Proliferation Tissue Repair - asht.org 2017_HTRC... · Tissue Repair Jane Fedorczyk, PT, PhD, CHT,...
Transcript of Proliferation Tissue Repair - asht.org 2017_HTRC... · Tissue Repair Jane Fedorczyk, PT, PhD, CHT,...
Tissue Repair
Jane Fedorczyk, PT, PhD, CHT, ATC
Curtis National Hand CenterBaltimore, MD
October 6-8, 2017
3 Stages of Tissue Repair
Inflammatory Response
Fibroplasia or Proliferation
Remodeling or Maturation
Inflammatory Response
• Necessary first step
• Clean up injured area before repair• Phagocytes remove
• bacteria, debris, • foreign material, necrotic tissue
so repair can begin
Inflammatory Response
Vascular Response & Cellular Response
occur simultaneously
Vascular Response
• Initial Vasoconstriction
• Vasodilation
• Edema
Vasodilation results from:
• Histamine
• mast cells and basophils release histamine
• Bradykinin (vasoactive peptide)
• Synthesized locally• Hageman Factor XII Kallikrein Kinins
• Arachidonic Acid Metabolites
• Prostaglandins (PGE1 and PGE2)• Leukotrienes
Arachidonic Acid Metabolites Vasodilation (continued)
• PGE2 and leukotriene B4 are chemotactic to neutrophils (WBC)
• ↑ vascular permeability
• Nitric Oxide (NO) and Endothelial‐derived Relaxing Factor (EDRF)• Relax smooth muscle
• Contraction of endothelial cells• ↑ areas of fenestra on
Normal Fluid Aspects• Hydrostatic forces within vessel push fluid out
• Osmotic forces exerted by plasma proteins balance hydrostatic force
• Fluid that does escape is collected by lymphatics
• When this mechanism is altered ‐> edema
Edema Formation
Edema = presence of excess fluid in interstitial space
Results from:Vasodilation
Increase vascular permeability
Injured or overwhelmed lymphatic vessels
Cellular Response
Platelets
Mast Cells
White Blood Cells
(WBCs)
Platelets
• Initially forms clot to stop bleeding immediately after injury
• Secrete platelet‐derived growth factor (PDGF) chemotactic to neutrophils, monocytes, fibroblasts, & smooth muscle cells
• PDGF contributes to re‐epithelialization• Secrete transforming growth factor β (TGF‐β) that stimulates synthesis of fibronectin and collagen; inhibits collagen degradation
• Secrete platelet‐derived angiogenesis factor (PDAF); contributes to neovascularization = angiogenesis=capillary budding
Mast Cells
• Located in connective tissue
• Major source of histamine and cytokines
(IL‐8, TNF‐α)
• Contribute to leukocyte activation
and adhesion
• Stimulates PGE synthesis
• Histamine release itching!
Neutrophils
• Granules noted in cytoplasm
• Granules contain enzymes to destroy/ degrade debris
• Phagocytic debridement
• Appear within 90 minutes after injury, high numbers in approximately 12 hours
Types of White Blood Cells (WBC) Leucocytes
• Eosinophils granules in cytoplasm
• Some degree of phagocytosis • High numbers found in allergic reactions and some parasitic diseases
• Basophils• Represent extremely low number of WBCs
• Not phagocytic• Contain heparin and histamine within granules • Contribute to early ↑ vascular permeability
Types of White Blood Cells (WBC) Leucocytes
• Monocytes – agranular
• Phagocytic cell • Arrive within 5 hours of injury • Predominant cell in area within 48 hours
• Monocytes ‐>macrophages
• (monocytes move from capillary to tissue)
Types of White Blood Cells (WBC) Leucocytes
• Macrophages
• Major role is phagocytosis –make enzymes (collagenase) that facilitate wound debridement
• Release chemotactic factors that attract fibroblasts to injured tissue to begin healing
Types of White Blood Cells (WBC) Leucocytes
• Lymphocytes: T and B cells
• Involved in the immune response • Enhance macrophage function
• Chemotactic to fibroblasts
Cellular Response • Neutrophils stick to endothelial lining of capillary wall called pavementing
• Neutrophils stick because ↓ blood flow due to fluid loss ↑ viscosity of blood
THE 5 CARDINAL SIGNS OF INFLAMMATION
• Warmth
• Edema
• Redness
• Pain
• Loss of Function
Originally described by the Roman Aulus Cornelius Celsus
http://www.nature.com/ni/journal/v6/n12/covers/ni1205_largecover1.gif
THE 5 CARDINAL SIGNS OF INFLAMMATION
• Local vasodilation REDNESS and WARMTH
• ↑metabolic activity WARMTH
• Fluid and cell leakage into the extravascular space EDEMA or EXUDATE
• Overwhelmed/blocked/damage to lymphatics EDEMA
THE 5 CARDINAL SIGNS OF INFLAMMATION
• Distention of tissue secondary to edema ↑ pressure and leads to PAIN
• Chemical irritation of nocioceptors leads to PAIN
• Secondary to PAIN, decreased motion due to EDEMA , there is LOSS OF FUNCTION
Redundancy in the Imflammatory Response
• Many cells contribute to the same process
• Several growth factors or cytokines perform same chemotactic activity
• Cells serve more than one purpose
Repair or Tissue Healing
Granulation Tissue Formation
Fibroplasia
Angiogenesis
Re‐epithelialization
Re‐epithelialization
• Concurrent with formation of granulation tissue; necessary for cell migration
• “Halted when centrally advancing fronts meet and contact inhibition is re‐established.”
• Crucial for remodeling phase of repair
Granulation Tissue Formation
• Macrophages
• Fibroblasts
• Myofibroblasts
• Neovasculature
• Matrix serves as framework for angiogenesis (capillaries and lymphatics)
• collagen, fibronectin, ground substance, hyaluronic acid, and proteoglycans
Fibroplasia or Proliferation
• 5‐28 days
• Fibroblasts attracted by cytokines and growth factors released from macrophages and other cells
• PDGF, TGF‐β, FGF, EGF
• Collagen Synthesis > Lysis (Degradation)
Fibroplasia or ProliferationCollagen Synthesis
• Type III Collagen synthesized about 72 hrs post‐injury with peak synthesis at 5‐7 days
• Type III Collagen is gel‐like, disorganized, and has poor tensile strength
Myofibroblasts
• Fibroblasts transformed to myofibroblasts
• Actin filaments allow for ameboid migration
• Involved in wound retraction
• Produce fibronectin, collagen, and ground substance
Ground Substance forms Extracellular Matrix
Gel‐like substance that contains
• Water
• Salts
• Glycosoaminoglycans (GAGS)
• Dermatan Sulfate,
• Chondroitin Sulfate • Hyaluronic Acid (Non‐sulfate)
• Proteoglycans
GROUND SUBSTANCE: Proteoglycans
• Negative Charge Attracts H2O
• “Hydrophillic”
• Spacing between fibers
• Lubricant between fibers
• GAGs are covalently bound
• Water aids nutrition and diffusion
Proteoglycan
Fibroplasia
• Covalent bonds = X‐Links begin to form
• Tensile Strength due to Tissue • Not X‐Linking
• Thickness greatest @ 14 Days
• Angiogenesis = capillary budding and perfusion
Angiogenesis = capillary budding and perfusion
The process is started by the degradation of the basement membrane and invasion of endothelial cells into the perivascular tissue.
Tensile Strength of Tissue during Fibroplasia
Remodeling or Maturation
• Day 28 – 1 or 2 Years
• Synthesis = Lysis
• Decreased Cellularity & Vascularity
• Increased: Matrix Density & Organization
Remodeling Maturation
• Collagen:• X‐Links – More Mature Covalent Bonds
• Conversion from Type III to Type I • More Organized Fiber Alignment Parallel Arrangement
• Increasing Tensile Strength 2° to X‐Links
Tensile Strength & ↓ Thickness Bone Healing (Fractures)• Inflammation
• Repair
• Remodeling
Fracture Healing
• Type of healing depends on method of fixation• Secondary Fracture Healing = callus formation=repair
• Fracture heals by forming callus that converts to bone
• Primary Fracture Healing = regeneration• Healing imposed due to mechanical stabilization
• Compression – lessens gap formation
• Stabilization – motionless environment
Inflammation
• Hematoma; protect with immobilization
• With fixation hematoma eliminated by compression; no need to avoid motion
Treatment During Inflammation
Repair
1. Immobilization
2. No motion
3. Maybe no therapy
Fixation
1. Support for soft tissues
2. Joints placed in functional position
3. Edema Control
4. Intermittent AROM
Repair/Fibrocartilage Phase (3‐6 wks)
• Hematoma converts to fracture callus
Regeneration with Fixation (1‐6 wks)
• With fixation, osteoclasts form cutting cone that moves across fracture gap forming haversian canals; revascularization fracture site
• Osteoblasts form new osteons to bridge fracture site
• No peripheral callus
• No chondral stage to convert to bone
• Fracture dependent on fixation implant strength
Therapy
Repair
1. Protect fracture
2. May use removable orthosis
3. May initiate intermittent motion
Fixation
1. Intermittent motion: AROM, PROM
2. May initiate orthoses to restore motion earlier
Remodeling: 6 wks ‐1 year • Wolf’s Law – exercise influences remodeling
• Resorption of peripheral callus
Boney Union• Clinical union
• fracture site becomes stable & painfree
• Radiographic union• sound boney union
Abnormal Fracture Healing
• Slow union• healing does not occur in expected time frame
• Delayed union• healing takes considerably longer time
• see widening of fracture site on x‐ray
• at risk for non‐union
Abnormal Fracture Healing
• Non‐union• failure of bone to heal
• fibrous union
• pseudoarthrosis
• Mal‐union• healing in unsatisfactory position with residual bone deformity
Wound Closure
• Primary intention• Surgical closure
• Secondary intention• Wound closes with production of connective tissue (contraction) and epithelialization
• Longer healing time
Wound Closure
• Delayed Primary Closure
• Tertiary or re‐epithelialization• Used when there is a significant loss of tissue and deformity or loss of function would result with skin closure
• Skin Grafts
• Skin Flaps
Clinical Decision Making
What not to wait for…
• Edema• Gliding resistance proportional to area and severity of edema; reduced with gentle motion
• Observation of edema should inform the range, frequency, and speed of exercise
• Cao et al., 2005‐2008
What not to wait for…
• Bony healing• Functional and physiologic stresses increase quality and rate of healing
• Feehan, 2003
• Statistically significant decrease in number of days to achieve functional range of motion in patients who started active range of motion at one week post‐op
• Valdes, 2009
Best case scenario…
• Close‐packed position• Optimal position for immobilization
• Ligaments maximally taut
• Joint surfaces maximally congruent
• Joint spaced minimized
• Wrist extension, maximal MP flexion, digital PIP/DIP extension, thumb palmar abduction and MP/IP extension
Protection Function
Factors that May Influence Tissue Healing: Patient Factors
• Age
• Nutritional Status
• Fitness Level
• General Health
• Sleeping
• Smoking
• ETOH or Drug Abuse
• Hygiene
• Language Barrier
• Associated Injuries
• Co‐morbidities
• Medications
• Home Life/ Support
• Motivation
• Occupation/Hobbies
• Economic Status
Factors that May Influence Tissue Healing: Co‐Morbidities
• Physical • Diabetes Mellitus
• Psychological • Depression
• Post Traumatic Stress
• Medications • Corticosteroids delay healing
• Allergies?
Factors that May Influence Tissue Healing: Skin/Superficial Soft Tissue
• Skin Integrity
• Skin Loss
• Type of Skin Coverage
• Tidy vs. Untidy
• Lymphatic Vessels
Factors that May Influence Tissue Healing: Vascular System
• Patent Vessels• Skin Color
• Skin Temperature
• Repair?
• Graft?
• Vascular Stability
• Edema
• Co‐Morbidities• Risk of Insufficiency
• Clotting History
• Patient Education• Cold
• Caffeine
• Nicotine
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Summary of Systems Review
When multiple systems are involved, the goals of treatment must protect the repaired structures according to their individual healing time frames.
What therapists need to know:
• All structures repaired
• Surgical specifics
• Perceived integrity of structures
Skin/Superficial Soft Tissue
• Skin Integrity
• Skin Loss
• Type of Skin Coverage
• Tidy vs. Untidy
• Vascularity
• Drainage
• Pins, Buttons, Drains
• Primary Healing
• Secondary Healing
• Delayed Healing
• Excessive Scar
• Skin Contracture
• Lymphatic Vessels
• Nails and Nailbeds
• Dressing Options
Vascular System
• Patent Vessels• Skin Color
• Skin Temperature
• Repair? Which? All?
• Graft?
• Vascular Stability
• Edema
• Co‐Morbidities• Risk of Insufficiency
• Clotting History
• Patient Education• Cold
• Caffeine
• Nicotine
Integrity of structures?Adequacy of blood supply?
Vascular
• Arterial or venous repair or graft• Vein grafts as particularly fragile
• Immediate concerns• Vasospasm
• Pale due to manipulation
• Venous insufficiency• Blue and tense to touch
• Arterial insufficiency• White or pale
Vascular
• Implications for therapy• Wound care and dressings
• Temperature• Choice of modalities
• Elevation/avoidance of dependent position
• Dietary issues• Nicotine/caffeine
• Orthotics and strapping• Avoidance of single digit
Nerves
• Repairs
• Level
• Type of Repair
• Tension
• Graft
• Transposition
• Decompression
• Injured not Repaired
• More than one level
• Type of Injury• Traction
• Laceration
• Neuromas
• Position and Duration of Immobilization
Nerves
• Sensibility
• Motor Loss
• Muscle Imbalance
• Sympathetic Fcn
• Sudomotor Fcn
• Proprioception
• Pilomotor Function
• Pain
• Sensory Re‐Ed
• Patient Education• Caffiene
• Nicotine
• Temperature
• Sharp Objects
• Pain• Phantom Limb/Digit
• Threshold/Tolerance
Nerve
• Questions to ask:• Tenuousness of repair?• Indications for protective immobilization?
• Timing of progression towards full range of motion?
“Limited, protected postsurgical motion does not affect the results of digital nerve repair”
(Yu et al., 2004)
Muscle and Tendons
Muscle
• Tear, Rupture, Loss
• Muscle Fibrosis
• Msle‐Tendon Length
• Status of Motor End Plates (nerve)
• Myositis Ossificans
• Trigger Points
Tendon
• Repair? Zone?
• Retraction? Tension?
• Sheath or Pulley Repairs
• Flexors/Extensors
• Balance
• Injury but no repair
Tendon Anastomosis
• Suture Technique
• Quality
• Gap
• Tension
• Retraction
Tendon
• Questions to ask:• Zone of injury?• Tendons repaired, partially lacerated, intact?• Number of strands?
• Integrity of repair?
Bone and Joints
Fracture
• Type
• Stability
• Fixation
• Bone Loss/Length
• Alignment/Congruity
• Location• Blood Supply
• Epiphysis
• Co‐morbidity• Metabolic Conditions
• Healing Potential
• Risk of: • Osteomyelitis
• Heterotopic Ossification