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Approximately 2.5 million Americans are diagnosed with chronic venous insufficiency, and approximately 20% will go on to develop venous leg ulcerations. Chronic venous leg ulcers (VLUs) account for 90% of all chronic ulcers of the lower limb region. Wound chronicity takes place in wounds that are stalled and/or remain unhealed after four to six weeks. Although evidence-based care has been established, it has been reported that 30% of patients still experience delayed healing, with wounds often failing to heal within a 24-week time frame. Identifying risk factors for VLUs is imperative in best outcomes.

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Venous leg ulcers can be slow to heal; the longer a wound is present, the less likely it is to heal. To move a venous leg ulcer through the phases of wound healing may require more than just basic wound care.

Chronic venous leg ulcers can be prone to chronic inflammation. Changes in the microcirculation down to the capillary level can elevate levels of cytokines and proteases, thus leaving the wound stuck in the inflammatory cycle. Controlling, reducing, or eliminating inflammation is necessary to move the wound toward closure.

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Of all the types of chronic wounds in lower extremities, venous leg ulcers are the most common, and they account for up to 70% of lower leg ulcers. Infection is a common complication in these wounds, however, and may contribute to chronicity. Biofilm is another common complicating factor. Preventing infection, removing unhealthy tissue from the wound, providing dressings that manage exudate, and using advanced modalities can help heal these chronic wound types and prevent a recurrence.

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Hard-to-heal venous leg ulcers (VLUs) comprise the most common type of leg ulcer and impose a major economic burden on the health care system. These wounds can be difficult to heal, and they often experience recurrence within three months of closure, thus further complicating treatment. When managing VLUs, it is important to select strategies that are evidence based and cost-effective. Early diagnosis and implementation of interventions can encourage best outcomes.

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Wounds typically heal in four sequential but overlapping phases — hemostasis, inflammatory, proliferative and remodeling — ultimately leading to tissue regeneration. Healing sometimes stalls for various reasons, a key one being extensive inflammation, which disrupts the normal cascade of healing and leads to chronic and hard-to-heal wounds. A vicious cycle of ongoing inflammation, pain and poor quality of life often follows. Understanding how to break this cycle is essential for wound care clinicians who want to optimize healing outcomes and patient quality of life.

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Wound healing can stall for a number of reasons. Wounds that have not healed or significantly reduced in size after four to six weeks are considered chronic. They are characterized by a multitude of impeding factors including biofilm, excess matrix metalloproteinases (MMPs) and extracellular matrix degradation, inflammation, fibrosis, unresponsive keratinocytes and fibroblasts, and atypical growth factor signaling.

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Biofilm: Colonies of multiphenotype, free-floating bacteria that secrete a polysaccharide matrix that protects the bacteria from immune response and antibiotics.

Chronic wounds: Wounds that stall in the inflammation phase and fail to progress toward healing within 3 months are considered chronic or hard to heal.

Continuous inflammation: When wound healing becomes stalled in the inflammatory phase because of the presence of bacteria and their endotoxins, the wound is unable to move out of the inflammatory phase and into the repair phase.

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As scientists and researchers have delved deeper into the causes of wounds and wound chronicity, matrix metalloproteinases, or MMPs, have come into sharper focus. MMPs are not just present in chronic wounds — they also play an essential role in acute wounds.

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An injury to the human body initiates a wound healing chain reaction that occurs in four sequential but overlapping phases: hemostasis, inflammatory, proliferative and maturation. This post focuses on the second (inflammatory) phase, which begins after blood flow stops (i.e., hemostasis) and defender white blood cells, or leukocytes, migrate to the site of the injury — a process known as chemotaxis.

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Wound bed preparation has been performed for decades in managing wounds of various etiologies. The wound healing process consists of a complex interlinked and independent cascade, which not all wounds follow in a consistent, organized manner. The TIMERS acronym, consisting of four general steps, has assisted clinicians globally to provide a systematic approach to wound bed preparation that includes Tissue debridement, Infection or Inflammation, Moisture balance, Edge effect, Regeneration and repair, and Social factors.1 Clinicians should have practical knowledge of the principles of advanced wound care management, as well as the challenges faced in treating complex wounds.

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