2.   Three Phases  Inflammatory response  Fibroblastic repair  Maturation remodeling phase Healing Process

3.   Begins immediately after injury  Signs of inflammation  Redness (rubor)  Swelling (Tumor)  Tenderness (dolor)  Increase in temperature (Calor)  Loss of function (functio laesa) Inflammatory response

4.   Very important to the healing process  If does not accomplish what it is supposed to or does not subside healing cant take place  First 48 hours after injury Inflammation Response

5.   Chemical mediators  Histamine- released from the injured mast causes vasodilation and increased cell permeability  Leukotrienes and prostaglandins cause margination (leukocytes adhere to cell walls ) Also increase cell permeability and exudate (accumulation of fluid that penetrates through vessel walls into extravascular space) Inflammation response

6.   Chemical Mediators continued  Vasodilation and active hyperemia important brings neutrophils (leukocytes)  As swelling increases vascular and lymphatic flow decreased Inflammation response

7.   Vascular reaction- immediate response is vasoconstriction causing local anemia in the area. This increase causes leukocytes to slow down and adhere to the injured cells  Function of platelets- platelets normally don’t adhere to vascular walls. However, injury exposes collagen and platelets adhere to collagen Inflammation response

8.   Formation of clot- thromboplastin to prothrombin to thrombin to fibrinogen to insoluble fibrin clot.  Begins around 12 hours after injury complete within 48 hours Inflammation response

9.   Occurs when the inflammatory response does not respond sufficiently to eliminate the injuring agent and restore tissue to its normal physiological state  This low grade inflammation causes tissue damage to connective tissue, prolonging healing and repair Chronic Inflammation

10.  Vascular reaction Vasoconstriction to Vasodilation toExudate create stasis Chemical mediator liberate Histamine, leukotrienes,Cytokines Injury to cell Inflammation Response

11.  Clots formation Phagocytosis Platelets and leukocytes adhere to vascular wall

12.   http://www.youtube.com/watch?v=Un9-vubdtmY http://www.youtube.com/watch?v=Un9-vubdtmY Inflammation response

13.   Treatment during this phase is RICE. Inflammation Response

14.   RICE  Rest-  Ice- 20 mins per hour  Compression- Ace wrap  Elevations- above the level of the heart Treatment during the inflamation phase

15.   Regenerative activity occurs during this stage  Fibroplasia- period of scar formation. Begins a few days after injury any last 4-6 weeks.  Granulation tissue breaks down the fibrin clot.  Collagen- a strong fibrous protein found in connective tissue Repair phase

16.  The normal sequence of events in the repair phase leads to the formation of minimal scar tissue Occasionally persistent inflammatory response will cause fibroplasia and excessive fibrogensis that lead to irreversible tissue damage Repair phase

17.   Long term process  Purpose of the phase is to realignment or remodeling of collagen fibers that make up scar tissue according to the tensile forces  Ongoing breakdown and synthesis of collagen occur with a steady increase in tensile strength  Increased stress and strain realign collagen for maximum efficiency  Rarely as strong as the normal uninjured tissue Maturation Remodeling Phase

18.   Rarely as strong as the normal uninjuried tissue  End of three weeks firm strong contracted nonvascular scar exist  Complete maturation phase may require several years to be complete Maturation Remodeling Process

19.   As the remodeling phase begins aggressive active range of motion and strengthening exercises should be incorporated  Pain dictates the rate of progression  If swelling increases need to decrease activity Maturation Remodeling Process

20.   Extent of injuryHumidity, Climate, oxygen tension  EdemaHealth, Age and Nutrition  HemorrhageInfection  Poor vascular supplyHypertrophic scars Corticosteroids  Separation of tissue  Muscle spasm  Atrophy Factors that impede Healing

21.   Cartilage healing- poor lack of blood supply so no clot  Ligament healing  first 72 hours loss of blood from damaged vessels.  during next 6 weeks new capillary growth begins  Initially scar is soft and viscous  Over next several months scar continues to mature. Take as long as 12 months  Limit immobilization Soft tissue Healing

22.   Muscle Healing- Least 6-8 weeks and considerable amount of patience  Tendon Healing- 2 weeks adheres to surrounding tissue. 3 weeks tendon separates tensile strength is not sufficient to permit a strong pull on the tendon for 4-5 weeks.  Nerve healing- can not regenerate once the nerve cell dies. Peripheral nerves can heal be slow process Soft tissue healing

23.   Antinflammatory drugs -NSAIDS- Nonstreroidal antiinflammatory drug  Therapeutic Modalities- Ultrasound, electrical stimulation  Exercise Rehabiliation Soft tissue healing

24.   Cutaneous- sharp, bright and burning  Deep somatic pain- pain in tendons, muscles, joints  Visceral pain originates from internal organs  Psychogenic pain- emotional causes PAIN

25.   Referred pain- occurs away for sight  Myofascial pain- Trigger points  Sclerotomic, Myotomic and dermatomical- Pain

26.   Gate control theory- pain is blocked by gate preventing message from getting to the brain. Pain Control

27.   Gate control theory- http://www.youtube.com/watch?v=ZfWO2wciIUY Pain

28.   Previous experiences, emotional influences and sensory perception influence the transmission of pain message and thus the perception of pain Descending pathway pain control

29.   Stimulate the release of opiate like chemical called endorphin from the hypothalamus and anterior pituitary Release of B endorphins

30.   Therapeutic modalities, medications, massage, acupuncture Treating pain

31. 