Illustration of (L) chronic co-morbidities associated with the obese patient and (R) the acute perioperative concerns important to the anesthetic management of the obese patient.
Obesity affects every organ system. Cardiovascular diseases include coronary artery disease, sudden cardiac death, obesity-related cardiomyopathy, hypertension, hyperlipidemia, and right-sided heart failure (cor pulmonale).[4,5] Pulmonary diseases include restrictive lung disease, obstructive sleep apnea (OSA), obesity hypoventilation syndrome (OHS)[5] and decreased residual lung volume.[4] Gastrointestinal diseases include hiatal hernia[4,5] and gastro esophageal reflux (GERD).[5] The most common endocrine disease is diabetes mellitus type II (DMII).[4] Musculoskeletal diseases include osteoarthritis of the weight-bearing joints and chronic back pain.[4,5] (See Table 47.1.) An increased incidence of postoperative complications detectable among obese surgical patients compared with lean controls includes myocardial infarction, peripheral nerve injury, wound infection, and urinary tract infection.[5] An increased incidence of difficult airway management in the perioperative period is controversial, with conflicting data in the medical literature.[5,6]
| Organ system | Disease | Potential postoperative complications |
|---|---|---|
| Cardiovascular |
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| Pulmonary |
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| Gastrointestinal |
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| Endocrine |
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| Musculoskeletal |
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Pulmonary complications
Obstructive sleep apnea: The prevalence of OSA is 5% among morbidly obese patients.[7] The incidence of OSA is 12 to 30-fold higher than in the general population.[8] OSA is defined as frequent episodes of apnea or hypopnea during sleep (apnea being greater than 10 seconds of cessation of airflow despite continuous effort against a closed glottis).[9] OSA may be associated with daytime somnolence and snoring, but definitive diagnosis can only be made by an overnight sleep study.[9] The morbidly obese patient is at risk for OSA owing to the anatomical and physiological changes associated with obesity: BMI >30 kg/m2, collar size >16.5 inches, and increased soft tissue surrounding the trachea.[8] OSA causes physiological changes such as hypoxemia and hypercapnia as well as pulmonary and systemic vasoconstriction leading to subsequent development of pulmonary and systemic hypertension.[5] The presence of OSA for patients undergoing total hip and knee arthroplasty increases the incidence of airway and pulmonary complications requiring Intensive Care Unit (ICU) admission and the length of inpatient hospitalization.[10]
Obesity hypoventilation syndrome: OHS is similar to but distinct from OSA. While the OSA patient is only hypercapneic while asleep, the OHS patient is hypercapneic at rest and while awake. OHS is defined as episodes of apnea without respiratory effort or “central apnea.”[5] The pathogenesis of obesity hypoventilation remains unclear but it is accepted that these patients have a decrease in central nervous system control of respiratory drive from hypercapnia and have an increasing reliance on hypoxemia as respiratory drive.[5,11] The hallmark used to differentiate OHS from OSA is the lack of respiratory effort against a closed glottis seen during periods of apnea in the OSA patient. The patient with OHS will desaturate, become hypoxic, and will have no physiological respiratory drive to mitigate the effect. A severe form of OHS is “Pickwickian syndrome,” characterized by obesity, hypersomnolence, hypoxia, hypercapnia, right ventricular failure, and polycythemia.[5,12]
The obese patient has impaired gas exchange secondary to mass loading on the thorax and abdomen. Implications of the excess mass means a significant reduction in functional residual capacity (FRC), expiratory reserve volume (ERV), and total lung capacity (TLC).[5] FRC decreases exponentially with increasing BMI. A decreased FRC leads to significant pulmonary complications such as ventilation–perfusion mismatch, right-to-left shunting, and arterial hypoxemia.[5] Anesthesia compounds the insufficiency. Data shows the FRC to be reduced by 20% in the non-anesthetized obese patient, and further reduced by 50% in the anesthetized patient.[13]
The obese patient is at risk for gas exchange abnormalities. The supine position of the obese patient under anesthesia leads to additional anatomical complications; increased work of breathing, increased carbon dioxide production, decreased compliance, and increased lung resistance.[5]
The post-anesthesia obese patient is potentially at risk for one or more of the above complications. Clinical guidelines have been developed for the obese patient with OSA:[5,13]
1. Identify OSA early;
2. Use continuous positive airway pressure (CPAP) postoperatively;
3. Anesthetic of choice is regional;
4. Judicious reversal of neuromuscular blockade;
5. Awake tracheal extubation following general anesthesia (if difficult airway);
Guidelines for the obese patient with OHS have not been developed, and the clinician must rely heavily on clinical judgment. Special attention to analgesia is prudent for patients with both obesity and OHS as increased sensitivity to opioid medications may have a profound impact upon ventilation.
After general anesthesia, to mitigate pulmonary complications in the morbidly obese patient, the following recommendations can be made:[4,5]
1. Always transport the patient sitting up at a 45-degree angle with oxygen.
2. Once in the PACU, respiratory rate and oxygen saturation should be monitored vigilantly, and opioid medication should be administered cautiously.[4,5]
3. Appropriate communication when transferring care to a PACU nurse or anesthesiologist should include documentation and communication of reversal of neuromuscular blockade; neostigmine/glycopyrrolate dosing and response.
4. Morbidly obese patients with significant co-morbid cardiopulmonary disease could potentially benefit from prolonged mechanical ventilation.[5]
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