Transcript Concepts of Healing

Concepts of
Healing
 https://www.youtube.com/watch?v=suCK
m97yvyk
Healing PhasesInflammation
 Injury occurs and body starts defense
 Goal of rehab clinicians is to allow
inflammation to happen, but minimize it
Inflammation-Vasoconstriction and
vasodilatation
 Vasoconstriction limits oxygen which
triggers the inflammation process by
causing hypoxia
 Vasodilatation releases blood and blood
products to injured site
Inflammation- Cellular
Response
 Chemicals are released and other cells
attracted
 Platelets
 release phospholipids (stimulate clotting)
 Bind to collagen
 Release fibronectin, growth factors, fibrinogen
 Fibronectin binds fibrin and collagen to
form web to stop bleeding
 Eventually replaced by Type III collagen
 Damaged lymph vessels also plugged
 Since they are plugged, can’t evacuate extra
fluid
 Once the area is stable, chemical released
to promote absorption of fibrin plug
 To remove debris, neutrophils (WBC)
come in 5-6 hours after injury
 Neutrophils replaced by phagocytes,
monocytes, and macrophages to remove
debris and dead tissue
 24-48 hours post injury
 Exudate formed from fluid escaping
vessels, dead tissue
 Debridement needed for healing to
continue
Inflammation- Chemical
Reactions
 Some cells produce chemicals, and some
chemicals stimulate the arrival or production of
specific cells.
 Chemotaxis- the process of attraction or stimulation
 Vascular permeability caused by histamine that
is released by mast cells
 Histamine is a chemotactic factor for WBC
 Kinins released by plasma
 Prostaglandin forms (continues vascular
permeability, attracting leukocytes). These permit
advancement to Proliferation Stage
Proliferation
 Fibroblasts- responsible for new
capillaries and extracellular matrix
 Matrix protects new blood vessels
 Collagen produced is Type III- weak, thin,
haphazard
 Tensile strength is directly related to amount,
type, & arrangement of collagen
Remodeling Phase
 Wound tissue converts to scar tissue
 Type I collagen synthesized, Type III
destroyed
 More resistant to destruction
 As fluid reduces, can create more cross links
Specific Tissue
 Ligaments
 Injured ligament stumps surrounded by fluid
Tendons
 Have support from
structures that aid  Revasularization
in healing
in first 3 weeks
 Periosteum
 Synovial sheath
 Collagen
synthesis weeks
1-4
 Week 2 cells begin
to align along lines
of stress
 Immobile until day
21
 Week 3 synovial
sheath
reconstituted
Muscles
 Satellite cells
 Larger muscles
resort to scar
 Unique to muscles
tissue
 Fuse with adjacent
myofibribers to
repair
 Occurs daily
Articular Cartilage
 Made of Type II
collagen
 Cartilage
regenerates
slower than scar
tissue
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Healing depends on
 Depth of defect
 Maturity of cartilage
 Location of defect
Surgical repair options
 Clean the joint
 Lavage or debridment
 Repair the joint
 Arthroplasty, drilling,
microfracture
 Restore the joint
 Plugs and transplantation
Bone
 Callus takes 3-4
weeks to form
 Eventually
becomes bone
 Immobilizes
fragment ends,
allows stress to be
applied without
harming fracture
site
Specific Tissue
Tissue
Inflam
Prolif
Remod
Final
Ligament 0-72 hrs 1-6wk
Tendon
0-1wk
Muscle
0-1wk
Articular 0-5d
cartilage
Bone
0-4d
6wk40-50wk
12mo
10d-42d 2mo40-50wk
112d
7-18d
6wk-6mo 6mo
2wk-1mo 2mo
6mo
1-6wk
12wk
3-4mo
Factors the Affect Healing
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Modalities
Drugs
Surgical repair- quality of technique, follow up, infection
Age
Disease
Wound size
Infection
Nutrition
Muscle spasm
Swelling
Healing & Rehab Timeline
Inflammation
Modalities for reduction of pain, muscle spasm,
edema.
No exercises to disrupt fibrin plug.
Exercise non-involved body parts, cardio
Proliferation
Modalities, non-involved and cardio
ROM to influence collagen arrangement- mild
PROM, AAROM, some AROM
Mild isometrics
Remodeling
Move from full motion to resistive exercises
Progress to balance and agility
Functional and sport-specific toward end
Aggressiveness inc as tissue strength improves