What is a wound?
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.
What is the wound physiopathology?
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.
What is the proliferative stage?
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.
For more information please visit the «Wound Healing Theory/Healing Process» section.
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.
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:
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 …
For more information please visit the «Wound Healing Theory/Infection» section.
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.