pathophysiology of wound healing

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+ Pathophysiology of wound healing and factors affecting it Dr.H.Fadaak Dr.Mariam Alqurashi King Fahd Hospital of The University 16 Nov 2011

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Pathophysiology of wound healing and factors affecting it.

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Page 1: Pathophysiology of wound healing

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Pathophysiology of wound healing and factors affecting itDr.H.FadaakDr.Mariam AlqurashiKing Fahd Hospital of The University16 Nov 2011

Page 2: Pathophysiology of wound healing

+Introduction

A wound is a disruption of the normal structure and function of the skin and underlying soft tissue.

Acute wounds in normal, healthy individuals heal through an orderly sequence of physiological events that include hemostasis, inflammation, epithelialization, fibroplasia, and maturation.

When this process is altered, a chronic wound may develop and is more likely to occur in patients with underlying disorders such as peripheral artery disease, diabetes, venous insufficiency, nutritional deficiencies, and other disease states.

Page 3: Pathophysiology of wound healing

+Wound mechanism

Wounds are generally classified as acute or chronic.

chronic wounds are generally associated with physiological impairments that slow or prevent wound healing.

Wounds may be caused by a variety of mechanisms including acute injury to the skin (abrasion, puncture, crush), surgery and other etiologies that cause initially intact skin to break down (eg, ischemia, pressure).

Page 4: Pathophysiology of wound healing

+Surgical wounds

Surgical wounds are a controlled form of trauma created in the operating room environment.

Classified according to the degree of bacterial load or contamination of the surgical wound.

The categories, clean, clean-contaminated, contaminated, and dirty are used to predict the risk of surgical wound infection which can impact wound healing.

The majority of clean and clean-contaminated wounds are closed primarily at the completion of the surgery.

Contaminated and dirty wounds (eg, fecal contamination, debridement for wound infection) are typically packed open

Page 5: Pathophysiology of wound healing

+Phases of wound healing

Wound healing occurs as a cellular response to tissue injury and involves activation of keratinocytes, fibroblasts, endothelial cells, macrophages, and platelets.

The process involves organized cell migration and recruitment of endothelial cells for angiogenesis.

Many growth factors and cytokines released by these cell types coordinate and maintain wound healing.

Page 6: Pathophysiology of wound healing

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Acute wounds transition through the stages of wound healing as a linear pathway, with clear start- and endpoints.

Chronic wounds are arrested in one of these stages, usually the inflammatory stage, and cannot progress further.

Page 7: Pathophysiology of wound healing

+Hemostasis

Immediately after injury to the skin, small vessels within the wound constrict to provide at least a measure of hemostasis for 5 to 10 minutes.

Platelets aggregate in severed vessels and trigger the clotting cascade and release essential growth factors and cytokines that are important 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 a provisional scaffold for the wound healing process.

Page 8: Pathophysiology of wound healing

+Hemostasis

Page 9: Pathophysiology of wound healing

+Inflammation

the lag phase because wound strength does not begin to return immediately.

The inflammatory phase is completed within 3 days, except in the presence 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 result in the abnormal production of metalloproteases which alter the balance of inflammation and impair the function of the cytokines

Page 10: Pathophysiology of wound healing

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Page 11: Pathophysiology of wound healing

+The healing progression of chronic wounds usually becomes arrested in this inflammatory stage

Page 12: Pathophysiology of wound healing

+Epithelialization

also called migration refers to basal cell proliferation and epithelial migration occurring in the fibrin bridgework inside a clot.

it continues until individual cells are surrounded by cells of similar type.

In a clean surgical wound, the epithelial cells migrate downward to meet deep in the dermis. Migration ceases when the layer is rejuvenated; this is normally completed within 48 hours of surgery.

The superficial layer of epithelium creates a barrier to bacteria and other foreign bodies. However, it is very thin, easily traumatized, and gives little tensile strength.

Page 13: Pathophysiology of wound healing

+Epithelialization

Page 14: Pathophysiology of wound healing

+Fibroplasia

Fibroplasia consists of fibroblast proliferation, accumulation of ground substance, and collagen production.

Fibroblasts are transformed from local mesenchymal cells, are usually present in the wound within 24 hours, and predominate by the 10th postoperative day.

They attach to the fibrin matrix of the clot, multiply, and produce glycoprotein and mucopolysaccharides, which make up ground substance.

Page 15: Pathophysiology of wound healing

+Fibroplasia

Fibroblasts produce contractile proteins. These contractile cells, which are designated myofibroblasts, are present in the wound by the 5th day and have characteristics of smooth muscle cells with the ability to contract.

Myofibroblastic cells are lost via apoptosis as repair resolves to form scar.

In pathological fibrosis, myofibroblasts persist and are responsible for fibrosis via increased matrix synthesis and for contraction. The exuberant scarring may impede normal organ function or, in the case of skin, result in keloid.

Page 16: Pathophysiology of wound healing

+Fibroplasia

Fibroblasts also synthesize collagen, the primary structural protein of the body.

Collagen production begins on the 2nd postoperative day, when it is secreted as an amorphous gel devoid of strength.

Maximum collagen production does not begin until day 5 and continues for at least 6 weeks.

The developing collagen matrix stimulates angiogenesis.

Granulation tissue is the result of the combined production of collagen and growth of capillaries

Page 17: Pathophysiology of wound healing

+Maturation

Key elements of maturation include collagen cross-linking, collagen remodeling, and wound contraction.

5 types of collagen have been identified; types I and III predominate in the skin and aponeurotic layers.

The tensile strength of the wound is directly proportional to the amount of collagen. As disorganized collagen is degraded and reformed, covalent cross-links are formed that enhance tensile strength.

Page 18: Pathophysiology of wound healing

+Maturation

Page 19: Pathophysiology of wound healing

+Maturation

Maximum strength depends upon the interconnection of collagen subunits.

Approximately 80% of the original strength of the tissue is obtained by 6 weeks after surgery, but the diameter and morphology of collagen fibers do not have the appearance of normal skin until 180 days.

Rest and immobility are important during the immediate postoperative period for successful healing to occur.

However, some physical activity is essential during the maturation phase because light tension increases tensile strength by remodeling, which may continue for many years.

Page 20: Pathophysiology of wound healing
Page 21: Pathophysiology of wound healing
Page 22: Pathophysiology of wound healing

+Tensile strength

The tensile strength of a wound is a measurement of its load capacity per unit area.

The bursting strength of a wound is the force required to break a wound regardless of its dimension. It varies with skin thickness.

Peak tensile strength of a wound occurs approximately 60 days after injury.

A healed wound only reaches approximately 80% of the tensile strength of unwounded skin.

Page 23: Pathophysiology of wound healing

+Impaired wound healing

There is usually not a single primary factor that contributes to impaired wound healing

There are multiple, smaller contributing issues that can disrupt the process.

As examples,

-local tissue ischemia and neuropathy can impair chemotaxis during the hemostasis and inflammatory stages.

-Tissue necrosis and infection alter the balance of inflammation and compete for oxygen.

-Uncontrolled periwound edema and wound instability disrupt myofibroblast activity, and collagen deposition and cross-linking.

Page 24: Pathophysiology of wound healing

+Risk factors for non-healing

Chronic wounds affect a substantial proportion of the population and contribute to a significant burden in the hospital setting.

Certain patients are at risk for development of a non-healing wound such as:

impaired arterial or venous circulation,

immunocompromised states,

the elderly,

diabetes, and

any patient with neuropathy or spinal cord injury

Page 25: Pathophysiology of wound healing

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The most common nonhealing wounds affecting the lower extremities are associated with peripheral artery disease, diabetes and chronic venous insufficiency.

Lipscomb, GH, Ling, FG. Wound Healing, Suture Material, and Surgical Instrumentation. In: TeLinde's Operative Gynecology, 9th edition, Rock, JA, Jones, HA, III (Eds), 2003. p.233.

Page 26: Pathophysiology of wound healing

+Peripheral artery disease

Severe peripheral artery disease (PAD) with multilevel arterial obstruction decreases arterial blood flow and diminishes the delivery of oxygen and nutrients to the tissues, and impairs removal of metabolic waste products.

Critical limb ischemia develops when blood flow does not meet the metabolic demands of tissue at rest, and manifests clinically with extremity pain, non-healing wounds or tissue loss.

Page 27: Pathophysiology of wound healing

+DM

Diabetes is a particularly important risk factor for the development of chronic wounds because it is associated with vasculopathy, neuropathy and immunopathy.

It is frequently associated with severe PAD with atherosclerosis developing at a younger age and affecting more distal arteries.

PAD in combination with diabetic neuropathy contributes to higher rates of non-healing ulcers and limb loss in diabetic patients compared with nondiabetic patients .

Page 28: Pathophysiology of wound healing

+DM..

Approximately 15% of patients with diabetes in the United States will develop a foot ulcer. Peripheral artery obstruction is present in about 20% of these patients, and diabetic neuropathy in about 50% with about 30% having both.

# Kurd SK, Hoffstad OJ, Bilker WB, Margolis DJ. Evaluation of the use of prognostic information for the care of individuals with venous leg ulcers or diabetic neuropathic foot ulcers. Wound Repair Regen 2009; 17:318.

Page 29: Pathophysiology of wound healing

+DM

Neuropathy alone can be responsible for the development of diabetic foot ulcers.

Neuropathy associated with diabetes affects sensory, motor, and autonomic nerves.

Sensory neuropathy diminishes the perception of pain that is protective when tissue injury has occurred.

The motor nerves to the intrinsic muscles of the foot are affected in approximately 50% of patients with diabetes resulting in claw deformities that transfer pressure to the plantar metatarsal heads.

The autonomic neuropathy causes the skin to become dry and susceptible to skin fissures, tearing and infection due to a loss of sweat and oil gland function.

Page 30: Pathophysiology of wound healing

+DM

Over 100 known cytologic factors contribute to impaired wound healing 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

Page 31: Pathophysiology of wound healing

+Aging

Skin is not excluded from the complex processes of aging.

The supply of cutaneous nerves and blood vessels decreases with age, and a general thinning of tissue including dermis and basement membrane.

There is a loss of collagen and ability to produce more collagen. These physiologic changes associated with aging contribute to slowed or impaired wound healing in the elderly

Page 32: Pathophysiology of wound healing

+Sickle cell disease

Sickle cell disease represents another form of local tissue ischemia at the specific location of the wound.

It is also obstructive in nature, similar to chronic peripheral artery disease, but is caused by dysmorphic RBCs physically occluding small vessels, usually of the lower extremities.

The location and appearance of sickle cell wounds may be similar to ischemic and venous ulcerations.

sickle cell wounds are known to progress much slower through wound healing and carry an increased risk of reoccurrence

Page 33: Pathophysiology of wound healing

+Chemotherapy

The administration of chemotherapy may have a detrimental effect on wound healing, specifically through its effects on vascular endothelial growth factor (VEGF).

VEGF is an important factor contributing to angiogenesis during the early stages of wound healing, but may also be an important regulator in malignancy, and thus, is a target of cancer therapy.

Similar to these effects, any patient on immunosuppressive therapy is at an increased risk for the development of chronic wounds and wound infection

Page 34: Pathophysiology of wound healing

+Radiation therapy

Radiation therapy has evolved as a powerful tool for tumor control as a sole therapy or administered perioperatively.

More than 50% of cancer patients receive some form of radiation treatment and, despite improvements in radiation technique, radiation-induced injury still contributes to poor wound healing.

The term “radiation injury” refers to the morphologic and functional changes that can occur in noncancerous tissue as a direct result of ionizing radiation and may include apoptosis with low doses of radiation, or outright tissue necrosis with higher doses of radiation.

Page 35: Pathophysiology of wound healing

+Radiation therapy

Irradiated skin in the chronic stage is thin, hypovascular, extremely painful, and easily injured by slight trauma or infection

Skin ulcers due to radiation injury are more commonly delayed in presentation and are due to ischemic tissue changes.

Characteristic features of delayed radiation injury include telangiectasia and eccentric myointimal proliferation in the small arteries and arterioles.

These ulcers heal very slowly and may persist for several years.

Page 36: Pathophysiology of wound healing

+Spinal cord disease & immobilization

Patients undergoing periods of prolonged immobilization, particularly those with spinal cord disease, are at an increased risk for the development of chronic wounds.

These are typically pressure wounds, similar in pathogenesis and appearance to neuropathic wounds occurring in areas of bony prominence such as the sacrum, knees, ankle malleoli and heels.

Page 37: Pathophysiology of wound healing

+Malnutrition

Nutrition is an important component of wound healing.

Several studies have indicated that nutrient deficiencies are more prevalent and cause delayed healing in patients with wounds.

The exact role for nutrition and nutritional supplementation in the management of wounds remains uncertain

Page 38: Pathophysiology of wound healing

+Malnutrition

Vitamin C is a cofactor for the collagen cross-linking

Lack of available vitamin C or scurvy impedes the hydroxylation and, consequently, the collagen fails to aggregate into fibers.

Vitamin A potentiates epithelial repair and collagen synthesis by enhancing inflammatory reactions, particularly macrophage availability.

Minerals also may affect healing; zinc deficiency reduces the rate of epithelialization and retards cellular proliferation and collagen synthesis.

Page 39: Pathophysiology of wound healing

+Infection

The presence of infection impairs several steps of the wound healing process.

Bacteria produce inflammatory mediators that inhibit the inflammatory phase of wound healing and prevent epithelialization.

Page 40: Pathophysiology of wound healing

+Recent developments that can expedite healing of wounds

Page 41: Pathophysiology of wound healing

+Negative Pressure Wound Therapy

also called vacuum-assisted wound closure, refers to wound dressing systems that continuously or intermittently apply subatmospheric pressure to the surface of a wound

NPWT has dramatically changed the surgical approach and time to heal a wide variety of complex and difficult wounds.

Page 42: Pathophysiology of wound healing

+Negative Pressure Wound Therapy

NPWT exerts its effect through direct and indirect effects of subatmospheric pressure.

These effects include

stabilization of the wound environment,

increased blood flow and deformation of the wound.

Deformation is a powerful stimulus for cellular processes that stimulate granulation tissue and accelerate wound healing.

Page 43: Pathophysiology of wound healing

+Negative Pressure Wound Therapy

Advantages:

provides a close to ideal environment for temporizing coverage.

provides a moist environment and promotes and accelerates the growth of healthy granulation tissue while decreasing the presence 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

Page 44: Pathophysiology of wound healing

+Technique of VAC fluid evacuation

Vacuum-assisted wound closure. The foam insert (sponge) within the wound and covered by a clear, vapor permeable, plastic dressing. Continuous subatmospheric pressure (suction) applied through the tube causes fluid to flow out of the wound (arrows).

Page 45: Pathophysiology of wound healing

+Contraindications..

Exposed vital structures

Ongoing infection

Devitalized tissue

Malignant tissue

Fragile skin

Adhesive allergy

Ischemic wounds

Page 46: Pathophysiology of wound healing

+Expedited Wound Healing with Noncontact, Low-Frequency Ultrasound Therapy in Chronic Wounds: A Retrospective Analysis Kavros SJ, Liedl DA, Boon AJ, Miller JL, Hobbs JA, Andrews KL. Advances in Skin & Wound Care. Vol. 21 no. 9. September 2008

Study Overview:

This was a retrospective observational study that assessed the clinical role of MIST Therapy® in the treatment of chronic lower-extremity wounds including venous leg ulcers, ischemic lower extremity ulcers, neuropathic lower extremity ulcers and multi-factorial ulcers.

It included 210 patients: 163 whose treatment included MIST Therapy plus standard of care and 47 who received only standard of care.

Page 47: Pathophysiology of wound healing

+Accelerating the Rate of Healing

MIST Therapy uses low-frequency ultrasound to stimulate cells at and below the wound surface to activate healing.

A painless procedure

The system creates low-frequency ultrasound waves that produce and propel a gentle mist of sterile saline into the wound bed. The saline mist improves the transfer of ultrasound from the device without 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

Page 48: Pathophysiology of wound healing

+MIST therapy..

Page 49: Pathophysiology of wound healing

+Key findings..

WOUND REDUCTION was achieved in 72% of patient using MIST therapy vs 46% of wounds treated using standard of care alone. (P=.002)

WOUND CLOSURE ws achieved in 70% of all wounds treated with MIST therapy as compared to 20% of wounds treated with SOC alone (P=.04)

50% of wound treated with thrice weekly MIST therapy healed over a mean of 147 days.

Just 32% of wounds treated with SOC alone healed over a mean 134 days. (P = .009)

Page 50: Pathophysiology of wound healing

+Summary

A wound is a disruption of the normal structure and function of the epidermis

Wounds may be caused by a variety of mechanisms including acute injury, surgery or other factors

There is no specific time frame that distinguishes between acute and chronic wounds.

Chronic wounds are associated with physiologic derangements that impair the wound healing process.

Page 51: Pathophysiology of wound healing

+Summary

After hemostasis has been achieved, acute wounds normally heal in an orderly and efficient manner characterized by four distinct, but overlapping, phases: inflammation, epithelialization, fibroplasia, and maturation.

Many disease states alter the process of wound healing, the most common of which are PAD, DM, and chronic venous disease.

vacuum-assisted closure, is an adjunctive therapy used in the management of open wounds that applies subatmospheric pressure to the wound surface.

Page 52: Pathophysiology of wound healing

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