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Podiatry Diabetes Workshop Module 5 D I A B E T E S P O D I A T R Y I N I T I A T I V E N I G E R I A T R A I N I N G M A N U A L 45 D I A B E T E S P O D I A T R Y I N I T I A T I V E N I G E R I A Module 5 46 T R A I N I N G M A N U A L Module 5 D I A B E T E S P O D I A T R Y I N I T I A T I V E N I G E R I A T R A I N I N G M A N U A L 47 D I A B E T E S P O D I A T R Y I N I T I A T I V E N I G E R I A Module 6: The Art of Wound Care The initial evaluation of the diabetic foot ulcer to bone (PTB) finding is highly predictive of must be comprehensive and systematic to osteomyelitis, although the frequency of false- ascertain the parameters that might have led to negative tests reduces its sensitivity. its onset as well as determine the presence of factors that can impair wound healing. Critical in Perhaps most importantly, the positive predictive this regard are assessments for vascular value for PTB falls off significantly when the perfusion (ischemia), infection/osteomyelitis, and prevalence of osteomyelitis decreases. The neuropathy. existence and character of odor or exudate should be noted. Cultures may be necessary As previously discussed, a thorough vascular when signs of inflammation are present. evaluation must be performed; this includes Generally, clinically uninfected ulcers without palpation of pulses, clinical evaluation of inflammation should not be cultured. Current capillary filling time, venous filling time, pallor on recommendations for culture and sensitivity elevation, and dependent rubor (283). If pulses include thorough surgical preparation of the are not palpable or if clinical findings suggest wound site with curettage of the wound base for ischemia, noninvasive arterial evaluation (eg, specimen or with aspiration of abscess material. segmental Doppler pressures with waveforms, ankle brachial indices, toe pressures, TcPO2 Wound Healing measurements and vascular surgical Phase 1-Inflammatory Phase Substrate or Lag consultation are warranted. When required, Phase : This stage lasts 3-4 days and has 3 these physiologic and anatomic data can be parts, vascular, hemostatic and cellular. supplemented with the use of magnetic a. Hemostasis is obtained via active resonance angiography or CT angiography vasoconstriction of blood vessels damaged in (CTA) and subsequent use of arteriography with the wound. Aggregation of platelets also leads digital subtraction angiography (DSA) as to the formation of a hemostatic plug. b. Platelet adhesion is in part stimulated by necessary. exposure of the platelets to the proline and Description of the ulcer characteristics on hyroxyproline matrix of mature collagen and presentation is essential for the mapping of the other connective tissue components ulcer’s progress during treatment. While some exposed by the injury. Muscle wasting occurs. The plantar fat pad characteristics are more important than others, becomes displaced and the metatarsal heads they all have prognostic value during become more prominent. Limited joint mobility management. The presumed etiology of the occurs and contributes to the potential for toe ulcer (i.e, chemical vs mechanical) and and foot injury. If Charcot foot is present, there character of the lesion (neuropathic, ischemic, or are severe bone and joint changes and the foot neuroischemic) should be determined. The is swollen and warm to the touch. evaluation should also describe the size and depth of the ulcer as well as the margins, base, c. Once platelets are exposed to and adhere to and geographic location on the extremity or foot. the connective tissue matrix, the platelets are All but the most superficial ulcers should be activated. This can only occur in the presence of examined with a blunt, sterile probe. The von Willebrand components of factor VIII which description should note whether the sterile probe is released from adjacent endothelial cells. detects sinus tract formation, undermining of the ulcer margins, or dissection of the ulcer into tendon sheaths, bone, or joints. A positive probe 48 T R A I N I N G M A N U A L Module 6 D I A B E T E S P O D I A T R Y I N I T I A T I V E N I G E R I A Activation endothelial cells and uncovering gaps between involves the release of ADP from the platelet. the cells. Histamine is also a powerful The ADP stimulates other platelets to stick to vasodilator. Serotonin released from the platelet one another platelet aggregation. and kinins made from plasma alpha globulins at d. Platelets store calcium and 5- the site of injury, also increase vascular ydroxytryptamine in intracytoplasmic granules as permeability. well as many other growth factors. These are i. Neutrophils, attracted by the chemotaxic released upon adhesion and promote further factors arrive in the wound about 6 hours after platelet aggregation and vasoconstriction. This the injury. They reach their highest numbers at 1- process is termed "degranulation” 2 days post injury. If no infection is present, their e. Platelet stimulation results in activation of numbers decline after this. Neutrophils are phospholipase and hydrolyzed membrane lipids responsible for wound debridement through the and the liberation of arachidonic acid. release of collagenolytic and fibrinolytic Arachidonic acid is converted by platelet enzymes. Additionally, neutrophils ingest cyclo-oxygenase into thromboxane A2. bacteria. Thromboxane A2 further stimulates platelet j. Lymphocytes reach their maximum number in aggregation and is also a potent vasoconstrictor. the wound at day 6. f. Contractile protein in the platelet, The most important role of the lymphocyte is the thrombosthenin, promotes clot retraction. Clot synthesis of lymphokines. Two of the best known retraction will not occur unless platelets are lymphokines are the migration inhibition factor present. (MIF) and macrophage activation factor (MAF). g. Coagulation occurs due to the activation of MIF attacts macrophages to the wound and clotting factors. MAF activates them. i. Intrinsic system k. The macrophages attracted to and activated ii. Extrinsic system in the wound are actually derived from The end result is the activation of factor X which monocytes in the blood. They are the most then converts prothrombin to thrombin. important inflammatory cells involved in Thrombin then converts fibrinogen to fibrin wound healing for the following reasons: monomers, which polymerize to form a fibrin I. They are the only cells able to tolerate the clot. Fibrin besides promoting hemostasis, low oxygen tensions at the wound edge. provides a scaffolding for the ingrowth of cells at ii. They appear in the wound during the first 5 a later stage. days and have a long life span (7-10 days). h. Platelets release a number of other factors at iii. Wound healing is severely inhibited in the this point which promote wound healing. These absence of monocytes. include: iv. They process and present antigens to the i. Proteolytic enzymes activate the complement lymphocytes to initiate immune response. system. Also released is 12-HPETE which in turn l. Migratory fibroblasts originate from stimulates the release of leukotriene B4 an mesenchymal cells near the wound edge. important chemotaxic agent. These cells become bound to the fibrin laid ii. Various platelet derived growth factors which down in the wound and proliferate. They then produce glycoproteins. Collagen promote various components of wound healing. synthesis begins on the 5th day post injury (See below) and lasts 2-4 weeks. h. Other substances in the plasma increase m. Eosinophil concentration reaches a peak in vascular permeability. Histamine is released by the injured area between days 7-14. mast cells. Histamine increases vascular They may be associated with collagen permeability by causing contraction of remodeling and synthesis occurring at the same T R A I N I N G M A N U A L 49 D I A B E T E S P O D I A T R Y I N I T I A T I V E N I G E R I A Module 6 time. There are very few and their role is unclear. capillary buds from blood vessels near the n. Fibronectin is a glycoprotein produced by wound occurs at the same time as the migration fibroblasts, endothelial cells and hepatocytes. of the epidermis. The development of capillaries Among the functions attributed to fibronectin towards the center of the wound may be are: under the influence of growth factors released by I. Fibronectin coats macrophages, aiding in macrophages. As oxygen tension increases with opsonization and the opening of new vascular channels, these phagocytosis. growth factors are inhibited and capillary growth ii. Fibronectin is found on the surface of slows and then stops. fibroblasts, where it may aid on the adhesion c. Collagen Synthesis: of these cells to the extracellular matrix. i. Within the injured dermis, fibroblasts iii. Fibronectin cross-links with collagen and (surgeon's cell) begin to appear at the end of glycosaminoglycans. This results in the inflammatory process, and adhere to the increased adhesion of epidermal cells and endothelial cells to the dermis. dermal collagen and fibrin. As the capillary iv. The matrix formed by fibroblasts and structure returns to the wound and oxygen fibronectin creates a framework over which tension increases, fibroblast replication slows. epidermal cells may migrate.
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