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SPMD3052 > Acute Injuries > Flashcards

Acute Injuries Flashcards

1
Q

Define acute meniscal injury (knee), signs/symptoms and how to examine.

A

It is shear stress damage to LAT and MED menisci and occurs when knee is flexed and compressed with femoral rotation (twisting with planted foot)
Signs:
- joint swelling
-popping/clicking within joint
-locking (“unlocking manoeuvre”)
Examined by
- joint line pain
- +ve McMurrary’s test

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2
Q

What is the Beighton Test and how to interpret score?

A

Beighton Test is a measure of how flexible certain joints in your body are.
0-3 = normal
4-9 = ligamentous laxity
5-9 = hypermobility

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3
Q

Why is there a higher risk of knee injuries in individuals with GJH (general joint hypermobility)?

A

greater flexibility in the knee increases the joints ROM due to ligamentous laxity. When applying force or producing the force, it may cause over stretching of structures and increase the amount of stress to withstand.

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4
Q

What are the statistics for GJH?

A

greater % of knee injuries
no significant difference in ankle injuries

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5
Q

Is stretching beneficial?

A

stretching by itself does not reduce LB injuries in endurance running
Stretching reduces risk of shoulder and elbow injuries e.g. baseball pitchers / fast bowling

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6
Q

What is the purpose of the stork test and how to interpret score?

A

Stork test designed to assess SL balance and observe for pelvic stability.
Score (in secs).
excellent >50
good 40-50
average 25-39
fair 10-24
poor <10

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7
Q

Why is it important to perform LB strength and balance exercises?

A

prevent LB injuries by increasing stability and force production/transmission.

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8
Q

What is a Grade 1 periosteal edema?

A

no associated bone marrow signal abnormalities

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9
Q

What is a Grade 2 periosteal oedaema?

A

periosteal oedaema and bone marrow visible only on T2 weighted images

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10
Q

What is a Grade 3 periosteal oedaema?

A

visible on both T1 and T2 weighted images

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11
Q

What is a Grade 4a periosteal oedaema?

A

multiple focal areas of intracortical signal abnormality and bone marrow oedaema visible on both T1 and T2 weighted images

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12
Q

What is a Grade 2 periosteal edema?

A

periosteal edema and bone marrow visible only on T2 weighted images

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13
Q

BME ratio is a useful tool for assessing severity of Lx stress fractures? What other factors can be used to assess?

A

location
extent of fracture
patient symptoms
medical history

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14
Q

What are the causes of BME?

A

interosseous hypertension (likely a factor)
- when bone experiences repetitve loading or increased activity, interosseous pressure increases = microdamage and inflammation within bone tissue

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15
Q

What effects does inflammation from BME have?

A

increase blood flow to bone and surrounding soft tissue = accumulation of fluid and development of oedema

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16
Q

What other factors along with interosseous hypertension cause?

A

disruption of vascular supply, change in bone metabolism, alterations in bone microstructure

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17
Q

Although MBE is common for locating stress fractures, what other image findings can suggest this?

A

cortical disruption
periosteal reaction

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18
Q

MED meniscus is at great risk of injury than LAT meniscus. True or False

A

True

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19
Q

What are the effects of displaced injured fragment and considerations to be made?

A
  • prevent full EXT
  • locking
  • pain (irritation of synovium)

Considerations
- vascularity (anatomical distribution)
- age (degenerative status)
- OA (prognosis)

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20
Q

What is the difference between the ‘red’ and ‘white’ zone of healing?

A

Red = vascular. This means excellent healing, fibroblast-like

Red and white = good healing, periphery of vascularised region

White = avascular = poor healing, fibrochondrocytes (organise matrix in response to mechanical stimuli) and type IV collagen (provides mechanical stimuli)

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21
Q

Define Arthroscopic

A

Suture repair

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22
Q

Define micro-fracturing

A

vacuum sucks out fragments. tool roughens up surface of missing cartilage and inserts small holes to improve receiving vascular supply for cartilage regrowth.

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23
Q

Define Mosaicplasty

A

removes section of bone from MED femoral condyle and inserts it into missing bone

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24
Q

Define partial meniscectomy

A

Take out small sections of inner meniscus

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25
Q

What happens in acute joint injuries?

A

traumatic ligament, meniscal, labral, cartilage and bone damage
increased intra-articular fluid
effusion
haemoarthrosis

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26
Q

What characteristics do acute articular cartilage injuries have?

A

chrondral and osteochondral fragments sheared from articular surfaces.

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27
Q

What are the long-term effects on acute injuries in the knee?

A

the increased risk of developing OA

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28
Q

What causes acute chondral injuries and why is the healing rate poor?

A

caused from high compressive/ shear forces
poor healing due to limited regenerative/repair capacity. Does not have blood vessels to receive blood and nutrients.

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29
Q

What are the causes of acute muscle contusions?

A
  • forceful impact
  • localised (blunt) trauma, local fibre damage and bleeding
  • pain
  • bruising (ecchymosis), oedema, haematoma
  • initially red due to heavy blood supply
  • after 1-2 days, appear blue/purple/black (haemoglobin)
  • after 5-10days, appear yellow/green (bilirubin)
  • after 10-14days, appear yellow/brown
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30
Q

What is mild “cork” characterised by?

A
  • usually able to continue playing
  • soreness after CD or following day

RTP 1-3wks

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31
Q

What is moderate “cork” characterised by?

A
  • may prevent continue play, min. stiffness/swelling with rest
  • ROM diminished by 50%

RTP 4+ WKS

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32
Q

What is severe “cork” characterised by?

A
  • rapid onset of swelling/obvious bleeding
  • severe functional deficit
  • difficulty bearing full weight (on affected leg)
  • muscle strength diminished
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33
Q

What are the common vulnerable sites to muscle contusions?

A

vastus lateralis
biceps brachii

34
Q

What are less common protected sites to muscle contusions?

A

thigh adductors
medial gastrocnemius

35
Q

How to manage acute muscle contusions?

A

ICE!!
- place in pain-free stretched position
- muscle fibres not shortened in position
- may reduce rate of myositis ossificans (bone forms inside of muscle) (heterotrophic ossification)

36
Q

What are the causes of myositis ossificans?

A
  • local factors (reserve of Ca2+ in adjacent skeletal tissue, vascular stasis hypoxia, mesenchymal cells with osteoblastic activity
  • unknown systemic factors
  • genetics
  • previous injuries
37
Q

What are the symptoms of acute muscle cramps?

A
  • painful, spasmodic, involuntary contractions
  • 1-3min duraction
  • late in game or post-exercise
38
Q

Where are the common locations for muscle cramps to occur?

A
  • calf (gastroc)
  • foot (intrinsic muscles)
  • thigh (quads/hamstrings)
39
Q

What are the causes of muscle cramps?

A
  • no particular reason.

Does not relate to metabolic/neurological/endocrine diseases. Electrolyte intake, stretching Hx, dehydration, or altered neuromuscular control (alpha motoneuron - increases/decreases excitation/inhibition

40
Q

What is the treatment for muscle cramps?

A
  • passive stretching
  • pickle juice, decrease cramp due to activation of oropharyngeal reflex (reduced alpha motor neuron activity of cramping muscle)
    -symptomatic relief within 10-20s
41
Q

What is the cause of DOMs?

A

soreness following vigorous, unaccustomed exercise 24-48hrs after exercise

42
Q

What are the underlying biological/biomechanical mechanisms of DOMs?

A

microtrauma of muscle cells and connective tissue followed by local inflammatory process within extracellular space which sensitises nerve endings

43
Q

Provide signs and symptoms of DOMs.

A
  • pain after unaccustomed ECC Ex between 24-72hr
  • local muscle swelling/muscle stiffness
  • muscle strength deficits
  • elevated plasma creatine kinase (marker of muscle breakdown)
44
Q

What is DOMs pain caused from?

A

1st pathway: Bradykinin-like substance released from muscle during ECC Ex triggers hyperalgesia by upregulating nerve growth factor through B2 receptors in exercised muscles

2nd pathway: activation of COX-2 glial cell line-derived neurotrophic factors likely generates muscle mechanical hyperalgesia directly by stimulating muscle nocirecpetors

45
Q

How to reduce Rx of DOMs?

A

-mass, cryotherapy, stretching, and active recovery
-curcumin (turmeric) may reduce inflammation and pain by modulating inflammation and cytokine flux by influencing COX-2 signal
-modify exercise regime (reduce intensity/train diff muscle group)

46
Q

Explain the 4 stages of overuse injuries.

A
  1. pain in affected area after Ex
  2. pain during Ex, not restricting performance
  3. pain during Ex, restricting performance
  4. chronic, persistent pain, even at rest
47
Q

What is the consequence of failed overuse injury healing?

A
  • morphology becomes more cartilaginous
  • increase prostaglandin E2 in tissues (decreased contraction strength)
  • increase collagenase, decrease collagen synthesis (breaks down native collagen, that holds muscle tissue together)
  • upregulation of genes for cartilage
  • downregulation of genes for tendon
48
Q

Explain the difference between long-term and short-term pathology in overuse tendinopathy.

A

Long = tendon is degenerative not inflamed
Short = involves inflammation / paratendonitis

49
Q

What are the three extrinsic factors of overuse injuries?

A
  1. training and technique errors (body positioning)
  2. surface and shoes
  3. equipment
50
Q

What are intrinsic factors of overuse injuries?

A
  • previous injury
  • flexibility
  • leg length discrepancy
  • malalignment
  • mal-tracking
  • patella alta
  • pes planus (flat-footed)
  • pes cavus (high foot arch)
  • muscle weakness
51
Q

Why is understanding the q-angle important?

A

“quadriceps ankle” = angle formed between quads and patella tendon

Assesses the lateral forces exerted onto the patella (how well it absorbs/transfers the force)

52
Q

Tendinopathy occurs due to failed healing. True or False

A

Trure

53
Q

What are the stages of Tendinopathy?

A
  1. reactive tendinopathy (tenocytes proliferate, increase proteoglycans, mild fusiform swelling)
  2. tendon Disrepair (collagen separates - matrix disorganised, ingrowth of vessels/nerves, tenocytes appear round)
  3. degenerative tendinopathy (areas of apoptosis, degenerative matrix with vascular changes, chronic pain)
54
Q

Why is it important to recognise tendinopathy early?

A

stage 1 = strong change of good outcome
stage 2 = good outcome unlikely
stage 3 = poor outcome likely

55
Q

What type of muscle contraction is best for tendinopathy Rx?

A
  • eccentric movements
56
Q

Compare different bone stress injury diagnostic tools.

A

x-ray: not sensitive to early changes
bone scan - high sensitivity, poor specificity, high radiation
CT: radiation issues, better in later stages (used to monitor healing process)
Ultrasound: needs further development
MRI = GOLD STANDARD

57
Q

Explain the Fredricson’s Grade for BSI and provide injury description.

A
  1. periosteal oedema, no bone marrow abnormalities
  2. periosteal oedema with mild bone marrow oedema
  3. periosteal oedema with extensive bone marrow oedema
    4a. periosteal oedema, extensive bone marrow oedema, multiple foci of intracortical signal change
    4b. periosteal oedema, extensive bone marrow oedema, fracture line
58
Q

Explain the Arendt grading in BSI.

A
  1. short-tau inversion Rx (STIR) signal change. T1/2 none. RTS 3wks
  2. STIR changes. T1 none, T2 present, 3-6wks RTS
  3. STI change. T2 present, T1 present 12-16WKS RTS
  4. STIR change. T1/2 fracture line, RTS 16+wks
59
Q

Why can’t pain be an indicator of fracture?

A

Fracture can be present in the absence of pain.

Meaning everyone has their own perception of pain.

60
Q

What is the difference between low risk vs high risk BSIs?

A

low: commonly heal w/o complication (if caught early), compression fractures, discourage use of NSAIDs (they mask the pain, cause athlete to feel normal and wanting to play/train)

high: require treatment, tension stress fractures! generally bending/tension side, risk of delayed non-union/progression to complete fracture

61
Q

Which sites heal faster, cortical bone (80% skeletal mass) or cancellous (20% skeletal mass)?

A

Cortical-rich injury sites (tibia, metatarsal) heal quicker than trabecular-rich injury sites (femoral neck, calcaneus and pelvis)

62
Q

List a few risk factors of BSIs that modify load applied to bone.

A
  • static (EXT hip ROT, pes cavus and planus) and dynamic (peak hip ADD, knee INT ROT)
  • muscle factors (weak or fatigue)
  • training errors
  • equipment and playing surface
  • shoes and insoles
63
Q

List a few risk factors of BSIs that modify ability of bone to resist load without damage accumulation.

A
  • bone mineral content/distribution
  • energy availability
  • vit D, Ca2+ deficiency
64
Q

Define osteochrondrosis, “little league’s elbow”.

A

overuse condition common in children and developing young athletes of the apophyseal or epiphyseal growth areas of bone.

65
Q

What is the 1st classification of osteochondrosis?

A
  1. non-articular
    e.g. OsGoodShlatter’s, Sinding Larsen Joahansson and Severs
66
Q

What is the 2nd classification of osteochrondrosis?

A

Spinal Physeal
e.g. Scheuermann’s
commonly associated with Schmorl’s (“small”) nodes - protrusions of nucleus pulposus through vertebral body endplate into adjacent vertebra

67
Q

What is the 3rd classification of osteochrondrosis?

A

Articular (within joint)
e..g Legg-Calve-Perthes
rare childhood hip disorder initiated by a disruption of blood flow to the femoral head (osteonecrosis or avascular necrosis) due to lack of blood flow.

68
Q

What is Osteitis Pubic, how can it be identified and what symptoms?

A

It is a painful overuse condition affecting pubic symphysis and parasymphyseal bone
MRI shows bone oedema
Symptoms: abnormal muscle forces and pelvic instability

69
Q

What is the recovery procedure for osteitis pubic?

A

Rest (activity modification)
Referral (diagnosis, potential causes)
Retraining (strengthening)
RTP (pain free)

70
Q

Summarise the stages of Osteitis Pubic

A

Pain: 1 is unilateral, 2&3 is bilateral and 4 = generalised
Site of P: 1&2 inguinal to/and adductors, 3 groin, adductors, suprapubic abdominal and 4 generalised, lumbar region
Characteristics of pain
1. pain alleviation after WU exacerbation after training
2. pain exacerbation after training
3. during training, kicking sprinting, unable to perform training
4. walking, getting up, simple ADLs.

71
Q

Why is OA a common risk factor for ACL injuries?

A

cartilage has poor healing capacity, increases matrix degrading enzymes, increase inflammatory cytokines

72
Q

Why are subchrondral bone injuries a major risk factor in ACL injuries?

A

may cause osteocyte necrosis in bone marrow, proteoglycan loss, chrondrocyte injury and matrix degeneration in overlying cartilage

changes in subchondral bone may initiate progression to PTOA following ACL injury

73
Q

True or False. 55% patients first-time ANT shoulder dislocation before 40y had some degree of arthropathy on radiographs after 25y follow up.

A

true

74
Q

What other complications arise due to overuse injuries?

A

Bone spurs, chronic bone impingement, periostitis

75
Q

What can cause bone spurs?

A

Chronic impingement due to overuse

76
Q

List a few characteristics of bone spurs.

A

Associated with chronic conditions - may restrict movement or be painful

Common in rugby front-rowers, sumo wrestlers and jockeys

77
Q

What is periostits?

A

inflammation of periosteum associated with chronic muscle activity

78
Q

Chronic compartment syndrome is a muscle/soft tissue injury. What are the characteristics of it?

A

It is the swelling and accumulation of fluid in interstitial spaces - impairs blood flow
Causes pain and compression of neural structural

Ex raises intracompartmental pressure

Commonly seen in long distance runners

To RELIEVE this syndrome = foot slap before/after run (activate intrinsic foot muscles)

79
Q

Chronic groin pain is a muscle/soft tissue injury. List a few characteristics of it.

A

caused by repetitive shear forces across hemipelvis involving abdominal and thigh muscles

Involves: ADD longs and rectus abdominis // conjoint INT oblique and transversus abdominis muscles

80
Q

Define Bursa. List cause, sites and common athletes that a likely to develop bursitis.

A

It is overuse damage to the site.

Sites: olecranon (student’s elbow), Prepatellar (cart-layers knees) and pes anserine (MED hamstring tendons)

Wrestlers (elbow/knees on ground), surfers (rubbing against board), cyclists (subacromial bursa in shoulder)

Mostly self-limited, often resolves with conservative management (RICE)

81
Q

Corticosteroid injections are beneficial to bursa injuries. True or False

A

False

Due increase infection risk (open wound)

82
Q

A Quad’ Ex performed with horizontal torso with 20kg chest weight (reverse nordic) using Sissy squat bench with feet rigidly fixed under ankle. What structures are injured/damaged?

A

patella tendon rupture!

Could also be caused by prevoius injury (e.g. ACL and tendinopathy)

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