NET Training Day: Whittington Hospital – 03/06/15

In June we congregated at the Whittington for a day focused on smoking cessation.

Introduction

Dr Myra Stern welcomed us and set the scene by giving some context to the quit smoking debate and reframing smoking cessation as treatment for tobacco dependance. She reminded us that there are diverse views on smoking, and prominent characters who are vocal in their defence of the right to smoke. Chairman Mao told his citizens “smoking is not an addiction, it is a breathing exercise.” Not quite the message we hope to give…

As a reminder, smoking kills.

• Doll, Richard, et al. “Mortality in relation to smoking: 50 years’ observations on male British doctors.” Bmj 328.7455 (2004): 1519.

With strong evidence of harm, it is therefore disappointing that 40% patients who are admitted to hospital with COPD continue to smoke. Perhaps this is not surprising when we consider how addictive nicotine is, and the fact that 40% of inpatients have no access to stop smoking services (BTS/RCP audit 2014). Also 33-70% asthma admissions to hospital are current smokers. 1/10 asthma deaths in under 10yr olds are a child smoker and 36% occurred in smoking households.

Dr Stern challenged us by asking why stop smoking is not a core part of every respiratory clinic? Stop smoking is a core treatment and provision of effective stop smoking is your clinical responsibility. To change the current situation every patient who smokes needs to be identified, acknowledged and advised, and offered pharmacotherapy and support from an expert advisor. This is in line with NICE guidelines.

She advised us to “know your sick smoker” and to take advantage of “the teachable moment”, using behaviour change skills. Key questions include: how many previous quit attempts; and what products have they tried? Barriers to quitting include co-morbid mental health diagnoses, and other household smokers. It is useful to quantify how addicted an individual is, using validated tools such as the Fagerstrohm score, and CO monitoring.

Finding optimal treatment for that individual patient takes an investment of time.The more time you spend with a patient, the more cost effective the outcome. Add pharmacotherapy = best results for lives saved and years gained.

• Hoogendoorn, Martine, et al. “Long-term effectiveness and cost-effectiveness of smoking cessation interventions in patients with COPD.” Thorax 65.8 (2010): 711-718.

TB – does it matter if you smoke or treat early

Dr Norman Johnson regaled us with “a tale of 2 smokers.”

Case 1:  an 18F visited her GP for low thoracic back pain. 2 months later she was no better and returned to her GP who sent a referred to Rheumatology. The referral was screened by the community team and she was triaged to see a physiotherapist. She was said to have “classical post birth back pain”. The pain persisted. 4 months following initial presentation she developed weakness in her legs. This was urgently investigated. She was diagnosed with a TB extradural abscess and vasculitis of the spinal cord. She underwent surgery but sadly had a poor outcome. She is now in a wheelchair.

Key learning point: thoracic back pain is unusual and requires investigation. This patient should have had an MRI. Costs of care now vs MRI then….

Case 2: a 45F smoker had breast ca and underwent a mastectomy, RTX, and hormonal therapy. At routine follow-up in a specialist Oncology clinic she felt well but had a cough productive of sputum. Her chest x-ray showed nodular shadowing. She was febrile. The diagnosis was thought to be multiple metastases. It was unclear why she was febrile and she was given antibiotics. She underwent a BAL which was negative. She then became drowsy, and fitted. She was transferred to a specialist ID unit. In fact the sputum sample from the original hospital was then reported as positive for AFBs. She had an LP and was started on anti-TB therapy. Sadly the result was that she had TB meningitis and is now in a wheelchair bound.

So how does smoking relate to TB? Smoking doubles the risk of pulmonary  TB and related mortality. There is increased risk of infection from exposure to second hand smoking and increased risk of relapse. 15% of pulmonary TB diagnosed in the UK may be attributable to smoking. Smoking cessation reduces the risk of premature death from TB by 50%, decreases the risk of infection in contacts, and decreases risk of relapse. Smokers also present later – perhaps due to not acting on a persistent cough.

We discussed whether stop smoking is likely to be part of the next TB guidelines? It was felt that it would probably not be as felt to be ‘outside scope of guidelines’ by NICE.  The guidelines out for consultation so why not comment now? Dr Restrick challenged the audience to consider how many TB clinics have stop smoking embedded? How many TB specialist nurses have had smoking cessation training?

HIV – does it matter if you smoke? Implications for treatment

Dr Marc Lipman helped us consider the impact of smoking on HIV.  He started with a case of a HIV+ patient with a CD4 count of 40 and a cough. They had an abnormal CXR and went on to have a CT which showed ground glass opacities. The working diagnosis was ?PCP. Presenting in this way, acutely unwell, has now almost gone. ART means the rate of significant life threatening acute infections have gone down (according to EuroSIDA data).

In the USA there are 1/2 million HIV infected individuals. Their life expectancy on ARVs is about the same as the general population. This is astonishing, considering where HIV care was just a few decades ago. Pulmonary admissions are falling in the HIV population. The START study may be a game-changer. It advocates for starting ARV at diagnosis to reduce AIDS events and non-AIDS events. This has economic implications and social/medical delivery implications. Overall however, we expect to have an increasing number of patients with HIV surviving to older age. Premature ageing is a problem in HIV patients. This is worsened by smoking. Lost-life years from smoking HIV patients vs never smoking HIV patients = 12.3yrs. The prevalence of smoking in cohorts of HIV patients has been found to be higher than in the general population.

• Helleberg, Marie, et al. “Smoking and life expectancy among HIV-infected individuals on antiretroviral therapy in Europe and North America.” AIDS (London, England) 29.2 (2015): 221.
• Smith, C. J., et al. “Cardiovascular disease risk factors and antiretroviral therapy in an HIV‐positive UK population.” HIV medicine 5.2 (2004): 88-92.
• Helleberg, Marie, et al. “Mortality attributable to smoking among HIV-1–infected individuals: a nationwide, population-based cohort study.” Clinical Infectious Diseases 56.5 (2013): 727-734

The pattern of pulmonary disease in HIV is changing. Interventions which reduce the risk of severe bacterial community acquired pneumonia include: take ART, stop smoking, 23-valent PS pneumococcal vaccine, treat pneumonia early, use CTM PCP prophylaxis.

• Crothers, Kristina, Laurence Huang, and Adeel A. Butt. “Risk and Incidence of Pulmonary Diseases among HIV-infected Patients in the Era of Combination Antiretroviral Therapy.” American Journal of Respiratory and Critical Care Medicine 184.9 (2011): 1087-1087.

When treating patients on ARV drug interaction must be considered. A patient newly diagnosed with COPD may be started on an inhaler including an inhaled steroid.  However, on ART there can be a massive steroid response as RTV increases inhaled budesonide & fluticasone. It is therefore important to cut down steroid use. Dr Lipman has seen at least 1 case of AVN bilateral hips and shoulder which was felt to have a contribution from HIV, ARTs, but also inhaled steroids for asthma. Importantly when considering how to support patients to stop smoking, varenicline does not interact, but bupropion does – watch out.

We moved on to consider lung cancer and HIV. Patients with HIV have similar tumour types and overall survival from lung cancer. In fact, lung cancer is now the most common cause of non-AIDS cancer death in the US.

• D’Jaen, Gabriela A., et al. “Human immunodeficiency virus–associated primary lung cancer in the era of highly active antiretroviral therapy: a multi-institutional collaboration.” Clinical lung cancer 11.6 (2010): 396-404.

Cannabis, Shisha and other recreational inhaled drug use – do these matter?

Dr Louise Restrick helped us consider other types of ‘smoking’, including cannabis and shisha. This was the subject of a recent editorial in the BMJ:

• Maziak, Wasim. “Rise of waterpipe smoking.” BMJ 350 (2015): h1991.
  

  from wikimedia.com

Cannabis smoking is very common. There is an estimated £1 billion yearly cannabis trade in the UK. Worryingly, a BLF survey in 2012 found that 32% population believe cannabis is not harmful to health.

Local data collection has shown that 1/3 smokers in an inner city hospital (the Whittington) also smoke cannabis. This data is not routinely collected, so wider use is unknown.  Cannabis use is associated with early emphysema, and with pneumothorax. A typical pattern is severe upper lobe bullous emphysema.

• “The impact of cannabis on your lungs” Ten years on from the British Lung Foundation’s A smoking Gun? report, this follow-up revisits the health effects of cannabis on your lungs and details the evidence published over the last decade. (Published June 2012)

Quantifying exposure is challenging as the equivalent in cigarettes is unknown. There a number of different ways to smoke cannabis. In London joints are most common. The pattern of inhalation is important for understanding exposure, so called “puff topology.” There are differences in the way people generally smoke cigarettes compared to joints. In a joint there is no filter, a shorter butt, a higher temperature. Users generally take a deeper inspiration, breath-hold and valsalva. Some studies have suggested there is 5 x tar deposition, 3 x carbon monoxide levels. Using a CO monitor in clinic may add value in this context.

• Joshi, Manish, Anita Joshi, and Thaddeus Bartter. “Marijuana and lung diseases.” Current opinion in pulmonary medicine 20.2 (2014): 173-179.
• Macleod, John, et al. “Cannabis, tobacco smoking, and lung function: a cross-sectional observational study in a general practice population.” British Journal of General Practice 65.631 (2015): e89-e95.

Data from Dr Paul Walker  in Liverpool (personal communication) shows the association between heroin use and asthma exacerbations. In one published cohort 31% asthma admissions in Boston were heroin users!

• Levine, Michael, et al. “The effects of cocaine and heroin use on intubation rates and hospital utilization in patients with acute asthma exacerbations.”CHEST Journal 128.4 (2005): 1951-1957.
• Levenson, Toby, et al. “Asthma deaths confounded by substance abuse: an assessment of fatal asthma.” CHEST Journal 110.3 (1996): 604-610.
• Walker, P. P., et al. “The association between heroin inhalation and early nset emphysema.” CHEST Journal (2015).

In the NRAD it was estimated that 46% deaths could have been prevented, and that substance misuse contributed to 6% deaths. Anecdotally, Prof Paul Corris from Newcastle sees an increasing number of young people referred for transplant assessment who have emphysematous lung disease due to cannabis and tobacco exposure.

New delivery methods for both tobacco and cannabis are emerging. It appears that the effects of exposure are not going away anytime soon.

Smoking and lung cancer

Dr Sara Lock increased our knowledge of the association between smoking and lung cancer. Around 90% lung cancers are attributable to smoking, and smokers have a 20x risk compared to non-smokers. 24-60% of patients with lung cancer are still smoking at diagnosis.
Post-diagnosis 6-83% continue to smoke – there is a wide variation.

We were reminded of the worldwide impact of smoking and the high rates of cancer in developed countries. We also considered the effect of smoking cessation on cancer risk.

• Peto, Richard, et al. “Mortality from tobacco in developed countries: indirect estimation from national vital statistics.” The Lancet 339.8804 (1992): 1268-1278.
• Peto, Richard, et al. “Smoking, smoking cessation, and lung cancer in the UK since 1950: combination of national statistics with two case-control studies.”Bmj 321.7257 (2000): 323-329.

It is very encouraging that “People who stop smoking, even well into middle age, avoid most of their subsequent risk of lung cancer, and stopping before middle age avoids more than 90% of the risk attributable to tobacco.” A great reason to embed smoking cessation into daily practice.

There is some evidence for a link between cannabis and lung cancer, so don’t forget to capture this when taking a history from patients.

• Aldington, Sarah, et al. “Cannabis use and risk of lung cancer: a case–control study.” European Respiratory Journal 31.2 (2008): 280-286.

Patients (and physicians) may have the opinion that “the damage has been done” when diagnosed with lung cancer, and therefore not prioritise smoking cessation. There are in fact numerous ways in which stopping smoking is beneficial to patients after a cancer diagnosis.

• Improved quality of life: Garces, Yolanda I., et al. “The relationship between cigarette smoking and quality of life after lung cancer diagnosis.” CHEST Journal 126.6 (2004): 1733-1741.
• Improved performance status: Baser, Sevin, et al. “Smoking cessation after diagnosis of lung cancer is associated with a beneficial effect on performance status.” CHEST Journal130.6 (2006): 1784-1790.
• Reduction in surgical complication rates: Møller, Ann M., et al. “Effect of preoperative smoking intervention on postoperative complications: a randomised clinical trial.” The Lancet 359.9301 (2002): 114-117.
• Improved effectiveness of some chemo/RTX in head and neck cancer: Browman, George P., et al. “Influence of cigarette smoking on the efficacy of radiation therapy in head and neck cancer.” New England Journal of Medicine328.3 (1993): 159-163.
• Improved effectiveness of some chemo/RTX in NSCLC: Fox, Jana L., Kenneth E. Rosenzweig, and Jamie S. Ostroff. “The effect of smoking status on survival following radiation therapy for non-small cell lung cancer.” Lung Cancer 44.3 (2004): 287-293.
• Greater erlotinib efficacy: Hamilton, Marta, et al. “Effects of smoking on the pharmacokinetics of erlotinib.”Clinical Cancer Research 12.7 (2006): 2166-2171. (since smoking induces CYP enzymes and therefore greater doses are required to achieve efficacious trough plasma levels.
• Lower mortality: Parsons, A., et al. “Influence of smoking cessation after diagnosis of early stage lung cancer on prognosis: systematic review of observational studies with meta-analysis.” Bmj 340 (2010). (NSCLC stage I-IIIa 5yr survival 33% ongoing smokers 70% quitters.)

Dr Lock advocated for a greater focus on smoking cessation in lung cancer. In one series only 42% of patients with lung cancer were advised to stop by any member of the team. This is despite the fact that many are motivated to quit when offered support. Of course introducing the subject must be done in a way that is support and does not add to the stigma felt by many patients.  Dr Lock advised that we focus on short-term and long-term benefits specific to patient circumstances. We must capitalise on the fact that diagnosis is a window of opportunity for behaviour change. Reframing smoking cessation as core treatment could help to move this forward.

• Cataldo, Janine K., Sarita Dubey, and Jodi J. Prochaska. “Smoking cessation: an integral part of lung cancer treatment.” Oncology 78.5-6 (2010): 289-301.

Smoking and ILD

Dr Melissa Heightman provided an overview of smoking and ILD. For some images of smoking-associated ILDs, see Radiopaedia:

The classification of ILDs has changed several times in our lifetimes. The current ATS statement puts smoking related ILDs into 4 groups.

1. ILDs directly linked to smoking e.g. RB-ILD, DIP, Langerhans Histiocytosis X.
2. Acute ILDs precipitated by smoking e.g. acute eosinophilic pneumonia.
3. ILDs more prevalent in smokers e.g. IPF, RA assoc-ILD.
4. ILDs less prevalent in smokers e.g. sarcoid. Th1 immune response.

• Travis, William D., et al. “An official American Thoracic Society/European Respiratory Society statement: update of the international multidisciplinary classification of the idiopathic interstitial pneumonias.” American journal of respiratory and critical care medicine 188.6 (2013): 733-748.

We increasingly pick up interstitial changes on CTs done for other reasons. In the COPDGene study Washko et al found that 8% of 2500 CTs in smokers had interstitial changes.

• Washko, George R., et al. “Lung volumes and emphysema in smokers with interstitial lung abnormalities.” New England Journal of Medicine 364.10 (2011): 897-906.

Garcio-Sancho et al found that current or former smoking was a risk et factor for IPF.

• García-Sancho, Cecilia, et al. “Familial pulmonary fibrosis is the strongest risk factor for idiopathic pulmonary fibrosis.” Respiratory medicine 105.12 (2011): 1902-1907.

A growing body of evidence suggests that aberrant activation of alveolar epithelial cells and fibroblasts plays a critical role in the pathogenesis of IPF. New theories propose that genetic factors are key in determining the effects of the aberrant repair mechanisms and the reasons why some people with prematurely aged lungs develop IPF whilst others develop emphysema.

• Selman, Moisés, and Annie Pardo. “Revealing the pathogenic and aging-related mechanisms of the enigmatic idiopathic pulmonary fibrosis. an integral model.”American journal of respiratory and critical care medicine 189.10 (2014): 1161-117

Combined pulmonary fibrosis and emphysema (CPFE) in increasingly recognised. It is characterised by characterized by exertional dyspnea, upper-lobe emphysema and lower-lobe fibrosis, preserved lung volume and severely diminished capacity of gas exchange. CPFE typically occurs in male smokers, and the mortality associated with this condition, particulary if pulmonary hypertension is present, is significant. It is theorised that the mechanism is aberrant lung ageing. Interestingly, a case report of familial CPFE identified telomerase mutations, helping to further understanding of potential mechanisms of disease.

• Nunes, Hilario, et al. “Is telomeropathy the explanation for combined pulmonary fibrosis and emphysema syndrome?: report of a family with TERT mutation.”American journal of respiratory and critical care medicine 189.6 (2014): 753-754.

e-cigarettes: pros, cons and controversy

Before lunch, Dr Laura-Jane Smith, Spr at the Whittington (please know I cringe as I talk about myself in the third person), presented an up to date review of the current evidence on the potential harms and benefits from ENDS (electronic nicotine delivery systems).

She reviewed the historical context of tobacco use, the invention of ENDS, and the current media interest in their safety and effects. She then examined a number of key areas in the current debate:

• are e-cigarettes safe?
• does e-cigarette use reduce tobacco harm at the level of the individual?
• does e-cigarette use reduce tobacco harm at the population level?
• is there a gateway effect, leading use of cigarettes by young people who would otherwise not smoke?
• what is the state of current legislation and policy?

You can access the slides, including all the links and references, on slideshare.

Key messages were:

• cigarettes kill half of regular users
• tobacco harm continues to be a major global problem, and huge contributor to inequality
• e-cigarettes appear to be significantly less harmful than cigarettes
• more research is needed on the safety of ENDS and regulation will improve safety
• long-term effects will not be known for many years
• e-cigarettes are being chosen by the public as harm reduction and as quit devices
• we have a responsibility to advise individual patients in informed and honest ways, so keep up to date with the evidence

Radiology Quiz

Dr Anna Gerratt shared some xrays and CT images of smoking-related pathology. Examples included:

• Apical bullae due to cannabis smoking
• Classical emphysema due to tobacco smoking
• Emphysema with fibrosis (CPFE) due to tobacco smoking
• Pneumothorax, a complication of bullae
• RB-ILD

For examples see Radiopedia 

Smoking, anti-CCP antibodies and Inflammatory Arthritis

Dr Mark Lazarus set out to convince us that Rheumatoid Arthritis is a lung disease! It then progresses to a systemic inflammatory disease, and takes hold in the joints, when patients finally present. He asked whether we should we be looking for RhF and anti-CCP antibodies in more of our lung clinic patients (and did not necessarily answer it!).

Patients with RA have a higher mortality due to infection and cardiovascular disease. Early diagnosis and treatment are important to prevent disability, and also since early intervention leads to higher rates of remission.

• Gullick, Nicola J., and David L. Scott. “Drug therapy of inflammatory arthritis.”Clinical Medicine 12.4 (2012): 357-363.

Current British Society of Rheumatology guidelines advise that patients newly diagnosed with RA should start DMARD therapy within 3 weeks. Diagnostic criteria have changed significantly in the last 30 years – some of the criteria from 1987 are now considered signs of chronicity, and should be prevented (eg
nodules and erosions).

Diagnosis now relies more on detection of autoantibodies. Anti-CCP is a useful test as it not only aids diagnosis but correlates with severity.

Should we screen people for anti-CCP antibodies? And if positive should we start them on a DMARD with a good side effect profile such as hydroxychloroquine? This is not advocated by guidelines and the clinical and cost effectiveness of such a strategy is unknown. So, no, for now.

Dr Lazarus shared some cases which highlighted the utility of anti-CCP.
1. 40M actor. Heavy smoker. Widespread polyarthritis. ESR 73, CRP 103, RhF 201, anti-CCP >200
Treated with steroids, MTX, SSZ. Suffered a ruptured biceps tendon. Was depressed and was started on an SSRI. Unable to work. Became homeless. Shows the devastating effects of a chronic disease. He had anti-TNF within 8/12, but failed etanercept. He had successful treatment with Rituximab.

2. 34F in fashion industry. Smoker. Fluctuating arthritis. Palindromic. NSAIDs. Steroid injections. DNA-ed clinic. Reappeared with multiple joint synovitis + boutonniere deformity. ESR 76, CRP 24, RhF 9, anti-CCP 49. With the autoantibody panel the diagnosis was much clearer. She agreed to try SSZ.

We considered how common Rheumatoid lung disease might be.

• Kelly, Clive A., et al. “Rheumatoid arthritis-related interstitial lung disease: associations, prognostic factors and physiological and radiological characteristics—a large multicentre UK study.” Rheumatology 53.9 (2014): 1676-1682.

The lung disease can exist without any evidence of lung damage – a precursor? 1 study examined 74 patients with lung disease and anti-CCP + ve but no RA or CTD symptoms.

• Fischer, Aryeh, et al. “Lung disease with anti-CCP antibodies but not rheumatoid arthritis or connective tissue disease.” Respiratory medicine 106.7 (2012): 1040-1047.

We were advised that we should check patients with bronchiectasis, ILD, and bronchiolitis for anti-CCP antibodies. However, the pick-up rate, and cost effectiveness of such as approach is unknown. Conversely if patients with RA have chest CTs we often find subclinical bronchiectasis and mild pulmonary fibrosis. What is the significance if they are asymptomatic?

It is not well understood how anti-CCP is generated. Smoking increases the risk of RA. The mechanism is thought to be due to citrillunation of peptides through PAD enzymes. Smoking increases PAD enzyme expression in the lungs.

• Reynisdottir, Gudrun, et al. “Structural Changes and Antibody Enrichment in the Lungs Are Early Features of Anti–Citrullinated Protein Antibody–Positive Rheumatoid Arthritis.” Arthritis & Rheumatology 66.1 (2014): 31-39.
• Lugli, Elena B., et al. “Expression of citrulline and homocitrulline residues in the lungs of non-smokers and smokers: implications for autoimmunity in rheumatoid arthritis.” Arthritis research & therapy 17.1 (2015): 9.

Some have postulated that the lung is the site of initiation of injury in Rhematoid arthriris. The effects of anti-CCP may be mediated through TLR-4 and Fcy receptors.

• Perry, Elizabeth, et al. “The lung in ACPA-positive rheumatoid arthritis: an initiating site of injury?.” Rheumatology 53.11 (2014): 1940-1950.
• Sokolove, Jeremy, et al. “Immune complexes containing citrullinated fibrinogen costimulate macrophages via Toll‐like receptor 4 and Fcγ receptor.” Arthritis & Rheumatism 63.1 (2011): 53-62..

Stop Smoking Training

Elizabeth Pang gave an interactive and interesting session of stop smoking training, upskilling us all to be better stop smoking champions. A lot was covered, but we have identified some highlights.

Elizabeth inspired us by demonstrating the huge impact of the smoke-free law: reduced MI admissions, premature births, and asthma admissions. Every patient contact is an opportunity to support someone to stop smoking, but what is the best way to go about it? When giving a brief intervention we were advised to “Ask Advise Act.”

CO monitors can be excellent motivational tools in smoking cessation. To use them effectively it is important to know the reasons for a falsely raised CO level. These include: HbSS; lactose intolerance; a defective exhaust.

It is important to really understand the smoker in front of you. Remind yourself that nicotine is very addictive. It takes just 7 seconds to hit the brain, stimulate receptors and release dopamine.

• “Nicotine: harder to kick than…heroin“

Withdrawal symptoms are common and include: feeling low; insomnia; irritability; poor concentration; restlessness; increased appetite and weight gain. However, you can reassure people that such symptoms are temporary and last around 10 weeks. This is the time when nicotine replacement therapies (NRT) are effective. We reviewed available preparations, and even tried some of them.

Elizabeth advised that a combination. e.g. patch + lozenge is most effective. Assessing the level of addiction can help ensure you prescribe the right dose of NRT. For this, the Fagerstrom Test for nicotine dependence is useful. If you do not have time to complete the whole test with your patient, the most important Qs are: how many cigarettes do you smoke a day?; and at what time do you have your first cigarette. <5min = highly addicted, >30min = moderate addiction; > 1hr low levels of addiction.

We then considered drug treatment to support smoking cessation:

Varenicline(Champix): Prescribed on a 12wk course. Contraindicated in those who are <18yrs, pregnant or breast feeding women. It acts by preventing nicotine binding to receptors. This reduces the reward and reinforcing aspects of smoking. It also releases a low level of dopamine which makes withdrawal less unpleasant. There are common misconceptions such as the risk of suicide which have led to underuse. The most common side effect is nausea which can lead to discontinued use. A recent meta-analysis found no evidence of an increased risk of suicide or attempted suicide, suicidal ideation, depression, or death with varenicline, providing reassurance for users and prescribers:

• Thomas, Kyla H., et al. “Risk of neuropsychiatric adverse events associated with varenicline: systematic review and meta-analysis.” bmj 350 (2015): h1109.

Only 3-5% can stop smoking cold turkey. There is a 4x better quit rate with behavioural support + varenicline / NRT. Combination therapy is better than monotherapy. You can use NRT in those who are 12yrs and above (important for our paediatric colleagues) in who you should choose a low dose patch or low dose oral monotherapy.

We then moved on to practice motivational interviewing techniques. Important elements were to ask permission before discussing behaviour change; explore importance of the change (if <7 not ready to change); and confidence in succeeding. Probing questions can be useful such as “why did you select a score of 6 rather than 5? What would need to happen to move up from 6 to 8?” Another useful technique is normalising: “a lot of people are concerned about that” “Yes some people do put on weight, but the increased appetite lasts only around 10wks” “that is not unusual, many people have had previous quit attempts.” Affirmation is helpful, but requires sincerity. Elizabeth told us that she congratulates people for coming to the 1st appointment in the stop smoking clinic, as many people DNA.
Ask “What do you know about the benefits of stopping smoking?” – then show the benefits and time after quitting – give quick wins. When asked about the motivation to stop smoking people answered: 8% health problems, 12% restrictions (e.g. smoking ban), 12% poster, 15% advert, 26% healthcare professional, 36% family and friends, so we as health professionals can help to influence people.

A useful acronym for motivational interviewing is OARS:

• Open-ended questions
• Affirmations
• Reflective listening
• Summarise

Go forth and save lives.