3.15 The impact of smoking on treatment of disease

Last updated: April 2020
Suggested citation: Just, J, Hurley, S, Greenhalgh, EM & Winstanley, MH. 3.15 The impact of smoking on treatment of disease. In Greenhalgh, EM, Scollo, MM and Winstanley, MH [editors].  Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2020. Available from  http://www.tobaccoinaustralia.org.au/3-15-smoking-and-complications-in-medical-treatmen

 

3.15.1 Surgery

Smoking increases the risk of intraoperative (anaesthetic) and postoperative complications. Smokers’ higher prevalence of chronic diseases, impaired pulmonary reserve and altered immune responses are thought to contribute to these complications. Poorer surgical outcomes result.1

In 2020, the World Health Organization released an updated review of tobacco and post-surgical outcomes that suggested that smokers who quit around 4 weeks prior to surgery have a lower risk of operative complications. However, the ideal cessation time varies according to the specific complication.2

3.15.1.1 Anaesthesia

The effectiveness of a number of commonly used anaesthetic drugs is reduced in smokers. Higher doses are therefore required. These drugs include opioids,3 neuromuscular blocking agents and some of the volatile agents that are administered by inhalation (via a mask or endotracheal tube). The polycyclic aromatic hydrocarbons in cigarette smoke induce the liver enzymes that metabolise anaesthetics, at least partly accounting for these effects.4 Smoking does however decrease postoperative nausea and vomiting, possibly because of the increased metabolism of volatile anaesthetics.4

Smoking also increases the risk of intraoperative respiratory complications, including bronchospasm, aspiration, hypoventilation and hypoxaemia.5-7

The Australian and New Zealand College of Anaesthetists recommends that patients who smoke be encouraged to quit at any time before surgery.8  Research suggests that recent quitters are no worse off than continuing smokers in terms of pulmonary complications. (see Section 3.15.1.3).9, 10

3.15.1.2 Postoperative complications

It is well-established that smoking results in a significantly increased risk of many postoperative complications. These complications include a higher risk of general morbidity, wound complications, lung complications, infections, neurological complications and an increased risk of intensive care unit (ICU) admission post-surgery.11

-Wound and surgical site complications

Smoking delays wound healing after surgery. Complications for which smokers have a greater risk include: wound infection;12 dehiscence (bursting of sutures);13 erosions (destruction of tissue surfaces) and necrosis (death of most of the cells of a piece of tissue or an organ);14 hernia (protuberance of organs through cavity walls); poor healing of broken bones and poor healing of fistulae (abnormal openings from body organs to the surface of the skin).15-17

Smoking has an impact on wound healing via several different pathophysiological mechanisms, including:18, 19

  • Reduced blood flow to, and oxygenation of, peripheral tissues
  • Impaired inflammatory processes that are part of normal healing
  • Impaired proliferation of fibroblasts and collagen production
  • Impaired immune function, which may increase the risk of wound infection2

Such wound complications are particularly problematic after plastic and reconstructive surgery, bariatric surgery,  bowel surgery, hernia repair surgery, dental surgery (see Section 3.11.4), microsurgery, and organ transplantation.14, 20-23

  

-Complications following cardiac surgery

A meta-analysis found smokers undergoing cardiac surgery were at increased risk of pulmonary complications and pneumonia following surgery, but had a reduced risk of kidney complications, compared to ex-smokers.24

A systematic review and meta-analysis of patients undergoing repair of an aneurysm (enlargement or ballooning of an artery due to a weakness in the artery wall) found that smoking was protective again endovascular leaks post-surgery.25 The paper proposed possible explanations for this; smokers are more likely to have extensive atherosclerosis, potentially protecting against leakage, and smoking increases aggregation of platelets, increasing clot formation, so leakage becomes less likely.

-Complications following orthopaedic surgery

Smokers have an increased risk of complications following several types of orthopaedic surgery (see Section 3.13.2), including shoulder surgery, and hip and knee arthroplasty.26-29

A meta-analysis found smokers had a higher risk of loosening of prostheses (artificial body parts inserted during surgery), deep infection, and the need for revision following total hip arthroplasty (hip replacement).26 Another study found an increased risk of periprosthetic joint infection (infection around the artificial body part) in smokers undergoing total hip or knee arthroplasty.28

A study also found smoking increases the risk of venous thromboembolism (VTE) (blood clots that form in veins) following anterior cruciate ligament (ACL) reconstruction surgery.30 Another study found smokers had higher rates of wound infection, VTE and subsequent ACL reconstruction compared to non-smokers.31

-Complications following plastic and reconstructive surgery

Following breast reconstruction, smoking has been associated with a doubling of the risk of complications (such as mastectomy flap necrosis and infection) and a five-fold increase in the risk of implant failure.32 Such poor surgical outcomes have led to a call for caution when undertaking breast reconstruction in smokers.33 Similarly, impaired wound healing and wound infection in smokers undergoing breast reduction surgery34, 35 have led to a suggestion that pre-operative smoking cessation be an essential eligibility criterion for this surgery.35 In another study of patients undergoing reduction mammaplasty (breast reduction), smoking was associated with an increased risk of wound complications including dehiscence.36, 37

-Complications following transplant surgery

Smokers undergoing organ transplantation have poorer outcomes,38 including increased mortality after liver transplantation,21 increased kidney transplant rejection,39 and poorer survival after heart transplantation if either the donor was, or the recipient is, a smoker.22, 40, 41

Unsurprisingly, solid organ transplant recipients who smoke post-transplant are at higher risk of newly diagnosed cardiovascular disease, cancer and overall shorter survival time, and  mortality.41

The poorer organ transplantation outcomes in smokers, combined with the high demand for donated organs, have led to suggestions that smokers be given lower priority for organ transplants and debate about the ethics of such a policy.42-44

-Complications following other types of surgery

Smoking increases the risk of complications following other types of surgery including: a higher failure rate for oral mucosa graft urethroplasty (repair of the urethra with a graft from the lining of the mouth);45 worse hearing and the need for repeat operations after ear surgery;46 increased complications post appendicectomy47 and hernia repair;23, 48 and increased risk of complications following bariatric surgery including prolonged intubation (insertion of a tube through the mouth to support artificial breathing) and organ space infection (a type of surgical site infection).49 Another study suggested that in patients undergoing sleeve gastrectomy (surgery involving removal of part of the stomach) for weight management, smokers had an increased risk of morbidity and mortality compared to non-smokers (of note, ‘smokers were those who had smoked  at least one cigarette in the year prior to surgery, ‘non-smokers’ were those that had not).50

 

3.15.1.3 Impact of smoking cessation

A systematic review published in 2012 explored the relationship between short-term preoperative smoking cessation and postoperative complications and concluded that at least four weeks of abstinence from smoking reduces respiratory complications, and abstinence of at least three to four weeks reduces wound-healing complications. Short-term (less than four weeks) smoking cessation did not appear to increase or reduce the risk of postoperative respiratory complications.51

A 2014 Cochrane Review examined interventions for smoking cessation preoperatively, and the impact of this on postoperative complications.52 Thirteen RCTs, with over 2000 participants, were included in the review. Intensive behavioural interventions (face-to-face counselling delivered over multiple sessions) were found to reduce the risk of any postoperative complications, and wound complications specifically. However, brief interventions did not have an impact. The authors concluded that although the ideal cessation time is not entirely clear, evidence suggests that interventions that commence at least four weeks before surgery, and that involve weekly counselling and pharmacotherapy, can reduce the risk of complications.

A study of over 6000 patients undergoing coronary artery bypass graft (CABG) surgery also found that cessation of at least four weeks’ reduced the risk of lung complications following surgery, including lung infection and reintubation.53 A further study demonstrated that smoking abstinence following CABG reduced the 5 year mortality rate by 35%.54

The Australian and New Zealand College of Anaesthetists recommend that, based on the current available evidence, anaesthetists and surgeons should not be dissuaded from advising patients to quit at any time before surgery.8

3.15.2 Drug interactions

Smoking alters the effects of a number of medications (see also Section 3.15.1.1 on interactions with anaesthetics). Doctors and other health professionals need to be aware of these interactions when medications are prescribed and also when patients quit smoking, as drug dosages may need to be adjusted.55

Drug interactions fall into two categories: (i) pharmacokinetic interactions, which occur when cigarette smoke alters a drug’s metabolism; or (ii) pharmacodynamic interactions, which occur when the physiological effects of cigarette smoke modify the physiological effects of the drug.56, 57

Pharmacokinetic interactions include increased metabolism of caffeine, heparin, warfarin, theophylline, beta-blockers (such as propranolol), a number of antipsychotic drugs (such as clozapine, chlorpromazine and olanzapine) and benzodiazepines.58-60 A meta-analysis of the interaction between smoking and warfarin, for example, found that smoking increased warfarin dosage requirements by about 12%.61

Although it is difficult to know which of the estimated 7000 compounds in cigarette smoke cause these interactions,62 the polycyclic aromatic hydrocarbons are suspected. These hydrocarbons induce liver enzymes (see Chapter 3, Section 13.15.1.1) and thereby hasten the clearance of any drug (or substance) whose metabolism requires the enzymes.56, 57 Conversely, upon smoking cessation, dosages of these medications may need adjustment, as clearance will slow. For example, upon stopping smoking, smokers may need to reduce caffeine consumption.58

The pharmacokinetic interaction between tobacco smoke and the antiplatelet medication clopidogrel has been described as a ‘smoking paradox’ as there is some evidence to suggest that smokers have higher clinical responsiveness to clopidogrel than non-smokers.58 A meta-analysis of over 70,000 patients with established cardiovascular disease found that smokers taking clopidogrel had a 25% lower risk of cardiovascular events compared to an 8% reduced risk in non-smokers.63  Another study suggested that doubling the dose of clopidogrel in smokers was effective in reducing the risk of cardiovascular events, without an increase in the risk of bleeding.64 Dosages of clopidogrel and other antiplatelet medications (such as prasugrel) may need to be adjusted upon stopping smoking.63

Pharmacodynamic interactions include: reduced response to corticosteroids in smokers who are asthmatic,65, 66 decreased effectiveness of benzodiazepines (a common sleeping medication) (possibly due to the stimulant effects of nicotine), slowed absorption of sub-cutaneous insulin among diabetics (possibly due to reduced blood flow to the skin, mediated by nicotine), and an increased risk of cardiovascular adverse effects in women taking oral contraceptives.56, 57

In the above examples, smoking modifies the effects of particular drugs. It has also been hypothesised that bronchodilator drugs (mainly beta-2-agonists), prescribed for people with chronic obstructive pulmonary disease (COPD), may worsen the effects of cigarette smoke. The theory is that bronchodilation improves smoke inhalation, and may increase the deposition of cigarette smoke on the lungs, thereby increasing cardiovascular disease morbidity and mortality. This hypothesis is yet to be tested.67

3.15.3 Cardiovascular disease

As detailed in Section 3.1, smoking causes cardiovascular disease, and generally, if a person continues to smoke after developing cardiovascular disease their prognosis is worse than if they had quit.

For example, a study of more than 18,000 patients who were receiving a statin drug for coronary disease found that over a five-year period those who continued to smoke had about a 50% higher chance of a major cardiovascular event (heart attack, stroke, cardiac arrest or death) than patients who quit.68  However, a more recent meta-analysis found that the risk of major cardiovascular events in people using statins was similar for smokers and non-smokers.69

Poorer treatment outcomes have been reported for people who continue to smoke after coronary artery bypass grafting (CABG)70 or a diagnosis of heart failure,71 compared with people who quit.

A 2019 meta-analysis involving over 120,000 patients undergoing either percutaneous coronary intervention (i.e. placement of a stent, a small device to open up an artery) or CABG found that smokers had a higher risk of all-cause mortality compared to non-smokers.72 However, there was no statistically significant difference in the rate of heart attacks, all cardiovascular events or cardiovascular deaths . The increased risk of all-cause mortality was also true of ex-smokers, compared to non-smokers.

3.15.4 Cancer

As detailed in Section 3.5, smoking causes numerous cancers.

The 2014 Surgeon General’s report was the first in its series to review the associations between cigarette smoking and health outcomes in cancer patients and survivors. It concluded that smoking causes adverse health outcomes in people with cancer, while cessation improves their prognosis. Smoking increases all-cause mortality and cancer-specific mortality in cancer patients and survivors, and increases the risk of second primary cancers that are caused by cigarette smoking, including lung cancer. Smoking may increase the risk of recurrence, result in a poorer response to treatment, and increase treatment-related toxicity.73

A 2018 review published by the World Health Organization identified some of the mechanisms by which smoking affects outcomes of cancer treatment.74 These mechanisms include increased cancer cell proliferation, migration and metastasis (development of secondary cancers), acceleration of systemic clearance of cancer therapies (potentially impacting efficacy of cancer treatment), increased complications associated with treatment, and an increased risk of co-morbidities related to tobacco.

The review also reinforced findings from the Surgeon General’s report, regarding the impact of smoking on cancer outcomes, including increased risk of all-cause mortality, cancer-specific mortality, recurrence, and reduced quality of life. Specifically, this included studies of patients with lung cancer, head and neck cancers, bladder cancer and breast cancer.74

A 2018 meta-analysis of patients with colorectal cancer found that current and former smokers had lower overall survival compared with never smokers. In the same study, smoking cessation, compared to current smoking, was linked with an improvement in overall and colorectal cancer-specific survival.75 Smoking has also been identified as a risk factor for superficial surgical site resections in patients undergoing rectal cancer resection.76

More severe pain has been associated with smoking in patients with cancer,77 and specifically for lung cancer78 and head and neck cancer.79 This may be because of the decreased effectiveness of opioids (due to increased drug metabolism caused by cigarette smoke components) described in Chapter 3, Section 13.15.1.1, and failure to increase the dose in response.

Of note, a 2019 meta-analysis did not find any difference in response to immunotherapy (for treatment of advanced solid organ cancers) between ever smokers and never smokers.80

Smoking cessation improves outcomes in cancer patients. Cessation is associated with  an improved quality of life (in patients with lung or head and neck cancers), reduced risk of cancer-specific mortality (in patients with breast cancer) and improvement in survival (for patients with lung cancer, head and neck, colorectal and bladder cancer).81 Patients who stop smoking also experience reduced treatment-related toxicity.81, 82

A 2019 retrospective study on patients with primary lung cancer who had undergone lung resection, found that smoking cessation reduced the risk of lung complications following surgery and mortality rate at 90 days. The longer the period of cessation, the lower the risk of lung complications.83

For an overview of smoking cessation interventions for people with cancer, see Section 7.19.5.

3.15.5 Treatment of infertility including assisted reproduction

As detailed in Section 3.6.2, women who smoke have reduced fertility, as smoking has been found to affect ovarian function and reserve,84 and there is emerging evidence that fertility may also be reduced in male smokers.62

 Smoking also has a negative impact on the outcomes of infertility treatment.85 In women participating in assisted reproduction programmes, smoking is associated with lower pregnancy rates, higher chances of miscarriage , and a lower probability of a live birth.85, 86  Another meta-analysis found that smokers had a lower number of oocytes retrieved compared to non-smokers, and a reduced rate of fertilisation.86

There is also evidence that smokers undergoing assisted reproduction also have an increased risk of ectopic pregnancy.87

 Interestingly, there is some evidence that paternal smoking can increase the rate of pregnancy loss, likely as a result of damage to spermatozoa.88

One study found that for couples who smoked (either female, male or both), the risk of not achieving a pregnancy was about twice as high as for non-smokers.89  Researchers have estimated that women who smoke need up to twice the number of in vitro fertilisation (IVF) cycles to conceive and suggest there is a correlation between the number of smoking years and the risk of not conceiving through IVF.90 Smoking cessation for both women and men is recommended for couples aiming to become pregnant91 and it has been suggested that access to fertility treatment should be conditional on quitting smoking.90

Of note, smoking appears to affect infant outcomes in assisted reproduction pregnancies in the same way as unassisted pregnancies.92

3.15.6 Contraception

As detailed in Section 3.2, smoking causes coronary heart disease, increasing the risk two- to four-fold.1 The ‘combined’ oral contraceptive pill (which contains the hormone oestrogen) also increases the risk of myocardial infarction two-fold.93 Women who take the oral contraceptive pill and smoke have a 20-fold increase in the risk of coronary heart disease, compared with non-smokers who are not taking the contraceptive pill.94 The impact of smoking and the contraceptive pill is therefore ‘synergistic’, meaning that the risk of disease is multiplicative rather than additive. Heavier smokers have an even higher risk of coronary heart disease.95

Although the newer ‘lower dose’ versions of the contraceptive pill may be associated with a lesser risk of developing coronary heart disease, risk is still elevated in smokers. There is insufficient evidence to evaluate the risk profile of the ‘third-generation’ pills (containing 30 μg or less of ethynyl estradiol and either gestodene or desogestrel) combined with smoking, but clinicians are advised to be wary when prescribing oral contraceptives to smokers aged in their mid-30s and to exercise extreme caution or avoid using them altogether in smokers aged over 40 years.95

In past decades the risk of stroke, particularly subarachnoid haemorrhage, has been significantly higher among smokers using the contraceptive pill. However research published since the 1990s following up women using lower dose pills is conflicting; some studies show increased risk, other studies have shown no significant effect.95

There is some evidence to suggest that the combined contraceptive pill has a higher failure rate in smokers than in non-smokers.94

3.15.7 Other conditions

A meta-analysis published in 2011 found that in patients receiving long-term haemodialysis (use of an artificial kidney machine to clean the blood) or peritoneal dialysis (an alternative to haemodialysis, uses the lining of the abdomen to clean the blood), smoking increased the death rate (all-cause mortality) by 65%.96

A 2019 meta-analysis and systematic review found that burns patients who smoke have higher rates of complications compared to non-smokers, including an increased risk of intubation (insertion of a tube through the mouth to support artificial breathing) and skin infections.97


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References

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