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Ch. 2 Tissue Healing. Introduction Tissue healing occurs and is influenced by several factors There are three phases: – Inflammatory response – Repair/regeneration.

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Presentation on theme: "Ch. 2 Tissue Healing. Introduction Tissue healing occurs and is influenced by several factors There are three phases: – Inflammatory response – Repair/regeneration."— Presentation transcript:

1 Ch. 2 Tissue Healing

2 Introduction Tissue healing occurs and is influenced by several factors There are three phases: – Inflammatory response – Repair/regeneration – remodeling

3 Inflammatory Response Cells remove debris Cells create groundwork for repair and regeneration phase

4 Repair/Regeneration Phase Cells restore the vascular and structural integrity of injured structures

5 Remodeling Phase Healed tissue adapts to functional loading Gets stronger based on the stress that is applied to it The three phases overlap one another Disruption of any one phase can cause an unsatisfactory outcome

6 Types of Tissue Epithelial tissue Connective Muscle nervous

7 Epithelial Tissue Composed of layers of cells Protect organs Secretions (glands) Absorption ( lining of the stomach )

8 Connective Tissue Most abundant and variable tissue in the body Attaching organs Support/structure Movement Physical protection Immune response, energy & mineral storage Heat generation and transportation (blood, etc.)

9 Connective Tissue Subtypes: – Fluid connective tissue=blood and lymph – Fibroconnective tissue=fat, tendons and ligaments – Supportive connective tissue=cartilage and bone

10 Nervous Tissue Located in brain and spinal cord and nerves Electrically exciteable Used to transmit and respond to various impulses and forms of information

11 Muscle Tissue Skeletal- striated or voluntary Cardiac – heart muscle Smooth- linings of organs and blood vessels

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13 Common Injuries

14 Puncture and Laceration

15 Incision

16 Acute vs. Chronic Acute – single forcefull event (ACL tear) Chronic – occur over a period of time (Tennis elbow)

17 Acute Injuries Contusions – bruises Strains – muscle or tendon injuries Sprains – ligamentous injuries

18 Contusions Caused by compressive forces or direct impacts and are graded by degrees of trauma 1 st degree-minimal swelling, no limits 2 nd – pain, bleeding, moderate functional limits 3 rd -hematoma formation,sever limitations

19 Sprains and Strains

20 Fracture Classifications Greenstick Transverse Oblique Spiral Comminuted Avulsion Impacted Depressed Epiphyseal (Salter-Harris classification)

21 Peripheral Nerve Injuries Neuropraxia-least severe, transient and reversible loss of nerve function Axontomesis- partial disruption, may cause atrophy or weakness for 2 – 52 weeks Neurotomesis – complete severance of a nerve resulting in permanent loss of function

22 Chronic Injuries Blisters – continuous friction Repetitive overload – tendinosis, tenosynovitis Chronic irritation –could cause neuralgia or neuroma

23 Soft Tissue Healing Phase 1: Inflammatory Response Phase 2: Repair/Regeneration Phase 3: Remodeling/Maturation

24 Phase 1 Signs and symptoms: – Redness – Heat – Pain – Swelling – Loss of function

25 Phase 1 con’t Lasts 7-10 days Initial damage is called “the primary injury” Caused by a release of proteins at the injury site Mast cells produce chemicals (histamines) which promote vasodilation This causes the redness and heat Vessels become more permeable which contributes to the swelling

26 Phase 1 Mast cells also release chemicals that attract neutrophils (immune cells) to come to the injury Neutrophils clear debris and regulate the early inflammatory process Injured area becomes ischemic and acidic which may cause secondary damage to otherwise healthy areas around the injury

27 Phase 1 Neutrophils die and are ingested by macrophages at the injury site When this happens the macrophages begin to produce proteins that promote tissue repair Early scar tissue forms Early rehab should focus on pain management, decreasing swelling, promote tissue healing

28 Phase 1 Immobilization or protection should be done RICE NSAIDS for decreased inflammatory symptoms Short term analgesic

29 Phase 2: Repair/Regeneration Repair- articular cartilage, meniscus, spinal cord (new tissue is not identical) Regeneration- bone, muscle, peripheral nerve, blood vessels (heal with identical tissue) Patients are still swollen and pain with motion Blends with the inflammatory phase and remodeling phase Day 7 to 21

30 Phase 2 Fibrin clots form Fibroblasts proliferate near the injury Capillary proliferation occurs (more oxygen needed) Fibroblasts produce fibronectin, collagens, glycoproteins Fibronectin begins dormant followed by type III collagen then to stronger type I

31 Phase 2 Initially patient has structural deficiency Treatment – early controlled mobilization This aligns collagen with areas of physical stress making it stronger Prevents atrophy

32 Phase 3: Remodeling/Maturation Lasts up to 24 months May have persistent swelling and pain with motion Fibroblast activity decreases throughout this phase Capillary density decreases Cellular matrix becomes more refined

33 Phase 3 More type I and type III collagen fibers are produced Tensile strength improves Rehab can increase the physical demands until patients return to their activities of daily living

34 Fracture Healing Four phases: – Inflammation – Soft callus formation – Hard callus formation – Bone remodeling

35 Phase 1: Acute Lasts up to a week Hematoma formation, inflammation, angiogenesis (new blood vessel formation), soft callus formation Dominated by immune cells Phagocytic cells remove debris Platelets form clots

36 Phase 2: Repair/Regeneration Lasts 8 to 12 weeks Remodeling of scar tissue through cartilage formation, calcification and bone formation Mesenchymal cells become cartilage cells Proliferate the soft callus Replace the scar tissue with cartilage Chondrycytes hypertrophy and release chemicals to promote bone formation

37 Phase 2 Osteoblasts produce new bone Revascularization of the region occurs Soft tissue is replaced by bone Casting is used to allow time for a proper callus to develop

38 Phase 3: Remodeling Starts during Phase 2 and continues for several years Starts 21 days post fracture Woven bone replaced by cortical or trabecular bone New bone is remodeled by osteoclasts and osteoblasts based on mechanical loading

39 Fracture Management Treatment varies by : type of fixation – No reduction – Closed reduction – Open reduction – Open reduction internal fixation (ORIF) Location of fx Involved bone Mechanical loads Surrounding soft tissue

40 Fracture Management ORIF – Surgical fixation – Uses metal implants to stabilize fx’s – May allow rehab to begin within first week after surgery ( edema control, wound management, early motion) – More aggressive rehab can begin in 6-8 weeks

41 Fracture Management Non-surgical fixation – ROM delayed for 3 weeks – Until callus has enough tensile strength to tolerate movement – At 6-8 weeks patient may begin strengthening exercises and increase mechanical loads – Upper extremity fx’s may begin ROM exercises sooner because of smaller loads and fear of atrophy

42 Delayed/Non Union Fx’s Causes – Nutritional deficiencies – Diabetes, anemia – Smoking – Pharmacological drug use – Pre-injury vascular status – Muscle around fracture – Inadequate immobilization – Infection – High energy fractures – Gap distance – Nerve injury

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44 Delayed / Non Union Fx’s Susceptible areas – Tibia – Ulna – Femoral neck – Scaphoid (most common)

45 Peripheral Nervous Healing More proximal injuries result in greater losses Within 3 -5 days, axons distal to the injury undergo a degenerative process called Wallerian degeneration This is promote by immune cells, Schwann cells(the cell that normally myelinate axons) and the distal axon

46 Nerve Healing Produce proteins that produce and inflammatory response and pain Schwann cells divide to create an optimal environment for regeneration Surgical repairs can be helpful but are not guaranteed Only one proximal branch will form a new axon the others will degenerate

47 Muscle Healing Tissue trauma Hematoma formation Inflammatory cell reaction Phagocytosis Capillary regrowth Scar formation remodeling

48 Muscle Healing Must balance regeneration with scar formation Scar tissue is weak and only serves as a “scaffold” for the healing process Site is still weak No active motion immediately after injury Could result in re-rupture However, prolonged immobilization could result in atrophy

49 Muscle Healing What do you do?

50 Muscle Healing Early mobilization and motion may be started within the first 24 hours It must be pain free to avoid overloading Pain is your guide

51 Tendon Healing Ruptured tendons often require surgery Once repaired the tendon ends can go through their normal healing stages

52 Tendon Healing Hematoma formation Platelet aggregation Recruitment of inflammatory cells Phagocytosis Angiogenesis Fibroblast proliferation remodeling

53 Tendon Healing Tensile strength increases at 4 weeks Continues to improve up to 1 year Strength of tendon never returns to pre-injury level

54 Factors Affecting Healing Healing process is variable Factors: – Extensive trauma – Blood supply – Infection – Diabetes – Age – nutrition

55 Critical Thinking In a rehab setting, patients want to return ASAP. As a result, some patients do extra exercises, stretch to a point of pain, or try aggressive exercises (e.g. running) too early. What are the potential hazards to this approach? How would you explain your concerns to the patient or athlete?

56 Critical Thinking Two patients that are 10 weeks post –fractures are exercising next to each other. One of the patients had a distal radius fracture and the other had a scaphoid fracture. Both were treated conservatively with immobilization. The patient with the scaphoid fracture notices that she is still not able to do a lot of the exercises her counterpart is able to perform. She then asks why she is not progressing at the same rate as the other patient. How would you explain the differences in their recovery?


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