Tissue Response to Injury
Inflammatory Response• Acute Inflammation  – Short onset and duration  – Production of exudate, leukocytes• Chronic Inflam...
Cardinal Signs of             Inflammation•   Rubor (redness)•   Tumor (swelling)•   Color (heat)•   Dolor (pain)•   Funct...
Phases of the Inflammatory           Response           (3 separate phases)• 1. Acute phase• 2. Repair phase• 3. Remodelin...
Phase I: Acute Phase• Initial reaction to an injury occurring 3  hours to 2 days following injury• Goal  –   Protect  –   ...
• External and internal injury result in  tissue death and cell death• Decreased oxygen to area increases cell  death• Res...
• First hour  – Vasoconstriction and coagulation occur to    seal blood vessels and chemical mediators    are released  – ...
• Second hour (continued)  – Exudate increases (high concentration of    RBC’s) due to increased vessel permeability  – Pe...
• Cellular response  – Mast cells (connective tissue cells) and    leukocytes (basophils, monocytes,    neutrophils) enter...
Phase II: Repair Phase• Phase will extent from 48 hours to 6  weeks following cleaning of fibrin clot,  erythrocytes, and ...
• Scar formation  – Less viable than normal tissue, may    compromise healing  – Firm, inelastic mass devoid of capillary ...
• Primary healing (healing by first intention)  – Closely approximated edges with little    granulation tissue production•...
• Regeneration  – Related to health, nutrition and tissue type  – Dependent on levels of:      • debris (phagocytosis)    ...
Phase III: Remodeling• Overlaps repair and regeneration• First 3-6 weeks involves laying down of  collagen and strengtheni...
Chronic Inflammation• Result of failed acute inflammation  resolution within one month termed  subacute inflammation• Infl...
Characteristics of Chronic        Inflammation• Proliferation of connective tissue and tissue  degeneration• Presence of l...
Factors That Impede Healing• Extent of injury       • Corticosteroids• Edema                  • Keloids and• Hemorrhage   ...
Soft Tissue Healing• Cell structure/function  – All organisms composed of cells  – Properties of soft tissue derived from ...
Soft Tissue Adaptations• Metaplasia - transformation of tissue from one type to               another that is not normal f...
Cartilage Healing• Limited capacity to heal• Little or no direct blood supply• Chrondrocyte and matrix disruption  result ...
Ligament Healing• Follows similar healing course as  vascular tissue• Proper care will result in acute, repair,  and remod...
Skeletal Muscle Healing• Skeletal muscle cannot undergo mitotic  activity to replace injured cells• New myofibril regenera...
Nerve Healing• Cannot regenerate after injury• Regeneration can take place within a nerve  fiber• Proximity of injury to n...
Modifying Soft-Tissue Healing• Varying issues exist for all soft tissues  relative to healing (cartilage, muscle,  nerves)...
Management Concepts• Drug utilization  – Anitprostaglandin agents used to combat    inflammation  – Non-steroidal anti-inf...
• Therapeutic Modalities  – Thermal agents are utilized     • Heat stimulates acute inflammation (but works       as a dep...
• Therapeutic Exercise  – Major aim involves pain free movement, full    strength power, and full extensibility of    asso...
Fracture Healing• Potential serious bone fractures are part  of athletics• Time is necessary for proper bone union  to occ...
• Bone undergoes constant remodeling  through osteocyte activity• Osteocytes cellular component of bone  – Osteoblasts are...
Acute Fracture of Bone• Follows same three phases of soft tissue  healing• Less complex process• Acute fractures have 5 st...
Callus Formation• Soft callus is a random network of woven  bone• Osteoblasts fill the internal and external  calluses to ...
• Hard callus formation occurs after 3-4  weeks and lasts 3-4 months• Hard callus is a gradual connection of  bone filamen...
Ossification• Ossification is complete when bone has  been laid down and the excess callus has  been resorbed by osteoclas...
Remodeling• Occurs following callus resorption and  trabecular bone is laid along lines of stress• Bioelectric stimulation...
Acute Fracture Management• Must be appropriately immobilized, until X-  rays reveal the presence of a hard callus• Fractur...
• Poor blood supply  – Bone may die and union/healing will not occur    (avascular necrosis)  – Common sites include:     ...
• Infection  – May interfere with normal healing,    particularly with compound fractures  – Severe streptococcal and stap...
• Gate Theory  – Area in dorsal horn of spinal cord causes    inhibition of pain impulses ascending to    cortex  – T-cell...
• Pain assessment  – Self report is the best reflection of pain and    discomfort  – Assessment techniques include:     • ...
• Heat/Cold  – Heat increases circulation, blood vessel    dilation, reduces nociception and ischemia    caused by muscle ...
Psychological Aspects of Pain• Pain can be subjective and psychological• Pain thresholds vary per individual• Pain is ofte...
Tissue healing
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Tissue healing

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Tissue healing

  1. 1. Tissue Response to Injury
  2. 2. Inflammatory Response• Acute Inflammation – Short onset and duration – Production of exudate, leukocytes• Chronic Inflammation – Long onset and duration – Presence of extensive scar tissue
  3. 3. Cardinal Signs of Inflammation• Rubor (redness)• Tumor (swelling)• Color (heat)• Dolor (pain)• Functio laesa (loss of function)
  4. 4. Phases of the Inflammatory Response (3 separate phases)• 1. Acute phase• 2. Repair phase• 3. Remodeling phase
  5. 5. Phase I: Acute Phase• Initial reaction to an injury occurring 3 hours to 2 days following injury• Goal – Protect – Localize – Decrease injurious agents – Prepare for healing and repair• Caused by trauma, chemical agents, thermal extremes, pathogenic organisms
  6. 6. • External and internal injury result in tissue death and cell death• Decreased oxygen to area increases cell death• Rest, ice, compression & elevation are critical to limiting cell death
  7. 7. • First hour – Vasoconstriction and coagulation occur to seal blood vessels and chemical mediators are released – Immediately followed by vasodilation or blood vessel• Second hour – Vasodilation decreases blood flow, increased blood viscosity resulting in edema (swelling)
  8. 8. • Second hour (continued) – Exudate increases (high concentration of RBC’s) due to increased vessel permeability – Permeability changes generally occur in capillary and venules
  9. 9. • Cellular response – Mast cells (connective tissue cells) and leukocytes (basophils, monocytes, neutrophils) enter area – Mast cells with heparin and histamine serve as first line of defense – Basophils provide anticoagulant – Neutrophils and monocytes are responsible for small and large particles undergoing phagocytosis - ingestion of debris and bacteria
  10. 10. Phase II: Repair Phase• Phase will extent from 48 hours to 6 weeks following cleaning of fibrin clot, erythrocytes, and debris• Repaired through 3 phases – Resolution (little tissue damage and normal restoration) – Restoration (if resolution is delayed) – Regeneration (replacement of tissue by same tissue)
  11. 11. • Scar formation – Less viable than normal tissue, may compromise healing – Firm, inelastic mass devoid of capillary circulation – Develops from exudate with high protein and debris levels resulting in granulation tissue – Invaded by fibroblasts and and collagen forming a dense scar and while normally requiring 3-14 weeks may require 6 months to contract
  12. 12. • Primary healing (healing by first intention) – Closely approximated edges with little granulation tissue production• Secondary healing (heal by secondary intention) – Gapping, tissue loss, and development of extensive granulation tissue – Common in external lacerations and internal musculoskeletal injuries
  13. 13. • Regeneration – Related to health, nutrition and tissue type – Dependent on levels of: • debris (phagocytosis) • endothelial production (hypoxia and macrophages stimulate capillary buds) • production of fibroblasts (revascularization allows for enhanced fibroblast activity and collagen production which is tied to Vitamin C, lactic acid, and oxygen –
  14. 14. Phase III: Remodeling• Overlaps repair and regeneration• First 3-6 weeks involves laying down of collagen and strengthening of fibers• 3 months to 2 years allowed for enhanced scar tissue strength• Balance must be maintained between synthesis and lysis• Take into consideration forces applied and immobilization/mobilization time frames relative to tissue and healing time
  15. 15. Chronic Inflammation• Result of failed acute inflammation resolution within one month termed subacute inflammation• Inflammation lasting months/years termed chronic – Results from repeated microtrauma and overuse – Proliferation of connective tissue and tissue degeneration
  16. 16. Characteristics of Chronic Inflammation• Proliferation of connective tissue and tissue degeneration• Presence of lymphocytes, plasma cell, macrophages(monocytes) in contrast to neutrophils (during acute conditions)• Major chemicals include – Kinins (bradykinin) - responsible for vasodilation, permeability and pain – Prostaglandin - responsible for vasodilation but can be inhibited with aspirin and NSAID’s
  17. 17. Factors That Impede Healing• Extent of injury • Corticosteroids• Edema • Keloids and• Hemorrhage Hypertrophic Scars• Poor Vascular • Infection Supply • Humidity, Climate,• Separation of Tissue Oxygen Tension• Muscle Spasm • Health, Age, and• Atrophy Nutrition
  18. 18. 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
  19. 19. Soft Tissue Adaptations• Metaplasia - transformation of tissue from one type to another that is not normal for that tissue• Dysplasia - abnormal development of tissue• Hyperplasia- excessive proliferation of normal cells in normal tissue arrangement• 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
  20. 20. Cartilage Healing• Limited capacity to heal• Little or no direct blood supply• Chrondrocyte and matrix disruption result in variable healing• Articular cartilage that fails to clot and has no perichondrium heals very slowly• If area involves subchondral bone (enhanced blood supply) granulation tissue is present and healing proceeds normally
  21. 21. Ligament Healing• Follows similar healing course as vascular tissue• Proper care will result in acute, repair, and remodeling phases in same time required by other vascular tissue• Repair phase will involve random laying down of collagen which, as scar forms, will mature and realign in reaction to joint stresses and strain• Full healing may require 12 months
  22. 22. Skeletal Muscle Healing• Skeletal muscle cannot undergo mitotic activity to replace injured cells• New myofibril regeneration is minimal• Healing and repair follow the same course as other soft tissues.
  23. 23. Nerve Healing• Cannot regenerate after injury• Regeneration can take place within a nerve fiber• Proximity of injury to nerve cell makes regeneration more difficult• For regeneration, optimal environment is required• Rate of healing occurs at 3-4 mm per day• Injured central nervous system nerves do not heal as well as peripheral nerves
  24. 24. Modifying Soft-Tissue Healing• Varying issues exist for all soft tissues relative to healing (cartilage, muscle, nerves)• Blood supply and nutrients is necessary for all healing• Healing in older athletes or those with poor diets may take longer• Certain organic disorders (blood conditions) may slow or inhibit the healing process
  25. 25. Management Concepts• Drug utilization – Anitprostaglandin agents used to combat inflammation – Non-steroidal anti-inflammatory agents (NSAID’s) – Medications will work to decrease vasodilatation and capillary permeability
  26. 26. • Therapeutic Modalities – Thermal agents are utilized • Heat stimulates acute inflammation (but works as a depressant in chronic conditions) • Cold is utilized as an inhibitor – Electrical modalities • Treatment of inflammation • Ultrasound, microwave, electrical stimulation (includes transcutaneous electrical muscle stimulation and electrical muscle stimulation
  27. 27. • Therapeutic Exercise – Major aim involves pain free movement, full strength power, and full extensibility of associated muscles – Immobilization, while sometimes necessary, can have a negative impact on an injury • Adverse biochemical changes can occur in collagen – Early mobilization (that is controlled) may enhance healing
  28. 28. Fracture Healing• Potential serious bone fractures are part of athletics• Time is necessary for proper bone union to occur and is often out of the control of a physician• Conservative treatment will be necessary for adequate healing to occur
  29. 29. • Bone undergoes constant remodeling through osteocyte activity• Osteocytes cellular component of bone – Osteoblasts are responsible for bone formation while osteoclasts resorb bone• Cambium (periosteum) – A fibrous covering involved in bone healing – Vascular and very dense• Inner cambium – less vascular and more cellular. – Provides attachments for muscle, ligaments and tendons
  30. 30. Acute Fracture of Bone• Follows same three phases of soft tissue healing• Less complex process• Acute fractures have 5 stages – Hematoma formation – Cellular proliferation – Callus formation – Ossification – Remodeling
  31. 31. Callus Formation• Soft callus is a random network of woven bone• Osteoblasts fill the internal and external calluses to immobilize the site• Calluses are formed by bone fragments that bridge the fracture gap• The internal callus creates a rigid immobilization early
  32. 32. • Hard callus formation occurs after 3-4 weeks and lasts 3-4 months• Hard callus is a gradual connection of bone filaments to the woven bone• Less than ideal immobilization produces a cartilagenous union instead of a bony union
  33. 33. Ossification• Ossification is complete when bone has been laid down and the excess callus has been resorbed by osteoclasts.
  34. 34. Remodeling• Occurs following callus resorption and trabecular bone is laid along lines of stress• Bioelectric stimulation plays a major role in completing the remodeling process• The process is complete when the original shape is achieved or the structure can withstand imposed stresses
  35. 35. Acute Fracture Management• Must be appropriately immobilized, until X- rays reveal the presence of a hard callus• Fractures can limit participation for weeks or months• A clinician must be certain that the following areas do not interfere with healing – Poor blood supply – Poor immobilization – Infection
  36. 36. • Poor blood supply – Bone may die and union/healing will not occur (avascular necrosis) – Common sites include: • Head of femur, navicular of the wrist, talus, and isolated bone fragments – Relatively rare in healthy, young athletes except in navicular of the wrist• Poor immobilization – Result of poor casting allowing for motion between bone parts – May prevent proper union or result in bony deformity
  37. 37. • Infection – May interfere with normal healing, particularly with compound fractures – Severe streptococcal and staphylococcal infections – Modern antibiotics has reduced the risk of infections – Closed fractures are not immune to infections within the body or blood• If soft tissue alters bone positioning, surgery may be required to ensure proper union
  38. 38. • Gate Theory – Area in dorsal horn of spinal cord causes inhibition of pain impulses ascending to cortex – T-cells will transmit signals to brain – Substantia gelatinosa functions as gate determining if stimulus sent to T-cells – Pain stimuli exceeding threshold results in pain perception – Stimulation of large fast nerves can block signal of small pain fiber input – Rationale for TENS, accupressure/puncture, thermal agents and chemical skin irritants
  39. 39. • Pain assessment – Self report is the best reflection of pain and discomfort – Assessment techniques include: • visual analog scales (0-10, marked no pain to severe pain) • verbal descriptor scales (marked none, slight, moderate, and severe)• Pain Treatment – Must break pain-spasm-hypoxia-pain cycle through treatment – Agents used; heat/cold, electrical stimulation-induced analgesia, pharmacological agents
  40. 40. • Heat/Cold – Heat increases circulation, blood vessel dilation, reduces nociception and ischemia caused by muscle spasm – Cold applied for vasoconstriction and prevention of extravasation of blood into tissue – Pain reduced through decrease in swelling and spasm• Induced analgesia – Utilize electrical modalities to reduce pain – TENS and acupuncture commonly used to target Gate Theory
  41. 41. Psychological Aspects of Pain• Pain can be subjective and psychological• Pain thresholds vary per individual• Pain is often worse at night due to solitude and absence of external distractions• Personality differences can also have an impact• A number of theories relative to pain exist and it physiological and psychological components• Athlete, through conditioning are often able to endure pain and block sensations of minor injuries

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