URGO MEDICAL

A wound interrupts skin continuity and integrity. It may be the result of trauma, minor or severe, or of a pathological process.

Wounds can be classified depending on the damage of the different skin layers.
The healing prognosis can be very different depending on the depth and lesions.

There are two types of wounds:

• acute wounds (post traumatic wounds, burns, skin tears etc)
• chronic wounds (leg ulcers, pressure ulcers, diabetic foot ulcers)

For more information please visit the "Wound Healing Theory/Types of Wounds" section.

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The complex healing process can be divided into 3 to 5 phases, depending on whether or not haemostasis is included in the inflammatory phase and wether the re-epithelialisation phase is included in the proliferative stage. Furthermore, these different phases overlap with one another, to a certain degree. However, all the different phases overlap with one another.

• Inflammation stage
• Granulation stage
• Remoduling stage

For more information please visit the "Wound Healing Theory/Healing Process" section.

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THE INFLAMMATORY PHASE begins immediately and lasts for a few hours to a few days in acute wounds. This process can last for several weeks or even months in chronic wounds (leg ulcers, pressure ulcers, diabetic foot ulcers) and is sustained by the disease that initiated the chronic wound.

The clot formed after the rupture of blood vessels covers the wound and forms a temporary extracellular matrix – composed of fibrin and fibronectin – which seals the wound and minimises blood loss and helps to guide cell migration. Platelets secrete and activate mediators to recruit inflammation cells (polynuclear neutrophils and macrophages), fibroblasts and endothelial cells. Bleeding is controlled at the end of the inflammatory phase, and the wound bed is cleaned through phagocytosis.

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THE PROLIFERATIVE PHASE can begin quickly with the proliferation of endothelial cells and fibroblasts to lead to the formation of new blood vessels (angiogenesis) and the synthesis of a new extracellular matrix (ECM). As the new ECM is re-modelled, the existing matrix is degraded by a number of Proteases, enzymes known as Matrix Metalloproteinase’s (MMP’s); MMP’s help with autolytic debridement (cleansing) of the wound, and cell migration. Their levels increase within the wound after injury & decrease when the wound is bacteria free. The fibroblasts then acquire the morphology and biochemical characteristics of smooth muscle cells to become myofibroblasts. This essential differentiation phenomenon takes place under the influence of cytokines and growth factors released during the previous phase. The myofibroblasts are the main cells responsible for synthesis of the extracellular matrix and contribute to reorganisation of this matrix as the wound contracts. The extracellular matrix plays an important controlling role because some factors may be stored in latent form and activated when they are released. Re-epithelialisation occurs to close the wound with the migration of epithelial cells starting from the edges of the wound and skin appendages. Differentiation of keratinocytes then helps to restore the barrier function of the epidermis.

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THE MATURATION PHASE will last for several months and will result in the final scar. This phase begins early, during the formation of the granulation tissue, with progressive reorganisation of the matrix under the influence of myofibroblasts. These cells contract their microfilament bundles, which are bonded to the extracellular matrix, causing compaction of the collagen network and contraction of the wound. New components are then secreted to increase the density of the matrix and to stabilise it. The proportion of the different types of collagen changes: the proportion of type I collagen increases, while the proportion of type III collagen decreases (from 30% to 10%). The cell density of myofibroblasts is reduced by apoptosis to leave room for fibroblasts, which will strengthen the extracellular matrix, giving better resistance to mechanical forces.

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Colonisation is caused by the presence of bacteria within the wound, without this leading to an inflammatory response. Most colonisation of acute wounds is composed of streptococci and staphylococci, which are already, present on normal healthy skin. The bacterial population in chronic wounds (leg ulcers, pressure ulcers, diabetic foot ulcers) is much more varied. It is composed of the commensal skin bacteria such as Staphylococcus (S. aureus, coagulase-negative staphylococci), corynebacteria, α-haemolytic streptococci.
After microorganisms have multiplied within the wound and bonded to epithelial cells, equilibrium is set up between the patient and his/her microbial flora.
Microorganisms remain on the surface of the wound and form a biofilm.
Quantitatively, normal colonisation is defined by a bacterial count of 10 ^<>5/mm3. If the number of bacteria exceeds this figure, it is referred to as critical colonisation, even if there is no obvious inflammation. The presence of large quantities of bacteria hinders the natural healing process and delays it.
Since routine examinations do not always include bacteriological sampling, clinical signs can also suggest bacterial colonisation : the abundance and thickening of foul-smelling exudate, spontaneous pain, erythema around the lesion and oedema.

For more information please visit the "Wound Healing Theory/Infection" section.

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The term infection is used when the presence of microorganisms leads to a local, regional or general inflammatory response with clinical symptoms.

This is due to several factors:

• Large quantities of microorganisms present
• Bacterial virulence
• Reduction in the patient’s immune defence mechanism

The local or systemic clinical symptoms are: local inflammation, heat, odour, pain, pus, fever, inflammatory response, healing halted, wounds that are worsening, deterioration of the wound …

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The antibacterial properties of silver have been widely recognized and exploited since ancient times. Modern medicine has made great use of silver in the form of silver nitrate sulphadiazine, in the prevention and treatment of infection in both acute and chronic wounds.
In the case of chronic wounds (leg ulcers, pressure ulcers, diabetic foot ulcers), secondary infection can delay healing as a result of local inflammatory reaction. In this context, silver salts are used in the treatment of wounds with a high bacterial colonisation due to their antibacterial and local anti-inflammatory properties. In recent years, numerous protocols have been recommended to treat acute or chronic wounds, in the form of creams or dressings containing silver.
The silver ion has a broad spectrum of activity that covers almost all microorganisms associated with the colonisation of chronic wounds. It acts on numerous targets and is bactericidal at very low concentrations, thereby minimising the potential risk of resistance.

Finally, Silver has no cytotoxicity that hinders the healing process.

For more information please visit the «Wound Healing Theory/Infection» section.

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Silver is only active in its Ag+ ionic form. It is neither a genuinely antiseptic nor a genuinely antibiotic treatment and for this reason it is classified as an antibacterial agent.

Several characteristics of the Ag+ ion are specific in making the emergence of resistant strains difficult:

• provides bactericidal action due to the Ag+ ion
• develops many actions targeted at the bacteria
• inhibits the bacterial DNA replication process
• reduces the wall strength
• increases the permeability of the bacterial cytoplasmic membrane inhibits the respiratory enzymes causing asphyxia of the bacteria  

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Systemic effects are rare, but one significant systemic occurrence should be noted: argyria (severe burn victims, infants).

Hyperpigmentation and argyria are due to deposition of Silver, usually characterised by a slate grey colour of the skin. The reported cases indicate that a large quantity of Silver needs to be absorbed through the skin.

To date, there have been no documented cases of resistance to silver ions.

For more information please visit our «Wound Healing Theory/Infection» section.

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An acute wound occurs on a site with normal trophicity at a specific time from a known mechanism (burn, cut, etc.). Its depth is variable depending on the type of trauma and it automatically leads to a loss of cutaneous substance.
Acute wounds are classified into several categories:

• Clean wounds with no loss of substance
• Extensive superficial wounds or skin abrasion
• Full thickness wounds with loss of substance

Examples: burns, dermabrasions, traumatic wounds, surgical wounds and etc.

For more information please visit our «Wound Healing Theory/Types of wounds» section

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A chronic wound is the loss of cutaneous substance resulting from a pathological process which progresses over an indeterminate time period.

There are different types of chronic wounds: leg ulcers (venous, arterial or mixed), pressure ulcers and diabetic foot ulcers

For more information please visit our «Wound Healing Theory/Types of wounds» section

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A pressure ulcer is an ischaemic necrosis of the skin and subcutaneous tissue caused by unrelieved and prolonged vascular compression on a specific area of the body, usually between a bony prominences and a supporting item such as a bed or chair

This external pressure is transmitted through the support (bed, armchair) and affects the part of the body bearing the support. The extent of the pressure ulcer depends on several factors, particularly the intensity of the pressure, the duration, the resistance of the tissue to pressure and the general condition of the patient.
Locally, tissue damage is the result of three forces:

• Shear
• Pressure
• Friction

For more information please visit our «Wound Healing Theory/Types of wounds/Chronic wounds» section

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Pressure
Pressure is a perpendicular force applied to a specific area of living tissue. This pressure is applied particularly on bony prominences. Where soft tissues between the bone relief and the underlying support are compressed. These forces correspond to the distribution of the body weight over the contact surface area.

Friction
These are forces applied between two surfaces in contact with each other and moving relative to each other. These forces are often responsible for the initial skin abrasion.

Shear
These are forces that cause slip and torsion of the subcutaneous layers. They exist especially in an unstable semi-seated position in which subcutaneous layers are subject to a kneading type force.

For more information please visit our «Wound Healing Theory/Types of wounds/Chronic wounds» section

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Age

• Elderly patients have a greater risk of developing a pressure ulcer.

Poor skin condition

• Skin resistance is reduced with age, long-term corticosteroid treatment and deficiency conditions.

Conditions that reduce sensitivity

• Impaired sensitivity and motor control
• Anaesthesia, hypaesthesia
• Spinal and neurological conditions
• Neurological disorders, which prevent pain signals, associated with excessive weight bearing and reflex actions leading to a position change

Concomitant diseases

• Hypoxia due to arterial disease and/or venous return anomalies, diabetes
• Cancer, infection, anaemia and hyperthermia are all risk factors.

Incontinence

• Maceration due to both urinary and faecal incontinence may cause skin abrasions.

Nutritional status

• Malnutrition appears to be a major risk factor in the development of pressure ulcers. All pressure ulcer treatment must be accompanied by appropriate dietary management.

For more information please visit our «Wound Healing Theory/Types of wounds/Chronic wounds» section

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Pressure ulcers can be broken down into four stages. It is important to consider the four stages as being four manifestations of the pressure ulcer, and not four phases that necessarily follow each other. In some patients, a pressure ulcer can begin with a phlyctena (blister) or a superficial wound, or even a deep lesion (ie a black necrotic patch on the heel). A pressure ulcer can sometimes develop into a black necrosed spot (deep pressure ulcer).

For more information please visit our «Wound Healing Theory/Types of wounds/Chronic wounds» section

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A leg ulcer is a loss of skin tissue usually originating from an arterial or venous circulatory disorder.

Other causes such as diabetic ulcers, angio-necrotic ulcers, blood diseases or cancers, are more unusual.

For more information please visit our «Wound Healing Theory/Types of wounds/Chronic wounds» section.

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Assessment of the condition of the vascular system will give information about blood perfusion in the lower limbs and concerns the narrow arterial, venous and microcirculation component. These examinations provide additional essential information complementary to the clinical examination. (continuous doppler, ultrasonography, arteriography).

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Chronic, painless and clean ulceration, usually located under the head of the 2nd or 3rd metatarsal bone in the foot or on any other point of normal or abnormal pressure on the underside of the foot. It is usually secondary to a reduction or disappearance in sensitivity, within the context of a diabetic angiopathy and neuropathy or deformation of the foot posture. It is readily complicated by infections, abscesses or osteitis.

For more information please visit our «Wound Healing Theory/Types of wounds/Chronic wounds» section »

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Wound healing, or wound repair, is the body's natural process of regenerating dermal and epidermal tissue. When an individual is wounded, a set of complex biochemical events takes place in a closely orchestrated cascade to repair the damage.

There are three main stages in wound healing:

• Inflammation stage
• Proliferative stage
• Maturation stage

To find out more please visit our «Wound Healing Theory/Wound healing principles» section.

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Natural healing takes place in a moist wound environment. Cellular and molecular elements migrate and develop more effectively in these conditions. This was demonstrated in 1962 by Winter, who proved that healing under a synthetic semi-occlusive dressing is faster than when a wound left open to the air.
Moist wound healing is 30% faster than wound healing in a dry environment.
Healing in a moist environment encourages the proliferation of fibroblasts, which synthesise the elements of the new Dermal Extracellular Matrix (collagen and elastin fibre) enabling wound healing.

To find out more please visit our «Wound Healing Theory/Wound healing principles» section.

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The required time for the complete healing of chronic wounds (leg ulcers, pressure ulcers, diabetic foot ulcers) remains extremely variable according to various clinical studies.

Nevertheless, it was observed that for certain wounds, this time may be abnormally prolonged and despite of an aetiological appropriate wound management. In some chronic wounds, complete healing can never be achieved.
Factors, which can "delay wound healing « have a negative effect on the evolution of the wound healing process and can lead to the risk of infection. They can also be responsible for the deterioration of patient’s quality of life and cause huge expenditure for the healthcare community. A certain number of local and general factors have now been identified, which allow an understanding of which type of wounds may present with a risk of delayed healing and which patients present with unfavourable conditions, which can also delay the healing process.

For more information please visit our section « Wound Healing Theory/Wound healing principles» or our website www.urgostart.com.

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Risk factors of delayed healing have been shown to have a negative influence on the wound healing process potentially resulting in a poor outcome. These factors can be modified to varying degrees and can be defined in two categories:

• Wound-related risk factors: wound surface area, depth, location, duration of the wound, recurrence, appearance of the wound bed (fibrin content > 50%, necrosed tissue content, presence of calcification), medical history (venous disease, DVT, varicose vein surgery, phlebitis, thrombosis, tissue hypoxia, arterial disorders (ABPI < 0.8), previous local treatments: lack of compression, inability to weight-bear, poor healing rate at 3-4 weeks.
• Patient-related risk factors: concomitant conditions (hip or knee surgery, poor joint mobility, ankylosis, difficulty walking, oedema of the lower limbs, etc.), general condition of the patient (Peripheral Arterial Occlusive Disease (PAOD), poor nutrition (obesity / malnutrition), sedentary lifestyle, poor hygiene, diabetes, immunodeficiency, etc.), age, sex.

And there are maybe other factors, such as infection, non-concordance with previous treatment, depression.

For more information please visit our section « Wound Healing Theory/Wound healing principles or our website www.urgostart.com.

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The clinician must ensure that the diagnostic process and evaluation is complete and that the origin of the wound has been determined.

APPLICATION PROTOCOL:

• The wound must be cleaned according to local protocol, with water or normal saline.
• Avoid the systematic use of antiseptics
• If an antiseptic is used, rinse the wound thoroughly with a normal saline before applying an appropriate dressing depending on the condition of the wound.
• If a non-adhesive dressing is used, hold this dressing in place with an elastocated bandage or multi-stretch adhesive plaster.

For more information please visit our «Wound Healing Theory/Wound healing principles» section.

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