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Tissue Response to injury

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Presentation on theme: "Tissue Response to injury"— Presentation transcript:

1 Tissue Response to injury

2 Injury Acute injury Overuse injury – microtrauma  macrotrauma
Macrotrauma - force that overwhelms the body with high force in a short time Microtrauma – repeated low-intensity forces Overuse injury – microtrauma  macrotrauma Chronic injury – failure of systems to continue healing process – “stuck”

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The Healing Process Essential for athletic trainer to possess in depth knowledge of healing process Understand phases Time frames physiological changes associated with each phase Must create a conducive environment for healing Healing is a continuum © 2011 McGraw-Hill Higher Education. All rights reserved.

4 Phases of the Inflammatory Response
(3 separate phases) 1. Inflammatory response phase 2. Fibroblastic repair phase 3. Maturation and remodeling phase © 2011 McGraw-Hill Higher Education. All rights reserved.

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Figure 10-1 © 2011 McGraw-Hill Higher Education. All rights reserved.

6 Phase I: Inflammatory Response Phase
Healing begins immediately Injury results in altered metabolism and liberation of various materials Initial reaction by leukocytes and phagocytic cells Goal Protect Localize Decrease injurious agents Prepare for healing and repair © 2011 McGraw-Hill Higher Education. All rights reserved.

7 Cardinal Signs of Inflammation
Rubor (redness) Tumor (swelling) Color (heat) Dolor (pain) Functio laesa (loss of function) © 2011 McGraw-Hill Higher Education. All rights reserved.

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Vascular Response Vasoconstriction and coagulation occur to seal blood vessels and chemical mediators are released Presses endothelial lining together to produce local anemia Followed by vasodilation of blood vessel 5-10 minutes later Initially increases blood flow Initial effusion of blood and plasma lasts hours © 2011 McGraw-Hill Higher Education. All rights reserved.

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Figure 10-3 © 2011 McGraw-Hill Higher Education. All rights reserved.

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Clot Formation Platelets adhere to exposed collagen leading to formation of plug (clot) Clots obstruct lymphatic fluid drainage and aid in localizing injury © 2011 McGraw-Hill Higher Education. All rights reserved.

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Chronic Inflammation Occurs when acute inflammatory response does not eliminate injuring agent Tissue not restored to normal physiologic state Cause for shift from acute to chronic is unknown Typically associated with overuse, overload, cumulative microtrauma © 2011 McGraw-Hill Higher Education. All rights reserved.

12 Phase II: Fibroblastic Repair Phase
Scar formation through 3 phases Resolution (little tissue damage and normal restoration) Restoration (if resolution is delayed) Regeneration (replacement of tissue by same tissue) Referred to as fibroplasia Complaints of pain and tenderness end © 2011 McGraw-Hill Higher Education. All rights reserved.

13 Phase III: Maturation & Remodeling
Long-term process Realignment of collagen relative to applied tensile forces Continued breakdown and synthesis of collagen = increased strength Tissue will gradually assume normal appearance May require several years to complete © 2011 McGraw-Hill Higher Education. All rights reserved.

14 Factors That Impede Healing
Extent of injury Edema Hemorrhage Poor Vascular Supply Separation of Tissue Muscle Spasm Atrophy Corticosteroids Keloids and Hypertrophic Scars Infection Humidity, Climate, Oxygen Tension Health, Age, and Nutrition © 2011 McGraw-Hill Higher Education. All rights reserved.

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Soft Tissue Healing Cell structure/function All organisms composed of cells Properties of soft tissue derived from structure and function of cells Cells consist of nucleus surrounded by cytoplasm and encapsulated by phospholipid cell membrane Nucleus contains chromosomes (DNA) Functional elements of cells (organelles) include mitochondria, ribosomes, endoplasmic reticulum, Golgi apparatus & centrioles © 2011 McGraw-Hill Higher Education. All rights reserved.

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Tissues of the Body Bone - not classified as soft tissue 4 types of soft tissue Epithelial tissue Skin, vessel & organ linings Connective tissue Tendons, ligaments, cartilage, fat, blood, and bone Muscle tissue Skeletal, smooth, cardiac muscle Nerve tissue Brain, spinal cord & nerves © 2011 McGraw-Hill Higher Education. All rights reserved.

17 Soft Tissue Adaptations
Atrophy- a decrease in the size of tissue due to cell death and re-absorption or decreased cell proliferation Hypertrophy - an increase in the size of tissue without necessarily changing the number of cells © 2011 McGraw-Hill Higher Education. All rights reserved.

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Cartilage Healing Limited capacity to heal Little or no direct blood supply © 2011 McGraw-Hill Higher Education. All rights reserved.

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Ligament Healing Follows similar healing course as other vascular tissues Proper care will result in acute, repair, and remodeling phases in same time required by other vascular tissues Repair phase will involve random laying down of collagen which, as scar forms, will mature and realign in reaction to joint stresses and strain © 2011 McGraw-Hill Higher Education. All rights reserved.

20 Skeletal Muscle Healing
Initial bleeding followed by proliferation of ground substance and fibroblast Myoblastic cells form = regeneration of new myofibrils Collagen will mature and orient along lines of tension Healing could last 6-8 weeks depending on muscle injured © 2011 McGraw-Hill Higher Education. All rights reserved.

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Tendon Healing Requires dense fibrous union of separated ends Abundance of collagen is required for good tensile strength Too much = fibrosis – may interfere with gliding Initially injured tendon will adhere to surrounding tissues (week 2) Week 3 – tendon will gradually separate Tissue not strong enough until weeks 4-5 © 2011 McGraw-Hill Higher Education. All rights reserved.

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Bone Healing Less complex process Acute fractures have 5 stages Hematoma formation Cellular proliferation Callus formation Ossification Remodeling © 2011 McGraw-Hill Higher Education. All rights reserved.

23 Healing of Stress Fractures
Result of cyclic forces, axial compression or tension from muscle pulling Electrical potential of bone changes relative to stress (compression, tension, or torsional) Constant stress axially or through muscle activity can impact bone resorption, leading to microfracture © 2011 McGraw-Hill Higher Education. All rights reserved.

24 Key Time Frames

25 Key Time Frames

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Pain Major indicator of injury Pain is individual and subjective Factors involved in pain Anatomical structures Physiological reactions Psychological, social, cultural and cognitive factors © 2011 McGraw-Hill Higher Education. All rights reserved.

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Pain Categories Pain sources Fast versus slow pain Acute versus chronic Projected or referred pain © 2011 McGraw-Hill Higher Education. All rights reserved.

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Pain sources Cutaneous, deep somatic, visceral and psychogenic Cutaneous pain is sharp, bright and burning with fast and slow onset Deep somatic pain originates in tendons, muscles, joints, periosteum and blood vessels Visceral pain begins in organs and is diffused at first and may become localized Psychogenic pain is felt by the individual but is emotional rather than physical © 2011 McGraw-Hill Higher Education. All rights reserved.

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Referred Pain Pain which occurs away from actual site of injury/irritation Unique to each individual and case May elicit motor and/or sensory response A-alpha fibers are sensitive to pressure and can produce paresthesia Three types of referred pain include: myofascial, sclerotomic, and dermatomic © 2011 McGraw-Hill Higher Education. All rights reserved.

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Pain assessment Self report is the best reflection of pain and discomfort Utilize multi- and uni-dimensional questionnaires Assessment techniques include: Visual analog scales (0-10, marked no pain to severe pain) Pain charts McGill Pain questionnaire Activity pain indicator profiles Numeric rating scale © 2011 McGraw-Hill Higher Education. All rights reserved.


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