Airway and pulmonary effects

Obesity imposes a restrictive ventilatory defect on the patient because of weight gain involving the chest wall and because of excessive diaphragmatic loading from abdominal fat, impeding the normal excursion of the diaphragm and significantly increasing the work of breathing. Both of these phenomena contribute to a decrease in pulmonary compliance. However, the major cause of the decrement in pulmonary compliance appears to be due to the increase in pulmonary blood volume. This restriction results in a decrease in total lung capacity and functional residual capacity (FRC), mainly from the loss of expiratory reserve volume. FRC decreases exponentially with increasing BMI, often reaching a point at which closing capacity is greater than FRC during tidal breathing, resulting in increased ventilation/perfusion mismatching in the awake state and increased shunt fraction (s/t) under general anesthesia. At rest, most morbidly obese patients experience only a modest decrease in PaO₂ and maintain PaCO₂ via hyperventilation (low tidal volume, increased respiratory rate). On average, a 1-mm Hg drop in PaO₂ and 1-mm Hg increase in PAO₂ − PaO₂ occur with each additional 10-kg weight gain. These patients tolerate apnea poorly and experience up to a 50% drop in FRC on induction of general anesthesia (vs. 20% in nonobese patients). Reported s/t for this group of patients undergoing general anesthesia can reach 10% to 25%, versus the normal 2% to 5%. The expanded pulmonary blood volume and loss of FRC also increase pulmonary vascular resistance, which then also contributes to the increased work of breathing. This loss of FRC can also accelerate the rate of uptake of inhalation anesthetic agents (shorter time constant in the lungs).

Airway anatomy becomes distorted and airway, management becomes more challenging for the anesthesia provider as the patient’s level of obesity becomes more extreme. Patients may have enlarged face and cheeks, large tongue, impaired mouth opening and cervical range of motion, increasing soft tissue encroachment in the palate and pharynx, short neck, and large breasts, all of which may contribute to difficult mask ventilation, difficult direct laryngoscopy, or difficult intubation. Difficult mask ventilation has been reported to occur in up to one third of morbidly obese patients. Although older literature has suggested an incidence of difficult intubation as high as 30% in these patients, more recent prospective trials document that, in general, this is not the case and that the only two variables that appear predictive of difficulty intubating patients in this population are an increased neck circumference and a Mallampati score of 3 or more.

As BMI exceeds 30 kg/m², the risk of a patient having obstructive sleep apnea increases. This syndrome is due to the normal reduction in upper airway tone seen during stage 4 and rapid eye movement sleep. The excessive deposition of soft tissue in the upper airway in the obese individual accentuates this tendency and can result in periodic obstruction of the airway during sleep. Obstructive sleep apnea consists of both apneas and hypopneas and is best delineated via formal sleep evaluations with polysomnography. For more information on this topic, see Chapter 108, Obstructive Sleep Apnea.

With progressive worsening of obstructive sleep apnea, desensitization of breathing control can evolve, resulting in degrees of chronic hypoxemia and hypercarbia. Up to 50% of individuals with a BMI greater than 50 kg/m² have evidence of daytime hypoventilation. Eventual physiologic changes develop that consist of secondary polycythemia, pulmonary hypertension, and right ventricular failure. This apnea hypoventilation syndrome has also been referred to as the pickwickian syndrome, although the term is no longer in use.

Gastrointestinal and hepatic effects

Study results have suggested that the obese patient is at increased risk of aspiration due to higher residual gastric volumes and lower gastric pH. However, recent studies have questioned these conclusions, indicating no greater increased aspiration risk per se. Obese individuals have normal or accelerated rates of gastric clearance, and the incidence of gastric reflux does not differ significantly from that of the general population. However, difficult airway management by mask may predispose some to an increased aspiration risk.

Short of significant liver dysfunction due to obesity (nonalcoholic steatohepatitis with cirrhosis), there is no evidence of impaired hepatic function in individuals with morbid obesity. Neither is there any proven greater tendency to inhalation agent–induced hepatitis.

Neurologic effects

Morbidly obese individuals have a significantly higher incidence of incurring positioning injuries involving the brachial plexus, sciatic nerve, and ulnar nerve. Special care needs to be exerted to achieve proper protection of these structures. Additionally, this population is at increased risk of developing decubiti with prolonged pressure under anesthesia.

Intraoperative anesthetic techniques

Modification of the anesthetic technique is necessary to minimize complications related to obesity. Because of physical limitations imposed by the patient’s girth, the anesthesia provider should ensure that proper “ramping” of the patient has been performed, such that the sternal notch is parallel to the angle of the mandible (Figure 163-1). This facilitates alignment of the intraoral axes for intubation. If a history of or major concerns regarding difficult intubation exist, awake fiberoptic intubation may be a reasonable option. Preoxygenation for 3 to 5 min with the patient in a mild reverse Trendelenburg position while using 10 cm H₂O of continuous positive airway pressure plus 10 cm H₂O of peak end-expiratory pressure with mask ventilation has been shown to significantly mitigate the initial drop in FRC on induction and to prolong time to desaturation. Appropriately sized oral and nasal airways should be available and used to maintain airway patency. An inability to use a mask should always be anticipated. The use of an intubating laryngeal mask airway can be highly effective in achieving successful airway maintenance when conventional mask techniques have failed.

Intraoperatively, alveolar recruitment using titrated peak end-expiratory pressure and some degree of head-up (beach-chair) positioning should be maintained. This is especially true when the operation requires introduction of a pneumoperitoneum. This technique has been proved to be more effective than the use of large tidal volume ventilation. Judicious use of colloids should be employed to maintain intravascular volume and prevent negative hemodynamic effects of excess peak end-expiratory pressure. Because of the mechanical limitations on the respiratory system and the increased sensitivity of morbidly obese patients to the effects of sedatives, opioids, and inhalation agents, spontaneous ventilation should not be used in these patients.

There is no evidence to support the use of one inhalation agent over another. Emergence times are essentially similar, especially when the agents are used in conjunction with processed electroencephalographic monitoring. The use of N₂O should be avoided, especially in the setting of pulmonary hypertension.

The dosing of intravenously administered anesthetic agents varies with lipid and solvent solubility. Lean body mass (ideal body weight + 20%) is a good estimate for determining the dose of hydrophilic drugs, such as nondepolarizing neuromuscular blocking agents, as well as remifentanil that, although lipid soluble, behaves similarly in obese and nonobese individuals. The dose of lipid-soluble drugs and succinylcholine (increased plasma cholinesterase activity) should be based on the patient’s current total body weight.

The use of multimodal analgesic agents that mitigate the use of opioids should be considered. The use of nonsteroidal anti-inflammatory agents, COX-2 inhibitors, intravenously administered lidocaine infusions, and subanesthetic doses of ketamine all help to prevent additive respiratory depression. Additionally, a marked sparing of the use of opioidergic agents without respiratory inhibition has been shown with the use of intraoperative and postoperative dexmedetomidine infusions.

Emergence from anesthesia

The inhalation agent should be titrated at the end of the operation to allow prompt emergence and return of airway reflexes and tone. Continuous monitoring of neuromuscular function to enable complete reversal of blockade at the conclusion of the operation is of paramount importance. The patient should be returned to the reverse Trendelenburg position if this position was not employed during the operation. Obese patients should be extubated when they are capable of maintaining a spontaneous airway with adequate tidal volume. The use of continuous positive airway pressure should be reinstituted as soon as possible.

Regional anesthesia

Regional anesthesia is more difficult to perform in the morbidly obese patient. Landmarks are obscured, increasing the number of attempts and the potential for complications. Nonetheless, a properly performed regional blockade (peripheral or neuraxial) circumvents many of the negative respiratory and hemodynamic effects of general anesthesia. The use of ultrasound guidance for both peripheral and neuraxial blocks can markedly enhance success and accuracy.

Determining the proper doses of local anesthetic agents is more unpredictable for neuraxial blocks because morbidly obese patients have smaller cerebrospinal fluid and epidural volumes because of venous epidural engorgement and potential epidural lipomatosis. The correct dose may be decreased by as much as 20% from normal. To avoid the potentially disastrous effects of an unintended high intrathecal block, consider using a combined spinal-epidural technique, which allows more conservative intrathecal dosing with the option to augment levels via an epidural catheter.