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MSK Flashcards

1
Q

What is a fracture?

A

Disruption in the integrity and continuity of bone associated with soft tissue injury

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2
Q

Why is there a unique fracture pattern in children?

A
  • Compressibility of bones
  • Increased fibrous strength of periosteum
  • Presence of physes (growth plates)
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3
Q

What fracture lies at an angle to the long axis of the bone?

A

Oblique fracture

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4
Q

What fracture involves more than 1 fragment?

A

Communited fracture

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5
Q

What fracture has more than 1 fracture along the bone?

A

Segmental fracture

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6
Q

What fracture lies perpendicular to the long axis of the bone?

A

Transverse fracture

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7
Q

What is a spiral fracture?

A

A severe oblique fracture with rotation along long axis of bone

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8
Q

What is a greenstick fracture?

A

Incomplete fracture with angulation on opposite side

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9
Q

What are the most common neonatal fractures?

A

Clavicle

  • From dystocia
  • Great prognosis, no specific tx needed

Humerus or femur

  • From breech delivery
  • Heals rapidly with immobilisation
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10
Q

What are the causes of a fracture?

A

Trauma

  • Direct force (penetrative, crushing)
  • Indirect force (tension, compression, rotation)

Pathological

  • Minor force causes fracture secondary to underlying bone weakness (malignancy, congenital)
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11
Q

What is the Salter-Harris classification?

A

Method used to grade fractures that occur in children and involve the growth plate.

The classification system grades fractures according to the involvement of the physis, metaphysis, and epiphysis.

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12
Q

What are the RFs for fracture?

A
  • Contact sports
  • Trampoline use
  • RTA
  • Osteogenesis imperfecta
  • > Consider NAI with every child fracture
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13
Q

What are the S/S of a fracture?

A

Usually hx of trauma

  • Assess if hx of NAI, time elapsed, force, possibility of glass contamination, associated head injury, medications and previous fractures

Closed fracture

  • Pallor and swelling over fracture site
  • Obvious deformity

Open fracture

  • Bleeding and bruising over fracture
  • Associated soft tissue injury

Neurovascular status

  • Assess for distal numbness, tingling, paralysis, or loss of pulse

MSK examination

  • Examine joint above and below for crepitus, effusion, and pain

Tuning fork test

  • Exacerbates pain over small stress fractures
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14
Q

What are the investigations for a fracture?

A
  • XR > usually in 2 views (frontal and lateral)
  • Repeat XR
  • MRI and bone scan
  • Genetics for bleeding disorders and osteogenesis imperfecta
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15
Q

What is the management for a fracture?

A

1. Pain mx

  • <16yrs = oral ibuprofen / paracetamol (IV if severe)
  • > 16yrs = paracetamol +/- codeine +/- IV morphine

2. Immobilise the fracture

  • Including proximal and distal joints

3. Sedation for manipulation

  • 1st line = intranasal/oral midazolam or NO
  • 2nd line / severe = intranasal ketamine

4. Manipulation and reduction

  • Radial fractures = elbow plaster cast or k-wire fixation
  • Femoral shaft fractures =
    Neonates = padded splints or Pavlik’s harness
    <18m = Gallows traction
    1-6yrs = straight less skin traction
    >4yrs = intramedullary nail (+ more support if >11yrs)

5. Manage infection including tetanus prophylaxis
6. IV broad spectrum abx for open injuries
7. Physiotherapy

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16
Q

What is Perthes’ Disease?

A

A neurodegenerative condition affecting the hip joints of children, due to idiopathic avascular necrosis of the femoral head, specifically the femoral epiphysis

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17
Q

What is the difference between Perthes’ and SUFE?

A

Perthes’ = Primary School
SUFE = Secondary School

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18
Q

When does Perthes’ occur?

A

Typically 4-8yrs
Far more common in boys

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19
Q

What are the RFs for Perthes’

A

Hyperactivity
Short stature

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20
Q

What are the S/S of Perthes’?

A

Classic presentation is a painless limp
Pain that progresses over a few weeks

  • Limp = early sign, intermittent, post-exercise
  • Pain = may have mild/intermittent pain in anterior thigh/hip (secondary to necrosis of affected bone)
  • Stiffness / reduced ROM in hip = particularly rotation and abduction, global in late stage
  • Limb shortening = leg length inequality
  • Gluteal wasting
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21
Q

What are the investigations for Perthes’?

A

Trendelenburg Test:

  • Positive

Roll test:

  • Supine, roll affected hip internally and externally > guarding or spasm (esp. on internal)

Bloods:

  • FBC, CRP/ESR (SA), Hb electrophoresis (sickle cell)

Joint aspiration

  • SA

XR +/- MRI

  • Early changes = widening of joint space / increased density of femoral head
  • Later changes = decreased femoral head size / fragmented and irregular/flattened femoral head
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22
Q

What system is used to classify Perthes disease based on radiographic features?

A

Cattarall Staging

Stage 1

  • Bone absorption changes visible only in anterior aspect of epiphysis
  • No sclerosis

Stage 2

  • Further bone resorption with slight femoral head collapse in the anterior aspect
  • Sclerosis

Stage 3

  • Almost entire femoral head involved in collapse with characteristic ‘head within head’ appearance
  • Sclerosis

Stage 4

  • Complete collapse of femoral head
  • Additional metaphyseal changes may be visible
  • Sclerosis
  • Posterior remodelling
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23
Q

What is the management of Perthes’ ?

A

<6yrs / mild: Conservative

  • Will heal well without any specific treatment
  • Kept under observation
  • PT or at home exercises
  • Keep femoral head within the acetabulum > cast, braces
  • Simple analgesia

>6yrs / severe: Surgery considered

  • Moderate results
  • Older children have a poorer prognosis
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24
Q

What is Osgood-Schlatter Disease?

A

A type of osteochondrosis characterised by inflammation of the tibial tuberosity (where the patellar tendon attaches to the top of the tibia) in growing adolescents

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25
Q

What are the causes of OSD?

A
  • Following growth spurt
  • Sports (esp with high knee impact e.g. jumping)
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26
Q

When does OSD occur?

A

Most common knee disorder in adolescence
10-15yrs
M > F

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27
Q

What are the symptoms of OSD?

A
  • Knee pain after exercise > gradual onset, relieved by rest / exacerbated by activity
  • Localised tenderness and swelling over tibial tuberosity
  • Hamstring tightness
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28
Q

What are the signs of OSD?

A

Pain reproducible on extending knee against resistance, stressing the quadriceps or squatting with knee in full flexion

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29
Q

What are the investigations for OSD?

A

Clinical diagnosis

+/- XR (indicated by Ottawa knee rules)

  • Fractures / fragmentation of the tibial tubercle
  • Overlying soft tissue swelling
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30
Q

What is the management for OSD?

A

Reassurance

  • Will resolve over time but may persist until end of growth spurt

Conservative

  • Avoidance/reduction of offending activity
  • Proper stretching before/after exercise may reduce symptoms
  • Analgesia (paracetamol or NSAIDs)
  • Ice packs (over tibial tuberosity, 10-15 mins, <=3/d, after exercise)
  • Protective knee pads (may relieve pain when kneeling)
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31
Q

What is Chondromalacia Patallae?

A

Anterior knee pain from softening of the cartilage on underside of the kneecap

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32
Q

What causes Chondromalacia Patallae?

A

> Common in young adults from overuse in physical activity

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33
Q

What are the S/S of Chondromalacia Patallae?

A
  • Anterior knee pain
  • Pain exacerbated by running, climbing stairs, getting up from chair
  • Characteristically anterior knee pain on walking up and down stairs and rising from prolonged sitting
  • Painless passive movements but repeated extension causes pain and grating sensation
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34
Q

What is the management of Chondromalacia Patallae?

A

Physiotherapy > strengthen quadriceps

35
Q

What is Osteochondritis Dissecans?

A

A problem that can happen in the joint, when a piece of bone and cartilage become loose.

This can cause pain, swelling and limited ROM.

36
Q

What are the symptoms of Osteochondritis Dissecans?

A
  • Subacute onset
  • Knee pain and swelling, typically after exercise
  • Catching, locking and giving way
  • Feeling a painful “clunk” when flexing or extending the knee
  • Joint effusion
37
Q

What are the signs of Osteochondritis Dissecans?

A
  1. Tenderness on palpation of the articular cartilage of the medial femoral condyle, when the knee is flexed
  2. Wilson’s sign for detecting medial condyle lesion > knee at 90 degree flexion and tibia internally rotated, gradual extension of the joint leads to pain at about 30 degrees, external rotation of the tibia at this point relieves the pain
38
Q

What are the investigations for Osteochondritis Dissecans?

A

Early dx is important

  • Bilateral XR > may show subchondral crescent sign or loose bodies
  • MRI > used to evaluate cartilage, visualise loose bodies, stage and assess the stability of the lesion
39
Q

What is the management of Osteochondritis Dissecans?

A
  • Pain relief (paracetamol or ibuprofen)
  • Initial 4-6w crutches to not fully weight bear
  • Then weight bare as tolerated with gentle strengthening exercises
  • Then supervised sports readiness programme
  • Sometimes surgical intervention is needed (to remove intra-articular loose bodies)
40
Q

What is osteomyelitis?

A

Inflammation of the bone, usually caused by bacterial infection

41
Q

What is the classification of osteomyelitis?

A

Haematogenous > Most common form in children

  • Results from bacteraemia
  • Is usually microbial

Non-haematogenous > Most common form in adults

  • Results from contiguous spread of infection from adjacent soft tissues to the bone or from direct injury / trauma to the bone
  • Is often polymicrobial
42
Q

What organisms cause osteomyelitis / SA?

A

Staph aureus (most common)
Salmonella species (sickle cell pts)

43
Q

What bones are most commonly affected in osteomyelitis?

A

Long bones including femur, tibia and humerus

Most commonly the distal femur and proximal tibia

44
Q

What are the S/S of osteomyelitis?

A
  • Fever
  • Bone pain, swelling, redness
  • Guarding of affected body part
45
Q

What are the investigations of osteomyelitis?

A
  • Septic screen + bloods (raised WCC, CRP, ESR)
  • Joint aspiration + MC&S
  • XR
  • MRI (imaging of choice)
46
Q

What is the management of osteomyelitis?

A

Acute osteomyelitis

  • Flucloxacillin for 6wks (Clindamycin if pen-allergic, Vancomycin if MRSA)
  • IV to oral once CRP returns to normal
  • Surgical debridement may be necessary if there is dead bone or a biofilm

Chronic osteomyelitis

  • Disease staging > Clerny-Mader classification
  • Surgical debridement
  • IV abx
  • Functional rehabilitation
47
Q

What is septic arthritis?

A

An infectious arthritis of a synovial joint (vs osteomyelitis of bone)

48
Q

Where does SA most commonly affect?

A
  • Hip (75%)
  • Knee
  • Ankle
  • Upper limbs
49
Q

When does SA occur?

A

Most common <2yrs
M > F

50
Q

What is the aetiology of SA?

A
  • Usually haematogenous spread > infection / direct inoculation
  • Can develop from osteomyelitis
51
Q

What are the RFs for SA?

A
  • RhA
  • Osteoarthritis
  • Joint prosthesis
  • Crystal arthritis
  • Chronic disease
  • Immunosuppression
52
Q

What are the S/S of SA?

A
  • Warm, red, swollen, tender, painful joint
  • Single joint affected
  • Reduced ROM
  • Limp
  • Infants will hold limb still
  • Fever / acutely unwell / lethargy
53
Q

What are the investigations for SA?

A
  1. Septic screen + bloods + blood culture
  • Raised WCC, CRP, ESR
  1. Joint aspiration + MC&S + culture
  2. XR of joint
  • Normal initially, evident >2/3wks of sx
  • Subluxation/dislocation, joint space narrowing, erosive changes
  1. MRI of joint
  • If dx in doubt > exclude osteomyelitis
  • Do not delay tx while awaiting MRI
  • Shows soft tissue and effusions/collections
54
Q

What is the Kocher Criteria?

A

For diagnosis of SA:

  • Fever > 38.5
  • Non-weight bearing
  • Raised ESR
  • Raised CRP
55
Q

What is the management of SA?

A

Immediate = Flucloxacillin

  • IV 2wks (until inflammatory markers normalise)
  • Oral 4wks
  • Pen-allergic > clindamycin
  • MRSA > vancomycin
  • Gram-negative > 3rd generation cephalosporin (e.g. cefotaxime)

+/- Surgical drainage

  • Low threshold for irrigation and debridement of joint (+drainage of any associated osteomyelitis)

Long-term = Physiotherapy

  • To avoid joint stiffness
56
Q

What is Juvenile Idiopathic Arthritis (JIA)?

A

Persistent joint swelling (>6wks) presenting before 16yrs, in the absence of infection or other defined cause

The most common chronic inflammatory joint disease in children

57
Q

What are the subtypes of JIA?

A

Based on number of joints affected in first 6m and presence of rheumatoid factor and HLA B27 tissue type

  • Systemic / Still’s Disease
  • Oligoarticular = <=4 joints
  • Polyarticular = >4 joints
  • Enthesitis-related arthritis
  • Psoriatic arthritis
  • Undifferentiated
58
Q

What are the S/S of JIA?

A

Acute joint swelling, pain, warmth, and stiffness

  • Worse in morning
  • Improves with activity
  • Intermittent limp
  • May present later with reduced ROM, overgrowth or contractures
  • Children tend to stop using affected joint

Systemic:

  • Pyrexia
  • Salmon coloured rash (Koebner phenomenon)
  • Uveitis / arthritis
  • Anorexia / WL
59
Q

What are the investigations for JIA?

A

Clinical diagnosis

Septic screen +/- joint aspirate +/- USS

  • Rule out SA

Bloods / imaging (to provide classification and prognostic information)

  • ANA may be positive
  • FBC, RhF (usually neg), CRP/ESR, anti-CCP
60
Q

What is the management of JIA?

A

1st line:

  • NSAID for pain and stiffness
  • OT and PT (inactivity leads to deconditioning, disability and decreased bone mass)

Intra-articular corticosteroids

  • Useful adjunctive agents whilst waiting for 2nd line agents to have an effect
  • High dose to induce remission > switch to low dose oral to maintain

DMARDs

  • Used when fail to respond to conventional tx
  • 1st line = oral/SC methotrexate
  • 2nd line = sulfasalazine

Biologics / cytokine modulators

  • I.e. TNF-alpha inhibitors
61
Q

What is reactive arthritis?

A

An arthritis that develops following an infection where the organism cannot be recovered from the joint

> HLA-B27 associated seronegative spondyloarthropathy

62
Q

What causes reactive arthritis?

A
  • Enteric bacteria > salmonella, shigella, campylobacter, Yersinia
  • Viral infections
  • STDs
63
Q

What are the S/S of reactive arthritis?

A

Cant see, can’t pee, can’t climb a tree

  • Arthriris, urethritis, uveitis

S/S generally start 1 to 4 weeks after exposure to a triggering extra-articular infection

  • Joint pain and stiffness
  • Transient joint swelling (<6wks)
  • Often ankles, knees, or feet
  • Low-grade fever
  • Conjunctivitis
  • Inflammation of tendons and ligaments where they attach to bone (enthesitis) - most often heels and soles of feet
64
Q

What are the investigations for reactive arthritis?

A

A diagnosis of exclusion as no +ve findings

Bloods > CRP normal or mildly elevated
Normal XR

65
Q

What is the management for reactive arthritis?

A

Self-limiting (sx rarely last more than 12m)

  • Symptomatic > NSAIDs, intra-articular steroids
  • Sulfasalazine and methotrexate are sometimes used for persistent disease
66
Q

What is Slipped Upper Femoral Epiphysis (SUFE)?

A

Displacement of the epiphysis of the femoral head postero-inferiorly

  • Ball at the head of the femur slips off the neck of the bone
  • Most common hip disorder in adolescence
  • Requires prompt treatment to prevent avascular necrosis
67
Q

When does SUFE occur?

A

10-15yrs (during growth spurts)

Caused by weakness in the proximal femoral growth plate

68
Q

What are the RFs for SUFE?

A
  • OBESITY
  • Metabolic endocrine disease > hypothyroidism, hypogonadism
  • Male
69
Q

What are the S/S of SUFE?

A
  • Limp
  • Hip pain +/- referred to the knee / groin / thigh
  • Insidious or acute onset (i.e. after minor trauma)
  • Loss of internal rotation of a flexed hip
  • Trendelenburg gait positive (lean on one side)
70
Q

What are the investigations for SUFE?

A

1. Physical examination of hip movement
2. Bilateral hip xrays

  • AP and frog-lateral view
  • Trethowan sign, loss of triangular sign of Capener, metaphyseal blanch sign
71
Q

What is the management of SUFE?

A

EMERGENCY (risk of avascular necrosis of femoral head)

Immediate:

  • Immediate referral to orthopaedics
  • Bed-bound / do not weight-bear
  • Analgesia

Definitive:

  • Urgent surgical repair
  • Internal fixation
  • Prophylactic fixation of contralateral hip
72
Q

What is transient synovitis?

A

“Irritable hip” – acute hip pain following a recent viral infection.

Commonest cause of hip pain in children

73
Q

When does transient synovitis occur?

A

Typically 3-10yrs
If <3yrs = urgent hospital assessment

74
Q

What are the S/S of transient synovitis?

A
  • Acute hip pain associated with viral infection
  • Limp / refusal to weight bare
  • Low-grade fever (high fever should raise suspicion of SA)
75
Q

What are the investigations for transient synovitis?

A

Clinical diagnosis

  • FBC, CRP, XR
  • If any doubt about septic arthritis: perform joint aspiration and blood cultures
76
Q

What is the management of transient synovitis?

A
  • Self-limiting
  • Rest and simple analgesia
  • Usually resolves after a few days
77
Q

What is developmental dysplasia of the hip (DDH)?

A

Abnormal growth of the hip resulting in dislocation or instability

78
Q

What are the RFs for DDH?

A
  • Female
  • FHx
  • Breech position
  • First born
  • Multiple pregnancy
  • Oligohydramnios
  • Macrosomia
79
Q

What is the screening protocol for DDH?

A

The following infants require a routine US examination

  • First degree FHx of hip problems in early life
  • Breech at or after 36wks gestation
  • Multiple pregnancy

All infants screened at both the newborn check and 6wk baby check using Barlow and Ortolani tests

80
Q

What are the S/S of DDH?

A
  • Positive Barlow test = attempts to dislocate an articulated femoral head
  • Positive Ortolani test = attempts to relocate a dislocated femoral head
  • Limp or abnormal gait, delayed crawling/walking, toe-walking
  • Asymmetrical skin folds
  • Limb-length discrepancy = Galeazzi sign (baby on back, legs together and knees flexed, look at leg length)
81
Q

What are the investigations for DDH?

A

<6m = Barlow and Ortolani tests at neonatal screen +/- USS if suspicion remains

>6m = XR

82
Q

What is the management for DDH?

A

> Most will spontaneously stabilise by 3-6wks

Pavlik harness (dynamic flexion-abduction orthosis)

  • In children younger than 4-5m
  • Keeps hips flexed and abducted
  • Worn constantly for several weeks
  • Progress monitored by repeat USS or XR

Older children may require surgery

83
Q

What investigation for child <3 with acute limp?

A

Urgent assessment by paediatrician
Rule out traumatic injury / SA

84
Q

Describe the Ortolani test

A
  • Flex the hips and knees to 90 degrees
  • Use index finger to apply pressure to the greater trochanters
  • Use thumb to abduct the legs

Positive test = distinctive clunk, as the femoral head is relocated anteriorly

(it relocates a dislocation of the hip joint if this has been elicited during the Barlow test)

Paeds (18 decks)

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