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May 2005
Volume 69
Number 5

What's New In...

Perioperative Respiratory Strategies for Morbidly Obese Patients

Juraj Sprung, M.D., Ph.D..


orbid obesity (MO) is associated with marked respiratory comorbidities such as restrictive lung disease, obstructive sleep apnea (OSA) and/or pulmonary hypertension. During anesthesia these patients experience large alveolar-to-arterial oxygen gradients requiring higher inspiratory oxygen concentrations to maintain adequate arterial oxygenation (PaO2) compared to normal-weight patients. All these issues may pose a significant challenge for the anesthesiologist.

Approximately 10 percent of MO patients suffer from hypoventilation syndrome,1 while more than 50 percent have moderate to severe sleep apnea.2 Intraoperative use of opioids in these patients may be associated with excessive postoperative respiratory depression. Almost intuitively the use of shorter-acting anesthetics, narcotics or regional techniques would be a desirable approach. A recent prospective, randomized study demonstrated that MO adult patients who underwent major abdominal surgery awoke significantly faster and had higher SpO2 on entry to the postanesthesia care unit after desflurane than after sevoflurane anesthesia.3 Theoretical advantages of using anesthetics with shorter pharmacokinetics properties on postoperative outcomes in MO patients, however, will require more formal studies.

Alternatives to narcotics, such as a2-agonists, have been used for sedation during awake fiberoptic intubation, and because these drugs are free of significant effects on respiratory function, they may be used during the course of anesthesia in MO patients, especially of those who suffer from OSA. An a2-agonist, dexmedetomidine, with sedative/hypnotic, anesthetic-sparing, analgesic and sympatholytic properties, has been approved for sedation in the intensive care unit; however, its role in intraoperative anesthesia practice has not yet been established, although sporadic case reports are being published that suggest its potential usefulness.4

Whether tracheal intubation is more difficult in obese patients is debatable. Juvin et al.5 report a difficult intubation rate of 15.5 percent in obese patients and 2.2 percent in lean patients. None of the risk factors for difficult intubation described in the lean population was satisfactory in obese patients. At the same time, Brodsky et al.6 found that neither obesity nor body mass index predicted problems with tracheal intubation. A high Mallampati score and large neck circumference, however, may increase the potential for difficult laryngoscopy and intubation. A conservative approach is to do fiberoptic intubation in all “questionable airway cases” or after assessment is made that mask ventilation may be difficult providing intubation fails. Having an array of alternative intubating devices readily available (intubating laryngeal mask airway, Bullard Scope, WU Scope, etc.) and an anesthesiologist who is proficient in these less-utilized techniques also makes the decision upon method of tracheal intubation in these patients easier.

Another challenge for anesthesia in MO patients may be intraoperative maintenance of PaO2. MO patients during anesthesia and paralysis experience a larger reduction in lung volume than the normal-weight patients, and this parallels more severe impairment of gas exchange.7-8 Once atelectasis has developed, using of positive end-expiratory pressure (PEEP) may not be sufficient to re-expand the atelectasis. Over the last several decades, different strategies were used to re-expand collapsed lungs during anesthesia in order to “optimize” oxygenation.

Strategy 1: Large tidal volume. By using large tidal volume ventilation, the mean lung volume is intermittently increased above closing volume, which may, at least theoretically, improve PaO2.9 Others10 demonstrated, however, that the strategy of using tidal volumes between 15 and 20 mL/kg ideal body weight has little or no beneficial effect on oxygenation in MO patients. It is possible that due to the intermittent nature of lung inflation despite use of high tidal volume, the collapsed alveolar units did not reopen.

Strategy 2: Use of PEEP. Isolated effects of PEEP on PaO2 during mechanical ventilation in either morbidly obese or normal-weight patients either has no beneficial effect11 or just slightly improves the PaO2.7 Its routine use is therefore not recommended. Application of PEEP early during induction of general anesthesia and before atelectasis develops prevents atelectasis and improves oxygenation in MO patients.12

Strategy 3: Alveolar recruitment maneuver. The physiologic background of the alveolar recruitment strategy lies in the fact that initial pressure needed to open collapsed alveoli during anesthesia is high;13 an “opening pressure” of at least 40 cm H2O is needed to fully reverse anesthesia-induced collapse of healthy lungs in normal-weight patients.14-17 In order to re-expand atelectatic lungs, three conditions need to be met: 1) insufflation pressure needs to exceed alveolar “opening pressure,” 2) pressure needs to be sustained as alveoli may not re-open by using intermittent pressure and 3) open recruitment needs to be followed by higher PEEP in order to maintain alveolar units.13 The recruitment maneuver has now been studied in MO patients by our group (unpublished data). Since MO patients have low respiratory system compliance,8-18 we use higher than usual recruitment pressures achieved by stepwise increase in PEEP up to 20 cm H2O, but at the same time, limiting maximum peak inspiratory pressure to 50 cm H2O. Upon achievement of expected PaO2, the lungs are ventilated with lower tidal volumes at 12 cmH2O of PEEP. This technique appears promising in maintaining excellent intraoperative PaO2.

Upon awakening from anesthesia, tracheal extubation needs to be performed after reaching satisfactory criteria for extubation and after the patient is “fully awake and cooperative.” Regardless of when or which nondepolarizing muscle relaxant was used, a full dose of reversal must always be given. In order to prevent atelectasis in the supine position, we may consider conducting tracheal extubation once the patients are in a semi-sitting position after they are transferred from the operating room table to their hospital bed. In order to prevent development of immediate postextubation hypoxia, uninterrupted administration of oxygen must be continued. Because of the fact that, in most of these patients, oxygenation during sleep (and especially after anesthesia) may be dependent on use of continuous positive airway pressure (CPAP) or bi-level positive airway pressure (Bi-PAP) devices, they should be considered soon after tracheal extubation. During monitored anesthesia care with sedation, one may consider using either CPAP or Bi-PAP instead of nasal cannula. Furthermore patients’ transport to the recovery room should be continuously monitored with pulse oximetry. Based on preoperative conditions and immediate postextubation assessment of respiratory risk, some of these patients may require admission to a telemetry unit for overnight respiratory observation.

Pulmonary embolism is a rare but devastating event. In patients who die after Roux-en-Y gastric bypass, clinically only 20 percent of patients were suspected to have pulmonary emboli; yet at autopsy, 80 percent of patients had pulmonary emboli. Therefore these patients have an unexpectedly high rate of clinically silent pulmonary emboli contributing to morbidity and mortality. Full measures of thromboprophylaxis is mandatory in this patient population.19

Duggan et al.20 have demonstrated in animal models that intraoperative atelectasis may increase pulmonary vascular permeability and that the recruitment maneuvers successfully prevent lung injury associated with hypoxemia caused by protracted atelectasis. While newer lung recruitment strategies — emerging for intraoperative respiratory management of MO patients — efficiently improve intraoperative oxygenation, it remains to be seen if they can improve outcomes and reduce postoperative pulmonary complications. Also more studies are needed to show if the use of shorter-acting anesthetics, narcotics or even neuraxial blockade can reduce postoperative respiratory risks in MO patients.



References:

1. Sugerman HJ. Pulmonary function in morbid obesity. Gastroenterol Clin North Am. 1987; 16:225-237.

2. Resta O, Foschino-Barbaro MP, Legari G, et al. Sleep-related breathing disorders, loud snoring and excessive daytime sleepiness in obese subjects. Int J Obes Relat Metab Disord. 2001; 25:669-675.

3. Strum EM, Szenohradszki J, Kaufman WA, et al. Emergence and recovery characteristics of desflurane versus sevoflurane in morbidly obese adult surgical patients: A prospective, randomized study. Anesth Analg. 2004; 99:1848-1853.

4. Hofer RE, Sprung J, Sarr MG, Wedel DJ. Anesthesia for a patient with morbid obesity using dexmedetomidine without narcotics: [L'anesthesie chez un patient obese morbide avec la dexmedetomidine sans narcotiques]. Can J Anaesth. 2005; 52:176-180.

5. Juvin P, Lavaut E, Dupont H, et al. Difficult tracheal intubation is more common in obese than in lean patients. Anesth Analg. 2003; 97:595-600.

6. Brodsky JB, Lemmens HJ, Brock-Utne JG, et al. Morbid obesity and tracheal intubation. Anesth Analg. 2002; 94:732-736.

7. Pelosi P, Ravagnan I, Giurati G, et al. Positive end-expiratory pressure improves respiratory function in obese but not in normal subjects during anesthesia and paralysis. Anesthesiology. 1999; 91:1221-1231.

8. Sprung J, Whalley D, Falcone T. The effects of tidal volume and respiratory rate on oxygenation and respiratory mechanics during laparoscopy in morbidly obese patients. Anesthesia Analgesia. 2003; 97:268-274.

9. Visick WD, Fairley HB, Hickey RF. The effects of tidal volume and end-expiratory pressure on pulmonary gas exchange during anesthesia. Anesthesiology. 1973; 39:285-290.

10. Bardoczky GI, Yernault JC, Houben JJ, d'Hollander AA. Large tidal volume ventilation does not improve oxygenation in morbidly obese patients during anesthesia. Anesth Analg. 1995; 81:385-388.

11. Salem MR, Dalal FY, Zygmunt MP, et al. Does PEEP improve intraoperative arterial oxygenation in grossly obese patients? Anesthesiology. 1978; 48:280-281.

12. Coussa M, Proietti S, Schnyder P, et al. Prevention of atelectasis formation during the induction of general anesthesia in morbidly obese patients. Anesth Analg. 2004; 98:1491-1495.

13. Lachmann B. Open up the lung and keep the lung open. Intensive Care Med. 1992; 18:319-321.

14. Rothen HU, Sporre B, Engberg G, et al. Re-expansion of atelectasis during general anaesthesia: A computed tomography study. Br J Anaesth. 1993; 71:788-795.

15. Rothen HU, Sporre B, Engberg G, et al. Reexpansion of atelectasis during general anaesthesia may have a prolonged effect. Acta Anaesthesiol Scand. 1995; 39:118-125.

16. Rothen HU, Sporre B, Engberg G, et al. Prevention of atelectasis during general anaesthesia. Lancet. 1995; 345:1387-1391.

17. Rothen HU, Sporre B, Engberg G, et al. Atelectasis and pulmonary shunting during induction of general anaesthesia — Can they be avoided? Acta Anaesthesiol Scand. 1996; 40:524-529.

18. Sprung J, Whalley DG, Falcone T, et al. The impact of morbid obesity, pneumoperitoneum, and posture on respiratory system mechanics and oxygenation during laparoscopy. Anesth Analg. 2002; 94:1345-1350.

19. Melinek J, Livingston E, Cortina G, Fishbein MC. Autopsy findings following gastric bypass surgery for morbid obesity. Arch Pathol Lab Med. 2002; 126:1091-1095.

20. Duggan M, McCaul CL, McNamara PJ, et al. Atelectasis causes vascular leak and lethal right ventricular failure in uninjured rat lungs. Am J Respir Crit Care Med. 2003; 27:27.



    Juraj Sprung, M.D., Ph.D., is Professor of Anesthesiology, Mayo Clinic College of Medicine, Rochester, Minnesota.

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