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Factors affecting claw lesion healing in cattle
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Objective
Wound healing is a complex process generally described in terms of 4 overlapping phases including: hemostasis, inflammation, proliferation and maturation. The objective of this session is to describe wound healing in the context of claw lesions with emphasis on the factors that may interfere with these events.
Materials and Methods
Information for this presentation has been derived from research observations and a review of pertinent literature on the subject of wound healing.
Wound Healing as it applies to Claw Lesions
Restoration of a new layer of epithelium (new hoof horn) on the surface of exposed corium is the primary objective in claw lesion healing. Wounds that result in significant tissue loss or those that are heavily contaminated are generally left open to heal by 2nd intention. Wound edges cannot be opposed as with sutures and lesions are generally contaminated requiring closure of the defect by granulation, and eventually re-epithelization of the granulating tissue surface. Bridging the gap between wound margins, depending upon size and depth of the lesion may be prolonged.
The 4 Phases of Wound Healing
Hemostasis
Hemorrhage plays a key role in wound repair as the source of blood platelets essential for blood clot formation. Within minutes, platelets enter the site of injury and begin to clump forming a clot. Coincident with the clotting process is the release of numerous cytokines and vasoactive mediators that cause vasoconstriction to reduce blood loss and activate inflammatory cells in preparation for the second phase of the healing process (Stadelmann et al, 1998; Auer and Stick, 2012).
Inflammation
The inflammatory phase is characterized by the influx of white blood cells that phagocytize bacteria and cellular debris within the site of injury. This phase is characterized by pain, swelling and loss of function at the wound site. Quite often, chronic lesions or wounds are those stuck (or stalled) in the inflammatory phase of healing.
Proliferation
The proliferative phase is characterized by angiogenesis, fibroplasia and granulation tissue formation and epithelialization. Any interference in these events has the potential to result in prolonged wound healing and a chronic lesion. The timing of topical treatments frequently coincides with key events that occur during this period.
Whereas hemostasis occurs within minutes and inflammation within minutes to hours after injury; the proliferative phase marked by the entry of fibroblasts and the formation of granulation tissue begins in 2-3 days of injury. Neovascularization supports the development of granulation tissue that fills the wound defect. Although less resistant to external factors than intact skin, granulation tissue provides an early, though imperfect, barrier to injurious agents from the environment (Stadelmann et al, 1998; Auer and Stick, 2012).
Re-epithelialization of the lesion is the ultimate objective in wound healing. The speed of re-epithelialization depends upon the severity and type of injury suffered. For example, re-epithelialization is rapid when the injury is superficial (i.e. such as an abrasion) and the basement membrane and basal cell layer are intact or minimally damaged. On the other hand, when a full thickness defect of the epithelium occurs the recovery process is prolonged. In this circumstance, residual keratinocytes at the wound site are not immediately available for recruitment to start the healing process. Instead, re-epithelialization must occur from the wound edges requiring centripetal movement of keratinocytes from the wound margins (O’Toole EA, 2001).
Persistent or Exuberant Granulation Tissue
The clinical indication of an interference with wound healing is the presence of exuberant granulation tissue (Auer and Stick, 2012). This is corroborated by the observations that ulcers with excessive granulation tissue healed more slowly compared with lesions free of granulation tissue (van Amstel et al, 2003). Re-epithelialization of mild to moderate lesions requires somewhere around 21-30 days with more severe lesions requiring as much as 40 days and potentially as long as 60 days.
Causes of Non-Healing Claw Lesions
One of the most frequent causes delayed claw lesion healing is infection of the exposed corium by organisms associated with digital dermatitis. The longer the corium remains exposed, the greater the likelihood of secondary infection. Complicating factors include bandaging and topical treatment of claw lesions among others. An understanding of the factors that affect claw lesion healing is important to assure a successful outcome from treatment.
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