Pressure sores What are they How do you prevent them How do you treat them

How can pressure ulcers develop Normally the skin is kept healthy by blood which is supplied through tiny blood vessels called capillaries. In some places large bones lie close to the skin especially at the shoulders,elbows,heels,hips and buttocks. When a person is lying/sitting down the skin gets compressed between the bones and the surface. This impedes the blood supply to the area of skin Then there is a risk of bedsores also known as decubitus ulcers

Factors

Shearing and friction Shearing force. This occurs when force or pressure is applied at an angle to the skin. The various skin layers move over one another causing tissue damage. Friction This occurs when the patient is slid over the sheet instead of being lifted.

Classification of pressure sores

Location of pressure sores Trunk 4% upper limbs 3% Sacrum 31% Trochanters 10% Buttocks 27% Lower limbs 5% Heels 20%

The prevention and management of pressure sores 1. Assess the patients risk of developing a pressure sore Using a valid assessment tool within two hours of admission. 2. Re-assess the risk whenever there is a change in the patients condition 3. Choose an appropriate patient support system. 4. Devise a mobility turning system appropriate to the patients risk. Keeping patient off damaged and high risk areas as much as possible.

5. Inspect high risk sites whenever repositioning patient, record treatment and healing. 6. Maintain skin integrity. Cleanse after patient is incontinent. Avoid using excessive soap and rubbing. 7. With the aid of the dietician assess the patients nutritional status and any special dietary requirements. 8.Alleviate the affects of other concurrent debilitating conditions if possible. 9. Don’t forget the importance of psychological support.

The results of pressure sores They can lead to: –1. Pain –2. Infection –3. An increase in the nurses workload –4.Extension to patients stay –5. Health trust being sued –6. Occasionally death.

Stage one. Wound healing time 0-6 days 1. Vasoconstriction and formation of a clot in severed blood vessels. 2.Vasodilatation around the wound causing redness and heat. 3. Escape of white corpuscles and fluid into the tissue around the wound causing swelling. 4. Clearance of any bacteria by the white corpuscles.

stage one cont. 5. Migration of Polymorphs and macrophages to the area. 6. Ingestion of cell debris and bacteria by the polymorphs and macrophages 7.Death of polymorphs and macrophages and creation of wound exudate. 8. Gradual drainage of exudate. Which shows that the first stage is over.

Stage two. The reconstruction proliferation stage. Time 4-15 days 1. Macrophages stimulate the production of fibroblasts and capillary buds. 2. Fibroblasts manufacture collagen to form the framework which gives strength to the wound. 3. Formation of granulation tissue to reduce the size of the wound.

Stage two cont. 4. Contraction of granulation tissue to reduce the size of the wound. 5. Migration of epithelial cells across the wound. 6. Joining of epithelial cells to complete the reconstruction stage.

Stage three. Remodelling 1. Collagen fibres randomly laid down during the reconstruction stage rearrange themselves along the line of tension to increase the strength of the scar. 2. Extra capillary buds needed for healing gradually disappear so the scar changes colour from red to pink to white.

Dressings Alginates. I.e. Sorbasan, kaltostat. –Used for heavily discharging/exudating wounds Beads. I.e. Debrisan. –Used for exudating wounds and debridement. Charcoal. I.e. Carbonet. –Used for Malodorous wounds. Foams. I.e. Lyofoam, Allevyn. –Used for Cavity wounds, moderately exudating wounds.

Dressings cont. Hydrocolloids. I.e. Granuflex. –Used for most wounds except heavily exudating ones. Hydrogels. I.e. Sherisorb. –Used for necrotic wounds and most other wounds. Enzymes. I.e. Varidase. –Used for hard black necrotic tissue. Films. I.e. Opsite, Bioclusive. –Used for small superficial/shallow wounds.