Anaesthesia for the Bariatric Patient

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Anaesthesia for the Bariatric Patient

INTRODUCTION

An estimated 63% of British adults are above normal weight; 26% of these are obese and around 2.5% are morbidly obese or higher. These figures are projected to rise, with nearly 50% of adults in the obese category by 2030. Britain’s obesity rates are not as high as in some other developed and developing countries. The scale of the demographic changes and the associated multisystem comorbidity mean that the obese patient is likely to present across the spectrum of healthcare and not simply to the specialist in the bariatric field.

MEASURING OBESITY

A patient’s mass varies with size and shape. Absolute mass can be important when considering factors such as equipment safety limits. However, it is more important to reference a person’s expected mass to height. The most widely used technique is calculation of Body Mass Index (BMI).

BMI has limitations and may not be representative in certain ethnic groups, or in those of athletic build. It cannot describe the distribution of weight, nor discriminate the nature of the excess tissue. However, calculation of BMI, from two ubiquitous measurements, requires the minimum equipment and expertise. Hence, it is likely to remain the measure of choice as a shorthand to express obesity (Table 25.1, Fig. 25.1).

TABLE 25.1

WHO Obesity Classes by BMI (Other Nomenclatures Included)

Category	BMI (kg m^–− 2)
Underweight	< 18.5
Normal	18.5–24.9
Overweight (pre-obese)	25–29.9
Obese Class I	30–34.9
Obese Class II (severe to morbid)	35–39.9
Obese Class III (morbid to super)	40 +
(Super obesity)	45–50 +

FIGURE 25.1 Body habitus and silhouettes by category. Left to right – normal, overweight and obese.

The limitations of BMI may account for some of the variability in obesity research. Other difficult measures such as hip to abdominal girth ratio and skin fold thickness may be better at describing more dangerous patterns of fat distribution. Central obesity (‘apple-shaped’, predominantly male) carries more associated risks than peripheral obesity (gluteofemoral or ‘pear-shaped’) often seen in females.

OBESITY PATHOPHYSIOLOGY, COMORBIDITY AND THE METABOLIC SYNDROME

Obesity is a multi-system disorder. The aetiology is complex and has long been oversimplified. The network of contributing factors includes socio-economic, ethnic, societal, social and psychological. The underlying and acquired pathophysiology cross the traditional boundaries of medicine to include endocrine, cardiovascular, respiratory, GI tract, locomotor and psychiatric disorders.

The Adipose Organ

The traditional view of fat tissue has been as a metabolically inert triglyceride energy store, with insulation from physical and temperature stress as a useful secondary effect. However, fat tissue actually exists as a continuum. In particular, hepatic and intra-abdominal visceral fat tissue is much more active than previously thought. It is known to excrete over 20 mediators. The observed effects are pro-inflammatory (cytokines, adipsin), pro-coagulant (plasminogen activator inhibitor 1) and endocrine (leptin, resistin, adiponectin).

The underlying biochemical state is probably responsible for the common patterns of accelerated comorbidity observed in morbid obesity. The ‘metabolic syndrome’ is the name applied to the pattern of central obesity associated with at least two of the following:

Hypertension

Hyperglycaemia/insulin resistance

Dyslipidaemia and atherogenesis

Non-alcoholic fatty liver disease

Pro-thrombotic and inflammatory state

COMORBIDITY AND ANAESTHETIC MANAGEMENT

Airway

The airway of the obese patient should be regarded with caution. Traditional teaching and audits of national practice predict that the management of the obese patient’s airway is likely to be difficult. However, a number of studies have demonstrated that, in experienced hands, certain aspects of airway management, in particular tracheal intubation, may be no more difficult than normal.

Anatomy: In the obese patient, the airway undergoes progressive adipose infiltration. This occurs at all levels from the oropharynx through to the glottis and vocal cords. Adipose infiltration causes progressive narrowing and reduction in airway diameter, which may reduce by 50% or more from the physiological male normal of about 20 mm in the hypopharynx.

The effect of adipose deposition on airway anatomy is not simply internal. External factors also need to be considered. The presence of a thoracic ‘hump’ can significantly affect supine posture, resulting in extension of the neck and flexion at the atlanto-occipital (AO) joint. Moreover, posterior adipose deposition between the occiput running inferior to the spine of T1, can hinder atlanto-occipital extension. Hence, in an unsupported supine position, the airway of the obese patient can easily become the opposite of ideal; neck extension and fixed AO flexion.

Careful positioning is key to successful management of the bariatric airway. This can be achieved either using specifically designed equipment, or special modifications to normal equipment. In urgent situations a number of aids to achieving the position have been suggested including multiple towels, fluid bags or inflatables. The key is to ensure true neck flexion and AO extension. This is best achieved by ensuring that the patient posture, in particular neck/head position is viewed from the side (Fig. 25.2A and B).

FIGURE 25.2 (A) Lateral CT Scout (supine, female, BMI 59 kg m^− 2). Note neck position, ‘free-floating’ head and the potential for neck, chest and breast adipose tissue to hinder airway management. (B) Sagittal cross-section (BMI 55 kg m^− 2). Note depth of both anterior and posterior airway structures and the extent of airway soft tissue around the 7.5 tracheal tube.

Airway Adjuncts: A range of products to assist in the management of difficult airways exists. Simple adjuncts such as oral and nasopharyngeal airways, and the use of CPAP can help to splint the airway open. Laryngeal mask airway products retain their role in airway salvage. Their routine use in the morbidly obese patient remains controversial, focusing on concerns around pulmonary aspiration and optimization of pulmonary function.

Standard laryngoscopes and blades remain the default equipment for tracheal intubation, particularly when combined with careful positioning. Video devices may help if additional risk factors exist. Many are designed with short-handled bodies, useful if a large chest and fixed neck posture limit space.

Respiratory Pathophysiology

Anatomy

Lung size is predicted by height or ideal body mass, rather than gross weight. The lung fields of obese patients often look small when assessed by chest radiography (Fig. 25.3). This is an artefact of accommodating the patient on the chest X-ray. Total lung capacity is usually nearly normal and it is functional spirometry which reveals the associated pathology (Fig. 25.4).

FIGURE 25.3 Anteroposterior chest X-ray of a morbidly obese patient.

FIGURE 25.4 Spirometric changes with obesity. Note the significant reduction in FRC. TLC, total lung capacity; IC, inspiratory capacity; FRC, functional residual capacity.

In obesity, there is heavy adipose infiltration of the chest wall and breast tissue, which leads to decreased chest wall compliance and damping of natural recoil expansion of the chest wall. This is further exacerbated by abdominal wall infiltration and a raised intra- abdominal pressure. Additionally, there is peribronchial parenchymal fat infiltration. Respiratory muscles demonstrate fat infiltration and the effect of inflammatory mediators. Diminished muscle power and respiratory endurance result.

Pathophysiology

Total lung capacity and vital capacity reduce in a gentle, linear manner with rising weight. The spirometric observations reflect the change in the balance between chest wall and parenchymal forces with rising obesity.

Functional residual capacity decreases (Fig. 25.5) and closing volume increases. Resulting atelectatic shunt reduces PaO₂. At higher levels of morbid obesity, tidal ventilation may impinge on closing volume even in the standing position.

FIGURE 25.5 Changes in functional residual capacity (FRC) with increasing body mass index (BMI). (Adapted from Pelosi et al (1998).)

FEV₁ decreases, although the FEV₁/FVC ratio is often preserved, particularly with central obesity patterns.

Work of breathing increases by 70% from low levels of obesity to an energy cost 300% higher in complicated, high BMI states. The energy cost of maintaining adequate minute ventilation is mitigated by a reduction in tidal volume, resulting in rapid, shallow breathing at rest.

The elastic load increases (reduced static compliance; Fig. 25.6). This is a reflection of both the reduced elastance of chest wall and parenchymal tissue and tidal ventilation occurring at lower lung volumes. Dynamic compliance (i.e. resistance to gas movement) also falls. In the lower airway, there is narrowing of the small conducting airways. This may be due to multiple factors:

FIGURE 25.6 Changes in static respiratory system compliance (Cst,rs) with increasing body mass index (BMI). (Adapted from Pelosi et al (1998).)

External compression from parenchymal fat deposition

A reduction in the part of the lung volume at which tidal breathing occurs.

Chronic inflammatory changes and increased smooth muscle reactivity/bronchospasm.

CLINICAL RESPIRATORY COMORBIDITY

Asthma

About 5% of the general population are diagnosed as asthmatic. Asthmatic symptoms such as wheezing, dyspnoea and reduced exercise capacity are reported by around 25% of the obese population; however, bronchodilator reversibility may not be found. Contradictions in the epidemiological data linking obesity and asthma may relate to exacerbating comorbidities in obesity such as gastro-oesophageal reflux or the interplay of the proinflammatory and endocrine mediators previously described.

Sleep-Disordered Breathing

Sleep-disordered breathing describes the spectrum of obstructive sleep apnoea, central sleep apnoea, obesity hypoventilation syndrome and pathological patterns of nocturnal ventilation.

Obstructive sleep apnoea can be diagnosed in 4% of the general population. However, 60% of these are in patients with a BMI > 30 kg m^− 2. Weight loss of a magnitude such as achieved with weight loss surgery is associated with symptomatic reduction or resolution in approximately 75% of patients. Clinical screening tools such as the self-assessed Epworth (sleepiness) score and the STOP–BANG criteria are helpful to target more specific investigations such as sleeping oximetry or full flow and effort-sensitive sleep studies.

Sleep-disordered breathing is associated with a number of comorbid conditions and their sequelae. These include systemic hypertension, pulmonary hypertension and the cardiovascular consequences of each.

The full implications of untreated sleep-disordered breathing on the perioperative patient are unresolved. Presentation as patients who display significant sensitivity to ventilatory depressants is well recognized. Prolonged apnoea/hypoventilation and narcolepsy can be found after relatively small doses of opioid.

ANAESTHETIC MANAGEMENT POINTS

All respiratory and sleep-related comorbidities should be identified, investigated and treated. At induction of anaesthesia, the use of the reverse Trendelenburg (head-up) or tipped beach chair positions maximize spontaneous and anaesthetized lung function. FRC on induction of anaesthesia can reduce by up to 50%.

Ventilation volumes should be calculated from ideal body weight. Recruitment manoeuvres and PEEP of 10 cmH₂O maximize lung function and minimize shunt. Pneumoperitoneum diminishes the benefit of postural changes.

Postoperatively, balanced analgesia, rapid mobilization, incentive spirometry and physiotherapy may help to avoid respiratory morbidity.

CARDIOVASCULAR PATHOPHYSIOLOGY

In common with other organs, cardiovascular changes in obesity are part of a continuum. The nature and extent of the pathophysiology relate to the extent and duration of being overweight and also the sequential effects of associated comorbid processes in other organs.

Oxygen Demand and Delivery

Oxygen demand increases in proportion to the increase in fat-free mass (FFM) rather than in relation to the patient’s BMI. FFM increases with total body weight (TBW), but with a decreasing curve gradient, to a ceiling of approximately 1 kg per centimetre of height.

Blood volume describes an inverse hyperbolic relationship with increasing BMI. The blood volume:TBW ratio decreases from around 70 mL kg^– 1 to 40 ml kg^– 1 at a BMI of 70 kg m^– 2.

Cardiac output increases with BMI in proportion to the square root of the ratio between actual BMI and ideal BMI. The increase is linear in relation to body surface area and fat-free mass gain. Indexed to adipose tissue mass, fat perfusion decreases as BMI increases. This decrease highlights the relatively poor vascular supply to peripheral adipose tissue (< 150 mL kg^– 1 min^– 1). Early stage increases in cardiac output appear to be achieved by blood volume-related preload increases in stroke volume, mediated by β-natriuretic peptide inhibition and aldosterone. The contribution of increased heart rate remains relatively minor.

Cardiac Pathophysiology

The heart of the obese patient may exhibit a number of pathological changes (Fig. 25.7). These may be related to either the primary obesity or associated comorbidity, e.g. hypertension, diabetes, hyperlipidaemia or sleep apnoea.

FIGURE 25.7 Effects of obesity-related cardiomyopathy.

Echocardiographic evidence suggests that three pathological patterns predominate in obesity. Concentric remodelling (LV wall thickening short of hypertrophy), concentric hypertrophy (hypertrophy with increased relative wall thickness) and eccentric dilated hypertrophy (thickened hypertrophic LV wall, but reduced wall:cavity ratio secondary to dilatation) occur. The practical application of these states is the recognition of the early existence of reduced ventricular wall compliance and ventricular diastolic dysfunction. As compensatory cardiac dilatation occurs, there is a progressive reduction in systolic contractility. The observed paradox of these states is discussed below.

Electrophysiology

A number of ECG changes may be recorded in obese patients. These may be related to habitus or pathology.

Atrial fibrillation is the commonest arrhythmia associated with obesity and the prevalence increases exponentially with BMI.

Voltage magnitudes vary and QRS complex size is not reliable for diagnosis.

Conduction axis is frequently left-shifted, but this may be caused by physical displacement of the heart from the normal position and rotation.

Conduction anomalies are relatively common and may relate either to fatty infiltration and fibrosis of the conduction system or underlying coronary artery disease. PR and QRS prolongation, through fascicle block to bundle branch block, are seen and may be benign. QTc prolongation appears to have a negative prognostic value.

Right Ventricular Pathophysiology

Right ventricular dysfunction is associated in particular with sleep-disordered breathing. The combined effects of chronic pulmonary hypertension (nocturnal hypoxaemia), with the effects of chronic volume overload (obesity) and progressive left ventricular changes lead to right-sided dilatation, systolic and diastolic dysfunction and failure.

VASCULAR DISEASE

Arterial disease is associated with both primary obesity and its comorbid diseases (hyperlipidaemia, diabetes mellitus, etc.). Some trials have suggested that there may be an absolute risk increase in coronary arterial disease of 50% between normal and overweight individuals, rising to a hazard ratio of > 2.5 in the severely morbidly obese. However, confusingly, lower cardiac mortality rates are reported in the mildly obese. The contradiction may lie partly in the limitations of BMI as a measure of the dangerous central obesity pattern. For example, controlled for comorbid conditions, peripheral vascular disease shows no correlation with BMI. However, obesity expressed as waist circumference, waist:hip ratio or waist:thigh ratio has a raised vascular risk profile. This unresolved effect is known as the obesity paradox. This is the term given to the lower mortality observed in obese patients in a number of conditions. These include critical illness, congestive cardiac failure and eccentric compared to concentric cardiac hypertrophy.

LIVER

Adipose tissue in the liver is highly metabolic endocrine and paracrine tissue. There is a close relationship between liver fat content and insulin resistance. In early obesity, insulin sensitivity returns with weight loss. Weight loss of 8% reduces liver fat content by 80%. Non-alcoholic steatohepatitis (NASH) or higher grades of non-alcoholic fatty liver disease (NAFLD) appear to uniformly precede the development of type 2 diabetes. Insulin resistance contributes to dyslipidaemia, hyperglycaemia and eventual pancreatic islet cell burn-out. The available data suggests that 20% of patients with NASH will progress to cirrhotic liver disease.

NAFLD alone, or as part of the metabolic syndrome (see above) is associated with accelerated atherogenesis, ischaemic heart disease and raised cardiovascular mortality.

Intra-abdominal pressure is raised in obesity and increases with BMI. Resting pressure is usually around twice normal, at 10 mmHg (Fig. 25.8). During laparoscopic procedures, the pneumoperitoneal pressure may need to be high to allow adequate vision. Care should be taken because pressures of 15 mmHg or higher have been shown to significantly reduce femoral vein, gut, visceral and portal blood flows. Measures such as positioning and adequate relaxation should be addressed first.

FIGURE 25.8 Relationship between body weight and intra-abdominal pressure. (Adapted from Pelosi et al (1999).)

Gastro-Oesophageal Reflux

Meta-analysis supports the traditional view that increasingly obese patients are at higher risk of gastro-oesophageal reflux. The direct causal nature of the relationship is ill-defined. However, reported symptoms are present 2–3 times more frequently in the obese compared to the general population. Detrimental factors such as higher gradient pressures, residual volumes and dysmotility may outweigh factors such as enhanced gastric emptying.

PHARMACOLOGY

Patients who are obese may display altered pharmacokinetics and pharmacodynamics (Table 25.2). These factors have clinical relevance. The application of basic concepts such as drug solubility, compartment volumes, transportation and metabolism may be helpful. However, the interactions are complex and reference to published data should be made. For these reasons, controversy remains and particular care should be taken with the use of target controlled infusion algorithms developed for patients of normal weight.

TABLE 25.2

Factors Which Affect the Pharmacokinetic and Pharmacodynamic Properties of Drugs in Obesity

Kinetic Property	Effect of Increasing Obesity
Blood volume and cardiac output	Increase
Adipose and lean body mass	Increase
Hepatic blood flow and glucuronidation rate	Increase
GFR and renal excretion	Increase
Cytochrome P450 isoenzymes	Variable
Renal tubular reabsorption	Decrease