Lecture 5: Tissue Types and Healing Flashcards
Why don’t we use the term acute anymore?
B/c all injuries are technically acute because something initiates them
Chronic injury
At some point, if injuries don’t heal, they are called chronic
Traumatic injuries
aka acute
- occur SUDDENLY and have a clearly DEFINED cause or ONSET (know exactly then it happened)
- occur when tissue loading is enough to cause sudden IRREVERSIBLE deformation of the tissue
- usually in high speed sports with or without contact
Overuse injuries
- occur slowly over time (secondary to repetitive movement)
- repeated overloading can accumulate over time to exceed tissue threshold (even if individual incidences don’t cause injury)
- in aerobic sports that need long training schedules or in technical sports where a movement is repeated many times
Extrinsic/External Injury Factors
- makes us SUSCEPTIBLE
- originating outside the anatomical limits of tissue/person
- ex. increased training duration, increase in FITT, not enough rest, inappropriate shoes, field conditions
Intrinsic vs Extrinsic Factors
Not enough rest
Extrinsic – could be due to practice too much or too much school
Intrinsic/Internal Injury Factors
- PREDISPOSES us to injury
- belonging to or lying within a given part person/tissue
- ex. flat feet, knee alignment, tight hamstrings
Muscle Characteristics
- contractile tissue with main function to generate power
- well vascularized = good O2 and nutrients; good for healing; bleeds lots
What structures are affected by strains?
Muscle
What structures are affected by contusions?
Muscle
Bone
Cartilage
What structures are affected by sprains?
Ligaments
What structures are affected by ruptures?
Muscle
Ligament
Tendon
What structures are affected by lacerations?
Muscle
Ligament
Tendon
What structures are affected by fractures?
Bones
What structures are affected by tendonosis/itis?
Tendons
Things to consider with strains
- % of fibres torn
- ability to move through range - stretch
- Oxford Scale (strength generated out of 5)
- pain – sometimes more is better (no pain could mean worse tear)
Oxford Scale
Grading Muscle STRENGTH
Out of 5
Oxford Scale
Grade 5
Normal
- Full strength
- can resist throughout available range compared to other side
Oxford Scale
Grade 4
Good
Near full strength through available range when compared to other side
Oxford Scale
Grade 3
FAIR
Full R.O.M against gravity only
- can’t take any resistance
Oxford Scale
Grade 2
Poor
Can complete full available range with GRAVITY ELIMINATED
- to eliminate gravity: change plane of movement (ex. biceps - go lateral to medial instead of up and down)
Oxford Scale
Grade 1
Trace
Able to palpate (feel) muscle contraction when patient tries to contract
Oxford Scale
Grade 0
Nothing happens when patient tries to contract
Isometric Contraction
muscle contraction where length of muscle is CONSTANT
Concentric Contraction
muscle SHORTENS while contracting against resistance
Eccentric Contraction
muscle LENGTHENES while contracting against resistance
- greater risk of injury
How do muscle injuries generally happen?
- Distension (strains/pulled muscle)
- Direct trauma (contusion/laceration)
Muscle strains
- usually happen at musculotendinous junction
- more common in 2 jt. msucle (sart
- strains happen due to forcible stretching of a muscle (either passively or when muscle is activated)
- active contraction + passive stretch = STRAIN
Ecchymosis
Bruising from strains (b/c muscle is well vascularized)
Grade I Strain
- usually 10-20% of muscle fibres torn/stretched
- near full ROM w/ some discomfort near the end
- good strength (4-5 on Oxford scale)
- slight pain/discomfort
- no palpable divot
Grade II Strain
- usually 20-80% of fibres torn
- significant DECREASE in ROM with discomfort near end
- poor strength (50% or 2-3 on Oxford scale)
- significant pain/discomfort
- can have palpable divot
Grade III Strain
- 80%+ of fibres torn to complete rupture
- Poor range of motion
- Poor strength (0-1 on Oxford scale)
- variable pain (complete rupture = no tension on muscle = no pain b/c no attachment)
- initial pain
- large gap or muscle retraction
Muscle Contusions
Bruising
- can be any muscle (most common in quads)
- ecchymosis is common due to vascularity of muscles
- all result in internal bleeding
- can be intramuscular or intermuscular
Intramuscular contusions
- NO injury to FASCIA = blood trapped in muscle
- significantly LONGER HEALING TIME
- increased compartment pressure = decreased flow/O2/nutrients
- chemical irritation (pain due to acidity of blood)
Intermuscular contusions
- fascia is injured
- blood flows out btwn muscles = ecchymosis faster
- HEALS FASTER (no increased pressure = more blood flow, increased healing)
- blood can be absorbed (no irritation)
Characteristics of Tendons
- connective tissue that attaches muscle to bone
- function: transfer force from muscle to skeleton
- 65-80% Type I collagen (less elastin than ligaments)
- arranged into parallel bundles of different sizes
Overuse Tendon Injuries
Tendinitis
Tenosynovitis
Paratenonitis
Tendinosis
Bursitis
Periotitis
Traumatic Tendon Injuries
hot, red and painful = inflmaed
laceration (skate)
penetrating injury (stab)
rupture (Achilles, quads)
acute tendon strain/tear
- tendonitis
Tendinitis
- inflammation of the tendon
- acute inflammation
relatively rare and over diagnosed
Paratenonitis
inflammation, pain and crepitation of the paratenon as it slides over the structure
Acute irritation of the tendon is usually triggered by
Extrinsic Factors: rub from equipment, “too much, too soon”, increase in FITT
Intrinsic Factors: rub over bone
Tendinopathy
general term used to refer to pain and reduced function in tendons
- could be traumatic or overuse injury
Tendinitis to Tendinosis
over time, tendinitis –> tendinosis
If repetitive overuse continues and an inflamed/irritated tendon fails to heal, the tendon begins to degenerate
Primary concern changes from tendon inflammation to tendon degeneration = tendinosis
Tendinosis
- chronic pathological changes due to repetitive micro-trauma (no time to heal = breakdown)
- NO inflammatory cells
- characteristic changes in collagen fibre structure
- abnormal vascularity
Tendinosis Collagen Changes
Normal tendon
- collagen fibres lined up
- many nuclei
Tendinosis (breaks down faster)
- collagen fibre disarray (not lined up)
- loss of parallel bundles
- fewer cell nuclei
Tendinosis Vascular Changes
Normal tendon
- well-developed, evenly spaced vasculature
Tendinosis (not evenly spaced)
- hyper vascularity
- increased # of poor-quality blood vessels (neovascularization)
Characteristics of Ligaments
- connect one bone to another
- made predominantly of collagen (higher amount of elastin than tendons
- passive stabilizers
- usually TRAUMATIC mechanism of injury
- well innervated = position, movement and pain (very important for proprioception and rehab)
Types of Ligaments
Intra-articular
Capsular
Extra-capsular
Intra-articular ligaments
inside a jt or jt capsule
- total rupture will NOT heal
- blood supply from ends - minimal to middle portion
- ex. ACL
Capsular ligaments
Ligament projects as a thickening of a jt. capsule
- total rupture = excellent healing
- good blood supply
- ex. MCL, ATFL (anterior talofibular lig.)
Extra-capsular ligaments
Outside of jt. capsule
- similar to intra-articular
- unlikely to heal total ruptures w/o surgery
- ex. LCL, CFL (calcaneofibular lig)
Structure/morphology of ligaments
- wave or crimp across ligament
- built into structure of ligament
- injury cam be closely correlated to load-deformation curve
- 3 phases of curve
3 phases of ligament curve
- Toe region
- Linear region
- Rupture region
Toe Region and Early Linear Region
Ligaments (stress vs strain curve)
- initial concave region
- represents normal physiological range of strain = 0-2% of length (crimp stays the same)
Early Linear Region = 2-4% of length
- due to flattening of crimp
Repeated cycling of stretch in this range is reversible
Late Linear Region
Ligaments
- pathological IRREVERSIBLE ligament elongation
- will see tears in ligament as cross-links are disrupted
- early part = mild/grade 1 sprain (<50% torn)
- 2nd part = grade 2 sprain (50-80% torn and obvious laxity)
Rupture Region
Ligaments
- failure point at about 10%
- complete rupture
- grade 3
- decreased pain (if totally torn)
Things to consider with sprains
- % of fibres torn
- ability to move through range - stretch
- laxity on testing and end point
- pain (sometimes more is better)
Grade I Sprain
- full ROM
- slight pain
- NO jt. laxity (good stability)
- has an endpoint
Grade II Sprain
- significant loss of ROM
- significant pain on palpation
- SOME jt. laxity
- has an endpoint
Grade III Sprain
- loss of motion (swollen)
- pain of palpation (variable)
- GROSS laxity
- has NO endpoint
Open Fractures
aka Compound fractures
- bone breaks through surrounding tissue
- usually a medical emergency
Closed Fractures
aka Simple fractures
- little or no displacement of bone through surrounding tissue
Greenstick fractures
incomplete fracture
common in CHILDREN
How to tell btwn a fracture and contusion?
Direct pressure = pain w/ contusion and fracture
Indirect pressure = pain with fracture (ex. fractured hand, pushing down on finger would tell; fractured fibula would be shown by pressure from rotating ankle)
Phases of Healing
- Inflammatory Phase
- Repair Phase
- Remodeling Phase
Inflammatory Phase
Phase 1 of Healing
- days 1 - 4 on injury
- cellular injury = altered metabolism + release of chemical mediators/proteins
- cause inflammatory response
Repair Phase
Phase 2 of Healing
- day 4 to 6 weeks after injury
- lay tissue down and repair
Remodeling Phase
Phase 3 of Healing
- week 6 to 2/3 years after injury
Primary Damage
- damage at a time of injury (immediately irreversible)
Secondary Damage
- damaged by released proteins (in tissues around)
- damage as a result of body processes (edema, damage due to decreased blood flow, decreased oxygen)
Steps of Injury
- Injury to cell
- Chemical mediators liberated (histamines, leukotrienes, cytokines)
- vascular rxns. (vascontsriction -> vasodilation/hyperemia -> exudate -> creates stasis)
- Margination (platelets and leukocytes (neutrophils) adhere to vascular wall)
- Diapedesis
- Phagocytosis
- Clot Formation
Histamines
cause vasodilation and cell permeabilitu
Leukotrines
responsible for margination/diapedesis
- stuff moving out of capillaries to tissue
Cytokines
helps attract phagocytes to remove waste from tissue
Diapedesis
Passage of fluid, proteins and neutrophils through cell wall
Forms exudate (fluid matrix where healing can start)
Signs/Symptoms of Inflammation
- redness
- swelling (b/c of exudate)
- pain
- local heat
- loss of function
Cycle of injury
pain, muscle spasm and ischemia increases the possibility of atrophy over time
Stop one and stop the rest
Repair (Fibroblastic) Phase
- 72 hours to 6 weeks
- proliferative and regenerative healing = formation of connective tissue repair and repair of injured tissue
- fibroplasia begins within the first few days and inflammatory signs should decrease
- growth of endothelial capillary buds into wound is stimulated by lack of O2 (new growth allows increased O2 and blood flow)
- body lays down Type 3 collagen (not as good as Type I)
- weak tensile strengtjh
Remodeling/Maturation Phase
- usually firm, strong non-vascular scar by end of 3 weeks
- long-term process (6 weeks to years)
- increased stress and strain = collagen changes to type I and begins realignment
- critical that injured structures be exposed to progressively increasing loads (work up to aggressive AROM and strengthening to facilitate remodeling and realignment)
- watch out for pain and swelling post-exercise
Wolf’s Law
Remodeling/Maturation phase
bone and soft tissue will respond to they physical demands placed on them = they will align
