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Abstract
The association between cigarette smoking and delayed wound healing is well recognized
in clinical practice, although extensive controlled studies have yet to be performed.
The documented effects of the toxic constituents of cigarette smoke—particularly nicotine,
carbon monoxide, and hydrogen cyanide—suggest potential mechanisms by which smoking
may undermine expeditious wound repair. Nicotine is a vasoconstrictor that reduces nutritional blood flow to the skin, resulting in
tissue ischemia and impaired healing of injured tissue. Nicotine also increases platelet
adhesiveness, raising the risk of thrombotic microvascular occlusion and tissue ischemia.
In addition, proliferation of red blood cells, fibroblasts, and macrophages is reduced
by nicotine. Carbon monoxide diminishes oxygen transport and metabolism, whereas hydrogen cyanide inhibits the enzyme systems necessary for oxidative metabolism and oxygen transport
at the cellular level. Slower healing has been observed clinically in smokers with
wounds resulting from trauma, disease, or surgical procedures. The reduced capacity
for wound repair is a particular concern in patients undergoing plastic or reconstructive
surgery. Compared with nonsmokers, smokers have a higher incidence of unsatisfactory
healing after face-lift surgery, as well as a greater degree of complications following
breast surgery. Smokers should be advised to stop smoking prior to elective surgery
or when recovering from wounds resulting from trauma, disease, or emergent surgery.
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References
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© 1992 Published by Elsevier Inc.