17. Acute Soft Tissue Flashcards

1
Q

There are two main areas that allow abduction in the shoulder: the glenohumeral joint and the abduction of the entire scapula. What is the ratio of the movement of these areas to allow complete abduction?

A

•Glenohumeral abduction motion to
scapulothoracic abduction motion is 2:1

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2
Q

Why is the shoulder a relatively unstable joint? (esp when compared to the hip, for example).

A

Anatomy: it is more of a shallow dish/ball than a socket/ball arrangement. Think about a golf ball’s relationship to a golf tee (the golf ball has a lot of potential movement)

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3
Q

Given that the bony anatomy offers inadequate stability, what provides the shoulder with stability?

A

Capsule, muscles, ligaments.

Balance between enough stability and enough motion.

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4
Q

Acute shoulder dislocations (aka glenohumeral joint dislocations): anterior or posterior dislocation more common?

A

Anterior dislocation - 98%

Posterior dislocation - 2%

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5
Q

With an anterior shoulder dislocation, what is a common sequelae in a younger person?

What about an older person (>40)?

A

Recurrence rate of dislocation is inversely related to age.

Young: more likely to re-dislocate several times due to a torn labrum and general loosening.

Older: dislocation is more likely to cause a rotator cuff tear.

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6
Q

What nerve is frequently injured/pinched by an anterior shoulder dislocation?

How to test fo rinjury to this nerve?

A

Axillary nerve: runs from brachial plexus to the posterior humerus.

Test via sensation of the lateral arm, and deltoid function.

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7
Q

What imaging view do we need to get to confirm a posterior dislocation?

A

Axillary view: looking up through someone’s armpit.

Challenging to get because this position may be painful for pt.

This image: axillary view, posterior dislocation. Note ball of humerus is below the glenoid.

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8
Q

Posterior dislocations of the glenohumerus are infrequent: what are the most frequent mechanisms of this dislocation?

A

Not generally due to trauma: generally due to seizure or electroconvulsive therapy.

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9
Q

Glenohumeral anterior instability: is it easier to diagnose recurrent dislocations or recurrent sublexations?

What treatment can often help with sublexation?

A

There is a spectrum of damage to this joint, from stable/normal, to sublexation, to dislocation. Sublexation is a loosened joint, feels to the pt like the humeral head is trying to slide out.

Sublexation condition much more difficult to diagnose.

PT can usually help.

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10
Q

What is a Bankart Lesion?

A

after most anterior dislocations, there is a labral tear aka Bankart Lesion.

Causes a loosened joint overall.

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11
Q

What is a Hill-Sachs Lesion?

A

Humeral head: has been displaced anteriorly, then impacted the head and is now gouged.

Reduction is not straightforward, have to disengage the structures first.

Basically the humeral head now looks like Pac-Man from the top.

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12
Q

Physical exam findings with anterior glenohumeral displacement?

A
  1. Apprehension Sign. Pt looks apprehensive when you move their arm in a way that will replicate the shoulder pain.
  2. Sulcus sign (see pic). Arm looks like it’s hanging low. Multidirectional instability.
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13
Q

What lesions are present on this MRI? (axial glenohumeral)

A

Arrows on the left side: Bankart Lesion (glenoid labrum has been stripped off the bone.

Right side: Hill-Sachs Lesion (pac-man).

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14
Q

What are the 2 main treatments for chronic recurrent anterior glenhumeral instability?

A
  • PT
  • Operative stabilization: 90% arthroscopic; the rest done via open procedure
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15
Q

Treatment for recurrent posterior multidirectional glenohumeral instability?

Word of caution?

A

Treat with PT. Surgical repair not as successful as for anterior instability.

Posterior instability occurs in ppl with ligamentous laxity (Ehlers-Danlos, for example - or just normal people who are loose-jointed.)

Caution: some people will present with this, but it may be self-inflicted –> factitious disorder, meds-seeking.

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16
Q

Clavicle: what is the most common site of fracture?

A

If you think of the clavicle as a bone with three equal parts, the middle third is the most frequently fractured.

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17
Q

Clavicle: what joint is medial to it? what joint is lateral to it?

What is the most uncommon location to fracture?

A

Medial: sternoclavicular joint

Lateral: acromioclavicular joint

Rare to fracture the medial third. Takes a lot of force (usually car crash = cause)

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18
Q

Clavicle: what causes the characteristic appearance of a pt who has fractured it? (bump under the skin)

A

The lateral clavicle is stabilized by the deltoid and trapezius, and the coracoclavicular ligaments

the medial part is pulled UP by the SCM muscle.

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19
Q

Clavicle fracture: treatment?

A

Supportive.

Figure of 8 brace holds a good anatomical position, but apparently is uncomfortable.

No difference in outcome for Fig of 8 vs simple sling.

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20
Q

When we casually call something a “shoulder separation” what joint are we talking about?

A

Acromioclavicular joint.

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21
Q

With an acromioclavicular separation, what ligments are torn?

A

The more medial ligaments: the coracoclavicular ligaments.

The acromioclavicular ligament is not very strong - is kind of inconsequential.

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22
Q

Acromioclavicular joint injuries: how are they classified? Why is this important?

A

Classified into 6 types by the extent of injury and the structures involved.

Treatment depends on type:

Types I and II: non-operative

Type III: usually non-operative

Types IV, V, VI: operative

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23
Q

Rotator cuff anatomy review: What are the 4 muscles of the rotator cuff? Where do they insert on the arm?

A

Subscapularis, Supraspinatus, Infraspinatus, Teres Minor.

All insert on greater tuberosity (posterior humerus) except Subscapularis, which inserts on the lesser tuberosity (anterior humerus).

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24
Q

Rotator cuff disorders: characteristic symptoms?

A

Night pain

Painful arc of motion (esp between 90’ and 120’)

Restriction of motion (if don’t get treatment)

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25
Q

What is impingement syndrome?

A

Rotator cuff disorder where the glenohumeral bursa can get pinched between the acromium and the greater tuberosity.

Leads to bursitis, tendonitis.

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26
Q

How can normal anatomic variants contribute to impingement syndrome?

A

acromion shapes that have more curve to them may allow less space in the joint and predispose pts to bursitis/impingement sx.

27
Q

Treatment options for impingement of the acromiohumeral joint?

A

PT, strengthen the muscles to functionally stabilize the joint.

Surgical: may need to remove some of acromion to increase space for the tendon/bursa.

28
Q

What is calcific tendinitis?

A

Rotator cuff disorder, idiopathic.

Deposits of Ca within tendons.

Picture: huge Ca deposit within the supraspinatus tendon.

29
Q

Calcific tendonitis: Etiology? Prognosis? Treatment?

A

Generally due to tendon overuse, impingment - but we don’t understand etiology.

Usually self-limiting.

Very painful: can inject steroids to stem the inflammatory response and alleviate pain. If very painful, may have to aspirate the Ca from the tendon.

30
Q

Define adhesive capsulitis.

Etiology?

Associations with other diseases?

A

Contracted, thickened capsule drawn tightly around the humeral head

Etiology unknown

Associated with diabetes, liver disease

31
Q

Adhesive capsulitis: how can you tell this is what’s going on?

What are the 3 stages?

Do we have treatments?

A

Diagnose partly with history: patient will have lost ROM in the joint over 3-4 days.

Partly with physical exam: both active and passive ROM limitations are equal. Ie, it is not due to muscle weakness - it is truly limited ROM.

3 stages: acute “freezing” phase (painful); later “frozen” phase, eventual “thawing” phase where it loosens up again.

Treatment is PT, possible manipulation under anesthesia to try to incr ROM, but these don’t work well and it will eventually loosen on its own (1yr)

32
Q

Rotator cuff tears: acute or chronic type more common?

Give an example for how each type can occur

A

Acute tears are rare, chronic tears are more common.

Acute: fall, shoulder dislocation.

Chronic: this is the end of the spectrum of impingment syndrome/tendonitis/bursitis. Ultimately the joint will fail and yield a tear.

33
Q

How can I diagnose an acute rotator cuff tear with physical exam?

A

The patient will have normal passive ROM, but limited active ROM.

Remember this is a problem of muscle/tendon, not bony joint.

34
Q

Rotator cuff tears: what is the treatment for acute? chronic?

A

Acute: early operative repair

Chronic: PT, anti-inflammatory meds. If they fail those, then operate. Surgery gives good pain relief but may not give functional improvement.

35
Q

What’s going on here?

A

(I think this is really hard to see)

End stage rotator cuff disease, with rotator cuff arthropathy.

The humeral head has risen so that it now arcitulates with the acromium rather than the glenoid.

36
Q

Biceps tendon lesions: what is it associated with?

What is treatment?

A

Remember the long head of the biceps attaches to the labrum at the top of the glenoid.

Associated with impingement/bursitis.

Treatment: not surgical, because the short head of the biceps is enough to maintain function.

Having the tendon rupture may actually reduce pain, since it makes the joint space less crowded

37
Q

What has happened to this dude?

Why don’t we need to repair it? (what is the function of this muscle)?

A

Biceps tendon rupture

Don’t need to repair since you still have the short head.

The muscle belly will become a single unit, rather than a biceps

Function is not primarily flexion, but supination. Might lose 15% of supination strength which is a bummer if you are a carpenter and use a screwdriver all the time but otherwise NBD.

38
Q

In terms of knee stability, what anatomical structures are static stabilizers? what are dynamic stabilizers?

A

Static stabilizers: ligaments, the capsule, the menisci

Dynamic stabilizers: quads, hamstrings.

The dynamic structures are the ones that you can build in order to increase strength

39
Q

Name the 4 major supporting knee ligaments

A
  1. Anterior Cruciate Ligament
  2. Posterior Cruciate Ligament
  3. Medial Collageral Ligament
  4. Lateral Collateral Ligament

(cruciates cross in the center of the joint; collaterals run parallel to the joint)

40
Q

How do the medial and lateral menisci provide stability to the knee? Which one is bigger?

A

The menisci “cup” the femoral condyles and proximal tibia, sort of like a dish.

The medial meniniscus is bigger, gives more stability.

41
Q

Classification of Ligament Injuries: What are the definitions of First, Second, and Third Degree injuries?

A
  • First Degree: Local tenderness, no instability with stress.
  • Second Degree: Joint will open with stress (indicates tear or stretch). Definite palpable endpoint to how far it will stretch open.
  • Third Degree: Joint opens with stress. No endpoint to how far it will stretch (indicates rupture).
42
Q

MCL injury: what is the mechanism?

A

Direct blow to the lateral aspect of the knee

aka “Valgus stress”

43
Q

MCL injury: what are the physical findings?

A
  • Pain on valgus stress
  • Laxity of medial structures with a valgus stress when leg is flexed 30’
  • Possible associated meniscal and ACL injuries

(“Terrible triad” = ACL, MCL, meninscus)

44
Q

MCL injury: Treatment?

Is it able to heal itself?

A

Grade I: treat symptoms via rest and ice

Grade II: use knee brace as protection

Grade III: either knee brace or surgical repair

It is able to heal itself depending on where it is torn: if by the femur, it is vascularized enough to heal. If at the proximal end, probably won’t heal itself.

45
Q

LCL injury: mechanism of injury?

Physical exam findings?

A

Mechanism = varus stress (as opposed to MCL, which is valgus stress)

Physical findings are same as those for MCL but in opposite direction (flex leg to 30’, then stress it in varus direction and see if there is incr movement)

46
Q

LCL: concern for damage to what nerve? how can I test for this?

A

Concern for peroneal nerve damage.

Test via dorsiflexion of the great toe, and sensation in the first toe web space.

47
Q

LCL Injury: treatment? ability to heal itself?

A

Treatment is the same as for MCL:

Grade I: treat symptoms via rest and ice

Grade II: use knee brace as protection

Grade III: either knee brace or surgical repair

LCL does not heal itself as well as MCL might.

48
Q

ACL: anatomy?

Capability to heal itself?

A

Runs from posterior femur to anterior tibia (roughly). It’s tense through the entire ROM of the knee.

It is an intra-articular structure, very little vascular nourishment. Bathed only in synovial fluid. Cannot self-heal. Hence we do a lot of reconstructions.

49
Q

ACL: mechanism of injury?

A

Mechanism is a rapid deceleration, hyperextension, or rotation on a planted foot.

Usually injury is done in a valgus position (knees in)

50
Q

ACL injury: what will the patient tell you happened?

A

Generally they were rotating around their planted foot or were hyperextended. They probably heard a loud pop and had immediate pain, swelling after the injury.

51
Q

ACL: what are the 3 tests we do to assess injury?

A

Lachman test, Anterior drawer test, Pivot Shift test.

Lachman: Most sensitive. Hold femur with one hand, tib-fib with other, see if they move relative to each other. Hard to do if you have small hands or a massive patient.

Anterior Drawer: sit on pt’s foot with their knee bent, pull forward on tib-fib. Make sure they relax their hamstrings

Pivot Shift Test: put valgus stress on knee while internally rotating it. (He glossed over this.)

52
Q

ACL injury: what imaging finding is pathnogmonic for ACL tear?

hint - image

A

“Lateral capsular sign” on plain Xray

Circle = the anterolateral ligament (ALL), and there is a small fragment there where the ALL attaches. Apparently this indicates ACL tear. Seriously?

Jen - the ACL tear was likely due to a really great force/impact that proably affected the stabilizing ligaments of the knee (the stabilizng ligaments have to be affected in order for the ACL that is in the middle of the knee to tear). Since those ligaments the tendons holding the knee in place are really strong, they can sometimes rip a piece of bone off rather than tearing themselves. Make sense??

53
Q

What is this?

A

That was a NORMAL ACL appearance on MRI.

This one is a torn ACL on T2-weighted MRI. This image: the patella is to the RIGHT. Note widened, fibrillar appearance of ACL.

54
Q

ACL Treatment: what are the options?

A

No universally accepted approach.

Bracing, PT, Activity Modification, or Reconstruction are all possibilities.

55
Q

If you are reconstructing an ACL, what are you goals for surgery? Can you prevent eventual OA in this joint?

A

Goals = create a more stable knee for pivoting/cutting movements, according to patient’s goals.

Probably don’t prevent eventual OA in the knee.

56
Q

ACL reconstruction: where can you take tendon from in order to reconstruct the ACL?

A

Often use the middle 1/3 of the patellar tendon. Use bone grafts to attach the two ends of the tendon to the femur and tibia

57
Q

ACL reconstruction: how long will it be before the pt is back to normal activity?

A

6 months to a year, depending on how intense the activity is.

Takes about a year to fully rebuild function and also confidence in the joint.

58
Q

ACL injury: risk to males vs females? Why?

A

Females are at greater risk for this injury because they naturally land from falls in a valgus position.

Can train to land more in a varus or straight position to try to reduce ACL issues.

Pretty sure he said that despite risk to females, males actually injure it ACL more frequently.

59
Q

Meninscal injury to the knee: what can it cause? What is the result of removing the meniscus?

A

Meniniscal injury to knee can cause very limited ROM, because the flap of meniniscus gets in the way like a doorstop.

If remove, immediately feel great and regain ROM. But in 20-30 yrs, they will get OA in that joint.

60
Q

Other:

How does PCL injury occur?

Diagnosis?

Treatment?

A

hyperextension + or dashboard injury (posterior stress applied to a flexed knee)

MRI

non-operative - only PCL

Operative - PCL + associated ligament injuries

61
Q

Other

How does Knee dislocation occur?

Risk?

Diagnosis?

Treatment

A

disruption of ACL+PCL AND one collateral ligament complex

increased risk of popliteal and/or peroneal nerve injury

arteriogram + Xray

Non-operative: closed reduction (cast)

Operative: arterial injury, open wound, irreversible injury

62
Q

Other

How does meniscal injury occur?

What is the patient at increased risk for?

PE?

Diagnosis?

Treatment?

A

flexion or rotary stress

increased risk for arthritis since meniscal injury results in increased chondral stresses and degenerative diseases

PE: tenderness, effusion, incomplete extension of the leg

MRI, Xray

Observation or Arthroscopic repair

63
Q

Other

How does patellofemoral injury occur? (4)

PE?

Diagnosis?

Treatment?

A
  1. articular cartilage pathology
  2. lateral patella dislocation due to trauma
  3. repetitive stres to patellar tendon (jumper’s knee)
  4. Osteochondritis Dessicans (separation of avascular bone fragment from the underlying bone with a layer of fibrous tissue - prevents revascularization)

PE:

  • knee giving way
  • peripatellar tenderness + pain
  • crepitus with knee flexion
  • quadriceps atrophy secondary to disuse because of painful patellofemoral joint
  • apprehension sign

Xray + operative measures for dislocation and osteochondritis dessicans

Otherwise - non-operative measures (PT, ice, rest) for the rest