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Wound physiology cf
- 1. Clare Fenwick Griffith Univeristy Gold Coast 2010 Wound Physiology and Assessment Dr. Clare Fenwick 2010
- 2. Clare Fenwick Griffith Univeristy Gold Coast 2010 Aspects of wound care? What causes wounds (pathophysiology)? Can I eliminate the cause? How do wounds heal (healing physiology)? What am I looking for (clinical assessment)? How will I treat the wound (product knowledge)? What skills do I need (clinical knowledge)? Did it work (evaluation)? If not, why not
- 3. Clare Fenwick Griffith Univeristy Gold Coast 2010 What causes/exacerbates wounds? Wounds are generally classified as acute or chronic Trauma/Surgery Underlying conditions Medications Lifestyle risks
- 4. Clare Fenwick Griffith Univeristy Gold Coast 2010 How do wounds heal? Haemostasis - vasoconstriction - platelet creation - biochemical response Tissue Repair - inflammation (inflammatory phase) - reconstruction (proliferative phase) - maturation (remodeling phase)
- 5. Clare Fenwick Griffith Univeristy Gold Coast 2010 Haemostasis Vasoconstriction response: Arteries, arterioles and capillaries spasm to cease bleeding Platelet response: Damaged endothelium exposes collagen fibres, platelets adhere resulting in a plug Biochemical response: Clotting factors released causing clot formation, retraction and breakdown
- 6. Clare Fenwick Griffith Univeristy Gold Coast 2010 Tissue Repair - inflammation Inflammation stage (0-5 days) Capillaries spasm, a clot forms and the wound becomes ischemic Histamine is released causing vasodilation in surrounding tissue Oedema and pressure initiates the pain pathway Defence cells migrate protecting from bacteria and clearing debris HEAT OEDEMA ERYTHEM A PAIN
- 7. Clare Fenwick Griffith Univeristy Gold Coast 2010 Tissue Repair - reconstruction Reconstruction stage (2-24 days): a time of cleaning and healing Defence cells continue to clean up bacteria and clear debris Granulation or angiogenesis appears (bumpy red new tissue) Contraction occurs Epithelialisation commences
- 8. Clare Fenwick Griffith Univeristy Gold Coast 2010 Tissue Repair - maturation Maturation stage (24days – 1 year) Remodelling of the wound occurs. Previously laid collagen fibres are broken down and new stronger collagen fibres are laid down Rosy pink scar is still remodelling; scar similar to the surrounding skin has finished this stage A scar has only 80% of strength and elasticity Contracture Remodelling (Myers, 2004)
- 9. Clare Fenwick Griffith Univeristy Gold Coast 2010 Stage I – Nonblanchable erythema of intact skin Stage II – Partial thickness, involving loss of the epidermis and/or dermis Stage III – Full thickness, involving loss of the epidermis, dermis and subcutaneous Stage IV – Full thickness, involving loss of the epidermis, dermis, subcutaneous and exposing muscle bone or supporting structures Wound staging STAGE ISTAGE IISTAGE IIISTAGE IV
- 10. Clare Fenwick Griffith Univeristy Gold Coast 2010 Are you totally lost yet?
- 11. Clare Fenwick Griffith Univeristy Gold Coast 2010 What am I looking for? General client assessment Assessment of the wound Assessment of environmental and local factors
- 12. Clare Fenwick Griffith Univeristy Gold Coast 2010 General client assessment Overall health Co-morbidities Mobility status Nutritional status Sensory functioning status Psychosocial status Pain Current medication
- 13. Clare Fenwick Griffith Univeristy Gold Coast 2010 Assessment of the wound Wound aetiology Wound location Wound dimensions Wound bed Wound drainage Wound temperature Wound infection Peri-wound
- 14. Clare Fenwick Griffith Univeristy Gold Coast 2010 Wound aetiology
- 15. Clare Fenwick Griffith Univeristy Gold Coast 2010 Wound location PRESSURE ULCERS
- 16. Clare Fenwick Griffith Univeristy Gold Coast 2010 Wound dimensions 4.2cm length3.6cm width Wound bed 12 o’clock 3cm 9 o’clock 4cm 6 o’clock 4.5cm 3 o’clock 3.2cm 16cm circumference TUNNELLING WOUND
- 17. Clare Fenwick Griffith Univeristy Gold Coast 2010 Wound Bed: Five tissue colours Pearly pink colour – Epithelial tissue Beefy red colour – Granulating tissue Stringy yellow colour – Sloughy tissue Hard black colour – Necrotic tissue Pus green colour – Infected tissue EPITHELIASING TISSUE GRANULATING TISSUE SLOUGHY TISSUE NECROTIC TISSUE INFECTED TISSUE
- 18. Clare Fenwick Griffith Univeristy Gold Coast 2010 Wound drainage Exudate is assessed by; Type Amount Colour Consistency Odour
- 19. Clare Fenwick Griffith Univeristy Gold Coast 2010 Wound Temperature Wounds heal best at constant temperatures of 37 - 38 º C Wounds left to cool down take about 3- 4 hours to restore to healing temperature (Shultz 2002) Keep it warm, keep it moist
- 20. Clare Fenwick Griffith Univeristy Gold Coast 2010 Peri-wound Attached or unattached Indistinct or well defined Macerated or dry Thickened and calloused Irregular or round Red, white or blue
- 21. Clare Fenwick Griffith Univeristy Gold Coast 2010 Nothing is how it seems
- 22. Clare Fenwick Griffith Univeristy Gold Coast 2010 Assessment of environmental and local factors INTRINSIC (inherent to the person) EXTRINSIC (control from outside person) Age Pressure, friction, shearing Underlying disease processes Temperature Nutritional status Infection Gender Hydration Psychological state Foreign bodies
- 23. Clare Fenwick Griffith Univeristy Gold Coast 2010 Modes of Healing Primary Intention Secondary Intention Tertiary Intention Skin Graft Skin Flap Primary Intention Secondary Intention (Surgeries and procedures 2003) Skin Flaps
- 24. Clare Fenwick Griffith Univeristy Gold Coast 2010 QUESTIONS???
- 25. Clare Fenwick Griffith Univeristy Gold Coast 2010 References Carville, K. (2001). Wound Care Manual. Western Australia: Silver Chain Foundation. Coleman, K. (2004). Wonderful World of Wounds. In C. Fenwick (Ed.). Gold Coast. Hand-Surgical Approaches, Skin Flaps. (2003). Retrieved 17 February, 2004, from http://www.orthoteers.co.uk/Nrujp~ij33lm/Images9/flaps3.jpg Edwards, S. L. (1998). High Temperature. Professional Nurse, 13(8), 521-526. Fierer, J., & Goldberg, C. (2002). Gangrene of the hand. Retrieved 2004, 2 February, from http://medicine.ucsd.edu/Clinicalimg/extremities- diabetic-foot-infection.html Helmerd, D. (2003). Brown Recluse Spider Bite. In C. Fenwick (Ed.). Gold Coast.
- 26. Clare Fenwick Griffith Univeristy Gold Coast 2010 References Morgan, S. (1990). A comparison of three methods of managing fever in the neurologic patient. Journal of Neuroscience Nursing, 22(1), 19-24 Myers, B. A. (2004). Wound Management Principles and Practice. New Jersey: Prentice Hall. Shultz, M. (2002). Wound Care. Retrieved 17 February, 2004, from http://www.medpharm.co.za/sapj/2002/july/wound.html SpinalNet. (2004). Skin and Wound Healing. Retrieved February 4, 2004, from http://www.spinalnet.co.uk/EEndCom/GBCON/Homepage.nsf/0/98BEE0 4F593CFD2D00256C46004B1D74?OpenDocument Surgeries & Procedures, Skin Grafts. (2003). Retrieved 17 February, 2004, from http://health.allrefer.com/health/skin-graft-skin-graft.html Wound Assessment. (2000). Retrieved 13 February, 2004, from http://www.medpharm.co.za/nursing/2000/sec2000/wound.html
Editor's Notes
- Introduction Never forget this is a whole person we are discussing although it will appear at times that we are only focusing on the wound. If you become distracted try to at least remember this fact; keep it warm, keep it moist
- Familiar with the nursing process or a plan of management Enquiring mind, what do you need to be asking yourself What causes wounds (pathophysiology)?Can I eliminate the cause? How do wounds heal (healing physiology)? What am I looking for (clinical assessment)? This will be discussed in the next group of wound lectures How will I treat the wound (product knowledge)?. What skills do I need (clinical knowledge)? Did it work (evaluation)? If not, why not!
- Trauma – gunshot, MVA, falls, stabbing We have all sustained some small traumatic injury within our lives Surgery – major, minor Most requires some form of incision or invasive process Underlying conditions Pressure – Elderly and immobile at great risk Malnutrition - various nutrients are essential to wound healing. Carbohydrates are required to fuel the cells, if none is available they will burn off the protein. Protein is needed for repair. Vitamin C collagen synthesis and infection reduction (lack of fruit will cause vitamin C deficiency) Vitamin A for epithelization etc. Obesity – adipose tissues is poorly vascularised Diabetes – Diabetics develop calcification of the arterial walls, this affects the oxygen and nutritional exchange. High blood sugar impairs wound healing including collagen synthesis, angiogenesis, tensile strength, and infection response (elevated glucose levels encourages bacterial growth)., consider the stress response Stress response - Stress response – release of adrenalin causes activation of adrenocorticotrophic hormone (ACTH) which stimulates adrenal cortex hormones. ACTH regulates glucocorticoids, cortisol, and hydrocortisone. Glucocorticoids cause breakdown of body stores of glucose, raising BSL, reducing mobility of granulocytes/macrophages impeding their migration to wound bed. This suppresses immune system and hinders the inflammatory response, rate of healing slows and infections rise Cardiovascular disease – poor blood flow (ineffective pump, anaemia, venous/arterial insufficiency) leads to diminished nutrients reaching the site and reduced oxygenation Respiratory disease - O2 is required for all areas of wound healing Immunocompromised – Aids, HIV, cancer, increasing age. Increasing age Fragile thinning skin Reduction in oil/sweat glands causing dryness and barrier breakdown Pain perception is diminished increasing injury risk Inflammatory response is slowed, vasoconstriction and dilatation are not as fast as they used to be Immune defences become impaired. Medications Steroids impair all stages of wound healing (suppress inflammation & immune systems, affect the wound contraction and tensile strength) Chemotherapy agents (immunosuppression) NSAID do not suppress wound healing (no evidence to support that) Lifestyle risks Alcohol abuse – malnutrition, impaired judgement, less likely to self care Smoking abuse – Vasoconstriction and reduced oxygenation, Increased platelet aggregation, reduced oxygenation
- HaemostasisVasoconstriction Platelet creation Biochemical response Tissue Repair InflammationReconstruction Maturation
- Vasoconstriction response: Arteries, arterioles and capillaries spasm to cease bleeding Platelet response: Damaged endothelium exposes collagen fibres, platelets adhere resulting in platelet aggregation. Serotonin and prostaglandins are released enhancing vascular spasm. Phospholipids and adenosine diphosphate (ADP) are released attracting more platelets Biochemical response: Clotting factors are released causing clot formation, retraction and (fibrinolysis) breakdown
- Inflammation stage (0-5 days) Depends on the individual and text book Inflammation is NOT infection Capillaries spasm, clot form, wound becomes ischemic Histamine released, vasodilation occurs in surrounding tissue causing redness and heat Swelling results from fluid collection (blood) in the tissue as well as vasodilation. Pressure exerted will compress peripheral nerve endings setting off the pain pathway Defence cells migrate from the permeable blood vessels into the wound area. Neutrophils arrive releasing enzymes to breaking up devitalised tissue and destroy bacteria, they have a short lifespan, they die after they phagocytose (these make up pus) Monocytes are activated ingested foreign bodies then transforming into macrophages. Macrophages long life span and produce a large number of substances which aid in wound healing processes i.e. growth factors that will stimulate growth of new tissue.
- Reconstruction phase (2-24 days) Defence Cells Neutrophils and macrophages continue to digest the bacteria and clean up the wound. Macrophages also stimulate fibroblastic cells to make collagen (protein for connective tissue that provides strength to tissues) becoming part of the granulation phase Granulation or Angiogenesis Angiogenesis is activated by tissue hypoxia from the disruption of blood flow at the time of injury. Angiogenesis are the new capillaries that sprout from the vessel walls of existing capillaries within 36 hours of initial damage. Growth factors released by macrophages stimulate these endothelial cells lining the walls of capillaries near the injured area, to divide and branch out forming new capillary loops. At the same time fibroblasts start to divide and collect at the wound margin producing a latticework of collagen fibres that provide strength to the wound Fibroblasts are dependent on an adequate intake of Vitamin C, iron and copper from the diet. Granulation is a good indicator effective wound bed healing. In wounds healing by primary intention (suture lines) collagen formation usually reaches its peak at approx 6 –7 days. Contraction Fibroblasts become myofibroblasts (similar properties to smooth muscle cells and fibroblasts) drawing the wound edges reducing the surface area of the wound, thereby reducing the amount of tissue replacement required. Contraction is dependant on the size and depth of the wound as it has a limited function Square, rectangular wounds contract the fastest and circular wounds the slowest Epithelialisation The growth of new epithelial cells across the surface of the wound occurs during the final stages of healing. Epithelial cell migration occurs granulating the wound bed, this appears as a thin translucent film across the wound bed. Epithelial cells are easily dislodged by abrasive cleaning hence why we do it gently Epithelial cells (keratinocytes) will not migrate over deoxygenated non viable tissue. To migrate over nonviable areas, the epithelial cells secrete enzymes breaking down debris in their path. Hence the rationale behind wound bed preparation
- Maturation stage Remodelling of the wound occurs. Previously laid collagen fibres are broken down and new stronger collagen fibres are laid down Rosy pink scar is still remodelling; scar similar to the surrounding skin has finished this stage A scar has only 80% of strength and elasticity as it previous had Image Myers, B. A. (2004). Wound Management Principles and Practice. New Jersey: Prentice Hall, photo C5 ) This image shows a wound in both the reconstruction stage and the maturation stage. This wound, located anteriorly below the patella, is actively contracting toward the center while the perimeter is remodeling. Near the wound edge, less granulation tissue has been formed and the scar is less mature and more pink in color, farther out, the scar is closer to the patient’s natural
- Stage I Nonblanchable erythema of intact skin Stage II Partial thickness, involving loss of the epidermis and/or dermis Presents as an ulcer, abrasion or blister Stage III Full thickness, involving loss of the epidermis, dermis and subcutaneous Extends to the fascia but not through it Presents as a deep crater, often with undermining Stage IV Full thickness, involving loss of the epidermis, dermis, subcutaneous Exposing muscle, bone or supporting structures
- Three main aspects to wound assessment General patient assessment Assessment of the actual wound Assessment of the environmental factors
- General patient assessment This assessment is done regardless of wounds, it is something you will develop over time. Critically observe people to notice health status and determine the things that will effect the achievement or maintenance of this health status. Overall health State the obvious ABC Traumatic injury sustained to the right gluteus maximus Gender (assumption this is a male) Age (older we are the less well things work) General appearance, clean, mentally intact, other obvious injuries Co-morbidities What sort of diseases will impact on this injury Endocrine diseases – Diabetes (poor vascular supply, sugar load in wound) Neuromuscular disease - motor-neuron disease (reduced sensation, immobility) Psychiatric illnesses – schizophrenia, psychosis (self care issues) Cardiovascular disease – CHF, venous/arterial insufficiency, anaemia (poor blood supply and oxygenation) Gastrointestinal disease – malnutrition, anorexia related to other illnesses, malabsorption (poor nutrition) Genitourinary disease – CRF(uraemia retards wound granulation), incontinence Integumentary disease – Friability of the skin, lesions, abrasions (breech in the barrier) Musculoskeletal disease – immobility, arthritis (steroids) Respiratory disease – COAD (poor oxygenation) Mobility status Immobility elevates the risk of poor wound healing due to pressure and deoxygenation This client will be a high risk due to extensive muscle damage especially to a weight bearing muscle Nutritional status Wound healing needs adequate nutritional intake. This client appears well fed. Obesity can impair healing due to the poorly vascularized adipose tissue and wound dehiscence Anorexia can significantly lack the essential vitamins required for healing. Know what foods are available to your client. Central Australian Aboriginal people lack zinc (zinc comes from seafood, organ meats, mushrooms, soybeans) it is required for the proliferation stage Sensory functioning status Impaired eyesight leads to falls Hearing impairment leads to miscommunication Diminished peripheral sensation such as in diabetes leads to undetected injury Rare condition where pain sensation is absent – poor life expectancy Psychosocial status Social determinants you would have learnt in health promotion Support systems, individual coping styles Living/home environment Work environment Education level Developmental level Cultural preferences Lifestyle choices (smoking, drugs, alcohol) Pain Next week we will explore pain physiology Would this be painful? What type of pain would the client be experiencing Current medication What types of drugs could hamper the client’s healing abilities Corticosteroids (impair the immune and inflammatory response) Anti-neoplastic (prevent cell growth) Anti-coagulants (prevent clot formation) Chemotherapeutics (impair the immune system) Anti-prostaglandins (prostaglandin is part of the inflammatory process) Penicillin (penicillamine released from penicillin prevents collagen cross-linking hence reduces wound strength) Radiation therapy (destroys health cells as well as malignant) Wound aetiology How did it happen? Type of wound (acute, chronic) What are the appropriate treatments? Could it be prevented?
- Wound aetiology Wound location Wound size Wound bed Wound edges Wound drainage Peri-wound
- Wound aetiology How did it happen? Mechanism of injury is a really important point. How did the elderly woman sustain a skin tear at home is as important as knowing how the child sustained a head injury. As both may be preventable. How long has the wound been there? Duration of wound provides an indication of acuity and chronicity cycles What are the appropriate treatments? Always consider at the start how you will be treating this wound, it lays the foundation of a wound lifespan plan Brown recluse spider bite Day 4 of a bite injury Day 6 of a bite injury Day 10 of a bite injury
- Wound location Try to use anatomical terms Location gives insight to the type of wound Pressure ulcers occur over bony prominences Arterial ulcers occur at the distal ends of toes Peripheral wounds will be slower to heal
- Wound size Indicator of improvement or deterioration of the wound, wound progress Wound debridement might provide measurements that increase the wound size Direct measurement Measure the length and width and depth of the wound 12 o’clock measurements are used for depth measurements Easy inexpensive quick To measure the depth, place a moist cotton tip into the wound and mark on the stick the level Other measurements Wound tracings – easy to use, kept as a clinical record, very abstract in interpretation Photographic record – take a photo at various stages, photos are real images Volumetric record – Using a wound moulds can be painful and unsure about damage done to wound bed. Inserting saline into the wound cover it with opsite then withdraw fluid; can be inaccurate and contradicted in sinus wounds Body Surface Area – discuss this with the burns lecture Dead space or dead space Where the wound edges have come away from the wound base, it appears grey/purplish in colour and should be probed carefully to determine the extent of the undermining. Use the clockwise method to determine the breadth of tunnelling Carville, K. (2001). Wound Care Manual. Western Australia: Silver Chain Foundation Page 46 explains the clock measurement
- The wound bed tissue reveals the phase and progress of wound healing. Five main tissue colours pink, red, yellow, black and green. Epithelial TissuePartial-thickness wounds heal by epithelialisation. Deeper, full-thickness wounds heal by contraction, filling with granulation tissue, and epithelial migration from the wound edges. Epithelial tissue is "pearly pink" in colour. Granulation TissueClassical "shiny, beefy, red" granulation tissue is a healthy sign. Tissue that appears grey or purple indicates an inadequate blood supply. Sloughy Tissue Yellow or tan coloured stringy mucous material called slough, is non viable tissue or yellow necrosis Necrotic TissueNecrosis delays healing and is a focus for infection. It must be removed by debridement, thick, hard, black necrotic material is called eschar. Infected Tissue All wounds are contaminated, this does not mean infection. Infection occurs when an imbalance of normal flora numbers occurs and the body’s normal defences cannot confine or control them. Wound swabs or cultures are only useful in confirming one’s clinical diagnosis. Infection is indicated by pain, oedema, heat, erythema, exudate (purulent) at the wound site and an elevated temp and WBC The area and depth of a wound cannot be properly assessed until this debris is cleared.
- Exudate/Wound DrainageExudate is rich in white blood cells and growth factors that facilitate healing. When drainage increases or has a foul odour and purulent appearance it is problematic, signifying bacterial growth, and a inhibited inflammatory response delaying healing. Dry wounds don’t heal well. Epithelizing cells need a crust free environment to migrate Type of exudate Serous (clear straw coloured) Haemoserous (slight blood stained) Sanguineous (heavy blood stained) Purulent (pus laden, infected) Amount of exudate None Minimal (normal) Moderate (normal) Copious (infective, especially if not proportion to wound size) The body weeps to rid itself of foreign bodies Colour Clear (normal) Pale Yellow (normal) Red (fresh blood) Dark brown (old blood) Blue-green (Pseudomonas Aeruginosa) Consistency Thin watery (normal) Thick (probable infected) Odour Is subjective and should only be documented as present or absent Proteus infections smell ammonia-like Pseudomonas infections have a sickly sweet smell
- Wounds heal best at constant temperatures of 37 - 38 º C Wounds left to cool down take about 3- 4 hours to restore to healing temperature (Shultz 2002) If you remember nothing from this lecture at least take away this message, keep it warm and keep it moist
- Peri-wound Attached or unattached Attached edges generally mean good vascularisation and wound healing is rapid Unattached edges are usually seen in deep wounds and will have slowed healing times. Observe unattached edges as they can discolour, indicating non-viable tissue. Indistinct or well defined Superficial wounds generally have blurred indistinct edges where the wound moulds into good skin Well defined wounds are usually partial or full thickness wounds Macerated or dry Dry wounds heal slower, if exposed to the air a crust will form within 2-3 hours. The epithelial cells need the crust to be broken down by enzymes before it can progress its migration. Maceration is where the wound edges are allowed to become too moist, this area is very fragile and can lead to widening the wound edges Thickened and calloused Usually indicate a chronic wound, often seen in diabetic ulcers and peripheral neuropathies Irregular or round Irregular shaped wounds on the lower peripheries are usually venous ulcers Round or regular shaped wounds on the lover peripheries are usually arterial ulcers Red, white or white Red wound edges can indicate wound infection White edges can indicate maceration Bluey grey edges can indicate non viable unattached edges
- Assessment of environmental and local factors explores the different intrinsic and extrinsic factors that effect healing Intrinsic means within the organ (human body) Extrinsic means outside of the organ Age Physiological changes already discussed Polypharmacy Increased chance of co-morbidities Reduced mobility Reduced financial resources, possibly effecting nutritional status Underlying disease processes What other diseases are taking up valuable resources for wound healing? A wound needs a blood supply to carry nutrients, oxygen and various cells to enable healing Nutritional Status What type of nutritional intake is there? Does the client have teeth? Are they obese or cachexic? What cultural influences is there on the clients nutritional intake? Do they have the finances to buy nutritional food? Carville, K. (2001). Wound Care Manual. Western Australia: Silver Chain Foundation.Page 38 and 104-105 for further reading Gender Females are less likely to injure themselves compared to males Males are more likely to be risk takers and take a ‘she’ll’ be right attitude Psychological state Altered body image – client can suffer depression and poor self esteem, reducing the motivation to get well and keep well Socialisation issues – client can become isolated due to the wound’s appearance, odour or effect on activity. Isolation can result in depression Availability of health care – not everybody is afford equality of health or access Compliance – What goals have been mutually set between you and the client to achieve healing? What motivates the client to be well. Compliance is about giving purpose to actions and empowerment back to the client Pressure, friction, shearing Pressure, friction and shearing all contribute to wound aetiology Temperature The importance of maintaining wound temperature has been previously discussed If you have a client with an elevated systemic temperature (hyperpyrexia) there is usually an underlying infective process NB Hyperthermia is not caused by infection but related to a damage hypothalamus or an inability to lose heat normally A body temp of 40.9 ºC will kill pneumococci and gonococci organisms (Edwards, 1998) A body temp of 38 - 40 ºC activates phagocytes and leukocytes and prevent vial cell replication (Edwards, 1998) A body temp of 41 – 43 ºC causes nerve damage, coagulation, convulsions and death (Edwards, 1998) Always prevent shivering as it can accelerate the body temp to four times the normal rate (Morgan 1990) Infection Bacteria lives normally on the human body All wounds are contaminated, this does not mean infection. Infection occurs when an imbalance of normal flora numbers occurs and the body’s normal defences cannot confine or control them. A wound is considered infected if there is 100 000 (105) organisms per gram of tissue (Carville, 2001) Infection is indicated by pain, oedema, heat, erythema, exudate (purulent) at the wound site and an elevated temp and WBC Hydration Exudate is rich in white blood cells and growth factors that facilitate healing. Dry wounds don’t heal well. Epithelizing cells need a crust free environment to migrate Too much exudate can cause maceration of wound edges. Moisture can provide a covering to exposed nerve endings thus reducing pain. Think of when you get burnt and you place your hand under cold water. The cold water not only cools the area but the seal of water protects the exposed nerves reducing pain allow it to dry out and the pain recommences. Foreign bodies Foreign bodies can include sutures, dirt, innate objects, dressing products such as cotton wool and wound debris. Foreign bodies will initiate the infective process References Edwards, S. L. (1998). High Temperature. Professional Nurse, 13(8), 521-526. Morgan, S. (1990). A comparison of three methods of managing fever in the neurologic patient. Journal of Neuroscience Nursing, 22(1), 19-24.
- Primary Intention Simplest and fastest way of healing Primary intention is when the wound edges can be physically approximated Secondary Intention A wound that doesn’t have wound edges to join so that healing will occur through wound bed granulation Tertiary Intention Also known as delayed primary closure. This is when a wound has approximated edges but there is a concern foreign bodies or an infection is present. Closure is delayed for 3-5 days Skin Graft Skin Flap