Surgery for Cancer: Does Anesthesia Matter?

Surgery for Cancer: Does Anesthesia Matter? Skip to main page content

HOME CURRENT ISSUE PAST ISSUES CME SUBSCRIBE ONLINE HELP SUBMIT TO A&A ACTIVATE MY ACCOUNT Search GO Advanced Search ? User Name Password Sign In Surgery for Cancer: Does Anesthesia Matter? James G. Bovill, MD, PhD, FCARCSI, FRCA

From the Department of Anaesthesiology, Leiden University Medical Centre, Leiden, The Netherlands. Address correspondence to James G. Bovill, MD, PhD, FCARCSI, FRCA, Hugo de Grootlaan 31, 1422 BR Uithoorn, The Netherlands. Address e-mail to jgbovill{at}gmail.com. As anesthesiologists, we often assume that once the immediate effects of our drugs dissipate, the body returns to the preanesthetic state without long-term sequelae. However, in addition to profound immediate effects, anesthesia can also have long-term consequences. In this issue of Anesthesia & Analgesia, 2 articles deal with 1 potentially devastating consequence: an increased risk of metastatic spread of malignant cells after cancer surgery. Gottschalk et al.1 review the pathophysiology of cancer recurrence after surgery, the potential role of anesthesia on the risk of recurrence, and discuss how this might affect clinical practice. Their review is an opportune reminder that not all consequences of anesthesia disappear after the immediate postoperative period. The authors of the second article report findings from an analysis of tumor recurrence after surgery for breast cancer.2 The results suggest that intraoperative administration of the nonsteroidal antiinflammatory drug (NSAID) ketorolac significantly decreases the incidence of cancer recurrence compared with non-NSAID analgesics.

Cancer is second only to cardiovascular disease as the most frequent cause of death among adults in the developed nations. Although cancer does occur in children and young adults, nearly 75% of cases occur in individuals aged 60 years and older, and more than one-third in those aged 75 years and older.* Populations in the developed countries are aging, with a concomitant increase in age-related diseases, including cancer. As a consequence, anesthesiologists will be confronted with increasing numbers of patients presenting for cancer surgery.

Surgical removal of a malignant tumor is the primary treatment for most cancers. However, surgical manipulation can release isolated cancer cells into the bloodstream and lymphatic system. Whether these develop into metastases depends on the balance between the patient's immune defenses and the ability of the tumor cells to seed, proliferate, and attract formation of new blood vessels. Several factors can upset this balance. The immune system, by specifically identifying and destroying malignant cells (tumor immune surveillance), is a primary defense against cancer.3 Major surgery is associated with immunosuppression which, together with the release of cytokines, chemokines, and prostaglandins, can facilitate angiogenesis, tumor metastasis, and tumor invasion.4 In particular, surgery inhibits the natural killer (NK) cells that are critical in limiting the spread of malignant cells.5 They are the only cell type able to recognize and lyse cells lacking self human leukocyte antigen class I molecules. Because many tumor cells inhibit the expression of these molecules, NK cells are the major first-line defense against the development of primary tumors and the metastatic spread of established tumors.

James Cottrell defined anesthesiologists as “… doctors who keep patients alive while surgeons do things that would otherwise kill them.”6 But could our choice of anesthesia increase the risk of cancer recurrence that could kill the patient, or could a more appropriate choice of drug decrease the risk of recurrence after cancer surgery? There is increasing evidence from experimental studies and a limited number of clinical studies that some anesthetics and opioids may be contributing factors to the development of metastases after cancer surgery.1 Inhaled anesthesia, independent of other factors, may increase the risk of malignant cells escaping from immune control. Volatile anesthetics induce apoptosis in lymphocytes, reduce NK cytotoxicity, and alter the release of cytokines by NK cells in response to tumor cells.7 On the positive side, some anesthetics are cytotoxic to poorly differentiated human carcinoma cell lines and might help counteract the spread of cancer cells.8 On balance, however, it would seem prudent to limit the use of inhaled anesthesia in patients undergoing cancer surgery. Gottschalk et al.1 propose 2 alternatives: regional anesthesia and total IV anesthesia (TIVA) with propofol. Although several studies have suggested that regional anesthesia preserves immune defenses against tumor progression by attenuating the surgical stress response, most have been retrospective and have investigated regional combined with general anesthesia.9 Propofol, the most popular hypnotic used in TIVA, attenuates the surgical stress-induced adverse immune response to surgery and has antitumor activity, possibly related to inhibition of cyclooxygenase.10,11 Unfortunately, propofol is not a complete anesthetic and needs to be combined with an opioid when used in TIVA.

Opioids have several actions that can promote the dissemination of malignant cells. They stimulate angiogenesis, a key factor in the growth and dissemination of cancers, in part by activating cyclooxygenase-2 (COX-2), increasing production of prostaglandin E2, which promotes angiogenesis and tumor progression.12 Opioids also significantly influence the functioning of the immune system indirectly via the hypothalamic-pituitary axis and directly through opioid receptors, especially ?3 receptors expressed on immunocytes. These receptors are involved in signaling pathways that modulate antibody production and the activity of NK cells.13 Now, there is compelling evidence that animals, including humans, synthesize morphine and related morphinan alkaloids, and that these endogenous opioids are involved in morphinergic signaling in immune cells.14 The ?3 receptors are also expressed on human cancer cell lines, where they are coupled to constitutive nitric oxide release.15 Opioid alkaloids such as morphine bind strongly to the ?3 receptor, whereas binding of synthetic opioids such as fentanyl and the endogenous opioid peptides is considerably weaker. This explains why alkaloids such as morphine are predominantly immunosuppressive, whereas the endogenous opioid peptides are predominantly immunostimulatory.

An accepted method of reducing the dose of an opioid while maintaining satisfactory analgesia is to combine the opioid with an NSAID. The combination can decrease postoperative pain and opioid requirements by 20% to 50%. NSAIDs, especially those with COX-2 inhibitory activity, have been shown in a number of major epidemiological studies to reduce significantly the risk of several types of cancer, including colon, breast, and prostate cancers. However, those studies were related to the chronic use of NSAIDs. The article by Forget et al.2 is of particular interest because their results suggest that an NSAID, given as a single dose during surgery, may also significantly reduce cancer recurrence after surgery. They reviewed 319 consecutive patients who had mastectomy for breast cancer during a 4.5-year period. Just more than half (55%) of the patients were given ketorolac IV immediately before skin incision. Cancer recurrence after surgery was lower (P < 0.001) in patients given ketorolac (6%) compared with the 17% recurrence in patients who did not receive ketorolac. The authors acknowledge several important limitations of their study. It was retrospective, nonrandom, and patients also received a number of other drugs that could have influenced recurrence, including diclofenac administered postoperatively for pain relief to more than half of the patients. Rather surprisingly, the authors found no association between cancer recurrence and the use of diclofenac, which, similar to ketorolac, is an NSAID with approximately equal activity at COX-1 and COX-2, so it would be expected to have a similar influence on cancer recurrence. Despite these reservations, the analysis of their data is sufficiently robust that the implications of their findings cannot be ignored.

Increased expression of COX-2 occurs in many types of cancers and is a crucial element not only in the pathogenesis and dissemination of tumors but also in increasing their resistance to apoptosis, and with the generation of prostaglandins and related compounds that support carcinogenesis.16 Blocking overexpression by COX-2–selective NSAIDs can induce apoptosis and tumor regression and inhibits the angiogenesis important for tumor growth and metastasis.17 In addition to the inhibition of COX-2 and prostaglandin synthesis by NSAIDs, recent studies have suggested that COX-independent pathways may also contribute to the anticancer actions of COX-2–selective NSAIDs.18,19 This may be an action specific to celecoxib because it inhibited the growth of human prostate cancer cell lines at concentrations comparable with those achieved clinically, whereas rofecoxib had no effect over the same concentration range.19 Therefore, there are good arguments for using COX-2–specific inhibitors in anesthesia; in addition to providing analgesia thereby reducing the amount of opioids needed for optimal pain relief, they can contribute to minimizing the risk of tumor spread and growth.

Although some cancers progress very rapidly, the majority progress slowly, at least in the early stages. For some patients, malignant cells may have been present in the body for years without any clinical sign of cancer. Indeed, some individuals may never develop overt signs of cancer despite cancer cells being present. This is tumor dormancy, a phenomenon whereby cancer cells persist below the threshold of diagnostic detection for months to decades. Patients who are free of clinically detectable disease for >20 years after treatment may still have circulating tumor cells.20 Some dormant cancer cells may remain in an asymptomatic, nondetectable, and occult state for the life of the individual.21 Autopsies of victims of trauma have revealed that most apparently healthy individuals harbor microscopic primary cancers.22

Dormant tumors are kept in check by the immune system, but any disruption of this equilibrium can allow them to escape from immune control and proliferate.23,24 In addition, for a tumor to progress beyond a diameter of 1 to 2 mm requires an “angiogenic switch” characterized by an imbalance between pro- and antiangiogenic factors, allowing the development of angiogenesis. This interrupts the dormant state, triggering invasive tumor growth.25 The implication is that many, indeed perhaps the majority, of our patients may be harboring a dormant cancer. Any factor that upsets this imbalance, such as surgery and anesthesia, could trigger activation of these cells leading to the development of overt cancer. Unfortunately, at this time, there is no reliable method for detecting the presence of dormant cancer cells.

In conclusion, even though the evidence is inconclusive and at times conflicting, we cannot ignore the possibility that anesthesia may contribute to the recurrence of cancer, months or even years after cancer surgery. Less clear, but equally worrying, is the possibility that anesthesia could activate dormant cancer cells in an individual undergoing noncancer surgery, with the development of an overt cancer that otherwise might never have materialized in the lifetime of that individual. So what should we do? An obvious choice is to use regional anesthesia when feasible, alone or in combination with general anesthesia, to minimize the amount of opioid administered, and to consider using NSAIDs, especially specific COX-2 inhibitors. Of course, what we really need are good prospective, randomized, and controlled clinical trials. These studies will be difficult, requiring large numbers of patients and considerable effort. However, without the results from such studies, we cannot make the informed judgments that will allow us to offer safe anesthesia to our patients while avoiding the devastating consequences of cancer long after the anesthetic has worn off.

 Next Section Footnotes Reprints will not be available from the author.

?* Office for National Statistics. MB1 No 37—Cancer Registration Statistics 2006 England. Available at: http://www.statistics.gov.uk/. Accessed January 19, 2010.

Accepted February 7, 2010. Copyright ? 2010 International Anesthesia Research Society Previous Section  REFERENCES 1.? Gottschalk A, Sharma S, Ford J, Durieux M, Tiouririne M . The role of the perioperative period in recurrence after cancer surgery. Anesth Analg 2010;110:1636–43 Abstract/FREE Full Text 2.? Forget P, Vandenhende J, Berliere M, Machiels J-P, Nussbaum B, Legrand C, De Kock M . Do intraoperative analgesics influence breast cancer recurrence after mastectomy? A retrospective analysis. Anesth Analg 2010;110:1630–5 Abstract/FREE Full Text 3.? Swann JB, Smyth MJ . Immune surveillance of tumors. J Clin Invest 2007;117:1137–46 CrossRefMedline 4.? Demicheli R, Retsky MW, Hrushesky WJ, Baum M, Gukas ID . The effects of surgery on tumor growth: a century of investigations. Ann Oncol 2008;19:1821–8 Abstract/FREE Full Text 5.? Ben-Eliyahu S, page GG, Yirmiya R, Shakhar G . Evidence that stress and surgical interventions promote tumor development by suppressing natural killer cell activity. Int J Cancer 1999;80:880–8 CrossRefMedline 6.? Cottrell JE . View from the head of the table: against putting people to sleep. Surg Rounds 1989;12:81–8 7.? Kurosawa S, Kato M . Anesthetics, immune cells, and immune responses. J Anesth 2008;22:263–77 CrossRefMedline 8.? Kvolik S, Glavas-Obrovac L, Bares V, Karner I . Effects of inhalation anesthetics halothane, sevoflurane, and isoflurane on human cell lines. Life Sci 2005;77:2369–83 CrossRefMedline 9.? Sessler DI . Regional analgesia and cancer recurrence. Anesthesiology 2009;111:1–4 CrossRefMedline 10.? Kushida A, Inada T, Shingu K . Enhancement of antitumor immunity after propofol treatment in mice. Immunopharmacol Immunotoxicol 2007;29:477–86 Medline 11.? Inada T, Kubo K, Kambara T, Shingu K . Propofol inhibits cyclooxygenase activity in human monocytic THP-1 cells. Can J Anaesth 2009;56:222–9 Medline 12.? Amano H, Ito Y, Suzuki T, Kato S, Matsui Y, Ogawa F, Murata T, Sugimoto Y, Senior R, Kitasato H, Hayashi I, Satoh Y, Narumiya S, Majima M . Roles of a prostaglandin E-type receptor, EP3, in upregulation of matrix metalloproteinase-9 and vascular endothelial growth factor during enhancement of tumor metastasis. Cancer Sci 2009;100:2318–24 CrossRefMedline 13.? Martin-Kleiner I, Balog T, Gabrilovac J . Signal transduction induced by opioids in immune cells: a review. Neuroimmunomodulation 2006;13:1–7 Medline 14.? Zhu W, Stefano GB . Comparative aspects of endogenous morphine synthesis and signaling in animals. Ann N Y Acad Sci 2009;1163:330–9 Medline 15.? Cadet P, Rasmussen M, Zhu W, Tonnesen E, Mantione KJ, Stefano GB . Endogenous morphinergic signaling and tumor growth. Front Biosci 2004;9:3176–86 Medline 16.? Eisinger AL, Prescott SM, Jones DA, Stafforini DM . The role of cyclooxygenase-2 and prostaglandins in colon cancer. Prostaglandins Other Lipid Mediat 2007;82:147–54 CrossRefMedline 17.? Farooqui M, Li Y, Rogers T, Poonawala T, Griffin RJ, Song CW, Gupta K . COX-2 inhibitor celecoxib prevents chronic morphine-induced promotion of angiogenesis, tumour growth, metastasis and mortality, without compromising analgesia. Br J Cancer 2007;97:1523–31 CrossRefMedline 18.? Gr?sch S, Tegeder I, Niederberger E, Br?utigam L, Geisslinger G . COX-2 independent induction of cell cycle arrest and apoptosis in colon cancer cells by the selective COX-2 inhibitor celecoxib. FASEB J 2001;15:2742–4 FREE Full Text 19.? Patel MI, Subbaramaiah K, Du B, Chang M, Yang P, Newman RA, Cordon-Cardo C, Thaler HT, Dannenberg AJ . Celecoxib inhibits prostate cancer growth: evidence of a cyclooxygenase-2-independent mechanism. Clin Cancer Res 2005;11:1999–2007 Abstract/FREE Full Text 20.? Meng S, Tripathy D, Frenkel EP, Shete S, Naftalis EZ, Huth JF, Beitsch PD, Leitch M, Hoover S, Euhus D, Haley B, Morrison L, Fleming TP, Herlyn D, Terstappen LW, Fehm T, Tucker TF, Lane N, Wang J, Uhr JW . Circulating tumor cells in patients with breast cancer dormancy. Clin Cancer Res 2004;10:8152–62 Abstract/FREE Full Text 21.? Hedley BD, Chambers AF . Tumor dormancy and metastasis. Adv Cancer Res 2009;102:67–101 CrossRefMedline 22.? Udagawa T . Tumor dormancy of primary and secondary cancers. APMIS 2008;116:615–28 CrossRefMedline 23.? Koebel CM, Vermi W, Swann JB, Zerafa N, Rodig SJ, Old LJ, Smyth MJ, Schreiber RD . Adaptive immunity maintains occult cancer in an equilibrium state. Nature 2007;450:903–7 CrossRefMedline 24.? Quesnel B . Tumor dormancy and immunoescape. APMIS 2008;116:685–94 CrossRefMedline 25.? Indraccolo S, Favaro E, Amadori A . Dormant tumors awaken by a short-term angiogenic burst: the spike hypothesis. Cell Cycle 2006;5:1751–5 Medline ? Previous | Next Article ?Table of Contents This Article doi: 10.1213/?ANE.0b013e3181d8d183 A & A June 2010 vol. 110 no. 6 1524-1526 ? Full Text Full Text (PDF) Classifications Editorial Services Email this article to a colleague Alert me when this article is cited Alert me if a correction is posted Similar articles in this journal Similar articles in PubMed Download to citation manager Request Permissions Citing Articles Load citing article information Citing articles via Google Scholar Google Scholar Articles by Bovill, J. G. Search for related content PubMed PubMed citation Articles by Bovill, J. G. Related Content Anesthetic Techniques Complications Preoperative Evaluation Outcomes Patient Safety Load related web page information Navigate This Article Top Footnotes REFERENCES Current Issue June 2011, 112 (6) Alert me to new issues of A & A Join the IARS About A&A Mission Editorial Board For Authors For Reviewers Cover Art Sign up Sign up for eTOCs Sign up for RSS feeds Browse by Topic Permissions and Copyright Press Room OpenAnesthesia Advertise in A&A Career Center Most Read Special Article: 2010 Anesthesia & Analgesia Guide for Authors: 2009-2010 Editorial Board, Anesthesia & Analgesia Hand Contamination of Anesthesia Providers Is an Important Risk Factor for Intraoperative Bacterial Transmission Review Article: The Role of the Perioperative Period in Recurrence After Cancer Surgery Postoperative Sore Throat: More Answers Than Questions Electrical Safety in the Operating Room: Dry Versus Wet ? View all Most Read articles Cited The comparative effects of postoperative analgesic therapies on pulmonary outcome: cumulative meta-analyses of randomized, controlled trials ASE/SCA Guidelines for Performing a Comprehensive Intraoperative Multiplane Transesophageal Echocardiography Examination: Recommendations of the American Society of Echocardiography Council for Intraoperative Echocardiography and the Society of Cardiovascular Anesthesiologists Task Force for Certification in Perioperative Transesophageal Echocardiography Consensus Guidelines for Managing Postoperative Nausea and Vomiting Cerebral Autoregulation and Flow/Metabolism Coupling during Cardiopulmonary Bypass: The Influence of Paco2 A Postanesthetic Recovery Score ? View all Most Cited articles Copyright ? 2011 by the International Anesthesia Research Society

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Review Article: The Role of the Perioperative Period in Recurrence After Cancer Surgery

The Role of the Perioperative Period in Recurrence After Cancer Surgery Skip to main page content

HOME CURRENT ISSUE PAST ISSUES CME SUBSCRIBE ONLINE HELP SUBMIT TO A&A ACTIVATE MY ACCOUNT Search GO Advanced Search ? User Name Password Sign In The Role of the Perioperative Period in Recurrence After Cancer Surgery Antje Gottschalk, MD*?, Sonal Sharma, MD*, Justin Ford, MD*, Marcel E. Durieux, MD, PhD* and Mohamed Tiouririne, MD*

From the *Department of Anesthesia, University of Virginia, Charlottesville, Virginia; and ?Department of Anesthesiology and Intensive Care Medicine, University Muenster, Muenster, Germany. Address correspondence to Mohamed Tiouririne, MD, Department of Anesthesiology, University of Virginia, Charlottesville, VA. Address e-mail to mt9y{at}virginia.edu. Abstract A wealth of basic science data supports the hypothesis that the surgical stress response increases the likelihood of cancer dissemination and metastasis during and after cancer surgery. Anesthetic management of the cancer patient, therefore, could potentially influence long-term outcome. Preclinical data suggest that beneficial approaches might include selection of induction drugs such as propofol, minimizing the use of volatile anesthetics, and coadministration of cyclooxygenase antagonists with systemic opioids. Retrospective clinical trials suggest that the addition of regional anesthesia might decrease recurrence after cancer surgery. Other factors such as blood transfusion, temperature regulation, and statin administration may also affect long-term outcome.

Footnotes Marcel E. Durieux is section Editor of Anesthetic Pre-Clinical Pharmacology for the Journal. The manuscript was handled by Sorin J. Brull, section Editor of Patient Safety, and Dr. Durieux was not involved in any way with the editorial process or decision.

Disclosure: The authors report no conflict of interest.

Reprints will not be available from the author.

Accepted February 24, 2010. Copyright ? 2010 International Anesthesia Research Society ? Previous | Next Article ?Table of Contents This Article Published online before print April 30, 2010, doi: 10.1213/?ANE.0b013e3181de0ab6 A & A June 2010 vol. 110 no. 6 1636-1643 ? Abstract Full Text Full Text (PDF) CME Classifications Series: Review Article Patient Safety Services Email this article to a colleague Alert me when this article is cited Alert me if a correction is posted Similar articles in this journal Similar articles in PubMed Download to citation manager Request Permissions Citing Articles Load citing article information Citing articles via Google Scholar Google Scholar Articles by Gottschalk, A. Articles by Tiouririne, M. Search for related content PubMed PubMed citation Articles by Gottschalk, A. Articles by Tiouririne, M. Related Content Mechanisms Outcomes Patient Safety Pharmacology Load related web page information Current Issue June 2011, 112 (6) Alert me to new issues of A & A Join the IARS About A&A Mission Editorial Board For Authors For Reviewers Cover Art Sign up Sign up for eTOCs Sign up for RSS feeds Browse by Topic Permissions and Copyright Press Room OpenAnesthesia Advertise in A&A Career Center Most Read Special Article: 2010 Anesthesia & Analgesia Guide for Authors: 2009-2010 Editorial Board, Anesthesia & Analgesia Hand Contamination of Anesthesia Providers Is an Important Risk Factor for Intraoperative Bacterial Transmission Review Article: The Role of the Perioperative Period in Recurrence After Cancer Surgery Postoperative Sore Throat: More Answers Than Questions Electrical Safety in the Operating Room: Dry Versus Wet ? View all Most Read articles Cited The comparative effects of postoperative analgesic therapies on pulmonary outcome: cumulative meta-analyses of randomized, controlled trials ASE/SCA Guidelines for Performing a Comprehensive Intraoperative Multiplane Transesophageal Echocardiography Examination: Recommendations of the American Society of Echocardiography Council for Intraoperative Echocardiography and the Society of Cardiovascular Anesthesiologists Task Force for Certification in Perioperative Transesophageal Echocardiography Consensus Guidelines for Managing Postoperative Nausea and Vomiting Cerebral Autoregulation and Flow/Metabolism Coupling during Cardiopulmonary Bypass: The Influence of Paco2 A Postanesthetic Recovery Score ? View all Most Cited articles Copyright ? 2011 by the International Anesthesia Research Society

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Global Warming Potential of Inhaled Anesthetics: Application to Clinical Use

Global Warming Potential of Inhaled Anesthetics: Application to Clinical Use Skip to main page content

HOME CURRENT ISSUE PAST ISSUES CME SUBSCRIBE ONLINE HELP SUBMIT TO A&A ACTIVATE MY ACCOUNT Search GO Advanced Search ? User Name Password Sign In Global Warming Potential of Inhaled Anesthetics: Application to Clinical Use Susan M. Ryan, MD, PhD* and Claus J. Nielsen, CSc?

From the *Department of Anesthesia and Perioperative Care, University of California, San Francisco, San Francisco, California; and ?Department of Chemistry, Centre for Theoretical and Computational Chemistry, University of Oslo, Oslo, Norway. Address correspondence to Susan M. Ryan, MD, PhD, 505 Parnassus Ave., Box 0648, University of California, San Francisco, San Francisco, CA 94143. Address e-mail to ryans{at}anesthesia.ucsf.edu. Abstract BACKGROUND: Inhaled anesthetics are recognized greenhouse gases. Calculating their relative impact during common clinical usage will allow comparison to each other and to carbon dioxide emissions in general.

METHODS: We determined infrared absorption cross-sections for sevoflurane and isoflurane. Twenty-year global warming potential (GWP20) values for desflurane, sevoflurane, and isoflurane were then calculated using the present and previously published infrared results, and best estimate atmospheric lifetimes were determined. The total quantity of each anesthetic used in 1 minimal alveolar concentration (MAC)-hour was then multiplied by the calculated GWP20 for that anesthetic, and expressed as “carbon dioxide equivalent” (CDE20) in grams. Common fresh gas flows and carrier gases, both air/oxygen and nitrous oxide (N2O)/oxygen, were considered in the calculations to allow these examples to represent common clinical use of inhaled anesthetics.

RESULTS: GWP20 values for the inhaled anesthetics were: sevoflurane 349, isoflurane 1401, and desflurane 3714. CDE20 values for 1 MAC-hour at 2 L fresh gas flow were: sevoflurane 6980 g, isoflurane 15,551 g, and desflurane 187,186 g. Comparison among these anesthetics produced a ratio of sevoflurane 1, isoflurane 2.2, and desflurane 26.8. When 60% N2O/40% oxygen replaced air/oxygen as a carrier gas combination, and inhaled anesthetic delivery was adjusted to deliver 1 MAC-hour of anesthetic, sevoflurane CDE20 values were 5.9 times higher with N2O than when carried with air/O2, isoflurane values were 2.9 times higher, and desflurane values were 0.4 times lower. On a 100-year time horizon with 60% N2O, the sevoflurane CDE100 values were 19 times higher than when carried in air/O2, isoflurane values were 9 times higher, and desflurane values were equal with and without N2O.

CONCLUSIONS: Under comparable and common clinical conditions, desflurane has a greater potential impact on global warming than either isoflurane or sevoflurane. N2O alone produces a sizable greenhouse gas contribution relative to sevoflurane or isoflurane. Additionally, 60% N2O combined with potent inhaled anesthetics to deliver 1 MAC of anesthetic substantially increases the environmental impact of sevoflurane and isoflurane, and decreases that of desflurane. N2O is destructive to the ozone layer as well as possessing GWP; it continues to have impact over a longer timeframe, and may not be an environmentally sound tradeoff for desflurane. From our calculations, avoiding N2O and unnecessarily high fresh gas flow rates can reduce the environmental impact of inhaled anesthetics.

Footnotes Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Web site (www.anesthesia-analgesia.org).

Disclosure: The authors report no conflicts of interest.

Reprints will not be available from the author.

Copyright ? 2010 International Anesthesia Research Society ? Previous | Next Article ?Table of Contents This Article Published online before print June 2, 2010, doi: 10.1213/?ANE.0b013e3181e058d7 A & A July 2010 vol. 111 no. 1 92-98 ? Abstract Full Text Full Text (PDF) Classifications Anesthetic Pharmacology Services Email this article to a colleague Alert me when this article is cited Alert me if a correction is posted Similar articles in this journal Similar articles in PubMed Download to citation manager Request Permissions Citing Articles Load citing article information Citing articles via Google Scholar Google Scholar Articles by Ryan, S. M. Articles by Nielsen, C. J. Search for related content PubMed PubMed citation Articles by Ryan, S. M. Articles by Nielsen, C. J. Related Content Economics and Health Care Research Mechanisms Ethics Pharmacology Load related web page information Current Issue June 2011, 112 (6) Alert me to new issues of A & A Join the IARS About A&A Mission Editorial Board For Authors For Reviewers Cover Art Sign up Sign up for eTOCs Sign up for RSS feeds Browse by Topic Permissions and Copyright Press Room OpenAnesthesia Advertise in A&A Career Center Most Read Special Article: 2010 Anesthesia & Analgesia Guide for Authors: 2009-2010 Editorial Board, Anesthesia & Analgesia Hand Contamination of Anesthesia Providers Is an Important Risk Factor for Intraoperative Bacterial Transmission Review Article: The Role of the Perioperative Period in Recurrence After Cancer Surgery Postoperative Sore Throat: More Answers Than Questions Electrical Safety in the Operating Room: Dry Versus Wet ? View all Most Read articles Cited The comparative effects of postoperative analgesic therapies on pulmonary outcome: cumulative meta-analyses of randomized, controlled trials ASE/SCA Guidelines for Performing a Comprehensive Intraoperative Multiplane Transesophageal Echocardiography Examination: Recommendations of the American Society of Echocardiography Council for Intraoperative Echocardiography and the Society of Cardiovascular Anesthesiologists Task Force for Certification in Perioperative Transesophageal Echocardiography Consensus Guidelines for Managing Postoperative Nausea and Vomiting Cerebral Autoregulation and Flow/Metabolism Coupling during Cardiopulmonary Bypass: The Influence of Paco2 A Postanesthetic Recovery Score ? View all Most Cited articles Copyright ? 2011 by the International Anesthesia Research Society

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Surgical Site Infections and the Anesthesia Professionals' Microbiome: We've All Been Slimed! Now What Are We Going to Do About It?

Surgical Site Infections and the Anesthesia Professionals' Microbiome: We've All Been Slimed! Now What Are We Going to Do About It? Skip to main page content

HOME CURRENT ISSUE PAST ISSUES CME SUBSCRIBE ONLINE HELP SUBMIT TO A&A ACTIVATE MY ACCOUNT Search GO Advanced Search ? User Name Password Sign In Surgical Site Infections and the Anesthesia Professionals' Microbiome: We've All Been Slimed! Now What Are We Going to Do About It? Raymond C. Roy, MD*, Sorin J. Brull, MD? and John H. Eichhorn, MD?

From the *Department of Anesthesiology, Wake Forest University School of Medicine, Winston-Salem, North Carolina; ?Department of Anesthesiology, Mayo Clinic College of Medicine, Jacksonville, Florida; and ?Department of Anesthesiology, College of Medicine, University of Kentucky, Lexington, Kentucky. Address correspondence and reprint requests to Raymond C. Roy, MD, Department of Anesthesiology, Wake Forest University School of Medicine, Winston-Salem, NC. Address e-mail to rroy{at}wfubmc.ed. Dr. Peter Venkman: “Someone blows their nose and you want to keep it? …” —Ghostbusters (1984)

We are grossly outnumbered! Each of us consists of approximately 10 trillion human cells, accompanied by our personal “microbiome” of 100 trillion microorganisms that live symbiotically inside and on our bodies. Surgical site infections are but one of the many complex features of this usually peaceful coexistence. These microorganisms have influenced our evolution. They are essential to our digestion, metabolism, and immunity. However, they also serve as the source of our infectivity. Since 2007, the National Institutes of Health has supported the international Human Microbiome Project in its effort to understand the extent to which our microbiomes are unique to each one of us as individuals and common to all of us as a species.1,2

Our microbiota are organized as biofilms, impressively structured communities within 3-dimensional matrices of extracellular polymeric substances, the “slime” attached to epithelial membranes.3 Chronic bacterial infections are now recognized as biofilms that limit access by host antibodies and macrophages and resist diffusion of antibiotics.3–6 Biofilms of the same species of bacteria may be nonpathogenic in one location and pathogenic in others. For example, the most common cause of surgical site infections, defined as infections occurring within 30 days postoperatively or within 1 year if the surgery involved an implant, is Staphylococcus aureus.7 Yet, 20% of us are persistent asymptomatic carriers of S aureus in our anterior nares; 30%, intermittent carriers.8 Because we are constantly shedding bacteria from our biofilms,6,9 we as patients and health care providers contaminate every operating room we enter.9–14

How should our personal microbiomic “slime” affect our efforts to reduce surgical site infections? A report in this issue of Anesthesia & Analgesia by Loftus et al.15 addresses bacterial transmission via the hands of anesthesia practitioners. This is part of the growing knowledge of the etiology of surgical site infections, and complements previous work by Loftus and his group,12 Koff et al.,16 Comp?re et al.,17 Call et al.,13 and Haessler et al.18

In 2005, the Centers for Disease Control and Prevention established the National Healthcare Safety Network by combining the National Nosocomial Surveillance System, the Dialysis Surveillance Network, and the National Surveillance System for Healthcare Workers to benchmark and study health care–associated infection surveillance data.19 The National Healthcare Safety Network provides national rates for 5 such health care–associated infections: central line–associated blood infection, urinary catheter–associated infection, ventilator-associated pneumonia, postprocedure pneumonia, and surgical site infection. Surgical site infection data are divided into risk groups. Each patient is graded by 3 criteria and assigned a 0- to 3-point score (Table 1): 1 point if the patient is an ASA physical status III or higher, 1 point if the surgical site is known to be contaminated before incision, and 1 point if the procedure duration is in the longest quartile for the specific operation being performed. In 2 recent studies of surgical site infections in older patients, S aureus was the responsible pathogen in 51% to 56% of cases, more than half of which were methicillin-resistant S aureus (MRSA). Other common pathogens included coagulase-negative staphylococci (in 8%–12% of cases), other Gram-positive bacteria (8%–13%), Escherichia coli (4%–5%), and other Gram-negative organisms (5%–13%).7,20

View this table: In this window In a new window Table 1. Percent Surgical Site Infections for Common Inpatient Surgical Procedures

Because of the enormous cost of surgical site infections,21 it is reasonable to ask if a change in practice can lower the national rate of infection seen in the data collected by the National Healthcare Safety Network. The report by Loftus et al. supports this assertion. Haessler et al.18 linked a systemic breakdown in operating room handwashing compliance caused by an institutional change in the hand antiseptic product to an increase in the rate of surgical site infections, exceeding both internal and national benchmarks. Koff et al.16 documented that increased handwashing frequency by anesthesia providers decreased the rate of health care–associated infections.

Because the responsible pathogen for most surgical site infections typically originates from the infected patient's own microbiota8,14 and contaminates through bacteremia, skin migration, or bacterial airborne dispersal (“cloud” formation), it is appropriate to wonder whether anesthesia providers could be directly implicated as the cause of a surgical site infection. Three case reports are particularly instructive. In 1969, an anesthesiologist was reported as the individual directly responsible for 2 clusters of group A Streptococcus pyogenes surgical site infections involving 20 patients.22 The route by which the bacteria arrived in the surgical wounds was not established, but it was clearly demonstrated that bacteria in the rectum of the carrier became airborne (as measured by the number of colony-forming units in operating room air samples) with physical activity, friction with clothing, or flatulence.9 Once airborne, the wound could be contaminated directly by the bacterial “cloud” or indirectly by transmission of bacteria lodged on surgical instruments or gloves.9–11 If this was the route of contamination, handwashing by the anesthesiologist would not have prevented infection. Alternatively, the anesthesiologist could have practiced poor personal hygiene and touched patients with his contaminated hands or contaminated endotracheal tubes, catheters, syringes, or IV injection ports such as stopcocks. In that bygone era (experienced by the 3 authors of this editorial), anesthesia providers generally did not wear gloves and washed their hands infrequently. Herpetic whitlow and paronychia were, at the time, occupational hazards for anesthesia professionals.

In 2000, 2 pediatric intensive care unit nurses were identified as nasal carriers of MRSA and were treated.23 Hygienic measures in the unit were tightened, closely monitored, and reinforced frequently. Two months later, a blood culture positive for MRSA prompted a reexamination of the hospital environment. MRSA recolonization of the anterior nares was documented in 1 nurse, but she was not involved in the care of the index patient. The other nurse was the source of contamination, but her nasal cultures were negative for MRSA. However, cultures from her hands, forearms, elbows, axillae, neck, perineum, and anus were all positive, because she had extensive eczema. Despite apparently demonstrating excellent hygienic practice, she contaminated the sample of blood she collected from the patient. Skin typically resists S aureus colonization.24 When there is loss of skin integrity, however, as occurs with eczema, atopic dermatitis, psoriasis, furunculosis, or a wound, colonization readily occurs, especially in patients who are known nasal carriers.25,26

There is also the case of an orthopedic surgeon with chronic hepatitis C virus infection who did not infect any of his patients with the hepatitis C virus. However, during the year in which he was treated with interferon-?, his surgical site infection rate increased from 1% to 9%. After his hepatitis C therapy was completed, his surgical site infection rates returned to 1%.27 Interferon-? produces flu-like symptoms. Fatigue could have caused lapses in adherence to operating room asepsis protocol. Such lapses have been associated with an increase in the rate of surgical site infections.14,28 Alternatively, the flu-like symptoms he exhibited could have been premonitory of an increase in airborne dispersal of bacteria (the “cloud”). When healthy asymptomatic nasal carriers of S aureus were deliberately infected with a rhinovirus, a 2-fold increase in airborne dispersal of coagulase-negative staphylococci was observed.29 Histamine-induced sneezing caused almost a 5-fold increase in airborne dispersal of S aureus from healthy nasal carriers.30

Much of the airborne cloud associated with cloud-forming patients was reduced by having the patients change from street clothes to surgical scrubs. Adding surgical masks did not provide any additional reduction in the number of colony-forming units collected.31,32 The primary value in wearing surgical facemasks is to protect health care workers from splashes of body fluids from patients, rather than reduce the risk of airborne dispersal of bacteria by the health care worker. Evidence supporting the effectiveness of surgical masks in decreasing surgical site infections is equivocal at this time.33 To date, most of the effectiveness research regarding the use of high-efficiency particulate air filters as surgical masks has focused on prevention of health care–associated infections related to viral transmission and not on reduction of surgical site infections related to the airborne dispersal of bacteria.

If we accept that we are “slimed” by our personal bacteria, constantly contaminate our environment, and cause some surgical site infections, then we must also accept responsibility for reducing our personal contributions to surgical site infections. The obvious answer is “as simple as washing your hands.”34 Sadly, our documented compliance with handwashing guidelines is abysmal.35 There are multiple explanations for the wildly variable rates in our compliance with one of the most basic (and effective) procedures to decrease surgical site infection: hand hygiene. Self-protection of health care workers is a major subliminal driver for performance of hand hygiene, such that the rates of handwashing are significantly lower before patient contact than after.36 Lack of a positive role model leads medical students, residents, and nurses to copy the (negative) behavior of their supervisors.37 The length of professional education seems to be inversely correlated with the rate of hand hygiene compliance, with nurses having a higher rate of compliance than physicians.38 Knowledge of being observed (Hawthorne effect) doubles the rate of compliance with handwashing requirements,39 but the effect is transient. Translation of community handwashing behavior (i.e., inherent behavior learned in the community) to hospital settings seems to be the predominant driver of all handwashing behavior.40 Implementation of a Six Sigma process to increase compliance was effective and sustained for a 9-month observation period,41 although a significant incidence of unintentional noncompliance remained. Finally, there are nihilistic data to suggest that although many health care–associated infections may be prevented by improved handwashing compliance, they will not be completely eradicated42 because health care providers also contaminate the perioperative environment in ways not involving their hands, and because the patient's own microbiota are a prominent source of pathogenic bacteria.

Based on these data, we suggest it is time for us as individuals, and as a profession, to address the following questions: Should we obtain and monitor anesthesia provider–specific data regarding surgical site infections? What should we do with such data? How would we apply them? Equally importantly, is it reasonable to assume, if the occurrence of surgical site infections and care from a specific health care provider are temporally related, that this evidence is causative? Should all operating room personnel (surgeons, nurses, and anesthesiologists) be routinely cultured (anterior nares, skin lesions) for S aureus and MRSA? Would such cultures suffice, or should more invasive cultures, such as those obtained from the axillae, perineum, and rectum be required? Should known nasal carriers of S aureus be required to wear high-efficiency particulate air masks routinely or when they are sneezing frequently from respiratory allergens or have an upper respiratory infection? Should anesthesia providers with active eczema, atopic dermatitis, or furunculosis be restricted from administering (or even from directing or supervising) anesthesia to patients receiving implants or from placing central lines? Focusing on the data in this current article from Loftus et al., should we eliminate the routine use of stopcocks in our IV lines? Likewise, should we be developing better disinfecting protocols for our anesthesia equipment, including pagers, stethoscopes, and operating room–based computer keyboards? And should we ban all other equipment and accessories (such as personal bags and purses, portable radios, cell phones, lab coats, iPods, and speakers) from the operating rooms?

The cost of surgical site infections to patients and to all health care delivery systems is very high. We assume that the increased cost of implementing effective processes, however significant, will be more than offset by the reduced cost of treating surgical site infections, but this remains an unproven hypothesis. Lastly, we must avoid the trap of treating only surrogate end points, such as making expensive decisions to reduce bacterial contamination, without also documenting that these decisions lead to a reduction in surgical site infections and improve patient outcome.

 Next Section ACKNOWLEDGMENTS We thank P. Samuel Pegram, Jr., MD, and Robert J. Sherertz, MD, Section on Infectious Disease, Department of Internal Medicine, Wake Forest University School of Medicine, for their thoughtful discussions during the preparation of this editorial.

Previous SectionNext Section Footnotes The authors report no conflict of interest.

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