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Understanding the Barriers to Healing

Hess, Cathy Thomas BSN, RN, CWOCN

Advances in Skin & Wound Care: May 2012 - Volume 25 - Issue 5 - p 240
doi: 10.1097/01.ASW.0000414709.35053.f9
Departments: Practice Points

Cathy Thomas Hess, BSN, RN, CWOCN, is President and Director of Clinical Operations, Well Care Strategies, Inc (WCS). WCS specializes in focused software solutions, Your TPS® EMR, and mapping best clinical, operational, and technology practices.

Please address correspondence to: Cathy Thomas Hess, BSN, RN, CWOCN, 4080 Deer Run Court, Suite 1114, Harrisburg, PA 17112; e-mail:

After decades of published clinical practice guidelines, research results, and documented best practices for wound care, one has to ask: Why are there so many chronic, nonhealing wounds?

Despite our best clinical coordination of efforts, wounds stall in the healing process and become chronic wounds. When skin integrity is altered and a wound results, the healing process begins. Typically, this process is well orchestrated, leading to repair of the injury. However, chronic wounds do not follow this complex healing model. Because of an impediment to the healing process, the wound is often thought to be “stuck” in the inflammatory or proliferative phase.Over time, key cells become senescent. Understanding and correcting the barriers to healing will spark the formation of granulation tissue, leading to the next stage of healing.

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Hemostasis occurs right after initial injury. The key cell responsible for this function is the platelet, which causes the body to form a clot to prevent further bleeding. In addition, platelets also release key cytokines, such as platelet-derived growth factor, which call in cells to participate in later phases of healing. Following hemostasis, the inflammatory phase begins.

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Inflammatory Phase (Defensive or Reaction Phase)

The inflammatory phase is characterized by a host of cells infiltrating the wound sites. Many of these are inflammatory cells, such as leukocytes and macrophages. The inflammatory phase begins right after injury and typically lasts 4 to 6 days. Bleeding is controlled by hemostasis, and any bacteria present are destroyed by leukocytes, particularly the polymorphonuclear neutrophils. About 4 days after the injury, macrophages (tissue cells derived from circulating monocytes that migrate to the area) also work to destroy bacteria, cleansing the wound of cellular debris. Macrophages replace the leukocytes (which phagocytize bacteria in the wound, stimulate the inflammatory response, and trigger other biochemical actions) and produce a host of cytokines and growth factors that act as chemoattractants to other cells needed for tissue repair. Macrophages also convert macromolecules into the amino acids and sugars necessary for wound healing.

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Proliferative Phase (Fibroblastic, Regeneration, or Connective Tissue Phase)

The proliferative phase typically lasts several weeks. In an open wound, granulation tissue is generated, which can be seen clinically as the production of red, beefy buds (or granules) of tissue. Granulation tissue consists of macrophages, fibroblasts, immature collagen, blood vessels, and ground substance. As this type of tissue proliferates, fibroblasts stimulate the production of collagen, which gives the tissue its tensile strength and, ultimately, its structure.

As the wound site fills with granulation tissue, its margins contract, or pull together, decreasing the wound’s surface. During epithelialization, the final step of this phase, keratinocytes migrate from the wound margins. Subsequently, they divide and, ultimately, become contiguous. Metalloproteinases (MMPs), such as collagenase 1, are critical in epidermal migration, whereas other MMPs, such as MMP8 and MMP9, are important in the normal healing process. The proteins are regulated by a set of inhibitors. Epithelialization can occur only in the presence of viable, vascular tissue. When epithelialization is complete, a scar results.

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Maturation Phase (or Remodeling Phase)

During the maturation phase, which can last from 21 days to months or years, collagen fibers reorganize, remodel, and mature, gaining tensile strength. Fibroblasts, MMPs, and their inhibitors play a crucial role in this process, as do certain growth factors, such as transforming growth factor β. This process continues until the scar tissue has regained about 80% of the skin’s original strength. This tissue will always be at risk for breakdown because its tensile strength is less than that of uninjured skin.

Wound repair occurs by primary intention, secondary intention, or tertiary intention. Many acute wounds, such as surgical wounds, are closed by primary intention, meaning that the skin edges are approximated (brought close together). Such wounds have a lower risk of infection, involve little tissue loss, and heal with minimal scarring after 4 to 14 days. Chronic wounds, such as pressure ulcers, heal by secondary intention; the skin edges are not approximated. Because of the delay in healing, chronic wounds are at a greater risk of becoming infected.

Surgical wounds that are left open for 3 to 5 days to allow edema or infection to resolve or exudate to drain are then closed with sutures, staples, or adhesive skin closures heal by tertiary intention. This is also called delayed primary intention.

The patient with a chronic wound generally presents with a host of factors that impede the healing process. Our job is to find out why.

Source: Hess CT. Clinical Guide to Skin and Wound Care. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008.

© 2012 Lippincott Williams & Wilkins, Inc.