smoking and pain vaping? · 11/7/2019 2 low back pain shiri et al. (2010) metanalysis both...

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Smoking and pain

Alan Kaplan MD CCFP(EM) FCFP

Chair, Family Physician Airways Group of Canada

Member, Chronic Pain SIFP

Chronic Pain consultant, York Region

Vaping?

Learning Objectives

Review the epidemiology of pain and smoking

Identify the relevant pharmacology of nicotine

to pain

Explain how nicotine exposure affects pain

Hopefully, be able to integrate tobacco

cessation strategies within patients suffering

with pain in clinical practice

Faculty/Presenter Disclosure

Faculty: Alan Kaplan MD CCFP(EM) FCFP

Chair Family Physician Airways Group of Canada

Past Chair of Special Interest Focused Practice, College of Family Physicians in Respiratory Medicine.

Honorary Professor of Primary Care Respiratory Medicine, OPRI

Chronic pain consultant, Brampton Civic Hospital

Relationships with commercial interests:

Grants/Research Support: none

Speakers Bureau/Honoraria: Astra Zeneca, Boehringer Ingelheim, Griffols, Pfizer, Purdue, Merck Frosst, Novartis, sanofi, Takeda.

Consulting Fees: Aerocrine, Behring, Novartis, Takeda, Purdue, Pfizer

Other:

Member of Health Canada Section on Allergy and Respiratory Therapeutics.

Member of Public Health Agency of Canada section on Respiratory Surveillance

Disclosure of Commercial Support

This program has received no financial support from .

This program has received no other in-kind support

Potential for conflict(s) of interest:

none

Mitigation of potential bias: There is no bias other than being an anti-smoking activist!

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Low Back pain

Shiri et al. (2010) metanalysis

Both cross-sectional and prospective studies also demonstrated evidence of a dose-response relation between number of cigarettes smoked per day and LBP (with confounders removed)

Mechanism?

The most widely accepted explanation for the association between smoking and low back pain is disc degeneration via malnutrition of spinal disc cells by carboxy-hemoglobin-induced anoxia or vascular disease (Akmal et al., 2004).

Smoking as a Risk Factor

for developing chronic pain

Rheumatoid Arthritis

Smoking may also influence RA disease severity, possibly in a dose-dependent fashion (Albano, et al., 2001; Harrison & Silman, 2000; Masdottir et al., 2000; Mattey et al., 2002; Papadopoulos et al., 2005)

Smoking and genetic predisposition may be independent risk factors in the development of RA, with smoking causing earlier disease expression in patients without a genetic predisposition (Hutchinson, Shepstone, Moots, Lear, & Lynch, 2001).

Possible Mechanism:

Smoking acts synergistically with other RA risk factors, including IgM-rheumatoid factor, anti-CCP, and shared epitopes (Christensen, Lindegaard, & Junker, 2008).


for developing chronic pain Headache:

In a population-based survey (N = 51,383) revealed that smokers were 1.5 times (95% CI = 1.3–1.6) more likely to report headaches than were never smokers, after controlling for sex, age, and education (Aamodt, et al., 2006). -Smokers in this sample were also 1.7 times more likely (95% CI = 1.3–2.2) to endorse experiencing headache activity on more than 14 days per month.

In two prospective studies, the first of which revealed that both smoking status and nicotine content of the preferred cigarette adversely influenced headache activity, with smokers reporting greater weekly peak headache intensity than nonsmokers (Payne et al., 1991)

Initiation of smoking behavior usually occurs prior to the onset of clusterheadache for both men and women, providing some indication of temporal precedence and suggesting that smoking may prime the inception of cluster headache activity (Rozen, et al., 2001).

Mechanism:

smoking that might also induce headache activity, including: changes in levels of nitric oxide in the brain, carbon monoxide-induced anoxia, decreased monoamine oxidase (MAO) activity, and a reduction in the efficacy of common headache medications because they may be metabolized more quickly by smokers



Associations between tobacco smoking and the prevalence/ severity of several other painful conditions, including:

Fibromyalgia (Lee et al., 2010; Weingarten, Podduturu, et al., 2009; Wolfe & Hawley, 1998; Yunus, Arslan, & Aldag, 2002),

Dyspepsia (Wildner-Christensen, Hansen, & De Muckadell, 2006)

Menstrual pain (Allen, Hatsukami, Christianson, & Brown, 2000; Gold et al., 2007),

Pregnancy-related pelvic pain (Biering, Aagaard Nohr, Olsen, Nybo Andersen, & Juhl, 2010)

Buerger’s disease (Quintas & Albuquerque, 2008), HIV-related bodily pain (Patel et al., 2006; Turner et al., 2001)

Painful temporomandibular joint disorders (Melis et al., 2010; Weingarten, Iverson, et al., 2009)

Pain associated with osteoarthritis (Amin et al., 2007)

Pain associated with sickle cell disease (Cohen, DeBaun, Blinder, Strunk, & Field, 2010).



Resource article of use:

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Findings from multinomial logistic regression models indicated that

RR 2.1 TO NON SMOKERS

adjusting for sex, own occupational class, educational level, body mass index, leisure

time physical activity, alcohol intake, long-standing illness and symptoms of anxiety and depression.

No association was observed between smoking history and CRP,

so mechanism unclear.

Smoking and Pain: A Paradox

Nicotine has analgesic properties likely resulting from effects at both

central and peripheral nicotine acetylcholine receptors (nAChRs)

BUT....

Smoking is a risk factor for chronic pain

Numerous studies demonstrate evidence of covariation between smoking

and the prevalence of a variety of chronically painful conditions

Recent meta-analytic support for smoking as a causal factor in the

development of chronic LBP & RA (Shiri et al., 2010; Sugiyama et al.,

2010)

Pharmcotherapy of Nicotine

Acetylcholine Receptors NAChR’s

Shows a wide distribution in the central and peripheral nervous system

Involved in sleep, arousal, anxiety, cognition and pain

Activation can trigger the release of neurostransmittors such as GABA,

glutamate, serotonin, histamine, and norepinephrine

Tally et al, 2009

Gotti et al, 2004

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Smoking and pain intensity

Smokers report greater pain and functional impairment than

nonsmokers ( Weingarten et al., 2008)

Smokers use substantially more analgesic medication (e.g.,

opioids) than nonsmokers

(Broekmans et al., 2010, Woodside, 2000)

Effects of pain on smoking:

Pain as a motivator of smokingCross-sectional & qualitative evidence (pain patients):

Reported increased smoking in response to pain

Endorsed pain-induce desire to smoke (Hooten et al., 2011) “My smoking

is extremely related to my pain…instead of rubbing my knee I’ll go smoke a cigarette”; “If I have a flare-up…I’ll…go for a cigarette”

Endorsed smoking for pain-coping (e.g., via

distraction) “I’m thinking of the cigarette…puffing it, and lighting it, and holding it…so it diverts me away from the

pain”; “Smoking is a great distraction tool”

Reported that opioid use increased urge to smoke “When I

was on…opioids it would make me a chain smoker”

Jamison et al., 1991

It goes both ways..Pain as a barrier to smoking cessation

Smokers in pain report greater difficulty and

less confidence in quitting (e.g., Waldie et

al., 2008; Hooten et al., 2011)

Pain as a barrier to smoking cessation:

WHY?

Pain factors (pain severity, functional impairment, disability status, pain-coping outcomes)

Psychiatric comorbidity (depression/anxiety, substance use,

personality disorders)

Medication interactions (effects of increasing/decreasing opioid use)

Pain-induced relapse (painful stressors can reinstate extinguished drug-

seeking)

Smoking abstinence-induced hyperalgesia

“I’d be afraid of the pain getting worse if I quit smoking” (Hooten et al., 2011)

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So,what to do

about it?

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How about comorbid psychiatric illness and smoking cessation:

Does that make it worse?

Opioid Risk Tool

1. Webster LR, et al. Pain Med. 2005;6:432-442. 2. Chou R, et al. J Pain. 2009;10(2):113-130.

3. Jovey RD, ed. Managing Pain – The Canadian Healthcare Professional’s Reference. 2008.

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Opioid Risk Tool

1. Webster LR, et al. Pain Med. 2005;6:432-442. 2. Chou R, et al. J Pain. 2009;10(2):113-130.

3. Jovey RD, ed. Managing Pain – The Canadian Healthcare Professional’s Reference. 2008.

How does it do this?

Nicotine effects on pain responses may represent

treatment of nicotine withdrawal, rather than from direct

analgesic effects in studies of smokers deprived of

nicotine experimentally

Schacter 1978, Shin 2010

When is the best time to quit?

At least pre-operatively!

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Nicotine Replacement Therapy and

Wound Healing

0%

5%

10%

15%

20%

25%

30%

Infection rate

Non-abstinent

Abstinent, active patch

Abstinent, placebo

•48 smokers randomized to

continuous smoking or

abstinence, with or without

nicotine replacement

•Standardized surgical wounds

over a 12 week period

Sorensen et al, Ann Surg 238:1, 2003

Smokers do less well

postoperatively

Short Term

- Worse wound healing

(Mastectomy flap necrosis

18.9% v 9.0 in NS) (DW

Chang Plastic & Reconstr

Surg. 2000 p2374)

- More infections (12% in

smokers, v 2% NS)

(Sorensen, Ann Surg, 2003)

Long Term

- Worse outcome (more pain, poorer function) one year after ACL repair (Karim, JBJS, 2006)

“We found that smoking was the single

most important risk factor for the

development of postoperative

complications”

(Moller JBJS 2002)

120 patients for elective joint replacementRandomised to control or smoking cessation intervention:

Control Routine preoperative preparation4 stopped smoking anyway

Intervention Routine preoperative preparation plusweekly meetings with nurse, NRT therapy36 stopped smoking, 14 reduced, 6 continued

Results

Control Intervention

Wound problems: 31% 5%

CV Insufficiency 10% 0%

Avg. days in hospital 13 11

Total days in ICU 32 2

Stopping smoking reduces risk:

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When to stop? Ideally 6 – 8 weeks or longer

Definite advantage of 4 weeks

For carbon monoxide elimination, 4 -8 hours

“No smoking after midnight”?

Risk of stopping shortly before surgery?

Postoperative quitting aids wound healing

Case study

Wanda is a 62 year old married pharmacist

Wanda wants to quit smoking, but is asking for your help

Started smoking at age 15, quit at 32 with birth of her child, but restarted at age 40 when diagnosed with Crohn’s disease and reactive arthritis.

Smoked to help deal with stress of illness and raising three kids, but has found that when she stopped smoking in past quit attempts, her pain worsened.

On Arthrotec for arthritis pain and Oxycocet for her abdominal pain.

Needs a bowel resection for active Crohns segment with obstruction despite optimal therapy

40 lb overweight and restricted in activities d/t pain.

On waiting list for biologic therapies........which I agree would help!!

Case study: Questions

1) What are the central issues in this case?

2) What are the patient’s barriers to change

3) Where would YOU start if you were seeing Sue?

4) What interventions would you perform in addressing smoking

cessation recognizing the other co-existing risk factors/issues?





Chronic pain and smoking

Smoking may well have some benefits in patients with IBD

Smoking helps her stress and potentially her mood

Surgical outcomes in smokers much worse

Analgesic needs pre and post op




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Pain

Stress

Anxiety re surgery

Coping mechanisms

Surgical outcomes

Long term benefits













Explanation of issues so she is prepared

Smoking cessation strategies that she can work with

Multimodal, eg NRT + Buproprion(anxiety and mood?)

E cig etc for coping skills?

Analgesics available for worsening pain?

NRT post-op aggressively

What about Vaping?

Case patients defined as persons who reported use of e-cigarette devices and related products in the 90 days before symptom onset and had pulmonary infiltrates on imaging and whose illnesses were not attributed to other causes.

There were 53 case patients, 83% of whom were male; the median age of the patients was 19 years.

The majority of patients presented with respiratory symptoms (98%), gastrointestinal symptoms (81%), and constitutional symptoms (100%).

All case patients had bilateral infiltrates on chest imaging (which was part of the case definition).

A total of 94% of the patients were hospitalized, 32% underwent intubation and mechanical ventilation, and one death was reported.

A total of 84% of the patients reported having used tetrahydrocannabinol products in e-cigarette devices, although a wide variety of products and devices was reported.

Syndromic surveillance data from Illinois showed that the mean monthly rate of visits related to severe respiratory illness in June through August of 2019 was twice the rate that was observed in the same months in 2018.

Case definition per CDC

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Initially the culprit: vitamin E acetate.

But the U.S. Food and Drug Administration soon dampened that enthusiasm, noting that not all tested samples even contain the oily substance. In fact, no candidate substances have consistently turned up across samples so far.

And then there is the question of what people are actually vaping: although most cases involve pods containing THC (the active ingredient in cannabis), not all of them do.

Vaping-product manufacturers have sought to distinguish their goods from counterfeits acquired on the street and to blame the latter, but investigators have not yet confirmed the provenance of many of the products involved in the disease.

In a good chunk of cases, patients say the one they vaped contained only nicotine.

Although it is possible patients do not want to admit to THC use in states where it is not decriminalized, there is no evidence they are lying.

Flavored e-cigarettes have been successful in the marketplace; the rates of vaping among teenagers

are increasing at an alarming rate

“We think the FDA should simply ban the sale of flavored nicotine products for use in e-cigarettes.

The public health problem that e-cigarettes can help solve — by helping people who are users of combustible tobacco products stop smoking by switching to vaping — is adequately addressed by

liquids that are not flavored to appeal to adolescents”

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What do I say?

Smoking is bad

E cig are bad, especially with THC and Nicotine

E cig may be more dangerous than we had thought

E cigarettes use for the ‘HABIT’ component of smoking cessation may be of benefit in

quitting

If recommended to assist smoking cessation (and I do!) use with NO flavour, NO

nicotine, NO colour, and NO THC and under MEDICAL SUPERVISION

HARM REDUCTION!

Not SAFER for pregnancy!

Document warnings when making the recommendation!

Most recent

Deaths reported from illicit fentanyl being place in Vaping devices

And the story continues…..

Summary

Pathophysiologic reasons for why smoking helps pain

Smoking does worsen conditions and cause pain

Does it induce pain sensitivity, like opioids do?

Clinically pain may be worse if smoking stopped in short term

Outcomes undoubtedly better in long term

When is the best time?

Especially if they are preop!

Use E cigarettes to help. NO flavour, colour, nicotine, THC, or anything else!!

Pain in patients with COPD…another issue!

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smoking and pain vaping? · 11/7/2019 2 low back pain shiri et al. (2010) metanalysis both...

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