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Preventing or reducing smoking-related complications in otologic and neurotologic surgery

Golub, Justin S.a,b; Samy, Ravi N.a

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Current Opinion in Otolaryngology & Head and Neck Surgery: October 2015 - Volume 23 - Issue 5 - p 334-340
doi: 10.1097/MOO.0000000000000184
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In this review of smoking-related issues and otologic surgery, we assess the newest research in an era of electronic (e-) cigarettes and debate for legalization of marijuana. With a steady accumulation of evidence over previous decades for smoking's negative effects on surgical complications and patient outcomes, largely from other surgical fields, our review addresses clinical data and physiologic evidence for its particular impact on otologic outcomes.

Smoking remains one of the greatest problems in medicine today. Numerous high-quality studies have shown a causal effect between smoking and heart disease, cerebrovascular disease, and chronic obstructive pulmonary disease – the three leading causes of death worldwide [1–3]. Other harmful conditions, such as alcohol dependence [4] and certain types of cancers occur in greater rates among smokers. Smoking is the number one preventable cause of premature death [5].

The relationship between smoking and otologic surgery has been less robustly studied. However, data exist in other fields of surgery on the negative impact of smoking on surgical complications and outcomes. A steady accumulation of evidence over the past few decades has suggested that smoking is associated with poorer otologic outcomes in many, but not all, situations. Although there have been no breakthrough studies in the past year, we assess the available literature with emphasis on newer research. Aside from clinical data, there is ample physiologic evidence that smoking should negatively impact otologic outcomes on a theoretical basis. This includes the local, regional, and systemic effects of cigarette smoke and its chemical contents.

Recently, there has been a trend from traditional paper-based cigarettes to electronic cigarettes that deliver purified nicotine via water vapor. Although this activity is too new for studies on its relationship to otologic surgery, there is great interest on whether this represents a positive or negative public health phenomenon. For example, while electronic cigarettes might lead to decreased rates of traditional cigarette smoking (which is probably more harmful), they may also cause an increased rate in nicotine use overall. Finally, the effect of marijuana on otologic surgery is becoming more relevant as several American states have recently legalized its use.

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The Medline database was searched for titles/abstracts containing smok* and the following terms: otology*, Eustachian tube, tympanoplasty, ear surgery, mastoidectomy, mastoid surgery, staped*, stapes surgery, cochlear implant, skull base surgery, neurotolog*, translab*, retrosig*, middle fossa*, CSF leak. Additional studies of interest were obtained from references of relevant articles. Emphasis was given to recent studies, particularly within the last year. When data were not available or conclusive, recommendations were based on our subjective experience.


The biologic effects of tobacco smoking on tissues of the ear are well known. These can be divided into three categories: local, regional, and systemic.

Local effects are those that directly influence the ear. Cigarette smoke affects goblet cells and, in turn, the quality and amount of mucus [6,7]. Middle ear ciliary function may also be adversely affected [8]. Of note, mucociliary dysfunction is due to the toxic byproducts of tobacco combustion, rather than the nicotine chemical itself [9]. Vasoconstriction, in contrast, is directly caused by nicotine consumption [10]. Nicotine can also decrease blood perfusion to local flaps whereas carbon monoxide in smoke can reduce the carrying capacity of oxygen to the healing tissue.

Regional effects include alteration of Eustachian tube and adenoid function. Smoke-induced inflammation of the Eustachian tube could induce poor middle ear aeration. Dysfunction of the adenoid tissue could cause hyperplasia, further obstructing the Eustachian tube, and also harbor bacteria [11].

Systemic effects include lung dysfunction, particularly the development of chronic obstructive pulmonary disease. Chronic obstructive pulmonary disease may lead to coughing and bucking on extubation, which could disrupt delicately arranged middle ear grafts. Finally, smoking may adversely affect the immune system, increasing the risk of postoperative infections [12].

In summary, cigarette smoking should negatively affect otologic outcomes because of a variety of biologic mechanisms from a theoretical standpoint. For higher-level evidence, we next assess clinical studies.


Myringoplasty and tympanoplasty

The association between smoking and otologic surgery has been mostly examined for repair of tympanic membrane perforations. The success rate for graft healing in smokers seems dependent on the graft material. Several articles have shown inferior results with smokers when a thin, pliable material, such as fascia, is used.

In a retrospective study from 1970 involving 86 participants who underwent myringoplasty with either temporalis fascia or, less commonly, vein, smokers had a 44% graft take rate (i.e., presence of an intact tympanic membrane on follow-up) versus 96% for nonsmokers. Patients with coinciding trauma and infection had the lowest take rate overall (33%), and all of these participants happened to be smokers [13].

In another study using temporalis fascia grafts, smokers had a comparable rate of graft healing problems with nonsmokers in the first 6 months postoperative. However, after 6 months, there was a higher risk of perforation or atelectasis of the graft in smokers (60%) versus nonsmokers (20%) [14].

The nicotine metabolite cotinine has been used as a more accurate measure of active smoking than history alone. In patients with a serum cotinine level higher than 17.5 ng/ml, temporalis fascia grafts were significantly less likely to succeed (52%) than in patients with cotinine levels lower than 17.5 ng/ml (77%) [15].

A more sophisticated study of temporalis fascia grafts using multivariate analysis found smoking to be a significant risk factor for graft failure, with a large odds ratio of 11.4 [16]. Because of suboptimal results with fascia in both smokers and some nonsmokers, many contemporary otologists employ cartilage for tympanic membrane reconstruction.

Cartilage possesses a number of advantages compared with temporalis fascia. First, because of its rigidity, cartilage does not easily deform and is resistant to recurrent retraction. Second, cartilage has low nutrient requirements, thereby allowing a scarcer blood supply during healing to the surrounding tympanic membrane. Both qualities would seem uniquely suited for smokers. For example, smoking exacerbates Eustachian tube dysfunction, leading to negative middle ear pressure, and a tendency for graft material to retract. In addition, nicotine also causes vasoconstriction, which may adversely affect blood supply and graft healing.

A recent study examined ‘butterfly’ inlay cartilage myringoplasty, where the cartilage is circumferentially scored and placed into the tympanic membrane perforation. In multivariate analysis, smoking was the only independent factor for increased graft failure (odds ratio 8.16) [17]. Despite the discouraging result, this was the only study in our review that showed worse graft survival in smokers when using cartilage.

A series of contrasting studies cite cartilage as an incredibly resilient and durable material that essentially negates the injurious effects of smoking. However, several of these studies also include a mastoidectomy, which makes it less clear whether it is the cartilage or the mastoidectomy responsible for the improved outcomes. Cartilage tympanomastoidectomy is discussed in the subsequent section.

In the previously mentioned study that used cotinine levels as a biomarker for smoking, cartilage grafting in patients with suprathreshold cotinine had a success rate of 89% compared with only 25% with temporalis fascia [15].

A similar result was obtained using a perichondrium-cartilage island graft. Smokers had an 80% success rate compared with 93% in nonsmokers, a nonsignificant difference [18▪]. (A similar ratio was found between smokers and nonsmokers with temporalis fascia grafting, however with lower success in both groups.)

Finally, a recent study examined taste function with whole-mouth gustatory testing after myringoplasty. There was no difference in taste before or after surgery between smokers and nonsmokers [19].


A large review of 329 smokers and more than 1000 nonsmokers or former smokers examined a variety of outcomes after otologic surgery. The vast majority of procedures performed were tympanomastoidectomies; however, the tympanic membrane grafting material was not specified. Smokers were significantly more likely to have cholesteatoma present, and on revision, more extensive disease. They were also significantly more likely to require canal wall down procedures, ossicular reconstruction, or revision surgery. Furthermore, smokers had worse hearing outcomes. Although this study made no attempt to control for severity of disease at surgery, it provides evidence that overall, smoking leads to worse otologic outcomes. Interestingly, former smokers who quit for less than 5 years have similar outcomes to smokers, whereas those who quit for more than 5 years were similar to never-smokers [20].

In a study focused on cartilage tympanoplasty and tympanomastoidectomy, graft take was equivalently high in both smokers (93%) and nonsmokers (91%). Hearing improvements were also similar [21]. Even more dramatic equivalence was obtained in a similar study that showed 100% take rate with cartilage in both smokers and nonsmokers [22].

Most of the above studies have examined graft incorporation (take rate), which is a measure of successful surgical healing. Dornhoffer followed patients with cholesteatoma for a mean of 8 years who underwent a retrograde (inside-out) mastoidectomy followed by cartilage reconstruction. This longer follow-up period should allow the assessment of long-term tympanic membrane health, rather than simply postoperative healing. The disease recurrence rate for smokers was 32% compared with 6% for nonsmokers. The rate of all complications (recurrence, need for intubation, perforation, need for second look because of poor hearing) was 79% for smokers compared with 16% for nonsmokers. Although statistics were not reported for the smoking data, the differences are certainly large [23].

In conclusion, cartilage seems to be a better reconstructive material for smokers as evidenced by graft integration rates approaching that of nonsmokers. Long-term data (i.e., beyond the healing period) are more limited, but smokers who have cholesteatoma may have complications at a higher rate.

Other otologic surgery

There is a paucity of studies on the risk of smoking related to otologic surgery for indications other than tympanic membrane perforation, chronic otitis media, or cholesteatoma. For patients without Eustachian tube dysfunction, the risk of smoking-induced middle ear dysfunction is less relevant. The primary concerns relate to poorer healing after raising tympanomeatal and other flaps as well as bucking/coughing during awakening from anesthesia.

For example, in stapedectomy, an elective procedure with a low level of tolerance for error, heavy coughing during extubation could potentially displace the prosthesis. In cochlear implantation, wound-healing complications (i.e., breakdown, infection) are a primary postoperative concern. With many surgeons using smaller incisions that do not extend beyond the postauricular sulcus, this may be less of an issue today. However, it is still prudent for surgeons to recommend that patients abstain from perioperative smoking when skin flap issues are possible.


Studies of smoking and neurotologic/related cranial surgery are uncommon. In a retrospective review of patients who underwent elective neurosurgery, multivariate analysis identified cigarette smoking as a significant predictor of surgical site infection (odds ratio 2.20) [24]. In neurotologic cases, smoking cessation is advisable when wound healing can be problematic. Relevant procedures may include the translabyrinthine approach (which involves an abdominal fat graft), auditory brainstem implantation (with similar concerns as discussed above with cochlear implantation), and in patients who had or will undergo regional radiation. Finally, in two studies that examined the rate of cerebrospinal fluid leak, smoking was not associated with an increased risk [25,26].


The preoperative period represents a unique and opportune time period to discuss smoking cessation with patients. The most discussed effects of smoking are chronic conditions or diseases caused by long-term exposure. To the unmotivated patient, these nebulous, faraway risks may not provide a strong enough stimulus to quit. For a patient about to undergo surgery, quitting may offer real, immediate benefits. It is the surgeon's responsibility to impart this urgency to the patient. Surprisingly, less than a quarter of surgeons consistently counsel about how to quit [27].

In addition to surgical complications related to smoking, a greater concern is perhaps the risk of perioperative systemic morbidity and mortality as a result of the stress of surgery. Perioperative smoking cessation measures lower this risk.

The strongest evidence comes from the nonotologic literature. In a randomized controlled trial from Denmark, patients who underwent knee or hip replacement were assigned to cessation counseling along with nicotine replacement therapy (NRT) versus a control group. The cessation/NRT group had fewer overall complications (18%) versus the control (52%), including fewer cardiac complications (0 versus 10%, respectively, although marginally significant) [28]. In another randomized trial with a similar design, the relative risk reduction for all complications (wound as well as systemic) was 49% [29]. Although general and orthopedic surgeries tend to be higher risk than ear surgery, one could extrapolate that there should be an analogous, even if smaller, risk reduction for otology.

Direct physician-to-patient counseling makes a difference. Smokers are more likely to quit when advised by a health professional [30]. However, the choice of which pharmacologic adjuvants to prescribe preoperatively is less clear. NRT along with counseling increases short-term smoking cessation. Varenecline, a nicotine receptor antagonist, has been shown to improve long-term cessation; however, a randomized controlled trial did not show an effect on early quitting or surgical complications [31▪,32].


Traditional cigarette smoking involves combustion, or burning, of tobacco rolled within paper. The resulting smoke contains nicotine and a variety of other chemicals. The smoke passes into the pharynx, is inhaled into the lungs, and then is absorbed into the bloodstream.

In contrast, electronic cigarettes (e-cigarettes) do not produce smoke. Instead, purified nicotine (and often flavor additives) within a solution is heated to produce water vapor. This water vapor is then inhaled. Unlike traditional cigarettes, there is no smoke produced from the combustion of tobacco and paper. Because it is the tobacco combustion products rather than the nicotine itself believed to be responsible for most of the deleterious and carcinogenic effects of smoking, electronic cigarettes are probably safer [33,34▪] (Fig. 1). Many e-cigarette users state that they are ‘vaping’, rather than ‘smoking’ because water vapor, not smoke, is produced.

Medical infograph comparing the negative effects and the contents of electronic cigarettes versus traditional tobacco cigarettes. Nicotine in e-cigarettes will still cause vasoconstriction during otologic surgery; however, the other harmful chemicals in combusted tobacco are not present in e-cigarettes (reprinted with permission from CASAA,

Nicotine-replacement products, such as gum and transdermal patches, have been available for years; however, e-cigarettes seem the most promising solution because they mimic many of the habits and social rituals associated with smoking. This minimizes the behavioral modifications necessary to quit. However, the superiority of e-cigarettes as a tobacco cessation tool awaits more convincing data [34▪,35▪].

The risk of e-cigarettes before or after otologic surgery is probably similar to that of nicotine gum and patches. In terms of local effects, nicotine itself does not adversely alter ciliary function or mucus production [9,36]. However, one relevant pharmacologic effect of nicotine will remain, namely vasoconstriction. For integration of free fascia grafts, e-cigarettes may still reduce blood flow to the graft site, possibly decreasing the take rate. Although studies are needed to substantiate this theory, cartilage may be preferred because of its lower metabolic requirements. The regional effect of Eustachian tube inflammation should be minimal with e-cigarettes. Finally, systemic effects of tobacco smoking, such as lung dysfunction leading to coughing/bucking on extubation, should also be less of a concern with e-cigarettes.

Compared with traditional cigarette smoking, e-cigarettes seem to have a strong theoretical advantage for the perioperative period. Therefore, it seems reasonable to encourage cigarette smokers who will not quit to switch to e-cigarettes before surgery.

Recommending e-cigarettes walks a fine line, however. The long-term health effects of inhaling nicotine vapor are unknown and may not be known for decades. The nicotine content can vary widely and regulation is nascent. Because e-cigarette vapor may be colorless and odorless (or pleasantly scented), it is possible to use e-cigarettes in locations where smoking is unacceptable. Even more concerning, e-cigarette cartridges may contain sweetly flavored vapors that appeal to children [35▪]. The latter two features may eventually propel e-cigarette use to far surpass that of traditional cigarettes. A final concern is whether e-cigarettes might serve as a gateway to traditional cigarettes or illicit substances. Answers are not currently available, but the modern otologist must be prepared to counsel patients on these issues.


In the United States, marijuana is the most commonly used illicit substance [37]. As several states have recently legalized its use and others are debating its legalization, the perioperative consequences of marijuana smoking are increasingly important to assess. In our review, we found no studies on marijuana use and surgical outcomes. Like tobacco and nicotine, marijuana contains a variety of substances aside from the active chemical tetrahydrocannabinol. Marijuana smoke may affect the respiratory tract and is associated with respiratory complications [38]. In otologic surgery, in which a smooth emergence from anesthesia without bucking and coughing is important, advising patients against smoking in any form seems prudent.


Smoking can adversely affect otologic surgical outcomes from both a theoretical/mechanistic standpoint as well as based on data from clinical studies. The strongest data demonstrate inferior results for tympanoplasty in smokers when temporalis fascia is used as the graft material. However, most studies show a similar short-term result when cartilage is used in smokers. For this reason, we recommend cartilage as the preferred grafting material in patients with a significant smoking history.

We also recommend preoperative smoking cessation counseling and, if needed, NRT. Electronic cigarettes represent a new alternative to tobacco cigarette smoking by delivering nicotine in water vapor, thus eliminating any combustion products. Other than the vasoconstrictive effects of nicotine, e-cigarettes are likely safer than smoking traditional cigarettes before and after otologic surgery. However, their efficacy and safety compared with NRT is currently unknown.


The authors thank Mary Kemper for editing the manuscript.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


Papers of particular interest, published within the annual period of review, have been highlighted as:

  • ▪ of special interest
  • ▪▪ of outstanding interest


1. World Health Organization. The top 10 causes of death [Internet]. 2014. [Accessed 2 June 2015]
2. Surgeon General's Report: The Health Consequences of Smoking. 2004. [Accessed 2 June 2015]
3. Doll R, Peto R, Boreham J, Sutherland I. Mortality in relation to smoking: 50 years’ observations on male British doctors. BMJ 2004; 328:1519.
4. Leao RM, Cruz FC, Vendruscolo LF, et al. Chronic nicotine activates stress/reward-related brain regions and facilitates the transition to compulsive alcohol drinking. J Neurosci 2015; 35:6241–6253.
5. World Health Organization. Tobacco fact sheet. [Internet]. 2015. [Accessed 2 June 2015]
6. Kuo HP, Rohde JA, Barnes PJ, et al. Cigarette smoke-induced airway goblet cell secretion: dose-dependent differential nerve activation. Am J Physiol 1992; 263 (2 pt 1):L161–L167.
7. Lamb D, Reid L. Goblet cell increase in rat bronchial epithelium after exposure to cigarette and cigar tobacco smoke. Br Med J 1969; 1:33–35.
8. Simet SM, Sisson JH, Pavlik J, et al. Long-term cigarette smoke exposure in a mouse model of ciliated epithelial cell function. Am J Respir Cell Mol Biol 2010; 43:635–640.
9. Hahn HL, Kleinschrot D, Hansen D. Nicotine increases ciliary beat frequency by a direct effect on respiratory cilia. Clin Investig 1992; 70:244–251.
10. Hock CE, Passmore JC. Mechanisms mediating canine renal vasoconstriction induced by nicotine infusion. Life Sci 1985; 37:1997–2003.
11. Lee I-W, Goh E-K, Roh H-J, et al. Histologic changes in the Eustachian tube mucosa of rats after short-term exposure to cigarette smoke. Otol Neurotol 2006; 27:433–440.
12. Shiels MS, Katki HA, Freedman ND, et al. Cigarette smoking and variations in systemic immune and inflammation markers. JNCI J Natl Cancer Inst 2014; 106:dju294.
13. Cantrell RW. Myringoplasty failure related to smoking: a preliminary report. Otolaryngol Clin North Am 1970; 3:141–145.
14. Becvarovski Z, Kartush JM. Smoking and tympanoplasty: implications for prognosis and the Middle Ear Risk Index (MERI). Laryngoscope 2001; 111:1806–1811.
15. Uguz MZ, Onal K, Kazikdas KC, Onal A. The influence of smoking on success of tympanoplasty measured by serum cotinine analysis. Eur Arch Oto-Rhino-Laryngology 2008; 265:513–516.
16. Onal K, Uguz MZ, Kazikdas KC, et al. A multivariate analysis of otological, surgical and patient-related factors in determining success in myringoplasty. Clin Otolaryngol 2005; 30:115–120.
17. Lin Y-C, Wang W-H, Weng H-H, Lin Y-C. Predictors of surgical and hearing long-term results for inlay cartilage tympanoplasty. Arch Otolaryngol Head Neck Surg 2011; 137:215–219.
18▪. Salviz M, Bayram O, Bayram AA, et al. Prognostic factors in type I tympanoplasty. Auris Nasus Larynx 2015; 42:20–23.

This recent article agrees with prior data that in smokers cartilage tympanoplasty is more effective than temporalis fascia tympanoplasty. It also shows that results for cartilage tympanoplasty are similar between smokers and nonsmokers.

19. Karatayli-Ozgursoy S, Ozgursoy OB, Muz E, et al. Evaluation of taste after underlay technique myringoplasty using whole-mouth gustatory test: smokers versus nonsmokers. Eur Arch Oto-Rhino-Laryngology 2009; 266:1025–1030.
20. Kaylie DM, Bennett ML, Davis B, Jackson CG. Effects of smoking on otologic surgery outcomes. Laryngoscope 2009; 119:1384–1390.
21. Coelho DH, Peng A, Thompson M, Sismanis A. Cartilage tympanoplasty in smokers. Ann Otol Rhinol Laryngol 2012; 121:657–663.
22. Kyrodimos E, Stamatiou GA, Margaritis E, et al. Cartilage tympanoplasty: a reliable technique for smokers. Eur Arch Oto-Rhino-Laryngology 2013; 271:255–260.
23. Dornhoffer JL. Retrograde mastoidectomy with canal wall reconstruction: a follow-up report. Otol Neurotol 2004; 25:653–660.
24. Walcott BP, Neal JB, Sheth Sa, et al. The incidence of complications in elective cranial neurosurgery associated with dural closure material. J Neurosurg 2014; 120:278–284.
25. Bien AG, Bowdino B, Moore G, Leibrock L. Utilization of preoperative cerebrospinal fluid drain in skull base surgery. Skull Base 2007; 17:133–139.
26. Litvack ZN, West GA, Delashaw JB, et al. Dural augmentation: part I – evaluation of collagen matrix allografts for dural defect after craniotomy. Neurosurgery 2009; 65:890–897.
27. Warner DO, Sarr MG, Offord KP, Dale LC. Anesthesiologists, general surgeons, and tobacco interventions in the perioperative period. Anesth Analg 2004; 99:1766–1773.
28. Møller AM, Villebro N, Pedersen T, Tønnesen H. Effect of preoperative smoking intervention on postoperative complications: a randomized clinical trial. ACC Curr J Rev 2002; 11:13–14.
29. Lindström D, Sadr Azodi O, Wladis A, et al. Effects of a perioperative smoking cessation intervention on postoperative complications: a randomized trial. Ann Surg 2008; 248:739–745.
30. Fiore MC. A clinical practice guideline for treating tobacco use and dependence: a US Public Health Service report. J Am Med Assoc 2000; 283:3244–3254.
31▪. Thomsen T, Villebro N, Møller A. Interventions for preoperative smoking cessation [review]. Cochrane Database Syst Rev 2014; 3:CD002294.

This high-quality review discusses methods to increase smoking cessation in the perioperative period. The conclusions are relevant to any centers attempting to establish effective smoking cessation programs into their practice.

32. Wong J, Abrishami A, Yang Y, et al. A perioperative smoking cessation intervention with varenicline: a double-blind, randomized, placebo-controlled trial. Anesthesiology 2012; 117:755–764.
33. Polosa R, Rodu B, Caponnetto P, et al. A fresh look at tobacco harm reduction: the case for the electronic cigarette. Harm Reduct J 2013; 10:19.
34▪. Rahman MA, Hann N, Wilson A, et al. E-cigarettes and smoking cessation: evidence from a systematic review and meta-analysis. PLoS One 2015; 10:e0122544.

One of the few early papers assessing the role of e-cigarettes and smoking cessation. The authors conclude that e-cigarettes are associated with smoking cessation and reduction.

35▪. Lee AHY, Stater BJ, Close L, Rahmati R. Are e-cigarettes effective in smoking cessation? Laryngoscope 2015; 125:785–787.

Another early article discussing the role of e-cigarettes and smoking cessation. This review does not find e-cigarettes to be more effective than existing smoking cessation products.

36. Bende M, Burian P, Danielsson GP, et al. Evaluation of side effects after nicotine nasal spray in patients with chronic rhinitis. Rhinology 1998; 36:98–100.
37. NIH/NIDA. What is the scope of marijuana use in the United States? 2015; Available from: [Accessed 2 June 2015]
38. Rummell CM, Heinberg LJ. Assessing marijuana use in bariatric surgery candidates: should it be a contraindication? Obes Surg 2014; 24:1764–1770.

cigarette; electronic cigarette; marijuana; myringoplasty; nicotine; otologic surgery; smoking; tobacco; tympanomastoidectomy; tympanoplasty

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