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MSK > Cortex Spine and Paediatric Orthopaedics > Flashcards

Cortex Spine and Paediatric Orthopaedics Flashcards

1
Q

describe an acute disc tear, its symptoms and management

A

a tear in the outer annulus fibrosis of an intervertebral disc

classically happens after lifting heavy object

periphery of disc highly innervated so pain can be severe- characteristically worse on coughing

symptoms last for 2-3 months, analgesia and physio treatment

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2
Q

where is the most common site for a disc tear with disc material impinging on exiting nerve root to occur

A

L4,5 and S1- sciatica

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3
Q

describe sciatic pain

A

neuralgic burning or severe tinging, radiating down the back of the thigh to below the knee

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4
Q

what tests can you do to prove sciatica

A

sciatic nerve stretch test

cross over sign- sciatic test on other side produces pain on affected side

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5
Q

what pattern of symptoms will an L3/4 prolapse produce

A

L4 root entrapment, pain down to medial ankle, loss of quadriceps power, reduced knee jerk

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6
Q

what pattern of symptoms will an L4/5 prolapse produce

A

L5 root entrapment, pain down dorsum of foot, reduced power to the extensor hallucis longus and tibialis anterior

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7
Q

what pattern of symptoms will an L5/S1 prolapse produce

A

S1 root entrapment, pain to the sole of the foot, reduced power plantarflexion, reduced ankle jerks

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8
Q

what is a radiculpathy

A

impinged nerve

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9
Q

what is the management for a disc prolapse

A

analgesia, maintain mobility, physio

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10
Q

mane a drug that can be used for severe neuropathic pain

A

gabapentin

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11
Q

what surgery might be indicated in severe or non improving cases of a disc prolapse

A

discectomy

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12
Q

in OA of the facet joints what can impinge on nerve roots- what is a possible surgical management

A

osteophytes- surgical depression, trimming of the osteophytes

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13
Q

what is ligamentum flavum

A

ligament that connects the laminae of adjacent vertebrae from C2 to S1

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14
Q

what spinal stenosis

A

narrowing of the spinal canal cause root ischaemia and neurogenic claudication

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15
Q

what can cause spinal stenosis of the cauda equina

A

bulging discs, bulging ligamentum flavum, osteophytosis

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16
Q

who gets spinal stenosis

A

usually over 60s

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17
Q

how is neurogenic claudication different from vascular

A

claudication distance more inconsistant

pain is burning rather than cramps

pain in less walking uphill

pedal pulses are preserved

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18
Q

what surgery can be done if conservative treatment for spinal stenosis (physio and weight loss) doesnt help

A

decompression

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19
Q

what cause cauda equina syndrome

A

a very large central disc prolapse that compresses all nerve roots of the cauda equina

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20
Q

why is cauda equina syndrome a surgical emergency

A

as sacra nerves affected (S4 and 5) controlling defaecation and urination- prolonged compression can cause permanent nerve damage= colostomy, urinary diversion

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21
Q

what is the treatment for cauda equina syndrome

A

urgent MRI to determine the level of the prolapse

urgent discectomy

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22
Q

what are the symptoms of cauda equina syndrome

A

bilateral leg pain, paraesthesia/ numbness, saddle anaesthesia, altered urinary function (urinary retention/ incontinence) or faecal incontinence and constipation

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23
Q

what is considered negligence in cauda equina syndrome

A

not doing a rectal exam

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24
Q

despite surgery, many patients with CA syndrome still have what

A

residual nerve injury with permanent bladder and bowel dysfunction

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25
Q

name 5 red flags an they might indicate

A

back pain in younger patients- osteomyelitis, discitis, (younger children)
spondylolisthesis, benign (osteoid osteoma) and malignant (osteosarcoma) tumours (adolescents)

new backpain in older patients (>60); 
arthritic change (crush fracture), neoplasia- metastatic, multiple myeloma

constant serve pain that is worse at night:
tumour

systemic upset:
(fevers, weight loss, fatigue, malaise) tumour or infection

cauda equina symptoms

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26
Q

what potential investigations could be done if you suspect an infection or tumour

A

bloods (CRP, FBC, U&Es, bone biochemistry, plasma protein electrophoresis, PSA for males, blood culture if suspecting infection), spine xray (may show vertebral collapse of loss of a pedicle on AP view), chest xray, bone scan and MRI scan

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27
Q

what causes crush fractures and what symptoms are produced

A

a result of severe osteoporosis

acute pain and kyphosis

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28
Q

what is the management for a crush fracture

A

conservative

sometimes- balloon vertebroplasty (involves inserting a balloon into the vertebral body under fluoroscopic guidance, inflating a balloon to lift the corticies of the vertebral body) and injecting cement to fill the void)

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29
Q

what is spondylosis

A

degeneration of the intervetebral discs

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30
Q

what are the symptoms and management of spondylosis in the cervical spine

A

slow onset stiffness and pain in the neck which can radiate locally to the shoulders and occiput

physio and analgesics

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31
Q

when can symptoms be felt in cervical spin root impingement

A

upper limb and neck

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32
Q

what is a myelopathy

A

injury to the spinal cord due to severe compression that may result from trauma, congenital stenosis, degenerative disease or disc herniation

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33
Q

what can atraumatic cervical spine instability occur in

A

down syndrome and RA

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34
Q

in RA what can cause atlanto-axial subluxation to occur

A

destruction of the synovial joint between the atlas and then den causing the rupture of the transverse ligament

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35
Q

what is the dens

A

ondontoid process on the axis (C2)

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36
Q

why is subluxation of the cervical spine dangerous

A

can cause fatal chord compression

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37
Q

what is the management for cervical spine suluxation

A

depends on severity: colloar to prevent flexion, surgical fusion

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38
Q

what are unconvertebral joints

A

(from C3 to C7)
as intervetebral discs degenerate the ucinate processes approximate with body of next highest vertebra causing degenerative joint changes

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39
Q

what can cause lower cervical spine subluxations

A

destruction of synovial facet joints and uncovertebral joints

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40
Q

what are upper neuron signs

A

wide based gait, weakness, increased tone, upgoing plantar response

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41
Q

what will peripheral nerve root compression cause

A

symptoms and signs affecting peripheral nerve sensory and motor territories rather than dermatomal and myotomal distributions

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42
Q

what forms the carpal tunnel of the wrist

A

carpal bones and the flexor retinaculum

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43
Q

what passes through the carpal tunnel

A

median nerve and 9 flexor tendons (FDS and FDP to 4 digits + FPL)

have a synovial covering

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44
Q

what happens if there is a swelling in the carpal tunnel

A

median nerve gets compressed

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45
Q

what causes carpal tunnel

A

idiopathic (most cases)

can occur secondary to:
RA (synovitis)
fluid retention (pregnancy, diabetes, chronic renal failure, hypothyroidism (myxoedema))
fractures around wrist (esp colles fracture)

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46
Q

who gets carpal tunnel

A

women 8x more likely than men

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47
Q

what are the symptoms of carpal tunnel

A

parathesiae in the median nerve innervated digits (thumb and radial 2 1/2 fingers)

usually worse at night

loss of sensation and sometime weakness of the thumb

clumsiness in the areas supplied by this nerve

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48
Q

what might be seen on examination of carpal tunnel

A

loss of sensation
weakness
muscle wasting of the thenar eminence

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49
Q

what tests can reproduce symptoms of carpal tunnel

A

Tinel’s (precussing over the median nerve)

phalens (holding the wrists hyper flexed (decreased space in the carpal tunnel)

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50
Q

what is the treatment for carpal tunnel

A

non operative- wrists splints at night to prevent flexion, injection of corticosteroids can help

surgical: carpal tunnel decompression- division of the transverse carpal tunnel ligament under local anaesthetic

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51
Q

what is cubital tunnel syndrome

A

compression of the ulnar nerve at the elbow behind the medial epicondyle (funny bone)

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52
Q

what are the symptoms of cubital tunnel syndrome

A

paraesthesiae in the ulnar 1 1/2 fingers

weakness of ulnar innervated muscles (1st dorsal interosseous (abduction index finger) and adductor pollicis)

tinel’s test usually positive over cubital tunnel

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53
Q

what test can asses the adductor pollicis

A

froments test

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54
Q

what can cause compression of the ulnar nerve

A

tight band of fascia forming the roof of the tunnel (osbornes fascia)

tightness at the intermuscular septum as the nerve passes through the two heads at the origin of flexor carpi ulnaris

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55
Q

what confirms the diagnosis of cubital tunnel and what it the managment

A

nerve conduction studies

may need surgery to release tight structures

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56
Q

what is brittle bone disease

A

osteogenesis imperfecta- defect of the normal maturation and organisation of type 1 collagen (most of bone)

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57
Q

what is the inheritance pattern of the majority of cases of osteogenesis imperfecta

A

autosomal dominant

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58
Q

what are clinical features of osteogenesis imperfecta

A

multiple fragility fractures of childhood, short stature with multiple deformities, blue sclerae, loss of hearing

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59
Q

what are the recessive osteogenesis imperfecta cases

A

rarer- associated with fatality in perinatal period or spinal deformity

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60
Q

what can multiple fractures in childhood be mistaken for

A

child abuse/ non accidental injury

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61
Q

what is osteopenia

A

mid point between healthy bones and osteoporosis

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62
Q

what can cause osteopenia in children and what can it result in

A

prematurity

low energy fractures

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63
Q

what are bones like in osteogenesis imperfecta

A

thin (gracile) with thin cortices and osteopenic

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64
Q

how do fractures tend to heal in osteogenesis imperfecta and how are they treated

A

with abundant but poor quality callus

splintage, traction or surgical stabilisation

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65
Q

what is skeletal dyspalsia

A

short stature, a genetic disorder resulting in abnormal development of bone and connective tissue

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66
Q

what is the inheritance pattern of skeletal dysplasia

A

most common type is achondroplasia- autosomal dominant

80% of cases though sporadic

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67
Q

what is achondroplasia

A

type of skeletal dysplasia causing disproportionately short limbs with a prominent forehead and widened nose

joints are lax and mental development normal

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68
Q

what can skeletal dysplasia other than achondroplasia be associated with

A 
learning difficulties, 
spine deformity, 
limb deformity, 
internal organ dysfunction, 
craniofacial abnormalities, 
skin abnormalities, 
tumour formation (especially haemangiomas), 
joint hypermobility, 
atlanto‐axial subluxation, 
spinal cord compression (myelopathy) 
intrauterine or premature death
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69
Q

what causes connective tissue disorders

A

genetic disorders of collagen synthesis (mainly type 1 found in bone, tendon and ligaments) resulting in joint hypermobility

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70
Q

what type of collagen does osteogenesis impertfecta affect

A

type 1 of bone

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71
Q

what is generalised (familial) joint laxity and what is its inheritance pattern

A

hypermobility of normal joints, seen in 5% of normal people (double jointed)

runs in families in dominant manner

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72
Q

what are people with generalises ligamentous laxity more prone to

A

soft tissue injuries (ankle sprains) and recurrent dislocation of joints (esp shoulder and patella)

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73
Q

what gene mutation causes marfans and how it is passed on

A

mutation of fibrillin gene

autosomal dominant or sporadic mutation

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74
Q

what are the clinical signs of marfans

A

tall stature
disproportionately long limbs
ligamentous laxity
high arched palate
scoiliosis
flattening of the chest (pectus excavatum)
eye problems (lens dislocation, retinal detachment, glaucoma)
aortic aneurysm
cardiac valve incompetence (prolapse and regurgitation)
lungs- spontaneous pneumothorax

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75
Q

what is ehlers danlos syndrome and how is it inherited

A

abnormal elastin and collagen formation causing hypermobility, vascular fragility, easy bruising, joint instability, scoliosis

autosomal dominant

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76
Q

what are the musculoskeletal manifestations of trisomy 21

A

(downs syndrome)

short stature, joint laxity, possible recurrent dislocation (esp patella dislocation and atlanto axial instability)

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77
Q

what is the usual pattern of inheritance of muscular dystrophies

A

x- linked recessive hereditary disorders

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78
Q

who gets x linked disorders

A

boys

79
Q

what are muscular dystrophies

A

genetic ( x linked) disorders resulting in progressive muscle weakness and wasting

80
Q

what mutation cause duchenne muscular dystrophy

A

defect in the dystrophin gene involved in calcium transport

81
Q

what are the clinical signs of duchenne musclar dystrophy

A

progressive muscle weakness, usually noticed when boys start to walk and have difficulty standing (gowers sign) and going up stairs

unable to walk by 10 or so

by the age of 20 will have progressive cardiac and respiratory failure

life expectancy early 20s

82
Q

how can you diagnose duchenne muscular dystrophy

A

raised serum creatinine phosphkinase and abnormalities

83
Q

what can prolong mobility in duhenne musclar dystrophy

A

physio, splintage, deformity correction (severe spinal stenosis)

84
Q

what is becker musclar dystrophy

A

similar to DMD, boys able to walk in teens, LE 30s to 40s

85
Q

what causes neuromusclar disorders

A

abnormal or deficient motor neuron signals to skeletal muscle due to a defect in either the brain, spinal chord, peripheral nerve, NMJ or muscle

86
Q

what is cerebral palsy (cause and onset)

A

neuromuscular disorder with onset before 2-3 years of age due to an insult to the immature brain before, during or after birth

87
Q

what are the causes of cerebral palsy

A

genetic problems, brain malformation, intrauterine infection in early pregnancy, prematurity, intracranial haemorrage, hypoxia during birth, menigitis

88
Q

what are the clinical features of cerebral palsy

A

depends on area of brain affected- can be mild (limited to one limb) or total body involvement with profound learning difficulties. developmental milestones may be missed

89
Q

what is spina bifida

A

congenital disorder where there the two halves of the posterior vertebral arch fail to fuse- probably in the first 6 weeks of gestation

90
Q

what is polio

A

a viral infection which affects motor anterior horn cells in the spinal chord or brainstem resulting in a lower motor neuron deficit- joint deformities and growth defects can occur with shortening of the limb (sensation is preserved)

91
Q

what increases the chances of obstetric brachial plexus injury

A

larger babies (macrosomia in diabetes), twin deliveries, shoulder dystocia (difficult delivery of the shoulder after the head with compression of the shoulder on the pubic symphysis

92
Q

what is Erb’s palsy

A

the commonest type of obstetric brachial palsy- injury to the upper (C5,6) nerve roots resulting in loss of motor innervation of the deltoid, supraspinatus, infraspinatus, biceps and brachialais muscles

93
Q

what are the clinical signs of Erb’s palsy

A

internal rotation of the humerus (from unopposed subscapularis) and may lead to waiter’s tip posture

94
Q

what is the treatment for erb’s palsy

A

physio to prevent contractures- return of biceps function by 6 months in 80-90%

surgical release of contractures and tendon transfers may be required if no recovery

95
Q

what is klumpke’s palsy

A

rarer form of obstetric brachial plexus palsy

lower brachial plexus injury (C8 and T1 roots)

caused by forceful adduction which results in paralysis of the intrinsic muscles of the hand +/- finger, wrsit flexors and possible horners syndrome

poorer prognosis than Erb’s

96
Q

what causes horners syndrome

A

disruption of the first sympathetic ganglion from T1

97
Q

what are the clinical features of klumpkes

A

fingers flexed (due to paralysis of the interossei and lubricals which assist extension at the PIP joints

98
Q

what are the normal neuromuscular landmarks

A 
sits alone, crawls- 6-9 months 
stands- 8-12 months 
walks- 14-17 months 
jumps- 24 months 
manages stairs independently age 3
99
Q

what are the neurological development landmarks

A

loss of primitive reflexes (moro, stepping rooting, grasp, fencing posture) by 1-6 months
head control 2 months
speaking few words 9-12 months
east with fingers, uses spoon 14 months
stacks 4 blocks 18 months
understands 200 words, learns around 10 words/day- 18-20 months
potty trained 2-3 years

100
Q

children are born naturally varus, at what age does the alignment first become neutral

A

14 months

101
Q

when do children become naturally vagus

A

age 3

102
Q

when is valgus or varus pathological

A

when alignment is +/- 6 degrees from mean value for age

103
Q

what can cause a varus or valgum deformity

A

idiopathic, familial

underlying skeletal disorder (skeletal dysplasia, blount’s disease)
physeal injury with growth arrest (usually unilateral)
biochemical disorder (rickets)

104
Q

what is blounts disease

A

growth disease of the medial proximal tibial physis- results in marked and persisting (beyond 4-5 years) varus deformity

105
Q

what are rare causes of genu varum

A

rickets, tumour (osteochondroma), traumatic physeal injury, skeletal dysplasia

106
Q

what are rare causes of geum valgum

A

rickets, tumours (enchondromatosis), trauma and neurofibromatosis

107
Q

how can excessive valgum or varum deformities be corrected

A

osteotomy or growth plate manipulation surgery

108
Q

what is intoeing

A

when a child walks and stands and their feet point toward the midline

109
Q

what exaggerates intoeing

A

running

110
Q

what are additional signs of intoeing

A

parents think they are clumsy, they go through shoes quickly

111
Q

name the 3 causes of intoeing

A

femoral neck anteversion
internal tibial torsion
forefoot adduction

112
Q

describe femoral neck anteversion

A

when the femoral neck points excessively inwards (anteverted) (is naturally anteverted but not to extremes) and gives the appearance of intoeing and knock knees

113
Q

why are internal tibial torsion and forefoot adduction not as important in in toeing

A

surgery should not be considered, they will resolve naturally

114
Q

is flat feet normal

A

everyone born with flat feet, arch develops as you start to walk

some flat feet in adults normal variation

115
Q

what are the types of flat feet and how are they distinguished

A

mobile and fixed

jack test- medial arch forms with dorsiflexion of the great toe

flatfootness may only by dynamic (present on weight bearing)

116
Q

what can cause flexible flat feet in adults

A

ligamentous laxity, may be familial or idiopathic

normal variant in children

117
Q

what might mobile flat feet in adults be related to

A

tibialis posterior tendon dysfunction

118
Q

what can cause rigid flat feet in adults

A

tarsal coalition- where bones of hindfoot have an abnormal bony or cartilaginous connection
inflammatory disorder
neurological disorder

119
Q

what are curly toes and how are they managed

A

minor overlapping of the toes
common
fifth toe most frequently affected
most correct without intervention, can require surgery if cause discomfort or of they persist into adolescence

120
Q

what is developmental dysplasia of the hip

A

dislocation or subluxation of the femoral head during the perinatal period which affects the subsequent development of the hip joint

121
Q

what gender is more likely to get DDH (developmental dysaplasia of the hip)

A

girls

122
Q

which hip is more commonly affected in DDH

A

left, 20% of cases are bilateral

123
Q

what are the risk factors for DDH

A

familial history, breech presentation, first borns, downs syndrome, congenital disorders (talipes, athrogryposis)

124
Q

what happens in DDH is left untreated

A

acetabulum is very shallow

in severe cases a false acetabulum occurs proximal to the original one with a shortened lower limb

severe arthritis due to reduced contact area can occur at a young age and gait/mobility may be severely affected

125
Q

what are signs of DDH on examination after birth

A

shortening, asymmetric groin/ thigh skin creases

click or clunk on the ortolani or barlow maneouvres

126
Q

what is the ortolani test

A

reducing a dislocated hip with abduction and anterior displacement

127
Q

what is barlow test

A

dislocatable hip with flexion and posterior displacement

128
Q

what needs to be done if ortolani or barlow tests are positive

A

ultrasound- should detect dislocated hip, an unstable hip or a shallow acetabulum

x rays after 4-6 months as before this femoral head epiphysis unossified

129
Q

what is the treatment for DDH

A

early diagnosis
mild cases- serial examination to ensure hip remains reduced
pavlik harness for dislocated or persistently unstable hips

persistent dislocation over 18 months= open reduction +/- osteotomy to shorten and rotate femur and pelvic osteotomy

130
Q

what can over flexing and abducting the hip result in in DDH

A

avascular necrosis

131
Q

what is transient synovitis of the hip

A

self limiting inflammation of the synovium of the hip joint

132
Q

what is the typical history preceding transient hip synovitis

A

lips or reluctance to weight bear on affected side
follows URT infection (usually viral)
typically between 2 and 10
boys more commonly affected
range of motion restricted
may have low grade fever but is not systemically unwell

133
Q

what is the commonest cause of hip pain in children

A

transient synovitis

134
Q

what pathologies can cause hip pain in children

A

transient synovitis, septic arthritis, perthes disease, juvenile idiopathic arthritis, RA

135
Q

what investigations can be done into transient synovitis of the hip

A

radiographs can exclude perthes
normal/ near normal CRP can exclude septic arthritis
joint aspiration if doubts of infection
MRI as osteomyelitis possible further diagnosis

136
Q

what is the treatment for transient synovitis of the hip

A

short course of NSAIDs and rest (pain should resolve within a few weeks)

137
Q

what is perthes disease

A

idiopathic osteochondritis (inflammation of cartilage) of the femoral head where the femoral head transiently loses its blood supply resulting in necrosis with subsequent abnormal growth

femoral head may collapse in fracture

138
Q

who gets perthes disease

A

boys (5:1) between 4 and 9

particularly very active boys of short stature

139
Q

what happens if the femoral head collapses in fracture in perthes disease

A

is remodelled- the shape of femoral head and congruence of the joint is determined by age of onset (older= worse prognosis) and amount of collapse

140
Q

what will an incongruent joint cause in perthes

A

early onset arthritis - may require early hip replacement

141
Q

hows does perthes present

A

pain and a limp
loss of internal rotation followed by loss of abduction
positive trendellenburg test from gluteal weakness

142
Q

what might bilateral perthes suggest

A

underlying skeletal dysplasia or a thrombophilia

143
Q

what is the treatment for perthes

A

regular x ray observation, avoidance of physical activity

144
Q

what is the prognosis for perthes

A

50% do well
some cases femoral head becomes aspherical, flattened and widened
lever arm of abductor muscles is altered= weakness= trendellenburg positive
occasionally femoral head maay sublux (partially dislocate) requiring an osteotomy of femur or acetabulum

145
Q

what is SUFE (slipped upper femoral epiphysis)

A

where femoral head epiphysis slips inferiorly in relation to the femoral neck

146
Q

who gets SUFE

A

overweight pre pubertal adolescent boys (more likely than girls)

147
Q

what can predispose to SUFE

A

hypothyroidism and renal disease (puberty may be delayed in hypothyroidism as growth spurt can cause SUFE)

148
Q

what is the pathology of SUFE

A

the growth plate (physis) is not strong enough to support body weight and the femoral head epiphysis slips due to the strain

149
Q

is SUFE uni or bi lateral

A

2/3rds unilateral

150
Q

what is the onset of SUFE

A

can be acute, chronic or acute on chronic

151
Q

what is the presentation of SUFE

A

pain and a limp
pain may be felt in the groin however can purely be pain in knee
loss of internal rotation predominant clinical sign

152
Q

why is SUFE can pain be felt purely in the knee

A

obturator nerve supplying both the hip and knee joint

153
Q

what is the treatment for SUFE

A

urgent surgery to pin femoral head
early hip (teens/ young adult) replacement in severe slip
osteotomy for chronic severe slip

154
Q

what must be examined in patients with knee problems (paeds and adolescents)

A

hip

155
Q

what causes knee extensor mechanisms problems

A

fairly common in adolescence as body weight and sporting activity increases

156
Q

what is jumpers knee and how is it treated

A

patellar tendonitis- self limiting, requires rest ans physio

157
Q

what is apophysitis

A

inflammation of a growing tubercle where a tendon attaches

158
Q

what is patellofemoral dysfunction

A

anterior knee pain

159
Q

who gets anterior knee pain and why

A

adolescent girls (more likely)

unknown- muscle imbalance, ligamentous laxity, subtle skeletal predisposition (genu valgum, wide hips, femoral neck anteversion)

160
Q

what is chondrolmalacia patellae

A

softening of the hyaline cartilage of the patella in anterior knee pain

161
Q

what is the treatment for anterior knee pain

A

most self limiting
physio to re-balance muscles
resistant cases may need tibial tubercle transfer surgery to shift the forces on the patella

162
Q

when in dislocation and subluxation of the patella most common

A

in adolsence

163
Q

what is patellar instability associated with

A

trauma with a tear in the medial patellofemoral ligament

predisposed by ligamentous laxity and variations in bony anatomy

164
Q

what is osteochondritis dissecans

A

an osteochondritis where a fragment of hyaline cartilgae with variable amounts of bone fragments breaks off the surface of the joint

happens most commonly in adolescence

presents with localised pain, effusion, sometimes locking

can predispose to OA

165
Q

can meniscal repair help menisclar tears

A

yes, younger patients have a higher chance of healing

166
Q

what are the most common types of meniscal tears

A

peripheral or bucket handle meniscal tears

167
Q

what is talipes equnovarus

A

club foot

congenital deformity of the foot

168
Q

what causes clubfoot

A

in utero abnormal alignment of the joints between the talus, calcaneus and navicular

this alignament causes contractures of the soft tissues (ligaments, capsule and tendons)

169
Q

how many talipes equinovarus cases are bilateral

A

50%

170
Q

what deformities make up club foot

A

ankle equinus (plantarflexion)

supination of the forefoot

varus alignment of the forefoot

171
Q

which gender is more likely to get club foot

A

boys 2x more likely

172
Q

what can increase chances of club foot

A

male
genetic link
common in breech presentation
oligohydramnios (low amniotic fluid content)
occasionally part of another skeletal dysplasia

173
Q

how is talipes equinovarus treated

A

early splintage- ponseti =technique

80% need tenotomy of achilles tendon for full correction

brace (boots and a bar) worn 23 hours a day for 3 months and then whilst sleeping untill 3/4 years old

late presentations (unlikely) difficult to correct can result in fixed deformity. might need extensive surgery

174
Q

describe the ponseti technique

A

commenced asap after birth

deformities corrected progressively in stages with plaster casts with 5 or 6 weekly cast changes

175
Q

what is tarsal coalition

A

abnormal bridge (bony, fibrous or cartilage) between the calcaneus and navicular or between the talus and calcaneus

can cause fixed flat foot deformity

176
Q

what is scoliosis

A

lateral curvature of the spine (and rotational deformity)

177
Q

what can cause scoliosis

A

idopathic

secondary to neuromusclar disease, tumour (osteo osteoma), skeletal dysplasia or infection

178
Q

how can severe scoliosis affect the lung

A

cause a restrictive lung defect

179
Q

why might surgery be required for scoliosis

A

in large curves for cosmesis or to improve wheelchair posture

180
Q

what is spondylolithesis

A

slippage of one vertebra over another and usually occurs at the L4/5 or L5/S1 level

181
Q

what can cause spondylolithesis

A

developmental defect, recurrent stress fracture which fails to heal

182
Q

true or false: Around the age of 3, children commonely have a valgus knee alignment of around 10-15 degrees?

A

true

183
Q

how does polio enter the body

A

via GI tract with a flu like illness

184
Q

True or false: Osteogenesis imperfecta is a genetic disorder with both autosomal dominent and recessive models of inheritance

A

true

(majority dominant, rarer recessive- fatal in perinatal period or associated with spinal deformity

185
Q

what is internal tibial torsion

A

bone rotated inwards about its vertical axis- should be ignored

186
Q

what is the most common form of cerebral palsy and what area of the brain is affected

A

spastic CP (80%)

injury to the motor cortex, upper motor neurons or corticospinal tract resulting in weakness and spasticity which may worsen as the child grows

187
Q

what area of the brain is affected in ataxic CP

A

cerebellum (reduces coordination and balance)

188
Q

what area of the brain is affected is athetoid CP

A

extrapyramidal motor system, pyramidal tract, basal ganglia

(uncontrolled writhing motion, sudden changes in tone and difficulty controlling speech

189
Q

when and how does spondylolisthesis usually present

A

in adolescence (increased body weight and sporting activity)

low back pain, radiculopathy (pinched nerve) with severe slippage, flat back due to muscle spasm, waddling gait

190
Q

True or false: ‘Spina bifida occulta’ describes the milder end of the spina bifida spectrum.

A

true

191
Q

what are the tell tale signs of spina befida occulta

A

dimple and tuft of hair on skin overlying the defect

192
Q

what nerve will a lateral L4/5 disc prolapse afffect

A

L4 exiting nerve

193
Q

True or false: Patients with rheumatoid arthritis are at greater risk of atraumatic cervical spine instability.

A

true (also true for downs syndrome)

MSK (71 decks)

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