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Concepts of Diagnosis of Sports Injuries

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Title: Concepts of Diagnosis of Sports Injuries Author: Honeywell Last modified by: Lenovo User Created Date: 5/5/2008 1:43:25 AM Document presentation format – PowerPoint PPT presentation

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Title: Concepts of Diagnosis of Sports Injuries


1
Concepts of Diagnosis of Sports Injuries
Site of injury
2
Truism
  • If you hear hoof beat donot think Zebras.
  • Eliminate the Zebras first
  • Always look for pathology first.
  • Example In calf pain consider DVT
  • In Shoulder Pain consider lung pathology

3
(No Transcript)
4
Priorities
  • The best things in life are not things
  • Harry Bertsch
  • Hermy Bavier
  • Ron Boris
  • Amanda Driscoll
  • Josh Bertsch
  • Dad

5
Ron Boris
6
Concepts of Diagnosis of Sports Injuries
Cause as it relates to exceeding the tensile
strength of the tissue
7
Fracture dislocation
8
Concepts of Diagnosis of Sports Injuries
Biomechanical concepts of causation
9
Concepts of Diagnosis of Sports Injuries After
you eliminate the Zebra
Motion deficits as major causative factor In
Physical Diagnosis look for soft tissue
restrictions and Fascial Adhesions
10
  • If dysfunction alters the efficiency of the
    musculoskeletal system, there is an increase
    demand for energy. Not only for increased
    activity but for normal activity.
  • Increase demands on the cardiovascular system

11
Evaluation of the Kinetic Chain
  • Lower limb Ankles, Knees, and hips
  • Upper limb Core Stability, Endurance, Balance,
    Range of Motion
  • Scapula Stability, Rhythm
  • Shoulder Clinical examination

12
Concepts of inflammation and repair
13
Treatment Protocols
  • Phase 1 Acute Inflammatory Phase
  • Question Does inflammation cause pain or does
    pain cause inflammation?
  • For a long time pain has been summarily dismissed
    as the outcome of direct stimulation of sensory
    nerve endings by injury and the pressure of
    inflammation exudates. This opinion completely
    neglects the observation that pain often
    initiates the inflammatory response and may
    become less severe as that process gains speed.
    Robbins pg.44
  • Goal is to control the pain and inflammation
  • PRICE
  • Protection
  • Rest
  • Ice
  • Compression
  • Elevation

14
Inflammation and Repair
  • Tissues respond to injury with a set of
    genetically programmed mechanisms to replace the
    damaged components and to restore normal function.

15
Inflammation and Repair
  • Cardinal signs of inflammation
  • Heat
  • Swelling
  • Pain
  • Redness
  • Loss of Function

16
Inflammation
17
Inflammation and Repair
  • Two types of Inflammation
  • Acute
  • Chronic More then 3 months cause central
    pathway changes.

18
Acute Inflammation
  • Vascular
  • Exudative
  • PMN

19
Proliferative stage Healing stage
  • Vascular
  • Proliferative
  • Fibroblast

20
Chronic Inflammation, pathological stage
  • Increase type 3 collagen formation
  • No cellular matrix
  • Increased neovascularization
  • Increased fibrosis
  • Central pathway changes
  • Result of improper healing and continued
    irritation of tissue

21
Acute Inflammation
22
Chronic Inflammation
23
Inflammation and Repair
Acute Inflammation
  • Characterized by the release of chemical
    mediators by mast cells,platelets and basophils
    at the site of the injury.
  • Vasoactive mediators regulate the vascular
    response to the injury and affect the recruitment
    of PMNs from the vascular component.
  • These in turn produce chemotactic factors that
    control the damage and remove debris by
    phagocytosis.

24
Inflammation and Repair
  • Granulation Tissue
  • Lead to the restoration of the vascular supply
    and connective tissue matrix.
  • Chronic Inflammation is the result of unresolved
    acute inflammation

In the case of sports related injuries removal of
the trauma and successful management of the
injury may result in the reduction of fibrosis
and restoration of normal function.
25
Inflammation and Repair
  • Repair
  • The repair phase of healing ideally result in the
    restoration of normal living tissue.
  • Repair by regeneration of injured tissue
  • Repair by second intention is characterized by
    the formation of scar tissue at the site of the
    injury.

26
Inflammation and Repair
  • Remodeling and Maturation
  • Process begins about 6 days after the fibroblasts
    begin to lay down collagen tissue.
  • Collagen is laid down randomly initially
  • Depends on the appropriate mechanical loading.
  • The hallmark of remodeling is the orientation of
    new fibers

27
Inflammation and Repair
  • Immobilization of a healing wound has been shown
    to compromise wound strength as a result of the
    failure of collagen to be oriented along lines of
    stress.
  • Mobilization and loading has been shown to result
    in stronger healed tissue.

28
Inflammation and Repair
  • Time Frame of Healing
  • Inflammation Phase is relatively brief. 24-48
    hours.
  • Proliferative Phase 3-7 days after the injury
  • Repair Phase Few days to a few weeks
  • Remodeling Phase Several months and may continue
    up to 12 months.

29
Inflammation and Repair
  • Repair Mechanisms in Soft Tissue Injuries
  • Muscle Tissue
  • Healing of skeletal muscle is dependent on the
    integrity of the vascular system and nervous
    system
  • Has considerable regenerative properties
  • Both regeneration and repair by scar tissue.
  • Capacity for regeneration is determined
    genetically but the success is determined
    primarily by the extent and type of injury.

30
Inflammation and Repair
  • Except for injuries in which the continuity of
    the muscle fiber is preserved, and the
    innervation, vascularity and extracellular matrix
    muscle will regenerate with a loss of normal
    tissue architecture and function.
  • Most muscle injuries are a result of exceeding
    the tensile strength of the tissue and are
    labeled indirect muscle injury.

31
Inflammation and Repair
  • Muscle Strain Injuries
  • Consists of a partial or complete tear at or near
    the musculotendinous junction.
  • When the force is sufficiently high the tendon
    has been shown to avulse from the muscle with
    only a few fibers left intact.
  • The greater the amount of injured tissue involved
    the more scar tissue with be deposited at the
    sight of the wound.

32
Inflammation and Repair
  • Ischemia- Induced Muscle Damage
  • Usually seen in compartment syndromes. Results
    from damage to vessels causing ischemic injury.
  • Seen in exhaustive endurance activities.
  • Extent of the injury is proportional to the
    duration of the pressure.
  • Nerve injury may result as a result of increase
    pressure.
  • Healing will be achieved with little or no damage
    if the damage is limited to individual fibers and
    blood supply is restored without delay.
  • Can result in significant scar tissue formation
    if delayed resulting in excessive cell death.

33
Tendon Injuries
  • Structure of Tendon
  • Pathology
  • Pain
  • Treatment Strategies

34
Tendon Structure
  • Ground Substance 68
  • Collagen 30
  • Elastin 2
  • Tenocytes Found between collagen fibers
  • 1. Collagen, proteogylcans, glycoproteins,
    Respond to loads.

35
Extracellular Matrix
  • Collagen Gives tendon tensile strength
  • Ground substance Nutrition, allows for
    elongation and friction free movement of tendon
  • Glycoproteins energy storage

36
Tendon Function in Athletes
  • Provide movement to Joints
  • Store energy to be released with activity
  • Afferent proprioception
  • Protect muscle from strain

37
Tendon Pathology
  • Result of exceeding the tensile strength of the
    tendon or not allowing sufficient time between
    loading.
  • Increases fibrosis and cross links in matrix
  • Increased neovascularization
  • Replacement of Type 1 with Type 3 Collagen.
  • Pain can be independent of pathology and
    inflammation.

38
Stages of Tendon Pathology
  • Reactive tendinopathy
  • a . Short term adaptive thickening as a result of
    acute tensile overload or compressive overload
  • b. Can return to normal if overload is
    discontinued or sufficient time between overload.

39
Stages ( continued)
  • 2. Tendon Dysrepair
  • a. Ongoing load to a reactive tendon
  • Separation of collagen
  • Increased vascularity
  • Increased proteogylcan and collagen production
    without a normal matrix structure

40
Stage 3
  • Degenerative Tendinopathy
  • a. Extreme changes to the matrix and cells
    including death and apoptosis
  • b. Large areas of the matrix are disordered and
    filled with debris, vessels, and little collagen
  • .

41
Cause Intrinsic
  • Intrinsic Motion deficits in kinetic chain
  • Asymetry pronation
  • Muscle weakness or tightness
  • Age, flexibility, previous injury, somatotype.
  • Genetic profile ABO. Vitamin C deficiency
  • Strength, BMI.

42
Cause extrinsic
  • Training Errors Load/volume
  • Overload Eccentric overload
  • Underload Immobilization
  • Tendons cannot rupture unless pathological
  • Tensile strength 1364-2310 pounds/cm2
  • Ex. Achilles goes through a prerupture
    tightness.

43
Treatment Not Pain by Numbers
44
Law of Least Action
  • Maupertius The quantity of action necessary to
    effect any change is the least possible, the
    decisive amount is always the minimal, the
    infintesimal.

45
Goal of Treatment
  • Restore normal Function to dysfunctional region.
  • Function must be the focus of treatment
    protocols.
  • Must be Evidenced Based.

46
Treatment
  • Deal with tissue pathology
  • Look for motion deficits in kinetic chain
  • A. subluxations causing afferent proprioception
    deficits and overload.
  • Begin to load the tendon progressively
  • Emphysis on eccentric loading
  • Eliminate provocative activities

47
Incidence of injury according to the American
Journal of Sports Medicine
  • Football players in a 5 year program at the Div.
    1 level have a 100 chance of being inured
  • High School 50-80
  • Swimming 50 men 70 women will develop shoulder
    problems.
  • Jogging, running 60
  • Tennis 60 Musculotendinous overload injuries

48
Duration of Injury
  • Tri-athlete 30 days
  • Cyclists 2 weeks
  • Swimming 2 weeks
  • Runners 40 days

49
Predictor of Injury
  • No previous injury 40 chance of experiencing a
    sports related injury
  • Previous Injury 65 chance of a re-injury in the
    Kinetic chain
  • a. Mostly due to incomplete rehabilitation
  • b. Rehab stopped at symptom reduction.

50
Effects of Immobilization
  • For each week of immobilization there is a 20
    loss of strength in joint.

51
Immobilization
  • Type 1 fibers are most affected
  • Cartilage deterioration, bone and ligament
    strength loss and increased stiffness.
  • Rehabilitation can counteract these changes by
    introducing motion with protection and loading.

52
Classification of Injury
  • Acute Injury Normal anatomy and normal
    physiology followed by abnormal anatomy and
    abnormal physiology.
  • a. One-Time microtrauma.
  • Chronic Injury Building up for a period of time.
  • a. Represents the tip of the iceberg of entire
    derangement of physiology
  • Repetitive microtrauma overload
  • a. Rotator Cuff Tendonitis
  • b. Plantar fascitisc.
  • c. Achilles Tendonitis

53
Adaptation
  • Body adapts over a period of time to chronic
    injuries. The Dx must look for these adaptations
  • Weakness and tightness in gastrocnemius in
    Achilles tendonitis
  • Elbow tendonitis tightness of wrist extensors
  • Rotator Cuff tendonitis Infexibility in
    posterior RC muscles and weakness in scapular
    stabilizers and post cuff muscles.

Note Entire Kinetic Chain must be searched and
evaluated
54
Adaptation
  • Acute exacerbation of a chronic injury Result
    from symptomatic treatment leading to return to
    athletic activity. Results in a recurrence of
    previous symptoms or new symptoms as a result of
    acute injury in kenetic chain.
  • 1. Ankle Sprain
  • - return to competition- Groin strain
  • 2. Rotator Cuff tendonitis
  • - return to competition- lateral epicondylitis

55
Adaptation
  • Injections cause very poor healing and a return
    of symptoms with activity

56
Adaptation
  • Chronic Adaptations
  • 1. No overt symptoms
  • 2. Pattern of abnormalities that lead to
    decreased function and performance

57
Negative Feedback Vicious Cycle
Tissue Overload Complex
Sub-clinical Adaptation Complex
Tissue Injury Complex
Functional Biomechanical Deficit Complex
Clinical Symptom Complex
58
Negative Feedback Vicious Cycle
  • 1. Tissue overload complex
  • a. Failure of Tensile strength
  • b. Subject to microtrauma
  • 2. Tissue Injury complex
  • a. Disrupted
  • b. Producing Symptoms

59
Negative Feedback Vicious Cycle
  • 3. Clinical Symptom Complex
  • Pain
  • 4. Functional Biomechanical Deficit Complex
  • a. Decreased flexibility
  • b. Decreased Strength
  • c. Muscle imbalances

60
Negative Feedback Vicious Cycle
  • 5. Sub-clinical adaptation complex
  • a. Activities the athlete uses to compensate for
    altered mechanics.
  • 1. Running on the outside of foot to compensate
    for heel pain.
  • 2. Over reaching in swimming to compensate for
    decreased ROM in the low back
  • 1. Tissue overload complex

Cycle begins again
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