L-25 Wounds and Wound Healing Stages

Wounds and Wound Healing

• A wound is a disruption of normal anatomic relationships resulting from an injurious process
• The injury may be intentional, like a surgical incision, or accidental after trauma.
• Biochemical and physiologic healing processes are identical regardless of the cause

Wound Types

• There are three distinct types of wounds, based on the timing of epithelium replacement: primary, secondary, and tertiary

Wound Healing Stages/Phases

• Wound healing can be divided into stages, based on the physiologic process
• The stages are: Hemorrhagic, Substrate, Proliferative, and Remodeling

Hemorrhagic Phase (Hemostasis)

• The first stage of wound healing involves stopping the bleeding
• Hemostasis and clotting occur within seconds to minutes of suffering a wound
• The body activates its emergency repair system to block drainage and prevent blood loss by forming a dam
• Clotting helps close and heal the wound, making a scab

Inflammation

• Inflammation is a basic physiologic process common to all wounds
• Redness (rubor), heat (calor), swelling (tumor), pain (dolor), and loss of function are cardinal signs of inflammation
• These signs can also be seen in wound infections, potentially leading to wound disruption
• The physiology underlying clinical signs is a complex mix of biochemical and cellular events

Biochemical Aspects

• Trauma activates a cascade of chemoattractants and mitogens to recruit phagocytes, fibroblasts, and endothelial cells
• Chemoattractants are produced during blood clotting, degradation of surrounding tissue, and entering cells
• Platelet-derived growth factor (PDGF) is a primary factor released only at the injury site
• PDGF has chemotactic and mitogenic activity toward fibroblasts and smooth muscle cells, appearing as a wound hormone
• Arachidonic acid (AA) is in cell walls and released when cells are injured
• Degradation of AA into prostanoid derivatives like Prostaglandins and thromboxanes triggers inflammatory responses, like vasodilation (rubor), swelling (tumor), and pain (dolor)

Physiologic Aspects

• Leukocytes marginate, stick to vessel walls, and move toward the injury site as biochemical events develop
• Venules dilate, and lymphatics are blocked

Substrate Phase

• The second phase of wound healing is also known as the inflammatory, lag, or exudative phase
• Polymorphonuclear leukocytes (PMN) and macrophages are the primary cells involved
• PMNs appear shortly after wounding and remain predominant for about 48 hours
• Small numbers of bacteria are handled by the macrophages present
• Large numbers of bacteria cannot be controlled, and a neutropenic state leads to a clinical wound infection
• Macrophages are crucial for normal wound healing, not neutrophils
• Monocytes enter the wound after PMNs, reaching maximum numbers about 24 hours later, and evolve into macrophages for wound debridement
• Macrophages secrete substances that cause fibroblasts to replicate (macrophage-derived growth factor (MDGF)) and blood vessels to approach the wound (wound angiogenesis factor (WAF))
• The clot, debris, and bacteria are removed, and substrates for collagen synthesis are arranged
• The process occurs over approximately a 4-day period in primary wound healing
• The wound appears edematous and erythematous, which may be difficult to distinguish from early signs of wound infection
• Healing by secondary or tertiary intention indefinitely continues this phase until the wound surface is closed by ectodermal elements

Proliferative Phase

• The wound appears less edematous and inflamed, but the scar itself may appear raised, red, and hard
• Collagen production in the wound characterizes this phase
• Fibroblasts, which makes the collagen, are the main cells in this phase
• Collagen is the principal structural protein of the body and is ubiquitous through all tissues
• Collagen synthesis begins with amino acid chain production in the cytoplasm
• In the primary wound, collagen production begins about day 7 and continues until approximately day 60
• Collagen production is not constant; slow at first, then a rapid spurt from day 18 to approximately day 50 occurs
• Increased collagen proliferation reflects a rapid gain in tensile strength during this period

Maturation Phase

• The fourth and final phase of wound healing is the remodeling or maturation phase
• Collagen maturation with intermolecular cross-linking characterizes it
• The wound scar gradually flattens, becomes less prominent, paler, and more supple
• Metabolic activity remains high, although there is no net collagen production
• Maturation corresponds clinically to scar flattening and requires approximately 9 months in the adult
• Phases are divided into categories to describe the predominant physiologic process

Classification of Healing Wounds: Primary

• In primary healing (healing by first intention), the wound is closed by direct approximation of the wound edges
• Larger defects use pedicled flaps or skin grafts that still result in primary wound healing via immediate coverage with epithelial elements

Classification of Healing Wounds: Secondary

• Secondary healing (spontaneous wound closure) heals spontaneously by leaving the wound open
• Spontaneous wound closure occurs by wound contraction and epithelialization
• Contraction occurs by a centripetal force in the margin of the wound that is generated by myofibroblasts
• Contraction is a normal process
• Contracture, pathological deformity caused by contraction of scar, is not desirable
• Epithelialization is another component of healing by secondary intention
• The inflammatory phase continues unabated in the middle of the open wound
• Granulation tissue is the product of prolonged inflammatory process
• Granulation tissue, consisting of inflammatory cells and capillary proliferation, is the "proud flesh" that was viewed as a sign of healthy wound healing in the past

Classification of Healing Wounds: Tertiary

• Tertiary wound healing (healing by third intention) involves closing a wound by active means after a delay of days to weeks
• This occurs when a granulating, open wound is closed with sutures or sterile tape before it heals
• Closing the wound interrupts the secondary healing process
• Delayed closure should only be performed in wounds with bacterial balance

Factors Affecting Wound Healing

• The goal of all wound closure is expedient, precise, and definitive tissue approximation
• The goal is to also prevent infection, fibrosis, and secondary deformities (wound contracture)
• The amount of tissue trauma that the wound has sustained is extremely important
• A laceration with a knife is minimally damaging, while crush or avulsion injuries are harder to evaluate and manage
• In a crush, large areas of tissue adjacent to the wound are tenuous and difficult to assess for ultimate viability
• Hematoma impedes wound healing, as the collection of clot in the wound does not allow for orderly removal of debris or collagen laying
• Hematoma acts a perfect medium for bacterial proliferation possibly fostering clinical wound infection
• Bacterial contamination and wound infection are factors of extreme importance in local control of wound and proper closure
• All wounds contain varying amounts of bacteria with a biologic balance (or equilibrium)
• Factors that affect equilibrium: blood supply to wound, necrotic debris, local wound care, and use of systemic or topical antimicrobial agents
• Wounds can tolerate 100,000 (10^5) organisms per gram of tissue to be closed successfully
• If more than 100,000 bacteria/g are present, closure leads to clinical wound infection
• Streptococci are the only exception to this and its presence in any quantity is a contraindication to wound closure
• Tetanus prophylaxis is an important consideration
• Prevention focuses on toxoid immunization, thorough cleansing, and debridement

Dressings

• Functions of dressings:
• Protect the wound
• Immobilize the area
• Compress the area evenly
• Absorb secretions
• Be aesthetically acceptable