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.