Anaesthesia for the Bariatric Patient

Published on 27/02/2015 by admin

Last modified 27/02/2015

Print this page

This article have been viewed 1833 times

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.