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Anaesthesia for the obese patient


Obesity rates have increased from 15% in 1993 to 27% in 2015, and morbid obesity has tripled to affect 2% of men and 4% of women. Figures are projected to rise, with 50% of UK adults expected to be obese by 2030. The scale of demographic changes and associated multisystem comorbidity means that the obese patient presents 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. The most widely used obesity measurement is BMI = (mass in kg) / (height in m) 2 . Body mass index was first devised more than 100 years ago and has several limitations:

  • It is not representative of certain ethnic groups or those of athletic build.

  • It cannot describe the distribution of weight ( Fig. 32.1 ).

    Fig. 32.1, Apples and pears body morphology description.

  • It is unable to discriminate the nature of the excess tissue—that is, muscle or fat.

However, calculation of BMI, from two simple, universal measurements, requires minimum equipment and expertise, and will therefore continue to be used to express degrees of obesity despite its flaws ( Table 32.1 ).

Table 32.1
World Health Organization classification of obesity (other nomenclatures included)
Category BMI (kg m −2 )
Underweight <18.5
Normal 18.5–24.9
Overweight (preobese) 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+
BMI, Body mass index.

Not all types of fat are the same. Intra-abdominal fat is metabolically active and is associated with a higher incidence of myocardial ischaemia, congestive cardiac failure, sleep-disordered breathing and respiratory problems; it is vital to identify this patient group, and the use of BMI in isolation will not do this. Fat distribution can be described using the fruit analogy of apples and pears (see Fig. 32.1 ). The apple distribution describes central abdominal obesity, whereas the pear shape describes the peripheral, benign-type buttock and thigh distribution of fat. Measurement of waist circumference provides a measure of this distribution. A waist circumference greater than 88 cm in women and 102 cm in men identifies individuals with intra-abdominal fat and associated higher risk profiles.

Obesity and the metabolic syndrome

Obesity is a multisystem disorder. The aetiology is complex but in the main is driven by excess nutrient intake (of the wrong type of foods), with little in the way of energy expenditure. There is an associated complex network of contributors, including socioeconomic, ethnic, societal, social and psychological factors. The underlying and acquired pathophysiological changes include the endocrine, cardiovascular, respiratory, gastrointestinal tract, locomotor and psychiatric systems.

The adipose organ

The traditional view of fat tissue has been as a metabolically inert triglyceride energy store that provides protection from physical insults and temperature changes. However, fat tissue is not uniform or benign. Hepatic and intra-abdominal visceral fat tissue is metabolically active and should be considered an endocrine organ; it is known to excrete more than 20 chemical mediators. The observed effects are proinflammatory (cytokines, adipsin), procoagulant (plasminogen activator inhibitor 1) and endocrine (leptin, resistin, adiponectin).

The generated underlying biochemical state is probably responsible for the common patterns of accelerated comorbidity observed in morbid obesity. Metabolic syndrome is the name applied to the pattern of atherosclerotic disease and diabetes mellitus associated with the presence of at least three of the following:

  • Hypertension

  • Hyperglycaemia/insulin resistance

  • Raised cholesterol

  • Visceral obesity

  • Low high-density lipoprotein (HDL) concentrations

Development of the metabolic syndrome is associated with a significant increase in perioperative organ dysfunction, resulting in increased mortality. It is vital to identify the presence of the syndrome and optimise each component before surgery to reduce risks. This includes smoking cessation. Cigarette smoking is a powerful catalyst to the development of adverse atherosclerotic events in those with the metabolic syndrome.

Obesity pathophysiology, comorbidity and anaesthetic management

Airway

The airway of the obese patient should be approached with caution. Traditional teaching and audits of national practice suggest that airway management in obesity is likely to be difficult. However, several studies have demonstrated that tracheal intubation is no more difficult than for normal-weight individuals, but face-mask ventilation is more likely to be difficult. The association of a large abdomen and increased neck circumference with the presence of a beard increases the risk of difficulty. Beard removal before surgery may need to be considered to facilitate safe airway management.

Obesity results in progressive airway infiltration by adipose tissue. This occurs at all levels from oropharynx to vocal cords, causing narrowing and reduction in airway diameter. A reduction of 50% or more from the physiological normal can be encountered. 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 joint.

Careful positioning is key to successful management of the bariatric airway. This can be achieved using specifically designed equipment such as the Oxford HELP ( Fig. 32.2 ). However, positioning can also be achieved by ramping with pillows and blankets. The key component of positioning is to place the patient in the reverse Trendelenburg position with the tragus of the ear level with the manubrium sterni. This position facilitates all aspects of airway manoeuvres.

Fig. 32.2, Oxford HELP (head elevating laryngoscopy pillow).

Airway adjuncts

Simple adjuncts such as oral and nasopharyngeal airways should be used routinely. Continuous positive airway pressure during preoxygenation and PEEP during face-mask ventilation can help to splint the airway open. Supraglottic airway devices (SADs) have a role in airway salvage. Their routine use in the morbidly obese patient remains controversial, focusing on concerns around pulmonary aspiration and optimisation of pulmonary function. The use of SADs in the obese patient should be limited to airway rescue.

Standard laryngoscopes and blades remain the default equipment for tracheal intubation in obese patients. Videolaryngoscopes may help if additional risk factors for difficult tracheal intubation are present (see Chapter 23 ). Many are designed with short-handled bodies which can be useful if a large chest and fixed neck posture limit space.

Respiratory system

Anatomy

The lung fields of obese patients often look small when assessed by chest radiography. This is an artefact of accommodating the patient onto the plate for the radiograph. Obesity results in compromised lung function. This function will change with location of fat mass, patient position and presence of other pathological conditions. Adipose deposition around the chest wall and in breast tissue leads to decreased chest wall compliance and damping of the natural recoil and expansion. Abdominal wall infiltration and raised intra-abdominal pressure with peribronchial and paren­chymal fatty infiltration further exacerbate this. Respiratory muscles demonstrate fat infiltration, which, when combined with effects from inflammatory mediators, results in diminished muscle power and respiratory endurance.

Pathophysiology

  • Total lung capacity and vital capacity decrease in a linear manner with rising weight. The spirometric observations ( Fig. 32.3 ) reflect the change in the balance between chest wall and parenchymal forces with rising obesity.

    Fig. 32.3, Spirometric changes with obesity. Note the significant reduction in FRC. FRC, Functional residual capacity; IC, inspiratory capacity; TLC, total lung capacity.

  • Functional residual capacity (FRC) decreases ( Fig. 32.4 ) and closing volume increases. Resulting atelectatic shunt reduces P a o 2 . At higher levels of morbid obesity, tidal ventilation may impinge on closing volume even in the standing position.

    Fig. 32.4, Changes in functional residual capacity (FRC) with increasing body mass index (BMI).

  • Forced expiratory volume in 1 s (FEV 1 ) decreases, although the FEV 1 /forced vital capacity (FVC) ratio is often preserved, particularly with central obesity patterns.

  • Increased metabolic rate is associated with increasing fat and muscle mass. This results in a doubling of metabolic rate compared with lean individuals, causing increased oxygen consumption and carbon dioxide production.

  • Work of breathing increases by 70% from low levels of obesity to an energy cost 300% higher in 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. 32.5 ). This reflects both the reduced elasticity of chest wall and parenchymal tissue and tidal ventilation occurring at lower lung volumes. Dynamic compliance (i.e. resistance to gas movement) also falls.

    Fig. 32.5, Changes in static respiratory system compliance (Cst, rs) with increasing body mass index (BMI).

  • In the lower airway there is narrowing of the small conducting airways. This may be due to multiple factors:

    • external compression from parenchymal fat deposition;

    • reduction in the part of the lung volume at which tidal breathing occurs; and

    • chronic inflammatory changes and increased smooth muscle reactivity/bronchospasm.

The consequences of these changes for the anaesthetist include:

  • shortened apnoea to desaturation time;

  • increased oxygen requirements;

  • increased shunt fraction and ventilation/perfusion mismatch;

  • increased work of breathing resulting in difficulty with spontaneously breathing general anaesthesia tech­niques; and

  • increased incidence of atelectasis.

Obstructive sleep apnoea

Sleep and associated snoring is a normal physiological process. Snoring occurs as a result of soft tissue collapse of the upper airway and vibration of these tissues and associated turbulent airflow. Snoring becomes abnormal when associated with apnoeas and hypopnoeas to produce obstructive sleep apnoea (OSA). This occurs in up to 25% of the adult population. Obstructive sleep apnoea occurs in up to 60% of obese individuals; the majority of these cases are undiagnosed. Obstructive sleep apnoea is not a benign condition; cyclical occlusion of the upper airway with associated hypoxaemia results in sympathetic nervous system activation, endothelial dysfunction and inflammation. Development of hypertension, myocardial ischaemia and failure, strokes and sudden cardiac death are increased.

Patients in the perioperative period will acquire an abnormal sleep cycle because of anaesthesia, surgery and administered drugs; this has adverse effects. A patient with OSA is at increased risk of respiratory failure and desaturation, emergency tracheal reintubation, delirium, cardiac arrhythmias, unplanned ICU admission and increased duration of hospital stay. Perhaps surprisingly, OSA is not associated with an increase in postoperative mortality.

It is vital to screen for OSA preoperatively to treat and reduce risk. Basic clinical history and examination are poor at identifying OSA. The STOP Bang tool (see Chapter 19 ) is a simple screening questionnaire designed for use in surgical patients to identify the presence of predictive factors in those with OSA. It is well validated, and its use is supported by experts in bariatric anaesthesia. However, the STOP Bang questionnaire has a greater sensitivity than specificity. Specificity can be improved with measurement of plasma bicarbonate. High STOP Bang scores or the presence of risk factors (large neck, high Mallampati score, bicarbonate concentration > 28 mmol L –1 or oxygen saturations of less than 95% on room air) will require referral to a sleep clinic before elective surgery for further investigation and management.

Anaesthetic management points

At induction of anaesthesia, the use of the reverse Trendelenburg position maximises lung function, as the FRC can reduce by up to 50% after induction of anaesthesia. Head-up positioning to ensure the tragus is level with the manubrium ( Fig. 32.6 ) increases apnoea to desaturation time, facilitates face-mask ventilation and assists with tracheal intubation.

Fig. 32.6, Head-up patient position.

Lung ventilation volumes should be based on ideal body weight (IBW; see Pharmacology section later in this chapter) and should be 6–8 ml kg –1 . Recruitment manoeuvres (50 cmH 2 O for 10 s or a vital capacity volume) and maintenance PEEP concentrations of 10 cmH 2 O have been demonstrated to maximise lung function by reducing atelectasis and shunt reduction. The presence of a pneumoperitoneum further worsens respiratory function. Optimising patient position, deep neuromuscular blockade and limiting pneumo­peritoneum pressures all reduce the adverse consequences. Postoperatively, balanced analgesia (including the use of regional techniques), avoiding long-acting opioid administration, rapid mobilisation, and use of incentive spirometry and physiotherapy may combine to reduce respiratory morbidity.

Cardiovascular system

In common with other organs, cardiovascular changes in obesity are part of a continuum. The nature and extent of the pathophysiology relates to the extent and duration of being overweight and the sequential effects of associated comorbid processes in other organs ( Fig. 32.7 ).

Fig. 32.7, Effects of obesity on the cardiovascular system.

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