Wound Healing and Cosmetic Outcome

CHAPTER 4

Wound Healing and ­Cosmetic Outcome Key Practice Points nn All

lacerations produce scars. function of a scar is to repair a wound with collagen, not to restore the original appearance of the injured tissue. nn The tensile or breaking strength of a repaired laceration is only 5% of normal skin at the time of suture removal. nn Final scar appearance and tensile strength are not reached for several months. nn The appearance and size of a scar can vary according to the mechanism of injury, anatomic location, wound infection, poor technique, and other factors. nn Visibly embedded grit in the epidermis must be removed to prevent permanent tattooing. nn Sutures can produce permanent marks in the skin if left longer than 7 to 14 days. nn Some people can react to wounds by producing excessive, hypertrophic or keloid, scars. nn There are no chemical or surgical methods to eliminate scars. nn Current research using growth factors has shown that regeneration of injured tissue, rather than collagen deposition, may be possible in the future.   nn The

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.1 True scar reduction, or even elimination, may become a valid therapy for lacerations and wounds. 15

16

CHAPTER 4  Wound Healing and Cosmetic Outcome Activity of Wound Healing Components

Time of incident

Time of incident

Immediate injury response (vasospasm/clot formation) 6h

24h Granulocyte activity (inflammatory phase)

6h

24h

3d

5d

7d

Epithelial cell growth

6h

24h

3d

5d

7d Macrophage activity (inflammatory phase)

24h

3d

5d

7d

14d

30d

60d New vessel formation

3d

5d

7d

14d

30d

60d Fibroblast activity (collagen formation)

3d

5d

7d

14d

30d

60d

Figure 4-1.  The various components of wound healing and their time frames.

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

CHAPTER 4  Wound Healing and Cosmetic Outcome

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

17

CHAPTER 4  Wound Healing and Cosmetic Outcome 100 90 % Wound tensile strength

18

80 70 60 50 40 30 20 10 0 0 2 3 7 1014

18

20 25 30 40 50 60 70

100

150

200

300

1 year

Days post injury

Figure 4-2.  Percentage of tensile strength that develops in a wound in the days and months after injury.

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.2 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.3 These included extremity wounds, wide wounds, incompletely apposed wound edges, significant tissue injury, and infection. 3 Below is a more complete discussion of the mechanisms and factors that ultimately can affect the cosmetic result.

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.4,5 Table 4-1 lists the various causes of emergency department wounds and their frequency.

Shearing

Shearing injuries, which result in a simple dividing of tissues, are caused by sharp objects, such as knives or glass (Fig. 4-3). This mechanism accounts for most lacerations seen in the emergency department.6 The skin is divided traumatically, but little energy is imparted to the tissues and minimal cell destruction occurs. These lacerations can be repaired primarily (primary intention), and they have a low incidence of wound infection. The resulting scar usually is thin and cosmetically acceptable.

CHAPTER 4  Wound Healing and Cosmetic Outcome

BOX 4-1  Interference with Wound Healing 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

TABLE 4-1

  Etiology of Traumatic Wounds

Cause of Wound

No. of Cases (%)*

Blunt object

417 (42)

Sharp (nonglass)

338 (34)

Glass

133 (13)

Wood

35 (4)

Bites: Human Dog Other

5 (1) 29 (3) 15 (2)

Totals

972 (99)

*Taken from a study of 1000 wounds. The etiology of the wound was not described in 28 cases. From Hollander JE, Singer AJ, Valentine S, Henry MC: Wound registry: development and validation, Ann Emerg Med 25:675–685, 1995.

19

20

CHAPTER 4  Wound Healing and Cosmetic Outcome

Figure 4-3.  Examples of injuring objects and a resulting laceration caused by shearing forces.

Tension

Tension injuries occur as a result of a blunt or semiblunt object striking the skin at a glancing angle (Fig. 4-4). Under these conditions, a triangular flap, a partial avulsion, of skin often is created. Because the blood supply is interrupted on two sides of the flap, ischemia can occur, leading to devitalization and necrosis. The remaining blood vessels entering the flap from the base have to be preserved by careful handling and special suturing techniques, which are described in Chapter 11. If the flap base is distally based (i.e., the flap tip points back against the regional arterial flow), the compromise is even greater. The energy necessary to create this type of wound is greater than that caused by shearing forces. The combination of potential ischemia and greater cell destruction can increase the risk of wound infection. These wounds also tend to lead to greater scar formation.

Compression

Crushing or compression injuries occur when a blunt object strikes the skin at right angles (Fig. 4-5). These lacerations often have ragged or shredded edges and are accompanied by significant devitalization of skin and superficial fascia (subcutaneous tissue). Under these conditions, there is increased susceptibility to infection.7 These wounds require extensive cleansing, irrigation, and débridement. Despite a meticulous primary repair, the resulting scars can be cosmetically poor in appearance.

CHAPTER 4  Wound Healing and Cosmetic Outcome

Figure 4-4.  Example of the mechanism of injury and the resulting flaplike laceration caused by tension forces.

Wound Infection

The most common and serious complication of wound and laceration repair is infection. Because all accidentally induced wounds occur in unsterile conditions, they have to be considered contaminated with bacteria and debris on arrival to the emergency department. The epidermis normally acts as an effective barrier against the penetration of bacteria into the deeper layers of the skin and superficial fascia. Any violation of the epidermis provides a pathway for bacterial invasion. Not only do environmental microorganisms find their way into wounds, but also the skin, which is populated with a variety of indigenous microflora, can harbor a potentially infective inoculum of pathogenic bacteria.8 Areas of the body with high concentrations of bacteria include scalp, perineum, axillae, mouth, feet, and nail folds. The trunk and proximal extremities are sparsely populated with bacteria. A crucial factor in determining whether contaminating bacteria go on to cause an established wound infection is the time elapsed from injury to cleansing and repair. It has been established that 100,000 (105) bacteria per gram of tissue constitute an infective inoculum.6 Wounds with counts less than that number heal without event. If bacterial counts are greater than that number, the risk of infection increases manyfold.9 In a series of patients studied in an emergency department, it was observed that wounds less than 2.2 hours old contained 100 (102) bacteria per gram of tissue.10 Wounds that were 3 hours old harbored 102 to 106 bacteria per gram of tissue. Wounds more than 5 hours old consistently grew more than 106 bacteria per gram of tissue. Despite experimental support for bacterial growth and invasion early after injury, the true clinical significance has not been established. It remains prudent, however, to cleanse and irrigate wounds in a timely manner. If antibiotics are considered necessary, early administration is appropriate.

21

22

CHAPTER 4  Wound Healing and Cosmetic Outcome

Figure 4-5.  Example of the mechanism and result of an injury caused by compression forces.

Technical Factors

Soil, in particular clay, can impair healing in two ways.11 First, the threshold infective inoculum is reduced to 102 bacteria, even in the presence of a small amount of dirt.12 Second, soil and grit of any kind can lead to permanent tattooing if not aggressively removed. Consultation with a plastic surgeon may be indicated if wound cleansing and débridement cannot eliminate grit that is visibly embedded in the epidermis and superficial dermis. Excessive tension when tying the suture knot created by improper suture technique can cause unnecessary wound ischemia.13 Ischemia promotes cellular necrosis with greater inflammatory and scarring responses. Deep sutures, undermining, and increasing the number of sutures per laceration are methods that can reduce the danger of excessive tension. Because tissue reactivity and inflammation vary with different suture materials, these materials can have differing effects on the healing process.14 Although silk has excellent mechanical properties, it has a propensity for causing marked tissue reactivity. Nylon and polypropylene are the least reactive of the nonabsorbable materials. Absorbable sutures act as foreign material, and excessive numbers can increase the risk of infection and may provoke a greater scarring response.15,16 Wound tapes and staples are the least reactive of wound closure alternatives and are associated with low infection rates even in contaminated wounds. Experiments have shown that local anesthetics can cause retardation of wound healing.17 This negative effect is enhanced by increasing concentrations of local anesthetics and the use of epinephrine in anesthetic solutions.12 There is no question, however,

CHAPTER 4  Wound Healing and Cosmetic Outcome

that local anesthetics need to be used in wound care. Judicious amounts at the lowest concentrations possible are recommended.

Anatomic Factors

Body region and skin tension lines have a significant effect on wound healing, specifically on final scar morphology (see Chapter 3). Wounds over the anterior thorax or the extremities heal with the most evident scars, whereas wounds of the eyelid heal with the least obvious scars. Pigmented and oily skin also tends to heal with greater scar formation than fairer, less oily skin.

Associated Conditions and Diseases

Several conditions and diseases cause an alteration in wound healing. Advanced age has been implicated in slower healing of wounds.18 If an older patient is basically healthy, however, normal healing and scar formation ultimately take place.19 Wound healing can be retarded in a patient with chronic alcoholism who has advanced liver disease and impaired protein synthesis. Acute uremia has long been thought to impede healing.20 In patients with uremia, there is an inhibition of fibroblast growth and a decrease in tensile strength during wound healing. Patients with diabetes also have numerous problems with wound healing.21 Not only do they have an increased chance of wound infection, but also there is retardation of neovascularization and collagen synthesis. A rare disease that causes problems with collagen formation and wound healing is Ehlers-Danlos syndrome.22 Any condition that leads to failure of oxygen and nutrient delivery to the wound profoundly affects wound healing.23 Shock, severe anemia, peripheral vascular disease, and malnutrition all fall into this category. Patients with severe underlying diseases, such as advanced cancer, hepatic failure, and severe cardiovascular disease, are subject to poor wound healing. Victims of major trauma, particularly individuals who have undergone prolonged shock and complicated resuscitations, also are at risk for poor wound healing.

Drugs

Numerous drugs and pharmacologic preparations alter wound healing.24 Drugs that seem to have negative effects include corticosteroids, nonsteroidal antiinflammatory drugs (aspirin, phenylbutazone), penicillamine, colchicine, anticoagulants, and antineoplastic agents. Of these drugs, corticosteroids have the most profound effect on healing and interfere with the process at many points. They adversely alter the inflammatory response, fibroblast activity, neovascularization, and epithelialization. Nonsteroidal antiinflammatory drugs depress the normal inflammatory response and can decrease overall wound tensile strength. Anticoagulants and aspirin increase the possibility of wound hematoma formation with subsequent delays in healing time. Although in theory antineoplastic agents would be expected to inhibit wound healing, in actual practice it is not clear that they do so in a clinically significant manner. Vitamins C and A, zinc sulfate, and anabolic steroids have a generally positive effect on wound repair.25 Vitamin C deficiency profoundly impairs collagen formation, but normal synthesis can be restored with administration of ascorbic acid. Vitamin A and anabolic steroids are able to reverse corticosteroid-induced suppression of the inflammatory response. Zinc deficiency seems to play a role in slowing the healing process. Correction of the deficiency reverses that effect. Use of zinc ointments in non–zincdeficient patients can cause a cross-linking failure during collagen maturation.25 Experimental evidence that zinc sulfate can retard wound contraction supports this observation.25

23

24

CHAPTER 4  Wound Healing and Cosmetic Outcome

SUTURE MARKS Skin suture marks can be an unsightly and unnecessary complication of laceration repair. There are several causes of suture marks, some within and some out of the control of the operator.26 The causes are as follows: Skin type: Some areas of the skin, including the skin of the back, chest, upper arms, and lower extremities, are more prone to retaining suture marks than others. On the face, skin of the lower third of the nose and cheeks adjacent to the nasal alae also is vulnerable. Suture marks are unusual on the eyelids, palms of the hands, and soles of the feet. Keloid tendency: Keloid formers have a higher risk of suture mark formation. Suture tension: Excessive suture tension during knot tying can cause tissue constriction, which increases the risk for larger, more obvious suture marks. Stitch abscess: Occasionally a small abscess forms adjacent to the suture itself. Because suture material is a foreign body, the risk of abscess formation, although small, is inherent. Silk and braided sutures are more likely to provoke an inflammatory response at the suture site than monofilament nylon or metallic staples.13 Duration sutures left in place: Sutures remaining in place for 14 days or longer uniformly leave behind suture marks.26 By 14 days, epithelialization of the suture track occurs, and a permanent epithelial “plug” is left behind. Conversely, no suture marks remain if sutures are removed before 7 days. The period between 7 and 14 days is less predictable with regard to retention and permanency of suture marks. These findings are independent of needle type or suture size.

• •• • •

KELOID AND HYPERTROPHIC SCARS A keloid is an inappropriate accumulation of scar tissue that originates from a wound and extends beyond its original boundaries (Fig. 4-6). Keloids are more common in blacks but can occur in darkly pigmented skin areas of people of different races. These scars more commonly tend to be located on the ears, upper extremities, lower abdomen, and sternum. Eventual outcome and treatment depend on early recognition of keloid formation and prompt therapy. Hypertrophic scars also have excessive bulk, but in contrast to keloids, they are confined to the original borders of the wound (Fig. 4-7). They tend to occur in areas of tissue stress, such as flexion creases across joints. The cause of this excessive scar response is not known. Physical therapy and splinting can be used during healing in patients who have a history of hypertrophic scarring. Interventions to minimize these abnormal scar formations are discussed in the next section on scar management and revision.

SCAR MANAGEMENT AND REVISION Currently, there is no chemical or surgical intervention that can eliminate scars. There are many ointments, dressings, vitamins, and herbal preparations that have been used to reduce scar size, color, and symptoms such as itching.27 To date, the small number of clinical trials to compare these products has not shown a clear advantage of one product over another. 27 In the small but significant number of cases where the scar is unsightly after several months, there are many surgical and nonsurgical techniques to modify that result. Z-plasty and dermabrasion are surgical interventions that have been shown to alter scar appearance effectively and favorably.28,29 At the time of wounding, it is important to identify patients who have a history of keloid or hypertrophic scar formation. For these patients, interventions need to be started shortly after the initial repair. Nonsurgical techniques include cryotherapy, pressure dressings, radiation therapy, and antimitotics.30 Other techniques shown to be effective for these patients are laser therapy and intralesional corticosteroids.30,31

CHAPTER 4  Wound Healing and Cosmetic Outcome

Figure 4-6.  Example of a keloid scar. The scar extends beyond the margins of the original wound.

Figure 4-7.  Example of a hypertrophic scar. The scar remains confined to the original borders of the wound.

25

26

CHAPTER 4  Wound Healing and Cosmetic Outcome

These patients need to be referred to specialists skilled in these therapies during the initial phases of wound healing. In the future, regenerative therapy may replace traditional scar formation as a true advance in wound healing and cosmetic outcome.

References

1. Rhett MJ, Ghatnekar GS, Palatinus, et al: Novel therapies for scar reduction and regenerative healing of skin wounds, Trends Biotech 26:173-180, 2008. 2. Hollander JE, Blasko B, Singer AJ, et al: Poor correlation of short- and long-term cosmetic appearance of repaired lacerations, Acad Emerg Med 2:983–987, 1995. 3. Singer AJ, Quinn JV, Thode HC, et al: Determinanats of poor surgical outcome after laceration and surgical incision repair, Plast Reconstr Surg 110:429–435, 2002. 4. Edlich R, Rodeheaver G, Thacker J: Technical factors in the prevention of disease. In Simmons RL, Howard RJ, Henriksen AI, editors: Surgical infectious diseases, New York, 1982, Appleton-Century-Crofts. 5. Trott AT: Mechanisms of surface soft tissue trauma, Ann Emerg Med 17:1279–1283, 1988. 6. Edlich RF, Rodeheaver GT, Morgan RF, et al: Principles of emergency wound management, Ann Emerg Med 17:1284–1302, 1988. 7. Cardany R, Rodeheaver GT, Thacker TG, et al: The crush injury: a high risk wound, J Am Coll Emerg Physicians 5:965–970, 1976. 8. Marples M: Life on the human skin, Sci Am 220:108–115, 1969. 9. Krizek TJ, Robson MC, Kho E: Bacterial growth and skin graft survival, Surg Forum 18:518–520, 1967. 10. Robson MC, Duke WF, Krizek TJ: Rapid bacterial screening in the treatment of civilian wounds, J Surg Res 16:299–306, 1974. 11. Rodeheaver GT, Pettry D, Turnbull V: Identification of the wound infection-potentiating factors in soil, Am J Surg 128:8–14, 1974. 12. Haury BB, Rodeheaver GT, Pettry D, et al: Inhibition of nonspecific defenses by soil infection-­potentiating factors, Surg Gynecol Obstet 144:19–24, 1977. 13. Price P: Stress, strain, and sutures, Ann Surg 128:408–421, 1948. 14. Swanson N, Tromovitch T: Suture materials: properties, uses and abuses, Int J Dermatol 21:373–378, 1982. 15. Edlich RF, Rodeheaver G, Kuphal J, et al: Technique of closure: contaminated wounds, J Am Coll Emerg Physicians 3:375–381, 1974. 16. Losken HW, Auchincloss JA: Human bites of the lip, Clin Plast Surg 11:773–775, 1984. 17. Morris T, Appleby R: Retardation of wound healing by procaine, Br J Surg 67:391–392, 1980. 18. Grove G: Age-related differences in healing of superficial skin wounds in humans, Arch Dermatol Res 272:381–385, 1982. 19. Goodson W, Hunt T: Wound healing and aging, J Invest Dermatol 73:88–91, 1979. 20. Colin J, Elliot P, Ellis H: The effect of uraemia upon wound healing: an experimental study, Br J Surg 60:793–797, 1979. 21. Hunt T: Disorders of wound healing, World J Surg 4:271–277, 1980. 22. Cohen I, McCoy B, Biegelmann R: An update on wound healing, Ann Plast Surg 3:264–272, 1979. 23. Hotter A: Physiologic aspects and clinical implications of wound healing, Heart Lung 11:522–530, 1982. 24. Pollack S: Systemic medications and wound healing, Int J Dermatol 21:491–496, 1982. 25. Soderberg T, Hallmans G: Wound contractions and zinc absorption during treatment with zinc tape, Scand J Reconstr Surg 16:255–259, 1982. 26. Crikelair GF: Skin suture marks, Am J Surg 66:631–639, 1958. 27. Shih R, Waltzman J, Evans GRD, et al: Review of over the counter topical scar treatment products, Plast Reconstr Surg 119:1091–1095, 2007. 28. Hove CR, Williams EF 3rd, Rodgers BJ: Z-plasty: a concise review, Facial Plast Surg 17:289–294, 2001. 29. Poulos E, Taylor C, Solish N: Effectiveness of dermasanding (manual dermabrasion) on the appearance of surgical scars: a prospective, randomized, blinded study, Am Acad Dermatol 48:897–900, 2003. 30. Chang CW, Ries WR: Nonoperative techniques for scar mangement and revision, Facial Plast Surg 17:283–288, 2001. 31. Alster T: Laser scar revision: comparison study of 585-nm pulsed dye laser with and without intra-­lesional steroids, Dermatol Surg 29:25–29, 2003.