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AD ABOS PART ONE > peds > Flashcards

peds Flashcards

1
Q

Question

A

Answer

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2
Q

genetic inheritance of achondroplasia

A

AD, 80% spontaneous mutation, FGFR3, champagne pelvis, lumbar lordosis and stenosis, short pedicles with decreased interpedicular distance. Foramen magnum stenosis- central apnea. radial head subluxation and trident hands

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3
Q

genetic defect of pseudoachondroplasia

A

COMP

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4
Q

genetic defect of spondyloepiphyseal dysplasia

A

type II collagen

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5
Q

spinal manifestations of pseudoachon

A

lumbar lordosis and cervical instability

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6
Q

genetic defect of Jansen metaphyseal chondrodysplasia

A

PTHRP

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7
Q

genetic defect of McCune Albright

A

cAMP.(cafe au lait spots in coast of Maine pattern)endocrine abnormalities (precocious puberty)\renal phosphate wasting due to FGF-23 (oncogenic osteomalacia) unilateral polyostotic fibrous dysplasia obtain AP spine radiographs to look for scoliosis

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8
Q

abnormal epiphyseal development with concomitant spine involvement

A

SED

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9
Q

abnormal epiphyseal development with no concomitant spine involvement

A

MED

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10
Q

non-ortho manifestation of the disease with abnormal epiphyseal development and concomitant spine involvement

A

retinal detachment is common with SED

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11
Q

dumbbell shaped bones, especially femur

A

Kniest syndrome - COL2A1 defect. Dwarf, retinal detach,

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12
Q

genetic defect of Schmid’s metaphyseal chondrodysplasia

A

type X collagen, AD, Severe coxa vara, gene varrem like rickets

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13
Q

gene defect of disease with flattened femurs, valgus knees

A

COMP, (MED)

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14
Q

found in the urine of Morquios

A

keratan sulfate

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15
Q

Morquios mnemonic

A

AR, Most common, Odontoid hypOplasia, Keratan sulfate, I is clOudy, Intelligent. C Spine instability

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16
Q

inheritance of Hurlers

A

AR

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17
Q

inheritance of Hunters

A

XLR

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18
Q

diastrophic dysplasia

A

autosomal recessive, mutation in DTDST gene (SLC26A2) on chromosome 5 , encodes for sulfate transporter protein. cervical kyphosis. Common in Finnish. Cauliflower ears, hitchhiker thumb. Hip/knee contractors

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19
Q

genetic defect in cleidocranial dysplasia

A

CBFA1, RUNX2 which are transcription factors for osteocalcin

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20
Q

this is thought to be related to COL6A1 in Down syndrome

A

type 6 collagen abnormality = joint laxity, hip/patellar dislocation

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21
Q

Factors for Hemaphilia A & B

A

VIII, IX. X linked recessive

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22
Q

abnormal factor VIII

A

von Willebrands

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23
Q

squared patella, femoral condyles

A

hemophilia

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24
Q

when is synovectomy for hemophilia indicated

A

recurrent hemarthroses despite medical mgmt. Can be done arthroscopically. VIII must be 50% normal

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25
Q

this is a relative contraindication for surgery in hemophilia

A

presence of IgG inhibitors

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26
Q

spinal manifestation of OI

A

basilar invagination common in severe OI

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27
Q

this can occur from bisphosphonate use in OI

A

iatrogenic osteopetrosis

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28
Q

radiologic findings of marfan’s

A

scoliosis and acetabular protrusio

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29
Q

two differences b/t marfans and homocystinuria

A

superior lens in marfans, and no osteoporosis

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30
Q

non-ortho manifestation of JIA

A

iridocyclitis; slit lamp exam q 6 mos

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31
Q

Two findings following birth plexus injury that carry poor prognosis

A

lack of biceps function at 3-6 mos and presence of a horners syndrome are both bad.Preganglionic will have no rhomboid

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32
Q

surgical option for birth plexus injury

A

lat and teres major transfer to the shoulder external rotators. If done before age 2 can also release subscap

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33
Q

imaging for torticollis

A

ultrasound; predictive of failure of nonop mgmt if severe fibrosis present

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34
Q

physiologic classes of CP

A

spastic, athetotic, ataxic, mixed

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35
Q

most common type of CP

A

spastic, characterized by slow, restricted movements bc of simultaneous agonist/antagonist action

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36
Q

this type of CP shows involvement of the lower extremities more than the uppers

A

diplegic CP involves the lowers more than the uppers

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37
Q

in this type of CP pts are usually unable to walk

A

quadriplegic CP, in contrast to hemi or diplegic

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38
Q

surgery for stiff-leg gait in CP

A

rectus transfer to hamstrings

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39
Q

scissor gait problem

A

adductor contracture

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40
Q

risk for scoli in CP highest with

A

spastic quads

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41
Q

general rule for surgery in CP

A

none before age 3, unless hip at risk

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42
Q

this can be done if there is a loss of knee flexion during the swing phase of gait

A

out-of-phase rectus femoris transfer to the semi-T or gracilis muscle

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43
Q

indication for an out-of-phase rectus femoris transfer to the semi-T or gracilis muscle

A

loss of knee flexion in swing phase of gait in CP

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44
Q

this foot deformity is most common in spastic diplegia

A

equinovalgus foot

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45
Q

this foot deformity is most common in spastic hemiplegia

A

equinovarus foot

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46
Q

cause of equinovalgus foot in spastic CP

A

overpull of the peroneal muscles

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47
Q

cause of equinovarus foot in spastic CP

A

overpull of the AT, PT, or both

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48
Q

two basic rules about surgical mgmt of most common foot deformity in spastic hemiplegia

A

this is equinovarus. You can’t just lengthen, and you can’t just transfer a whole muscle. You have to split transfer

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49
Q

when are split-muscle transfers helpful in spastic CP foot deformities

A

when the muscle is spastic in both swing and stance phases of gait

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50
Q

no flexion creases

A

arthrogryposis

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51
Q

multiple joint contractures, decreased anterior horn cell activity, normal intelligence

A

arthrogryposis

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52
Q

upper extremity mgmt in arthrogryposis

A

anterior triceps transfer, posterior soft tissue release

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53
Q

surgical mgmt of bilateral hip dislocation in arthrogryposis

A

usually left unreduced because ambulation is preserved

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54
Q

surgical mgmt of bilateral elbow pathology in arthrogryposis

A

leave one in extension for hygiene, flex one for feeding

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55
Q

knee contractures, hip dislocation in arthrogryposis

A

correct the knee first

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56
Q

initial and recurrent treatment for foot deformities in arthrogryposis

A

soft tissue release first, but recurrence may need bony procedure (talectomy). Goal is stiff, plantigrade foot.

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57
Q

important level in myelodysplasia and why

A

L4 gives quad function, important bc allows some community ambulation

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58
Q

change in function, UTI, or new deficit in spina bifida

A

this can be associated with tethered cord or hydrocephalus

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59
Q

can be confused with infection in myelodysplasia

A

fractures can mimic infection in ages 3-7 in spina bifida

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60
Q

perioperative concern in myelodysplasia

A

many myelodysplastics are latex allergic

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61
Q

only instance in which hip containment is not controversial in myelodysplasia

A

in myelodysplasia pts that have a functioning quadriceps

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62
Q

what has no bearing on the functional outcome of a myelomeningocele

A

whether the hips are reduced or not

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63
Q

since hip position does not affect myelo outcomes, mgmt consists of

A

soft tissue releases

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64
Q

how are the surgical mgmts of valgus deformity in mature and immature pts different

A

in skeletally immature pts you do a distal tibial hemiarrest or Achilles tendodesis to the fibula. In mature pts you do a distal tibial osteotomy

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65
Q

this is typically avoided in myelodysplastics

A

triple arthrodeses reserved for severe deformities and sensate feet

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66
Q

surgical mgmt of rigid clubfoot in myelodysplastics

A

subtalar release, TAL and tib post lengthening, AT transfer to the dorsal midfoot

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67
Q

mgmt of scoliosis in dz with high serum levels of creatine phosphokinase

A

in muscular dystrophy, scoliosis can progress rapidly due to lack of muscle support. This can have significant effect on respiratory function, and therefore is treated earlier. Curves of 25-30*.

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68
Q

scapulothoracic fusion

A

FSH, facioscapulohumeral muscular dystrophy

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69
Q

Nystagmus, wide gait, cardiomyopathy

A

Friedrich’s ataxia, cavus foot, scoliosis

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70
Q

CMT aka…

A

peroneal muscle atrophy. Defect Chr17, PMP22

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71
Q

first foot deformity of dz caused by defective PMP22 and its etiology

A

Plantarflexed first ray occurs first in CMT, due to the weakened anterior tib (as well as PL/PB)

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72
Q

algorithm for surgical mgmt of CMT foot

A

if the hindfoot varus is flexible, you can get away with post tib transfer. If not you have to do a calcaneal osteotomy at a minimum, possibly a triple arthrodesis

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73
Q

hallmark of polio

A

motor weakness with normal sensation

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74
Q

site of destruction of poliovirus

A

anterior horn cells and brainstem motor nuclei

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75
Q

survival motor neuron gene

A

spinal muscular atrophy

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76
Q

mgmt of hip instability in dz with autosomal recessive loss of the anterior horn cells in the spinal cord

A

hip dislocation or subluxation in SMA is treated nonoperatively

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77
Q

what to tell parents of a child with SMA considering spinal fusion about the mgmt of the extremities

A

there may be a transient decrease in the function of the uppers, and contractures in the lowers should be addressed prior to spine surgery (sitting balance)

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78
Q

hemihypertrophy

A

assoc with Wilms tumor (serial abd ultrasound) as well as more commonly with neurofibromatosis

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79
Q

threshold for scoli evaluation

A

7*

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80
Q

risk factors for AIS progression

A

Curve more than 20 in young, more than 45 if mature. Thoracic curves progress faster than lumbar, as do double curves in comparison to single curves

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81
Q

who gets MRI in peds scoli

A

painful scoli, left curves, onset before 11 (Juvenile), associated syndromes or neural deficits, congenital abnormalities

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82
Q

2 indications for anterior + PSF in scoli

A

very large curves (75*+) that may need anterior releases to improve flexibility, and very young pts that still have spinal growth remaining (crankshaft)

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83
Q

stable vertebra

A

most proximal vertebra that is most closely bisected by the center sacral line

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84
Q

end vertebra

A

the most tilted vertebra

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85
Q

neutral vertebra

A

has no rotation in the axial plane

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86
Q

structural curve

A

either the largest curve or one that does not bend to less than 25*

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87
Q

acute infection following PSF for scoli

A

D/I, abx suppression, hardware retention until fusion. Typically Staph aureus

88
Q

delayed infection following PSF for scoli

A

Typically P acnes or Staph epi. Hardware removal, check for pseudoarthrosis, abx.

89
Q

treatment for pseudoarthrosis in spine fusion (maybe just scoli)

A

compression instrumentation and bone grafting

90
Q

differences between infantile and adolescent idiopathic scolis

A

Infantile is more common in boys. More commonly has a left curve. Associated more with congenital defects. And most curves resolve spontaneously, although there are exceptions (RVAD scale…)

91
Q

these radiographic parameters are indicative of high risk for progression of infantile scoli

A

if there is overlap of the medial rib relative to the apical vertebra, or Rib Vertebral Angle greater than 20*

92
Q

indication for casting scoliosis

A

Mehta casting can be done for young pts with flexible curves

93
Q

this type of scoli routinely has progression of their curves

A

juvenile idiopathic scoli has high rate of curve progression, ages 3-10

94
Q

why are MRI’s routinely ordered in JIScoli

A

there is 25% rate of spinal cord abnormalities in JIS

95
Q

who commonly gets a cardiac workup for scoli surgery

A

Pts with duchennes muscular dystrophy get cardiomyopathy, and commonly have scoli due to loss of muscle support

96
Q

nutritional lab markers for successful scoli surgery

A

leukocyte counts above 1500, albumin > 3.5

97
Q

two additional concerns in congenital scoliosis, after MRI

A

renal ultrasound, (25% GU defect rate) and cardiac workup (echo? 10% cardiac anomalies)

98
Q

two main types of congenital scoli

A

failure of segmentation (bar) or failure of formation (hemivertebra)

99
Q

worst prognosis in congenital scoli

A

unilateral bar with contralateral fully segmented hemivertebra

100
Q

this type of hemivertebra has higher risk of progression

A

if a hemivertebra is fully segmented, rather than unsegmented, its risk for progression is higher

101
Q

when resection is indicated in congenital scoli

A

if a hemivertebrae is fully segmented, it has high risk of progression and can be resected

102
Q

sole (?) indication for fusion anteriorly only, in pediatric scoli

A

as part of surgical mgmt of fully segmented hemivertebral congenital scoli that has begun progressing. Combined with hemivert excision.

103
Q

this type of congenital kyphosis is most common

A

failure of formation

104
Q

this type of congenital kyphosis has the worst prognosis

A

type I, or failure of formation

105
Q

this type of congenital kyphosis has the highest risk for neuro complications

A

type I, or failure of formation

106
Q

indications for PSF in congenital kyphosis

A

Favored in kids

107
Q

indications for PSF plus anterior procedure in congenital kyphosis

A

Older than 5, or with curves > 50*. If there are neuro deficits: vertebrectomy/decompression PLUS ASF then PSF.

108
Q

most common site of skeletal involvement in neurofibromatosis

A

spinal involvement common in NF

109
Q

two types of NF related scoli

A

nondystrophic (which is treated like AIS) and dystrophic (tight sharp curves, vertebral scalloping, rib penciling)

110
Q

why is rib penciling important in NF dystrophic scoli

A

Penciling of 3 or more ribs prognostic of rapid deformity

111
Q

thresholds for surgical treatment of dystrophic NF scoli

A

surgery for curve progression, and when above 40*. Also kyphosis.

112
Q

diastematomyelia

A

tissue bar that causes cleft in the spinal cord

113
Q

treatment of diastematomyelia

A

unless spinal deformity present (has to be resected first) or a neuro deficit it can be observed

114
Q

earliest radiographic finding of discitis

A

loss of the normal lumbar lordosis

115
Q

indication for repair of a pars defect

A

pars defects at L4 and above

116
Q

this spondylolisthesis has the highest risk for progression

A

dysplastic type of spondy has highest risk of progression

117
Q

spondy slip of less than 50% treated with

A

after failure of non-op (bracing, PT, activity mod), arthrodesis +/- instrumentation

118
Q

spondy slip of more than 50% treated with

A

usually surgery as there is pain and risk of progression; L4-S1 fusion. Decompression performed if there is high-grade slip or neurologic symptoms

119
Q

additional imaging study besides AP and Lat lumbar spine films when pediatric pars defect suspected

A

SPECT scanning done for equivocal cases of peds spondy

120
Q

definition of kyphosis

A

45* curve, 3 sequential vertebra with >5* of wedge

121
Q

frequency of MRI in Scheuermann’s kyphosis

A

neurologic changes are rare, so are MRI’s. But if present get MRI.

122
Q

Non-op treatment for scheuerman’s kyphosis

A

bracing done for progressive curves in pts that have at least one year of growth (

123
Q

Indications for surgery in scheuerman’s kyphosis

A

Pain after PT, skeletal maturity, curve >75*. Cosmesis is relative indication

124
Q

klippel-feil etiology

A

failure of formation or segmentation in multiple cervical segments during 3rd-8th weeks of gestation

125
Q

conditions associated with klippel-feil

A

congenital scoliosis, renal aplasia, sprengel deformity, congenital heart deformities

126
Q

although not often seen, classic triad of klippel-feil

A

low posterior hairline, webbed neck, decreased cervical motion

127
Q

atlantoaxial instability assoc with these

A

down syndrome, JRA, various osteochondrodystrophies

128
Q

grisel dz

A

retropharyngeal inflammation, leads to rotatory atlantoaxial instability

129
Q

indications for surgical mgmt of os odontoideum

A

Instability (>10mm ADI,

130
Q

distinguishing pseudosubluxation from true subluxation

A

in pseudo, the posterior spinolaminar line is not disrupted. This is a normal finding in kids younger than 8

131
Q

cervical spine, disc calcification, elevated ESR, pain, decreased ROM

A

disc calcification syndrome, conservative mgmt, self-limiting

132
Q

sprengel’s deformity

A

undescended scapula, winging. Most common congenital shoulder deformity of children.

133
Q

common causes for in-toeing in peds

A

metatarsus adductus in infants, tibial torsion in toddlers, and femoral anteversion up to 10 yrs

134
Q

common causes for out-toeing in peds

A

external hip contractures in infants, from the tibia or femur in older children or adolescents

135
Q

normal foot progression angle and its significance

A

-5 to 20. Abnormal is non-specific rotation problem

136
Q

normal prone hip rotation angle and its significance

A

>70* internal rotation, or

137
Q

normal thigh foot angle and its significance

A

normal 0-20.

138
Q

when surgery is done for tibial torsion

A

7-10 years old, supramalleolar osteotomy

139
Q

Congenital DDH can be associated with

A

other uterine packaging defects, such as torticollis and metatarsus adductus

140
Q

risk factors for DDH

A

breech first-born females with a family history. Most often the leFt.

141
Q

Ortolani/Barlow

A

Can’t both be positive. Ortolani, out and you can get it in. Barlow, back in but you can get it out

142
Q

anterior straps of pavlik

A

flexion

143
Q

posterior straps of pavlik

A

abduction

144
Q

when does ossific nucleus of femoral head appear

A

~ 6 mos

145
Q

radiographic position of femoral ossific nucleus in DDH

A

superior to hilgengreiners, lateral to perkins

146
Q

Up to 6 months, DDH treatment consists of

A

Pavlik. Recheck reduction in 3 weeks by ultrasound. If reduced, continue harness until exam and U/S are normal. If it is out, reduce it, get arthrogram, and spica cast

147
Q

From 6-18 months, DDH treatment consists of

A

perform hip arthrography, percutaneous adductor tenotomy, closed reduction, and spica casting.

148
Q

After walking age up to age 6-8, DDH treatment consists of

A

open reduction

149
Q

Unilateral DDH after age 8

A

leave it alone.

150
Q

after age 6, DDH unilateral

A

consider osteotomy (until age 8…)

151
Q

after age 4 this isn’t an option for treatment of DDH anymore

A

femoral osteotomy not successful that late

152
Q

bilateral DDH after age 6

A

leave it alone

153
Q

filling defect on arthrogram of unsuccessful DDH reduction attempt

A

superior limbus

154
Q

this position can result in femoral nerve palsy in pavlik treatment of DDH

A

excessive flexion

155
Q

this position can result in femoral head osteonecrosis in pavlik treatment of DDH

A

excessive abduction

156
Q

approach for open reduction of DDH

A

anterior (less risk of damage to MFCA)

157
Q

these pelvic osteotomies require periacetabular metaplasia for success

A

Chiari, shelf

158
Q

this pelvic osteotomy leaves the posterior column intact

A

PAO

159
Q

triangular ossification defect inferomedial femoral neck

A

congenital coxa vara

160
Q

treatment of congenital coxa vara

A

depends on the Hilgengreiner-Epiphyseal angle: 60*.

161
Q

predictors of poor outcome in noninflammatory dz causing deformity of the proximal femur secondary to vascular insult

A

These Perthes pts do worst: females with bone age older than 6, decreased ROM, and lateral column classification (C)

162
Q

treatment regimen for Perthes

A

NSAIDs, traction, protected weightbearing, maintain ROM

163
Q

Herring proposed surgery for these Perthes pts

A

B/C and C pts older than 8

164
Q

radiographic signs of poor prognosis in noninflammatory dz causing deformity of the proximal femur secondary to vascular insult

A

Perthes: lateral calcification, Gage sign (v-shaped defect at the lateral physis, lateral subluxation, metaphyseal cysts, horizontal growth plate

165
Q

SCFE occurs here

A

weakness of the perichondrial ring and slippage through the hypertrophic zone of the growth plate

166
Q

ROM exam finding in SCFE

A

obligate ER with flexion

167
Q

Difference in stable vs unstable SCFE with respect to AVN rates

A

No pts with stable develop AVN; Half of those with unstable slips do

168
Q

Indications for prophylactic SCFE pinning

A

Endocrinopathies,

169
Q

SCFE pin placement in this location has the highest rate of joint penetration

A

placing screws in the anterior superior part of the head = highest joint penetration

170
Q

threshold for amputation in femoral deficiency

A

if the femur is less than 50% of the contralateral side

171
Q

Indication for CT in LLD

A

knee flexion contracture

172
Q

rough guide for length per year in mm in the leg

A

5-9-6-3, from prox femur to distal tibia

173
Q

LLD less than 2 cm

A

lifts, non-op

174
Q

LLD more than 5 cm

A

lengthening

175
Q

ESR value in transient synovitis

A

typically less than 20mm/hr

176
Q

Utility of CRP in peds infections

A

should decline within 48-72 hrs of treatment; if not change the treatment

177
Q

indications for operative mgmt of peds osteomyelitis

A

failure to respond to abx, frank pus (MRI or aspiration), or sequestered abscess

178
Q

when does periosteal new bone form in peds osteomyelitis

A

5-7 days

179
Q

these help distinguish septic arthritis from transient synovitis

A

refusal to bear weight, WBC > 12,000, Fever >101.5, ESR > 40 are not found in transient synovitis. These are Kocher criteria

180
Q

This pathogen does not need surgical drainage if it causes septic arthritis

A

Neisseria, can be treated with penicillin (need to verify…)

181
Q

metaphyseal beaking

A

infantile blounts

182
Q

non-op treatment in blounts dz from 0-4 yrs

A

Stage I and II: KAFO for pts under 3. Surgery for higher stages and stage II older than 3. Overcorrect into a little valgus. In stage III the epiphysis looks like it is melting into the metaphysis

183
Q

this amount of genu valgum is gon’ be foine

A

up to 15* from 2-6 yrs

184
Q

indications for surgery in genu valgum

A

more than 10cm between medial mals, more than 15* valgus, and only if older than 10 yrs

185
Q

posteromedial tibial bowing

A

physiologic, intrauterine packaging. Commonly associated with calcaneovalgus feet and LLD

186
Q

anteromedial tibial bowing

A

associated with fibular hemimelia, equinovarus, tarsal coalition, and LLD

187
Q

anterolateral tibial bowing

A

most common cause is congenital pseudoarthrosis of the tibia. 50% of pts with anterolateral bow have NF. Only 10% of pts with anterolateral bow have NF.

188
Q

initial treatment for tibial bowing associated with NF

A

anterolateral = total contact brace

189
Q

only long bone deficiency with a known inheritance pattern

A

tibial hemimelia, autosomal dominant

190
Q

other deformity often present with tibial hemimelia

A

lobster claw hand

191
Q

most frequent location OCD

A

lateral aspect of MFC

192
Q

indications for OCD lesions

A

loose or little growth remaining

193
Q

indications for discoid meniscus

A

only if symptomatic and torn: saucerization

194
Q

clinical features of clubfoot

A

forefoot adductus and supination, combined with hindfoot varus and equinus

195
Q

radiographic appearance of talus / calcaneus in clubfoot

A

parallel

196
Q

CAVE in clubfoot Ponseti method

A

order of correction, cavus, adductus, varus, then equinus.

197
Q

common deformity after clubfoot treatment, its cause, and treatment

A

persistent supination of the forefoot, which is believed to be from overpull of the anterior tibialis and a weak peroneus, or undercorrection of forefoot supination. This often requires transfer of the AT laterally

198
Q

possible gene cause for clubfoot

A

PITX-1

199
Q

treatments for clubfoot after ponseti casting

A

achille’s tenotomy at 6-8 weeks, braces for 2-4 years

200
Q

clinical appearance of metatarsus adductus

A

heel bisector line that hits lateral to the 2nd webspace

201
Q

treatment for metatarsus adductus

A

supple feet can be stretched, stiff feet can be casted

202
Q

treatment for skewfoot

A

non-operative treatment does not work

203
Q

test in pes cavus

A

besides full neuro workup, a Coleman block test tells you whether hindfoot corrects or not

204
Q

treatment for pes cavus

A

after neuro workup, assess whether supple or not (Coleman block) If flexible, plantar release, metatarsal osteotomy, posterior tib transfer. If hindfoot varus is RIGID, add a calcaneal osteotomy as well.

205
Q

this is not the answer in pes cavus that does not correct with Coleman block testing

A

Avoid triple arthrodesis; use calcaneal slide instead

206
Q

irreducible dorsal dislocation of the navicular on the talus, and fixed equinus hindfoot

A

CVT

207
Q

radiographic findings in CVT

A

long axis of the talus hits posterior to the metatarsal axis

208
Q

irregular middle facet on Harris heel view

A

talocalcaneal coalition

209
Q

most common tarsal coalition in children 10-12

A

calcaneonavicular

210
Q

most common tarsal coalition in children 12-14

A

subtalar

211
Q

surgical treatment for subtalar coalition

A

only after failing non-op, if there is 50%, subtalar fusion (verify this with foot talk)

212
Q

juvenile bunions

A

don’t operate unless skeletally mature

213
Q

radiographs in this condition mimic CVT

A

flexible pes planus, except a plantar-flexed view shows talar axis passing above the metatarsal cuneiform axis

214
Q

this view is helpful in accessory navicular

A

external oblique

215
Q

threshold for spine surgery in OI

A

treated at 35* if crappy bone, with PSF.

AD ABOS PART ONE (3 decks)

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