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Wounds and Wound Healing

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Kerraboot® Aetiology of Wounds Trauma Infection Vascular Thermal Chemical Radiation • • • • • •

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Kerraboot® Wound Pathology Ischaemia Venous stasis Oedema Neuropathic Infection (systemic) Malignancy Connective tissue disorders Blood dyscrasias • • • • • • • •

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Kerraboot® Wound Types Puncture Surgical Laceration Ulceration Burn Contusion (bruise) Avulsion Abrasion • • • • • • • •

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Wound Healing

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Kerraboot® Introduction Following injury, wounds progress through a series of stages. Many of these stages may be occurring in different areas of the wound at the same time. The stages are: • Vascular response • Inflammation • Proliferation - Angiogenesis - Granulation • Contraction • Epithelialisation • Maturation •

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Kerraboot® Vascular Response Haemostasis is achieved by clotting at the wound surface. • Platelets contact molecules from damaged endothelium such as collagen and fibronectin. • The platelets stick to the endothelium and flatten out in matter of seconds, increasing their surface area. • The platelets release factors (ADP) to produce thrombin and cause further platelet aggregation. • The thrombin activates fibrinogen to fibrin and with tissue factors from the clotting cascade create irreversible links between platelets. • A platelet/fibrin plug is formed. •

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Kerraboot® Inflammation Vasodilation and increased vascular permeability is initiated by factors and serum proteins from the clotting and complement cascades. The platelets release growth factors and chemical attractants into the wound site. This enables more cells to move through the endothelium . • • •

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Kerraboot® Inflammation continued... Immune cells migrate into the wound through the endothelium. • Neutrophils (leukocytes) engulf bacteria through phagocytosis and produce chemotactic molecules and growth factors. • Macrophages phagocytose bacteria and damaged tissue and produce chemotactic molecules and growth factors. • Lymphocytes produce antibodies (B cells) and mediate the bodies response to viruses, fungus and foreign material (T cells). • The growth factors (cytokines) cause inflammation – redness, swelling, heat and pain. •

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Kerraboot® Proliferation- Angiogenesis and Granulation Fibroblasts migrate into the wound and divide in response to macrophage Platelet Derived Growth Factor (PDGF). New extra cellular matrix (ECM) is formed by fibroblasts. ECM comprises collagen, elastin, glycoproteins, proteoglycans and glygosaminoglycans Collagenase (an Matrix Metaloprotease) is produced by fibroblasts to remodel ECM The new ECM forms a scaffold into which capillaries can grow. The new capillary growth is stimulated by growth factors (19 known growth factors) from macrophages, fibroblasts, neutrophils, mast cells, keratinocytes and platelets.

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Kerraboot® Proliferation continued... - Angiogenesis and Granulation Blood vessels may be new extensions to existing vessels. The capillaries form loops in the naïve tissue which have a red/pink granular appearance – granulation tissue. The granulation tissue produces increased exudate from the wound bed. The granulation tissue must form a flat bed and fill the wound to enable epithelialisation. • • • •

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Kerraboot® Contraction Specialised fibroblasts (myofibroblasts) draw the edges of the wound together allowing wound contraction. Contraction reduces the size of the wound reducing the potential for infection and helping to bring damaged tissue together. • •

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Kerraboot® Epithelialisation Epithelial cells (keratinocytes) migrate across the wound bed from the wound edge. The peri-wound surface is extremely fragile. The keratinocytes divide and form layers or strata. Once the stratified layer is complete, the keratinocytes undergo a morphological change to become the epidermis, the normal barrier layer of the skin. The new tissue continues to be remodelled. Numbers of fibroblasts fall and capillary bundles become organised. • • • • •

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Kerraboot® Maturation Remodelling of tissue continues for months or up to 2 years. Collagen fibres are reorganised to increase tensile strength. The type of collagen produce changes ( type III to type I). The scar initially has about 5% of the tissue’s pre-injury strength. The scar may mature to 80% of its original strength. • • • •

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Kerraboot® Primary Intention Healing Wounds healing by primary intention have minimal loss of tissue and apposing edges to the wound. These wounds occur following injury or an operation. Edges of the wound are brought together (approximation) by suturing or application of adhesive strips. The wound surface normally forms initial closure within 24 to 48 hours. Primary intention healing can lead to linear scarring. • • • • •

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Kerraboot® Secondary Intention Healing Wounds healing by secondary intention have some loss of tissue at the wound site. These wounds occur following injury or an operation where tissue is excised. The wound is left open to allow exudate to drain, removing bacteria and proteases that slow wound healing. Necrotic tissue must be debrided. The wound base is treated to encourage granulation tissue to provide a base to support re-growth of epithelium. Skin grafting may be applicable when granulation tissue has formed. • • • • • •

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Kerraboot® Tertiary Intention Healing Wounds healing by tertiary intention have gross loss of tissue at the wound site. These wounds occur following injury or an operation where tissue is excised and foreign material or infection is present. Necrotic tissue must be debrided. Often revision surgery to remove dead tissue is necessary. The wound is kept open to allow exudate to drain, preventing the spread of deep infection and aiding granulation. • • • •

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Kerraboot® Tertiary Intention Healing continued... The wound base is treated to encourage granulation tissue growth. The edges of the wound will begin to contract aiding closure. When foreign material has been removed, necrotic tissue debrided and infection is no longer present, the wound edges are brought together to achieve closure (delayed primary closure). • • •