Perioperative Smoking Cessation and Anesthesia: A Review

Talmage D. Egan, MD,* K. C. Wong, MD, PhDj_ Departments of Anesthesia, Stanford University School of Medicine, Stanford, CA, and University of Utah School of Medicine, Salt Lake City, UT.

Perioperative smoking causes acute changes in cardiopulmonary function that can have unfavorable implications for patients undergoing

anesthesia.

These cardiopulmonary

Keywords: Smoking; smoking cessation; carbon monoxide; carboxyhemoglobin.

anesthesia;

ef-

fects are carbon monoxide and nicotine mediated changes in oxygen (OJ delivery and myocardial 0, balance. Smokers also are at increased risk for postoperative pulmonary corn,-

Introduction

plications

Although no formal consensus has ever been reached regarding the appropriate ASA physical status classification for asymptomatic smokers, anesthesiologists have long recognized that patients who smoke are often at increased risk for both intraoperative and postoperative complications.’ Data from a recent report of the Surgeon General indicate that, despite a dramatic decline in numbers over the past two decades, smokers still constitute nearly one-third of the U.S. adult population and thus present frequently for a wide variety of surgical procedures.’ Successful an_.rl-r:_ ___-__-____c r_-_c:__._ .Wll” ..1-_ SIIIVKC ___,._ ___..:___ cs111e11c IIlaIla~wlcIlL 101 piLlrIlLb 1 equ,, cs

function.

that are secondary Smoking-induced

ary function preoperative

to chronic

changes

in lung

acute changes in cardiopulmon

can be largely avoided

by a brief period

smoking abstinence. Bringing

in postoperative pulmonary

of

about a decrease

complications requires a much

longer period of preoperative

abstinence. Because

the per-

ioperative period is in many ways an ideal time to abandon the smoking

habit permanently,

anesthesiologists,

in coop-

eration with other health professionals, can perhaps play a more active role in facilitating this process.

*Fellow, Department tProfessor

of Anesthesia, Stanford University

and Chairman,

Department

of Anesthesiology,

Univer-

sity of Utah Address reprint requests to Dr. Egan at the Department of Anesthesia, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA 94305, USA. Received for publication December 7, 1990; accepted for publication June 25, 1991. 0 1992 Butterworth-Heinemann J. Clin. Anesth. 4~63-72,

1992.

revised manuscript

careful consideration of the pathophysiologic changes induced by smoking and prudent implementation of steps to prevent or mitigate complications. Among the many clinical issues requiring consideration, one of the most controversial is the question of smoking cessation. The optimal advice to patients regarding the timing of their preoperative smoking cessation has been confusing. Furthermore, the anesthesiologist’s role in helping patients embark on a course of long-term smoking cessation beginning with the perioperative period has remained largely unexplored. More conclusive preoperative advice based on recently available scientific data is now possible. Moreover: an expanding role of the anesthesiologist as a J. Clin. Anesth.,

vol. 4, January/February

1992

63

member of a multidisciplinary perioperative medical team in helping patients permanently abandon smoking is perhaps an appropriate wave of the future in anesthetic practice.

Physiologic Effects Data outlining the ill effects of tobacco smoke on the human organism have been collected over may decI‘:____&&‘ . __.. I... L”llLall,b _--r..:-.. “A_, Clllll -,A dlt: ___ _.,. _,...^ US;aI ClUCJ ““‘1..-.: UIIIIII”US. CLLC S111UKC well over 3,000 identified constituents, many of which have toxic or tumorogenic effects.” This wide variety of biologically active compounds accounts for tobacco’s broad and profound impact on health. Although virtually every organ system in the body is perturbed in some way, the cardiovascular and pulmonary systems are the primary targets of the most serious smoking-induced derangements.

Cardiovascular

System

Exacerbation of any existing imbalance between myocard.ia! nxvcwn CO.,\ 2nd d&very is per-..,u-_. \.-L, cnnsilmntion --__I-___r‘_l~~ -__haps the most significant acute cardiovascular effect of smoking. Nicotine, a ganglionic stimulant with widespread physiologic action, is the principal chemical mediator of smoking’s effects on the cardiovascular system. Due in part to stimulating the release of catecholamines from the adrenal medulla, nicotine acts as a potent adrenergic agonist and thus produces an increase in blood pressure, heart rate (HR), and systemic vascular resistance that persists for approximately 30 minutes after smoking just one cigarette.* An important new finding is that nicotine stimulates an increase in coronary artery vascular resistance, particularly in diseased arteries with severe proximal stenoses, further limiting blood flow to areas that may already be predisposed to ischemia? These effects mediated by nicotine combine to alter adversely the balance of myocardial 0, supply and demand. Compounded over many years, this disruption of normal myocardial 0, balance may be partly responsible for smoking’s association with ischemic heart disease. Like nicotine, carbon monoxide is another of the tobacco smoke by-products responsible for adverse aiterations in myocardiai 0, baiance. Carbon monoxide is a colorless, odorless gas produced by incomplete combustion of the organic material found in cigarettes. Because hemoglobin has a much higher affinity for carbon monoxide than it does for O,, smokers develop levels of carboxyhemoglobin (COHb) reaching as high as 15%, despite the relatively low 64

J. Clin. Anesth., vol. 4, January/February 1992

It:\els of carbon monoxide inhaled in cigarette smoky. It is commonly knmvn that high (:OHb levels result in correspondingly lower oxyhemoglobin levels, lvith a net decrease in blood 0, content. It is perhaps less commonly kncnvn that carbon monoxide shifts the oxyhemoglobin dissociation curve to the lef‘t, theret)\ increasing hemoglobin’s affinity for O,.” A leftwar; shift in the oxyhemoglobin dissociation curve car1 result in a decreased release of 0, to the tissues. Thus, the carbon monoxide inhaled by smokers can produce tissue-ievei hypoxia by MO mechanisms. Evidence aiso indicates that carbon monoxide may have a weak, direct, negative inotropic effect on the heart.” The net clinical effects of nicotine and carbon monoxide in disrupting the normal myocardial 0, balance have been con\,incinglv demonstrated in numerous human laboratory studies. It has been shown, for example, that the time to onset of angina during exercise in patients with known coronary artery disease ((XI)) is significantly shorter when patients breathe air containing enough carbon monoxide to produce CX)Hb levels of 4.5% .I” The duration of angina1 episodes produced under such conditions also is prolonged. Other investigators have reported that physical work ca1Kl’ A.L.) Cl1P~~IXlEPE -b-L LL..>,_., ..* --.,.,. ‘._.^ 2-s 2. function of HP r”-“,citv, tllP2cIIrfVi markedly when recent smoking has produced average COHb levels approaching 10%. 11Yet COHb levels of less than 10’S are modest compared with the levels some frequent smokers may develop and maintain.12 Furthermore. a long suspected association between high (X)Hh levels and cardiac arrhythmias has recently been confirmed in patients with CAD. When patients with known CAD breathed an air-carbon monoxide mixture sufficient to produce COHb levels of’ 6%, investigators noted a significant increase in both simple and complex ventricular arrhythmias.“< Interestingly, this increase in cardiac ectopy was not observed when carbon monoxide levels were adjusted to 4%. Thus, the combined phvsiologic effects of tobacco smoke’s carbon mon;x&ie and nicotine can translate clinically into decreases in cardiopuhnonar) reserve. ‘I-his impairment of cardiopulmonary function can be understood in more practical terms when considering that the physiologic impact of carboxvhemoglobinemia of 5% has been equated with tl;e impact of moving from sea level to an altitude of 10,000 feet.” Another aspect of smoking-induced carboxyhemoglobinemia of special importance to anesthesiologists is the effect of high COHb levels on pulse oximetry. Carboxyhemoglobinemia to any degree is known to result in a proportional overestimation of arterial hemoglobin 0, saturation as determined by pulse OXimetry. Because currently available pulse oxirneters

Perioperative smoking cessation and anesthesia: Egan and Wong

measure light absorbance at only two wavelengths, they cannot discriminate between more than two species of hemoglobin .I4 Hence, pulse oximeters respond to COHb as if it were oxygenated hemoglobin; the oximeter reading is roughly the sum of the COHb and the oxygenated hemoglobin.15 At high levels of COHb, the oxyhemoglobin saturation can be grossly overestimated. In a patient with 10% COHb, for example, the pulse oximeter may display a saturation of close to lOO%, when in fact the actual saturation is less than 90%. This COHb-related problem with pulse oximetry has obvious implications for the anesthesiologist responsible for ensuring adequate oxygenation of the unconscious patient under general anesthesia. Reversal of these smoking-induced changes in cardiopulmonary function and pulse oximetry monitoring depends almost entirely on the biotransformation and/or elimination of the principal chemical mediators, nicotine and carbon monoxide. The bulk of nicotine is transformed in the liver to conitine, which is excreted in the urine, while carbon monoxide depends entirely on the lungs for elimination. The halflives of nicotine and carbon monoxide are such that the acute decreases in work capacity and threshold to angina1 pain demonstrated in these human laboratory studies are reversible with relatively brief periods of abstinence from smoking. This is consistent with the observation from the anesthesia literature that COHb levels and P,, values (partial pressure of oxygen at which hemoglobin is 50% saturated) in patients who smoke fall to near nonsmoker levels after a i2-hour period of smoking abstinence, as shown in Table 1 .I6 The acute hemodynamic effects of smoking, therefore, appear to be largely reversible with a simple overnight preoperative fast. There is new evidence, however, that the half-life of carbon monoxide is longer in men than in women, and thus a period of abstinence longer than I2 hours may be desirable in men. I7 Mean Total Hemoglobin, Carboxyhemoglobin, and P,,, Values in 15 Smokers Before and After a IZ-Hour Smoking Fast

Table 1.

Variable

Before

After

Hb (g/dl) COHb (%) Pj, WmHg)

15.74 6.55 22.92

15.56 1.06 26.41

Hb = hemoglobin; pressure of oxygen

COHb = carboxyhemoglobin; P?,, = partial at which hemoglobin is 50% saturated.

Source: Adapted from Kambam JR, Chen LH, Hyman SA: Effect of short-term smoking halt on carboxyhemoglobin levels and Pj, values. Anesth Analg 1986;65:1186-8.

Pulmonary System In view of tobacco’s well-described association with chronic obstructive pulmonary disease (COPD), it is not surprising to discover that smoking’s effect on the lungs is not limited to an impairment of hemoglobin saturation secondary to a decrease in the amount of 0, available for alveolar gas exchange. Smoking also may cause hypersecretion of mucus and dysfunction of ciliary activity secondary to the irritant and ciliostatic factors found in cigarette smoke. These functional abnormalities result in a marked impairment of tracheobronchial clearance.ls While chronic smokers with COPD show an obstructive pattern on standard spirometric pulmonary function tests (PFTs), asymptomatic smokers usually have grossly normal PFT values.1g,20 However, even in asymptomatic patients, smoking is known to cause increases in closing volume, which is thought to be an indicator of small airway disease. 21 This increased closing volume can usually be documented by sensitive testing (singlebreath argon technique) in smokers who exhibit completely normal values on conventional spirometric PFTs. Other tobacco-induced changes in lung function may include increased bronchial reactivity, alterations in pulmonary macrophage function, and changes in pulmonary surfactant.7 In contradistinction to smoking’s acute cardiopulmonary effects, many of these disturbances of lung function are chronic, necessitating a long period of abstinence before any return toward normal function. Although somewhat controversial, there is general consensus that in COPD patients with grossly abnormal PFT values, no dramatic improvement can be expected upon cessation of smoking, although the rate of further decline in PFT values appears to normalize.20 Similarly, in relatively asymptomatic smokers whose PFT values are already normal, little if any improvement in spirometric PFT values is observed after quitting cigarettes, though some increase in the maximal expiratory flow rates may be noted in some subjects. lg However, significant improvement in these asymptomatic patients is seen after smoking cessation in tests of small airway function such as closing volume. These expected improvements in closing volumeLg and small airway function,zO along with _l_.. ___ 111 1._~purum _._~~L~~.__ ._.._ 3 ~uanges prouuction’ ? and tracheobronchiai clearance,‘3 appear to require a minimum of 6 to 8 weeks.

Other Organ Systems -._. .

W bile the perturbations in cardiopuimonary function are perhaps the changes most relevant to anesthetic J. Clin. Anesth., vol. 4, January/February

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65

practice, smoking’s impact on other organs car1 SOIIKfor the anesthesiologist. times have implications Smoking, for example, can induce hepatic microsomal enzyme systems and thereby increase the metabolism of certain drugs (~.g., barbiturates and benzodiazepines).‘” This is consistent with the observation that patients who smoke require larger doses of opioid for coronary artery bypass operations when a high-dose opioid technique is used. 25 In addition, alterations in blood components such as polycythemia, increased platelet aggregability, decreased natural killer cell activity, and low immunoglobulin levels have potential implications for smokers undergoing anesthesia and surgery.‘“-“” The issue of smoking-associated changes in gastric volume and acidity has special relevance to anesthesia. Laboratory studies addressing this topic have yielded conflicting results. Some studies have demonstrated rl~1-a.r 11, in fi”0’ m-act,-;,.amnt.i;nrr xanrl U‘ ‘an1 111L1X_U.J1 ;~r,>l “U0UI while other studies have come gastric acid secretion?’ to opposite conclusions. 32.33There also have been reports that smoking may decrease lower esophageal sphincter pressure.:“’ In any case, two recent clinical studies assessing the effect of perioperative smoking on gastric volume and acidity have failed to show a significant difference between smokers and nonsmokers; even when smokers were allowed to smoke two cigarettes at the time of premeditation administration.““,“” Thus, although smoking had once been considered a potential risk factor for anesthesiaassociated aspiration pneumonia, there does not appear to be compelling laboratory or clinical evidence to support this notion. Unfortunately, the reversibility of many of these pathologic changes secondary to smoking has not yet been adequately studied. In view of smoking’s farreaching impact on various physiologic systems, it is little wonder why tobacco use has been associated with CAD, hypertension, COPD, peripheral vascular disease, and numerous cancers, all of which may at times have important implications for anesthetic management. Interestingly, because tobacco smoke is often involuntarily inhaled by nonsmokers, frequent “passive” smokers may be predisposed in some unknown degree to many of the same diseases and perioperative risks as smokers.“’

Clinical

Effects

Postoperative Pulmonary Comfdications The suggestion that smoking-induced physiologic derangements demonstrated in the laboratory can ac66

J. Clin. Anesth., vol. 4, January/February 1992

tually produce increased perioperative morbidit\, III ;I clinical setting is supported by an impressive arra\ 01 evidence. ‘I-he observation that smokers are at greatI\ increased risk for postoperative pulmonary complications such as ateiectasis and pneumonia dates back to as early as 15144.“HIn this early report, smoking was associated with a sixfold increase in postoperative pulmonary morbidity. More recent studies and revie\cs have repeatedly confirmed this initial observation that smokers are predisposed to postoperative pulmonary morbidity.--,,I”’‘VI .. “I The definition of pulmonar), morbidity in these studies varied and included problems such as atelectasis. pneumonia, and bronchospasm, among others. Nonetheless, a common denominator in all of these investigations lvas a strong correlation between smoking and postoperative respirator) complications, however defined or determined. Kecognition that hospital-acquired pneumonia, though less rr,mmnn th.>n t-,. L&L lllUl I tr’ II >,-t ‘ALL “, WI”U&IU XLLI\Ib-L..,,..., acounts for more fatalities than nosocomial infections at any other site underscores the potentially catastrophic significance of postoperative complications in the lung. iI Surprisingly, because smokers exhibit significantly decreased expiratory flow rates and volumes under subarachnoid block when compared with nonsmoker controls, it has been suggested that smokers mav be at increased risk for postonerativr I -~ ~~~~ respiratory morbidity even when anesthesia is provided by spinal block.” When compared with nonsmokers. smokers appear to be at increased risk for hypoxemia in the recovery period whether they are anesthetized with general or regional techniques. although hypoxia episodes in smokers are more common after general anesthesia.“” Unfortunately, a simple preoperative overnight smoking fast is not effective in reducing postoperative pulmonary morbidity in smokers who undergo surgery and anesthesia. The failure of short periods ofpreoperative abstinence in prophylaxing against smoking-related lung complications was first noted in a retrospective study of 500 patients undergoing coronary artery bypass grafting (CABS), as shown in Figuw 1. 14 A threefold decrease in the rate of postoperative pulmonary complications was observed in patients who had stopped smoking more than 8 weeks before surgery when compared with those whose period of abstinence was less than 8 weeks. Patients who had abandoned their smoking habit for more than 8 weeks had a pulmonary complication rate approaching those of patients who had never smoked. Curiously, patients whose period of preoperative smoking abstinence was less than 8 weeks actually had pulmonary complication rates slightly higher than smokers who had smoked up to the day of surgerv.

Perioperative smoking cessation and anesthesia: Egan and Wong

The essence of these provocative findings was recently reproduced in a blinded, prospective study patterned after the original study at the same institution and involving 192 patients undergoing CABG procedures.45 The investigators found that postoperative pulmonary complications occurred in 33% (6 of 18) of current smokers, 57% (12 of 21) of patients who had quit for less than 8 weeks, and an average of about 12% (18 of 153) for both ex-smokers who had quit for more than 8 weeks and nonsmokers, as shown in Figure 2. This constitutes a nearly fourfold increase in pulmonary morbidity in patients who quit smoking less than 8 weeks preoperatively compared with patients who quit for a longer period. As in the original study, pulmonary complications were defined as lung problems requiring therapy beyond their standard postoperative care, including pneumonia, bronchospasm requiring dilator therapy, and pleural effusion requiring drainage. This important new study prospectively confirmed the futility of brief preoperative smoking cessation in preventing postoperative pulmonary complications in patients undergoing CABG. These findings are consistent with what is known about the recovery speed of various chronic abnormalities of lung function.

100

J

1

s-

70

.r-

so -

fl

50

-

.x

N-21

-

SYOK

< 5 WKS Smoking

NONSYOK History

Figure 2. Percentage of patients who suffered postoperative pulmonary morbidity grouped according to preoperative smoking history. The data were gathered prospectively

ir? 142 ~“““AL” ngtient~

whn IV...,

,,nrl.wuien+ U.IYCI I,..11L

,-n~--cln~v-.~ _“a “l&U1

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h.rew.. “J p.70

grafting. SMOK = patients who smoked up until the day of surgery; 8 WKS = patients who quit smoking more than 8 weeks before surgery; NONSMOK = patients who never smoked; N = total number of patients in each group. (Source: Compiled from data in Warner MA, Offord KP, Warner ME, Lennon RL, Conover A, JanssonSchumacher U: Role of preoperative smoking cessation and .,+c-.. laCL”l C”,+,,,,J 111 :, pvxvpc, __.-* ____ PLI”lz ,.+:..- t)UIIII”ll‘ -..I ___^_.I ^^__ 1:--r: ^_^. a “CllLl ll y C”lllt)ll‘ dLI”IIS. blinded prospective study of coronary artery bypass patients. Mayo Clin Proc 1989;64:609-16.)

Other Complications

SMOK

< 8 WKS Smoking

>

8 WKS

NONSMOK

History

1. Percentage of patients who suffered postoperative pulmonary morbidity grouped according to preoperative smoking history. The data were gathered retrospectively in 500 patients who underwent coronary artery bypass grafting. SMOK = patients who smoked up until the day of surgery; 8 WKS = patients who quit smoking more than 8 weeks before surgery; NONSMOK = patients who never smoked; N = total number of patients in each group. (Source: Compiled from data in Warner MA, Divertie MB, Tinker JH: Preoperative cessation of smoking and pulmonary complications in coronary artery bypass patients. Anesthesiology 1984;60:380-3.)

Figure

Although investigators have focused primarily on acute postoperative lung disturbances, smoking-related complications in other organ systems also have been described. Smokers who undergo femoropopliteal bypass grafting procedures, for instance, exhibit markedly lower graft patency rates and higher limb loss rates when followed from the immediate postoperative period for up to 5 years.46 Similarly, the risk of skin flap necrosis after a face-lift procedure is known to be more than ten times higher in smokers than in nonsmokers.47 Serving as a dramatic example of the adverse effects of smoking in the immediate perioperative period, other investigators reported the acute loss of previously viable revascularized digits that appeared to be directly precipitated by smoking postoperatively.48 These illustrative studies and reports emphasize the impact that perioperative smoking may have on specific measures of operative outcome. Complications attributed to smoking are not limited to problems traditionally linked to recovery from anesJ. Clin. Anesth., vol. 4, January/February

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67

Armed with knowledge about the anesthetic implications of smoking, particularly with respect to cardiopulmonary fitness, the anesthesiologist should find

proving adverse effects secondary to smoking in I ht immediate preoperative period are not available, it iz only logical to extend intraoperative efforts to ensure favorable myocardial 0, balance into the preoperative period as well. I Ience, because perioperative smoking is likely to be particularly dangerous to patients with ha r\nr**,\lr,A if I, r,.,t;u.,t L1__,_ LclJCJ I.,.r-r ,h,,..li Jll”LJlU “L ywL~“IILu II a plUL.111 CAI> , 3”lllL with CAD has been smoking prior to a procedure. Cancellation of a procedure. of course, would not always be in the patient’s best interest depending on the urgency of the planned procedure, among other considerations.

theoretical advantages of a preoperative overnight smoking fast. Unfortunately, specific outcome studies proving the usefulness of a preoperative fast in reducing intraoperative complications such as hypoxemia or myocardial ischemia are not available. It is clear, however, that the combined effects of nicotine and carbon monoxide on myocardial 0, balance are unfavorable. And, of course? other organ systems in addition to the heart also must subsist on the reduced blood 0, content produced by smoking. Furthermore, the increased frequency of ventricular arrhythmias and the inaccuracy of pulse oximetry associated with increased COHb are no doubt detrimental to the patient under anesthesia. It is fortunate that these acute effects on cardiac function, blood 0, content, and pulse oximetry are largely reversible with an overnight smoking fast. While certainly not an important issue in every case, providing a more favorable myocardial 0, balance or a higher blood 0, content may be important in selected patients when considering the patient’s coexisting disease or the magnitude of the proposed surgical procedure. It would be difficult, for example, to argue against preoperative smoking cessation in a patient with stable angina scheduled for hernia repair. Similarly, it would be unwise to argue against a preoperative smoking fast in an otherwise healthy smoker scheduled for radical hysterectomy. In such patients, if not in all patients, the improvement in cardiovascular fitness alone is probably ample justification for a preoperative 12- to 24-hour smoking fast.i.lz.4Y Available data suggest that a preoperative smoking fast is particularly important in patients with CAD. Much of the accumulated evidence outlining the deleterious effects of cigarette smoking on cardiac rhythm, blood 0, content, and myocardial ischemia L_” L_,.,..-*l-,.-,.-l I‘ c-,.-. ....L bfi,u. rr\n TL..” Ild> “CC,, g;dLllts1cu “111 --r:,.-+)JdLICIILS.WlLll I1111>, these data are especially applicable to such patients. Anesthesiologists are careful to take steps to ensure a favorable myocardial 0, balance in patients with CAD during the course of an anesthetic. While studies

esthetist should consider spending a few minutes explaining the possible benefits of a preoperative smoking fast. After coming to an agreement with the patient, an order in the chart making the patient’s nurse aware of the plan regarding preoperative smoking abstinence would be appropriate. Because a large proportion of surgery is done on an outpatient basis, some mention of the ovrrnig_ht __ ..-u--- smnking ._____.___0 f;lst ---- should be made in the correspondence sent to patients by the outpatient clinic. In a recent study, written advice sent to the patient prior to admission requesting that the patient quit smoking 5 days prior to an operation was successful in convincing nearly 50% of the patients to quit for at least 1 day preoperatively.io Sadly, evidence suggests that a simple overnight smoking fast will not be effective in reducing postoperative pulmonary morbidity such as atelectasis or pneumonia. As noted, two clinical anesthesia studies bv Warner et (IL.,~‘,~”the most recent of which was prospective and blinded, G have verified what was suspected on the basis of numerous pulmonology studies designed to establish the time course of lung recovery after quitting cigarette smoking. Accordingly, preventing postoperative respiratory morbidity in patients undergoing CABG necessitates a minimum of’ 8 weeks’ preoperative smoking cessation. These findings are based on data from patients who underwent sternotomy and were thus predisposed to postoperative pulmonary complications. ‘I’heir generalizability with respect to other types of procedures is a matter of judgment. The results of these clinical outcome studies, however, are difficult to ignore. They clearly suggest that smoking cessation for at least 8 weeks is necessary for a reduction in postoperative lung complications and that smoking cessation for a shorter period may actually be undesirable. At the very least, it is iikely that these findings appiy to any procedure that is associated with a high rate of pulmonary complications. For the vast majority of patients who smoke, promoting a prolonged period of preoperative smoking

thesia, such as hypoxia and atelectasis. Beyond these anesthetic-related complications, smoking may at times directly foil the specific goals of the surgical procedure.

Advice to Smokers Preoperative

Abstinence

IittL L “““L”“, riiffTrxlltxi 1.1 in .,““““““b d11f-3tinc7 IILL‘

68

J. Clin. Anesth.,

vol.

natif=nt< ‘ reuarrlina y-L.%““” -a”‘““‘b

4, January/February 1992

the

Perioperatiue

abstinence is logistically impossible.51 The process of patient identification and education, followed by patient support and compliance verification, is difficult. Any such effort is further complicated by the fact that preoperative smoking cessation for a period of less than 8 weeks may actually be associated with increased chances of postoperative lung complications. However, because of severe ongoing cardiopulmonary disease or the unusually ambitious nature of the contemplated procedure, there may be patients for whom extraordinary efforts in promoting a long period of smoking abandonment might be fruitful. Surgeons could no doubt be more effective in this effort than anesthesiologists because they often are aware of a patient’s forthcoming procedure many months in advance. It might at times be appropriate to cancel or postpone an elective procedure in a heavy smoker who, for whatever combination of factors, appears to be particuiariy vuinerabie to postoperative respiratory complications. In geographic regions or hospital systems where a long waiting period is an unavoidable part of the surgery scheduling process, anesthesiologists or surgeons could advise patients by mail regarding the planned perioperative management of smoking.5o As a practical matter, because of obvious logistical -L-r--l__ _-__~l__.:_1--:_._ -__- ___L,I,.-1.. *L-..- -‘-. OUSLdClCS, iillf3LIl~S1OIU~l~l~ ii1.C IIUL IlKClY LU IlLtVfZ Slgn&ant success in fostering smoking cessation for the long period required to achieve a reduction in perioperative lung complications. When it is possible to foster smoking cessation for more than 8 weeks preoperatively, it is not surprising to find that such patr. .-0,,;, c...,,,,..~..l tients are much more 1;1,,1., llhrly L” ‘r;lllalll JucccDJlu, quitters indefinite1y.j’

Postoperative

Cessation

While preventing perioperative complications is a worthwhile aim, perhaps an even more important goal :” l.,l,:,n,_t:,._+n ,..__,,Tl ;, l,,, +-rm c.he-rlfi---s+ I3 UcqJu’g plLlCllLJ DUCCCCU 111 I”‘lgJj-&;I 111 cl”allu”IIIIIc;IIL of the smoking habit. Smoking is unquestionably the most important preventable cause of mortality in the United States and is thought to be responsible for one physicians have of every six deaths. 2 Collectively, largely failed to optimize the impact they could have in promoting smoking cessation. It has been repeatedly suggested that the power of the medical profession to curb tobacco use has not been fully realized.53 Indeed, a review of studies on physician intervention for smoking cessation reveals that nearly two-thirds of physicians do not regularly advise patients who smoke to quit. 54 In a recent survey of smokers seen by a physician during the 12-month period prior to

smoking cessation

and anesthesia: Egan and Wong

being surveyed, only 44% reported that they had ever been told to quit smoking by a physician.55 This collective failure of physician willingness to intervene persists despite a plethora of data showing that simple physician advice to patients can contribute to successful abandonment of habitual smoking.54 One representative study demonstrated that when survivors of myocardial infarction were given a detailed explanation reinforced with written advice outlining the merits of smoking cessation, 62% were able to quit smoking when followed up for 1 to 3 years.56 In fact, even minimal physician counseling consisting of brief, simple education and advice has been shown to be efficacious in convincing some patients to quit.j7 A meta-analysis of 39 controlled trials of smoking cessation concluded that a team of physicians and nonphysicians delivering individualized advice on multiple occasions would likely be most successful in motivating patients to quit smoking.j* Such physician advice takes on greater importance in view of the fact that, although a wide variety of commercial programs exist to assist patients with quitting smoking, most patients quit on their own, and many are influenced to do so because of advice from a physician.5” Fortunately, physicians are presented with ample opportunity to counsel patients to quit smoking. It is estimated that smokers average 4.3 physician visits per year,60 and at least 70% of smokers see a physician each year.54 These estimates do not include contact patients have with anesthesiologists in preoperative and postoperative visits. The perioperative period clearly serves as an ex--11--* L,,a‘ _L--__ _.._.._*:-.. Cll”, -IX,.-+L.?fil Lel,el,L lLe *L” L-Lvegm ^ * ..-,.I.:->m”nlllg CC>&iLI”II “_Hospitalized patients are not allowed to smoke for any number of reasons, including the proximity of 0, in use and hospital policy prohibiting smoking except in designated areas. Hence, smoking within the hospital is inherently inconvenient. Moreover, some patients may actually present for surgery to repair or mitigate the effects of a smoking-related illness. The w~li~at~nn I LUllLcACI”IIthat Cl-UCtnharrn CVYU..LVIIEP . . ..I hzs rpSgitpd

jp_ ap_ iiip_pss

requiring surgery may contribute to the patient’s motivation for giving up cigarettes. All these factors present the anesthesiologist, as a member of a multidisciplinary perioperative team comprising surgeons, nurses, respiratory therapists, and others, with an excellent opportunity to help the patient initiate a trial of smoking cessation. The perioperative setting is unique in its intensity and pervasiveness. Primary care physicians rarely have any other chance to encourage their patients repeatedly to quit smoking in an environment in which smoking is inconvenient and at a time during which patients are more likely to be concerned about perJ. Clin. Anesth.,

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sonal health. Working in conjunction with other professionals, physicians can repeatedly educate and encourage patients. Follow-up encouragement can easily be arranged by the operating surgeon. This is an aspect of anesthesia practice that has not received the attention it deserves. fi2 It is a simple, safe, inexpensive change in anesthesia practice that, if implemented, could have a positive impact on patient health. Perhaps anesthesiologists should consider including a brief segment of education and encouragement intended to foster smokitig cessaiiori in all pi-eoperative and postoperative visits. At the very least, simply pointing out to patients that the perioperative period is an ideal time to quit might be a worthwhile change in practice routine. A potential disadvantage of advocating permanent smoking cessation at the preoperative visit is the effect that such dogmatic advice may have on patient rapport. Some patients may be embarrassed or angered by such personal counseling from a physician whom they have only recently met. There will occasionally be particularly anxious or hostile patients for whom such advice should be prudently tempered as circumstances dictate. Still other patients may respond better to f+lJcrcreftic>nc revarclincr sE_Qkip_g ccssa[iQp. jp_ [he bb _I__V._Y --n----_--b postoperative period when they have had more perience with the anesthesiologist and surgeon. course, there may be some patients from whom, a variety of reasons, advice regarding smoking sation should be withheld altogether.

exOf for ces-

Summary Smokers present frequently for surgical procedures of all types. The widespread physiologic effects of tobacco smoke pose certain risks to smokers who undergo anesthesia and surgery. In particular, the disruption of normal myocardial 0, balance mediated by the nicotine and carbon monoxide found in tobacco smoke may decrease a patient’s cardiopulmonary fitness for anesthesia. High COHb levels also interfere with the accuracy of pulse oximetry. Furthermore, smokers are clearly at increased risk for postoperative respiratory morbidity, including nosocomial pneumonia, which can frequently be a lethal complication. Other smoking-related physiologic derangements such as polycythemia, hepatic enzyme induction, immune system inhibition, or coagulation system disruption can conceivably predispose patients to a variety of intraoperative and postoperative complications. Finally, for certain operations, particularly vascular procedures, smoking may actually lead to failure of the specific goals of surgery, such as necrosis 70

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of a reimplanted finger or thrombosis of a prosthetic vascular graft. Because many of the pathologic effects of smoking are largely reversible, smoking-related perioperative complications can perhaps be mitigated with appropriate planning. A 12- to 24-hour preoperative smoking fast, which is essentially an overnight fast begun in the early evening, can be expected to yield a bettrl state of preoperative cardiovascular fitness. This is obviously more important in patients with compromised cardiopuimonary systems. Bringing about a decrease in postoperative pulmonary complications requires a much longer period of smoking cessation. At least 8 weeks of smoking abstinence appears to be necessary to decrease the risk of postoperative problems in the lung. There is some question that abandoning cigarettes for a period of less than 8 weeks may actually increase the predisposition to postoperative lung problems. With respect to long-term smoking cessation, the perioperative period is in many ways an ideal setting to initiate a tr\; at kicking the smoking habit. There is ample evidence that physicians of all specialties arc not participating as actively as possible in advising n~t;entc thqt t/““._“‘” t,, 1.1 n,,;t ‘i”” -, * he .*.. effect LLlrr. r~f,-imr~tt~ .,&._‘b”.._‘“-

KM: CIttiting ph\stc ians ag,tittst smoking: tlt~ ttcctl tot- a c~ootxlit~a~etl tiatioti;rl stratcg:\. ,/.\:21A 198X:L’i!J: ‘Lwo- I ,FA. Okene JK: Phvsician tleii\eretl tnterventiotts tilt- htrtol\ing cmsation: ~trairgirs for increasing et‘lecti\-eness. I’vi 1987: 16:723-37. :Md 5.5. Anda RF, Remingtott PL. Sienko I)(;, Davis KM: :\tt physicians advising smokers to quit? The patient’s pet-spective.JA:ZlA 1987:2.57: 1916-9. 56. Burt I1, Illing:M’orth I), Shaw I‘RD, ~I’hornley I’, \Vhitr P. furner R: Stopping stnoking after m~ocardial intnt-ction. fxlrrcc~t 1074; 1:X)4-6. 57. Russel MAH, Wilson Cl. ‘I‘aylor C. Baket- CD: Effect cut w~~~=rxl sp_c~!&g. _K! l?~p~!,/ ,,_“_ ._.. nr.xtitionrl.‘ *,~“_ . . . .E _._. ,, :~1~1viw . . . .._ scninst “,,_~..“‘

smoking on skin-flap survival in the face lift patient. Plast Reconstr Sulg 1984;73:91 l-5. Wilson GR, Jones BM: The damaging effect of smoking on digital revascularization: two further case reports. Br J Plast Sur;c: 1984;37:613-4. Jones RM: Smoking before surgery: the case for stopping. Br Med J 1985;290: 1763-a. Shah MV, Watkins G, Latto IP: The effect of written “A.,;,.- n.5 R LIU”,LL “I1 VxraC..Vz.r~t;.,u ~l~l,~~laUYc r;,Vrrp+ry 11#U‘~LCc-,,\~,,%mr.t;~,, \\,,,0U”L~CL”“. ‘Ann lll,L II Co11 Swg Engl 1984;66:436-7. Gomez MN, Tinker JH: Smoking, anesthesia, and coronary bypass operation: a witches’ cauldron? Mayo Clin Proc 1989;64:708-11. Berg GA, Kirk .?JB, Bain WH: Stnoking habits after coronary artery bypass surgery. BY,\ Clin Pratt 1988; 42: 1X1-3.

1979:2:231-r,. :i8. Kortke I‘E, Battista RN. DeFriese GH, Brekke ML: Atribures of successful smoking cessation interventions in medical pr-actice. A meta-analysis of 39 controlled trials. ]AIZIA 19X8:259:288%9. 59. Fiat-e MC:, No\otny I‘E, Pierce JP, et al: Methods used to quit smoking in thr L‘nited States. Do cessation programs help? ,];i,LIA 1990;263:2760-5. 6!!, TA~,t.,lD*UP , I‘ r,,C.cr !)I;: Se!!-;,I epc>r!ed nh,,c;r-,>I hw>lth ,,._IL,L, 111 \IIcL._.7., y”,““‘““’ LICU,LII practices and health care utilization: findings from the national health inter\,iew surcev. Ant 1 Public Hmlth 1985.75: 1._ ‘(‘V-w.~ ,, 6 1. Jones KM, Rosen M, Seymour 1,: Smoking and anaesthesia. A~wetlhccicz 19X7:42: l-2. 62. Callandet- (XZ: Smoking and anaesthesia [Letter]. At(rLlJ.\thu.ticr 1987;32:7701.

44. Warner MA, Divertie MB, ‘linker-,]H: Preoperative cessation of smoking and pulmonar-y complications in coronary artery bypass patients. AwsUtesiolo,~ 1984;60:3803. 45. Warner MA, Offord KP, Warner ME, Lennon RL, Conover A, Jansson-Schumacher I’: Role of preoperative smoking cessation and other factors in postoperative pulmonary complications: a blinded prospective study of coronary artery bypass patients. ;Vn?o Ch Proc 1989;64:609-16. 46. Ameli FM, Stein M, Aro L, Pro\an JL, Prosser R: ‘[‘he effect of postoperative smoking on femoropopliteal laypass grafts. .4n,t I’asc Surg 1989:3:20-5. A7 I,.

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