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MSK & Rheum > Mohammad-MSK-Core > Flashcards

Mohammad-MSK-Core Flashcards

1
Q

What’s an antalgic gait?

A

Painful gait

Not wanting to spend time on the affected limb

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2
Q

Differential for an antaglic gait in a 1-3 yr? (6)

A 
Septic Arthritis
Osteo
Fracture
Diskitis 
Neoplasm
Trauma
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3
Q

Causes of abnormal gait? (5)

A 
Pain and limp
Joint abnormalities 
Leg length discrepancies 
Neuromuscular
Toe walking
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4
Q

What’s the most common organism causing Septic arthritis?

A

Staph aureus

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5
Q

Which age group is more likely to get

  • Strep Pneumo
  • Kingella Kingae
  • GBS
  • Gonorrhea
A
  • Strep pneum: <2 yr
  • Kingella Kingae: <5 yrs
  • GBS: neonates
  • Gonorrhea: sexually active adolescents and neos
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6
Q

What are the most commonly affected joints in septic arthritis?

A
  1. Knee
  2. Hip
  3. Ankle
  4. Elbow
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7
Q

What would septic arthritis be commonly associated with in neonates and infants?

A

osteomyelitis: Transphyseal transfer of organisms

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8
Q

Manifestations of septic arthritis?

A
  • Nonspecific in younger children

- Fever, joint swelling, erythema and warmth (seen earlier than in Osteo)

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9
Q

Management of septic arthritis?

A
  • If Hip: surgical emergency
  • Blood culture
  • Joint aspirate for Gram stain and c/s and fluid analysis
  • BW: CBC, CRP and ESR (which might be normal)
  • US
  • Abx in neo: amp/cefotax. In Older: Ancef/Vanco
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10
Q

What’s the most sensitive way of detecting Kingella Kingae?

A

PCR

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11
Q

What position would a septic hip be in?

A

Flexed
Abducted
Externally rotated

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12
Q

What’s metatarsus adductus?

Metatarsus varus?

A

Adductus: Adduction of the forefoot ONLY
Varus: Adduction and supination of the forefoot

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13
Q

what’s a:
forefoot
Midfoot
hindfoot

A

F: toes and matatarsals
M: cuneiforms, navicular, cuboid
H: talus and calcaneus

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14
Q

What causes metatarsus adductus?

A

Intrauterine molding

50% it’s bilateral

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15
Q

What’s the effect of uncorrected metatarsus adductus?

A

In-toe gait
abnormal shoe wear
May have hallux varus (no Tx needed)

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16
Q

Tx of metatarsus adductus?

A

Depends on the rigidity

  • If flexible and overcorrect into abduction w passive
    manipulation: Observe
  • If can correct just to neutral position, provide stretching exercises in the office.
  • If child walking, parents can try reversing shoes
  • If still not working, reverse last shoes prescribed and worn 22hr/day w reassessment in 4-6 wks
  • If no improvement, serial plaster casts should be considered
  • If foot cannot be corrected to neutral position from the beginning, serial casting. Best results before 8 months

-Sx if still no response. Usually delayed until 4-6 yrs

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17
Q

Newborn w metatarsus adductus. Cannot bring foot to neutral position. What to do? Goal behind this Tx?

A

Serial casting
Best results before 8 months

Goal: Stretching, alter physeal growth to promote permanent correction

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18
Q

Patient with Hallux varus. what to do?

A

No Tx.

Improves on its own

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19
Q

What’s Calcaneovalgus foot?

A

Excessive dorsiflexion and eversion of hindfoot.
May have abducted forefoot
May have external tibial torsion

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20
Q

Which deformities has the highest association with Developmental Dysplasia of the hip?

A

Calcaneovalgus foot (19.4%)

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21
Q

Which conditions can lead to calcaneovalgus foot deformities?

A

Polio
Myelomeningocele

Weakness of the gastrocsoleus muscle

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22
Q

Tx of calcaneovalgus foot?

A

if full ROM, observe. Usually resolves in 1wk
Stretching if some restriction
Casting is rarely required

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23
Q

What’s club foot?

A

congenital talipes equinovarus:
Malalignment of the Calcaneotalarnavicular complex

More commonly in males 2:1
50% bilateral

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24
Q

What’s the pathoanatomy of club foot?

A 
CAVE:
Cavus
Adductus
Varus
Equinus

All have calf atrophy
Higher association of DDH
Tibial shortening
leg length discrepancy (shorter ipsilateral)

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25
Q

Causes of club foot?

A
  • Positional
  • Congenital
  • Underlying diagnosis (neuromuscular, syndromic)
  • focal dysplastic
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26
Q

What congenital conditions are associated w club foot?

A

22q11

T18

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27
Q

Risk of clubfoot if one parent and one sibling has clubfoot?

A

25%

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28
Q

Child has clubfoot. What else should he/she be examined for?

A

spinal dysraphism

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29
Q

Treatment of clubfoot?

A 
-OLD: Nonoperative post birth:
Taping and strapping
Manipulation
Serial casting
Functional treatment.

-New: Ponseti method

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30
Q

What are some common long term complication/sequalea of club feet?

A
  • Stiffness

- Pain in adulthood

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31
Q

What’s the Ponseti tx for club foot?

A

CAVE

  • Cast: weekly, usually 5-10x
  • Tenotomy of the heel as an outpatient
  • Long leg cast w foot in maximal abduction and dorsiflexion x 3-4wks
  • Bracing: fulltime for 3 months, nighttime only for 3-5 yrs.
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32
Q

T or F

Most patients w clubfoot require sx.

A

True

Eventually they do

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33
Q

What’s the most common cause of in-toeing in children younger than one year?

A

Metatarsus adductus

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34
Q

What should children with Metatarsus adductus be examined for?

A

DDH

Torticollis

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35
Q

What are some focused physical exam manuever for a child with in toeing?

A
  • Heel bisector line
  • Flexibility of metatarsus adductus
  • Thigh-foot angle
  • Hip rotation
  • DDH
  • Torticollis
  • Ankle ROM
  • Limb length
  • Gait
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36
Q

Indications for surgical referral in a child with intoeing? (6)

A
  • Semiflexible metatarsus adductus post 6 months
  • Rigid metatarsus adductus (at any age)
  • Children ≥8 years with activity limiting or cosmetically unacceptable in-toeing due to tibial torsion
  • Children ≥11 years with activity limiting or cosmetically unacceptable in-toeing due to increased femoral anteversion
  • In-toeing that does not follow the expected course
  • unilateral or asymmetric in-toeing with findings suggestive of cerebral palsy or developmental dysplasia/dislocation of the hip
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37
Q

By what age does metatarsus adductus tend to resolve by

A

-Usually by 1 yr

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38
Q

Most common cause of in toeing in age 1-4?

>3?

A

1-3: Internal tibial rotation. Tends to resolve by 5yr

>3: Increased femur antiversion. Resolves by 11yr. They tend to prefer to sit in W…which should be discouraged

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39
Q

Etiology of Legg Calve Perthes disease ?

A

Unknown etiology

Interruption of blood supply to the proximal fem head/epiphysis leading to osteonecrosis

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40
Q

Most common age for Legg Cave Parthes?

A

Boy more affected than girls
Usually boys 4-8yrs
10% have bilat involvement
Highest in white

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41
Q

Manifestations of Legg Cave Parthes?

A

Limp is most common
Pain w activity
Antalgic gait
May have atrophy of the muscles of the thigh, calf or buttock, from disuse

Limited Hip internal rotation and abduction

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42
Q

how to make the diagnosis of Legg Cave Parthes?Best imaging modality?

A

Imaging
**Need AP and frogleg but xray can only detect later disease and not early

Best imaging:
MRI
If no MRI, Bone scan

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43
Q

What are the radiographic findings in Legg Cave Parthes? (5)

A
  • Decreased size of ossification centre
  • Lateralization of the femoral head
  • Increased widening of the medial joint space
  • Sub chondoral #
  • Irregularity of physis
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44
Q

Differential for avascular necrosis of the femoral head? (5)

A
  • Sickle cell disease
  • Thal
  • Steroid
  • Trauma from hip dislocation
  • Septic arthritis
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45
Q

What endocrine disorder can cause epiphyseal dysplasia?

A

Hypothyroid

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46
Q

Tx for Legg Cave Parthes?

A
  • Activity limitation
  • protected weight bearing
  • NSAIDs
  • Casting (in abduction and internal rotation)
  • Sx
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47
Q

Who does SCFE affect? Pathology? Ethnicity?

A

Older children age 10-16
Failure of the physis and displacement of the femoral head relative to the neck.

Obese African american
More boys

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48
Q

Presentation of SCFE?

A

Chronic presentation is the most common w vague groin, thigh pain w limp

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49
Q

What’s a stable vs unstable SCFE?

A

If able to walk: Stable

Unable or need walking aids: Unstable; higher prevalence of osteonecrosis (likely from the displacement)

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50
Q

What conditions increase the risk of SCFE?

A
  • Hypothyrpoidism
  • Hypopit
  • Renal osteodystrophy
  • Obesity (one of the largest RF)
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51
Q

What’s the ROM like in SCFE? Legg Cave Parthes?

A

SCFE: limited internal rotation and limited abduction and limited flexion

LCP: limited internal rotation and limited abduction

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52
Q

Child w unstable SCFE. Which position would his leg be in?

A
  • Shortened
  • Flexed
  • Externally rotated.
  • Abducted
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53
Q

Which imagings are needed to diagnose SCFE?

A

AP and frog leg of the BOTH hips

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54
Q

What are the ragiographic findings in SCFE?

A
  • widening and irregularity of the physis
  • decrease in epiphyseal height.
  • crescent-shaped area of increased density in the proximal portion of the femoral neck
  • “blanch sign of Steel” :double density from the anteriorly displaced femoral neck overlying the femoral head.
  • Klein’s line no longer intersects the epiphysis
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55
Q

Management of SCFE?

A
  • Admit (MUST ADMIT)
  • Bed rest
  • If obese, investigate for endocrinopathy
  • Goal to close the physis and stabilize it
  • Gold Standard: Pinning the head
  • Prophylactic pinning of other side (20-40% develop contralateral SCFE)
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56
Q

What are the two most serious coplications of SCFE?

A

Osteonecrosis

Chondrolysis

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57
Q

Most common cause of anterior knee pain?

A

Patellofemoral stress syndrom

Diagnosis of exclusion
No explanation for pain.

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58
Q

Description of the pain in patelofemoral stress syndrome?

A
  • Difficult to localize.
  • Common to be bilateral.
  • Worse going up the stairs of after prolonged sitting running
  • No swelling
59
Q

What investigations are needed to diagnose Patelofemoral stress syndrome? How to confirm the diagnosis

A
  • Nothing specific
  • Rarely imaging
  • Diagnosis of exclusion
  • R/O hip pathology
  • Medial patellar tenderness or pain with compression of the patellofemoral joint confirms the diagnosis
60
Q

Tx of patelofemoral stress syndrome?

A
  • Conservative
  • Ice and NSAIDs
  • Reducing acitvity initially w limitation of flexion
  • Improving flexibility, strength and gait abnormalities
  • If there is midfoot hyperpronation (ankle varus) then new shoes to help with arch support might help
  • May consider theraputic taping
61
Q

What’s osgood shlatter disease?

A

Traction apophysitis at the insertion of the patellar tendon on the tibial tuberosity.

62
Q

Tx of Osgood Shlatter? How long does resolution take?

A
  • Protective padding; to protect against direct trauma.
  • Theraputic taping
  • Knee sleeves
  • NSAIDs
  • PRICE

-Resolution is slow taking about 12-18 months

63
Q

Potential complications of Osgood Shlatter? (3)

A

Growth plate arrest
recurvatum deformity
Rupture or avulsion of the patellar tendon

64
Q

Most common mechanism of forearm fracture?

A

Fall On Out Stretched Hand (FOOSH)

65
Q

What’s the most common type of fracture of the forearm?

Difference between buckle and bucket handle?

A

Torus (Buckle): Impacted; cast; heal in 3-4 wks.
Greenstick: one side of the bone; removable splint;

*** Bucket handle aka corner fracture is different and is more suspicious of child abuse in the appropriate context

66
Q

What’s a Colles fracture?

A

Fracture of the distal radius: Fork deformity

67
Q

What’s the most common heridatary neuromuscular disease?

A

Duchenne

68
Q

What are the characteristics of Duchenne? (4)

A
  • Progressive weakness
  • Intellectual impairment
  • Calf hypertrophy
  • Proliferation of connective tissues in muscles.
69
Q

What’s the mode of inheritance of Duchenne?

A

X-linked Ress

70
Q

What’s the difference btw Duchenne and Becker?

A

Essentially the same

Becker is milder.

71
Q

How does Duchenne present at birth/infancy?

A

Essentially normal
Some might have mild hypotonia

Normal facies.

72
Q

What might be the earliest sign of weakness in children with Duchenne?

A

Poor head control.

73
Q

When can Gower’s sign be evident? What’s the Gait like at 5-6 yrs?

A

Usually by 3 yrs.
Fully expressed by 5-6 yrs.
Trendelenburg gait

74
Q

Child suspcted to have Duchenne. Needs to go to Sx. What to worry about?

A

Malignant hyperthermia

75
Q

Manifestations of Duchenne?

A
  • Weakness (resp/pulmonary involvement = more infections, dec respiratory drive, ineffective drive, risk pf aspiration, airy or nasal voice qulity
  • MSK: Contractures and scoliosis. enlargement of calf muscles. Ankles tendons are preserved. Knee reflux eventually get lost.
  • Cardiomyopathies: Tachy and CHF
  • Intellectual impairment
  • Death at around 18-20
76
Q

What’s the second most common site for muscle hypertrophy after the calf in pt with duchenne?

A

The tongue.

77
Q

Features of Beckers that are different than Duchenne?

A
  • Less intellectual disabilities
  • Tend to live longer
  • Onset of weakness if later than duchenne

Rest same including labs

78
Q

Diagnosis of Duchenne?

A

PCR for dystrophin gene mutation
elevated CK

Can do muscle biopsy if blood PCR is negative despite high clinical suspicion.

79
Q

Why might patients with Duchenne have headache in the morning?

A

Due to CO2 retention from slower resp drive on top of poor resp effort.

80
Q 
Manifestation of Lyme disease?
Arthritis pattern
Rash type
Joint affected
ANA/RF
WBC
Presence of systemic symptoms
A
  • Monoarticular
  • Erythema migrans
  • Large joints
  • Negative negative
  • Normal WBC
  • Systemic manifestations: malaise, lethargy, fever, headache, stiff neck, myalgias, and lymphadenopathy. Can have early manifestations w nerve palsy
81
Q

Which organism causes Lyme disease ?

A

Borrelia burgdorferi

82
Q

When does symptoms manifest in Lyme disease?

A

7-14 days.

83
Q

Features of erythema migrans?

A

erythematous papule w red, raised border, and central clearing.
Can be very wide
Pruritic and painful

84
Q

Tx of Lyme disease?

A

Doxy or amox for 14-21 days

If arthritis, amox for 28 days

85
Q

Major complication of Lyme disease?

A

Cardiac: conduction abnormalities

and arthritis

86
Q

Complications associated with Scoliosis? (4)

A

Cardiopulmonary
Back pain
Adverse cosmesis
Poor sitting balance

87
Q

What are the major types/categories of scoliosis? (5)

A 
Idiopathic (most common)
Congenital
Neuromuscular
Syndromic
Compensatory (leg length discrapancy)
88
Q

What are the manifestations of adolescent idiopathic scoliosis? Physical exam findings?

A

Should be asymptomatic, if symptoms needs investigations and imaging.

-Physical exam:
Should height asymmetry
Scapular prominence
Flank crease asymmetry

89
Q

What’s adam’s forward bend test?

A

Test for evaluating for rib hump

90
Q

Management of Adolescent idiopathic scoliosis?

A

Observation:

  • Mild curves <25
  • Mod: 25-45 in patients who skeletally mature

Bracing:
-Mod: 25-45 in skeletally immature patients

Surgery: spinal fusion
-Severe >50

91
Q

What teratogens might be associated w scoliosis?

A

Alcohol

Valporic acid

92
Q

Pt found to have incidental congenital scoliosis. what should he be screened for?

A

VACTERAL

Need US kidney, Echo

93
Q

Treatment of congenital scoliosis?

A

Need close monitoring w serial imaging.

Bracing has poor efficacy

94
Q

Differential of congenital kyphosis?

A
  • Congenital vertebral abnormalities

- Spinal fracture

95
Q

What are two congenital dieases associated w kyphosis?

A

Mucopolysacharidosis

Achondroplasia

96
Q

Which pattern of scoliosis is most common: R or L

A

Right

97
Q

Best determinant of scoliosis on physical exam?

A

Adam’s test

asymmetric rib cage on exam.

98
Q

What’s Caffey’s disease? Onset? Presentation? Lab fingings?

A
  1. Cortical Hyperostosis
  2. Inflammation of the continguous fascia and muscle

Onset usually younger 6 months. Avg 10 wks

Sudden onset irritability
swelling of soft tissue with cortical hyperostosis of the underlying bone
Fever
Anorexia

Lab:
High ESR
High ALP
High IgE

99
Q

What’s the most common bone involved in Caffeys disease? which bones are spared?

A

The mandible
clavicle
ulna

Bone spared: Vertebral bodies and small bones of the phalanges

100
Q

Treatment of Caffeys disease?

A

Indomethacin

and if poor response to indomethacin, give prednisone.

101
Q

Indications for surgical correction of scoliosis?

A
  1. Skaletally immature w progressive curve angle >45
  2. Mature w curve >50
  3. Cardio resp compromise
  4. Cosmesis and functional impariment.
102
Q

T or F

DDH can occur after birth

A

True

103
Q

Risk factors for DDH

A 
Breech
Female
First newborn
FmHx
Oligophydroamnios
Postnatal infant position (lower extremeity swaddling)
Larger birth weight
104
Q

Conditions associated w DDH?

A

Club goot
metatarsus adductus
Cong muscular torticolis

105
Q

Types of DDH?

A

Typical: Normal no neuro concerns
Teratologic: genetic/syndrome occur before birth

106
Q

What maneuvers screen for DDH?

A
  • *Barlow: assessment for possibility of dislocating a non0-displaced hip
  • Adduct and push posteriorly

**Ortolani: Attempt to reduce hip

107
Q

What’s the diagnostic modality for DDH?

A

US

108
Q

Indications for DDH screening?

A

Risk factors for DDH
Suspicious exam
Must be done AFTER 3-4 wks of life

109
Q

Indications for DDH referral to ortho?

A
  1. Unstable, dislocated hip
  2. limited hip abduction or asymmetric hip abduction after
    the neonatal period (4 weeks)
110
Q

Treatment of DDH?

Risk of Tx?

A
  • Initiation of abduction brace (immediate or delayed)
  • if older child 6 months, then Sx (closed reduction)

Risk of Tx: avascular necrosis

111
Q

Causes of Torticollis?

A
  • *Congenital
  • Positional deformity
  • Absence of sternoclidomastoid
  • Vertebral abnormalities (failure of formation, segmentation)
  • Webbed neck
  • unilateral atlantooccipital fusion
  • *Trauma
  • Muscle injury
  • Antlantooccipital subluxation
  • Antlantoaxial subluxation
  • Cervical #
  • *Inflammation:
  • Cervical lymphadinitis
  • RPA
  • Cervical vertb osteo/diskitis
  • JIA
  • *Neurologic
  • Visual (superior oblique or lateral rectus paresis)
  • Cervical cord tumour
  • Posterior fossa tumour
  • Wilson’s
  • *Other
  • Soft tissue tumour
  • Pscyhocogenic
112
Q

Syndromes associated with cervical spine instability? Nongenitc causes?

A

T21
Marfan
Ehler Danlos
22q11.2

Other noncongenital:
Mucopolysaccharidosis
Rickets
Tumor
JIA
113
Q

Which gene is affected in Marfan? Mode of inheritance?

A 
Fibrillin-1 gene Ch 15
Aut Dom (high penetrance)
114
Q

Skeletal Manifestations of Marfans? (7)

A
  • Reduced upper segment to lower body ratio
  • Anterior chest deformity
  • Thoracolumbar scoliosis
  • Inward bulging of the acetabulum into the pelvic cavity
  • Ped planus
  • Joint hypermobility
  • Arachnodactyly (long selender fingers) (wrist sign)
115
Q

Facial manifestations of Marfans? (7)

A
  • Long narrow skull
  • Deep set eyes
  • Recessed lower mandible
  • Small chin
  • Flattening of the mid face
  • High arching palat
  • downeward slanting palpebral fissues
116
Q

What’s the leading cause of mobidity and mortality in children with Marfan?

A

Cardiovascular: Mitral valve prolapse.

This might lead to SVT or ventricular arrhythmias

117
Q

Cardiac manifestations in marfans?

A
  • Dilated cardiomyopathies (progressive dilatation of the aortic root)
  • Mitral valve prolapse
  • Predisposition to arrhythmias
118
Q

What are the three main systems involved in Marfans?

A
  • Skeletal
  • Cardiac
  • Ophthalmic
119
Q

What are the ophthomalgic findings in Marfan?

A
  • High myopia
  • Ectopia lentis
  • Cataracts
  • Increase axial length of the globe
  • Hypoplastic iris
  • Ciliary muscle hypoplasia causing decreased miosis
120
Q

What’s the most life threatening condition in Marfan? what are the two most important factors in predicting Marfans?

A

Aortic root disection

RF: FmHx of dissection and aortic root z-score.

121
Q

Diagnostic criteria for Marfans?

A
  • *Absence of FmHx:
    1. Aortic root z-score >2 AND ectopia lentis
    2. Aortic root z score >2 AND FBN1 gene mutation
    3. Aortic root z score >2 and systemic score >7
    4. Ectopia lentis AND FBN1 gene mutations known to cause aortic root dilatation.
  • *Presence of FmHx
    1. Ectopia lentis
    2. Systemic score >7
    3. Aortic root score >2 if older than 20 or >3 if <20yrs
122
Q

Systemic features (that are scored in Marfans) (12)

A
  1. Wrist AND thumb sign
  2. Pectus craniatum
  3. Dural ectasia
  4. Pneumothorax
  5. Decreased upper to lower limb ratio
  6. Skin striae
  7. Myopia
  8. Facial features
  9. Pes planus
  10. Scoliosis
  11. Reduced elbow extension
  12. Acitabuli protrusio
  13. Mitra valve prolapse
123
Q

Child w marfan wants to lift weight. Yes or NO

A

NO

  • Moderate aerobic exertion is recommended.
  • Strenuous, Contact, or ones w valsalva (wt lifting) NO
124
Q

Indications for aortic root sx in Marfan?

A
  • Diameter approaching 50mm
  • Rapid increase 5-10mm
  • FmHx of dissection
125
Q

Tx of Marfan?

A
  • Genetics counseling

- Evidence for ARB II; prevents pathologic aortic root growth

126
Q

What’s the pathology in a rocker bottom foot?

A

Congenital vertical Talus

Convex plantar surface of the foot. 
Prominent talus
Prominent medial part of the foot
Dorsiflexed forefoot
Hindfoot is equinus
127
Q

Conditions associated with rocker bottom foot?

A

myelodisplasia
Tethered cord
sacral agenesis
T13

128
Q

Tx of congenital vertical talus?

A
  • Serial manipulation and casting shortly after birth

- Surgical: open reduction and pin fixation (usually 6-12 months)

129
Q

Target age group for Legg Cave Parthes vs SCFE? Femoral head shape? Tx

A

LCPD younger
SCFE older

LCPD: smaller femoral head
SCFE: displaced

LCPD: mostly conservative
SCFE: surgical

130
Q

Pathoanatomy of nursemaid elbow? Age?

A

Subluxation of the ligament w Partially torn annular ligament.

Rarely older than 5

Subluxation of the ligament produces pain.
No swelling

131
Q

Tx of nursemaid elbow?

A
  1. Supination, stabilization of radial head and flexion

2. Hyper pronation

132
Q

What’s a bucket handle fracture?

A

Metaphyseal fracture
Aka corner fracture

More suspicious of inflected injury

133
Q

Which side would the neck turn to in Torticollis? Contralaterla or ipsilateral?

A

Contra

134
Q

When does the ligamentous arch develop?

A

5-10 yr

135
Q

Physical exam finding of flexible flat foot?

A
  1. Normal longtitudinal arch when non-weight bearing or when standing on toes.
  2. Arch disappears when standing flat.
  3. Hindfoot valgus
136
Q

Treatment of flexible flat foot?

A
  • Only those who are symptomatic.

- May benefit from non-prescription orthosis such as arch support

137
Q

What symptoms might people with flexible flat foot complain of?

A

Usually asymptomatic
might have hind foot pain
abnormal shoe wear
Fatigue after long walking

138
Q

Who with flat feet might benefit from custom orthosis?

A

Those w severe disease including Ehler danlos and T 21

139
Q

How to differentiate tenosynovitis from Septic arthritis?

A

Kocher criteria:

  • Temp >38.5
  • Not weight bearing
  • ESR >40
  • WBC >12
  • CRP >23.8 (not in original criteria)
140
Q

Manifestations of spina bifida occulta? What would xray show? Investigations?

A

Aka spinal dysraphysim

-Asymptomatic; no neuro findings
-Posterior vertebral body defect.
May have:
-Hemangioma
-Discoloration of the skin
-pit
-lump
-dermal sinus
-hairy patch
**Tend to be above the gluteal folds

Xray may be normal or may show fusion

Investigations:
May start w US
But must get MRI

141
Q

Indications for imaging of a sacral dimple or abnormalities?

A
  1. Subcutaneous mass or lipoma
  2. Hairy patch
  3. Dermal sinus
  4. Atypical dimples (deep, >5 mm, >25 mm from anal verge)
  5. Vascular lesion, e.g., hemangioma or telangiectasia
  6. Skin appendages or polypoid lesions, e.g., skin tags, tail-like appendages
  7. Scar-like lesions
142
Q

What’s a toddler’s fracture?
Age affected?
Mechanism?
Presentation?

A
  • Non-displaced oblique or spiral fracture of the distal tibia
  • No fibula #
  • No significant trauma.
  • No significant trauma
  • Happens in ambulatory kids 9 months - 3 yrs
143
Q

How to differentiate the location of Toddler’s fracture from that of a NAT?

A
  • Toddlers: Lower one third of the tibia

- NAT: Upper two thirds or midshaft.

MSK & Rheum (2 decks)

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