, including open abdominal wounds, wounds of lower extremities, pressure wounds/decubitus ulcers, and exposed bone.
1. +Pathophysiology of woundhealing and factorsaffecting itDr.H.FadaakDr.Mariam AlqurashiKing Fahd Hospital of The University16 Nov 2011
2. +Introduction A wound is a disruption of the normal structure and function of the skinand underlying soft tissue. Acute wounds in normal, healthy individuals heal through an orderlysequence of physiological events that include hemostasis,inflammation, epithelialization, fibroplasia, and maturation. When this process is altered, a chronic wound may develop and ismore likely to occur in patients with underlying disorders such asperipheral artery disease, diabetes, venous insufficiency, nutritionaldeficiencies, and other disease states.
3. +Wound mechanism Wounds are generally classified as acute or chronic. chronic wounds are generally associated with physiologicalimpairments that slow or prevent wound healing. Wounds may be caused by a variety of mechanisms including acuteinjury to the skin (abrasion, puncture, crush), surgery and otheretiologies that cause initially intact skin to break down (eg,ischemia, pressure).
4. +Surgical wounds Surgical wounds are a controlled form of trauma created in theoperating room environment. Classified according to the degree of bacterial load or contaminationof the surgical wound. The categories, clean, clean-contaminated, contaminated, and dirtyare used to predict the risk of surgical wound infection which canimpact wound healing. The majority of clean and clean-contaminated wounds are closedprimarily at the completion of the surgery. Contaminated and dirty wounds (eg, fecal contamination,debridement for wound infection) are typically packed open
5. +Phases of wound healing Wound healing occurs as a cellular response to tissue injury andinvolves activation of keratinocytes, fibroblasts, endothelial cells,macrophages, and platelets. The process involves organized cell migration and recruitment ofendothelial cells for angiogenesis. Many growth factors and cytokines released by these cell typescoordinate and maintain wound healing.
6. + Acute wounds transition through the stages of wound healing as alinear pathway, with clear start- and endpoints. Chronic wounds are arrested in one of these stages, usually theinflammatory stage, and cannot progress further.
7. +Hemostasis Immediately after injury to the skin, small vessels within the woundconstrict to provide at least a measure of hemostasis for 5 to 10minutes. Platelets aggregate in severed vessels and trigger the clottingcascade and release essential growth factors and cytokines that areimportant for the initiation and progression of wound healing (eg,platelet-derived growth factor, transforming growth factor- ).β The fibrin matrix that results stabilizes the wound and provides aprovisional scaffold for the wound healing process.
9. +Inflammation the lag phase because wound strength does not begin to returnimmediately. The inflammatory phase is completed within 3 days, except in thepresence of infection or other causes of wound chronicity. Key components of this phase are increased vascular permeability,and cellular recruitment. The presence of necrotic tissue, foreign material and bacteria resultin the abnormal production of metalloproteases which alter thebalance of inflammation and impair the function of the cytokines
11. +The healing progression of chronic wounds usuallybecomes arrested in this inflammatory stage
12. +Epithelialization also called migration refers to basal cell proliferation and epithelialmigration occurring in the fibrin bridgework inside a clot. it continues until individual cells are surrounded by cells of similartype. In a clean surgical wound, the epithelial cells migrate downward tomeet deep in the dermis. Migration ceases when the layer isrejuvenated; this is normally completed within 48 hours of surgery. The superficial layer of epithelium creates a barrier to bacteria andother foreign bodies. However, it is very thin, easily traumatized, andgives little tensile strength.
14. +Fibroplasia Fibroplasia consists of fibroblast proliferation, accumulation ofground substance, and collagen production. Fibroblasts are transformed from local mesenchymal cells, areusually present in the wound within 24 hours, and predominate bythe 10thpostoperative day. They attach to the fibrin matrix of the clot, multiply, and produceglycoprotein and mucopolysaccharides, which make up groundsubstance.
15. +Fibroplasia Fibroblasts produce contractile proteins.These contractile cells,which are designated myofibroblasts, are present in the woundby the 5thday and have characteristics of smooth muscle cellswith the ability to contract. Myofibroblastic cells are lost via apoptosis as repair resolves toform scar. In pathological fibrosis, myofibroblasts persist and areresponsible for fibrosis via increased matrix synthesis and forcontraction.The exuberant scarring may impede normal organfunction or, in the case of skin, result in keloid.
16. +Fibroplasia Fibroblasts also synthesize collagen, the primary structural proteinof the body. Collagen production begins on the 2ndpostoperative day, when it issecreted as an amorphous gel devoid of strength. Maximum collagen production does not begin until day 5 andcontinues for at least 6 weeks. The developing collagen matrix stimulates angiogenesis. Granulation tissue is the result of the combined production ofcollagen and growth of capillaries
17. +Maturation Key elements of maturation include collagen cross-linking, collagenremodeling, and wound contraction. 5 types of collagen have been identified; types I and III predominate inthe skin and aponeurotic layers. The tensile strength of the wound is directly proportional to theamount of collagen. As disorganized collagen is degraded andreformed, covalent cross-links are formed that enhance tensilestrength.
19. +Maturation Maximum strength depends upon the interconnection of collagensubunits. Approximately 80% of the original strength of the tissue isobtained by 6 weeks after surgery, but the diameter andmorphology of collagen fibers do not have the appearance ofnormal skin until 180 days. Rest and immobility are important during the immediatepostoperative period for successful healing to occur. However, some physical activity is essential during the maturationphase because light tension increases tensile strength byremodeling, which may continue for many years.
20. +Tensile strength The tensile strength of a wound is a measurement of its loadcapacity per unit area. The bursting strength of a wound is the force required tobreak a wound regardless of its dimension. It varies with skinthickness. Peak tensile strength of a wound occurs approximately 60days after injury. A healed wound only reaches approximately 80% of thetensile strength of unwounded skin.
21. +Impaired wound healing There is usually not a single primary factor that contributes toimpaired wound healing There are multiple, smaller contributing issues that can disrupt theprocess.As examples,-local tissue ischemia and neuropathy can impair chemotaxis duringthe hemostasis and inflammatory stages.-Tissue necrosis and infection alter the balance of inflammation andcompete for oxygen.-Uncontrolled periwound edema and wound instability disruptmyofibroblast activity, and collagen deposition and cross-linking.
22. +Risk factors for non-healing Chronic wounds affect a substantial proportion of the population andcontribute to a significant burden in the hospital setting. Certain patients are at risk for development of a non-healing woundsuch as: impaired arterial or venous circulation, immunocompromised states, the elderly, diabetes, and any patient with neuropathy or spinal cord injury
23. + The most common nonhealing wounds affecting the lowerextremities are associated with peripheral artery disease,diabetes and chronic venous insufficiency.Lipscomb, GH, Ling, FG. Wound Healing, Suture Material, and Surgical Instrumentation. In:TeLindes Operative Gynecology, 9th edition, Rock, JA, Jones, HA, III (Eds), 2003. p.233.
24. +Peripheral artery disease Severe peripheral artery disease (PAD) with multilevel arterialobstruction decreases arterial blood flow and diminishes thedelivery of oxygen and nutrients to the tissues, and impairs removalof metabolic waste products. Critical limb ischemia develops when blood flow does not meet themetabolic demands of tissue at rest, and manifests clinically withextremity pain, non-healing wounds or tissue loss.
25. +DM Diabetes is a particularly important risk factor for the development ofchronic wounds because it is associated with vasculopathy,neuropathy and immunopathy. It is frequently associated with severe PAD with atherosclerosisdeveloping at a younger age and affecting more distal arteries. PAD in combination with diabetic neuropathy contributes to higherrates of non-healing ulcers and limb loss in diabetic patientscompared with nondiabetic patients .
26. +DM.. Approximately 15% of patients with diabetes in the United Stateswill develop a foot ulcer. Peripheral artery obstruction is presentin about 20% of these patients, and diabetic neuropathy in about50% with about 30% having both.# Kurd SK, Hoffstad OJ, Bilker WB, Margolis DJ. Evaluation of the use of prognosticinformation for the care of individuals with venous leg ulcers or diabetic neuropathic footulcers. Wound Repair Regen 2009; 17:318.
27. +DM Neuropathy alone can be responsible for the development ofdiabetic foot ulcers. Neuropathy associated with diabetes affects sensory, motor, andautonomic nerves. Sensory neuropathy diminishes the perception of pain that isprotective when tissue injury has occurred. The motor nerves to the intrinsic muscles of the foot are affected inapproximately 50% of patients with diabetes resulting in clawdeformities that transfer pressure to the plantar metatarsal heads. The autonomic neuropathy causes the skin to become dry andsusceptible to skin fissures, tearing and infection due to a loss ofsweat and oil gland function.
28. +DM Over 100 known cytologic factors contribute to impaired woundhealing in patients with diabetes These include decreased or impaired: growth factor production, angiogenic response, macrophage function, collagen accumulation, epidermal barrier function, quantity of granulation tissue, etc
29. +Aging Skin is not excluded from the complex processes of aging. The supply of cutaneous nerves and blood vessels decreases withage, and a general thinning of tissue including dermis andbasement membrane. There is a loss of collagen and ability to produce more collagen.These physiologic changes associated with aging contribute toslowed or impaired wound healing in the elderly
30. +Sickle cell disease Sickle cell disease represents another form of local tissueischemia at the specific location of the wound. It is also obstructive in nature, similar to chronic peripheral arterydisease, but is caused by dysmorphic RBCs physically occludingsmall vessels, usually of the lower extremities. The location and appearance of sickle cell wounds may besimilar to ischemic and venous ulcerations. sickle cell wounds are known to progress much slower throughwound healing and carry an increased risk of reoccurrence
31. +Chemotherapy The administration of chemotherapy may have a detrimental effecton wound healing, specifically through its effects on vascularendothelial growth factor (VEGF). VEGF is an important factor contributing to angiogenesis during theearly stages of wound healing, but may also be an importantregulator in malignancy, and thus, is a target of cancer therapy. Similar to these effects, any patient on immunosuppressive therapy isat an increased risk for the development of chronic wounds andwound infection
32. +Radiation therapy Radiation therapy has evolved as a powerful tool for tumor control as a soletherapy or administered perioperatively. More than 50% of cancer patients receive some form of radiation treatmentand, despite improvements in radiation technique, radiation-inducedinjury still contributes to poor wound healing. The term “radiation injury” refers to the morphologic and functionalchanges that can occur in noncancerous tissue as a direct result of ionizingradiation and may include apoptosis with low doses of radiation, oroutright tissue necrosis with higher doses of radiation.
33. +Radiation therapy Irradiated skin in the chronic stage is thin, hypovascular, extremelypainful, and easily injured by slight trauma or infection Skin ulcers due to radiation injury are more commonly delayed inpresentation and are due to ischemic tissue changes. Characteristic features of delayed radiation injury includetelangiectasia and eccentric myointimal proliferation in the smallarteries and arterioles. These ulcers heal very slowly and may persist for several years.
34. +Spinal cord disease &immobilization Patients undergoing periods of prolonged immobilization,particularly those with spinal cord disease, are at an increased riskfor the development of chronic wounds. These are typically pressure wounds, similar in pathogenesis andappearance to neuropathic wounds occurring in areas of bonyprominence such as the sacrum, knees, ankle malleoli and heels.
35. +Malnutrition Nutrition is an important component of wound healing. Several studies have indicated that nutrient deficiencies are moreprevalent and cause delayed healing in patients with wounds. The exact role for nutrition and nutritional supplementation in themanagement of wounds remains uncertain
36. +Malnutrition Vitamin C is a cofactor for the collagen cross-linkingLack of available vitamin C or scurvy impedes thehydroxylation and, consequently, the collagen fails toaggregate into fibers. Vitamin A potentiates epithelial repair and collagensynthesis by enhancing inflammatory reactions, particularlymacrophage availability. Minerals also may affect healing; zinc deficiency reducesthe rate of epithelialization and retards cellular proliferationand collagen synthesis.
37. +Infection The presence of infection impairs several steps of the woundhealing process. Bacteria produce inflammatory mediators that inhibit theinflammatory phase of wound healing and preventepithelialization.
38. +Recent developments that canexpedite healing of wounds
39. +Negative Pressure Wound Therapy also called vacuum-assisted wound closure, refers to wound dressingsystems that continuously or intermittently apply subatmosphericpressure to the surface of a wound NPWT has dramatically changed the surgical approach and time toheal a wide variety of complex and difficult wounds.
40. +Negative Pressure Wound Therapy NPWT exerts its effect through direct and indirect effects ofsubatmospheric pressure. These effects include stabilization of the wound environment, increased blood flow and deformation of the wound. Deformation is a powerful stimulus for cellular processesthat stimulate granulation tissue and accelerate woundhealing.
41. +Negative Pressure Wound Therapy Advantages: provides a close to ideal environment for temporizing coverage. provides a moist environment and promotes and accelerates thegrowth of healthy granulation tissue while decreasing thepresence of infectious agents used effectively in a variety of wounds can be used as a longer-term dressing its use has decreased the need for secondary amputations remove excess fluid and promote wound contraction
42. +Technique of VAC fluid evacuationVacuum-assisted wound closure.The foam insert (sponge) within thewound and covered by a clear, vapor permeable, plastic dressing.Continuous subatmospheric pressure (suction) applied through thetube causes fluid to flow out of the wound (arrows).
44. +Expedited Wound Healing with Noncontact, Low-FrequencyUltrasound Therapy in Chronic Wounds: A RetrospectiveAnalysisKavros SJ, Liedl DA, Boon AJ, Miller JL, Hobbs JA, Andrews KL. Advances in Skin & WoundCare.Vol. 21 no. 9. September 2008Study Overview:This was a retrospective observational study that assessed theclinical role of MIST Therapy® in the treatment of chroniclower-extremity wounds including venous leg ulcers, ischemiclower extremity ulcers, neuropathic lower extremity ulcers andmulti-factorial ulcers. It included 210 patients: 163 whose treatment included MISTTherapy plus standard of care and 47 who received onlystandard of care.
45. +Accelerating the Rate of Healing MIST Therapy uses low-frequency ultrasound to stimulate cells atand below the wound surface to activate healing. A painless procedure The system creates low-frequency ultrasound waves that produceand propel a gentle mist of sterile saline into the wound bed.Thesaline mist improves the transfer of ultrasound from the devicewithout contact or pain to the patient. MIST Therapy promotes painless wound healing through:• Active cell stimulation • Decreased bioburden• Increased blood flow • Cleansing and gentle debridement
46. +MIST therapy..
47. +Key findings.. WOUND REDUCTION was achieved in 72% of patient usingMIST therapy vs 46% of wounds treated using standard ofcare alone. (P=.002) WOUND CLOSURE ws achieved in 70% of all wounds treatedwith MIST therapy as compared to 20% of wounds treatedwith SOC alone (P=.04) 50% of wound treated with thrice weekly MIST therapyhealed over a mean of 147 days. Just 32% of wounds treated with SOC alone healed over amean 134 days. (P = .009)
48. +Summary A wound is a disruption of the normal structure and function of theepidermis Wounds may be caused by a variety of mechanisms includingacute injury, surgery or other factors There is no specific time frame that distinguishes between acuteand chronic wounds. Chronic wounds are associated with physiologic derangementsthat impair the wound healing process.
49. +Summary After hemostasis has been achieved, acute wounds normally heal inan orderly and efficient manner characterized by four distinct, butoverlapping, phases: inflammation, epithelialization, fibroplasia,and maturation. Many disease states alter the process of wound healing, the mostcommon of which are PAD, DM, and chronic venous disease. vacuum-assisted closure, is an adjunctive therapy used in themanagement of open wounds that applies subatmospheric pressureto the wound surface.