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Peds > Miller's Review Peds > Flashcards

Miller's Review Peds Flashcards

Ortho Peds

1
Q

Type of femur fracture most common in NAT in non-ambulator patients

A

Transverse

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2
Q

Indications for physeal bar resection

A

> 2cm growth, <50% physeal involvement

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3
Q

Blocks to closed reduction of proximal humerus fractures

A

Biceps, deltoid, periosteum

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4
Q

Acceptable parameters for proximal humerus fractures in peds

A

<5 = 70 deg, 100% displaced

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5
Q

Humeral shaft fracture in patient <3

A

Think NAT

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6
Q

Common malunion in supracondylar humerus fractures

A

Cubitus varus and extension

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7
Q

Other injuries in patients with supracondylar humerus and ipsilateral distal radius fracture.

A

Increased incidence of nerve injury and acute compartment syndrome

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8
Q

X-ray needed to evaluate lateral conylde fractures

A

Internal rotation oblique

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9
Q

Malunion complications in lateral condyle fractures

A

Cubitus valgus with tardy ulnar nerve palsy

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10
Q

Associated injury in medial epicondyle fractures

A

Elbow dislocation

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11
Q

X-ray needed in medial epicondyle fracture

A

Distal humeral axial view

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12
Q

How to identify a transphyseal distal humeral fracture on x-ray

A

Looks like an elbow dislocation; however, the radius follows the capitellum

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13
Q

Most common displacement of transphyseal distal humerus fractures

A

Posteriomedial displacement, late complications include cubitus varus and AVN

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14
Q

Techniques to treat proximal radius fractures

A

Closed reduction (traction, varus in supination and extension, flex and pronate)

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15
Q

Forearm fracture acceptable angulation by age

A

<9 = 15 degrees angulation, 45 rotation

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16
Q

Malunion risk in pediatric acetabular and pelvis fractures

A

Early triradiate cartilage closure and acetabular dysplasia

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17
Q

Next step after closed reduction of pediatric hip dislocation

A

MRI to confirm reduction

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18
Q

Age base approach to pediatric femoral shaft fractures

A

<6 mos = Pavlik

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19
Q

Indications for flexible IMN of pediatric femur fractures

A

Age 5-11, wt <50kg

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20
Q

How does the proximal tibial physis close

A

Posterior -> Anterior and Medial -> Lateral

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21
Q

Complications of tibial spine fractures

A

Late anterior instability in stiffness

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22
Q

Distal tibia physeal gap that increases risk of physeal arrest

A

> 3mm, ORIF does not decrease the risk though

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23
Q

Acceptable displacement in Tillaux fractures

A

2.5mm

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24
Q

Order of distal tibia physeal closure

A

Central -> medial -> lateral

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25
Q

Triplane fracture

A

SH III on AP, SH II on lateral = SH IV

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26
Q

Halo pins in peds

A

6-8 pins at 2-4 lbs of torque

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27
Q

Diagnosis of atolantooccipital dissociation

A

BDI >12mm, Powers ratio >1

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28
Q

Most common type of pediatric odontoid fracture

A

Right at the dentocentral synchondrosis, this normally fuses around age 6. Treatment is with halo immobilization.

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29
Q

Management of pediatric thoracolumbar flexion distraction injuries

A

Assess for intra-abdominal injury (50%), most often operative stabilization for unstable bony or ligamentous injury, may consider extension bracing if stable bony injury

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30
Q

Most common mechanism of pediatric osteomyelitis

A

Hematogenous spread at the sluggish flow area in the metaphysis

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31
Q

Common osteomyelitis organisms in kids

A

S. aureus most common, GBS in neonates, K. Kingaei in delayed presentation

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32
Q

Involucrum

A

New bone formed around the infection

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33
Q

Sequestrum

A

Necrotic avascular bone that can be nidus for persistent infection

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34
Q

Risk of DVT in kids?

A

MRSA osteomyelitis with PVL gene

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35
Q

Joints commonly infected in kids

A

Those with intra-articular metaphysis: shoulder, elbow, hip and ankle. In other joints where the physis is extra-articular, it seems to be protective of a septic joint.

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36
Q

Kocher criteria

A

NWB, ESR >40, WBC >12k, fever >38.5.

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37
Q

Lyme symptoms other than erythema migrans

A

CN VI and VII palsy, migratory arthritis

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38
Q

Lyme tx

A

Doxy if >8 years old, amoxicillin if younger

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39
Q

Bug involved in foot puncture wounds

A

Pseudomonas

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40
Q

Concern for pediatric patient with back pain and loss of lordosis on plain films

A

Discitis

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41
Q

Chronic recurrent multifocal osteomyelitis

A

Multiple episodes of osteomyelitis at different sites, nothing ever grows on culture, associated with palmar/plantar pustules. Rheumatologic condition treated with NSAIDs.

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42
Q

Diagnostic criteria for cerebral palsy

A

Non-progressive upper motor neuron disorder onset before age two

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43
Q

Potential causes of cerebral palsy

A

Prematurity, intrauterine factors, perinatal infections, anoxic brain injury and meningitis

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44
Q

MRI findings of cerebral palsy

A

Periventricular leukomalacia

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45
Q

GMFCS classification

A

I: no assistive device needed. II: brace or assistive device needed III: ambulatory but use braces or walker IV: wheelchair dependent V: completely dependent

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46
Q

SEMLS in CP

A

Single Event Multi Level Surgery to limit trips to OR

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47
Q

Treatment of toe walking in CP

A

AFO, casting +/- botox

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48
Q

Treatment of crouch gait in CP

A

Release of tight iliopsoas and hamstring lengthening

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49
Q

Treatment of stiff knee gait in CP

A

Hamstring lengthening and rectus transfer

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50
Q

CP hips at risk for dislocation

A

Abduction < 45 degrees and uncovered femoral head

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51
Q

Tendon release for CP hip subluxation

A

Adductor and IP release

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52
Q

Late bone reconstruction for CP hip subluxation

A

Proximal femur VDRO +/- acetabulum osteotomy

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53
Q

Treatment for late recognized CP hip dislocation

A

Leave untreated, abduction osteotomy to take misshapen femoral head further from the pelvis and girdlestone procedure

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54
Q

Surgical treatment of equinovalgus foot in CP

A

Due to spastic peroneals

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55
Q

Surgical treatment of equinovarus foot in CP

A

Due to overpull of PT +/- AT

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56
Q

Cause of arthrogryposis

A

Decrease in anterior horn cells, non-progressive contractures in multiple joints

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57
Q

Arthrogryposis in upper extremities? Lower extremities?

A

Shoulder AD/IR, elbow extension, wrist flexion/ulnar deviation

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58
Q

Arthrogryposis UE treatment

A

Manipulation and casting -> posterior elbow release, can do osteotomies age 4-8, if bilateral put one hand up for eating and one down for perineal hygiene

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59
Q

Arthrogryposis LE treatment

A

Correct knees 1st to allow flexion needed for harness/brace/casting, then reduce hip if unilateral, cast for stiff and plantigrade foot

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60
Q

Cause of spina bifida, diagnosis?

A

Incomplete neural tube closure, can be secondary to low folate, valproic acid use, carbamazepine, maternal hyperthemia and maternal DM. Diagnosed with elevated maternal serum AFP

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61
Q

How to determine level of function in spina bifida

A

Lowest motor level, need L4 for community ambulation

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62
Q

Allergy in spina bifida patients

A

IgE mediated latex allergy

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63
Q

Other conditions to treat in spina bifida

A

Hip dislocations, knee flexion contracture, clubfoot, equinus, tethered cord

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64
Q

Treatment of hip dislocations in spina bifida

A

Often treated non-op unless they’re a low sacral level because there is a high rate of recurrence

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65
Q

Spina bifida patient with infected appearing leg, next step?

A

X-ray, fractures often present like infection in these patients

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66
Q

Things to check if acute change in function in spina bifida patient

A

Shunt malfunction, hydrocephalus, Arnold Chiari malformation, tethered cord

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67
Q

No of spina bifida pts with scoliosis?

A

100%, thoracic, high level of complications when treated with surgery

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68
Q

Patient has imperforate anus, GU and LE deformities with progressive kyphosis. Mother has history of diabetes. Why might this patient have a motor deficit?

A

Sacral agenesis is associated with maternal diabetes. Typically protective sensation remains intact.

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69
Q

Treatment of sacral agenesis

A

Spinal stabilization of types III and IV (no sacrum)

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70
Q

Genetic cause of Duchenne and Becher muscular dystrophy

A

XLR mutation in dystrophin gene results in progressive loss of motor proximal strength.

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71
Q

Indications for spine fusion in muscular dystrophy

A

20-25 degree curve

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72
Q

Medical management of muscular dystrophy

A

Corticosteroids slow progression

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73
Q

Fascioscapulohumeral muscular dystrophy

A

AD, normal CK, scapular winging, unable to whistle given weakness and paralysis of facial muscles

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74
Q

Diagnosis in patient with fever, muscle aches, elevated CPK and ESR with muscle biopsy showing inflammation. Treatment?

A

Polymyositis and dermatomyositis. Treat with anti-TNF medications for flares.

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75
Q

Staggering wide based gait, cardiomyopathy, cavus foot and die in their 50’s. Diagnosis?

A

AR Freidrich ataxia from GAA repeat in frataxin gene that causes spinocerebellar degeneration and degeneration in posterior columns of spinal cord

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76
Q

Cause of CMT

A

AD mutation in PMP 22 gene on chromosome 17

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77
Q

Cause of pes cavus in CMT. Nonop management?

A

TA and PB weak. PL flexes 1st ray and PT pulls fut into varus. Treat with lateral post and depression for plantarflexed 1st ray.

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78
Q

Op management for pes cavus in CMT?

A

Plantarfascia release and 1st MT dorsiflexion osteotomy

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79
Q

Dejerine-Sottas

A

AR hypertrophic neuropathy of infancy with delayed ambulation, cavus feet, stocking/glove dysesthesias

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80
Q

Riley Day syndrome

A

AR Ashkenazi Jewish disoerder with dysphagia, sweating, postural hypotension, sensory loss in infancy

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81
Q

Myasthenia gravis treatment

A

Cyclosporine, anti-Ach-ase agents or thymectomy to minimize Ab produced by the thymus that competitively inhibit Ach receptors

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82
Q

Treatment of post-polio syndrome

A

Limited exercise with large periods of rest (sub-exhaustion)

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83
Q

Types of SMA

A

All are AR mutation in SMN (survival motor neuron) causing lack of SMN-1 protein

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84
Q

Metaphyseal diaphyseal angle diagnostic of Blounts disease

A

> 16 degrees

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85
Q

Infantile Blount’s

A

Age < 4, seen more in early walkers and obese children

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86
Q

Deformities seen in Blount’s

A

Varus proximal tibia and internal tibial torsion

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87
Q

Treatment algorithm in Blount’s

A

HK AFO in age <3 and stage I-II.

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88
Q

Treatment of adolescent blount disease

A

Typically unilateral in morbidly obese patients. Treat with hemiepiphysiodesis or osteotomy. Bracing is not effective in this age group.

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89
Q

Causes of in-toeing

A

1) Femoral anteversion, usually resolves, consider derotation osteotomy if lack of 10 deg ER

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90
Q

Miserable malalignment syndrome

A

Femoral anteversion, external tibial torsion and patellofemoral syndrome

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91
Q

Causes of out-toeing

A

1) External tibial torsion, thigh foot angle > 40 deg, may consider supramalleolar osteotomy if age > 8-10, watch closely because it can get worse with growth

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92
Q

Test age for female growth cessation and male growth cessation

A

Females = 14, males = 16

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93
Q

Growth/year at lower extremity physes

A

Proximal femur = 3, distal femur = 9, proximal tibia = 6, distal tibia = 5

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94
Q

Limb length discrepancy treatment.

A

<2cm = observe

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95
Q

Posteromedial tibial bowing association

A

Associated with calcaneovalgus foot, both the foot and bow resolve on their own. May need limgb lengthening 3-4cm later on.

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96
Q

Anteromedial tibial bowing

A

Associated with fibular hemimelia, PFFD and equinovarus foot

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97
Q

Anterolateral tibial bowing

A

Pseudoarthrosis of the tibia seen in patients with neurofibromatosis. Try bracing to prevent fracture from occurring because fixing the fracture is very difficult.

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98
Q

Gene involved in fibular hemimelia

A

Sonic hedge hog gene

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99
Q

Deformity seen in fibular hemimelia

A

LLD, equinovalgus foot, ball and socket ankle, tarsal coalition

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100
Q

What determines treatment in fibular hemimelia

A

3 or fewer rays = amputation. 4-5 rays preserved limb lengthening and epiphysiodesis

101
Q

Tibial hemimelia associations

A

AD, associated with lobster claw hand, equinovarus foot

102
Q

Treatment of tibial hemimelia

A

Depends on quad function, knee disarticulation or BKA w/tib-fib synostosis

103
Q

Etiologies of clubfoot

A

Idiopathic (PITX-1 gene), syndromic

104
Q

Deformities associated with clubfoot

A

Limb length discrepancy, decreased musculature and deficient tibialis anterior

105
Q

X-ray findings in clubfoot

A

Talocalcaneal parallelism with talocalcaneal angle less than 35 degrees on lateral and 20 on AP

106
Q

Series of casts in the Ponseti method

A

1st cast corrects cavus, subsequent casts correct adductus and varus, then finally correct equinus with TAL

107
Q

Risk for recurrent clubfoot

A

Syndromic type and noncompliance with boot/bar bracing up to age of 3

108
Q

Residual dynamic deformity with clubfoot

A

Supination from tibialis anterior, treat with transfer of TA

109
Q

How does surgical posteromedial release compare with the Ponseti method

A

Surgery makes their feet more stiff with worse outcomes

110
Q

Etiologies of congenital vertical talus

A

50% associated with syndromes, spina bifida and chromosomal abnormalities

111
Q

X-ray findings in congenital vertical talus

A

The talus doesn’t line up with the 1st metatarsal or reduce to the navicular on plantarflexion views

112
Q

Management of congenital vertical talus

A

Manipulation and casting, perc TAL, talonavicular capsulotomy and TN pinning once the foot is in a better position from casting

113
Q

Management of calcaneovalgus foot

A

Stretching only, can be associated with posteromedial tibial bowing needing limb length correction later on

114
Q

Differentiate calcaneovalgus foot from congenital vertical talus

A

In calcaneovalgus foot there is excessive foot dorsiflexion but no dislocation of the talonavicular joint

115
Q

Management of metatarsus adductus

A

Check for DDH (associated), 85% resolve spontaneously, may treat with stretching and casting. Lateral closing wedge and medial midfoot opening wedge osteotomy reserved for persistent deformity after age 5

116
Q

Syndromes associated with tarsal coalition

A

FGFR-related craniosynostosis, there are also familial AD inheritance of coalitions

117
Q

Treatment of talocalcaneal coalitions

A

Resection and interposition if <50%, arthrodesis if >50%

118
Q

Treatment of Kohler’s disease

A

Conservative with decreased WB, most resolve

119
Q

Modified Kitner procedure

A

For accessory navicular, excision and PTT advancement

120
Q

Management of curly toe

A

Typically because lateral 3 toe flexors are tight, treat with 3-5 flexor tenotomies

121
Q

Management of pediatric pes planus

A

Conservative management, inserts don’t change the arch, surgical treatment may include lateral column lengthening (Evans) with or without medial column shortening (calcaneo-cuboid-cuneiform osteotomy)

122
Q

Most common scoliosis curve

A

Right thoracic

123
Q

Value threshold for referral in Adam’s forward bend test?

A

7 degree rotational deformity

124
Q

Risser score

A

Physis divided into quarters, fuses from front to back, each quarter is a stage. 1= 25%, 2= 50%, 3 = 75%, 4 = 100%, 5 = fused

125
Q

Indications for MRI in scoliosis

A

Left thoracic curves, apical kyphosis (AIS typically hypokyphotic with apical lordosis), pain, rapid curve progression, neurologic signs, congenital abnormalities, age<10

126
Q

When does peak height velocity occur?

A

Prior to Risser 1 and menarche

127
Q

Factors affecting scoliosis curve progression in adolescents

A

Peak growth velocity, skeletal maturity, curve >20, curve type (thoracic and double more likely to progress)

128
Q

Factors that predict scoliosis progression after skeletal maturity

A

Thoracic curve >50, lumbar curve >30, typically progress 1-2 degrees per year

129
Q

Treatment algorithm for AIS

A

<25 and skeletally immature, observe

130
Q

Indications for anterior and posterior fusion in AIS

A

Less than 10 to limit crankshaft phenomenon (shown below, growth pivots around fusion mass) and sometimes in curves >75

131
Q

Treatment for SMA syndrome after fusion for scoliosis

A

The SMA compresses the 1st/2nd segments of the duodenum between it and the aorta, treatment is NG tube

132
Q

Definition of early onset scoliosis

A

Onset <10 years old

133
Q

Typical curve properties seen in early onset scoliosis that are different from AIS

A

Left thoracic, male predominance

134
Q

Risk of curve progression in early onset scoliosis

A

RVAD > 20 degrees

135
Q

Phase I and phase II ribs

A

Phase I = no overlap on convex side of curve, these are more likely to resolve. Phase II = overlap of rib on convex side of curve, more likely to progress

136
Q

Treatment algorithm in infantile idiopathic scoliosis

A

<20 deg curve, RVAD <20 = observe, 3 mo f/u

137
Q

Effectiveness of casting in infantile idiopathic scoliosis

A

Rule of 1/3’s, 1/3 correct, 1/3 stabilize, 1/3 get worse

138
Q

Congenital spine deformity that is a failure of segmentation

A

Bar

139
Q

Congenital spine deformity that is a failure of formation

A

Hemivertebrae

140
Q

Conditions associated with congenital spine deformity

A

GU in 25%, cardiac in 10%, dysraphism in 25%

141
Q

Risk of family transmission in congenital spine deformity

A

1%

142
Q

Highest risk of curve progression in congenital scoliosis

A

Bar on one side, hemivertebra on the other, progression is near 100%

143
Q

Algorithm for treatment of congenital scoliosis

A

Pre-op MRI, surgery if progression >10 degrees, usually front/back fusion, hemivertebrectomy if large oblique take off

144
Q

Age to consider growing rod construct in scoliosis

A

Up to age 8 because alveoli tend to grow and expand up to this age and you don’t want to restrict lung growth by thoracic insufficiency from early fusion

145
Q

Congenital spine abnormality with highest risk of neurologic compromise

A

Congenital kyphosis

146
Q

Most common site of skeletal involvement in neurofibromatosis

A

Spine

147
Q

Types of scoliosis seen in neurofibromatosis

A

Non-dystrophic (like AIS) and dystrophic (vertebral scalloping, enlarged foramen, penciling of ribs, short segment, sharp curve and kyphoscoliosis)

148
Q

Treatment of scoliosis in neurofibromatosis

A

Non-dystrophic, treat like AIS.

149
Q

Physical exam findings in pediatric spondylolysis

A

Activity related low back pain, tight hamstrings (most common)

150
Q

Most sensitive test for pediatric spondylolysis

A

SPECT

151
Q

Management of spondylolysis

A

Limit activity and brace. If non-op management fails consider repair vs fusion

152
Q

Etiologies for spondylolisthesis

A

Dysplastic, isthmic/lytic, degenerative, traumatic and pathologic

153
Q

Management of pediatric spondylolisthesis

A

Fusion for:

154
Q

Most common complication following high grade spondylolisthesis reduction at L5-S1

A

L5 nerve root injury

155
Q

Scheuermann kyphosis definition

A

> 5 deg wedging in 3 consecutive vertebrae, disc narrowing, endplate irregularities and Schmorl’s nodes

156
Q

Management of Scheuermann kyphosis

A

Mostly non-op, surgery for curves >65-80 degrees

157
Q

Klippel-Feil syndrome triad

A

Low hairline, web neck and limited cervical ROM. X-rays will show abnormal cervical segmentation

158
Q

Conditions associated with Klippel-Feil syndrome

A

Sprengel’s, congenital scoliosis, cardiac and renal abnormalities

159
Q

Management of Klippel-Feil syndrome

A

Conservative, avoid collision sports

160
Q

Indication for fusion in atlanto-axial instability

A

5mm, 10mm if Down’s Syndrome

161
Q

Diagnosis and treatment?

A

Os odontoideum with C1-C2 instability. Confirm on MRI, if odontoid compresses cord then proceed to C1-C2 fusion.

162
Q

C1-C2 rotatory subluxation treatment algorithm

A

NSAID, benzo and collar for 2-3 weeks -> Halter traction -> halo vs C1-C2 fusion

163
Q

Diagnosis in a child less than 8 years old?

A

Pseudosubluxation. The facet orientation in kids <8 is more horizontal and you’ll see subluxation with c-spine flexion. Line drawn is Schwischuk’s line, note how the spinolaminar line of C1 and C3 intersect in the same place as the spinolaminar line of C2

164
Q

Torticollis work up

A

Palpable mass = SCM. If no palpable mass, get an x-ray to rule out other disorders.

165
Q

Risk factors for DDH

A

Breech (most important), first born, female, +FHx

166
Q

Conditions associated with DDH

A

Torticollis and metatarsus adductus

167
Q

Barlow and Ortolani tests

A

Ortolonai = hip is out and reducible. Barlow = hip is in and dislocatable

168
Q

Name the lines

A

A = Perkin’s, B = acetabular index, C = Hilgrenreiner’s, D = nothing, E = Shenton’s

169
Q

DDH management birth to 6 months

A

Pavlik harness, check on u/s at 3 weeks to make sure its reduced, if not, convert to arthrogram, closed reduction and abduction brace vs. spica cast

170
Q

How do you adjust a Pavlik harness

A

Anterior straps = flexion. Posterior straps = abduction.

171
Q

Pavlik disease

A

Posterior acetabulum deficiency from prolonged subluxation in Pavlik harness

172
Q

DDH management 6-12 months

A

Arthrogram, closed vs open reduction and spica casting

173
Q

What is indicated by the red arrow

A

This child had an arthrogram that shows a superolateral filling defect, indicated an inverted limbus blocking the closed reduction

174
Q

Obstructions to hip reduction in DDH

A

TAL, pulvinar, inferomedial capsule, iliopsoas tendon, inverted limbus

175
Q

DDH management >12-18 months

A

Likely open reduction +/- shortening femoral osteotomy to prevent AVN and correct excessive anteversion

176
Q

Up to what age is an isolated femoral osteotomy appropriate in DDH without performing a concomitant pelvic osteotomy

A

4

177
Q

DDH with bilateral dislocation over 6 years old treatment?

A

Leave them alone, non-op, can be well tolerated

178
Q

DDH with unilateral hip dislocation over 8 years old treatment?

A

Non-op, there is minimal remodeling capacity of the acetabulum after age 8

179
Q

Acetabular index indicating hip dysplasia

A

> 30-35 degrees

180
Q

Early treatment of hip dysplasia

A

Abduction brace

181
Q

Differences between Salter, triple, PAO and shelf osteotomies?

A

Salter: hinges on pubic symphysis

182
Q

Diagnosis and treatment?

A

Congenital coxa vara, noted the inverted Y sign and Hilgenreiner-Physeal line > 25 degrees.

183
Q

How to differentiate bilateral Perthes from MED?

A

Perthes with have femoral head collapse in different stages and at different times. MED will be symmetric (shown)

184
Q

Poor prognosis for Perthes

A

Onset 6 years old or later and involving entire femoral head

185
Q

Lateral pillar classification for Perthes

A

A = no hight loss, B = 50%, B/C = lateral pillar narrowed 2-3mm or poorly ossified with 50% height C= >50% height loss

186
Q

Perthes treatment

A

Age >8, bone age >6 and pillar A: abduction bracing to contain the femoral head, crutches to offload and therapy to preserve ROM

187
Q

Southwick classification

A

Slip angle < 30 = mild, 30-50 = moderate, >50 = severe

188
Q

Stable vs unstable SCFE

A

Stable = ambulatory (AVN risk <10%), unstable = unable to walk, AVN risk much higher if unstable

189
Q

Indications for bilateral pinning in SCFE

A

Age <10, endocrine etiology or open tri-radiate cartilage

190
Q

Associated conditions with PFFD

A

50% have fibular hemimelia

191
Q

Gene involved in PFFD

A

Sonic hedge-hog

192
Q

1 year old with bulky thigh, externally rotated femur and coxa vara on radiographs. What else should you look for on exam? Treatment?

A

This patient has congenitally short femur. The majority of these patients will have no ACL. You can lengthen them up to 30%.

193
Q

Why are disarticulations performed in peds but not so much in adults?

A

To limit overgrowth seen in kids after amputation (transmetaphyseal overgrowth > diaphyseal).

194
Q

When to fit kids for prosthetics

A

UE = 6 months (when sitting), LE =12 months (when walking)

195
Q

Treatment of congenital patella dislocation

A

Large open realignment procedure with semitendinosus autograft check rein

196
Q

Management of pediatric popliteal cysts

A

Typically not related to a meniscal tear and resolved with observation

197
Q

Genetic pathways that stimulate normal limb bud development

A

Homeobox (HOX) and sonic hedgehog genes trigger limb bud formation around 6-8 weeks

198
Q

Primary vs secondary ossification center

A

Primary = present at birth. Secondary = develops after birth.

199
Q

Zones of the physis

A

Resting

200
Q

FGFR3 mutation

A

Achondroplasia, rhizomelic dwarfism (proximal segment shorter than the distal segment), gene on Chr 4p16

201
Q

Disproportionate types of dwarfism

A

Short trunk (Kniest, SED) and short limb (Achondroplasia, diastrophic dysplasia)

202
Q

Proportionate types of dwarfism

A

Mucopolysaccharidoses, cleidocranial dysplasia, MED

203
Q

Abnormalities affecting primary ossification center

A

Primary = present at birth = typically diaphyseal defect

204
Q

Cleidocranial dysplasia mutation

A

AD mutation CBFA1 on Chr 6p21 causes mutation in transcription factor for osteocalcin and prevents osteoblast differentiation.

205
Q

Other conditions associated with cleidocranial dysplasia

A

Coxa vara, may need valgus osteotomy if neck shaft angle >100

206
Q

Genetic mutation in this disorder?

A

Rose bud hand seen in Apert’s syndrome. Mutation is FGFR2 causing hand/foot syndactyly and cranial synostosis.

207
Q

Dysplasias affecting secondary ossification centers

A

Secondary ossification = after birth = typically epiphyseal

208
Q

Genetic mutation in this disorder?

A

Note the valgus deformity and irregular bilateral epiphyses, this is MED. They’ll have mild disproportionate dwarfism , are prone to early osteoarthritis and do not have spine involvement (SED).

209
Q

Genetic mutation in this disorder?

A

Note the tongue like projections from the vertebral body. This is SED. Its associated with odontoid hypoplasia (shown), pectus carinatum, kyphosis, hip flexion contractures and equinovarus foot.

210
Q

Genetic mutation in this disorder?

A

This is diastrophic dysplasia with hitchhikers thumb and cauliflower ear. Associated conditions include club feet, dramatic kyphosis (shown, needs urgent tx), scoliosis, rhizomelic dwarfism, fused PIP joints.

211
Q

Zone of physis affected in Achondroplasia

A

AD mutation in FGFR-3 resulting in QUANTITATIVE defect of collagen in proliferative zone

212
Q

Spine findings in achondroplasia

A

Narrow foramen magnum and short/narrow pedicles that can lead to spinal stenosis. Infants have thoracolumbar kyphosis that usually resolves.

213
Q

Diagnosis?

A

Achondroplasia has a champagne glass outlet view of the pelvis

214
Q

MPS with accumulation of dermatan sulfate

A

Hurler’s syndrome, AR defect in alpha-L-iduronidase. Dermatan sulfate accumulation results in CNS toxicity and mental retardation. Treat with bone marrow transplant and enzyme replacement.

215
Q

MPS with accumulation of heparan sulfate

A

San Filippo’s, AR, accumulation of heparan sulfate leads to mental retardation, treat with marrow transplant

216
Q

MPS with accumulation of keratin sulfate

A

Morquio’s, AR mutation resulting in accumulation of keratin sulfate. Associated conditions include genu valgum, cloudy corneas, normal intellect, coxa vara and bullet shaped metacarpals.

217
Q

Spine findings in Morquio’s

A

Odontoid hypoplasia

218
Q

Diagnosis and treatment?

A

Dysplasia Epiphysealis Hemimelica (Trevor’s disease)

219
Q

Genetic defect seen in osteochondromas

A

EXT (loss of Shh regulation)

220
Q

Physeal zone involved in rickets

A

Provisional calcified zone in the hypertrophic zone

221
Q

Cause of vitamin D resistant rickets?

A

XLD. Proximal tubules in kidney unable to reabsorb PO4, Ca normal, PO4 low, Alk Phos elevated

222
Q

Genetic mutation?

A

Osteogenesis imperfecta is a COL1A2 mutation from Gly substitution on procollagen molecule that leads to abnormal crosslinking and weakened collagen. Physeal osteoblasts do not produce sufficient osteoid in the metaphyseal region.

223
Q

Spine association with OI

A

Basilar invagination

224
Q

Treatment of OI

A

IV pamidronate reduces fractures, may need osteotomies and IM implants to reduce fracture rate and deformity

225
Q

Diagnosis and treatment?

A

Scurvy. Occurs secondary to poor Vit C intake that limits conversion of proline to hydroxyproline. X-rays show lucent metaphyseal lines. Replete vitamin C

226
Q

Cause, diagnosis and treatment?

A

This is the rugger jersey spine seen in osteopetrosis. This is from an AR mutation on Chr 11q13 resulting in carbonic anhydrase dysfunction.

227
Q

Neurofibromatosis mutation and syndrome

A

NF1 on Chr 17q21. Café au lait spots, hemihypertrophy, Lisch nodules, scoliosis and anterolateral tibial bowing

228
Q

Marfan’s mutation and syndrome

A

AD mutation in fibrillin gene (FBN1) on Chr 15q21. Arm span greater than height, superior lens dislocation, mitral valve prolapse, hyperlaxity, scoliosis, dural ectasia (shown), protrusion hips and arachnodactyly.

229
Q

Down’s mutation and syndrome.

A

Trisomy 21. Hyperlaxity, heart disease, endocrine disorders, premature aging, C1-C2 instability, patellofemoral instability with high recurrence rate

230
Q

Operative indications for C1-C2 instability in Down’s syndrome

A

> 10mm ADI or neurologic symptoms present

231
Q

Larsen mutation and syndrome.

A

AD or AR mutation in filamin B (cytoskeletal structural protein). They have wide spaced eyes, cleft palate, cervical kyphosis (needs immediate tx because can progress rapidly to myelopathy), scoliosis with posterior element deficient and vertebral body hypoplasia, MULTIPLE JOINT DISLOCATIONS, an accessory calcaneal ossification center and equinovarus or equinovalgus foot deformity.

232
Q

Pediatric patient with Klippel-Feil and limited shoulder abduction

A

Sprengel’s deformity: failure of scapula to descend to thorax and attached to thorax via omovertebral bone.

233
Q

No hx of birth trauma or NF. Diagnosis?

A

Congenital pseudoarthrosis of the clavicle secondary to vascular disruption of medial and lateral ossification center fusion, so always on the right side unless they have dextrocardia.

234
Q

Patient presents with this x-ray. What is the next step?

A

Check a platelet count. Congential absence of the radius is associated with TAR syndrome (AR) and Fanconi’s anemia (AR). Can also have thumb hypoplasia.

235
Q

Contraindications to centralization procedure in congenital absence of radius.

A

Unacceptable anesthetic risk due to other organ disease, inadequate elbow flexion to get hand to mouth

236
Q

How is centralization performed in congenital absence of the radius?

A

Wrist extensors transferred to ECU and ulna is lengthened

237
Q

How do you determine treatment in patients with thumb hypoplasia?

A

CMC stability, needs to be stable enough to allow pinch for reconstruction. If not stable -> ablation and pollicization.

238
Q

Most common direction of congenital radial head dislocation

A

47% anterior, 43% posterior

239
Q

Treatment of congenital radial head dislocation

A

Observation. If they have pain then do radial head resection; however, this will have minimal impact on ROM.

240
Q

Key anatomic structure involved in Madelung’s deformity

A

Vicker’s ligament tethers the volar ulnar corner and causes growth disturbance of the distal radial physis resulting in excessive volar and ulnar angulation.

241
Q

Treatment of Madelung’s

A

If asymptomatic, no treatment.

242
Q

Etiology of proximal radioulnar synostosis?

A

Failure of segmentation as radius and ulna separate from distal to proximal in the neonate. Can be bilateral in up to 60%.

243
Q

Treatment of radioulnar synostosis?

A

If symptomatic, do not resect the synostosis. Perform osteotomy to put forearm in preferred range of motion (30 pronation)

244
Q

Causes of transverse failure of limb formation (congenital amputation)

A

Intrauterine vascular compromise to developing limb bud, misoprostol, EtOH, tobacco and cocaine.

245
Q

Surgical treatment of thumb duplication

A

Bilaut-Cloquet procedure. Fuse duplicated distal phalanx, risk is physeal arrest.

246
Q

When do pediatric trigger thumbs resolve?

A

30% by 1 year, if not resolved, do A1 pulley release

247
Q

Poor prognosis in obstetric brachial plexu palsy

A

No biceps return after 6 months and/or Horner’s syndrome

248
Q

Surgical management of obstetric brachial plexus palsy

A

Contracture release, muscle transfer (get CT pre-op to determine need for osteotomy of humeral head) and nerve grafting

Peds (1 decks)

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