Reduced Lung Volumes

As fat accumulates in the chest and abdomen, the chest wall becomes stiffer, diaphragmatic movement is impaired and pulmonary compliance falls. This causes an exponential decline in functional residual capacity (FRC) and expiratory reserve volume as BMI increases (Jones, 2006).

As FRC falls, small airway closure during tidal breathing leads to alveolar collapse and atelectasis. The result is a mismatch of lung ventilation and perfusion and a tendency to hypoxemia. The problem is compounded by general anaesthesia (Figure 18.2) (Adams and Murphy, 2000).

Figure 18.2 Schematic representation of the effects of severe obesity on FRC.

With permission from Adams 2000.

Decreased pulmonary compliance also increases the work of breathing. A significant proportion of obese patients have reduced respiratory muscle endurance compared to normal-weight subjects when measured on pulmonary function tests (PFTs) (Sebastian, 2013). Muscle fatigue may contribute to an increased risk of respiratory failure after major abdominal surgery.

Asthma

Weight gain and elevated BMI are associated with an increased risk of developing adult-onset asthma. The risk appears greater for obese women than for obese men (Sebastian, 2013).

Obese patients reporting episodic dyspnoea, wheeze or cough should undergo pulmonary function testing (PFTs), including bronchodilator challenge. Consider cardiac disease and gastro-oesophageal reflux disease (GORD) as differential diagnosis in obese patients with asthma-like symptoms and normal PFTs.

Obstructive Sleep Apnoea

Obstructive sleep apnoea (OSA) is characterised by recurrent episodes of upper airway obstruction during sleep. Obesity increases susceptibility to OSA by causing physical narrowing and impaired neuromuscular function of the pharynx (Sebastian, 2013). The severity of OSA is based upon the frequency of apnoea and hypopnoea per hour of sleep – Apnoea Hypopnoea Index (AHI).

The prevalence of OSA is estimated to be 40 per cent for obese women and 50 per cent for obese men (Chung, Yang and Liao, 2013). Most will be undiagnosed when they attend the pre-assessment clinic, so making the diagnosis and implementing CPAP therapy can have a positive impact on patients’ perioperative and long-term health.

Chronic untreated OSA causes systemic hypertension and has been associated with higher rates of cardiac arrhythmias, myocardial infarction, heart failure, stroke and diabetes mellitus (Jordan, McSharry, and Malhotra, 2014). Surgical patients with untreated OSA have higher rates of post-operative desaturation, respiratory failure, post-operative cardiac events, ICU transfers (Kaw et al., 2012) and increased length of stay (Gupta et al., 2001) compared to non-OSA patients. There are a large number of case reports describing perioperative complications in patients with OSA, including respiratory arrest, cardiac arrest and death (Chung, Yuan and Chung, 2008).

The easiest way to identify patients at risk of OSA in the pre-assessment clinic is to perform a screening questionnaire. The STOP-Bang questionnaire (Table 18.4) has the benefit of being easy to remember and has been validated for use in obese surgical patients (Chung et al., 2013). STOP-Bang has a sensitivity and negative predictive value approaching 100 per cent, meaning a score < 3 safely excludes the possibility the patient before you has moderate-to-severe OSA (Chung and Elsaid, 2009).

Patients with a STOP-Bang score 5–8 are at high risk of moderate-to-severe OSA, and will benefit most from diagnostic testing. The intermediate group (STOP-Bang score 3–4) should be referred for diagnostic testing if undergoing major surgery or surgery with high post-operative analgesic requirements.

The gold standard diagnostic test for OSA is overnight laboratory polysomnography. The result provides an accurate AHI index, allowing grading of OSA severity; however, it requires expensive equipment and trained staff and can be inconvenient for patients. Simplified diagnostics including overnight oximetry and home polysomnography are viable alternatives for most patients (Jordan et al., 2014).

Continuous positive airway pressure (CPAP) is effective in relieving the symptoms of OSA and reducing long-term respiratory and cardiovascular complications. Data on the efficacy of perioperative CPAP are poor. Preoperative CPAP therapy is effective in reducing the AHI, and there is a trend towards shorter length of stay post-operatively (Nagappa et al., 2015). Post-operative CPAP has been shown to reduce post-operative atelectasis, pneumonia and re-intubation after major abdominal surgery (Ireland et al., 2014).

We recommend a minimum 4-week trial of preoperative CPAP for patients with moderate to severe OSA. This allows time to optimise CPAP fitting and ventilation parameters. All patients on CPAP are required to bring their own machines and facemasks to hospital on the day of surgery.

Perioperative management of obese patients with OSA depends on the severity of disease, CPAP compliance, type of surgery and anticipated analgesic requirements. Table 18.5 describes one approach, with guidelines for the appropriateness of ambulatory surgery and post-operative care requirements for patients with OSA.

This guide relies on a coordinated approach to care by anaesthetists, surgeons, physicians and nursing staff. It should be modified to suit local conditions and resources.

Obesity Hypoventilation Syndrome

This is a sleep disorder characterised by obesity, daytime hypercapnia and hypoxemia. Although affecting only 0.15–0.03 per cent of the general population, the prevalence of OHS among obese patients with OSA is as high as 10 per cent (Chau et al., 2012).

Patients with OHS have a reduced central respiratory drive. This places them at higher risk of post-operative respiratory failure; a problem compounded by general anaesthesia and sedating analgesics. Chronic OHS also contributes to higher rates of pulmonary hypertension, coronary artery disease and heart failure (Berg et al., 2001).

The diagnosis should be considered in obese patients who report sleep disturbance and have low oxygen saturations on room air (SpO₂ ≤94%). Serum bicarbonate (HCO₃) is an easily performed and sensitive screening test for chronic hypercapnia. If HCO₃ is elevated, a resting arterial blood gas should be performed to quantify the degree of hypercapnia and hypoxemia.

It is appropriate to refer these complex patients to a sleep physician for assessment and treatment. They will require PFTs, polysomnography and titration of CPAP or bi-level positive airway pressure (BiPAP) preoperatively.

Respiratory Investigations and Optimisation

All obese elective surgical patients should have resting respiratory rate and room air pulse oximetry recorded at pre-assessment. Serum bicarbonate and arterial blood gas measurement should be performed in patients with low oxygen saturations as described previously.

Preoperative PFTs in obese patients without symptoms or signs of underlying lung disease are costly and are not beneficial. The same is true of routine chest radiographs, peek expiratory flow measurements and preoperative incentive spirometry (Cattano et al., 2010). PFTs are indicated for patients with unexplained dyspnoea at rest, symptoms of obstructive lung disease and obesity hypoventilation syndrome (OHS).

The principles of pulmonary optimisation in obese patients should include:

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  Minimum 6 weeks smoking cessation programme, including nicotine replacement therapy (Lee et al., 2015);

  
  
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  Inhaled corticosteroids, leukotriene inhibitors and long-acting beta agonists for treatment of asthma;

  
  
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  Antibiotics for patients with infected sputum;

  
  
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  Minimum 4 weeks titration of CPAP (or BiPAP) therapy for OSA and OHS;

  
  
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  Proton pump inhibitors for symptomatic GORD;

  
  
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  Preoperative dietary and exercise advice (see Weight loss and nutritional support).

Coronary Artery Disease

Obesity, particularly central obesity, is strongly associated with coronary artery disease. In a large meta-analysis of 302,296 participants, obese subjects were 80 per cent more likely than normal-weight subjects to have a coronary event during follow-up (adjusted relative-risk 1.81, 95% CI 1.56–2.10) (Bogers et al., 2007). Many obese patients will have occult CAD.

Measuring waist and hip circumference in the pre-assessment clinic is useful, as a low waist-to-hip ratio predicts myocardial infarction risk and related mortality better than BMI (Chrostowska et al., 2013). A 12-lead ECG is recommended for patients with at least one risk factor for CAD or poor exercise tolerance (Poirier et al., 2009). Left bundle branch block and S-T and T wave abnormalities may be indicative of underlying CAD.

The AHA/ACC recommends non-invasive cardiac testing for patients with ≥2 revised cardiac risk indices and poor functional status (Fleisher et al., 2014). There are no specific recommendations for obese patients who score poorly on measures of function because of physical limitations. A recommended approach is to perform stress testing for patients with a BMI >40 kg/m² with at least two or more CAD risk factors who cannot exercise or have unknown exercise tolerance (Poirier et al., 2009). The choice of stress test – exercise, pharmacological or combined – depends on the patient’s mobility and the facilities available.

Cardiopulmonary exercise (CPET) testing has been used to predict morbidity and length of stay after gastric bypass surgery (Hennis et al., 2012). In general, obese individuals have an anaerobic threshold only slightly less than normal-weight controls (Serés et al., 2003). If available, CPET testing can be recommended for obese patients undergoing high-risk procedures where functional status is unknown (Fleisher et al., 2014).

Heart Failure

In addition to the most common causes of heart failure – CAD, systemic hypertension and heart valve disease – prolonged obesity is associated with the development of a reversible obesity cardiomyopathy. This is initially characterised by diastolic dysfunction, but may progress to both diastolic and systolic dysfunction (Poirier et al., 2009) (Figure 18.3).

Figure 18.3 The aetiology of obesity cardiomyopathy and its association with right‐sided heart failure, systemic hypertension and ischaemic heart disease.

With permission from Adams 2000.

A history of dyspnoea, orthopnoea and peripheral oedema are non-specific in obese patients. On examination, heart sounds may be muffled and jugular venous pulses obscured. Right axis deviation and right bundle branch on ECG suggests right ventricular hypertrophy. This may be an important sign of pulmonary hypertension and deserves further cardiac investigation.

Transthoracic echocardiography windows may be poor quality in very obese patients. Alternative cardiac imaging includes nuclear imaging, magnetic resonance imaging and computed tomography (Poirier et al., 2009). MRI has the advantage of no radiation exposure; however, specialised large-bore MRI is required for very obese patients. The preferred modality will depend on local availability and expertise.

Systemic Hypertension

The Framingham Heart Study observed that obese subjects were twice as likely to develop systemic hypertension than the non-obese. The mechanisms are unclear, but have been shown to be reversible with weight loss (Wilson et al., 2002). Obese patients with hypertension are also more likely to be resistant to antihypertensive therapy (Chrostowska et al., 2013). Although grade 1 and 2 hypertension per se does not increase clinically significant perioperative complications, it is an important marker of end-organ damage (Howell et al., 1996).

Manual or automated blood pressure measurements should be taken with the cuff bladder encircling 80 per cent or more of the patient’s upper arm circumference. Undersized cuffs tend to overestimate blood pressure. Ideally two measurements should be taken at least 1 minute apart, with the average recorded.

Patients with average systolic pressures >140mmHg or diastolic pressures >90mmHg should be referred to their primary physician and managed according to primary care guidelines (Krause et al., 2011). First-line therapy is usually an angiotensin-converting enzyme inhibitor (ACE-I) or angiotensin II receptor blocker (ARB).

Cardiac Arrhythmias

Obesity is associated with diastolic dysfunction and atrial enlargement; both are risk factors for developing atrial fibrillation. In population-based cohort studies, obese individuals are at almost 50 per cent increased risk of developing AF than non-obese individuals (RR 1.49; 95% CI 1.36–1.64)(Wanahita et al., 2008). The likelihood of other cardiac arrhythmias and sudden death is also higher.

If OSA is present, the severity is an independent predictor of the incidence of atrial fibrillation (Cadby et al., 2015). The mechanism may be an increased sympathetic tone associated with recurrent episodes of apnoea and arousal.

Venous Thromboembolism

The relative risk of deep venous thrombosis and pulmonary embolism for obese patients is twice that of non-obese patients. The disparity is greatest for patients less than 40 years (Stein, Beemath and Olson, 2005). Despite this knowledge, pulmonary embolism (PE) remains a leading cause of morbidity and mortality in bariatric centres, with an estimated 2.4 per cent incidence of symptomatic venous thromboembolism and 0.3 per cent incidence of fatal PE (Gould et al., 2012).

Pro-coagulant changes in obesity include enhanced platelet activity, increased circulating pro-coagulants, impaired fibrinolysis and vascular endothelium activation. Obesity related hormones, insulin resistance, chronic inflammation and inactivity are contributing factors (Freeman, 2010).

The co-morbidities known to increase the risk of fatal VTE in bariatric surgery are a past history of VTE, BMI >60 kg/m², central obesity, venous stasis disease and a diagnosis of OSA/OHS (Sapala et al., 2003). Interventions recommended to reduce VTE risk are intermittent pneumatic lower-limb compression devices combined with anticoagulant prophylaxis.

Typical dosing regimens for unfractionated heparin and low molecular weight heparin (LMWH) may under-dose morbidly obese patients. Previous international guidelines recommended thrice-daily UH or twice-daily LMWH dosing (Geerts et al., 2008); however, a recent update recommended seeking pharmacy advice for bariatric dosing (Gould et al., 2012).

Insertion of a vena cava filter preoperatively may be considered in very high-risk patients. This includes obese patients with a history of prior PE, prior iliofemoral DVT, evidence of venous stasis disease, known hypercoagulable state or increased right-sided heart pressures (PAP >40mmHg) (Mechanick et al., 2008).

Predicting Difficult Intubation

It is debatable whether obesity alone increases the likelihood of difficult tracheal intubation. Clinical trials comparing direct laryngoscopy and intubation in obese and normal-weight subjects are conflicting (Brodsky et al., 2002; Juvin et al., 2003). A large cohort study of 91,332 surgical patients concluded a BMI >35 kg/m² was only a weak predictor of difficult and failed intubation (adjusted odds-ratio 1.34; 95% CI 1.19–1.51, P <0.0001) (Lundstrøm et al., 2009).

The best predictors of difficult airway management in obese patients are listed in Table 18.6. Absolute weight, BMI, gender, mouth opening and mandibular recession are not independent predictors of difficult intubation in obese patients, but taken together may assist with airway planning (Juvin et al., 2003). Please see also Chapter 7, page 87.

Predicting Difficult Mask Ventilation

The incidence of difficult mask ventilation (DMV) in surgical populations is 1–2 per cent (Han et al., 2004; Kheterpal et al., 2006). In obese populations, the incidence of DMV is reported as high as 14 per cent (Cattano et al., 2014).

A BMI > 30 kg/m² is the strongest independent predictor of DMV (Kheterpal et al., 2006). It seems that once the threshold BMI of 30 kg/m² is reached, further obesity does not substantially increase the risk (Leoni et al., 2014).

The independent predictors of DMV in obese populations are listed in Table 18.6. Other predictors of DMV from the general literature include male gender, lack of teeth, history of snoring or OSA, neck radiation changes and the presence of a beard (Kheterpal et al., 2006; Langeron et al., 2000).