most evidence suggests that muscle relaxants should be dosed according to IBW. Dosing based on TBW is likely to lead to profound block with prolonged duration of action. The exception is suxamethonium, a depolarizing agent, which should be dosed according to TBW in order to achieve satisfactory intubating conditions.
ANAESTHESIA AND INTENSIVE CARE MEDICINE 12:7
279
Ó 2011 Elsevier Ltd. All rights reserved.