Obesity’s impact on respiratory function (Table
2) is inversely related to BMI, with significant impairment observed once BMI exceeds 45 [
53]. Consistent with restrictive physiology, the pattern of distribution of excess weight - central vs. peripheral - is more consequential than BMI
per se. For further discussion, the reader is referred to the BMC Anesthesiology article by Fernandez-Bustamante
et al. [
54].
Table 2
Respiratory changes with obesity [
119‐
124]
Work of breathing (WOB) | Increased |
Functional residual capacity (FRC) | Decreased |
Expiratory reserve volume (ERV) | Decreased |
Total lung capacity (TLC) | Unchanged, though decreased in severe obesity |
Vital capacity (VC) | Decreased |
Forced expiratory volume in 1 s (FEV1) | Unchanged, though decreased in severe obesity |
Forced vital capacity (FVC) | Unchanged, though decreased in severe obesity |
FEV1/FVC | Unchanged, though decreased in severe obesity |
Diffusing capacity of the lung for carbon monoxide (DLCO) | Unchanged in simple obesity |
Obstructive sleep apnea
Magnetic resonance imaging studies confirm that pharyngeal structures (from the nasopharynx to the laryngopharynx) increase in size with deposition of adipose tissue [
55]. Additionally, King
et al. have documented a reduction in airway caliber (increase in airway resistance) with increasing weight [
56]. These changes in pharyngeal shape are associated with impairment of pharyngeal dilator activity and an increased risk of airway collapse [
57]. Although obstruction may occur at any point in the pharynx, it is most frequently observed in either the retropalatal and/or the retroglossal regions [
57].
Obstructive sleep apnea (OSA), a sleep-related breathing disorder, is estimated to affect between 40 % and 90 % of obese individuals [
57]. It is characterized by periodic reduction or cessation of breathing due to narrowing of the upper airways during sleep. Factors linking obesity and OSA include anatomical imbalance from excess upper airway fat deposition, changes in upper airway muscle tone [
58,
59], as well as alterations in the control of ventilation [
60]. Furthermore, OSA itself leads to changes that contribute to the development of obesity: decreased energy level, motivation, sleep fragmentation
etc. While the majority of individuals with severe obesity are able to maintain eucapnia, a significant minority will develop obesity hypoventilation syndrome (OHS), characterized by alveolar hypoventilation (PaCO
2 > 45 mmHg) unexplained by other disorders [
61,
62].
OSA can negatively affect perioperative outcome. The Longitudinal Assessment of Bariatric Surgery (LABS) study found that a history of OSA was significantly associated with a composite endpoint of death, VTE, reintervention, or failure to be discharged by 30 days after surgery [
63]. However, preoperative intervention may reverse this impact. Weingarten
et al. did not find an association between OSA and postoperative respiratory, cardiac, or surgical complications in affected patients who were treated preoperatively with continuous positive airway pressure (CPAP) or bi-level positive airway pressure (biPAP) for several weeks to months and were monitored with pulse oximetry postoperatively [
64].
As OSA is often undiagnosed, routine polysomnography (PSG) for patients undergoing bariatric surgery has been recommended [
32,
65]. Though this test is the gold standard for diagnosis, it is costly and time-consuming. Furthermore, whether or not routine screening improves safety and outcomes is debatable. A study of 1,058,710 patients undergoing elective orthopedic, abdominal, prostate, and cardiovascular surgery found that sleep-disordered breathing (SDB) was not associated with a clinically significant increase in in-hospital mortality, length of stay or total charges [
66]. However, patients with SDB were more likely to have cardiopulmonary complications such as AF, respiratory failure, emergency intubation, as well as non-invasive and mechanical ventilation.
A protocol for the evaluation of patients at risk for OSA is an integral component of the preoperative assessment of the obese [
67]. Questions regarding snoring, apneic episodes, frequent arousals during sleep, morning headaches, and daytime somnolence should be explored. The physical examination should include an evaluation of the airway, neck circumference, tongue size and volume, and nasopharyngeal characteristics. Despite varying sensitivities and specificities, tools such as the STOP-Bang questionnaire [
68], Epsworth Sleepness Scale [
69] or the Berlin questionnaire [
70] can facilitate the OSA screening process. The STOP-Bang questionnaire (Table
3) [
68], developed specifically for use in surgical patients, has been validated in patients with a BMI > 30 [
71]. In the obese, a STOP-Bang score of ≥ 3 has a sensitivity of 90.5 % for detecting OSA with a positive predictive value of 84.8 %. A score of ≥ 5 is associated with a sensitivity of 53 % and a specificity of 70.2 % for predicting moderate/severe OSA (defined as an apnea-hypopnea index [AHI] >15) and a sensitivity of 68.8 % and a specificity of 68.7 % for predicting severe OSA (AHI > 30).
Table 3
STOP-BANG questionnaire
Snoring | Do you Snore Loudly? |
Tired | Do you often feel Tired, Fatigued, or Sleepy during the daytime? |
Observed | Has anyone Observed you Stop Breathing or Choking/Gasping during your sleep? |
Pressure | Do you have or are you being treated for High Blood Pressure? |
Body Mass Index | BMI > 35 kg/m
2
|
Age | Age > 50 years |
Neck Circumference | Shirt collar > 17 in/43 cm for males |
Shirt collar > 16 in/41 cm for females |
Gender | Gender = male |
Table 4
Major obesity-related conditions and pertinent studies
Cardiovascular | | • ECG if cardiac disease is suspected |
| Coronary artery disease | • Use validated tools to estimate risk of perioperative MACE |
• If risk of MACE ≥ 1 % and functional status is poor, consider stress testing |
| Pulmonary hypertension | • Consider right ventricular hypertrophy, pulmonary hypertension if ECG shows right axis deviation, right bundle branch block |
• Echocardiogram to assess right and left ventricular function & morphology, valvular morphology, estimate pulmonary artery pressure |
• Right heart catherization |
| Congestive heart failure | • Chest radiograph |
• Echocardiogram |
Respiratory | | |
| Dyspnea | • Chest radiograph |
| Asthma | • Pulmonary function testing not recommended for routine screening |
| Obstructive sleep apnea | • Screen for OSA with history, physical exam, validated screening questionnaire |
• Consider polysomnogram |
• Consider initiating CPAP/biPAP preoperatively |
| Hypoventilation syndrome | • Arterial blood gas |
Gastrointestinal | | |
| GERD | • Upper endoscopy |
• 24-h pH monitoring |
• Esophageal manometry |
• Barium swallow (upper gastrointestinal series) |
| NAFLD | • Liver function tests (LFTs) |
• Triglyceride level |
• Liver ultrasound if LFTs elevated or symptomatic biliary disease |
| H. Pylori | • Stool antigen test |
• Urea breath test |
• Endoscopy – rapid urease test |
Endocrine | | |
| Diabetes mellitus | • Measure Hgb A1c |
• Optimize glycemic control |
Hematologic | | |
| VTE | • Assess VTE risk: degree of obesity, age, history of previous DVT or hypercoagulable state, history of malignancy, immobility |
Psychologic | | • Psychosocial-behavioral evaluation |
| Depression / anxiety | • Identify patients at risk for suicide |
| Binge eating disorder | |
Nutritional | | • Iron studies, B12, folate, 25-hydroxyvitamin D |
• Electrolytes, calcium, magnesium, phosphate levels |
When clinical screening identifies a patient as potentially having OSA, the decision whether to manage him clinically preoperatively or to obtain sleep studies and initiate OSA treatment prior to surgery should take into account the severity of OSA (based on clinical indicators or sleep study results), the invasiveness of the planned procedure, and the estimated postoperative narcotic requirement [
67]. A recent Cochrane review found no evidence that CPAP reduces postoperative mortality; however, it may offer benefit in preventing pneumonia, reducing atelectasis, and lowering the risk of reintubation [
72]. While studying the incidence of serious postoperative complications (e.g. cardiac events) in OSA patients, Gupta
et al. found a lower incidence in those treated with preoperative CPAP than in the untreated group [
73]. In a recent trial, OSA patients treated with CPAP for a 12-week period showed a reduction in mean arterial pressure whereas those who received only nocturnal supplemental oxygen or education did not [
74]. Despite insufficient data to conclusively establish the benefits of pre- and postoperative CPAP, the American Society of Anesthesiologists (ASA) [
67] recommends considering the perioperative initiation of CPAP, particularly if OSA is severe. In patients already treated with CPAP or non-invasive positive pressure ventilation (NIPPV), this treatment should be continued into the postoperative period unless contraindicated [
67].
Pulmonary hypertension
Obese patients have multiple risk factors for developing pulmonary hypertension (PH) such as OSA, OHS, left heart dysfunction, and chronic pulmonary thromboembolism. Patients with PH are at increased risk for morbidity and mortality with anesthesia and surgery. Kaw
et al. reported that 26 % of patients with PH (defined as a mean pulmonary artery pressure of > 25 mmHg) experienced postoperative morbidity or mortality as compared to a 2.6 % complication rate in patients without PH. Compared to controls, patients with PH had a significantly higher risk of developing congestive heart failure, respiratory failure, hemodynamic instability and sepsis. Factors associated with increased risk of complications included poor functional status (New York Heart Association functional class ≥ II), history of pulmonary embolism, OSA, and surgical complexity [
77]. Other risk factors included longer time under anesthesia (>3 h) and intraoperative vasopressor use.
Patients with PH should have a preoperative ECG, chest radiograph, and an echocardiogram to assess ventricular and valvular structure and function. Right-sided heart catheterization is indicated for patients with pulmonary arterial hypertension [
78]. The data should be reviewed for characterization of pulmonary hemodynamics (pulmonary artery pressures, pulmonary vascular resistance), cardiac output (looking for signs of right heart failure), and response to vasodilator therapy [
79]. Other guidelines for perioperative management include continuing baseline pulmonary vascular targeted therapy (i.e. phosphodiesterase type 5 inhibitors, soluble guanylate cyclase stimulators, endothelin receptor antagonists, and prostanoids) [
38]. Preoperative evaluation by a PH specialist can be invaluable in optimizing the patient’s condition prior to surgery and anesthesia.