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Medical-Surgical Nursing

28.1 Cellular Response and Adaptation in Wound Healing

Medical-Surgical Nursing28.1 Cellular Response and Adaptation in Wound Healing

Learning Objectives

By the end of this section, you will be able to:

  • Describe the anatomy and function of the skin
  • Define the four phases of the wound-healing process
  • Identify the major physiological aspects of wound healing

Let us understand the skin we are in. Aside from being the largest human organ, the skin is the first physical barrier a human body has against the external environment. In addition to protecting the underlying structures of the body, among other responsibilities, our skin must be able to protect itself and heal when an injury occurs. This module will explore the anatomy and physiology of our largest organ, review the phases of healing when a wound occurs, and discuss the physiological components that accompany the healing process.

Skin Anatomy and Physiology

The skin consists of three layers (see Figure 14.2). The outermost layer is the epidermis, the middle component is the dermis, and the deepest layer is subcutaneous tissue. Each layer plays an integral part in the external and internal roles of the skin. Therefore, in caring for different client populations, it is important to know and understand the skin’s underlying structures.

Structure and Function

As previously mentioned, there are three major layers that compose the skin: the epidermis, the dermis, and subcutaneous tissue (see Figure 14.2). The epidermis is the waterproof outermost layer. It is avascular, or lacks blood vessels, and contributes to an individual’s skin tone. Depending on its location in the body, the epidermis consists of four or five sublayers of cells. Moving from superficial presentation to deep, the typical four sublayers are the stratum corneum, stratum granulosum, stratum spinosum, and stratum basale. A fifth sublayer, typically found on thicker-skinned areas such as the palms of the hand or soles of the feet, is located between the stratum corneum and stratum granulosum and is called the stratum lucidum. This extra sublayer provides added strength and protection to the skin in regions where the skin is subject to constant pressure or rubbing. The melanocytes, which produce melanin, are located in the epidermis. It is the melanocytes that determine the pigment of skin, which can range from fair to dark with a variety of shades and hues.

The dermis contains hair follicles, blood vessels, lymphatic vessels, nerves, and sweat glands. This core layer is divided into two distinct sublayers, the papillary and reticular dermis. The subcutaneous layer, also known as the hypodermis, consists of fat and connective tissue. This layer links the skin to the underlying structures, which include fascia, muscles, and bones.

The functions of the skin include regulation of temperature, protection, mobility, sensation, endocrine activity, and exocrine activity (Table 28.1).

Function Description
Protection The layers of the skin work together to protect the body against microorganisms, dehydration, and mechanical damage. Skin pigmentation is a defense mechanism against UV radiation.
Temperature regulation The skin regulates body temperature and homeostasis by conserving or releasing heat.
Mobility The skin allows for smooth body movement. Damage to the skin (e.g., burns and scarring) and the healing process can cause restrictive movements.
Sensation Sensation begins with the skin. Pain, temperature, and pressure are all felt due to receptors within the skin.
Endocrine activity The skin is involved with biochemical processes such as production of Vitamin D and prevention of excessive water loss.
Exocrine activity The skin participates in exocrine activity by releasing water, urea, and ammonia. In addition, the skin secretes products including cytokines, pheromones, sweat, and sebum.
Table 28.1 General Functions of the Skin

Age Considerations

Skin development begins during the first trimester of gestation. The various structural features are formed by thirty-four weeks gestation, and maturation continues until full term. The dermal-epidermal junction acts as the barrier between the epidermis and the dermis. In preterm newborns, the dermal-epidermal junction is weaker, containing less collagen, water, and melanin than in older counterparts. As a result, newborn skin has a greater risk of heat loss and is more fragile, susceptible to infections, and vulnerable to toxicity from topical agents. The skin continues to mature through the first year of life and closely resembles adult skin by the time a person is two years old. Table 28.2 details how quickly a person’s epidermal cells are renewed throughout the life span.

Age Rate of Turnover in Days
Newborn to 3 months Approximately every 2 days, depending on site
Infant 14 days
Teens to 20s 14–30 days
Adults 30s–40s 28–42 days
Adults 50+ 45–85 days
Table 28.2 Epidermal Turnover Rates by Age (Rahma & Lane, 2022; Maeda, 2017)

At the opposite end of the care spectrum, aging results in the thinning of the epidermis and dermis as well as a potential decrease of the hypodermis. The thinning of the hypodermis may result in reduced support, increasing the risk for pressure injury development, and impaired temperature regulation. As we age, the skin loses its elasticity due to impaired barrier function and a decrease in sebum production, which may result in dry skin and wrinkles. Melanocytes decrease with age as do the numbers of sweat glands, blood vessels, and nerves. These normal consequences of aging make the skin more susceptible to damage and cause wounds to heal up to four times more slowly.

Life-Stage Context

Wound Healing in the Older Adult

Changes in the dermis in different age categories can affect how we approach treatment and support the patient in their wound-healing journey. Older adult patients generally heal more slowly than younger patients. Skin breakdown and delayed wound healing may result from comorbid conditions, inadequate nutrition intake, and dehydration. An individual’s body build can impair wound healing. For example, excessive adipose tissue impairs blood flow, while a lack of adipose tissue can delay healing due to lack of nutrition and oxygen transport.

Consider the following when caring for an older adult with a wound:

  • Older patients may be at risk for chronic wounds due to comorbid conditions and impaired circulation.
  • Nonsteroidal anti-inflammatory medications (NSAIDs), such as aspirin and ibuprofen, are often used to treat arthritis but may interfere with the inflammation stage of the healing process.
  • Dry skin is more vulnerable to excoriation and infection.

Phases of Wound Healing

The physiological process of wound healing includes four phases (Figure 28.2). These phases occur in a predictable manner that resembles a cascade of events as opposed to a series of distinct steps. Regardless of wound etiology, the biological repair process is the same for all wounds. As soon as damage occurs, the healing process begins. Keratinocytes, fibroblasts, vascular endothelial cells, and immune cells all play essential roles in supporting inflammation, cell migration, and angiogenesis.

A four-panel diagram showing the stages of healing. The stages include hemostasis (showing the bacteria and fibrin clot), inflammation (showing the neutrophil and macrophage), proliferation (showing the scab, fibroblast, and granulation tissue), and remodeling (showing the collagen fiber).
Figure 28.2 Wound healing is a physiological process that includes four phases: (a) hemostasis, (b) inflammation, (c) proliferation, and (d) remodeling. Each phase features cellular and molecular responses that resemble a cascade rather than a series of distinct steps. (attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

Hemostasis

The first phase in the wound-healing cascade, called hemostasis, is marked by the cessation of bleeding (Wallace et al., 2023). When injury occurs, such as a break in the skin, blood vessels contract and clotting factors, such as fibrin, are released, which help stop the bleeding. In addition, platelets release growth factors that signal cells to start the repair process at the wound location. Depending on the severity of the injury, the hemostasis phase can last as much as sixty minutes.

Inflammation

The second phase of the wound-healing cascade is the inflammation phase. Acute inflammation begins immediately after injury and is essential for the orderly and timely healing of a wound. This phase is marked by vasodilation, facilitating the movement of white blood cells (neutrophils, macrophages, lymphocytes, mast cells) to the wound bed, where they start cleaning. Typically, the inflammation phase lasts three to seven days, depending on the injury. During the inflammatory process, the wound can present with redness, pain, swelling (edema), and possibly exudate.

Proliferation

During the proliferation phase, the wound fills with new tissue, the wound margins contract, and the wound is covered. Proliferation does not have a specific starting point but can begin within a few days after the injury and last several weeks. This phase includes four distinct processes: epithelialization, angiogenesis, collagen formation, and contraction. The regeneration of the epidermis and the formation of granulation tissue is epithelialization. During epithelialization, various cell types actively proliferate to replace the damaged or loss tissue. For example, a keratinocyte is a cell that participates in the contraction and migration of cells across a wound bed to facilitate healing. They migrate from the wound edges, where they multiply until they meet in the middle of the wound bed. New connective tissue with fragile, thin-walled capillaries is called granulation tissue. In a healthy wound, granulation tissue can appear pink or red with an uneven texture. Healthy granulation does not bleed easily. If the granulation tissue appears dark and is friable (bleeds easily), it can be a sign of infection.

Proliferation also involves angiogenesis, the creation of new blood vessels. Additionally, cells called fibroblasts help to produce new collagen and repair the avascular epithelial tissue, causing the wound to contract.

Maturation and Remodeling

The maturation phase, also known as the remodeling phase, is the longest phase of wound healing, beginning around week three and lasting up to twelve months. Maturation involves the reorganization and transformation of collagen into scar tissue. Cellular activity slows, and the number of blood vessels in the wound is reduced. Collagen fibers continue to reorganize while the tissue remodels and matures. As a result, the tissue increases its tensile strength; however, the maximum strength is limited to 80 percent of the preinjured strength. During the maturation phase, any scarring may reduce in size, flatten, increase in strength, or change color.

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