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Physiology 2 > KIN 428 Midterm 2 > Flashcards

KIN 428 Midterm 2 Flashcards

1
Q

Why model the shoulder?

A
  1. Gain insight into a closed system 2. Difficult to measure muscle forces, joint contact forces, and ligament forces 3. Test untestable hypothesis such as unsafe loading conditions and trauma 4. Test hypothesis quickly and w/o volunteers to answer “what if” questions
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2
Q

Types of shoulder biomechanical models?

A
  1. External models 2. Geometric Models 3. Internal (musculoskeletal models) 4. Composites
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3
Q

What comprises an external model?

A

Moments and forces…121/221 rigid link model

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4
Q

What comprises a geometric model?

A

Orthodpaedic models (has bones, not just links) and muscles capability/moment arms

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5
Q

What comprises an internal/musculoskeletal model?

A

Individual muscle forces, tissue forces (ligaments, tendons, etc), and joint contact force

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6
Q

What comprises a composite model?

A

Complete mechanisms description…a combination of an external, geometric, and internal model

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7
Q

What is the input for an external dynamic shoulder model?

A

Subject data (who), task data (what), and motion data (how)

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8
Q

What is the output of an external dynamic shoulder model?

A

Joint torques and forces

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9
Q

What is the input for geometric shoulder modelling?

A

Motion data (how)

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10
Q

Considerations for motion data in a geometric reconstruction?

A

Collection protocol–>marker placement and sampling rate

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11
Q

What are the geometric/orthopedic orientations for a geometric reconstruction model?

A

Joint center location, shoulder rhythm, and global vs. local positioning

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12
Q

What is the output for geometric reconstruction modeling?

A

Shoulder geometry

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13
Q

What are the considerations when doing the shoulder geometry in a geometric reconstruction model?

A

Muscle attachment sites, muscle wrapping, and muscle element definition

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14
Q

3 things to take away form shoulder modeling?

A
  1. Everyone represents muscles differently (diff # of mechanical activators of a muscle…no 2 are the same) 2. All perform differently on different criteria (depends on what you really want to look at) 3. Model is only as good as its validation
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15
Q

Why is it important to study muscle forces?

A
  1. can provide an objective quantitative indication of tissue loading for a given task/activity 2. This quantity can be related to pain, discomfort, or effort associated with the task 3. Assists in design of worker interfaces that minimize potentially harmful loading muscles 4. Fatigue is a major mechanism of shoulder instability and subsequent tissue damage (to estimate fatigue, you need to know what the muscle is doing)
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16
Q

What do optimization prediction models do?

A

Use inverse dynamics to calculate joint loading (moments) and minimize a quantity of muscle loading while satisfying equilibrium around all joints

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17
Q

What are the contraints in an optimization models?

A

Segment muscle composition, muscle force limits, glenohumeral contact force constraints

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18
Q

What are the inputs in an optimization model?

A

Torque model outputs and geometric model outputs

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19
Q

Internal muscle model outputs show an instanteous and continuous prediction of?

A

Muscle force, GH stability, internal joint forces (NHJRF), and ligament tension

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20
Q

What is the shoulder stability constraint in an optimization model?

A

The GH internal joint force (NHJRF) must satisfy a directional stability requirement/ratio. Other models use an ellipoid constraint

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21
Q

When using optimization at the shoulder, what is important to remember?

A

You should incorporate your knowledge of GH stability into the model to make it more realistic

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22
Q

What are the model limitations of optimization models?

A
  1. Assume that the body is attempting to minimize some muscular loading quantity. This has not been proven 2. Historically, do no account well for co-contraction of muscles (Joint stabilization) 3. Do not account for changes in muscle cross-sectional area for different postures when calculating stresses 4. Predict muscles as on/off and the madgitude is touchy 5. Drives by (somewhat subjective) objective function decision
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23
Q

What is one of the most physiologically relevant optimization models?

A

Soft-saturation method

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24
Q

What are EMG muscle force prediction models, and what do they predict?

A

Measure recorded surface EMG to estimate muscular loading. Estimates sholder moment generated by predicted muscle forces. Uses external forces to calculate shoulder momente and compare to predicted moment to validate muscle force predictions. Basically and in-out system.

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25
Q

Laursen (‘98) showed that calculated EMG model moments ___________ measured external moments?

A

Slightly underestimated…but overall, a positive relationship exists.

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26
Q

Model limitations of EMG modelling?

A
  1. Inherent limitations of the strength of the EMG/muscle force relationship (EMG does NOT equal force) 2. Confounding factors associated with EMG recording and interpretation (EMG amplitude is related to muscle length. At low levels (<10% max), EMG reliability is questionable due to cross-talk and noise levels
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27
Q

.How do optimization-predicted muscle forces vs EMG compare?

A

A fairly good/imperfect relationship exists

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28
Q

Models have been developed using:

A

optimization, EMG, hybrid (EMG-assisted optimization)

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29
Q

Models ________ to predict useful muscle forces to assess exertions

A

have been shown

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30
Q

What details are largely overlooked by current shoulder models?

A
  1. CO-activation (antagonistic activation for stability) 2. Joint translation (GH joint translates, which changes moment arms of muscles, which change forces and moments at the joint) 3. Variation in muscle capabilities (fibre type changes with age and fitness and therefore amount of force produced at a joint changes, too) 4. Ligaments are ignored 5. Variation in the population (no one is average…dertminism vs stochasticity)
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31
Q

Incidence of humeral fractures?

A

~4-5% of all fractures

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32
Q

What happens to occurence of proximal fractures with age?

A

Increases with age; many are osteoporosis related (degrades trabecular bone, which increases risk of humeral head fractures)

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33
Q

What percentage of humeral fractures do proximal fractures account for?

A

45% (over age 40 = 76%)

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34
Q

What gender is more likely to get proximal humerus fractures?

A

Women

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35
Q

What are the 3 mechanisms of proximal humerus fractures?

A
  1. Fall onto an outstretched hand (FOOSH), particularly for elderly 2. Usually something traumatic like a car accident or getting shot in younger people (sometimes overlooked because more serious injuries have also occurred) 3. Electrical shock or convulsions (bone can’t handle all the muscle contracting at once!)
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36
Q

What is the worst place to fracture on the humerus?

A

The anatomical neck because it cuts off blood supply!

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37
Q

4 possible fragments of a proximal humerus fracture?

A

greater tuberosity, lesser tuberosity, head, shaft

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38
Q

What fracture classification is most common?

A

Neer classification

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39
Q

What is a minimal displacement fracture in the Neer Classification system?

A

Most common (85%0. NO segment displaced more than 1 cm, or angulated more than 45 degrees

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40
Q

What is an articular segment displacement n the Neer Classification system?

A

Through anatomical neck of humerus (uncommon). Separation of tuberosity rare. Malunion of osteonecrosis of humeral head possible because of poor vascularization.

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41
Q

What is shaft displacement fracture n the Neer Classification system?

A

At level of surgical neck. Fragment displacement of more than 1 cm or angulations over 45 degrees. Semi neutral head posture.

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42
Q

What is a greater tuberosity displacement n the Neer Classification system?

A

Any of 3 facets/entire tuberosity retracted >1cm, or angulated >45 degrees. 2 or 3 part injury. Blood supply to humeral head at some risk.

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43
Q

What is a lesser tuberosity displacement n the Neer Classification system?

A

Uncommon 2 part lesion. Avulsion fracture of lesser tuberosity. 3 part lesion if surgical neck is also fractured. Soft tissue attachments aid in blood supply to humeral head, but some risk. 4 part lesion if both tuberosities are involved. Definite blood supply risk to humeral head.

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44
Q

What is fracture dislocation n the Neer Classification system?

A

GH dislocation with a fracture. Very complex injury. Good potential for blood supply to humeral head to be lost.

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45
Q

WHat does AO stand for?

A

Association for the Study of Internal Fixation

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46
Q

In the AO fracture classification, what do the letters (A,B,C) and numbers (1,2,3) stand for?

A

Letters are for the amount of vascular supply (A has no vascular isolation, B has partial isoaltion but necrosis is unlikely, and C has total vascular isolation with high likelihood of necrosis). The number represent the number of parts the fracture has created.

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47
Q

Clinical features of proximal humerus fractures?

A

Pain, swelling, tenderness, crepitis (popping sounds caused by bones grinding on each other), ecchymosis (bruising/skin discoloration from ruptred blood vessels around fracture sight)

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48
Q

How are prximal humerus fractures diagnosed?

A

Radiographs using 3 views (anteroposterior, lateral, and axillary)

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49
Q

Treatment options for a proximal humeral fracture?

A
  1. Initial immobilization and early motion 2. Closed reduction (percutaneous pins and external fixation) 3. Splints and Casts 4. Skeletal traction 5. Open reduction and internal fixation (ORIF) 6. Internal prostheses/endoprostheses
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50
Q

Recommended treatment sequence for a minimally displaced proximal humerus fracture?

A

Sling and ROM exercises within 14 days

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51
Q

Recommended treatment sequence for a 2 part anatomical neck proximal humerus fracture?

A

ORIF, prosthesis in older patients (return to mobility)

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52
Q

Recommended treatment sequence for a 2 part surgical neck fracture?

A

Closed redcution (pinning if needed), next is ORIF

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53
Q

In pinning, how do you want to pins placed in the bone?

A

Obliquely to keep the fragments together and prevent long axis rotation

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54
Q

Recommended treatment sequence for a 2 part greater tuberosity fracture?

A

ORIF and usually required a rotator cuff repair

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55
Q

Recommended treatment sequence for a 2 part lesser tuberosity repair?

A

Very rare, sometime sling, sometimes internal fixation, sometimes removal and tendon transfer

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56
Q

4 muscles of rotator cuff?

A

Supraspinatus, Infraspinatus, Subscapularis, Teres Minor

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57
Q

2 components that are critical in rotator cuff injuries?

A

Subacromial space and joint stability

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58
Q

Percentage of cadavers >60 that present with rotator cuff tears?

A

~30%

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59
Q

Percentage of elite swimmers with RC tears?

A

42%

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60
Q

Percentage of shoulder pain complaints that result from subacromial impingement syndrome?

A

44-65%

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61
Q

What does SAIS cause?

A

disability, loss of function, and pain

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62
Q

Signs and symptoms of SAIS?

A

anterosuperior pain (>at night and overhead activity), stifness, decreased ROM, crepitus (humeral head grinding on acromion)

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63
Q

Superior border of subacromial space?

A

Anterior, lateral 1/3 of acromion and coracoacromial arch

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64
Q

Inferior border of subacromial space?

A

Superior aspect of humeral head and greater tuberosity

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65
Q

Contents of subacromial space?

A

Supraspinatus tendon, LH of biceps tendon, subacromial bursa

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66
Q

Neutral height of a subacromial space in a healthy individual?

A

7-13 mm

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67
Q

What happens to height of subacromial space during elevation and external rotation>

A

It is reduced

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68
Q

What reduces the height of the subacromial space?

A

decreased size with posture, fatigue, and injury

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69
Q

What is SIS?

A

a decreased subacromial space such that tissues are compressed/”impinged”

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70
Q

Who was the first person to recognize SIS?

A

Neer in 1972

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71
Q

What is Stage I SIS?

A

Edema and haemorrhage, reversible, common in people less than 25 who do overhead sport or work

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72
Q

What is Stage II SIS?

A

Fibrosis, tendinosis, affects tendon/bursa, pain with activity, found in 25-40 year olds

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73
Q

What is Stage III SIS?

A

Bone spurs and partial or full tendon tears affecting those over the age of 40, surgery is needed

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74
Q

2 main theories of SIS?

A

Intrinsic and Extrinsic methods

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75
Q

What is the intrinsic theory of SIS?

A

Partial or full thickness tendon tears occur as a result of the degenerative process that occurs over time with overuse, tension overload, or trauma of the tendons. Osteophytes, acromial changes, muscle imbalances, and weaknesses and altered kinematics leading to impingement will subsequently follow.`

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76
Q

What is the extrinsic theory of SIS?

A

Inflammation and degeneration of the tendon occur as a result of mechanical compression by some structure external to the tendon. Potential mechanisms for EI are faulty posture, altered ST or GH kinematics, posterior capsular tightness, acromial or coracromial arch pathology.

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77
Q

What are some causes/risk factors for SIS?

A

1) Compression of supraspinatus 2) Traumatic factors 3) Degenerative factors 4)Developmental factors (acromial morphology and glenoid version) 5) Capsuloligamentous factors (instability and contractures) 6) Neuromuscular dysfunction 7) Inflammatory disease (rheumatoid arthritis and bursitis)

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78
Q

What are the devlopmental factors that contribute to SIS, and how do they contribute?

A

Acromial morphology and glenoid version…contribute because they are key in determining the subacromial space

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79
Q

What are the capsuloligamentous factors that contribute to SIS, and how do they contribute?

A

Instability and contracture…influence how humeral head sits in glenoid

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80
Q

What are the three types of acromions?

A

Flat, curved, and hooked

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81
Q

What is the angle of a Type I/flat acromion?

A

0-12 degrees

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82
Q

What is the angle of a Type II/curved acromion?

A

13-27 degrees

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83
Q

What is the angle of a Type III/hooked acromion>

A

> 27 degrees

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84
Q

What type of acromion causes the greatest amount and most severe rotator cuff tears?

A

Hooked

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85
Q

Order of acromion types from least severe to most severe in terms of RC injuries?

A

Flat, curved, hooked

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86
Q

What is os acromiale?

A

Partially unfused acromion

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87
Q

What does os acriomiale cause?

A

Hypermobile/inferiorly slanted acromion, which causes a predisposition to SIS (ligaments pulled, can cause hooked acromion)

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88
Q

What two parts of the acromion don’t fuse in most cases of os acromiale?

A

Meso and meta-acromion

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89
Q

What are the two mechanisms that are likely to causes translation (particularly superiorly) in the GH joint?

A

Gleniod degeneration and fatigue

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90
Q

What is scapular dyskinesis?

A

Abnormal movement of the scapula with humeral movement

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91
Q

What is does healthy/normal elevation allow at the GHJ?

A

Allows for upward rotation, posterior tilt, and retraction/external rotation

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92
Q

In SAIS, what happens to movement of the scapula during humeral movement?

A

It allows downward rotation, anterior tilt, and protraction/internal rotation

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93
Q

After a global and external rotators fatigue protocol, what happens to upward scapular rotation and posterior scapular tilt?

A

They increase…“impingement sparing”

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94
Q

Is there one cause of SIAS?

A

NO…a multi-factorial condition whose symptoms may be attributed to many causes

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95
Q

What is the progression of deterioration in RC pathology?

A

Supraspinatus tendon, infraspinatus tendon, suscapularis tendon, and long head of biceps tendon

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96
Q

What are the clinical findings of rotator cuff tears?

A

Stiffness, weakness/pain on contraction (esp. overhead), instability, roughness (athropathy)

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97
Q

What is Apley’s Scratch Test?

A

Can indicate rotator cuff damage if range of motion is compromies. Bend arm behind neck to touch opposite shoulder to check for GH abduction, external rotation, and scapular upward rotation. Reach behind back and touch opposite shoulder to check for GH adduction, internal rotation, and scapular retraction with downward rotation

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98
Q

What is Neer’s Sign?

A

Examiner performs maximal passive abduction in hte scapular place with internal rotation, while stabilizing the scapular. Impingement indicator. Positive test if there is anterior pain.

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99
Q

What is the Hawkin’s Test>

A

Passive internal rotation in scapular pain. Impingement indicator. Positive test if pain is felt.

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100
Q

How does tissue thickness relate to SIAS?

A

People with SAIS have increases tissue thickness and decreased subacromial space…61.7% of the space is occupied versus 54.2% space occupied in healthy people

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101
Q

Recommended treatment sequence for 3 part fracture?

A

Almost always ORIF because the joint is very unstable

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102
Q

Recommended treatment sequence for 4 part fracture?

A

Prosthesis…very hard to fix surgically

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103
Q

3 phases for rehab for proximal humerus fractures?

A

1) Passive assistive exercises to maintain ROM, avoid adhesions, and capsular tightness 2) Active and early resistive exercises 3) Maintenance through advanced stretching and strengthening

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104
Q

Complications of humeral fractures?

A

vascular injury, brachial plexus injury, frozen shoulder, avascular necrosis, nonuion, malunion

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105
Q

WHat is nonunion?

A

Bones don’t reform as a single bone (translational issues)

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106
Q

What is a malunion?

A

“New” bone that isn’t like your original…rotational issues such that the HH in the glenoid is different, which affects elbows and muscle movement at the elbow. Usually a result of rushing movement post surgery.

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107
Q

Incidence of scapular fractures?

A

2% of all fractures, 5% shoulder fractures

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108
Q

Reasons for infrequency of shoulder fractures?

A

1) Protection by soft tissues posteriorly and rib cage anteriorly 2) Scapula mobility dissipates traumatic forces

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109
Q

Why are scapular fractures extremely rare?

A

1) protection by its surrounding musculature 2) Protection by the ribcage 3) Free mobility of the scpula–gliding plane with 5 DOF

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110
Q

Mechanisms for body or spine fractures?

A

direct blow with significant force

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111
Q

Mechanisms for acromion fractures?

A

Direct blow to shoulder or force transmitted through the humeral head

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112
Q

Mechanisms for neck fractures?

A

Anterior or posterior force (lack stability in these directions). Fall with outstretched UE causing impact of the humeral head against the glenoid process.

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113
Q

Mechanisms for glenoid rim fracture?

A

Lateral force drives humeral head against the periphery of the glenoid cavity. Small avulsion fractures can also occur when dislocating humeral head impacts the anterior part of the capsule/labrum.

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114
Q

Mechanisms for glenoid fossa fracture?

A

A violent force laterally to the humerus, causing it to be driven into the center glenoid cavity, transverse fracture of the glenoid fossa occurs, fracture spreads depending on the direction of the force applied to the humerus

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115
Q

High shear and low compression in the glenoid causes?

A

dislocation

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116
Q

High shear and high compression in the glenoid causes?

A

rim/face fracture

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117
Q

Areas of the scapula that have the most fractures?

A

Scapular body (45%), glenoid neck (10%), acromial process (8%), coracoid process (7%), scapular spine (5%)

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118
Q

What is the biggest problem with malunion of two bones?

A

It changes articular version, which changes stability.

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119
Q

Clinical indicators of scapular fractures?

A

pain (with resistance, particularly abduction), local tenderness, swelling, crepitus, not much ecchymosis (so deep, so don’t see bruising)

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120
Q

Diagnosis of scapula fractures?

A

Radiographs with the scapular trauma series, AP, axillary, lateral, and weight bearing AP

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121
Q

3 types of extra-articular glenoid neck fractures?

A

Anatomical neck, surgical neck, inferior neck

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122
Q

Causes of glenoid neck fractures?

A

direct blow to shoulder, fall onto outstretched arm, force to superior aspect of shoulder

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123
Q

Percentage of glenoid neck fractures that are Type I fractures? Type II?

A

90%, 10%

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124
Q

Treatment for glenoid neck fractures?

A

conservative (non-surgical), ORIF (very traumatic to tissues so usually only done in young people), depends on the specifics of the injury.

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125
Q

Classification for intrarticular glenoid cavity fractures, of which 90% are nonoperative?

A

Classification by Goss-Ideberg…progressively more serious from Type I to Type VI

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126
Q

Treatment for scapular body fractures?

A

Usually non-operative…limited bone stock to perform surgery on, but usually heal well

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127
Q

Treatment for isolated acromial fractures?

A

depending on displacement: nonsurgical, surgical

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128
Q

Treatment for isolated coracoid fractures?

A

usually non-surgical, occasionally grafting and compression screw fixation (generates fracture site opposition, which creates some force between fragments, promoting bone growth)

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129
Q

What is the SSSC?

A

Superior Shoulder Suspensory Complex…Bony and soft tissue ring comprising the glenoid process, the coracoid process, the coracoclavicular ligaments, the distal clavicle, the AC joint and the acromion. Its integrity is essential to the normal relationship between the upper extremity and the trunk.

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130
Q

Treatment for a double disruption of the SSSC?

A

surgical intervention if displacement too large at any/either site

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131
Q

What is the a floating shoulder?

A

Ipsilateral scapular neck and clavicular shaft fractures. Unstable injury with a considerable risk of significant displacement of scapular neck and/or the clavicular fracture.

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132
Q

Treatment for avulsion scapular fractures?

A

Many are treated without surgery, but surgery is needed if there is high displacement, poor opposition, or inadequate healing/

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133
Q

What is scapulothoracic dissociation?

A

Closed traumatic forequarter amputation…extremely rare…very difficult to treat because there are no orthopedic connections and muscle attachments are completely disrupted.

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134
Q

Incidence of clavicular fractures?

A

1 in 20 fractures, 44% shoulder girdle injuries

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135
Q

Clavicle injury mechanisms?

A

Direct and indirect force (FOOSH or direct impact through axial loading (semi-direct) or superior loading). Stress fractures (usually athletic and usually resolved with change in training routine)

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136
Q

3 major mechanisms for clavicular fractures?

A

Fall directly onto shoulder (87%), direct blow to point of shoulder (7%), fall with outstretched hand (6%)

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137
Q

3 basic mechanisms that elevate stress levels sufficiently in slender bones that lead to fractures?

A

bending, torsion, compressive loading

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138
Q

Most likely cause of clavicular fracture out of bending, torsion and compressiON>

A

Compression by a force transmitted through the point of contact with the acromion (semi-direct force)

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139
Q

Why aren’t torsion and bending likely causes of clavicular fractures?

A

Freedom of the clavicle at the SCJ makes bending unlikely mechanism of clavicle fracture during clavicular impact loading. Available rotation about the longitudinal axis of the clavicle (approx. 50 degrees) eliminates torsion as the mechanism of clavicular fracture

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140
Q

How many times bodyweight is needed to cause a buckle fracture at the clavicle?

A

5x BW

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141
Q

What type of clavicle is most likely to buckle?

A

Thinner and longer

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142
Q

The critical force for a clavicular fracture will depend on:

A

speed of contact with solid object or ground, duration of collision (energy transfer through contact), body weight of individual

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143
Q

Clavicular fracture is most likely to occur from what type of blow?

A

Direct blow when the impact energy is absorbed fast vs. a glancing blow where the energy is dissipated more slowly.

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144
Q

Direction of applied force in a FOOSH in a clavicular fracture?

A

Force directed through humerus head to scapula. Fx only component that will produce clavicular compression. Fy/Fz tend to move scapula up and back away from clavicle = dislocation rather than fracture. Only when outstretched arm in coronal plane relative to the body is Fx sufficient to produce compressive buckling.

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145
Q

Direction of applied force in a direct blow to the shoulder that results in a clavicular fracture?

A

Entire impact force transmitted along the clavicular axis via the acromion. Fz/Fy are equal to zero. Critical buckling forces are reach as values apporach BW. If blow more glancing, Fx will be decreased and Fy/Fz will increase = favorable conditions for dislocation rather than fracture.

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146
Q

Clinical findings of clavicle fractures?

A

skin tenting, dropping shoulder, tenderness, ecchymosis, angles head to reduce trapezius pull

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147
Q

3 groups/classifications of clavicle fractures?

A

Group I, Group II, Group III

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148
Q

What is a group I clavicle fracture?

A

In the middle of the clavicle

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149
Q

What is a group II clavicle fracture?

A

Distal clavicle/near AC joint

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150
Q

What is a group III clavicle fracture?

A

Promximal fracture/near SC joint

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151
Q

Ranking of clavicle fractures from least common to most common?

A

Group III (5-6%) < Group II (12-15%) < Group I (80%)

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152
Q

As the type number of a clavicle fracture increases, what happens to severity?

A

It also increases

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153
Q

What is the worst type of clavicular fracture?

A

Comminuted

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154
Q

For group I clavicular fractures, what is A in the CCF guidelines?

A

Transverse fracture…one fracture sight

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155
Q

For group I clavicular fractures, what is B in the CCF guidelines?

A

Wedge…wishbone fracture with 2 fracture sights

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156
Q

FOr group I clavicular fractures, what is C in the CCF guidlelines?

A

COmminution zone separation

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157
Q

What does CCF stand for?

A

Comprehenesice Classification of Fractures

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158
Q

What is a Group II Type I fracture?

A

Clavicle fracture distal to the coracoclaviculr ligaments

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159
Q

What is a Group II, Type IIA fracture?

A

Clavicular fracture proximal to coracoclavicular joint

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160
Q

What is Group II, Type IIB fracture?

A

Clavicular fracture between the conoid and trapezoid ligaments

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161
Q

What types of Group II clavicular fractures are the worst?

A

Group II Type IIA and IIB because they cause a lost connection between the scapular and clavicle

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162
Q

Treatment options for clavicle fractures?

A

1) Arm support (simple sling) 2) Reduction (also maintain reduction) 3) ORIF 4) OREF

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163
Q

Type I clavicular fracture treatment?

A

Usually conservative…sling/figure 8 sling. If displaced or shortened, ORIF (plate fixation and intermedullary fixation via a clavicle pin)

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164
Q

Why is a figure 8 sling used for a clavicular fracture?

A

Prevents anterior collapse of the fracture site by putting the shoulder in retraction

165
Q

Type II clavicular fracture treatment?

A

Medial to conoid = like type I. Lateral to conoid = usually with a sling. If there is AC joint damage, then ORIF is often needed because of SSSC disruption

166
Q

Type III clavicular fracture treatment?

A

ALmost always conservative, very rare (~5%), if S-C joint is implicated can be much more serious

167
Q

Complications of clavicle fractures?

A

nonunion, malunion, neurovascular sequelae (compression syndromes…carotid, subclavian vein, subclavian artery, aneurysm, brachial plexus), post-traumatic arthritis

168
Q

Circumstances classifications of joint instability?

A

Chronic, recurrent, traumatic, atraumatic

169
Q

Chronic joint instability?

A

repeatedly over a long time

170
Q

Recurrent joint instability?

A

more than once

171
Q

Traumatic joint instability?

A

specific event caused it

172
Q

Atraumatic joint instability?

A

no specific event

173
Q

Dislocation?

A

separation of joint surfaces

174
Q

Subluxation?

A

partial dislocation, some contact, but it isn’t right

175
Q

Apprehension?

A

fear of dislocation after having a dislocation

176
Q

Incidence of GH dislocation?

A

85% of dislocations in the shoulder and 45% of all dislocations

177
Q

GH dislocations from least common to most common?

A

superior < inferior < posterior < anterior

178
Q

Directions and causes of anterior GH dislocation?

A

abduction, extension, external rotation…hits elbow back posteriorly = anterior dislocation

179
Q

Directions and causes of posterior GH dislocation?

A

axial loading, adducted, internally rotated…getting hit with arm across tummy

180
Q

Directions and causes of inferior GH dislocation?

A

Hyperabduction of humerus

181
Q

Directions and causes of superior dislocation at the GH?

A

forward and upward force on an adducted arm

182
Q

Most common GH dislocation?

A

Anterior dislocation…95% of dislocations

183
Q

Anterior dislocation of GH mechanisms?

A

fall with arm in abduction and external rotation, FOOSH injury (common in older adults)

184
Q

Complications of anterior dislocation?

A

Bankart lesions, HIll-Sachs defect, increased laxity of joint, rotator cuff tears, vascular damage, berve damage, reccurence

185
Q

Bankart lesion?

A

avulsion of labrum at inferior ligament

186
Q

Hill-Sachs defect?

A

Fracture of posterolateral surface of humeral head due to impaction of humeral head against anterior rim and glenoid during dislocation.

187
Q

Percentage of recurrence of GH dislocations?

A

40%

188
Q

Nerve damaged during anterior dislocation?

A

Axillary nerve…as much as 45% of the time

189
Q

% of GH dislocations that are posterior?

A

4%

190
Q

Mechanisms of a posterior GH dislocation?

A

axial loading of the adducted, internally rotated arm (severe blow), seizure or electric shock, fall with arm in abduction and internal rotation

191
Q

Complications of posterior GH dislocations?

A

Bankart lesions (reverse…posterior tear of labrum). Hill-Sachs (reverse…defent on anterior portion of humeral head). Articular surface changes (increased retroversion of humeral head or retroversion of glenoid)

192
Q

Incidence of inferior GH dislocation?

A

0.5% of dislocation

193
Q

Mechanism of inferior GH dislocation?

A

shoulder is forced into hyperabduction with proximal humerus levered over the acromion process (pivot point). Direct loading on a fully abducted arm (dropping a piano on a waiter)

194
Q

Complications of inferior dislocation?

A

fractures (greater tuberosity, acromion, clavicle, coracoid process, and glenoid rim), brachial plexus injury (~in 60% of patients), axillary artery injury, rotator cuff tear, long term (include adhesive capsulitis and recurrent subluxations or dislocations). Humerus becomes locked (between 110-160 degree of abduction) with head below the glenoid fossa (luxation erecta). May force head of humerus through soft tissues and skin through elbow.

195
Q

Mechanisms of superior GH dislocation?

A

extreme forward and upward force on adducted arm. humeral head driven upward through rotator cuff. Associated with fracture of humerus, clavicle or acromion.

196
Q

Clinical findings in all GH dislocations?

A

pain, deformity, lack of arm control, swelling, and numbness

197
Q

Clinical findings of an anterior GH dislocation?

A

muscle spasms and posterior hollow

198
Q

Clinical findings of a posterior GH dislocation?

A

Limited external rotation, limited elevation, flattening of anterior shoulder, prominent coracoid

199
Q

Severity of GH dislocations from least to most severe?

A

anterior < posterior < inferior < superior

200
Q

3 steps in nonsurigical treatment of GH dislocations?

A

reduction, protection, and strengthening

201
Q

2 steps of surgical treatment of GH dislocation?

A

arthroscopic and open

202
Q

Why is reduction used regardless of the type of GH dislocation?

A

best method is quick, effectice, requires minimal assistance and causes no additional injury.

203
Q

Four basic methods of reduction?

A

Traction, leverage, scapular manipulation, combination

204
Q

Milch Technique?

A

70-95% successful. Gentle longitudinal traction, also can apply external rotation. Pressure to the humeral head may be required. Welll tolerated by patients.

205
Q

External Rotation reduction?

A

81% successful. One hand holds upper arm. Other hand dgently guides forearm at 90degrees through external rotation. Sometimes reduction occurs during internal rotation following complete external rotation. One operator. Little/no sedatives needed.

206
Q

Scapular manipulation reduction?

A

85% success among experienced operators. Reposition the glenoid rather than the humeral head. Assistant applies downward traction in prone posture. Operator uses 2 thumbs to adduct the inferior aspect of the scapula.

207
Q

Phase 1 of conservative rehab for GH dislocation?

A

Acute injury (1-5 days). Goal: control pain/swelling and regain range of motion. With shoulder immobilized, isometric rotator exercises and pendululm/sawing exercises can help with ROM.

208
Q

Phase 2 of conservative rehab for GH dislocation?

A

Repair (5-12 days). Goal: achieve full ROM and increase strength. Porgression form isometric to tubing and dumbbells. Continued ROM exercises.

209
Q

Phase 3 of conservative rehab for GH dislocation?

A

Remodeling (12 days to 3 weeks). Goal: regain normal strength and return to full activity. Weights and closed kinetic chain using weight shifting for neuromuscular control.

210
Q

What is a shoulder separation?

A

AC joint dislocation

211
Q

What is the most common shoulder injury?

A

AC joint separations…40-50% of all athletic injuries

212
Q

When do shoulder separations mostly occur?

A

Second decade of life

213
Q

In what gender do most shoulder separations occur in?

A

Male…male:female = 5:1

214
Q

Mechanisms of injury for AC joint disorders?

A

Direct force or indirect force (upward from falling on adducted arm or downward from a swift load change)

215
Q

Diagnosis of AC joint disorders?

A

articulation and palpitation and Xrays

216
Q

Class 1 AC joint disorder?

A

AC strain, but intact

217
Q

Class 2 AC joint disorder?

A

AC disrupted, but CC intact

218
Q

Class 3 AC joint disorder?

A

Both AC and CC disrupted

219
Q

Class 4 AC joint disorder?

A

Type III + posterior displacement of clavicle into trapezius

220
Q

Class 5 AC joint disorder?

A

Type III + detachment of deltoid and trap on clavicle

221
Q

Class 6 AC joint disorder?

A

Type III + inferior displacement to subcoracoid position.

222
Q

What type of AC joint disorder causes pulmonary injury?

A

Type IV separation…ipsilateral pulmonary contusion

223
Q

What type of AC joint disorder causes distal clavicle osteolysis?

A

Type III separation…microtrauma causing bone resorption with no bone remodeling

224
Q

Secondary pathologies of AC joint disorders?

A

fractures (acromial process, clavicle and ribs), sternoclavicular dislocation, pulmonary injury, distal clavicle osterolysis, AC joint osteoarthritis

225
Q

Incidence of AC joint disorders?

A

12% of shoulder dislocations.

226
Q

Age group that gets more AC joint disorders?

A

Younger&raquo_space; older

227
Q

Most common AC joint disorder?

A

III > I > II > IV > V > VI

228
Q

Treatment for Type I AC joint disorder?

A

Ice, resolves 7-10 days as a rule…want to make contracture of ligaments

229
Q

Treatment for Type II AC joint disorder?

A

Nonoperative (slings, casts, braces, and harnesses). 3-6 weeks continuous pressure on superior clavicle to promote ligament healing (want to keep distal clavicle down). Operative (athroplasty, removal of distal clavicle, joint debridement, and meniscetomy)

230
Q

What are operative treatment methods for Type II AC joint disorder?

A

arthroplasty (joint reconstruction), removal of distal clavicle (if degenerative), joint debridement (removal of dead tissue), meniscectomy (removal of meniscus)

231
Q

Treatments for Type III AC joint disorders?

A

Nonoperative (sling and harness and skillful neglect) and Operative (intra-articular, extra-articular coracoclavicular via suturing and screws)

232
Q

In suturing for a Type III AC joint separation, why would you use a double suture?

A

Try and act like conoid and trapezoid ligaments

233
Q

In the surigical vs conservative treatment which one is better?

A

Pretty much the same, except surgery had a slightly higher overall patient satisfactory outcome

234
Q

What are manual muscle tests?

A

Do a specific task to recruit a certain muscle to see what the condition that muscle is in

235
Q

What did the results of the thesis testing MMTs show?

A

For the most part, the tests are actually testing the muscles they are supposed to be testing. Pain can skew results. Can never get perfect isolation.

236
Q

What is the painful arc?

A

Abducting your arm, first part of the painful arc is from RC inflammation, top part of the acr is painful because you are relying on AC and SC joints more, so if they are inflammed, you will get pain up there.

237
Q

What is the drop arm test?

A

Bringing arm down in adduction, and all of the sudden the arm just drops because of a RC tear. A full tear will have a full drop, a partial tear will have pain and not as severe of a drop

238
Q

What is the shoulder dump test?

A

Adducting the arm, when all of the sudden, the scapula dumps due to scapular dyskinesis NOT rotator cuff

239
Q

What is a full can test?

A

Arms elevated in the scapular plane with thumbs up. Tester presses on arm, testee tries to resist force. Causes grinding of tubersoties under the arch. A postitive test is weakness.

240
Q

What is an empty can test?

A

Arms elevated in scapular plane, with thumbs facing downward. Tester presses on arm, while testee resists. Positive test is muscle weakness.

241
Q

When using an empty or full can test, which is a better evaluation, pain or muscle weakness?

A

Muscle weakness

242
Q

What test is better to use, empty or full can?

A

Full can…has about the same sensitivity as empty, but has a greater specificity

243
Q

Do you want sensitivity and specificity high or low? What is a good value in clinical trials?

A

Both high, above 50

244
Q

Rotator cuff injury classifications?

A

1) asympotomatic (common in low demand RC users) 2) posterior tightness 3) subacromial abrasion (SAIS…95% of RC tears are preceded by SAIS) 4) Partial-thickness cuff tear 5) Full thickness tear 6) Cuff tear arthripathy 7) Failed acromioplasty 8) Failed cuff surgery

245
Q

Conservative treatment for RC tears?

A

1) avoid repeated unjury 2) restore flexibility 3) restore strength 4) aerobic exercise 5) modification of work/sport

246
Q

Why is strengthening the subscap and infra good for RC tears?

A

Takes the load off of subscap, which helps to let it heal

247
Q

Priorities for surgical repair of RC?

A

1) reshape rather than remove acromion 2) do not damage deltoid origin 3) restore motion 4) release, mobilize and repair torn tendons 5) individualize treatment

248
Q

What is acromioplasty, and what does it do?

A

1) reshaping of anterioinferior acromion 2) increases subacromial space 3) removal of bone spurs 4) repair deltoid well

249
Q

Why is is so important to not damage the deltoid origin in a rotator cuff repair surgery?

A

Damage deltoid and supraspinatus is torn = little/no abduction

250
Q

Surgical treatment for a partial/full tear?

A

1) convert to a full tear 2) create firm attachment 3) reestablish tendon/bone contact

251
Q

What is a tendon transfer for a rotator cuff tear?

A

usually pec major or lat dorsi…for inoperable/failed repair of RCT elements. Changes mechanics, but eliminates instability

252
Q

What is the most important part of rehab for the “shoulder” joint injuries?

A

Get mobility back as soon as possible because if not joint adhesions develop and you lose it. Stretching is followed by strengthening.

253
Q

Rehab following RC surgery?

A

Very similar to conservative method–>mobility very quickly followed by increasing intensity over a period of weeks, 3 phases of intensity

254
Q

Phase I of RC tear rehab?

A

early mobility movements…passive and active

255
Q

Phase II of RC tear rehab?

A

active, passive stretching

256
Q

Phase III of RC tear rehab?

A

tubing instead of bands to increase resistance. Weights after 3 months.

257
Q

Gaps in understanding RCT?

A

casual relationships not confirmed conclusively (don’t know why some people get them, and others do not), repair strategies only partially driven by biomechanical considerations (surgically good, functionally poor), appropriateness, optimal nature of clinical screening tests, dose-response relationship (how much/what kind/when), establishment of work-relatedness, better quantification/understanding of RCT contributions to arm positioning and muscle activity.

258
Q

Why is new research needed when it comes to RCT?

A

1) Need better ways to quantify exposure to tissues (modeling through mathematical and animal models) 2) Large-scale workplace studies to show causality (monitored physical requirements, compared to incidence/compensation data) 3) Better ways to differentiate between treatment strategies (newer techniques…arthroscopic superior to open technique)

259
Q

Where can bicep disorders happeN?

A

proximally and distally

260
Q

Why do bicep insertion variations matter?

A

Influence failure mechanisms

261
Q

What is the “house” of the long head of the biceps tendon?

A

Coracohumeral ligament is the roof. Superior glenohumeral ligament is the floor.

262
Q

What does the long head of the biceps tendon do at the GH joint?

A

Acts as a stabilizer…particularly when supra is damaged

263
Q

Origin of Long head of biceps brachii?

A

Supraglenoid tubercle

264
Q

Biceps tendon pathologies?

A

SLAP lesions, tendinitis, subluxation, rupture

265
Q

Incidence of SC joint dislocations?

A

3% of dislocations

266
Q

Mechanisms of SCJ dislocations?

A

direct force or indirect force

267
Q

What is the most common SCJ dislocation?

A

anterior (about 20x more common than a posterior)

268
Q

What causes an anterior SCJ dislocation?

A

an indirect froce

269
Q

What causes a posterior SCJ dislocation>

A

Indirect force, but possible a direct force

270
Q

What is the problem with a posterior SCJ dislocation?

A

can puncture a lung or your trachae, or shred veins

271
Q

Mechanism of a posterior SCJ dislocation from an indirect force?

A

Arm is adducted and internally rotated, force is applied to shoulder and clavicle dislocates at SC joint posteriorly

272
Q

Mechanism of an anterior SCJ dislocation from a direct force?

A

Arm is adducted and behind back, force is applied at shoulder, and clavicle dislocates from SCJ anteriorly

273
Q

Clinical findings of a SCJ dislocation?

A

Pain (increases with arm movement and more pain in posterior direction). Subluxation of SCJ. Dislocation apparent by visible deformity.

274
Q

Treatment for anterior SCJ dislocation?

A

Closed reduction by putting pressure on medial clavicle

275
Q

Treatment for posterior SCJ dislocation?

A

Close reduction. Manipulation of medial clavicle, use of towel clips if necessary

276
Q

WHen is surgical treatment needed for a SCJ dislocation?

A

very rare. usually only if all ligaments are dirupted, goal is to reduce the joint and promote normal function (fusion.suturing + ligament repair)

277
Q

When does the long head of the biceps contribute the most to shoulder stability?

A

When there is a problem with the rotator cuff

278
Q

What are the identified bicep pathologies?

A

SLAP lesions, tendinitis, subluxation, rupture

279
Q

What is TLC for the general classification of bicep tendon pahologies?

A

T = state of tendon L = location along tendon C = cuff involvement/damage

280
Q

What are the provocative tests for bicep tendon pathologies, and what is their purpose?

A

Speed’s test, Yergasson’s test, and modified Neer’s test. Promote bicep activity (elbow flexion and supination) in a mechanically advantageous position and then put pressure on biceps tendon to compress a tendon with tension in it…a positive test is one that causes pain

281
Q

What is a SLAP lesioN?

A

acronym for Superion-labrum-anterior-posterior.

282
Q

How many flavors of SLAP lesions are there? Which are the worst?

A

Type I-IV…severity increases with type

283
Q

For what type of SLAP lesion is a tenotomy or a tendoesis performed?

A

Type IV lesions

284
Q

What is a tenotomy? When is it used?

A

Removal of biceps tendon…age >60 yrs, lower demand, minimal cosmetic concern, massive rotator cuff tear

285
Q

What is a boney tenodesis?When is a boney tenodesis performed?

A

Attach biceps tendon to bone…high demand age <50 years

286
Q

What is a soft tissue tenodesis? When is it performed?

A

Attach tendon to soft tissue (holds less than a boney tenodesis)Lower demand…age b/w 50 to 60 years

287
Q

Where is the biceps transferred during a tenodesis. and what is its intention?

A

Transfer of biceps to humerus. Intended to save remainder of labrum and maintain some elbow flexion capacity. No loner cross GH, so not a GH stabilizer any more

288
Q

What is biceps tendonitis?

A

Chronic shoulder pain with tenderness over bicipital groove. Positive Speed test. Includes 90% of all painful shoulders. Often in conjunction with RC tears/

289
Q

Why is biceps tendonitis typically in conjuction with RC tears?

A

There is more comrpession and tension put in the biceps tendon as a stabilizer because the RC isn’t working correctly…overloading of biceps tendon = tendonitis. If you don’t have biceps pain, your shoulder pathology isn’t advanced yet.

290
Q

What are the 2 types of subluxations of the biceps tendon?

A

1) Rupture of transverse ligament causes the biceps tendon to move up and out of bicipital groove and onto subscap, which affects its mechanical advantage. 2) Separation of subscap tendon and transverse ligament causes the biceps tendon to move between the subscap tendon and humeral head. Force into either tendon causes the biceps tendon to move down and cause destabilizing forces at the GHJ.

291
Q

Causes of a ruptured bicep?

A

Osteophyte tendon destruction or acute damage due to lifting heavy load

292
Q

Symptoms of a ruptured biceps?

A

biceps bulge (more for proximal), bruising, loss of flexion strength, a lot of pain

293
Q

Treatment for a ruptured biceps?

A

Usually only distal is repaired. Proximal not always treated unless you are young and active (this is a more intrinsic mechanism so repair won’t necessarily work)

294
Q

Overview of frozen shoulder?

A

inflammatory disorder, characterized by pain, decreased range of motion, shoulder stiffness, shrinkage of capsule

295
Q

Types of frozen shoulder?

A

Primary = idioathic. Secondary = traumatic or post surgery

296
Q

Anatomy of adhesive capsulitis/frozen shoulder?

A

inflammation and thickening of shoulder capsule with hypervascularization (shoulder wants to refresh itself)

297
Q

What movements are most limited in frozen shoulder?

A

internal rotation, abduction, and external rotation

298
Q

Why are IN, abd, and ER most limited in frozen shoulder?

A

shortening of capsule in primary posteriot and posterior IGHL

299
Q

Demographics of frozen shoulder?

A

Affects 3% of population, women are 2x more likely, 6-17% become bilateral within 5 years, present in 10-20% of diabetics (Type I 36%)

300
Q

3 stages of frozen shoulder and how long they last?

A

Painful (204 weeks), Frozen (3-6 months), Thawing (18-24 months)

301
Q

How does frozen shoulder go away?

A

It self resolves

302
Q

The pathogenic mechanisms proposed for frozen shoulder?

A

autoimmune, inflammatory, paralytic, degenerative, traumatic, pyschogenic, fibrogenic

303
Q

Predisposing factors to frozen shoulder?

A

Age (40-60 years), prior injuries, non-shoulder surgery, immobility, diabetes, thryroid disorders, neurological conditions, personality disorders

304
Q

Clinical findings of frozen shoulder?

A

Loss of ROM (judged to normal ROM), pain with movement, particularly end range, pain increased at night

305
Q

What movement of the GHJ is most affected by FS?

A

abduction

306
Q

Secondary pathologies of FS?

A

increased GH translation (RC pathologies from reduced intra articular pressure, which increases translation), very painful and stiff shoulder, shoulder arthritis, muscle atrophy, intra-articular lesion due to manipulation, persistent disability

307
Q

Treatment goals of FS?

A

eliminating pain source (if cervical disc related), treat stiffness, prevention of initiation (post-trauma must initiate movement)

308
Q

Non-surgical treatments of frozen shoulder?

A

1) supervised neglect (supportive therapy and passive stretching within pain limits) 2) pain relievers (NSAID, oral steroids, 1 intra-articular corticosteroid injections) 3) physiotherapy with NSAIDs (relieve pain, maintain active and passive ROM and regain function, best in thawing phase) 4) intra-articular injection of sodium hyaluronate 5) suprascapular nerve block (freeze suprascapular nerve with local anesthetic to relieve pain of mechanotransducers, which allows for more active ROM to prevent further joint restriction) 6) Capsular distension arthrogrpahy

309
Q

What is capsular distension arthrography?

A

numb the GHJ, and then keep injecting corticosteroid and saline until the capsule distends and ruptures, thus decreasing pain by reducing the stretch on pain receptors in capsule

310
Q

What is a non-surgical manipulation under anesthesia for FS going to do?

A

Move arm until rupture of capsule

311
Q

Iatrogenic complincation of manipulation of FS under anesthesia?

A

RC tears, rupture of anterior capsular structures, fracture of surgical neck and shaft of humerus, dislocation, and complete brachial plexus palsy.

312
Q

Surgical methods for FS if conservative methods fails?

A

1) arthroscopic capsular release 2) open surgical release (rare…lengthening of subscap and removal of bony spurs)

313
Q

What are the complications of an arthroscopic capsular release?

A

bones lesions and damage to axillary nerve

314
Q

Cervical/shoulder neuropathies?

A

thoracic outlet syndrome, axiallry, suprascapular, musculocutaneous, spinal accessory, long thoracic, “Saturday night” palsy, Erb’s Palsy

315
Q

5 parts of a nerve?

A

myelin, axon, endoneurium, perinerium, epineurium…Each type of nerve injury affects a progressive amount of the nerve as it gets worst

316
Q

What are the locations of thoracic outlet syndrome?

A

scalene triangle (most common), costoclavicular space, and pec minor space

317
Q

Sites implicated in TOS?

A

neurovascular bundle of the brachial plexus and subclavian artery/vein

318
Q

What are the general risk factors for TOS?

A

people with long necks and droopy shoulder, aging, obesity, repetitive injuries, sleep disorders, hormone imbalance, fibromyalgia, rheumatoid arthritis, lack of nutrition, tumors, infection, anemia, stress or depression

319
Q

All of the risk factors for TOS do what?

A

add pressure on blood vessels and nerves, cause tendon and muscle swelling in shoulders, change the structure or function of nerves/vessels = compression in thoracic outlet!!!

320
Q

Causes of TOS?

A

1) cervical hyperextension activities such as whiplash 2) working from repetitive stress of lifting heavy loads overhead and prlonged postures leading to slouching 3) idiopathic 4) developmental (rare, less the 1% populatio born with an extra rib)

321
Q

5 types of TOS?

A

1) true neurological TOS (birth defects of nerves in the thoracic outlet) 2) arterial TOS (also birth defects) 3) venous TOX (rare, causes unknown, develops suddenly) 4) traumatic TOS (MVA, sports) 5) disputed TOS (most commom, no clear causes)

322
Q

Most common cause of TOS?

A

disputed…no one knows and some doctors say it doesn’t exist

323
Q

Consequences of TOS?

A

painful tingling and numbness anywhere in U, persiscapular pain, motor weakness

324
Q

Diagnosis of TOS?

A

very difficult for non-neurological, but there are tests

325
Q

Treatments of TOS?

A

usually conservative such as posture correction and avoiding trigger activities…surgery usually only for confirmed neuro TOS (very rare)

326
Q

Diagnosis of TOS?

A

patchy neurological processes (interrupted signals) in electrodiagnosis and provocative manipulation

327
Q

Provocative manipulations for TOS diagnosis?

A

Costoclavicular maneuver (lift chest out, shoulder down and back with arm extension) and Allen’s test (horizontally abducted arm with external rotation, elbow at 90 degrees, turn head away)

328
Q

Positive test for provocative tests for TOS?

A

No radial pulse

329
Q

TOS treatments?

A

Generally conservative (supportive and anti-inflammatory) or surgery (less than 1/3, tnedon transfers, scalene resection, and rib removal if there is an extra one)

330
Q

Physical therapy program fro TOS treatment?

A

abdominal breathing, postural correction, nerve flossing to improve range of motion and break up adhesions/scar tissie, strengthening exercises for neck and shoulder

331
Q

Goal of surgical treatment for TOS?

A

releive compression on the brachial plexus and blood vessels

332
Q

3 procedures for surgical treatment of TOS?

A

1) partial scalene removal around nerves 2) first or extra rib removal 3) scalene and rib removal (scar tissue formation = numbness or tingling, prevention = cellophane type material to cover the nerves)

333
Q

Innervation of axillary nerve?

A

deltoids and teres minor

334
Q

2 types of axillary nerve problems?

A

1) Quadrilateral space syndrome (compression of nerve in the quadrilateral space…uncommon) 2) Iatrogenic injury (an injury induced inadvertently by a physician or surgeon or by medical treatment or diagnostic procedures)

335
Q

Clinical findings of axillary nerve problems?

A

paresthesis throughout the lateral arm, shoulder weakness in shoulder elevation and abduction, fatiguing quickly when exercising

336
Q

Diagnosis of axillary nerve problem?

A

can go undetected in from a traumatic injury because joint and/or bone injury dominates the clinical practice, nerve entrapment and compression, deltoid atrophy, EMG, nerve biopsy, MRI (most common)

337
Q

Consequences of axillary nerve disorder?

A

deltoid and teres minor paralysis, deltoid atrophy, weakness in abduction

338
Q

Diagnosis of axillary nerve disroder?

A

EMG recordings

339
Q

Treatments of axillary nerve disorders?

A

1) most cases resolve nonsurgically < 3 months 2) surgery for compression releaes/grafting/neurolysis

340
Q

Types of surgical treatments for axillary nerve disorder?

A

neurorrhaphy, neurotization, nerve grafting, neurolysis, nerve transfer, muscle transfer

341
Q

neurorrhaphy?

A

suture of divides nerve

342
Q

neurotization?

A

regeneration of a nerve

343
Q

nerve grafting?

A

new nerve tissue is inserted into gap

344
Q

neurolysis?

A

using radio frequency, heat, cutting, or chemical injection to release nerve from scar

345
Q

nerve transfer?

A

nerve is transferred to the area and replaces injured nerve roots

346
Q

muscle transfer?

A

functioning muscle, nerve and blood supply are grafted to the area to restore function

347
Q

Location/innervation of suprascapular nerve?

A

From c5,c6,cc7 nerve roots to supraspinatus and infraspinatus

348
Q

Causes of suprascapular nerve problems?

A

Blunt trauma, sudden shoulder twist, ganglionic cysts (labrum teaars), repetitive motion

349
Q

Consequences of a suprascapular nerve injury?

A

pain in posterior/lateral shoulder, weak abduction/external rotation

350
Q

Diagnosis of a suprascapular injury?

A

EMG/NCS (nerve conduction studies)

351
Q

Treatments for a suprascapular nerve injury?

A

chronic –> conservatively. Surgical decompression by removing the cyst. Supra repair works better than infra in general.

352
Q

Location and innervation of musculocutaneous nerve?

A

Obliquely below coracoid process. Passes through the coracobrachialis, also innervating biceps and brachialis

353
Q

Causes of injury to musculocutaneous nerve?

A

Severe trauma, surgery, occasionally GH dislocation

354
Q

Consequences of a musculocutaneous nerve injury?

A

biceps atrophy and numbness in lateral elbow and forearm (whre nerve travels)

355
Q

Diagnosis of a musculocutaneous injury?

A

nerve conduction

356
Q

Treatment for a musculocutaneous injury?

A

Many self-resolve in weeks to month by traction (keeping the nerve straight). Exploratory surgery is an option (nerve grafting, nerve transfer (over lesion), after > 1 year following injury = significantly less recovery)

357
Q

Common name for a spinal accessory nerve injury?

A

“stinger” or “burner”

358
Q

Location and innercation of spinal accesory nerve?

A

through sternocleidomastoid and into trapezius

359
Q

Causes of spinl acessory nerve injury?

A

Penetrating shoulder trauma (knife wounds), quick change in neck./shoulder angle, iatrogenic

360
Q

Consequences of spinal accessory nerve damage?

A

trapzius atrophy, pain, impingement (from lack of scapular rotation because the trapezius isn’t working correctly)

361
Q

Diagnosis of spinal accesory nerve injury?

A

Shoulder shrug

362
Q

treatments for spinal accessory nerve injury?

A

generally surgical (neurolysis, grafting, repair), nonsurgical only in extended cases if person learns to compensate for not being able to use traps, muscle transfer possible

363
Q

Location and innervation of long thoracic nerve?

A

From c5, c6, c7 nerve roots to serratus anterior

364
Q

Causes of long thoracic nerve injury?

A

crushed by scapula from a blow, surgical complication, idiopathic

365
Q

Consequencs of a long thoracic nerve injury?

A

Winging, serratus paralysis (come together)

366
Q

Diagnosis of a long thoracic nerve injury?

A

winging check

367
Q

Treatment for a long thoracic nerve injury?

A

may resolve nonoperatively, surgical (scapulothoracic fusion, tendon trandfers, pec major transfer)

368
Q

Cause of Saturday Night Palsy?

A

Radial nerve compression on humerus, often caused by falling asleep drunk in a chair with your arm slumped over it

369
Q

Effects of Saturday Night Palsy?

A

decreased sensation in hand, inability to flex wrist and fingers

370
Q

treatments for Saturday Night Palsy?

A

recovery in 2-4 weeks on its own, accelerated with physiotherapy, usually no surgery

371
Q

What are the 2 mechanisms of Erb’s Palsy?

A

Upper barchial plexus inury that occurs with excessive stretching og the neck during delivery OR excessive upper limb pulling causing a lower brachial plexus injury

372
Q

Signs of Erb’s Palsy?

A

Partial or complete arm parlysis (loss of movement or feeling)

373
Q

Treatment of Erb’s Palsy?

A

Asses child’s arm over time (looking for improvements in movement and feeling). Spontaneous recovery 90% of the time

374
Q

3 bones of the elbow

A

humerus, radius, ulna (olecranon)

375
Q

3 joints of the elbow?

A

ulnohumeral, radiohumeral, superior radioulnar…all in one synovial capsule

376
Q

What type of joint in the ulnohumeral joint?

A

hinge…important for force transmission

377
Q

Main joint at the elbow?

A

ulnohumeral joint

378
Q

What type of joint is the radiohumeral joint?

A

arthodial/planar (sliding in a plane)

379
Q

What is the role of the superior radoiulnar joint?

A

Enabler of pronation and supination

380
Q

Ligaments of elbow?

A

anterior, posterio, ulnar colalteral, medial collateral, annular

381
Q

Bursa in the elbow?

A

at the olecranon

382
Q

Nerves of the elbow

A

ulnar, radial, median

383
Q

Main blood vessel at elbow?

A

brachial artery

384
Q

2 major activities at the elbow

A

flexion/extension and pronation/supination

385
Q

ROM for flexion/extension at elbow?

A

0-145 degrees

386
Q

ROM for pronation/supination at the elbow?

A

-70 (pronation) to 85 (supination) degrees

387
Q

What type of glide happens at the radiohumeral joint during elbow flexion?

A

anterior glide

388
Q

What type of glide happens at the radiohumeral joint during elbow extension?

A

posterior glide

389
Q

Carrying angle measurement?

A

10-15 degrees valgus

390
Q

What is the carrying angle?

A

angle between long axis of humerus and forearm in full extension

391
Q

Abnormalities in the carrying angle usually result in?

A

joint dysfunction and radiohumeral dysfunction

392
Q

Why is joint contact so important at the elbow?

A

posturally sensitive joint…maintain static posture leads to focal tissue damage(arthritis)

393
Q

What is joint force influenced by at the elbow, and what does an imbalance in net ulnar joint reaction force cause?

A

influenced by contact points and muscle actions…inbalance in net ulnar joint reaction force increases the probabilty of a fracture

394
Q

People who did deterministic elbow models?

A

murray (1997 and 2000), Lan (2001), An (1987)

395
Q

Person how did stochastic elbow model?

A

Longenderfer (2005)

396
Q

Elbow stability work at Western using cadaver arms?

A

Cynthia Dunning

397
Q

What is a deterministic model?

A

No variability (one value), usually mean data is used.

398
Q

What is the number of inputs for a deterministic model?

A

single

399
Q

What is the number of outputs for a deterministic model?

A

single

400
Q

Type of output for a deterministic model?

A

one value/”case”

401
Q

What is a stochastic model?

A

accounts for variability (uses statistics_

402
Q

Number of outputs for a stochastic model?

A

many distributions

403
Q

Number of inputs for a stoachastic model?

A

many

404
Q

Type of ouput in a stochastic model?

A

population description…get a # of values that fall into a distribution

405
Q

Stability at the elbow?

A

Similar mechanisms as shoulder but overall more stable (and less flexible), bony socket (fossa) = deepers so increases contact area, ulnar processes to resist anterior/posterior translations, radiohumeral joint for anterior and valgus displacements

406
Q

Ligaments at the elbow prevent?

A

hyperextension, hyperflexion, varus/valgus

407
Q

Muscle contraction at the elbow does what

A

Increases compression, which increaes stability and joint contact force…co-activation really increases compression

408
Q

3 main contributors to stability at the elbow?

A

ligaments, muscle contraction, and bones

Physiology 2 (16 decks)

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