Physiologic Factors of Rehabilitation

primary injury

Occurs at the moment of trauma

Direct mechanical damage to cells and tissues

Cells may be disrupted, torn, crushed, or ruptured

examples of primary injury

• ligament fibers torn during ankle sprain

• muscle fibers damaged during a strain

• tissue crushed by a direct blow

secondary injury

Develops after the initial trauma

Results from the body’s physiologic response to injury

Reduced blood flow and oxygen delivery may damage cells that survived the initial trauma

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Often referred to as secondary hypoxic injury

local blood flow after trauma

• intial vasocontriction before vasodilation

• Cells surrounding the primary injury may become hypoxic

Prolonged oxygen deprivation can lead to:

Cell degeneration

Additional cell death

Expansion of the injured area

prolonged o2 deprivation can lead to

Cell degeneration

Additional cell death

Expansion of the injured area

what happens as damaged cells die?

Cellular contents and inflammatory mediators are released

Vascular changes are stimulated

The inflammatory response continues

tissue damages trigger the release of what?

inflammatory mediators such as

• histamine

• Plasma, proteins, and blood cells move from the vessels into the interstitial tissues

  
  

histamine

• natural chemical created by your immune system and nervous system

• acts as a messenger to trigger inflammation, control stomach acid, and wake up your brain

• increases capillary permeability (how easily tiny blood vessels let fluid, oxygen, and nutrients pass through their walls into body tissues)

  
  

plasma

Pale-yellow liquid (~55% of blood) that carries water, proteins, nutrients, hormones, and minerals

swelling

broad term for enlargement caused by fluid, injury, inflammation, infection, or abnormal tissue growth

edema

A specific condition defined strictly by fluid retention and leakage from tiny blood vessels into tissues

as inflammatory cells and injured cells break down, they may release:

Proteolytic enzymes

Additional inflammatory mediators

Cellular debris

proteolytic enzymes

a group of enzymes that break down proteins into smaller peptides and amino acids

break down of inflammatory cells can…

• break down proteins in nearby tissues

• Irritate surrounding structures

• Increase capillary permeability

• Sustain the inflammatory response

around a joint, prolonged inflammation can contribute to …

• Persistent swelling

• Joint irritation

• Loss of range of motion

• Muscle inhibition and weakness

• Delayed tissue repair and recovery

what happens as the histamine releases and increases capillary permeability?

• blood flow slows

• WBC move towards vessel walls

• WBC adhere to vascular lining

• WBC migrate through vessel into injured tissue

neutrophils

arrive first

• most common WBC

• make uo 50-70% of WBC

• first line of germ defense

• early cellular response

• many eventually die within injured tissue

macrophages

arrive after neutrophils

• large WBC

• finds, engulfs, and digests cellular debris, foreign substances, microbes, and abnormal cells through a process called phagocytosis

• removes dead neutrophils

• Remove fibrin, red blood cells, and other material

• Help prepare the tissue for repair

  
  

hematoma

a localized pool of clotted or partially clotted blood that forms outside of blood vessels due to a damaged wall of a vein, artery, or capillary

exudate

a fluid that leaks out of blood vessels into nearby tissues or surfaces due to inflammation or injury

excessive hematoma and edema

can delay progression into repair

structures affected by inflammation

Synovial membrane

Synovial fluid

Joint capsule

Ligaments

Articular cartilage

Menisci or labrum, when present

Tendons and bursae surrounding the joint

Subchondral bone

synovial joint

a freely movable joint enclosed by a capsule and containing synovial fluid

Articular cartilage

smooth cartilage covering the ends of bones within a joint

Labrum

fibrocartilaginous rim that deepens a joint socket, such as at the shoulder or hip

meniscus

fibrocartilage that helps distribute load and improve joint congruency, such as in the knee

after injury synovial changes

Surface cells may proliferate

Vascularity may increase

The membrane may become irritated and inflamed

Subsynovial tissue may gradually become fibrotic

Synovial fluid volume may increase

Protein content may increase

hyaluronic acid concentration or quality may change

joint effussion

synovitis

Inflammation of the synovial membrane

May follow acute trauma

May persist with repeated mechanical irritation

Can contribute to ongoing joint effusion

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once synovitis becomes chronic, the membrane itself can continue contributing to the inflammatory process even after the original trauma has passed.

consequences of joint effusion

Increases joint pressure

May limit ROM

Can contribute to pain

May inhibit surrounding muscles

Can alter joint mechanics

synovitis changes to synovial fluid

Increased protein concentration

Decreased viscosity with chronic inflammation

Reduced hyaluronic acid concentration

hemarthrosis

• bleeding into the joint

• blood and fibrin may accumulate

effects of blood in joint on articular cartilage

Decreased proteoglycan synthesis

Potential for prolonged or irreversible changes

joint capsule

connective tissue envelope surrounding a synovial joint

effects of persistant effusion on joint capsule

Intra-articular (inside the joint) pressure increases

The capsule may become stretched

Capsular tissues may become fibrotic over time

Associated ligaments may be stressed

Motion may become restricted

fxn of fibrocartilage

Improve joint congruency

Distribute load

Contribute to stability

Assist with force transmission

effect of injury or prolonged inflammation on fibrocartilage

Tissue may become irritated

Mechanical loading may be altered

Healing may be limited in poorly vascularized regions

Persistent inflammation may delay recovery

effects of inflammation on soft tissues

Tendon irritation

Bursitis (inflammation of a bursa)

Muscle inhibition (reduced ability to fully activate a muscle)

Protective spasm

Loss of extensibility

Altered movement patterns

uses of immobilization

Protect injured or repaired tissue

Reduce stress on healing structures

Control pain and symptoms

Maintain surgical or joint stability

physiologic effects of immobilization

Decreased joint motion

Reduced muscle activation

Reduced mechanical loading

Changes in connective tissue

Changes in cartilage and bone

loss of strength due to immobilization

↓ Muscle fiber cross-sectional area

↓ Muscle mass

↓ Tension produced per unit of muscle

• Structural and metabolic changes may occur within hours

  Muscle fiber size can decrease substantially within the first few days

  
  

type I slow twitch fibers

fatigue-resistant fibers used for endurance and postural activity

type II fast twitch fibers

larger, high-force fibers used for strength, power, and rapid movement

metabolic changes in muscle with immobilization

• energy stores decrease

• protein synthesis decreases rapidly

  • oxidative capicity decreases

  • mitochondrial activity decreases

  • lactate accumulation increases

• greater fatigue and reduced muscular endurance

ATP

immediate energy source

creatine phosphate

stored high energy comound used to rapidly regenerate ATP

glycogen

• stored form of glucose used for energy during muscle activity

oxidative capacity

muscles ability to use oxygen to produce energy

mitochondrial activity

reduced function of cell structures that produce aerobic energy

lactate

byproduct produced in greater amounts when energy demand exceeds aerobic energy production

muscle atrophy varies by

Muscle function

Joint position

Duration of immobilization

**extensors

shortened position for atrophy

greater loss of muscle length and size

• decreased sarcomere number

• increases connective tissue

• reduce extensibility

lengthened position for atrophy

better preservation of muscle size

early rehab of joints

Gentle stretching

Isometric contractions (muscle contraction without joint movement)

Restoration of normal joint position

Progressive return of active movement

arthrogenic muscle inhibition

reflexive reduction in muscle activation caused by joint injury

• can contribute to disuse atrophy

periarticular connective tissue (CT surrounding a joint)

Joint capsule and synovium

Ligaments and tendons

Fascia

changes in CT with immobilization

↓ Water content

↓ Glycosaminoglycans, or GAGs (molecules that attract water and help connective tissue stay hydrated)

↓ Collagen mass

↑ Collagen turnover (breakdown and rebuilding of collagen)

↑ Abnormal collagen cross-links (bonds between collagen fibers that restrict normal movement)

contracture

persistance shortening or stiffening of tissue that limits joint motion

arthrofibrosis

• excessive formation of fibrous scar tissue within or around a joint

  • joint capsule

  • synovium

  • intra articular tissues

cycle of stiffness

Trauma or surgery

Hemarthrosis (blood within a joint) + pain

↓ Motion and muscle activation

Adhesions (abnormal scar tissue connecting tissues that should normally move separately)

Synovitis (inflammation of the synovial membrane)

Fibrosis (excessive formation of fibrous connective tissue)

Further loss of ROM

how does cartilage recieve nutrition

• diffusion (increased with joint motion)

• osmosis

intermittent loading of cartilage promotes

• synovial fluid circulation

• chondrocyte nutrition

• cartilage health

appopriate stress on CT benefits

Stimulate proteoglycan synthesis (production of molecules that attract and retain water)

Maintain tissue hydration

Maintain lubrication

Align new collagen along lines of stress

Limit abnormal collagen cross-linking

when ROM is limited how do you apply stress?

Favor low-load, long-duration stretching

Progress motion gradually

Avoid repeatedly provoking inflammation

articular cartilage

• smooth tissue covering the ends of bones within synovial joints

• no direct blood supply

immobilization effects on cartilage

↓ Chondrocyte activity (activity of the cells that maintain cartilage)

↓ Proteoglycan/GAG content

↓ Cartilage thickness

Softer cartilage with less resistance to compression

prolonged immobilization effects on cartilage

Fibrillation (surface fraying)

Chondrocyte degeneration

Pressure necrosis (cell death caused by prolonged compression)

Adhesion formation

ligament remodeling

according to stress placed on them

appropriate loading on ligaments

Helps maintain strength

Helps maintain stiffness

Supports collagen organization

effects of immobilization on ligaments

↓ Tensile strength (ability to resist pulling forces)

↓ Stiffness

↓ Collagen fibril size and density

Disorganization of collagen fibers

↓ GAG content

Increased vulnerability at the bone-ligament junction

remobilization of ligaments

Progressive ROM

Gradual mechanical loading

Time

graft undergoes…

neovascularization

ligamentization

neovascularization

development of a new blood supply

ligamentization

remodeling of graft tissue toward ligament-like structure and function

healing of graft

Graft properties change over time

Tissue may be vulnerable even when symptoms are minimal

Graft type influences healing characteristics

return to sport considerations with graft

Strength

Dynamic control

Balance

Functional performance

Psychological readiness

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mechanical stability does not equal complete biologic healing

reduced weight effects on bone

↓ Bone formation

↑ Bone resorption (breakdown and removal of bone tissue)

• within weeks

over time bone may become with unloading

Less dense

Less mechanically strong

More susceptible to injury

primary goals of acute rehab

Manage excessive inflammation

Limit secondary tissue damage

Protect the injured area

Prevent complications associated with prolonged swelling or immobilization

what to watch out for with acute rehab

Decreased range of motion

Muscle inhibition and weakness

Persistent edema

Pain with excessive activity

Compensatory posture or gait patterns

early rehab interventions

Relative rest and protection

Cryotherapy for pain and symptom management

Gentle pain-free ROM

Isometric muscle activation

Appropriate positioning

Maintenance of normal movement and gait when safe

benefits of continuous passive motion

Maintain or improve ROM

Reduce stiffness and adhesion formation

Promote synovial fluid movement

Support articular cartilage nutrition

Reduce early pain and swelling

Benefits are generally greater in the short term than long term

effects of PRP

Angiogenesis and revascularization

Cell migration and proliferation

Collagen synthesis and remodeling

Support of tendon, muscle, cartilage, and connective tissue healing

Clinical effectiveness varies by tissue, condition, and PRP preparation