It has been shown to adversely affect bone mineral density, lumbar disk disease, the rate of hip fractures, and the dynamics of bone and wound healing.. Furthermore, some cases of low ba
Trang 1Cigarette smoking has come under
increasing attack by a number of
different groups both within the
United States and worldwide This
has been fueled, in part, by
recog-nition of the increasing number of
diseases with which smoking has
been directly or indirectly associated
Currently, there are more than 50
million smokers in this country,
and approximately 800 billion
ciga-rettes are smoked each year.1 The
adverse effects of smoking on the
cardiovascular system are common
knowledge.2,3 Smoking is implicated
in the etiology of a multitude of
cancers as well.2,4 Smoking is now
the leading avoidable cause of
mor-bidity and mortality in the United
States According to one report,
more than 500,000 deaths per year
in the United States alone can be
at-tributed to smoking.2
Cigarette smoke has two phases:
a volatile phase and a particulate phase The volatile phase is the longer phase and accounts for 95%
of the cigarette smoke Nearly 500 different gases are released during the volatile phase, including nitro-gen, carbon monoxide, carbon di-oxide, ammonia, hydrogen cyanide, and benzene The roughly 3,500 different chemicals released in the particulate phase include nicotine, nornicotine, anatabine, and anaba-sine.5 Stripped of water, the partic-ulate matter that remains, or “tar,”
contains the majority of the car-cinogens of cigarette smoke.6 Nico-tine, which is considered the addic-tive component of cigarette smoke, has been implicated in the patho-genesis of a variety of diseases.6
Nicotine has been shown to in-crease platelet aggregation,
de-crease microvascular prostacyclin levels, and inhibit the function of fibroblasts, red blood cells, and macrophages.6,7 Carbon monoxide has a stronger affinity for hemoglo-bin than oxygen, resulting in the displacement of oxygen from the hemoglobin and a lower oxygen tension in tissues.8
For years, orthopaedic sur-geons have known about the rela-tionships that putatively exist between smoking and an array of orthopaedic conditions and com-plications In the past, there have been many reports that deal with these relationships as separate entities but very few published comprehensive reviews This arti-cle will summarize the currently available literature regarding the relationships between smoking and musculoskeletal diseases, as well as the effect on the treatment
of those diseases, to provide infor-mation that can be used clinically
by both the practitioner and the patient
Dr Porter is Harry Winkler, Jr, Orthopaedic Surgery Research Fellow, Department of Orthopaedic Surgery, Carolinas Medical Center, Charlotte, NC Dr Hanley is Chair-man, Department of Orthopaedic Surgery, Carolinas Medical Center.
Reprint requests: Dr Porter, Department of Orthopaedic Surgery, Carolinas Medical Center, PO Box 32861, Charlotte, NC 28232 Copyright 2001 by the American Academy of Orthopaedic Surgeons.
Abstract
Currently, there are more than 50 million smokers in this country, and
approxi-mately 800 billion cigarettes are smoked each year Smoking is now the leading
avoidable cause of morbidity and mortality in the United States According to
one report, over 500,000 deaths per year in the United States alone can be
attrib-uted to smoking For years, orthopaedic surgeons have known about the
rela-tionships that putatively exist between smoking and an array of orthopaedic
con-ditions and complications It has been shown to adversely affect bone mineral
density, lumbar disk disease, the rate of hip fractures, and the dynamics of bone
and wound healing Although scientific and clinical information on smoking
and its consequences suggests differing degrees of correlation between smoking
and orthopaedic conditions, most available data do suggest a real and
repro-ducible relationship In the past, there have been many individual reports that
deal with these relationships separately but very few published comprehensive
reviews This summary of the current literature regarding the relationship
between smoking and musculoskeletal diseases and their treatment provides
information that can be used clinically by both the practitioner and the patient.
J Am Acad Orthop Surg 2001;9:9-17
Scott E Porter, MD, and Edward N Hanley, Jr, MD
Trang 2Osteoporosis is a common finding
in postmenopausal women and
elderly men It is a complex
disor-der that occurs earlier in life and
more often in women than in men
Osteoporosis is characterized by a
decrease in bone mass with a
resul-tant increased risk of fractures of the
radii, femoral necks, and vertebral
bodies.9,10 Honkanen et al11 have
warned against generic
compar-isons of studies that deal with
osteo-porotic fractures They emphasize
that the relationships between the
risk factors associated with
pre-menopausal, peripre-menopausal, and
postmenopausal fractures differ by
fracture type, which precludes their
general comparability
In an early study by Daniell,12
fractures of the weight-bearing spine
occurred more frequently in
os-teoporotic postmenopausal women
who smoked than in women of
similar age who did not smoke He
determined that smokers had an
ap-parent cortical bone loss of roughly
1.02% per postmenopausal year,
compared with only 0.69% for
non-smokers (P<0.001) This rate
in-creased to 1.19% for nonobese
osteo-porotic women who smoked.12 A
later study by Stevenson et al13
sup-ported the findings of Daniell by
also documenting that the vertebrae
of women who smoke have
appre-ciably less bone mass
Many authors believe that this
increase in the rate of osteoporosis
observed in women who smoke is
mediated by the complex and often
inhibitory interaction between
smoking and estrogen.14-18 The
effects of this interaction include
unfavorable lipid profiles, a
reduc-tion in the rate of endometrial
can-cer, earlier menopause, and reduced
rates of estrogen receptor–positive
breast cancers.16,17,19-21
Williams et al14 showed that
smoking adversely affected women
who were not users of exogenous
estrogen In their study, they dem-onstrated an increase in the rates
of hip and forearm fractures in postmenopausal women smokers
However, this increase was statisti-cally significant only for the subset
of thin women who smoked and were not estrogen users
In a recent prospective study of more than 115,000 nurses, Cornuz
et al17 demonstrated a small in-crease (1.3%) in the risk of sustain-ing a hip fracture in smokers and a greater increase (1.6%) in this risk for women who smoked more than
25 cigarettes per day This risk decreased to a level below that of control subjects after smoking ces-sation, but only after a mean of 10 years The authors concluded that their observed results might be attributable to the inhibitory effects smoking has on circulating estro-gen This inhibition would decrease the protective effects of estrogen on bone mass
La Vecchia et al19showed simi-lar results in their study of over 200 women They demonstrated that women smokers had a 1.6% in-crease in the relative risk of sus-taining a hip fracture compared with age-matched controls This risk increased to 2.8% for the women who smoked more than 25 ciga-rettes per day A smaller subset of women who were actively taking hormone replacement therapy (HRT) had a nonsignificant de-crease in their relative risk to 0.4;
however, the authors conjectured that the small numbers in this sub-set may have prevented the dem-onstration of statistical significance
Melhus et al15postulate that it is the increase in reactive oxygen intermediates, or free radicals, found in the circulation of smokers that is directly antagonizing to estrogen They were able to dem-onstrate a nearly fivefold increase
in the relative risk of hip fractures
in smokers with a low intake of the antioxidant vitamins C and E when
compared with a control group, after adjustment for other major osteoporosis risk factors
Jensen and Christiansen18 stud-ied oral and percutaneous HRT and the effects of smoking on these modalities Oral HRT resulted in a decrease in the rate of bone loss for nonsmokers, but this beneficial re-sponse to oral HRT was significantly
lessened for smokers (P<0.01)
In-cidentally, they also reported that smoking is antagonistic to the effect
of the favorable lipid profile shared
by women as a result of HRT Osteoporosis afflicts men as well Recent estimates based on bone den-sitometry studies suggest that be-tween 250,000 and 2,000,000 white men have osteoporosis of the femoral neck.22 The prevalence is roughly 1%
in white men over the age of 80.10
Grisso et al10 and Kanis et al23
have shown that many of the risk factors for hip fractures in women also apply to men Specifically, lean body mass, the absence of physical activity, and smoking were all associated with an increased risk
of hip fracture The authors of the National Health and Nutrition Examination Survey study exam-ined the possible risk factors for hip fracture in more than 2,500 white men.22 Although the differences failed to reach statistical signifi-cance, the results did demonstrate
an increase in the number of hip fractures sustained by men who smoke Forsén et al24 also demon-strated increases in the relative risk
of hip fractures for smokers in their study of 35,000 men and women (5.0 and 1.9, respectively) Further-more, they reported that this in-creased risk persisted in their subjects even if they had stopped smoking within 5 years of the in-ception of the study
De Vernejoul et al25suggest that
at the root of a decrease in bone mineral content is a defect in os-teoblast function that is caused by smoking They demonstrated a
Trang 3statistically significant decrease in
trabecular volume and thickness
(P<0.05) and mean wall thickness
(P<0.001) of iliac-crest biopsy
sam-ples from smokers compared with
samples from nonsmokers The
bone resorptive properties of these
individuals were normal The ability
to form bone, however, was
mark-edly decreased, and this uncoupled
resorption could result in
osteo-porosis
Galvin et al26demonstrated this
same relationship experimentally in
a study of the effects of smokeless
tobacco Tibias from chick embryos
were cultured in nicotine and
smoke-less tobacco extracts, and the effects
on bone glucose metabolism and
col-lagen synthesis were measured The
authors concluded that tobacco
extracts, in concentrations found in
saliva, resulted in a nearly 25%
de-crease in oxygen consumption and
an 88% reduction in collagen
synthe-sis This relationship between
smok-ing and osteoblast function could
explain the relationships between
smoking, osteoporosis, and altered
bone healing that many investigators
have shown.9,12,18,25,27-29
In contrast to these findings,
many other studies have not
demon-strated a relationship between
smok-ing and the risk of osteoporotic
frac-tures.9,16,24,30-33 In a recent study,
Christensen et al34 were unable to
support the conclusions drawn by de
Vernejoul et al25 implicating
osteo-blasts that have been rendered
defec-tive by nicotine as a cause of
osteo-porosis Admittedly, the cohorts and
purposes of the two studies differed
Nevertheless, Christensen et al found
no differences in the function of
osteoblasts harvested during
postero-lateral fusion procedures in smokers
and nonsmokers
In the Framingham Study,33 the
authors were unable to demonstrate
a relationship between smoking and
hip fractures in either men or
women They reexamined this
rela-tionship in a follow-up study
be-cause of the large amount of data that suggested some type of an association.9,10,12,13,16,17 They specifi-cally focused their efforts on women and were once again unable to prove a statistically significant dif-ference between smokers and non-smokers who were not receiving oral HRT This was true regardless
of the number of cigarettes smoked
There was a trend toward increased fracture rate in the heavy (>20 ciga-rettes per day) smokers, but this did not reach statistical significance
When they stratified the smokers and nonsmokers by their HRT
histo-ry, however, the women who had used HRT and were currently smok-ing had a substantially greater risk
of sustaining a hip fracture com-pared with women who had never smoked (adjusted odds ratio, 3.44).16
This, too, could be explained by the adverse effects of nicotine on estrogen
Hemenway et al32examined the data on 96,000 women in a prospec-tive study and found no difference in the rates of hip and forearm fractures
in smokers and nonsmokers The authors postulated that the relatively young age of the subjects, which ranged from 35 to 59 years, might have influenced the results In sepa-rate studies, Hemenway et al30,31also looked at the rates of hip and wrist fractures in men The researchers were unable to find a correlation between smoking and an increase in the rates of these fractures Again, the authors noted that the subjects in this study were young, with ages ranging between 44 and 75 years
Most of the 50,000 men who partici-pated were less than 70 years of age
Furthermore, very few (<3%) of the subjects in one study were heavy smokers.30
Low Back Pain Causal Link
Low back pain is a very com-mon complaint that can be costly in
time, money, and resources for the patient, the physician, and society
as a whole Studies indicate that in the Western world, 60% to 80% of the population will have an epi-sode of incapacitating low back pain at some point during their lives Fortunately, 80% to 90% of these persons will return to being functional within a period of 4 to 8 weeks and will not experience long-term disability However, in some individuals, the condition will progress to become chronic low back pain.35-38 A study con-ducted in The Netherlands demon-strated that as much as 1.5% of the Gross National Product was spent
on patients with low back pain Surprisingly, only 3% of that cost was actually medically related; the remainder of the costs were for such work-related events as leaves
of absence, early retirements, and job changes.39
In the recent era of antismoking campaigns waged by health advo-cates and lobbying groups, smok-ing has come under fire from the orthopaedic community as being a possible cause of low back pain There has been scientific evidence
to both support and refute this notion
The findings from several epi-demiologic studies have suggested
an association between smoking and low back pain.35,36,40-52 Using questionnaires, Frymoyer et al49,52
determined that low-back-pain sufferers were likely to be cigarette
smokers (P<0.001), particularly
when smoking was accompanied
by a chronic cough (P<0.001) The
authors postulated that the chronic cough of smokers might adversely affect intradiskal pressure, causing the symptom of low back pain Al-ternatively, smoking or one of the ingredients within cigarette smoke may directly and unfavorably af-fect the spine Later studies by Symmons et al51and Kelsey et al,53
however, were unable to support a
Trang 4link between chronic cough and
low back pain
Svensson et al54determined that
there was a weak relationship
be-tween smoking and low back pain,
but found other variables with a
stronger relationship to low back
pain, such as calf pain on exertion,
the degree of physical activity at
work, and worry or tension With
the exception of the latter, all of
these findings are common to other
smoking-related diseases, such as
heart disease and peripheral
vascu-lar disease.2,3
Smoking may simply be an
indi-cation of poor health and lifestyle
more than a direct cause of low
back pain Biering-Sørensen and
Thomsen55 felt that although there
is an apparent causal relationship
between cigarette smoking and low
back pain, it is not as strong as
ini-tially suggested In nearly 1,000
subjects, they found that the
contri-bution of smoking to the
develop-ment of low back pain was
statisti-cally significant (P<0.05), but that it
had no significance as a risk factor
for recurrent or persistent low back
pain Moreover, they postulated
that it might not necessarily be
smoking that contributes to low
back pain, but rather poor general
health
In a study by Cox and Trier,41it
was found that smokers were much
more likely to have low back pain
and were more likely to exclude
exercise from their daily routine
This finding was echoed by Deyo
and Bass,42 who suggested that
smoking might be indicative of a
complex interaction of personal and
social traits that together are
associ-ated with the increased risk of low
back pain purported to occur in
smokers
The complex etiology of low
back pain is supported by the work
of Heliövaara et al.50 In their study
of over 5,500 subjects, they
demon-strated a weak relationship between
smoking and low back pain and
proposed that the risk of low back pain seems to be better determined
by the overall quality of one’s work, lifestyle, and health behavior
Notably, they showed differences in the association between smoking and low back pain in groups gener-ated by sex, age, and quantity of cigarettes smoked The relationship was strong in men aged 50 to 64 who smoked 20 cigarettes a day or more (odds ratio, 1.9) Interestingly,
in women aged 30 to 49, there was
no association with any quantity of cigarettes smoked (odds ratio, 1.0)
Moreover, this apparent dichotomy was reversed for women aged 50 to
64 years In this age group, the women who smoked more than 20 cigarettes a day had an odds ratio for the development of low back pain of 2.7.50 This suggests that there may be some type of protection conferred on younger women This protection can also be appreciated in relation to cardiovascular disease.2
Boshuizen et al44suggest that the link between smoking and low back pain may never be fully elucidated
Leboeuf-Yde and co-workers con-ducted several studies to evaluate the relationship between smoking and low back pain.46-48,56 Their most recent study surveyed a popu-lation of 29,424 twins and found an association between smoking and low back pain (odds ratio, 2).47 The odds ratio increased to 3 for the group of subjects with long-standing (>30 days) complaints of low back pain Furthermore, the cessation of smoking did not reverse these ings More important were the find-ings in a large group of monozygotic twins who were discordant in their smoking histories (264 pairs of iden-tical twins composed of a smoking and a nonsmoking sibling) There was no difference in the prevalence
of low back pain in the chronic-smoker group compared with their siblings in the nonsmoker group
This supports earlier work by Battié
et al57on a much smaller sample of
identical twins The large popula-tion size in the study by Leboeuf-Yde et al47 also allowed a critical look
at the possibility of a dose response between total cigarette consumption and degree of low back pain It was obvious from their data that this rela-tionship did not exist This contra-dicts the earlier work by Frymoyer
et al,49Heliövaara et al,50and Kelsey
et al.53
Although these findings may appear to refute any biologic or causal link between smoking and low back pain, there is still a wealth
of epidemiologic, circumstantial, and anecdotal evidence supporting the earlier claims that smoking has adverse effects on the lumbar spine Furthermore, some cases of low back pain have recognizable etio-logic factors that may be linked to smoking.50,57-59
Disk Disease
Lumbar disk disease and hernia-tion has become a popular diagno-sis in cases of low back pain, in part because a potential cure can be sought with surgical intervention.58
Some authors believe that smoking adversely affects the intervertebral disks, predisposing patients to disk disease and low back pain.45,53,60
Ernst45 believes that the interverte-bral disks are “malnourished” due
to many of the vascular and hema-tologic changes that result from long-term smoking He postulates that tissues such as the vertebrae and vertebral disks have a tenuous blood supply and are not able to compensate for the decrease in blood flow that occurs in the micro-vasculature of chronic smokers Over time, the diffusion capacity for the delivery of oxygen and nutrients becomes insufficient, leaving the in-tervertebral disks more vulnerable
to insults.45
Kelsey et al53 determined in their epidemiologic study that ciga-rette smoking in the year prior to a patient’s presentation to a
Trang 5physi-cian increased the risk of having a
prolapsed disk (odds ratio, 1.7)
Furthermore, they discerned a
weak dose response for smoking
and the subsequent risk of disk
pro-lapse; for every 10 cigarettes that
were smoked per day, the risk of
having a prolapsed disk increased
by 20%
Hanley and Shapiro61
deter-mined that a smoking history
longer than 15 years was an
impor-tant factor in determining the
post-operative success of lumbar
diskec-tomies performed to treat severe
radiculopathies They postulate
that the persistent back pain after
the procedure may be a
manifesta-tion of the vascular effects of
nico-tine Furthermore, the metabolic
changes within the disk may render
it more susceptible to mechanical
problems.61
Battié et al57examined
differ-ences in magnetic resonance (MR)
imaging studies of the lumbar
spines of identical twins who were
highly discordant in their smoking
histories They found no differences
in the reported rate of occurrence of
low back pain between the
smok-ing and nonsmoksmok-ing groups but
did demonstrate a difference in the
disk degeneration scores (based on
MR imaging criteria) used to
evalu-ate the intervertebral regions of the
two groups
Stronger evidence comes from
An et al.60 In their study, the rates
of smoking in a population of
pa-tients with surgically confirmed
cer-vical or lumbar disk disease were
examined The relative risk values
for lumbar and cervical disk disease
for smokers were 2.2 (P = 0.00029)
and 2.9 (P = 0.0025), respectively.
When the authors excluded those
patients who had recently quit
smoking from the “smokers” group,
the relative risks increased to 3.0
and 3.9, respectively They
demon-strated that the association between
cigarette smoking and documented
disk disease, not just the subjective
complaint of low back pain, is quite significant Continued smoking in light of these problems could actually worsen the diskogenic or radicular symptoms that accompany disk disease
So how does smoking exert these changes in the intervertebral disks that render them more susceptible
to disease? As stated earlier, Ernst45
believes that the macrovascular and microvascular changes that occur in smoking may affect the blood sup-ply around intervertebral disks
The decreased blood flow renders the disks susceptible to pathologic changes
The study by Battié et al57 sup-ports this notion In that study, the authors used MR imaging to evalu-ate disk integrity in pairs of identi-cal twins discordant in their smok-ing histories Although there was
no difference in complaints of low back pain, the mean score for lum-bar spine disk degeneration was
18% higher for the smokers (P =
0.015) Furthermore, because their results demonstrated involvement
of the entire lumbar spine, the au-thors postulated that the mecha-nism of action must be systemic
In a recent article, Newby et al3
showed that smoking has dramatic adverse effects on the endogenous fibrinolytic capacity of the vascular endothelium of smokers, leading to
a systemic increase in the risk of atherothrombotic disease or micro-vascular occlusive disease Jayson and co-workers62-64have performed several studies demonstrating that
a decrease in fibrinolytic activity is common in many chronic back pain syndromes It is feasible that this mechanism is active in a large num-ber of patients who smoke and have low back pain It is also feasi-ble that this is a mechanism that results in the local hypoperfusion of the lumbar spine, as well as the alterations in disk metabolism that some authors believe occur in smokers.3,45,60-64
Wound Healing
The effects of cigarette smoking on soft-tissue wound healing, skin physiology, and the complex vari-ables that control these entities have been studied by several groups
of researchers In a review by Leow and Maibach,8 most of the studies analyzed showed a de-crease in cutaneous blood flow in subjects exposed to nicotine or cig-arette smoke Jensen et al65noted
an acute decrease in the subcuta-neous tissue oxygen tension in the forearms of subjects after smoking cigarettes The authors attributed these effects to the pharmacologic actions of nicotine
In 1977, Mosely and Finseth66
were among the first to demonstrate that smoking impairs wound heal-ing in the soft tissues of the hand They postulated that the vasocon-striction and moderate blood levels
of carbon monoxide secondary to smoking could retard proper wound healing, especially in the extremi-ties It was noted that severe digital vasoconstriction can occur after smoking a single cigarette The fol-lowing year, they demonstrated that systemic nicotine given to rabbits re-sulted in decreased wound healing
in an established rabbit-ear injury model.67
Several authors have noted changes in the blood flow and oxy-gen tension of the cutaneous and subcutaneous tissues that can be related to smoking.8,65-67 Forrest et
al68 specifically examined the skin hemodynamics of random-pattern skin flaps from rats that had been given either low-dose or high-dose subcutaneous nicotine for the 24 weeks prior to a surgical procedure The capillary blood flow and distal perfusion were lessened in these animals, resulting in flaps with a much smaller area of viability When the nicotine was withheld during the 2 weeks before surgery, the hemodynamics of the skin flaps
Trang 6returned to near-control levels.
Nolan et al69 and Lawrence et al,70
in separate studies, also showed
that the survival of skin flaps in rats
exposed to a cigarette smoke–filled
environment was appreciably less
than the survival of skin flaps in
control rats
Abidi et al71 demonstrated a
dif-ference in wound healing after open
reduction and internal fixation of
calcaneal fractures in smokers who
either were or were not allowed to
smoke perioperatively A major
complication associated with this
surgery is poor healing of the lateral
surgical wound; although the
differ-ence was not statistically significant,
the authors noted that those who
continued to smoke perioperatively
had prolonged wound healing times
Nicotine has been shown to
me-diate many other actions within the
body In their review, Sherwin and
Gastwirth1 note that the
prolifera-tion of cells within the extracellular
matrix and the process of epithelial
regeneration are decreased by the
damaging effects of nicotine and
carbon monoxide In a prospective
human trial, Jorgensen et al7showed
that collagen synthesis was
hin-dered in the wounds of those
sub-jects who smoked more than a pack
per day compared with the matched
nonsmoking group Mature
colla-gen is the main determinant of the
tensile strength in a healing wound,
and its assembly is dependent on
sufficient perfusion and
oxygena-tion The authors concluded that
wound healing is definitely impeded
by smoking
It is believed by many that this
interference with the natural process
of wound healing may lead to higher
rates of postoperative wound
infec-tions in smokers Calderone et al72
determined that the additional costs
involved in treating deep
postopera-tive spinal infections could increase
the total cost of caring for a patient by
more than four times Capen et al73
included smoking as a preoperative
risk factor for postoperative wound infections after lumbar fusion
Thalgott et al74 retrospectively reviewed the cases of 32 patients in order to develop a classification scheme for identifying populations
at risk for postoperative spinal wound infections and for guiding therapy In their classification scheme, cigarette smokers, patients with systemic diseases, and immu-nocompromised patients are con-sidered to be at high risk for post-operative wound infections In the group of patients who sustained an infection after elective spinal fusion and instrumentation, 90% were cig-arette smokers Furthermore, the only patients to have a superficial
or deep infection worsen to an in-fection that included myonecrosis were heavy smokers The findings
of these authors led them to clude that patient smoking is a con-trollable variable that should be stopped in the perioperative period
Fracture Healing
In addition to its effects on the soft tissues and vasculature of the body, it
is believed that cigarette smoking also retards the healing of bone
Silcox et al75reported that union did not occur in the lumbar spines of rab-bits after a single-level lumbar fusion with use of autologous iliac-crest bone graft if the rabbits were subse-quently exposed to systemic nicotine
Cobb et al76 evaluated the rela-tive risk of nonunion in smokers versus nonsmokers in a case-control study Although they had a rela-tively small study group, and their results only approached statistical significance, they demonstrated that the relative risk of progression to a nonunion after ankle arthrodesis was 16 times greater for smokers than for nonsmokers
Brown et al77 reported that the pseudarthrosis rate for lumbar ar-throdesis in 50 of their patients
approached 40% The rate for the 50 nonsmokers in that study was only 8% Carpenter et al78 furthered the work presented by Brown et al and reported that the outcomes of repeat procedures for pseudarthrosis that developed after an attempted local arthrodesis of the lumbar spine were significantly more favorable
for nonsmokers (P = 0.02) Patients
who stopped smoking also had a better mean outcome score and were more likely to return to work than those who continued to smoke These findings have led several inves-tigators to recommend periopera-tive cessation of smoking as a
gener-al measure to improve the outcome
of surgical procedures.1,7,71,79,80
De Vernejoul et al25have identi-fied a possible explanation for these findings They demonstrated that smoking impairs osteoblast func-tion in osteoporotic individuals The quantity of bone resorbed re-mained normal, but the rate of bone formation was decreased This could result in the defective healing response demonstrated clinically in the previously mentioned studies Campanile et al80 suggest that the effects of smoking are mediated by the vasoconstrictive and platelet-activating properties of nicotine, the hypoxia-promoting effects of car-bon monoxide, and the inhibition of oxidative metabolism at the cellular level by hydrogen cyanide
There are no conclusive studies that have generated definite guide-lines about perioperative cessation
of smoking Campanile et al80note that suggestions range from 1 day
to 3 weeks preoperatively and from
5 days to 4 weeks postoperatively Sherwin recommends that smoking
be stopped at least 12 hours before surgery because it takes the body roughly this amount of time to clear the carbon monoxide.1 Abidi et al71
noted that cessation of smoking 5 days before surgical procedures had
a favorable outcome on subsequent wound healing Lind et al81
Trang 7recom-mend 1 week of cessation, on the
basis of the pharmacokinetics of free
radicals and thrombotic
compo-nents Mosely et al67 demonstrated
that healing was impaired for a
period of 4 to 10 days after wound
creation in rabbits After 12 days, the
wounds of rabbits either exposed or
not exposed to nicotine contracted at
nearly the same rate
Whitesides based his
recommen-dations concerning perioperative
smoking on studies showing that a
nonsmoker can make 1 cm of bone
in 2 months, but that it takes a
smok-er an avsmok-erage of 3 months to make
the same amount of bone.82 He,
therefore, feels that it is not prudent
to perform elective spinal surgery on
smokers unless they demonstrate
abstinence from smoking for a period
of 60 days In contrast, Hanley
of-fers the argument that many of the
effects of chronic smoking are
irre-versible and that medical care should not be withheld from patients with-out firm evidence.82
Summary
Tobacco smoking has come under relentless attack as more and more medical and social ills have been proved to be the direct result of smoking, which is now the most preventable cause of morbidity and mortality in the United States The scientific and clinical information on smoking and its consequences sug-gest varying degrees of correlation between smoking and musculo-skeletal conditions Smoking has been shown to adversely affect bone mineral density, lumbar disk health, the relative risk of sustaining hip and wrist fractures, and the dynam-ics of bone and wound healing
In response to these findings, many surgeons have recommended that some type of smoking cessa-tion program be instituted in con-junction with musculoskeletal treatment for patients with a signif-icant smoking history The physi-cian should not necessarily delay
or withhold elective treatment from such patients At the very least, however, a detailed smoking history should be obtained from all patients who present with muscu-loskeletal conditions Furthermore, the risks and complications that appear to be associated with smok-ing should be discussed in detail, and assistance in smoking cessa-tion should be offered The patient and the physician should both thoroughly understand the impli-cations and effects of smoking on a disease process or planned medical intervention
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1998;16:545-556.
3 Newby DE, Wright RA, Labinjoh C, et
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