- Email: [email protected]
Postoperative Hypoxemia: Common, Undetected, and Unsuspected After Bariatric Surgery1
Journal of Surgical Research 159, 622–626 (2010) doi:10.1016/j.jss.2009.09.003
ASSOCIATION FOR ACADEMIC SURGERY Postoperative Hypoxemia: Common, Undetected, and Unsuspected After Bariatric Surgery1 Scott F. Gallagher, M.D., F.A.C.S.,*,2 Krista L. Haines, M.A.,* Lynette G. Osterlund, M.D.,* Matt Mullen, B.S.,* and John B. Downs, M.D., F.C.C.M., F.C.C.P.† *Department of Surgery, USF Health, University of South Florida College of Medicine, Tampa, Florida; and †Department of Anesthesiology, University of Florida College of Medicine, Gainesville, Florida Submitted for publication July 9, 2009
Background. Patients undergoing gastric bypass are at greater than ordinary risk for postoperative respiratory insufficiency, presumably related to obstructive sleep apnea (OSA) and patient-controlled analgesia (PCA). This study was proposed to quantify the magnitude of the problem. Methods. Fifteen patients undergoing gastric bypass had oxygen saturation (SpO2) recorded continuously, but not displayed, for 24h postoperatively; eight also had arterial blood analysis every 4h. All received narcotic PCA. SpO2 < 90% lasting more than 10 s was reviewed. Results are mean ± SEM. Results. Mean age was 44 ± 4 y, and mean BMI was 48 ± 2kg/m2; 77% had OSA. Every patient had more than one episode with SpO2 < 90% for longer than 30s undetected by routine monitoring; most had multiple episodes. Nadir SpO2 averaged 75% ± 8%. Mean longest duration of desaturation below 90% averaged 21 ± 15min. Mean PaCO2 was 37 ± 3mm Hg; maximum PaCO2 was 47mm Hg. Conclusions. Severe and prolonged episodes of hypoxemia were a consistent finding, despite aggressive preoperative diagnosis and treatment of OSA, including use of CPAP postoperatively. Although some postoperative hypoventilation was expected, the degree and frequency of desaturation were surprising. No patient exhibited arterial PaCO2 evidence of hypoventilation. No patient experienced cardiopulmonary arrest/instability, in spite of severe, repeated episodes of hypoxemia. In no instance was a significant hypoxemic 1 Presented at the 2008 Association for Academic Surgery–Academic Surgical Congress in Huntington Beach, CA, and published as an abstract in the Journal of Surgical Research, 2008;144:370. 2 To whom correspondence and reprint requests should be addressed at Department of Surgery, USF Health, University of South Florida College of Medicine, 1 Tampa General Circle, Suite F145, Tampa, FL 33606. E-mail: [email protected].
0022-4804/09 $36.00 Ó 2010 Elsevier Inc. All rights reserved.
episode suspected or detected. Continuous pulse oximetry monitoring, with an audible alarm set for a saturation less than 90% for 10 s, would have alerted providers to 100% of significant hypoxemic episodes. Our recommendation is routinely monitoring (with alarm capability enabled) every bariatric surgical patient, to prevent such occurrence. Ó 2010 Elsevier Inc. All rights reserved. Key Words: hypoxemia; hypoventilation; obesity; gastric bypass; bariatric surgery; obstructive sleep apnea; postoperative; pulse oximetry.
INTRODUCTION
Obesity has grown to epidemic proportions in this country. The National Health and Nutrition Examination Survey revealed that at least one-third of the population is obese, i.e., exceed their ideal body weights by more than 20% [1]. Bariatric surgery for clinically significant obesity is common. Postoperatively, these patients present a higher risk for respiratory complications than the normal weight population [2–4]. One such complication is hypoventilation, defined by decreased minute ventilation as a result of decreased rate and/or depth of respiration. Extremely obese individuals may exhibit evidence of chronic hypoventilation with mild hypercarbia in the resting, preoperative state [5, 6]. Postoperatively patients are at risk for hypoventilation secondary to respiratory depression and/or the inability to maintain an adequate airway [7, 8]. Respiratory depression may stem from impaired respiratory drive from residual volatile anesthetics, sedatives, or opioid analgesics [9]. Inadequate airway maintenance may develop due to decreased muscle tone from muscle relaxants, incomplete neuromuscular blockade
622
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reversal, or blunted airway reflexes. Poor positioning, reduced thoracic compliance, the supine position, obstruction due to secretions or mucous plugs, and bronchospasm are additional factors that can contribute to full or partial airway obstruction and produce acute hypoventilation and/or arterial hypoxemia that place the obese patient at significant risk for pulmonary issues, ventilatory failure, and hypoventilation. The obese individual may be at further pulmonary risk from coexisting obstructive sleep apnea (OSA) [10]. This syndrome is an abnormality of respiratory mechanics during sleep in which full or partial upper airway obstruction occurs repeatedly, predisposing the patient to frequent episodes of acute hypoventilation and hypoxemia [11]. Sleep apnea is quite common in the obese population. Indeed, the gastric bypass surgery patient population at our institution demonstrates an OSA prevalence of at least 60% [12–14]. The incidence of hypoventilation in a large population given general anesthesia has been reported as 0.2%, with obesity noted as a risk factor for the development of this condition [15]. The actual incidence of hypoventilation in that obese subset was not reported. Thus, the incidence of postoperative hypoventilation in the obese, particularly in patients with clinically significant obesity (BMI > 35%), has not been well documented in the literature. We undertook this investigation to determine how often and to what degree hypoventilation occurs in patients with clinically significant obesity immediately after undergoing the same operation (gastric bypass). Further, we wished to determine the postoperative incidence of arterial hypoxemia caused by acute airway occlusion in this population. METHODS This is a prospective, double blind, single-center pilot study of 15 patients undergoing elective Roux-en-Y bypass (RYGB). All patients who qualify for bariatric surgery at this institution are screened for obstructive sleep apnea (OSA) using Epworth Sleepiness Scale (ESS) as part of their preoperative evaluation. The ESS is a validated screening tool for daytime sleepiness and somnolence [16]; patients scoring 6 on the ESS were referred for consultation with a pulmonologist and subsequently for standard polysomnography and CPAP titration [12, 13]. After hospital administrative review and University of South Florida Internal Review Board (IRB) approval, patients scheduled to undergo RYGB were interviewed to determine willingness to participate in this study; procedures followed were in accordance with the ethical standards of the committee on human experimentation at both institutions, and the study is registered at clinicaltrials.gov as required. Patients provided written informed consent to participate in the study, if the following inclusion criteria were met: 18 to 65 y of age, with clinically significant obesity (BMI from 40– 85 kg/m2), and qualified as Physical Status Classification American Society of Anesthesiologists (ASA) no greater than III. The first eight patients were dually-assessed for hypoventilation by arterial blood analysis preoperatively (baseline) before any sedatives were administered, postoperatively within one-half h after arrival to the post-anesthesia care unit (PACU), and then every 4 h for the first 24 h after surgery. Arterial blood samples (3 mL each) were collected
from a radial artery catheter placed preoperatively and maintained for the initial 24 h postoperative period. In accordance with agreements made with the Hospital and IRB committee, a physician remained at the bedside of patients with in-dwelling arterial catheters during the entire 24 h postoperative duration of the study after leaving the PACU. Every attempt was made to not disturb sleeping patients during arterial blood sampling. The patients’ SpO2 and heart rate were monitored continuously in the preoperative holding area, in the operating room, and in the PACU by conventional as well as the study pulse oximeter (N600; Nellcor Puritan Bennett LLC; Boulder, CO); only study monitors (blinded and silenced) were in place continuously on the floor. Patients at our institution are not routinely monitored with continuous oximetry in the 24-h period following their operation. Continuous oximetry is used in the post-anesthesia care unit; however, routine monitoring used when patients go to the floor is per hospital policy (spot check pulse oximetry and vitals are done every hour for 2 h, every 2 h for 4 h, then every 4 h until discharge, unless otherwise ordered or specified). The portable study pulse oximeter supplied continuous 24-h monitoring and data storage without display of SpO2 data, which was recorded and stored in the machine every 4 s. The SpO2 data from the study oximeter were blinded and inaccessible until downloaded with proprietary software (Profox; Escondido, CA) at the conclusion of the study period. All oximeter data were reviewed for SpO2 < 90%, for >10 s and for >30 s; to account for possible artifact, only data that included heart rate and oxygen saturation simultaneously were included. Results are reported as mean 6 SEM.
RESULTS
Fifteen patients consented to the study; for the safety of one patient, the blinded/study ABG results were revealed to the clinical care providers in the recovery room, so this patient was not included in the analysis since the blinded study ABG was used to guide, and clearly influenced, patient care [17]. All (14) patients underwent laparoscopic operations and completed the study; but only several minutes out of 24 h of data were recovered from the study machine of another patient, leaving 13 patients for analysis. Mean age was 44 6 4 years, 84% were female, and mean BMI was 48 6 2 kg/m2. Most (77%) had sleep study confirmed OSA prior to participation in this study (Table 1). Of the 10 patients preoperatively diagnosed with OSA, seven patients were treated with CPAP (9 6 1 cm H2O); one was treated with BiPAP (12/8 cm H20). All eight patients diagnosed with obstructive sleep apnea used CPAP/BIPAP preoperatively and used CPAP/ TABLE 1 Demographics and Patient Characteristics
n Age (years) Male Female BMI (kg/m2) OSA
Study patients
Comparable bariatric patients with ESS > 6
13 44 6 4 16% 84% 48 6 2 77%
349 45 6 1 20% 80% 52 6 1 83%
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was 47 mmHg. Many patients were snoring while arterial blood samples were drawn; no episodes of apnea were observed by the monitor or recorded.
DISCUSSION
FIG. 1. Illustrates a 30-min time period in one patient with three separate episodes of desaturation (SpO2 < 90%). Of particular note, the rapidity with which oxygen saturation (SpO2) can fall is quite significant.
BIPAP postoperatively, usually their own machine; unfortunately, the hospital records and patient charts do not indicate precise times or duration of usage with any consistency. Postoperatively, four patients breathed room air and nine received supplemental oxygen, with two concurrently through the CPAP machines. Analysis of the data revealed that hypoxemia occurred in every patient, including those who received supplemental oxygen. Every patient (100%) had more than one episode of significant desaturation (SpO2 < 90%) lasting more than 30 s, which was otherwise undetected by routine monitoring; an example is shown in Fig. 1. Most patients had multiple similar episodes of prolonged desaturation. Nadir SpO2 averaged 75% 6 8%, and the mean longest duration of saturation below 90% was 21 6 15 min for each patient. The mean time with SpO2 < 90% was 165 6 49 min (median ¼ 114 min with SpO2 < 90%, range 1–555 min with SpO2 < 90%). There were five patients with less than 10 min with SpO2 < 90% during the entire 24 h (1, 3, 3, 3, and 8 min). For the remaining patients, the mean time with SpO2 < 90% was 266 6 54 min (median ¼ 231 min with SpO2 < 90%, range 95–555 min with SpO2 < 90%). The mean percentage of time during the 24 h study period with SpO2 < 90% was 18% 6 4% (median time ¼ 16% with SpO2 < 90%, range 7%–38% with SpO2 < 90%). Per patient, the mean total number of events with SpO2 < 90% for longer than 10 s was 112 6 34 (range 3–429 events). The mean total number of events with SpO2 < 90% for longer than 30 s was 62 6 16 (range 2–184 events). This degree of arterial hypoxemia was unappreciated clinically in every patient. In the six patients with an arterial catheter, arterial blood analyses revealed a mean postoperative PaCO2 value of 37 6 4 mmHg, and the highest PaCO2 value measured for any patient
While most of the patients had OSA diagnosed and treated preoperatively for at least 6 wk, all of the patients experienced more than one episode of desaturation in the first 24 h postoperatively with SpO2 < 90% for more than 30 s. Even more significant was the fact that the mean longest duration of desaturation for each patient lasted more than 21 min. The bariatric surgical population is known to be at high risk for respiratory complications in the postoperative period. Significant attention and resources are dedicated to minimize the risk of complications. These complications can be severe and even life-threatening [17]. In fact, they can be fatal. The study population is very similar to the other gastric bypass patients operated on at this Surgical Review Corporation designated Bariatric Surgery Center of Excellence, including mean age, demographics, sex, and those with OSA, as shown in Table 1 [14, 17]. We consider the observed average desaturation nadir of 75% a very clinically significant finding. A concern to us is that each of these events was otherwise clinically unsuspected; moreover, there were multiple, recurrent episodes despite use of CPAP and supplemental oxygen. All of the patients were monitored by continuous pulse oximetry in the PACU and then with the measurement of vital signs on the ward with no oxygen desaturation detected, including review of nursing records, which lack documentation of any desaturation episodes. Perhaps the transient nature of the episodes caused the lack of appreciation of their significance, assuming that they were even detected clinically. This study is the first investigation to report 100% of patients with significant periods of arterial hypoxemia, despite aggressive diagnosis and treatment of obstructive sleep apnea in the preoperative and perioperative period [14]. All patients with OSA were required to bring their own CPAP machine and use it postoperatively, per preprinted gastric bypass orders. If the patient’s CPAP machine was unavailable, one was provided. Hypoxemic episodes occurred despite supplemental oxygen administration in some patients. The degree of desaturation may have been decreased, at least temporarily, by supplementing inspired oxygen; however, these patients still experienced significant durations of oxygen desaturation similar to the room air patient’s mean nadir saturation of 75%, even while on supplemental oxygen. The route of delivery and flow rate of oxygen were variable and determined by the
GALLAGHER ET AL.: POSTOP HYPOXEMIA HYPOVENTILATION AFTER GASTRIC BYPASS
clinician. Although ordered routinely, it is possible that oxygen supplementation was inconsistent; however, our data confirm that supplementation of inspired oxygen alone is not reliable for preventing significant hypoxemic episodes. Reduction in functional residual capacity (FRC) routinely accompanies induction of general anesthesia and causes atelectasis [18, 19]. Merely assuming the supine position causes up to a 20% reduction in FRC, observed in normal subjects [20]. This reduction in FRC stems from compression atelectasis and is accentuated in obese individuals [21]. Supine positioning of the obese individual causes significant cephalad displacement of the diaphragm and reduced thoracic compliance; this creates a restrictive ventilatory defect, further increasing the potential for atelectasis formation [22]. Obese patients demonstrate lower resting lung volumes compared with normal individuals. Functional residual capacity, vital capacity (VC), and total lung capacity (TLC) are all reduced, although closing capacity (CC) usually is normal [23]. Thus, any condition that further lowers FRC, such as the supine position or general anesthesia, may alter the favorable relationship between FRC and CC, even during normal tidal ventilation, leading to collapse of small airways and atelectasis. Mismatching of ventilation and pulmonary perfusion (V/Q mismatch) is a common cause of postoperative arterial hypoxemia. Acute airway occlusion results in rapid arterial oxygen desaturation and rapid recovery with relief of the obstruction. In contrast, prolonged hypoventilation will result in a much slower desaturation and recovery. For example, as PaCO2 climbs from 40 to 80 mmHg, the PaO2 will decrease gradually and recovery will occur as the PaCO2 returns to baseline [24]. In our study population, PaCO2 never indicated significant hypoventilation, as the highest observed PaCO2 was 47 mmHg. Thus, desaturation is unlikely to have been caused by carbon dioxide accumulation decreasing PaO2 via the effect described by the alveolar gas equation [24]. This suggests that these patients did not hypoventilate, at least not at the time arterial blood samples were drawn. The common explanation for acute postoperative hypoxemia is hypoventilation. However, using the alveolar air equation, in order for hypoventilation to cause hypoxemia, even breathing room air, PaCO2 levels in excess of 70 mmHg must occur. According to arterial blood analyses, the highest PaCO2 observed in our 35 samples was 47 mmHg. One limitation of this study was our inability to have continuous PaCO2 monitoring for every patient. Since all six patients had repeated and severe episodes of arterial hypoxemia with rapid recovery, we conclude that transient airway obstruction, rather than hypoventilation, V/Q mismatch, or intrapulmonary shunting of blood, was the much more
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FIG. 2. With acute airway occlusion, oxygen is extracted at a rate equal to oxygen consumption but is not replaced by atmospheric oxygen. As a result, the partial pressure of oxygen decreases and the partial pressure of nitrogen increases; this creates the hypoxic alveolar gas mixture.
likely cause of desaturation. This phenomenon is well-known to occur in patients with obstructive sleep apnea, and is likely explained as follows. With acute airway obstruction, oxygen is drawn from the functional residual capacity at a rate equal to total body oxygen consumption, normally 250 mL/min. Assuming an FRC of 1000 mL at the time of airway obstruction, and further assuming an alveolar oxygen concentration of 16%, carbon dioxide of 5%, and nitrogen of 79%, one can appreciate the rapidity with which a hypoxic gas mixture will occur at the alveolar level as illustrated in Fig. 2. Within 30 s, 125 mL of oxygen will be withdrawn from alveolar gas, leaving 35 mL of oxygen at a PAO2 of approximately 40 mmHg, which incidentally equates to a SpO2 of about 70%! We proposed this pilot study to determine if hypoventilation is present in this population and to what extent. Our data suggest that this condition, as a classic cause of arterial hypoxemia, does not occur commonly for extended periods of time. Obviously, the data showed that there were two cohorts of patients with different durations of postoperative hypoxemia; owing to the limited sample size in this pilot study, there were too few patients to fully evaluate the differences, if any, between the groups. Further investigation through direct observation and follow-up studies is warranted to better determine which factors offer the greatest contribution to the development of arterial hypoxemia and how it might be ameliorated. Currently, most pulse oximeters use a ‘‘buffer’’ (rolling average) or report a rolling average in order to minimize frequent false alarms. We suspect that this method of data processing limits the ability of the pulse oximeter to be used to detect severe, acute desaturations as detected in our case report—and likely occurring elsewhere. Clearly, this methodology decreases the utility of pulse oximetry to detect and alert practitioners in a timely fashion. Furthermore, alarms can
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be set at the discretion of the clinician or respiratory therapist, often for saturation less than 90%. Our recommendation is that alarms be set at a significantly lower threshold to further decrease frequent and false alarms, which can lead to complacency. We also recommend that the alarm settings allow for longer duration of desaturation to permit appropriate patient arousal, while further minimizing false alarms. Pulse oximetry, an alarm set for saturation less than 90%, for 10 s, would have detected 100% of significant hypoxemic episodes, thus permitting appropriate diagnosis and early intervention [15]. We believe we have merely uncovered the tip of an iceberg. Some patients do suffer cardiopulmonary arrest, postoperatively. Often, it is assumed that narcotic-induced respiratory depression is the etiologic factor, albeit rare. Our results suggest that there may be an even more common cause, likely secondary to some degree of airway obstruction, with narcotic-induced decreased arousal. Our recommendation is to routinely monitor every patient with clinically significant obesity and/or a history or suspicion of obstructive sleep apnea using narcotic analgesics and PCA, as has been suggested by the Anesthesia Patient Safety Foundation Whitepaper, with pulse oximetry, in order to detect that occurrence and institute appropriate therapy until hypoxemia resolves [25]. CONCLUSIONS
Severe and prolonged arterial hypoxemia was a consistent finding in this surgical population, despite aggressive perioperative diagnosis and treatment of obstructive sleep apnea. Although we expected some degree of postoperative hypoventilation due to patients’ underlying co-morbidities, we were amazed to discover the degree and frequency of desaturation, when the data were unblinded. No patient experienced cardiopulmonary arrest or even a significant alteration in clinical vital signs, in spite of severe and repeated arterial hypoxemia. In no instance was a significant hypoxemic episode even suspected. It is clear that a significant change in monitoring is warranted in order to detect significant hypoxemic episodes and prevent those that lead to catastrophic events in the perioperative period, especially with the use of narcotic analgesics and PCA [25]. ACKNOWLEDGMENTS The authors thank Taylor Martin, M.A. and Tracy Torrella, M.A. for assisting with the research components and IRB application. They also thank Nikolas Gravenstein, M.D. and Michel Murr, M.D. for their critical review of the manuscript. The 4 Nellcor N600 oximeters were loaned by Nellcor Puritan Bennett LLC, doing business as Covidien. S.F.G. has served on a Consultant Advisory Board for Covidien.
REFERENCES 1. Kuczmarski RJ, Flegal KM, Campbell SM, et al. Increasing prevalence of overweight among U.S. adults. The National Health and Nutrition Examination Surveys, 1960 to 1991. JAMA 1994;272:205. 2. Rose DK, Cohen MM, Wigglesworth DF, et al. Critical respiratory events in the postanesthesia care unit. Patient, surgical, and anesthetic factors. Anesthesiology 1994;81:410. 3. Marti Valeri C, Sabate A, Masdevall C, et al. Influence of the severity of obesity on morbidity and mortality after gastric bypass surgery. Rev Esp Anestesiol Reanim 2004;51:195. 4. Choban PS, Flanchaum L. The impact of obesity on surgical outcomes: A review. J Am Coll Surg 1997;185:593. 5. Gozal D. Determinants of daytime hypercapnia in obstructive sleep apnea. Chest 2002;121:320. 6. Golpe R, Jimenez A, Carpizo R. Diurnal hypercapnia in patients with obstructive sleep apnea syndrome. Chest 2002;122:1100. 7. Marshall BE, Wyche MQ, Jr. Hypoxemia during and after anesthesia. Anesthesiology 1972;37:187. 8. Hines R, Barash PG, Watrous G, et al. Complications occurring in the postanesthesia care unit. A survey Anesth Analg 1992;74:503. 9. Nunn JF. Effects of anesthesia on respiration. Br J Anaesth 1990;65:54. 10. Benumof JL. Obstructive sleep apnea in the adult obese patient: Implications for airway management. Anesthesiol Clin North Am 2002;20:789. 11. Strollo RJ, Rogers RM. Obstructive sleep apnea. N Engl J Med 1996;334:99. 12. Rasheid S, Banasiak M, Gallagher SF, et al. Gastric bypass is an effective treatment for obstructive sleep apnea in patients with clinically significant obesity. Obes Surg 2003;13:58. 13. Serafini F, Anderson WM, Rosemurgy A, et al. Clinical predictors of sleep apnea in patients undergoing bariatric surgery. Obes Surg 2001;11:28. 14. Haines KL, Nelson LG, Gonzalez R, et al. Objective evidence that bariatric surgery improves obstructive sleep apnea. Surgery 2007;141:354. 15. Johns MW. Reliability and factor analysis of the Epworth Sleepiness Scale. Sleep 1992;15:376. 16. Rose DK, Cohen MM, Wigglesworth DF, et al. Critical respiratory events in the postanesthesia care unit. Patient, surgical, and anesthetic factors. Anesthesiology 1994;81:410. 17. Gallagher SF, Haines KL, Osterlund L, et al. Life-threatening hypoventilation after bariatric Surgery. Surgery for Obesity and Related Disorders, SOARD 2009 epub May 2009, and doi:10.1016/j.soard.2009.04.009, (In press). 18. Bergman NA. Distribution of inspired gas during anesthesia and artificial ventilation. Appl Physiol 1963;18:1085. 19. Hendenstierna G. Causes of gas exchange impairment during general anesthesia. Eur J Anaethesiol 1988;5:221. 20. Lundquist H, Hedenstierna G, Strandberg A, et al. CT-Assessment of dependent lung densities in man during general anesthesia. Acta Radiol 1995;36:626. 21. Pelosi P, Croci M, Ravagman I, et al. The effects of body mass on lung volumes, respiratory mechanics, and gas exchange during general anesthesia. Anesth Analg 1998;87:654. 22. Paul DR, Hogt JL, Boutros AR. Cardiovascular and respiratory changes in response to change of posture in the very obese. Anesthesiology 1976;45:73. 23. Blass NH. Morbid obesity and other nutritional disorders. In: Katz J, Benumof J, Kadis LD, Eds. Anesthesia and uncommon disease. Philadelphia: WB Saunders, 1981. 24. Complete Alveolar Gas Equation (AGE) Interactive Model http:// vam.anest.ufl.edu/simulations/alveolargasequation.php. University of Florida, 2009. 25. Weinger MB. Dangers of postoperative opioids: APSF workshop and whitepaper address prevention of postoperative respiratory complications. APSF Newsletter 2007;21:61.
ASSOCIATION FOR ACADEMIC SURGERY Postoperative Hypoxemia: Common, Undetected, and Unsuspected After Bariatric Surgery1 Scott F. Gallagher, M.D., F.A.C.S.,*,2 Krista L. Haines, M.A.,* Lynette G. Osterlund, M.D.,* Matt Mullen, B.S.,* and John B. Downs, M.D., F.C.C.M., F.C.C.P.† *Department of Surgery, USF Health, University of South Florida College of Medicine, Tampa, Florida; and †Department of Anesthesiology, University of Florida College of Medicine, Gainesville, Florida Submitted for publication July 9, 2009
Background. Patients undergoing gastric bypass are at greater than ordinary risk for postoperative respiratory insufficiency, presumably related to obstructive sleep apnea (OSA) and patient-controlled analgesia (PCA). This study was proposed to quantify the magnitude of the problem. Methods. Fifteen patients undergoing gastric bypass had oxygen saturation (SpO2) recorded continuously, but not displayed, for 24h postoperatively; eight also had arterial blood analysis every 4h. All received narcotic PCA. SpO2 < 90% lasting more than 10 s was reviewed. Results are mean ± SEM. Results. Mean age was 44 ± 4 y, and mean BMI was 48 ± 2kg/m2; 77% had OSA. Every patient had more than one episode with SpO2 < 90% for longer than 30s undetected by routine monitoring; most had multiple episodes. Nadir SpO2 averaged 75% ± 8%. Mean longest duration of desaturation below 90% averaged 21 ± 15min. Mean PaCO2 was 37 ± 3mm Hg; maximum PaCO2 was 47mm Hg. Conclusions. Severe and prolonged episodes of hypoxemia were a consistent finding, despite aggressive preoperative diagnosis and treatment of OSA, including use of CPAP postoperatively. Although some postoperative hypoventilation was expected, the degree and frequency of desaturation were surprising. No patient exhibited arterial PaCO2 evidence of hypoventilation. No patient experienced cardiopulmonary arrest/instability, in spite of severe, repeated episodes of hypoxemia. In no instance was a significant hypoxemic 1 Presented at the 2008 Association for Academic Surgery–Academic Surgical Congress in Huntington Beach, CA, and published as an abstract in the Journal of Surgical Research, 2008;144:370. 2 To whom correspondence and reprint requests should be addressed at Department of Surgery, USF Health, University of South Florida College of Medicine, 1 Tampa General Circle, Suite F145, Tampa, FL 33606. E-mail: [email protected].
0022-4804/09 $36.00 Ó 2010 Elsevier Inc. All rights reserved.
episode suspected or detected. Continuous pulse oximetry monitoring, with an audible alarm set for a saturation less than 90% for 10 s, would have alerted providers to 100% of significant hypoxemic episodes. Our recommendation is routinely monitoring (with alarm capability enabled) every bariatric surgical patient, to prevent such occurrence. Ó 2010 Elsevier Inc. All rights reserved. Key Words: hypoxemia; hypoventilation; obesity; gastric bypass; bariatric surgery; obstructive sleep apnea; postoperative; pulse oximetry.
INTRODUCTION
Obesity has grown to epidemic proportions in this country. The National Health and Nutrition Examination Survey revealed that at least one-third of the population is obese, i.e., exceed their ideal body weights by more than 20% [1]. Bariatric surgery for clinically significant obesity is common. Postoperatively, these patients present a higher risk for respiratory complications than the normal weight population [2–4]. One such complication is hypoventilation, defined by decreased minute ventilation as a result of decreased rate and/or depth of respiration. Extremely obese individuals may exhibit evidence of chronic hypoventilation with mild hypercarbia in the resting, preoperative state [5, 6]. Postoperatively patients are at risk for hypoventilation secondary to respiratory depression and/or the inability to maintain an adequate airway [7, 8]. Respiratory depression may stem from impaired respiratory drive from residual volatile anesthetics, sedatives, or opioid analgesics [9]. Inadequate airway maintenance may develop due to decreased muscle tone from muscle relaxants, incomplete neuromuscular blockade
622
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GALLAGHER ET AL.: POSTOP HYPOXEMIA HYPOVENTILATION AFTER GASTRIC BYPASS
reversal, or blunted airway reflexes. Poor positioning, reduced thoracic compliance, the supine position, obstruction due to secretions or mucous plugs, and bronchospasm are additional factors that can contribute to full or partial airway obstruction and produce acute hypoventilation and/or arterial hypoxemia that place the obese patient at significant risk for pulmonary issues, ventilatory failure, and hypoventilation. The obese individual may be at further pulmonary risk from coexisting obstructive sleep apnea (OSA) [10]. This syndrome is an abnormality of respiratory mechanics during sleep in which full or partial upper airway obstruction occurs repeatedly, predisposing the patient to frequent episodes of acute hypoventilation and hypoxemia [11]. Sleep apnea is quite common in the obese population. Indeed, the gastric bypass surgery patient population at our institution demonstrates an OSA prevalence of at least 60% [12–14]. The incidence of hypoventilation in a large population given general anesthesia has been reported as 0.2%, with obesity noted as a risk factor for the development of this condition [15]. The actual incidence of hypoventilation in that obese subset was not reported. Thus, the incidence of postoperative hypoventilation in the obese, particularly in patients with clinically significant obesity (BMI > 35%), has not been well documented in the literature. We undertook this investigation to determine how often and to what degree hypoventilation occurs in patients with clinically significant obesity immediately after undergoing the same operation (gastric bypass). Further, we wished to determine the postoperative incidence of arterial hypoxemia caused by acute airway occlusion in this population. METHODS This is a prospective, double blind, single-center pilot study of 15 patients undergoing elective Roux-en-Y bypass (RYGB). All patients who qualify for bariatric surgery at this institution are screened for obstructive sleep apnea (OSA) using Epworth Sleepiness Scale (ESS) as part of their preoperative evaluation. The ESS is a validated screening tool for daytime sleepiness and somnolence [16]; patients scoring 6 on the ESS were referred for consultation with a pulmonologist and subsequently for standard polysomnography and CPAP titration [12, 13]. After hospital administrative review and University of South Florida Internal Review Board (IRB) approval, patients scheduled to undergo RYGB were interviewed to determine willingness to participate in this study; procedures followed were in accordance with the ethical standards of the committee on human experimentation at both institutions, and the study is registered at clinicaltrials.gov as required. Patients provided written informed consent to participate in the study, if the following inclusion criteria were met: 18 to 65 y of age, with clinically significant obesity (BMI from 40– 85 kg/m2), and qualified as Physical Status Classification American Society of Anesthesiologists (ASA) no greater than III. The first eight patients were dually-assessed for hypoventilation by arterial blood analysis preoperatively (baseline) before any sedatives were administered, postoperatively within one-half h after arrival to the post-anesthesia care unit (PACU), and then every 4 h for the first 24 h after surgery. Arterial blood samples (3 mL each) were collected
from a radial artery catheter placed preoperatively and maintained for the initial 24 h postoperative period. In accordance with agreements made with the Hospital and IRB committee, a physician remained at the bedside of patients with in-dwelling arterial catheters during the entire 24 h postoperative duration of the study after leaving the PACU. Every attempt was made to not disturb sleeping patients during arterial blood sampling. The patients’ SpO2 and heart rate were monitored continuously in the preoperative holding area, in the operating room, and in the PACU by conventional as well as the study pulse oximeter (N600; Nellcor Puritan Bennett LLC; Boulder, CO); only study monitors (blinded and silenced) were in place continuously on the floor. Patients at our institution are not routinely monitored with continuous oximetry in the 24-h period following their operation. Continuous oximetry is used in the post-anesthesia care unit; however, routine monitoring used when patients go to the floor is per hospital policy (spot check pulse oximetry and vitals are done every hour for 2 h, every 2 h for 4 h, then every 4 h until discharge, unless otherwise ordered or specified). The portable study pulse oximeter supplied continuous 24-h monitoring and data storage without display of SpO2 data, which was recorded and stored in the machine every 4 s. The SpO2 data from the study oximeter were blinded and inaccessible until downloaded with proprietary software (Profox; Escondido, CA) at the conclusion of the study period. All oximeter data were reviewed for SpO2 < 90%, for >10 s and for >30 s; to account for possible artifact, only data that included heart rate and oxygen saturation simultaneously were included. Results are reported as mean 6 SEM.
RESULTS
Fifteen patients consented to the study; for the safety of one patient, the blinded/study ABG results were revealed to the clinical care providers in the recovery room, so this patient was not included in the analysis since the blinded study ABG was used to guide, and clearly influenced, patient care [17]. All (14) patients underwent laparoscopic operations and completed the study; but only several minutes out of 24 h of data were recovered from the study machine of another patient, leaving 13 patients for analysis. Mean age was 44 6 4 years, 84% were female, and mean BMI was 48 6 2 kg/m2. Most (77%) had sleep study confirmed OSA prior to participation in this study (Table 1). Of the 10 patients preoperatively diagnosed with OSA, seven patients were treated with CPAP (9 6 1 cm H2O); one was treated with BiPAP (12/8 cm H20). All eight patients diagnosed with obstructive sleep apnea used CPAP/BIPAP preoperatively and used CPAP/ TABLE 1 Demographics and Patient Characteristics
n Age (years) Male Female BMI (kg/m2) OSA
Study patients
Comparable bariatric patients with ESS > 6
13 44 6 4 16% 84% 48 6 2 77%
349 45 6 1 20% 80% 52 6 1 83%
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was 47 mmHg. Many patients were snoring while arterial blood samples were drawn; no episodes of apnea were observed by the monitor or recorded.
DISCUSSION
FIG. 1. Illustrates a 30-min time period in one patient with three separate episodes of desaturation (SpO2 < 90%). Of particular note, the rapidity with which oxygen saturation (SpO2) can fall is quite significant.
BIPAP postoperatively, usually their own machine; unfortunately, the hospital records and patient charts do not indicate precise times or duration of usage with any consistency. Postoperatively, four patients breathed room air and nine received supplemental oxygen, with two concurrently through the CPAP machines. Analysis of the data revealed that hypoxemia occurred in every patient, including those who received supplemental oxygen. Every patient (100%) had more than one episode of significant desaturation (SpO2 < 90%) lasting more than 30 s, which was otherwise undetected by routine monitoring; an example is shown in Fig. 1. Most patients had multiple similar episodes of prolonged desaturation. Nadir SpO2 averaged 75% 6 8%, and the mean longest duration of saturation below 90% was 21 6 15 min for each patient. The mean time with SpO2 < 90% was 165 6 49 min (median ¼ 114 min with SpO2 < 90%, range 1–555 min with SpO2 < 90%). There were five patients with less than 10 min with SpO2 < 90% during the entire 24 h (1, 3, 3, 3, and 8 min). For the remaining patients, the mean time with SpO2 < 90% was 266 6 54 min (median ¼ 231 min with SpO2 < 90%, range 95–555 min with SpO2 < 90%). The mean percentage of time during the 24 h study period with SpO2 < 90% was 18% 6 4% (median time ¼ 16% with SpO2 < 90%, range 7%–38% with SpO2 < 90%). Per patient, the mean total number of events with SpO2 < 90% for longer than 10 s was 112 6 34 (range 3–429 events). The mean total number of events with SpO2 < 90% for longer than 30 s was 62 6 16 (range 2–184 events). This degree of arterial hypoxemia was unappreciated clinically in every patient. In the six patients with an arterial catheter, arterial blood analyses revealed a mean postoperative PaCO2 value of 37 6 4 mmHg, and the highest PaCO2 value measured for any patient
While most of the patients had OSA diagnosed and treated preoperatively for at least 6 wk, all of the patients experienced more than one episode of desaturation in the first 24 h postoperatively with SpO2 < 90% for more than 30 s. Even more significant was the fact that the mean longest duration of desaturation for each patient lasted more than 21 min. The bariatric surgical population is known to be at high risk for respiratory complications in the postoperative period. Significant attention and resources are dedicated to minimize the risk of complications. These complications can be severe and even life-threatening [17]. In fact, they can be fatal. The study population is very similar to the other gastric bypass patients operated on at this Surgical Review Corporation designated Bariatric Surgery Center of Excellence, including mean age, demographics, sex, and those with OSA, as shown in Table 1 [14, 17]. We consider the observed average desaturation nadir of 75% a very clinically significant finding. A concern to us is that each of these events was otherwise clinically unsuspected; moreover, there were multiple, recurrent episodes despite use of CPAP and supplemental oxygen. All of the patients were monitored by continuous pulse oximetry in the PACU and then with the measurement of vital signs on the ward with no oxygen desaturation detected, including review of nursing records, which lack documentation of any desaturation episodes. Perhaps the transient nature of the episodes caused the lack of appreciation of their significance, assuming that they were even detected clinically. This study is the first investigation to report 100% of patients with significant periods of arterial hypoxemia, despite aggressive diagnosis and treatment of obstructive sleep apnea in the preoperative and perioperative period [14]. All patients with OSA were required to bring their own CPAP machine and use it postoperatively, per preprinted gastric bypass orders. If the patient’s CPAP machine was unavailable, one was provided. Hypoxemic episodes occurred despite supplemental oxygen administration in some patients. The degree of desaturation may have been decreased, at least temporarily, by supplementing inspired oxygen; however, these patients still experienced significant durations of oxygen desaturation similar to the room air patient’s mean nadir saturation of 75%, even while on supplemental oxygen. The route of delivery and flow rate of oxygen were variable and determined by the
GALLAGHER ET AL.: POSTOP HYPOXEMIA HYPOVENTILATION AFTER GASTRIC BYPASS
clinician. Although ordered routinely, it is possible that oxygen supplementation was inconsistent; however, our data confirm that supplementation of inspired oxygen alone is not reliable for preventing significant hypoxemic episodes. Reduction in functional residual capacity (FRC) routinely accompanies induction of general anesthesia and causes atelectasis [18, 19]. Merely assuming the supine position causes up to a 20% reduction in FRC, observed in normal subjects [20]. This reduction in FRC stems from compression atelectasis and is accentuated in obese individuals [21]. Supine positioning of the obese individual causes significant cephalad displacement of the diaphragm and reduced thoracic compliance; this creates a restrictive ventilatory defect, further increasing the potential for atelectasis formation [22]. Obese patients demonstrate lower resting lung volumes compared with normal individuals. Functional residual capacity, vital capacity (VC), and total lung capacity (TLC) are all reduced, although closing capacity (CC) usually is normal [23]. Thus, any condition that further lowers FRC, such as the supine position or general anesthesia, may alter the favorable relationship between FRC and CC, even during normal tidal ventilation, leading to collapse of small airways and atelectasis. Mismatching of ventilation and pulmonary perfusion (V/Q mismatch) is a common cause of postoperative arterial hypoxemia. Acute airway occlusion results in rapid arterial oxygen desaturation and rapid recovery with relief of the obstruction. In contrast, prolonged hypoventilation will result in a much slower desaturation and recovery. For example, as PaCO2 climbs from 40 to 80 mmHg, the PaO2 will decrease gradually and recovery will occur as the PaCO2 returns to baseline [24]. In our study population, PaCO2 never indicated significant hypoventilation, as the highest observed PaCO2 was 47 mmHg. Thus, desaturation is unlikely to have been caused by carbon dioxide accumulation decreasing PaO2 via the effect described by the alveolar gas equation [24]. This suggests that these patients did not hypoventilate, at least not at the time arterial blood samples were drawn. The common explanation for acute postoperative hypoxemia is hypoventilation. However, using the alveolar air equation, in order for hypoventilation to cause hypoxemia, even breathing room air, PaCO2 levels in excess of 70 mmHg must occur. According to arterial blood analyses, the highest PaCO2 observed in our 35 samples was 47 mmHg. One limitation of this study was our inability to have continuous PaCO2 monitoring for every patient. Since all six patients had repeated and severe episodes of arterial hypoxemia with rapid recovery, we conclude that transient airway obstruction, rather than hypoventilation, V/Q mismatch, or intrapulmonary shunting of blood, was the much more
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FIG. 2. With acute airway occlusion, oxygen is extracted at a rate equal to oxygen consumption but is not replaced by atmospheric oxygen. As a result, the partial pressure of oxygen decreases and the partial pressure of nitrogen increases; this creates the hypoxic alveolar gas mixture.
likely cause of desaturation. This phenomenon is well-known to occur in patients with obstructive sleep apnea, and is likely explained as follows. With acute airway obstruction, oxygen is drawn from the functional residual capacity at a rate equal to total body oxygen consumption, normally 250 mL/min. Assuming an FRC of 1000 mL at the time of airway obstruction, and further assuming an alveolar oxygen concentration of 16%, carbon dioxide of 5%, and nitrogen of 79%, one can appreciate the rapidity with which a hypoxic gas mixture will occur at the alveolar level as illustrated in Fig. 2. Within 30 s, 125 mL of oxygen will be withdrawn from alveolar gas, leaving 35 mL of oxygen at a PAO2 of approximately 40 mmHg, which incidentally equates to a SpO2 of about 70%! We proposed this pilot study to determine if hypoventilation is present in this population and to what extent. Our data suggest that this condition, as a classic cause of arterial hypoxemia, does not occur commonly for extended periods of time. Obviously, the data showed that there were two cohorts of patients with different durations of postoperative hypoxemia; owing to the limited sample size in this pilot study, there were too few patients to fully evaluate the differences, if any, between the groups. Further investigation through direct observation and follow-up studies is warranted to better determine which factors offer the greatest contribution to the development of arterial hypoxemia and how it might be ameliorated. Currently, most pulse oximeters use a ‘‘buffer’’ (rolling average) or report a rolling average in order to minimize frequent false alarms. We suspect that this method of data processing limits the ability of the pulse oximeter to be used to detect severe, acute desaturations as detected in our case report—and likely occurring elsewhere. Clearly, this methodology decreases the utility of pulse oximetry to detect and alert practitioners in a timely fashion. Furthermore, alarms can
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be set at the discretion of the clinician or respiratory therapist, often for saturation less than 90%. Our recommendation is that alarms be set at a significantly lower threshold to further decrease frequent and false alarms, which can lead to complacency. We also recommend that the alarm settings allow for longer duration of desaturation to permit appropriate patient arousal, while further minimizing false alarms. Pulse oximetry, an alarm set for saturation less than 90%, for 10 s, would have detected 100% of significant hypoxemic episodes, thus permitting appropriate diagnosis and early intervention [15]. We believe we have merely uncovered the tip of an iceberg. Some patients do suffer cardiopulmonary arrest, postoperatively. Often, it is assumed that narcotic-induced respiratory depression is the etiologic factor, albeit rare. Our results suggest that there may be an even more common cause, likely secondary to some degree of airway obstruction, with narcotic-induced decreased arousal. Our recommendation is to routinely monitor every patient with clinically significant obesity and/or a history or suspicion of obstructive sleep apnea using narcotic analgesics and PCA, as has been suggested by the Anesthesia Patient Safety Foundation Whitepaper, with pulse oximetry, in order to detect that occurrence and institute appropriate therapy until hypoxemia resolves [25]. CONCLUSIONS
Severe and prolonged arterial hypoxemia was a consistent finding in this surgical population, despite aggressive perioperative diagnosis and treatment of obstructive sleep apnea. Although we expected some degree of postoperative hypoventilation due to patients’ underlying co-morbidities, we were amazed to discover the degree and frequency of desaturation, when the data were unblinded. No patient experienced cardiopulmonary arrest or even a significant alteration in clinical vital signs, in spite of severe and repeated arterial hypoxemia. In no instance was a significant hypoxemic episode even suspected. It is clear that a significant change in monitoring is warranted in order to detect significant hypoxemic episodes and prevent those that lead to catastrophic events in the perioperative period, especially with the use of narcotic analgesics and PCA [25]. ACKNOWLEDGMENTS The authors thank Taylor Martin, M.A. and Tracy Torrella, M.A. for assisting with the research components and IRB application. They also thank Nikolas Gravenstein, M.D. and Michel Murr, M.D. for their critical review of the manuscript. The 4 Nellcor N600 oximeters were loaned by Nellcor Puritan Bennett LLC, doing business as Covidien. S.F.G. has served on a Consultant Advisory Board for Covidien.
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