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Health Protocols

Trauma and Wound Healing

Classification of Wounds

There are several ways wounds are classified. In the hospital setting, surgeons often classify wounds according to their degree of apparent contamination and infection risk (CDC 2017):

  • Clean wounds are generally surgical wounds in which no inflammation or infection are encountered.
  • Clean-contaminated wounds, also typically surgical wounds, are those in which the gastrointestinal, respiratory, genital, or urinary tract are entered without resulting in unusual contamination.
  • Contaminated wounds include fresh accidental wounds as well as surgical wounds in which acute inflammation is encountered or sterile procedure is not properly followed.
  • Dirty wounds include accidental wounds that retain dead tissue or are infected, and surgical wounds complicated by existing infection or organ perforation.

Acute Versus Chronic Wounds

Acute wounds can result from surgery or accidental trauma (Ubbink 2015; Bowler 2001). Examples include clean incisions and common uncomplicated traumatic lacerations, abrasions, and punctures that heal with standard care (Ghafouri 2012; Worster 2015; Anderson 2016).

An acute injury can become a chronic wound (Sood 2014). Chronic wounds are defined by their persistence, often failing to heal for weeks or months (Nunan 2014; Kyaw 2017; Gould 2015).

Chronic wounds often fail to progress through the normal healing stages because of an underlying disease process. Common causes include reduced oxygen supply to the wound site due to poor blood flow, prolonged inflammation, poor cellular response to reparative stimuli, and infection (Guo 2010; Demidova-Rice 2012). Infections from chronic wounds can spread to surrounding tissues or enter the bloodstream and become widespread (Gardner 2008; Leaper 2015; Wolcott 2016).

Mitochondrial dysfunction may also impair wound healing. Because they provide energy for all cellular metabolic processes, including cell division, mitochondria play a critical role in the healing process. They also produce reactive oxygen species, which kill bacteria and participate in cell signaling during wound healing (Gould 2015).

Common types of chronic wounds include (Sen, Chandan 2009):

  • Diabetic foot ulcers
  • Venous ulcers (such as from venous insufficiency)
  • Arterial ulcers (such as from atherosclerosis)
  • Bedsores (pressure ulcers)

Primary and Secondary Intention

Wounds can also be classified by the way they are managed:

  • Primary intention involves closure of the wound or surgical incision such that the edges of the wound are in direct contact and can reconnect with minimal need for new tissue synthesis. Primary intention best preserves the integrity of tissues surrounding the wound and reduces scarring, but can only be performed on surgical and some limited other wounds soon after they are inflicted (Mercandetti 2017; Velnar 2009).
  • Secondary intention is used for wounds with edges that cannot be brought together because of extensive tissue loss. This is a longer process in which the open wound heals through the formation of new connective tissue and small blood vessels (granulation tissue) and the laying down of new superficial (epithelial) cells (Velnar 2009). Healing by secondary intention results in more inflammation and susceptibility to infection than healing by primary intention (Simon 2016). Examples of wounds generally left to heal by secondary intention include pressure ulcers and diabetic ulcers. Secondary intention healing leads to more scar formation.
  • Delayed primary intention (sometimes called tertiary intention) is a technique used for contaminated wounds, in which the wound edges are not brought together right away. This allows time for the cells of the immune system to remove dead and contaminated tissue from the wound before it is closed (Mercandetti 2017). Delayed primary intention involves aspects of both primary and secondary wound management.

The Phases of Healing

During otherwise healthy conditions, wound healing proceeds through four overlapping phases (Mercandetti 2015; Simon 2016; Guo 2010).

The healing process begins with hemostasis or coagulation immediately after injury, at which time the body attempts to reduce blood loss from the site of injury (Velnar 2009). Vasoconstrictive signaling reduces blood flow, and coagulation proteins and platelets are activated to promote blood clotting at the injury site (Dashty 2012; Nurden 2008).

Inflammation is initiated by cytokines released by activated platelets and cells in the surrounding tissues. Cytokines attract immune cells from circulation to the wound site. The arriving immune cells release additional cytokines, attracting more immune cells to the site of injury and leading to swelling and inflammation (Velnar 2009). Inflammation overlaps with coagulation and can last for several days (Mercandetti 2017; Velnar 2009).

The proliferative phase begins after resolution of the inflammatory phase, usually 48‒72 hours after injury (Gonzalez 2016; Li 2016). Cells known as fibroblasts infiltrate the site and deposit extracellular matrix, the scaffolding that holds the injured tissues together. Small blood vessels (capillaries) grow into the site bringing oxygen and nutrients and removing waste from the healing tissue. Proliferation can last for 2‒4 weeks (Mercandetti 2017; Velnar 2009).

The last phase of healing is remodeling, which can last for years after the initial injury. As the wound site is remodeled, it begins to adopt a normal tissue structure at the molecular level. In adults, the extracellular matrix deposited during the proliferative phase often lacks the original structure of the damaged tissue it replaces, but its organization and strength are improved over time (Eming 2014; Velnar 2009).

Pathological scarring results from overactive cell growth and disproportionate extracellular matrix deposition during the proliferation and remodeling phases of wound healing. Excessive inflammation (Sarrazy 2011; Block 2015; Eming 2014) and genetic factors may influence scarring (Sidgwick 2015). Pathological skin scars include hypertrophic scars and keloids. Hypertrophic scars are raised scars from surgery or trauma that do not extend beyond the site of the initial injury, while keloids are excessive growths of connective tissue that grow beyond the margins of the original wound and do not regress over time (Sidgwick 2015; Gauglitz 2011). 

Scarring can cause functional disability by restricting mobility and psychological stress because of their cosmetic appearance. Although there are many scar treatment techniques, such as surgical revision, steroid injections, laser therapy, pressure therapy, anti-tumor drugs, cryotherapy, and others, their effectiveness is limited (Eming 2014).