Download The Musculoskeletal effects of Cigarette Smoking and Nicotine

Dr. R Tyler Boone
1960’s- U>S. Surgeon General
warned of association between
smoking and lung cancer
 Smoking rates have declined but
20% of American adults smoke
 Smokeless tobacco use
increasing

Volatile phase (500 gases) carbon
monoxide, carbon dioxide, ammonia,
hydrogen cyanide, benzene
2. Particulate phase (3500 chemicals)
nicotine, nornicotine, antabine,
anabasine.
• Most of the carcinogens
• 2 to 3mg of nicotine, 20-30ml of carbon
monoxide inhaled per cigarette.
1.
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The addictive component of tobacco
“The cigarette should be conceived not
as a product but as a package. The
product is nicotine. Think of the
cigarette pack as a storage container for
a day’s supply of nicotine. Think of a
cigarette as a dispenser for a dose unit of
nicotine.” (Phillip Morris Executive)
 Named
after tobacco plant
Nicotania tabacum
 Frenchman Jean Nicot de
Villemain
 16th century
 Alkaloid

17th century use as insecticide
 Neurotoxin lethal to insects
 2008 EPA banned use in
pesticides
 30 to 60mg lethal to humans (1
to 3 in cigarettes)

Nervous system effect
 Decreases appetite, boosts mood,
relieves depression, improves
cognition and memory
 Stimulates intestinal motility,
increases salivation, increases heart
rate and blood pressure
 Nausea, vomiting
1mg stimulates brain
 Masks neurotransmitters, deceives neurons by
replacing acetylcholine on receptors
 Stimulates abnormal, extra production of dopamine
 Euphoria
 After finishing cigarette, the nicotine effect ceases
and euphoria disappears
 Attempt to recover feeling with another cigarette
 Cycle of addiction
 Maybe the most addictive drug known to man
 Every drag delivers via lungs to brain a dose of
nicotine that acts more rapidly than heroin injected
via veins

Intense craving
 Anxiety, drowsiness, insomnia,
frustration, headaches, weight gain,
difficulty with concentration
 Symptoms peak at 2-3 days
 No physical pain---mainly mental
pangs caused by illusion of pleasure
deprivation
 “feeling normal”

1.
2.
3.
Physical
Habitual
Emotional
 Vasoconstriction
thus hypoxia
 Platelet adhesion, microvascular
thrombosis
 Carbon monoxide reduces the
amount of oxyhemoglobin
 One pack per day leads to 15-20
hrs. tissue hypoxia

Immune suppression
 Decreased WBC function, reduced
serum immunoglobulins, reduced
antibody response, decreased
lymphoid tissue, inhibits T-cell
lymphocytes.
 Negatively impacts wound healing
and increases infection rates.
Reduced blood supply and tissue
hypoxia leads to reduced bone
metabolic activity
 4-fold increased risk of AVN of femoral
head.
 Osteoblast function stimulated at low
levels of circulating nicotine and
inhibited at high levels.

 Osteoclastic
function/formation
stimulated by nicotine
 Decreased calcium absorption in
smokers leads to increased bone
resorption and decreased
formation

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Increased fracture rates of hip, spine and distal
radius (osteoporosis)
Exacerbates postmenopausal and age-related bone
loss
Decreased peak BMD in adolescents and young
adults who smoke
Lifestyle variable associated with smoking
 Decreased appetite
 Lower calcium intake
 Higher consumption of caffeine and alcohol
 Lower levels of physical activities


Nonunion and delayed union
increased
Lower Extremity Assessment Project
(J. Orthopedic Trauma 2005)
 Smokers with open tibial fractures
 37% increased nonunion
 3.7 times more osteomyelitis
 Twice as likely to develop acute
post-op infection
 Delayed time to union (4 weeks)

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Numerous studies show 2.7 to 3.8
times more likely nonunion in
ankle/foot procedures
Spinal Fusions
 Increased pseudoarthuosis rates
 Brown et ‘al (Spine 1986)
 100 pts with lumbar fusion
 Pseudoarthrosis rates in smokers
40% vs. 8% in non-smokers.

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Bohlman (TBJS 2001)
 Lower fusion rates in smokers
undergoing multilevel anterior
cervical interbody fusions.
Increased infection rates for all spine
surgical procedures (Boakye et’al
Spine 2006)
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Poor wound healing from cigarette
smoking due to alteration of normal
process of healing
Fibroblasts, stem cells, acute phase
proteins and growth factors diminished
in forming granulation tissue.
Nicotine increases catecholamines
(dopamine, epinephrine) which inhibit
epithelialization.
Free-radicals created that damage cells.
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Tendon and ligament healing
affected
Poorer outcomes in ACL
reconstruction
Higher prevalence of degenerative
rotator cuff tears

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Smoking associated with increased
risk of back pain and degenerative
disc disease.
Twin Spine Study (Spine J. 2009)
 18% greater disc degeneration
 Reduced perfusion and
malnutrition from
vasoconstriction/hypoxia
Chronic Pain
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No definitive guidelines on preoperative cessation
Encourage/mandate all patients
contemplating elective procedures
quit 4 to 6 weeks in advance
Immune function recovers after 2-6
weeks
Wound healing after 3-4 weeks
Pulmonary function after 6-8 weeks

Orthopedists ability to express
importance of quitting tobacco can
have profound effect
 Chrin (Spine 2000)
 35.6% quit rate in pts. Whose
surgeon placed “high priority”
 19.5% quit rate in “low priority”
group


1-800-QUIT-NOW
www.smokefree.gov

Nicotine replacement therapy (gum,
transdermal patches, nasal spray, inhalers,
sublingual tablets, lozenges)
 Bupropion
(Wellbutrin)
 Atypical antidepressant
 Reduces severity of nicotine
cravings

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Chantix/Varenicline Tartrate
Partial agonist of nicotine receptor
Reports of severe cardiovascular events
and neuropsychiatric side effects

Electronic or e-cigarettes
Produce aerosol by heating a humectant (propylene
glycol) containing nicotine and flavoring
 When inhaled aerosol delivers nicotine
 Long-term health effects unknown
 Not FDA regulated


Most effective smoking cessation
program has yet to be determined
but probably includes a combination
of the following:
 Counseling
 Dedicated “quit line”
 Regular follow-up contact
 NRT
 Pharmaceutical support
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Nicotine and it’s major breakdown
product cotinine can be tested for in
urine, blood, saliva and hair.
Chewing or inhaling tobacco introduces
nicotine into the body where it is
metabolized by the liver and excreted in
urine.
Cotinine is the primary method of
nicotine detection because it has a halflife up to 10 times that of nicotine.


Hair
 rare use because of cost
 Can evaluate long-term use because it
can detect nicotine exposure up to 10
days before sample taken
Saliva
 Simple, noninvasive
 Difficult to get large enough sample
 Rely on very recent exposure and fails
to differentiate light active smokers
from passive smokers

Blood
 Allows detection of cotinine in
blood plasma
 Requires more processing
 More time consuming and
expensive

Urine
 Very sensitive and will detect even
small levels of second hand smoke
 Most common method used by
insurance companies to differentiate
active smokers from passive smokers
 Can test for anabasine
 Alkaloid present in tobacco but not
NRT

When tobacco and nicotine
product use stopped
 > 2 weeks for blood cotinine to
drop to level of non-user
 >5-6 weeks for urine level of
cotinine to clear