Wound Healing and Repair
Christopher J. Brandys
Tim M. Brandys
A 17-year-old man is brought to the emergency room directly from the local high school track and field meet. While running in the 100-yard hurdles, he was injured on the last hurdle, sustaining a 15 by 3-cm laceration down the medial aspect of his right thigh. You are consulted regarding the best management of the local track star’s injury.
What are the key features of your initial assessment?
View Answer
Proper initial management of the wound promotes healing, reduces infection, and prevents complications. Critical considerations include identification of factors that potentiate infection, such as the elapsed time from injury, the degree of contamination, the depth of injury, and the presence of devitalized tissue or foreign material in the wound. Injuries by animal or human bite also need accurate and prompt identification. The patient’s ability to respond to potential infection is also important. Significant medical problems that affect wound healing include diabetes, cardiovascular disease, immunocompromised states, and medications that suppress the immune system. Tetanus status and nutritional status are also critical. Important features on examination of the wound include neurovascular compromise, function distal to the injury, the depth of wound and any involved structures (e.g., compound fracture, tendon injury), and the presence of devitalized tissue or foreign material.
What is the best method to close the wound?
View Answer
There are three options for wound closure: primary (immediate suture closure), secondary (healing by secondary intention), or tertiary closure (delayed primary closure). When deciding, significant factors include the potential for wound infection, the condition of the soft tissues and the tension required to approximate them, and the need for hemostasis. Most wounds that are less than 6 hours old are in “the golden period” and contain less than 105 colonies of organisms per gram of tissue and can be closed primarily (1). Acute wounds can also be classified into four categories: clean, clean-contaminated, contaminated, and dirty and infected (2). Do not close puncture wounds, human bites, wounds with inadequate hemostasis, and wounds under excessive tension. Devitalized tissues and foreign bodies must be removed before primary closure. Diabetics and immunocompromised patients will have a higher risk of infection and subsequent dehiscence.
Does this patient require tetanus prophylaxis?
View Answer
The risk of tetanus is increased if the wound is more than 6 hours old, is deeper than 1 cm, or is contaminated. Crush or missile injuries and bite wounds also require a tetanus shot (3). Assess the patient’s tetanus immune status and give appropriate tetanus toxoid with or without immunoglobulin as indicated.
Does this patient require prophylactic antibiotics?
View Answer
Prophylactic antibiotics are indicated for contaminated wounds in patients who are immunocompromised, are diabetic, or have indwelling prosthetic devices such as heart valves or joint prostheses. Bite wounds, necrotic wounds, and wounds contaminated with gastrointestinal or urologic organisms also should receive prophylactic antibiotics (4).
What are the four phases of wound healing?
View Answer
The four phases that acute and chronic wounds must pass through are hemostasis, inflammation, proliferation, and remodeling (Table 2.1).
The platelet is the most important component of the hemostasis phase. Not only does it help to form the wound clot (or temporary matrix) but also its alpha granules release growth factors, which play a critical role in accelerating wound healing.
TABLE 1.2. Phases of Wound Healing | ||||||||||||||||||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
|
Neutrophils, monocytes, and macrophages direct the inflammatory phase by removing devitalized tissue and destroying bacteria. They phagocytose bacteria and release proteases (matrix metalloproteinases [MMPs]).
The fibroblast and myofibroblast produce collagen during the proliferative phase and initiate wound contraction. By 6 weeks, collagen synthesis has peaked and the wound has achieved approximately 75% of its eventual tensile strength (5). Keratinocytes re-epithelialize the wound.
Fibroblasts then regulate remodeling as immature collagen (type 3) is broken down and mature collagen (type 1) is synthesized and re-aligned to increase the tensile strength of the wound.
In the wound center, you are asked to assess a 25-year-old man from a long-term care facility who has a chronic wound on his right ischial region. He has a history of spinal cord injury from a motor vehicle accident 5 years earlier. The majority of his day is spent in a wheelchair. On examination, he has a dry eschar with surrounding erythema over the right ischial tuberosity and redness over the left ischial tuberosity.
What are the underlying etiologic factors of this wound?
View Answer
This patient’s functional status clearly plays a large role in his predisposition to ulcer formation. Decubitus ulcers (from the Latin decumbere– “to lie down”) result from pressure, shear, friction, and moisture. Tissue necrosis can result when interface pressure on soft tissues between a bony prominence and support surface exceeds 32 mm Hg (6), the pressure at which tissue capillaries collapse. Other factors to consider include the patient’s nutritional and immune status.
What stage are these wounds?
View Answer
Staging of decubitus ulcers is critical to allow for effective communication between members of the health care team and to document progress of the wound as it heals. The right ischial wound cannot be staged until it is débrided to healthy tissue. The left ischium has a stage I wound. The National Pressure Ulcer Advisory Panel (NPUAP) classification is useful:
Stage I: redness of the skin
Stage II: ulceration of the epidermis with or without dermis
Stage III: ulceration into the subcutaneous tissue
Stage IV: ulceration to bone, tendon, or fascia
Why has this chronic wound failed to heal?
View Answer
Chronic wounds are defined as wounds that have been present more than 12 weeks and are not progressing through the four phases of wound healing. Most chronic wounds are stuck in phase 2, the inflammatory phase.
The prolonged inflammatory phase appears to be triggered by the presence of necrotic debris, bacterial infection (or bioburden), cellular debris (senescent cells) (7), and decreased levels of cytokines and growth factors (8). These stimuli result in an exaggeration and prolonged release of proteases (including MMPs), which degrade the extracellular matrix faster than it can take hold in the wound bed. Wound exudate analysis has shown the level of MMPs to be up to 116 times normal compared to the acute healing wound (9). These proteases include collagenases (MMP1, MMP8, MMP13), gelatinases (MMP2, MMP9), and stromelysins (MMP3, MMP10, MMP11). The activity of these enzymes appears to be regulated by several tissue inhibitors of metalloproteinases (TIMP), which are decreased in the chronic wound (10).
What is the role of debridement?
View Answer
Frequent debridement of the chronic wound bed has been shown to accelerate wound healing (11). Debridement is intended to remove necrotic debris, the cellular burden (senescent cells), and the biofilm of contaminated or infected matrix from the wound bed (12). In doing so the stimulus for white cell migration and the inflammatory process within the wound is removed (13). Debridement can be performed by surgical debridement, mechanical debridement (whirlpool, pulsed lavage), enzymatic means (papain-urea or collagenase), or autolytic means.
How is the bioburden managed?
View Answer
Quantitative tissue cultures reveal whether the wound is contaminated or infected (more than 105 colonies per g of tissue) (14). Specific organisms can be addressed with topical agents such as ionic silver or cadexomer iodine. Agents such as povidone iodine (Betadine), 3% hydrogen peroxide, and 0.5% sodium hypochlorite (Dakin solution) kill fibroblasts and keratinocytes (15) and should be avoided. Systemic antibiotics may be required if extensive soft tissue, bone, or systemic infection is present.