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The healing process is divided into three broad stages which are not mutually exclusive and overlap considerably. 1.Initial vascular reaction 2.Inflammatory response 3. Proliferative phase 4. Remodeling Wound healing refers to the body’s replacement of destroyed tissue by living tissue (Walter & Israel 1987). It comprises of two essential components whose differentiation is based on resultant tissue: Regeneration specialised tissues replaced by proliferation of surrounding undamaged specialised cells e.g lung,liver tissue and meniscus (O’Brien 1990) Repair Injured tissue replaced by granulation tissue which matures to form scar tissue.
INJURY: Tissue damage produces capillary bleeding inhibiting cell metabolism resulting in cell death. Dead cells contain Iysosomes which release digestive enzymes. Within 10-15 mins the damaged soft tissues contain disrupted extracellular tissues, dead and dying cells and extravastated blood. The extravasated blood contains platelets and plasma. The platelets die due to lack of oxygen and release thrombin which changes fibrinogen to fibrin. The fibrin deposits an irregular network of fibers to form a clot.
INFLAMMATION: Inflammation is a normal and necessary pre- requisite to healing (Hardy 1989). It may be a non- immunological or immunological event, whether by injury or virus. Inflammation is a localised protective response to injury” Triple Response”. There is disagreement as to specific duration of this phase but it is reported to last between 3-5 days. It is stimulated by “a cascade chemical effect’ and its extent is dependent upon the area of damage and severity of injury. The cardinal signs of inflammation are: Calor Rubor Tumor Dolor Functiolasea Calor /Rubor: Initial V/C is followed by V/D. Blood vessels: : Increase calibre ( histamine,bradykinin, PGE)
Increase permeability (serotonin, bradykinin, histamine, leukotrines) Increase blood flow / decrease flow
WBC + platelets marginate to walls endothelial cells swell. (4hrs)
Tumor: Swelling is due to inflammatory exudate as chemicals released increase permeability of local capillaries. Fluid exudate contains gammaglobulins and fibrinogen (antibodies) Gammaglobulins fight infection. Fibrin is formed from fibrinogen to construct a fibrin lattice. Platelets, mast cells and basophils are present in all tissue. Chemical mediators modulate the action of the cells. Leucocytes ( neutrophils, basophils, oesinophils) and macrophages enter area and act as debriders (phagocytosis) Mast cells release hylauronic acid which draws water into the site and creates a gel which limits local fluid flow, and further traps various particles and debris (Hardy 1989) Dolor: Pain is caused by mechanical and chemical nociception Mechanical tissue pressure. Chemical increase sensitivity of nerve endings ( bradykinin, PGE and histamine)
Functiolasea: Loss of function is a result of: Neurological reflex inhibiting movement due to pain Oedema mechanically restricting movement
PROLIFERATIVE PHASE: This develops from around the third day while inflammation is still going on. It consists of two fundamental processes 1. Fibroplasia 2. Angiogenesis (new cells). Macrophages, fibroblasts and capillaries infiltrate the wound. Fibroplasia involves activation of fibroblast proliferation. Fibroblasts initially produce predominantly type 111 collagen fibres which will become type I as the repair process matures ( 7-12 days)
Angiogenesis involves mitosis in the cells surrounding the capillaries. Capillary buds sprout and communicate with existing capillaries. This new capillary system + fibroblasts = granulation tissue. The tensile strength of the new tissue is at its lowest level at this stage. Myofibroblasts are derived from fibroblasts and are responsible for wound contraction. Some authors believe that this phase lasts approx 21 days REMODELING PHASE: This phase will have the longest duration extending a year or more.
Macrophages, fibroblasts, capillaries and water content all decrease. Sensitivity is reduced and collagen is primarily type I. Initial deposition of collagen produces fibrils with random orientation, which in time becomes more orientated in line with local stresses. Tensile strength correlates with maturity of collagen. TENSILE STRENGTH
Restoration to near normal tensile strength (NNTS) varies with different tissues. Muscle may reach NNTS in 7 II days ((Garrett 1990). The extent and duration of inflammation is reportedly longer in experimental contusion injuries compared with strains (Stauber1990).
Ligaments & tendons may take 4 months for 85-95 % of NNST or some say 40-50 weeks. There ~s yet no uniform answer.
Ligaments may differ in their repair process. The ACL does not heal well but the collaterals do. The cell arrangement & blood supply differ between them. The ACLs main nutrition is from synovium. Synovial fluid has been shown to adversely affect ACL fibroblast proliferation.(Andrish 1979) Synovial fluid washes away the clot from the site of injury This may deplete growth factors necessary for stimulating the healing response.
Tendon healing is very controversial but generally day 5 is considered to be the weakest point for tendon tensile strength (Gillman 1968) Complete immobilization of a tendon results in reduction in glycosaminoglycan content and in the strength of the tendon. Too early mobilisation can result in rupture. Poor nutrition is proposed to contribute to poor healing. Articular cartilage: Avascular has limited powers of repair and tends towards calcification following injury.
FACTORS THAT MAY RETARD HEALING:(Walter Israel 1978) General causes: -Old age -Starvation -lack of vit C (Scurvy) -Steroids (inhibitory effect) -temperature (lower rate when cooler) Local causes: lschaemia irritation (infection or haematoma) drying of the wound excessive movement (restarts inflammation) adhesion to underlying bone or other tissues.
MODIFYING FACTORS: NSAIDs will enhance the healing process.
However they act by inhibiting prostaglandin production (is this a good thing?) There is evidence that they may also increase collagen strength. NSAID have side effects such as: Gastrointestinal (upto 1-2% get ulcers) Skin eruptions. Patients with asthma, nasal polyps and aspirin intolerance should not be treated with these drugs. Approximately 50% of patients who receive NSAID may experience an adverse reaction. NSAID’s use may be justified in a professional athelete as opposed to a recreational athelete. The most important time to use them is during the first stage as Herring 1990 reported that extended dosages may actually impair tissue repair. REHABILITATION PROGRAMME Avoid a cookbook approach. Acute phase: Ice, Compression, Elevation and gentle movement. Ultrasound has been shown to have beneficial results in early stages of healing (Dyson 1978). lt is believed to affect cell membrane permeability. Restoration phase: Mobility Flexibility
Strength/ Endurance Balance & coordination Confidence. Evidence exists that stress on forming collagen encourages the alignment of greater scar tissue strength than without application of stress.
It is easier to mechanically affect young scars than it is to change old scars
REFERENCES: 1.Evans P. (1980) “The healing proces” Physiotherapy 66: 8 256-259 2,Barlow Y. Willoughby J. (1992) “Pathophysiology of soft tissue repair” British Medical Bulletin 48: 3 698-711 3.Burroughs P, Dahners L (1990) “The effect of enforced exercise on the healing ligament” American Journal of Sports medicine 18: 4 376-378 4.Houglum PA (1992) “Soft tissue healing and its impact on rehabilitation Journal of Sport Rehabilitation 119-39
5. Watson T. (1996) “Wound healing” Lecture notes.
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