Pediatric Orthopedics Flashcards
1
Q
Why do kids gets certain fractures?
A
■ thicker, more active periosteum results in pediatric-specific fractures: greenstick (one cortex), torus (i.e. ‘buckle’, impacted cortex) and plastic (bowing)
adults fracture through both cortices
2
Q
Most common fractures in children
A
distal radius fracture most common in children (phalanges second), the majority are treated with closed reduction and casting
3
Q
Epiphyseal growth plate
A
■ weaker part of bone, susceptible to fractures
■ plate often mistaken for fracture on x-ray and vice versa (X-ray opposite limb for comparison), especially in elbow
■ tensile strength of bone < ligaments in children, therefore clinician must be confident that fracture and/or growth plate injury have been ruled out before diagnosing a sprain
■ intra-articular fractures have worse consequences in children because they usually involve the growth plate
4
Q
Role of anatomic reduction in children
A
■ gold standard with adults
■ may cause limb length discrepancy in children (overgrowth)
■ accept greater angular deformity in children (remodelling minimizes deformity)
Greenstick fractures are easy to reduce but can redisplace while in cast due to intact periosteum
5
Q
When should you have a higher suspicion of child abuse
A
■ high index of suspicion with fractures in non-ambulating children (<1 yr); look for other signs, including X-ray evidence of healing fractures at different sites and different stages of healing
■ common suspicious fractures in children: metaphyseal corner fracture (hallmark of non-accidental trauma), femur fracture < 1 yo, humeral shaft < 3 yo, sternal fractures, posterior rib fractures, spinous process fractures
6
Q
Stress fracture mechanism
A
• insufficiency fracture
■ stress applied to a weak or structurally deficien bone
• fatigue fracture
■ repetitive, excessive force applied to normal bone
• most common in adolescent athletes
7
Q
Stress fracture most common site
A
tibia
8
Q
Stress fracture diagnosis
A
- localized pain and tenderness over the involved bone
- plain films may not show fracture for 2 wk
- bone scan positive in 12-15 d
9
Q
Stress fracture treatment
A
rest (can take several months)
10
Q
Epiphyseal injury classification
A
Salter-Harris
11
Q
Salter-Harris I description and treatment
A
Straight through; stable
Transverse through growth plate
Closed reduction and cast immobilization (except SCFE – ORIF); heals well, 95% do not affect growth
12
Q
Salter-Harris II description and treatment
A
Above
Through metaphysis and along growth plate
Closed reduction and cast if anatomic; otherwise ORIF
13
Q
Salter-Harris III description and treatment
A
Low
Through epiphysis to plate and along growth plate
Anatomic reduction by ORIF to prevent growth arrest, avoid fixation across growth plate
14
Q
Salter-Harris IV description and treatment
A
Through and through
Through epiphysis and metaphysis
Closed reduction and cast if anatomic; otherwise ORIF
15
Q
Salter-Harris V description and treatment
A
Ram
Crush injury of growth plate
High incidence of growth arrest; no specific treatment
16
Q
What Salter Harris types are more likely to cause growth arrest and progressive deformity
A
III-V
17
Q
Slipped Capital Femoral Epiphysis definition and risk factors
A
- type I Salter-Harris epiphyseal injury at proximal hip
- most common adolescent hip disorder, peak incidence at pubertal growth spurt risk factors: male, obese (#1 factor), hypothyroid (risk of bilateral involvement)
18
Q
Slipped Capital Femoral Epiphysis etiology
A
• multifactorial
■ genetic: autosomal dominant, black children at highest risk
■ cartilaginous physis hypertrophies too rapidly under growth hormone effects
■ sex hormone secretion, which stabilizes physis, has not yet begun
■ overweight: mechanical stress
■ trauma: causes acute slip
19
Q
Slipped Capital Femoral Epiphysis clinical features
A
• acute: sudden, severe pain with limp
• chronic (typically): groin and anterior thigh pain, may present with knee pain
■ positive Trendelenburg sign on affected side, due to weakened gluteal muscles
• tender over joint capsule
• restricted internal rotation, abduction, flexion
■ Whitman’s sign: obligatory external rotation during passive flexion of hip
• Loder classification: stable vs. unstable (provides prognostic information)
■ unstable means patient cannot ambulate even with crutches
20
Q
Slipped Capital Femoral Epiphysis investigations
A
• X-ray: AP, frog-leg, lateral radiographs both hips
■ posterior and medial slip of epiphysis
■ disruption of Klein’s line
■ AP view may be normal or show widened/lucent growth plate compared with opposite side
21
Q
Slipped Capital Femoral Epiphysis treatment
A
• operative
■ mild/moderate slip: stabilize physis with pins in current position
■ severe slip: ORIF or pin physis without reduction and osteotomy after epiphyseal fusion
22
Q
Slipped Capital Femoral Epiphysis complications
A
• AVN (roughly half of unstable hips), chondrolysis (loss of articular cartilage, resulting in narrowing of joint space), pin penetration, premature OA, loss of ROM
23
Q
What is Klein’s Line
A
On AP view, line drawn along supero-lateral border of femoral neck should cross at least a portion of the femoral epiphysis. If it does not, suspect SCFE
24
Q
Developmental Dysplasia of the Hip definition
A
- abnormal development of hip, resulting in dysplasia and subluxation/dislocation of hip
- most common orthopedic disorder in newborns
25
Developmental Dysplasia of the Hip etiology
• due to ligamentous laxity, muscular underdevelopment, and abnormal shallow slope of acetabular roof
• spectrum of conditions
■ dislocated femoral head completely out of acetabulum
■ dislocatable head in socket
■ head subluxates out of joint when provoked
■ dysplastic acetabulum, more shallow and more vertical than normal
• if painful, suspect septic dislocation (normally painless)
26
Developmental Dysplasia of the Hip physical exam
• diagnosis is clinical
■ limited abduction of the flexed hip (<60°)
■ affected leg shortening results in asymmetry in skin folds and gluteal muscles, wide perineum
■ Barlow’s test (checks if hips are dislocatable ◆ flex hips and knees to 90° and grasp thigh ◆ fully adduct hips, push posteriorly to try to dislocate hips
■ Ortolani’s test (checks if hips are dislocated ◆ initial position as above but try to reduce hip with fingertips during abduction
◆ positive test: palpable clunk is felt (not heard) if hip is reduced
■ Galeazzi’s sign
◆ knees at unequal heights when hips and knees flexed
◆ dislocated hip on side of lower knee
◆ difficult test if child <1 yr
◆ Trendelenburg test and gait useful if older (>2 yr)
27
Developmental Dysplasia of the Hip investigations
* U/S in first few months to view cartilage (bone is not calcified in newborns until 4-6 mo)
* follow-up radiograph after 3 mo
* X-ray signs (at 4-6 mo): false acetabulum, acetabular index >25°, broken Shenton’s line, femoral neck above Hilgenreiner’s line, ossification centre outside of inner lower quadrant (quadrants formed by intersection of Hilgenreiner’s and Perkin’s lines)
28
Developmental Dysplasia of the Hip treatment
* 0-6 mo: reduce hip using Pavlik harness to maintain abduction and flexion
* 6-18 mo: reduction under GA, hip spica cast x 2-3 mo (if Pavlik harness fails)
* >18 mo: open reduction; pelvic and/or femoral osteotomy
29
Developmental Dysplasia of the Hip complications
* redislocation, inadequate reduction, stiffness
| * AVN of femoral head
30
Developmental Dysplasia of the Hip risk factors
5 Fs that Predispose to Developmental Dysplasia of the Hip
```
Family history
Female
Frank breech
First born
LeFt hip
```
31
Legg-Calve-Perthes Disease (Coxa Plana) definition
* idiopathic AVN of femoral head, presents at 4-8 yr of age
* 12% bilateral, M>F = 5:1, 1/1,200
• associations
■ family history
■ low birth weight ■ abnormal pregnancy/delivery
■ ADHD in 33% of cases, delayed bone age in 89%
■ second-hand smoke exposure
■ Asian, Inuit, Central European
• key features
■ AVN of proximal femoral epiphysis, abnormal growth of the physis, and eventual remodelling of regenerated bone
32
Legg-Calve-Perthes Disease (Coxa Plana) clinical features
* child with antalgic or Trendelenburg gait ± pain
* intermittent knee, hip, groin, or thigh pain
* flexion contracture (stiff hip): decreased internal rotation and abduction of hip
* limb length discrepancy (late)
33
Legg-Calve-Perthes Disease (Coxa Plana) investigations
* X-ray: AP pelvis, frog leg laterals
* may be negative early (if high index of suspicion, move to bone scan or MRI)
* eventually, characteristic collapse of femoral head (diagnostic)
34
Legg-Calve-Perthes Disease (Coxa Plana) treatment
• goal is to preserve ROM and keep femoral head contained in acetabulum
• non-operative
■ physiotherapy: ROM exercises
■ brace in flexion and abduction x 2-3 yr (controversial)
• operative
■ femoral or pelvic osteotomy (>8 yr of age or severe)
◆ prognosis better in males, <6 yr, <50% of femoral head involved, abduction >30°
* 60% of involved hips do not require operative intervention
* natural history is early onset OA and decreased ROM
35
Osgood-Schlatter Disease definition
inflammation of patellar ligament at insertion point on tibial tuberosity
* M>F
* age of onset: boys 12-15 yr; girls 8-12 yr
36
Osgood-Schlatter Disease mechanism
repetitive tensile stress on insertion of patellar tendon over the tibial tuberosity causes minor avulsion at the site and subsequent inflammatory reaction (tibial tubercle apophysitis)
37
Osgood-Schlatter Disease clinical features
* tender lump over tibial tuberosity
* pain on resisted leg extension
* anterior knee pain exacerbated by jumping or kneeling, relieved by rest
38
Osgood-Schlatter Disease investigations
• X-ray lateral knee: fragmentation of the tibial tubercle, ± ossicles in patellar tendon
39
Osgood-Schlatter Disease treatment
• benign, self limited condition, does not resolve until growth halts
• non-operative (majority)
■ may restrict activities such as basketball or cycling
■ NSAIDs, rest, flexibility, isometric strengthening exercises
■ casting if symptoms do not resolve with conservative management
• operative: ossicle excision in refractory cases (patient is skeletally mature with persistent symptoms)
40
Congenital Talipes Equinovarus (club foot) definition
* congenital foot deformity
* muscle contractures resulting in CAVE deformity
* bony deformity: talar neck medial and plantar deviated; varus calcaneus and rotated medially around talus; navicular and cuboid medially displaced
* 1-2/1,000 newborns, 50% bilateral, occurrence M>F, severity F>M
41
Congenital Talipes Equinovarus (club foot) etiology
* intrinsic causes (neurologic, muscular, or connective tissue diseases) vs. extrinsic (intrauterine growth restriction); may be idiopathic, neurogenic, or syndrome-associated
* fixed deformity
42
Congenital Talipes Equinovarus (club foot) physical exam
* examine hips for associated DDH
* examine knees for deformity
* examine back for dysraphism (unfused vertebral bodies)
43
Congenital Talipes Equinovarus (club foot) treatment
• largely non-operative via Ponseti Technique (serial manipulation and casting)
■ correct deformities in CAVE order
◆ change strapping/cast q1-2wk
◆ surgical release in refractory case (rare) – delayed until 3-4 mo of age
* 3 yr recurrence rate = 5-10%
* mild recurrence common; affected foot is permanently smaller/stiffer than normal foot with calf muscle atrophy
44
CAVE deformity
Midfoot cavus
Forefoot adductus
Hindfoot varus
Hindfoot equinus
45
Scoliosis definition
• lateral curvature of spine with vertebral rotation • age: 10-14 yr • more frequent and more severe in females
46
Scoliosis etiology
* idiopathic: most common (90%)
* congenital: vertebrae fail to form or segment
* neuromuscular: UMN or LMN lesion, myopathy
* postural: leg length discrepancy, muscle spasm
* other: osteochondrodystrophies, neoplastic, traumatic
47
Scoliosis clinical features
* ± back pain
* primary curve where several vertebrae affected secondary curves above and below fixed 1° curve to try and maintain normal position of head and pelvis
* asymmetric shoulder height when bent forward
* Adam’s test: rib hump when bent forward
* prominent scapulae, creased flank, asymmetric pelvis
• associated posterior midline skin lesions in neuromuscular scolioses
■ café-au-lait spots, dimples, neurofibromas
■ axillary freckling, hemangiomas, hair patches
* associated pes cavus or leg atrophy
* apparent leg length discrepancy
48
Scoliosis investigations
• X-ray: 3-foot standing, AP, lateral
■ measure curvature: Cobb angle
■ may have associated kyphosis
49
Scoliosis treatment
• based on Cobb angle
■ <25°: observe for changes with serial radiographs
■ >25° or progressive: bracing (many types) that halt/slow curve progression but do NOT reverse deformity
■ >45°, cosmetically unacceptable, or respiratory problems: surgical correction (spinal fusion)
50
What is used to monitor the progression of the scoliotic curve
Cobb angle
51
Scioliosis screening in Canada
Scioliosis screening is not recommended in Canada
52
In structural or fixed scoliosis bending forward does what
makes curve more obvious
53
Most common population to see primary bone tumours
rare after 3rd decade
54
Most common population to see metastases to bone
After 3rd decade
55
Clinical features of bone tumours
* malignant (primary or metastasis): local pain and swelling (wk – mo), worse on exertion and at night, ± soft tissue mass
* benign: usually asymptomatic
* minor trauma often initiating event that calls attention to lesion
56
Bone tumour red flags
Persistent sksletal pain
Localized tenderness
Spontaneous fracture
Enlarging mass/soft tissue swelling
57
Distinguishing benign from malignant bone lesions on xray
Benign
- No periosteal reaction
- Thick endosteal reaction
- Well developed bone formation
- Intraosseous and even calcification
```
Malignant
- Acute periosteal reaction
Codman's triangle
Onion skin
Sunburst
- Broad border between lesion and normal bone
- Varied bone formation
-Extraosseous and irregular calcification
```
58
X-ray findings
* lytic, lucent, sclerotic bone
* involvement of cortex, medulla, soft tissue
* radiolucent, radiopaque, or calcified matrix
* periosteal reaction
* permeative margins
* pathological fracture
* soft tissue swelling
59
Bone tumours diagnosis
• malignancy is suggested by rapid growth, warmth, tenderness, lack of sharp definition
```
• staging should include
■ blood work including liver enzymes
■ CT chest
■ bone scan
■ bone biopsy
◆ should be referred to specialized centre prior to biopsy
◆ classified into benign, benign aggressive, and malignant
■ MRI of affected bone
```
60
What is Codman's triangle
A radiographic finding in malignancy where the partially ossified periosteum is lifted off the cortex by neoplastic tissue
61
Benign active bone-forming bone tumours
Osteoid osteoma
62
Osteoid osteoma description and symptoms and treatment
* bone tumour arising from osteoblasts
* peak incidence in 2nd and 3rd decades, M:F = 2:1
* proximal femur and tibia diaphysis most common locations
* not known to metastasize
* radiographic findings: small, round radiolucent nidus (<1.5 cm) surrounded by dense sclerotic bone (“bull’s eye”)
* symptoms: produces severe intermittent pain from prostaglandin secretion and COX1/2 expression, mostly at night (diurnal prostaglandin production), thus is characteristically relieved by NSAIDs
* treatment: NSAIDs for night pain; surgical resection of nidus
63
Benign active bone tumours fibrous lesions
Fibrous cortical defect
Osteochondroma
Enchondroma
64
Fibrous cortical defect
* or non-ossifying fibroma; fibrous bone lesion
* most common benign bone tumour in children, typically asymptomatic and an incidental finding
* occur in as many as 35% of children, peak incidence between 2-25 yr old higher prevalence in males
* femur and proximal tibia most common locations, 50% of patients have multiple defects that are usually bilateral, symmetrical
* radiographic findings: diagnostic, metaphyseal eccentric ‘bubbly’ lytic lesion near physis; thin, smooth/ lobulated, well-defined sclerotic margin
* treatment: most lesions resolve spontaneously
65
Osteochondroma
* cartilage capped bony tumour
* 2nd and 3rd decades, M:F = 1.8:1
* most common of all benign bone tumours – 45%
* 2 types: sessile (broad based and increased risk of malignant degeneration) vs. pedunculated (narrow stalk)
* metaphysis of long bone near tendon attachment sites (usually distal femur, proximal tibia, or proximal humerus)
* radiographic findings: cartilage-capped bony spur on surface of bone (“mushroom” on x-ray)
* may be multiple (hereditary, autosomal dominant form) – higher risk of malignant change
• generally very slow growing and asymptomatic unless impinging on neurovascular structure (‘painless mass’)
■ growth usually ceases when skeletal maturity is reached
* malignant degeneration occurs in 1-2% (becomes painful or rapidly grows)
* treatment: typically observation; surgical excision if symptomatic
66
Enchondroma
* hyaline cartilage tumour; majority asymptomatic, presenting as incidental finding or pathological fracture
* 2nd and 3rd decades
* 60% occur in the small tubular bones of the hand and foot; others in femur (20% - Figure 56), humerus, ribs
• benign cartilaginous growth, an abnormality of chondroblasts, develops in medullary cavity
■ single/multiple enlarged rarefied areas in tubular bones
■ lytic lesion with sharp margination and irregular central calcification (stippled/punctate/popcorn appearance)
* malignant degeneration to chondrosarcoma occurs in 1-2% (pain in absence of pathologic fracture is an important clue)
* not known to metastasize
* treatment: observation with serial x-rays; surgical curettage if symptomatic or lesion grows
67
Benign active bone tumours cystic lesions
Unicameral/solitary bone cyst
68
Unicameral/solitary bone cyst
* most common cystic lesion; serous fluid-filled lesion
* children and young adults, peak incidence during first 2 decades, M:F = 2:1
* proximal humerus and femur most common
* symptoms: asymptomatic, or local pain; complete pathological fracture (50% of presentations) or incidental detection
* radiographic findings: lytic translucent area on metaphyseal side of growth plate, cortex thinned/ expanded; well-defined lesion
* treatment: aspiration followed by steroid injection; curettage ± bone graft indicated if re-fracture likely
69
Benign Aggressive Bone Tumours
Giant Cell Tumours
Aneurysmal Bone Cyst
Osteoblastoma
70
Osteoblastoma location
found in the distal femur, proximal tibia, distal radius, sacrum, tarsal bones, spine
71
Location of metastases in giant cell tumour
pulmonary metastases in 3%
72
Aneurysmal bone cysts are constituted of what
either solid with fibrous/granular tissue, or blood-filled
73
Giant cell tumour radiographic findings
eccentric lytic lesions in epiphyses adjacent to subchondral bone; may break through cortex; T2 MRI enhances fluid within lesion (hyper-intense signal)
74
Aneurysmal bone cyst radiographic findings
expanded with honeycomb shape
75
Osteoblastoma radiographic findings
often nonspecific; calcified central nidus (>2 cm) with radiolucent halo and sclerosis
76
Benign aggressive bone tumours symptoms
local tenderness and swelling, pain may be progressive (giant cell tumours), ± symptoms of nerve root compression (osteoblastoma)
77
Benign aggressive bone tumours recurrence
15% recur within 2 yr of surgery
78
Benign aggressive bone tumours treatment
* intralesional curettage + bone graft or cement
| * wide local excision of expendable bones
79
Osteosarcoma population
most frequently diagnosed in 2nd decade of life (60%), 2nd most common primary malignancy in adults
80
Osteosarcoma risk factors
history of Paget’s disease (elderly patients), previous radiation treatment
81
Osteosarcoma sitess
predilection for sites of rapid growth: distal femur (45% - Figure 58), proximal tibia (20%), and proximal humerus (15%)
■ invasive, variable histology; frequent metastases without treatment (lung most common)
82
Osteosarcoma symptoms
painful symptoms: progressive pain, night pain, poorly defined swelling, decreased ROM
83
Osteosarcoma radiographic findings
radiographic findings
■ characteristic periosteal reaction: Codman’s triangle (Figure 55) or “sunburst” spicule formation (tumour extension into periosteum)
■ destructive lesion in metaphysis may cross epiphyseal plate
84
Osteosarcoma management
management: complete resection (limb salvage, rarely amputation), neo-adjuvant chemo; bone scan – rule out skeletal metastases, CT chest – rule out pulmonary metastases
85
Osteosarcoma prognosis
prognosis: 70% survival (high-grade); 90% survival (low-grade)
86
Chondrosarcoma difference between primary and secondary
primary (2/3 cases)
■ previous normal bone, patient >40 yr; expands into cortex to cause pain, pathological fracture
• secondary (1/3 cases)
■ malignant degeneration of pre-existing cartilage tumour such as enchondroma or osteochondroma
■ age range 25-45 yr, better prognosis than primary chondrosarcoma
87
Chondrosarcoma symptoms
progressive pain, uncommonly palpable mass
88
Chrondrosarcoma radiogrpahic findings
in medullary cavity, irregular “popcorn” calcification
89
Chondrosarcoma treatment
unresponsive to chemotherapy, treat with aggressive surgical resection + reconstruction; regular follow-up X-rays of resection site and chest
90
Chrondrosarcoma prognosis
10 yr survival 90% for low-grade, 20-40% for high-grade
91
Ewing's sarcoma population
most occur between 5-25 yr old
92
Ewing's sarcoma description
malignant, small round cell sarcoma
florid periosteal reaction in metaphyses of long bone with diaphyseal extension
93
Ewing's sarcoma complication
metastases frequent without treatment
94
Ewing's sarcoma signs/symptoms
signs/symptoms: presents with pain, mild fever, erythema, and swelling; anemia, increased WBC, ESR, LDH (mimics an infection)
95
Ewing's sarcoma radiographic findings
moth-eaten appearance with periosteal lamellated pattern (“onion-skinning”)
96
Ewing's sarcoma treatment
resection, chemotherapy, radiation
97
Ewing's sarcoma prognosis
70% survival, worst prognostic factor is distant metastases
98
Most common primary malignant tumour of bone in adults
Multiple myeloma
99
Multiple myeloma epidemiology
90% occur in people >40 yr old, M:F = 2:1; twice as common in African-Americans
100
Multiple myeloma clinical presentation
localized bone pain (cardinal early symptom),
compression/pathological fractures,
renal failure,
nephritis,
high incidence of infections (e.g. pyelonephritis/pneumonia),
systemic (weakness, weight loss, anorexia)
101
Multiple myeloma radiographic findings
multiple, “punched-out” well-demarcated lesions,
no surrounding sclerosis,
marked bone expansion
102
Multiple myeloma diagnosis
serum/urine immunoelectrophoresis (monoclonal gammopathy)
■ CT-guided biopsy of lytic lesions at multiple bony sites
103
Multiple myeloma treatment
chemotherapy,
bisphosphonates,
radiation,
surgery for symptomatic lesions or impending fractures – debulking,
internal fixation
104
Multiple myeloma prognosis
5 year survival 30%; 10 year survival 11%
105
Bone metastases most common tumours metastatic to bone
BLT with Kosher Pickle
```
Pickle
Breast
Lung
Thyroid
Kidney
Prostate
```
Melanoma
2/3 from breast or prostate
106
Bone metastases common characteristics
Usually osteolytic
Prostate occasionally osteoblastic
107
Bone metastases clinical presentation
may present with mechanical pain and/or night pain, pathological fracture, hypercalcemia
108
Bone metastases investigations
bone scan for MSK involvement, MRI for spinal involvement may be helpful
109
Bone metastases treatment
pain control,
bisphosphonates,
stabilization of impending fractures if Mirel’s Critera >8 (ORIF, IM rod, bone cement)
110
Mirel's Criteria for impending fracture risk and prophylactic internal fixation
Site
Upper arm = 1
Lower extremity = 2
Peritrochanteric = 3
Pain
Mild = 1
Moderate = 2
Severe = 3
Lesion
Blastic = 1
Mixed = 2
Severe = 3
Size
<1/3 bone diameter = 1
1/3-2/3 diameter = 2
>2/3 diameter = 3
