Key Practice Points
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All lacerations produce scars.
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The function of a scar is to repair a wound with collagen, not to restore the original appearance of the injured tissue.
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The tensile or breaking strength of a repaired laceration is only 5% of normal skin at the time of suture removal.
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Final scar appearance and tensile strength are not reached for several months.
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The appearance and size of a scar can vary according to the mechanism of injury, anatomic location, wound infection, poor technique, and other factors.
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Visibly embedded grit in the epidermis must be removed to prevent permanent tattooing.
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Sutures can produce permanent marks in the skin if left longer than 7 to 14 days.
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Some people can react to wounds by producing excessive, hypertrophic or keloid, scars.
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There are no chemical or surgical methods to eliminate scars.
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Current research using growth factors has shown that regeneration of injured tissue, rather than collagen deposition, may be possible in the future.
Many of the elements of scar formation are beyond the control of the operator repairing a traumatic wound. In contrast to surgical incisions, wounds and lacerations are not planned with regard to location, length, depth, or cosmetic concerns. Wounds caused at random present a variety of biologic and technical problems that need to be solved to produce the best cosmetic outcome. Age, race, body region, skin tension lines, associated conditions and diseases, drugs, type of wound, and technical considerations all affect scar formation. The choice of repair strategy depends on these and other factors. Finally, knowledge of the spectrum of wound healing ensures that patients with traumatically induced wounds receive the proper advice and counseling. A key biologic reality in wound healing is that the wounded tissue is replaced by collagen scar tissue. By definition, the scar will look different than uninjured skin. Only recently has tissue regeneration research, studied in the lab, been tried with some success on animals. True scar reduction, or even elimination, may become a valid therapy for lacerations and wounds.
Normal Wound Healing
Although wound healing is commonly described as a discrete event, it is actually a continuum of overlapping phases. For the sake of clarity, these phases are described separately and their interrelationships are graphically depicted in Figure 4-1 .
Hemostasis
At the moment of injury, several events take place that culminate in rapid hemostasis. The traumatic insult causes changes in skin architecture that result in wound edge retraction and tissue contraction, which lead to compression of small venules and arterioles. Vessels also undergo intense reflex vasoconstriction for 10 minutes. Platelets begin to aggregate in the lumens of the severed vessels and on the exposed wound surfaces. The clotting cascade is activated by tissue clotting factors, and within minutes, the wound begins to fill with a hemostatic coagulum.
Inflammatory Phase
When hemostasis has been achieved and exudation begins, the inflammatory response rapidly follows. The complement system is activated, and chemotactic factors, which attract granulocytes to the wound area, are released. These cells are followed shortly by lymphocytes. Peak granulocyte numbers can be found 12 to 24 hours after the injury is sustained. The chief function of granulocytes and lymphocytes seems to be the control of bacterial growth and the suppression of infection. These cells are aided by immunoglobulins that are included in the wound exudate. In most simple wounds, granulocyte counts diminish markedly after 3 days.
After 24 to 48 hours, macrophages can be detected in large numbers, and by day 5, they are the predominant inflammatory cells in the wound area. These cells play a major role in the inflammatory responses and in the early fibroblast and collagen formation.
Epithelialization
While the inflammatory response proceeds, epithelial cells undergo morphologic and functional changes. Within 12 hours, intact cells at the wound edge begin to form pseudopod-like structures that facilitate cell migration. Replication takes place, and the cells begin to move over the wound surface. An advancing layer can be seen traveling over the damaged dermis and under the hemostatic coagulum. When these cells reach the inner wound area, they begin to meet other advancing epithelial extensions. The original cuboidal shape of the epithelial cells is regained, and desmosomal attachments to other cells are made. Continued replication eventually reestablishes the normal layers of epidermis. After repair of lacerations, initial epithelialization can take place within 24 to 48 hours, but the architecture and thickness of this layer continually change over the months of the wound maturation process.
Neovascularization
The phenomenon of new vessel formation is crucial to wound repair. These vessels replace the old injured network and bring oxygen and nutrients to the healing wound. Neovascularization is evident by day 3 and is most active by day 7; this explains the marked erythematous appearance of the wound at the time of suture removal. Vascularity decreases rapidly by day 21, with continued regression as the wound matures. New vessels form loops of capillaries that are surrounded by actively growing fibroblasts. These two components on the wound surface give it the classic appearance referred to as granulation.
Collagen Synthesis
With the establishment of a vascular supply and stimulation by macrophages, fibroblasts rapidly undergo mitosis. They begin to produce new collagen fibrils by day 2. Peak synthesis occurs between days 5 and 7, and the wound has its greatest collagen mass by 3 weeks. By then, the wound is devoid of inflammatory infiltrate and edema.
New collagen is laid down in a random, amorphous pattern. It is a gel with little tensile strength. Over the months, however, this gel continually remodels itself, creating an organized basket-weave pattern that is achieved by the cross-linking of collagen fibers. The balance between synthesis and lysis of collagen creates a vulnerable period approximately 7 to 10 days after injury, when the wound is most prone to unwanted opening or dehiscence. The wound has only 5% of its original tensile strength at 2 weeks and 35% at 1 month ( Fig. 4-2 ). Final tensile strength is not achieved for several months.
Wound Contraction and Remodeling
Every wound undergoes scar remodeling over several months. With this remodeling comes some degree of wound contraction. It is most pronounced in full-thickness skin losses. The scar that forms gradually contracts centripetally over the wound defect through the action of specialized fibroblasts called myofibroblasts. Contraction pulls normal surrounding skin over the defect. Practically speaking, a properly everted suture line contracts to a flat, cosmetically acceptable scar, whereas a wound closed with the edges already inverted forms an unsightly depression in the epidermis that stands out because of shadow formation from incident light (see Chapter 10 ).
As scars remodel, they change in appearance as well. In a study of scar appearance at suture removal versus appearance 6 to 9 months later, there was little correlation in appearance. Patients need to be advised that the final appearance may not be evident for 6 months to 1 year after suture removal.
Factors Affecting Cosmetic Outcome ( Box 4-1 )
There are numerous biologic and nonbiologic causes of scar and cosmetic outcome. In a study of 800 patients, followed for 3 months, who sustained traumatic lacerations or were surgically incised, several factors were found to be associated with a suboptimal wound appearance. These included extremity wounds, wide wounds, incompletely apposed wound edges, significant tissue injury, and infection. Below is a more complete discussion of the mechanisms and factors that ultimately can affect the cosmetic result.
Technical Factors
Inadequate wound preparation
Excessive suture tension
Reactive suture materials
Local anesthetics
Anatomic Factors
Static skin tension
Dynamic skin tension
Pigmented skin
Oily skin
Body region
Associated Conditions and Diseases
Advanced age
Severe alcoholism
Acute uremia
Diabetes
Ehlers-Danlos syndrome
Hypoxia
Severe anemia
Peripheral vascular disease
Malnutrition
Drugs
Corticosteroids
Nonsteroidal antiinflammatory drugs
Penicillamine
Colchicine
Anticoagulants
Antineoplastic agents
Mechanism of Injury
The mechanism of injury is important because it is a significant determinant in the choice of management technique and in estimating the probability of wound infection. The injury mechanism also plays a role in scar formation and in the eventual cosmetic outcome. The mechanism of injury can be described as three forces that are applied to the skin under injury conditions: shearing, tension, and compression forces. Table4-1 lists the various causes of emergency department wounds and their frequency.
| Cause of Wound | No. of Cases (%) ∗ |
|---|---|
| Blunt object | 417 (42) |
| Sharp (nonglass) | 338 (34) |
| Glass | 133 (13) |
| Wood | 35 (4) |
| Bites: | |
| Human | 5 (1) |
| Dog | 29 (3) |
| Other | 15 (2) |
| Totals | 972 (99) |
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