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PT10121 MedSurg3 > L3.3 Spina Bifida > Flashcards

L3.3 Spina Bifida Flashcards

1
Q

Intro to Spina Bifida

Main cause of Spina Bifida

A

Congential Malformations of the vertebral column and spinal cord

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2
Q

Intro to Spina Bifida

Failure of the neural tube to close spontaneously between the ___ and ___ week of in-utero development

A

3rd and 4th Week

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3
Q

Intro to Spina Bifida

Cases are highest amongst this race and gender

A

Whites and Females

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4
Q

Intro to Spina Bifida

Can Spina Bifida be prevented?

A

Yes it can with the use of folic acid

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5
Q

Intro to Spina Bifida

Most infants born myelomeningocele are born to whom?

A

Mothers with no previously affected children

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6
Q

Intro to Spina Bifida

Women with what have a 2-10 fold higher risk

A

Pregentational Diabetes

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7
Q

Intro to Spina Bifida

What are other factors of Spina Bifida?

A
  1. Maternal obesity
  2. Gestational diabetes
  3. Hyperthermia/Maternal Febrile
  4. Intrauterine exposure to antiepileptic drugs
  5. Drugs used to induce ovulation
  6. Low socioeconomic class
  7. Midspring concepttion
  8. Increase maternal age

Intrauterine exposure to antiepileptic drugs (Most Important)

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8
Q

Intro to Spina Bifida

Examples of antiepileptic drugs with teratogenic

A

Valporate and carbamazepine

Both are maintenance for seizure, so change the antipileptic drugs

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9
Q

Intro to Spina Bifida

Recommended Amount of Folic Acid Intake and Time

A

400 nng or 0.4 mg for at least 1 month before conception and during 1st trimester of pregnancy

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10
Q

Intro to Spina Bifida

Recommended Amount of Folic Acid Intake and Time for mother that already has a child with neural tube defect

A

4mg

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11
Q

Pathogenesis

Development of the nervous system during embryonic phase

A

Neurulation

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12
Q

Pathogenesis

Closure of the neural tube thus forming brain and spinal cord (until Day 25)

A

Phase 1

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13
Q

Pathogenesis

Formulation of the caudal structures of the neural tube

Forms the sacral and coccygeal portions (26th day of gestation)

A

Phase 2

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14
Q

Pathogenesis

Failure of closure of the sacral and coccygeal portions results in what?

A

Varying degree of spinal dysraphism

Dysraphism = Incomplete fusion

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15
Q

Pathogenesis

(?) appears as the groove in the epiblast layer

A

Primitive Streak (Week 2)

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16
Q

Pathogenesis

Cells migrate and form 3 germ layers namely: (From most outer layer to most inner)

A
  1. Ectoderm
  2. Mesoderm
  3. Endoderm

By 3rd week, the ectoderm will have a neural tube

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17
Q

Pathogenesis

Week the notochord appears in the mesoderm

A

3rd Week

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18
Q

Pathogenesis

The notochord is what secretes growth factor that stimulates what?

A

Differentiation of the ectoderm to neuroectoderm forming the neural endplate

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19
Q

Pathogenesis

Process of how the neural tube is formed

A

From the neural plate, edges rise to form neurla folrd meetin in the midline and fuse to become the neural tube

This becomes the brain and spinal cord

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20
Q

Pathogenesis

This becomes the peripheral nervous system and autonomic spinal nerves

A

Neural Crest

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21
Q

Pathogenesis

What usually occurs on the 24th day of gestation?

A

Closure of the cranial end

(Also called 38 days from LMP or last menstrual period)

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22
Q

Pathogenesis

What is the result of the failure of closure of the rostal neuropore

Rostal Neuropore - Cranial open end of the neural tube

A

Anencephaly

Defect where the brain and spinal cord have missing parts; Can die early

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23
Q

Pathogenesis

What occurs on the 26th day of gestation?

(40 days of LMP)

A

Closure of the caudal end

Also called Posterior (Caudal) Neuropore

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24
Q

Pathogenesis

Most common lesions when there is defect at the closure of the caudal end?

A

Through mid-lumbar

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25
Q

Pathogenesis

What results from the failure of fusion or closure of the caudal neuropore?

A

Initiates Spina Bifida Cystica or Myelomeningocele

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26
Q

Pathogenesis

Process of the formation of the Spinal Cord

A

Caudal regression and rostral extension

Occurs by Day 53

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27
Q

Pathogenesis

Site of lesion if neural tube does not close by Day 53

A

Lesions at the Lumbosacral Region

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28
Q

Clinical Types & Associated Malformation

Two major types of Spina Bifida

A

Spina Bifida Occulta and Spina Bifida Cystica/Manifesta

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29
Q

Clinical Types & Associated Malformation

Type of Spina Bifida that manifests no symptoms; unidentifiable until seen in an xray

A

Spina Bifida Occulta

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30
Q

Clinical Types & Associated Malformation

Type of Spina Bifida that is dependent on what contains in the cyst

A

Spina Bifida Cystica/Manifesta

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31
Q

Clinical Types & Associated Malformation (Spina Bifida Occulta)

Site of lesion due to the failure of fusion

A

Posterior elements of the vertebrae alone

XRay shows skin is close/tuft of hair at site of lesion

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32
Q

Clinical Types & Associated Malformation (Spina Bifida Cystica)

Type of SB Cystica: Producing sac contains meninged and spinal fluid

A

Meningocele

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33
Q

Clinical Types & Associated Malformation (Spina Bifida Cystica)

Type of SB Cystica: Producing sac contains meninges, spinal cord, spinal fluid

A

Myelomeningocele

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34
Q

Clinical Types & Associated Malformation (Spina Bifida Cystica)

Type SB Cystica: Cystic cavity is in front of the anterior wall of the spinal cord

A

Myelocele

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35
Q

Clinical Types & Associated Malformation (Spina Bifida Occulta)

Associated Findings (seen in 50%)

A
  1. Pinevus Nevus (mole)
  2. Angioma (Blood vessels)
  3. Hirsute Patch (hairy patch)
  4. Dimple or Dermal Sinus Overlying Skin (Tuft of Hair)
  5. Cafe Au Lait Spots (Birthmarks)
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36
Q

Clinical Types & Associated Malformation (Spina Bifida Occulta)

Spinal Cord Level Involved

A

Lumbosacral/Sacral Region (L5 & S1)

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37
Q

Clinical Types & Associated Malformation (Spina Bifida Occulta)

Population Affected

A

5-10% of the Population

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38
Q

Clinical Types & Associated Malformation (Meningocele)

____ and form a cystic sac

A

Meninges herniate

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39
Q

Clinical Types & Associated Malformation (Meningocele)

Contents of Cystic Sac

A

Spinal Fluid Meninges

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40
Q

Clinical Types & Associated Malformation (Meningocele)

Associated Findings

A
  1. W/wo intact skin site of sac
  2. INC skin coverage leads to leakage of CSF
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41
Q

Clinical Types & Associated Malformation (Meningocele)

Clinical Sx

A
  1. Neurological Signs are normal
  2. <10% of cases of SB Cystica
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42
Q

Clinical Types & Associated Malformation (Meningocele)

Spinal Cord Level

A

75% - Lumbar-Lumbosacral
25% - Thoracic

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43
Q

Clinical Types & Associated Malformation (Myelomeningocele)

Contents of Cystic Sac

A
  1. Spinal Fluid
  2. Meninges
  3. Spinal Cord
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44
Q

Clinical Types & Associated Malformation (Myelomeningocele)

Associated Findings

A

Arnold Chiari

Complicated by hydrocephalus in over 90%

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45
Q

Clinical Types & Associated Malformation (Myelomeningocele)

Clinical Sx

A
  1. Motor Paralysis
  2. Sensory Deficits
  3. Neurogenic Bowel and Bladder
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46
Q

Clinical Types & Associated Malformation (Myelomeningocele)

Spinal Cord Level

A

75% at lumbar and lumbosacral segments

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47
Q

Clinical Types & Associated Malformation (Myelomeningocele)

Population affected

A

Majority of the group w/ Spina Bifida Cystica

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48
Q

Clinical Types & Associated Malformation (Myelomeningocele)

What makes the abnormal transmission of nervous impulses impossible resulting in loss of motor and sensory function below the lesion?

A

Abnormal growth of the cord and the tortuous pathway of neural elements

Common in lumbosaral

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49
Q

Clinical Types & Associated Malformation (Myelocele)

Where is the cystic cavity located?

A

In front of the anterior wall of the spinal cord

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50
Q

Clinical Types & Associated Malformation (Myelocele)

Spinal Cord Level

A

75% at the lumbar and lumbosacral

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51
Q

Clinical Types & Associated Malformation (Myelocele)

Cyst pushes the spinal cord out which causes what?

A

Tethered cord and other sx

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52
Q

Clinical Types & Associated Malformation

Occurs when excessive fatty (lipomatous) tissue is within the vertebral canal attached to the spinal cord or filum terminale

A

Lipomeningocele

Development of motor and sensory deficits & can pull spinal cord

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53
Q

Clinical Types & Associated Malformation

Complete absene of skin and sac with exposure of the muscle and presence of a dysplastic spinal cord w/o evidence of a covering

A

Rachischisis

54
Q

Clinical Types & Associated Malformation

Affectation of the caudal part where there is no covering of the spinal cord or skin did not fuse (exposed spinal cord)

A

Craniorachischisis

55
Q

Clinical S/Sx and Course

Clinical Manifestations

A
  1. Motor Loss
  2. Sensory Loss (Neurogenic Bladder)
  3. Learning Disability
  4. Hydrocephalus
56
Q

Clinical S/Sx and Course

Increase level of affectation = ______ IQ

A

Dec IQ

57
Q

Clinical S/Sx and Course

Sacral Affectation =

A

No learning disability

58
Q

Clinical S/Sx and Course

Abnormal accumulation of CSF in the cranial vault d/t overproduction or failure in absorption of fluid/obstruction in the normal CSF flow

A

Hydrocephalus

Accumulation of CSF in the brain & cause pressure

59
Q

Clinical S/Sx and Course

Motor and sensory deficits vary according to?

A

Level and extent of spinal cord anomaly

60
Q

Clinical S/Sx and Course

Affectation @ these sites:
1. Thoracic Lesion leads to

A
  1. Paraplegia
  2. Hyperreflexia (UMNL Sx)
61
Q

Clinical S/Sx and Course

Motor paralysis is usually the what type?

A

LMN type

62
Q

Clinical S/Sx and Course

T/F: Neurogenic bowel and bladder is a common clinical sx

A

True

63
Q

Clinical S/Sx and Course (Thoracic Lesions)

Spares which areas

A

UEs and Abdomen

Everything below will be absent = total paralysis of LE

64
Q

Clinical S/Sx and Course (Thoracic Lesions)

Manifestations in the T6-T12

A
  1. Weakness of intercostals (late sitting), abdominals, and back muscles
  2. Kyphosis and kyphoscoliosis
  3. Flaccid legs/ little spasticity
  4. Flail Paralysis
65
Q

Clinical S/Sx and Course (Thoracic Lesions)

Flail Paralysis Manifestation

A
  1. Hip ER & Abd
  2. Ankle PF d/t gravity
66
Q

Clinical S/Sx and Course (Thoracic Lesions)

Common Findings

A
  1. Contracture of hip & knee flexion + ankle PF
  2. Foot in equinus (PF)
67
Q

Clinical S/Sx and Course (Thoracic Lesions)

L1-L3 Segment Spared

A
  • (+) Hip flexors and Add which can develop early paralytic hip dislocation
  • Gravity-related equinus foot deformity
68
Q

Clinical S/Sx and Course (Thoracic Lesions)

L4 (+) Knee Extensors Spared

A
  • Hip extensors and abductors remain weak
  • Coxa Valga and acetabular dysplasia (slow hip dislocation)
69
Q

Clinical S/Sx and Course (Thoracic Lesions)

L5 (+) Gluteal Max, Medius & Hamstrings Spared

A
  • Less knee extension contracture (possible hip)
  • Knee flexion contracture is possible
  • Foot is in calcaneus attitude
70
Q

Clinical S/Sx and Course (Sacral Lesions)

Manifestations

A
  1. (+) PF Weak
  2. Intrinsic foot muscles still weak; pes cavus with clawing of toes
71
Q

Clinical S/Sx and Course (Associated Malformations)

Not associated with SB occulta but is common in cystica (myelomeningocele)

A

Arnold Chiari Type II

72
Q

Clinical S/Sx and Course (Associated Malformations)

Arnold Chiari Type II Manifestation

A

Caudal displacement or herniation into the cervical spinal canal of the medulla, lower pons, causing an elongation of the 4th ventricle and cerebellar vermis

Associated with hydrocephalus

73
Q

Clinical S/Sx and Course (Associated Malformations)

Sx of Arnold Chiari II

A
  1. Stridor
  2. Apnea
  3. Gastroesophageal reflux
  4. Paralysis of vocal cords
  5. Tongue fasciculations
  6. Facial Palsy
  7. Ataxia

Marami pa pero these are the ones na most likely na lumabas (feeling ko)

74
Q

Clinical S/Sx and Course (Associated Malformations)

Caused by tissue attachments that limit the movement of the spinal cord within the spinal column

Causes abnormal stretching of the spinal cord

A

Tethered Cord Syndrome

20-50% of children

75
Q

Clinical S/Sx and Course (Associated Malformations)

Polymicrogryria, Heterotropia, Hypoplasia of the hypothalamus, and Angenesis of oflactory bulb, tracts, and corpus callosum

A

Forebrain Malformation

76
Q

Clinical S/Sx and Course (Primary Functional Deficits)

Depends on the level and extent of spinal cord anomaly (Motor problem paralysis)

A

Paraplegia

The higher the lesion, the more weakness the patient has

77
Q

Clinical S/Sx and Course (Primary Functional Deficits)

Low IQ, concentration and attention deficits, lower performance scores on visual perception and visual motor task, and personality problem

A

Mental Retardation

78
Q

Clinical S/Sx and Course (Primary Functional Deficits)

Weak fo absent detrusor muscle contraction (Cannot release urine)

Under Neurogenic Sphincter Dysfunction

A

Hypotonic Bladder (LMN)

Emptying is incomplete causes overdistention results to retrograde flow

79
Q

Clinical S/Sx and Course (Primary Functional Deficits)

Voiding bladder is intact w/ detrussor contractions are uninhibited d/t loss of central control

A

Hypertonic Bladder (Spastic)

High intravesical pressure leads to reflux (Incontinence)

80
Q

Clinical S/Sx and Course (Primary Functional Deficits)

Specific severe disturbance of voiding function where bladder and sphincter contractions occur simultaneously

A

Detrusor-Sphincter Dyssynergia

High intravesical pressure leads to reflux

81
Q

Dx and Prognosis

Info from Prenatal Diagnosis

A
  1. (+) Familial History
  2. Measurement of maternal serum and amniotic fluid
  3. Fetal ultrasouns
82
Q

Dx and Prognosis

Alphafetoprotein is normally extreted into?

A

Fetal Urine by babies (found in amniotic fluid)

Peaks at around 6-14 weeks and dec afterwards

83
Q

Dx and Prognosis

Open tube defects allow leakage of fetal CSF leading to?

A

Elevated serum AFP by 13-15th post conceptual week

84
Q

Dx and Prognosis

Usual time of testing in maternal serum is ?

A

16th to 18th week of gestation

85
Q

Dx and Prognosis

Amniocentesis may be done by?

A

16th to 18th week for confirmation

86
Q

Dx and Prognosis

Fetal Ultrasound can be done by

A

16th to 24th weeks of gesatation

87
Q

Dx and Prognosis

Finding in fetal skull d/t loss of normal convex shape of frontal bone and appears flat in patients with SB

A

Lemon Sign

88
Q

Prognosis

Children with prenatally Dx myelomeningocele suggests?

A

Less severe ventroculomegaly

89
Q

Prognosis

Lower anatomic level of lesion on prenatal ultrasonogram predict what?

A

Better developmental outcomes in childhood

90
Q

Prognosis

When can fetal surgery be done

A

20-25 weeks of gestation

Can be done as soon as they diagnose it at 16-24 wks

94% reversal in hindbrain herniation (Arnold Chiari Malformation)

91
Q

Management (Rehabilitation Treatment)

MSK System Treatments

A
  1. Management begins in the newbron
  2. PROM to all joint below level of paralysis
  3. Emphasis on joints with evident muscle imbalance
  4. Frequent turning to avoid contractures and pressure sores
  5. Strengthening exercises for partially innervated muscles
92
Q

Management (Rehabilitation Treatment)

Motor function is close to normal during when?

A

1st half year of life unless complications

Delays are obvious in 2nd half of the 1st year of life

93
Q

Management (Rehabilitation Treatment)

T/F: Provision of adaptive equipment for assisting in early motor milestone and exploratory behavior is not necessary

A

False. It is important

Ex. Chair - to develop balance

94
Q

Management (Rehabilitation Treatment)

When does rolling start if the site of lesion is in the thoracic area?

A

18mo. with compensatory strategies using arm

95
Q

Management (Rehabilitation Treatment)

Patient is able to perform what, if the site of lesion is at the mid lumbar and L5 or sacral region?

A

Get up on hands and knees to crawl

96
Q

Management (Rehabilitation Treatment)

What is needed when the patient has diff in sitting (Lesion at T12)

A

(+) Trunk control

97
Q

Management (Rehabilitation Treatment)

What sitting level is achieved when the site of lesion is mid lumbar?

A

Sit with some delay and increased lordosis

98
Q

Management (Rehabilitation Treatment)

What sitting level can the patient perform when the site of lesion is L4-L5 spared?

A

Child can sit normally

99
Q

Management (Rehabilitation Treatment)

What level of ambulation can the aptient do when the site of lesion is within the thoracic region?

A

Child require assistive devices for passive standing (braces)

Started at 18mos.

100
Q

Management (Rehabilitation Treatment)

What is required of the patient if the site of lesion is at the lower thoracic and lumbar region?

A

Often require devices (reciprocal gait orthosis)

Used after 3yrs old

101
Q

Management (Rehabilitation Treatment)

how is tension created during ambulation?

A

Created by forward stepping which generates extension moment at the contralateral hip

102
Q

Management (Rehabilitation Treatment)

When the L3 is spared, what orthosis is recommended?

A

AFO

103
Q

Management (Rehabilitation Treatment)

In low lumbar lesions, the child should be able to pull to stand and cruise at the usual age like ??

A

10 months

104
Q

Management (Rehabilitation Treatment)

In low lumbar lesions, the child walks at 2y/o with what manifesations?

A
  1. Trendelenburg Lurch (Lurching Gait)
  2. Gastrocnemius limp
105
Q

Management (Rehabilitation Treatment)

At what age can a patient achieve crutch walking when the site of lesion is at the low thoracic lesion and upper lumbar lesion?

A

4-5 years

106
Q

Management (Rehabilitation Treatment)

T/F: Sitting balance and motor level are early predictors of walking.

A

True

The higher the lesion is, the poorer is the prognosis of walking

107
Q

Management (Rehabilitation Treatment)

Unfavorable factors for ambulation

A
  1. Deformities of the spine and lower extremities
  2. Obesity (Harder to lift themselves up)
108
Q

Management (Rehabilitation Treatment)

This orthosis enhances function and mobility of children with T11-L3 deficits from 6-15 y/o

A

Hip Guidance Orthosis

109
Q

Management (Neurological Treatment)

Delay closure for the spinal defect until 3 to 6 mos of age results to what?

A

High mortality rate due to infection

110
Q

Management (Neurological Treatment)

What would an open defect enable?

A

Infection to enter the CNS

111
Q

Management (Neurological Treatment)

What are the criteria for not performing immediate surgery?

A
  1. Complete paralysis of both legs with lesions L1
  2. Significant hydrocephalus with enlarged head present on the first day of life
  3. Serious associted malformation of other organs
  4. Evidence of cerebral birth injury
112
Q

Management (Urologic Treatment)

When does urologic assessment and treatment of bladder dysfunction start?

A

Neonatal period

113
Q

Management (Urologic Treatment)

Primary aims of urologic treatment

A
  1. Control incontinence
  2. Prevent and control infections
  3. Preserve kidney function (most common cause of death)
114
Q

Management (Urologic Treatment)

When should intermittent catherization program begin?

A

Whn residual volume is >/ 20cc

115
Q

Management (Urologic Treatment)

Self-independent catherization may be achieved in what age?

A

5-6 yrs old

116
Q

Management (Urologic Treatment)

T/F: Girls learn intermittent catherization more easily than boys

A

False

117
Q

Management (Urologic Treatment)

When is ICP recommended?

A

Age of 2 years

118
Q

Management (Orthopedic Treatment)

Goal of orthopedic treatment

A

Maintain a stable spine with best possible correction

119
Q

Management (Orthopedic Treatment)

Spinal deformities occur most commonly where?

A

In thoracic lesions with 80-100% of patients affected by the age of 14-15 years

120
Q

Management (Orthopedic Treatment)

Common orthopedic deformities to be addressed

A

Kyphosis, Scoliosis, knee flexion contracture, rigid club foot

121
Q

Management (Orthopedic Treatment)

Orthosis for treatment of mild scoliosis

A

TLSO

122
Q

Management (Orthopedic Treatment)

Treatment for rapidly progressive scoliosis

A

Check for tethered cord which can cause rapid scoliosis (surgical correction)

123
Q

Management (Orthopedic Treatment)

Treatment for Gibbous (Kyphotic) Deformity

A

Kyophectomy

124
Q

Management (Orthopedic Treatment)

Common manifestation in paralytic scoliosis

A

Hip dislocation and pelvic obliquity

125
Q

Management (Orthopedic Treatment)

What is the best course of action when there is bilateral hip dislocation w/o restriction of joint mobility

A

Best left alone if the child will not stand up

Common in upper thorasis lesion

126
Q

Management (Orthopedic Treatment)

Unilateral dislocation or asymmetric contractures may be treated as these can lead to what?

A

Lead to pelvic obliquitym difficulty in sitting, and decubiti (pressure ulcurs)

127
Q

Management (Orthopedic Treatment)

Knee flexion contracture can occur due to?

A

Weak quadriceps, positional factors or poor posture, fx, spasticity

128
Q

Management (Orthopedic Treatment)

Equinus deformity is often treated with?

A

Stertching of the achilles tendon or lengthening (surgical procedure)

129
Q

Management (Orthopedic Treatment)

Treatment for Calcaneus Foot Deformity (Calcaneal Gait)

A

Posterior transfer of tibialis anterior is performed at >5 years of age

130
Q

Management (Orthopedic Treatment)

Treatment used to correct severe claw toe deformity and pes cavus?

A

Flexor tenodesis or transfer and plantar fascia fasciotomy

PT10121 MedSurg3 (8 decks)

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