Cortex Spine and Paediatric Orthopaedics Flashcards
describe an acute disc tear, its symptoms and management
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
where is the most common site for a disc tear with disc material impinging on exiting nerve root to occur
L4,5 and S1- sciatica
describe sciatic pain
neuralgic burning or severe tinging, radiating down the back of the thigh to below the knee
what tests can you do to prove sciatica
sciatic nerve stretch test
cross over sign- sciatic test on other side produces pain on affected side
what pattern of symptoms will an L3/4 prolapse produce
L4 root entrapment, pain down to medial ankle, loss of quadriceps power, reduced knee jerk
what pattern of symptoms will an L4/5 prolapse produce
L5 root entrapment, pain down dorsum of foot, reduced power to the extensor hallucis longus and tibialis anterior
what pattern of symptoms will an L5/S1 prolapse produce
S1 root entrapment, pain to the sole of the foot, reduced power plantarflexion, reduced ankle jerks
what is a radiculpathy
impinged nerve
what is the management for a disc prolapse
analgesia, maintain mobility, physio
mane a drug that can be used for severe neuropathic pain
gabapentin
what surgery might be indicated in severe or non improving cases of a disc prolapse
discectomy
in OA of the facet joints what can impinge on nerve roots- what is a possible surgical management
osteophytes- surgical depression, trimming of the osteophytes
what is ligamentum flavum
ligament that connects the laminae of adjacent vertebrae from C2 to S1
what spinal stenosis
narrowing of the spinal canal cause root ischaemia and neurogenic claudication
what can cause spinal stenosis of the cauda equina
bulging discs, bulging ligamentum flavum, osteophytosis
who gets spinal stenosis
usually over 60s
how is neurogenic claudication different from vascular
claudication distance more inconsistant
pain is burning rather than cramps
pain in less walking uphill
pedal pulses are preserved
what surgery can be done if conservative treatment for spinal stenosis (physio and weight loss) doesnt help
decompression
what cause cauda equina syndrome
a very large central disc prolapse that compresses all nerve roots of the cauda equina
why is cauda equina syndrome a surgical emergency
as sacra nerves affected (S4 and 5) controlling defaecation and urination- prolonged compression can cause permanent nerve damage= colostomy, urinary diversion
what is the treatment for cauda equina syndrome
urgent MRI to determine the level of the prolapse
urgent discectomy
what are the symptoms of cauda equina syndrome
bilateral leg pain, paraesthesia/ numbness, saddle anaesthesia, altered urinary function (urinary retention/ incontinence) or faecal incontinence and constipation
what is considered negligence in cauda equina syndrome
not doing a rectal exam
despite surgery, many patients with CA syndrome still have what
residual nerve injury with permanent bladder and bowel dysfunction
name 5 red flags an they might indicate
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
what potential investigations could be done if you suspect an infection or tumour
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
what causes crush fractures and what symptoms are produced
a result of severe osteoporosis
acute pain and kyphosis
what is the management for a crush fracture
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)
what is spondylosis
degeneration of the intervetebral discs
what are the symptoms and management of spondylosis in the cervical spine
slow onset stiffness and pain in the neck which can radiate locally to the shoulders and occiput
physio and analgesics
when can symptoms be felt in cervical spin root impingement
upper limb and neck
what is a myelopathy
injury to the spinal cord due to severe compression that may result from trauma, congenital stenosis, degenerative disease or disc herniation
what can atraumatic cervical spine instability occur in
down syndrome and RA
in RA what can cause atlanto-axial subluxation to occur
destruction of the synovial joint between the atlas and then den causing the rupture of the transverse ligament
what is the dens
ondontoid process on the axis (C2)
why is subluxation of the cervical spine dangerous
can cause fatal chord compression
what is the management for cervical spine suluxation
depends on severity: colloar to prevent flexion, surgical fusion
what are unconvertebral joints
(from C3 to C7)
as intervetebral discs degenerate the ucinate processes approximate with body of next highest vertebra causing degenerative joint changes
what can cause lower cervical spine subluxations
destruction of synovial facet joints and uncovertebral joints
what are upper neuron signs
wide based gait, weakness, increased tone, upgoing plantar response
what will peripheral nerve root compression cause
symptoms and signs affecting peripheral nerve sensory and motor territories rather than dermatomal and myotomal distributions
what forms the carpal tunnel of the wrist
carpal bones and the flexor retinaculum
what passes through the carpal tunnel
median nerve and 9 flexor tendons (FDS and FDP to 4 digits + FPL)
have a synovial covering
what happens if there is a swelling in the carpal tunnel
median nerve gets compressed
what causes carpal tunnel
idiopathic (most cases)
can occur secondary to:
RA (synovitis)
fluid retention (pregnancy, diabetes, chronic renal failure, hypothyroidism (myxoedema))
fractures around wrist (esp colles fracture)
who gets carpal tunnel
women 8x more likely than men
what are the symptoms of carpal tunnel
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
what might be seen on examination of carpal tunnel
loss of sensation
weakness
muscle wasting of the thenar eminence
what tests can reproduce symptoms of carpal tunnel
Tinel’s (precussing over the median nerve)
phalens (holding the wrists hyper flexed (decreased space in the carpal tunnel)
what is the treatment for carpal tunnel
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
what is cubital tunnel syndrome
compression of the ulnar nerve at the elbow behind the medial epicondyle (funny bone)
what are the symptoms of cubital tunnel syndrome
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
what test can asses the adductor pollicis
froments test
what can cause compression of the ulnar nerve
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
what confirms the diagnosis of cubital tunnel and what it the managment
nerve conduction studies
may need surgery to release tight structures
what is brittle bone disease
osteogenesis imperfecta- defect of the normal maturation and organisation of type 1 collagen (most of bone)
what is the inheritance pattern of the majority of cases of osteogenesis imperfecta
autosomal dominant
what are clinical features of osteogenesis imperfecta
multiple fragility fractures of childhood, short stature with multiple deformities, blue sclerae, loss of hearing
what are the recessive osteogenesis imperfecta cases
rarer- associated with fatality in perinatal period or spinal deformity
what can multiple fractures in childhood be mistaken for
child abuse/ non accidental injury
what is osteopenia
mid point between healthy bones and osteoporosis
what can cause osteopenia in children and what can it result in
prematurity
low energy fractures
what are bones like in osteogenesis imperfecta
thin (gracile) with thin cortices and osteopenic
how do fractures tend to heal in osteogenesis imperfecta and how are they treated
with abundant but poor quality callus
splintage, traction or surgical stabilisation
what is skeletal dyspalsia
short stature, a genetic disorder resulting in abnormal development of bone and connective tissue
what is the inheritance pattern of skeletal dysplasia
most common type is achondroplasia- autosomal dominant
80% of cases though sporadic
what is achondroplasia
type of skeletal dysplasia causing disproportionately short limbs with a prominent forehead and widened nose
joints are lax and mental development normal
what can skeletal dysplasia other than achondroplasia be associated with
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
what causes connective tissue disorders
genetic disorders of collagen synthesis (mainly type 1 found in bone, tendon and ligaments) resulting in joint hypermobility
what type of collagen does osteogenesis impertfecta affect
type 1 of bone
what is generalised (familial) joint laxity and what is its inheritance pattern
hypermobility of normal joints, seen in 5% of normal people (double jointed)
runs in families in dominant manner
what are people with generalises ligamentous laxity more prone to
soft tissue injuries (ankle sprains) and recurrent dislocation of joints (esp shoulder and patella)
what gene mutation causes marfans and how it is passed on
mutation of fibrillin gene
autosomal dominant or sporadic mutation
what are the clinical signs of marfans
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
what is ehlers danlos syndrome and how is it inherited
abnormal elastin and collagen formation causing hypermobility, vascular fragility, easy bruising, joint instability, scoliosis
autosomal dominant
what are the musculoskeletal manifestations of trisomy 21
(downs syndrome)
short stature, joint laxity, possible recurrent dislocation (esp patella dislocation and atlanto axial instability)
what is the usual pattern of inheritance of muscular dystrophies
x- linked recessive hereditary disorders
who gets x linked disorders
boys
what are muscular dystrophies
genetic ( x linked) disorders resulting in progressive muscle weakness and wasting
what mutation cause duchenne muscular dystrophy
defect in the dystrophin gene involved in calcium transport
what are the clinical signs of duchenne musclar dystrophy
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
how can you diagnose duchenne muscular dystrophy
raised serum creatinine phosphkinase and abnormalities
what can prolong mobility in duhenne musclar dystrophy
physio, splintage, deformity correction (severe spinal stenosis)
what is becker musclar dystrophy
similar to DMD, boys able to walk in teens, LE 30s to 40s
what causes neuromusclar disorders
abnormal or deficient motor neuron signals to skeletal muscle due to a defect in either the brain, spinal chord, peripheral nerve, NMJ or muscle
what is cerebral palsy (cause and onset)
neuromuscular disorder with onset before 2-3 years of age due to an insult to the immature brain before, during or after birth
what are the causes of cerebral palsy
genetic problems, brain malformation, intrauterine infection in early pregnancy, prematurity, intracranial haemorrage, hypoxia during birth, menigitis
what are the clinical features of cerebral palsy
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
what is spina bifida
congenital disorder where there the two halves of the posterior vertebral arch fail to fuse- probably in the first 6 weeks of gestation
what is polio
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)
what increases the chances of obstetric brachial plexus injury
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
what is Erb’s palsy
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
what are the clinical signs of Erb’s palsy
internal rotation of the humerus (from unopposed subscapularis) and may lead to waiter’s tip posture
what is the treatment for erb’s palsy
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
what is klumpke’s palsy
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
what causes horners syndrome
disruption of the first sympathetic ganglion from T1
what are the clinical features of klumpkes
fingers flexed (due to paralysis of the interossei and lubricals which assist extension at the PIP joints
what are the normal neuromuscular landmarks
sits alone, crawls- 6-9 months stands- 8-12 months walks- 14-17 months jumps- 24 months manages stairs independently age 3
what are the neurological development landmarks
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
children are born naturally varus, at what age does the alignment first become neutral
14 months
when do children become naturally vagus
age 3
when is valgus or varus pathological
when alignment is +/- 6 degrees from mean value for age
what can cause a varus or valgum deformity
idiopathic, familial
underlying skeletal disorder (skeletal dysplasia, blount’s disease)
physeal injury with growth arrest (usually unilateral)
biochemical disorder (rickets)
what is blounts disease
growth disease of the medial proximal tibial physis- results in marked and persisting (beyond 4-5 years) varus deformity
what are rare causes of genu varum
rickets, tumour (osteochondroma), traumatic physeal injury, skeletal dysplasia
what are rare causes of geum valgum
rickets, tumours (enchondromatosis), trauma and neurofibromatosis
how can excessive valgum or varum deformities be corrected
osteotomy or growth plate manipulation surgery
what is intoeing
when a child walks and stands and their feet point toward the midline
what exaggerates intoeing
running
what are additional signs of intoeing
parents think they are clumsy, they go through shoes quickly
name the 3 causes of intoeing
femoral neck anteversion
internal tibial torsion
forefoot adduction
describe femoral neck anteversion
when the femoral neck points excessively inwards (anteverted) (is naturally anteverted but not to extremes) and gives the appearance of intoeing and knock knees
why are internal tibial torsion and forefoot adduction not as important in in toeing
surgery should not be considered, they will resolve naturally
is flat feet normal
everyone born with flat feet, arch develops as you start to walk
some flat feet in adults normal variation
what are the types of flat feet and how are they distinguished
mobile and fixed
jack test- medial arch forms with dorsiflexion of the great toe
flatfootness may only by dynamic (present on weight bearing)
what can cause flexible flat feet in adults
ligamentous laxity, may be familial or idiopathic
normal variant in children
what might mobile flat feet in adults be related to
tibialis posterior tendon dysfunction
what can cause rigid flat feet in adults
tarsal coalition- where bones of hindfoot have an abnormal bony or cartilaginous connection
inflammatory disorder
neurological disorder
what are curly toes and how are they managed
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
what is developmental dysplasia of the hip
dislocation or subluxation of the femoral head during the perinatal period which affects the subsequent development of the hip joint
what gender is more likely to get DDH (developmental dysaplasia of the hip)
girls
which hip is more commonly affected in DDH
left, 20% of cases are bilateral
what are the risk factors for DDH
familial history, breech presentation, first borns, downs syndrome, congenital disorders (talipes, athrogryposis)
what happens in DDH is left untreated
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
what are signs of DDH on examination after birth
shortening, asymmetric groin/ thigh skin creases
click or clunk on the ortolani or barlow maneouvres
what is the ortolani test
reducing a dislocated hip with abduction and anterior displacement
what is barlow test
dislocatable hip with flexion and posterior displacement
what needs to be done if ortolani or barlow tests are positive
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
what is the treatment for DDH
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
what can over flexing and abducting the hip result in in DDH
avascular necrosis
what is transient synovitis of the hip
self limiting inflammation of the synovium of the hip joint
what is the typical history preceding transient hip synovitis
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
what is the commonest cause of hip pain in children
transient synovitis
what pathologies can cause hip pain in children
transient synovitis, septic arthritis, perthes disease, juvenile idiopathic arthritis, RA
what investigations can be done into transient synovitis of the hip
radiographs can exclude perthes
normal/ near normal CRP can exclude septic arthritis
joint aspiration if doubts of infection
MRI as osteomyelitis possible further diagnosis
what is the treatment for transient synovitis of the hip
short course of NSAIDs and rest (pain should resolve within a few weeks)
what is perthes disease
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
who gets perthes disease
boys (5:1) between 4 and 9
particularly very active boys of short stature
what happens if the femoral head collapses in fracture in perthes disease
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
what will an incongruent joint cause in perthes
early onset arthritis - may require early hip replacement
hows does perthes present
pain and a limp
loss of internal rotation followed by loss of abduction
positive trendellenburg test from gluteal weakness
what might bilateral perthes suggest
underlying skeletal dysplasia or a thrombophilia
what is the treatment for perthes
regular x ray observation, avoidance of physical activity
what is the prognosis for perthes
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
what is SUFE (slipped upper femoral epiphysis)
where femoral head epiphysis slips inferiorly in relation to the femoral neck
who gets SUFE
overweight pre pubertal adolescent boys (more likely than girls)
what can predispose to SUFE
hypothyroidism and renal disease (puberty may be delayed in hypothyroidism as growth spurt can cause SUFE)
what is the pathology of SUFE
the growth plate (physis) is not strong enough to support body weight and the femoral head epiphysis slips due to the strain
is SUFE uni or bi lateral
2/3rds unilateral
what is the onset of SUFE
can be acute, chronic or acute on chronic
what is the presentation of SUFE
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
why is SUFE can pain be felt purely in the knee
obturator nerve supplying both the hip and knee joint
what is the treatment for SUFE
urgent surgery to pin femoral head
early hip (teens/ young adult) replacement in severe slip
osteotomy for chronic severe slip
what must be examined in patients with knee problems (paeds and adolescents)
hip
what causes knee extensor mechanisms problems
fairly common in adolescence as body weight and sporting activity increases
what is jumpers knee and how is it treated
patellar tendonitis- self limiting, requires rest ans physio
what is apophysitis
inflammation of a growing tubercle where a tendon attaches
what is patellofemoral dysfunction
anterior knee pain
who gets anterior knee pain and why
adolescent girls (more likely)
unknown- muscle imbalance, ligamentous laxity, subtle skeletal predisposition (genu valgum, wide hips, femoral neck anteversion)
what is chondrolmalacia patellae
softening of the hyaline cartilage of the patella in anterior knee pain
what is the treatment for anterior knee pain
most self limiting
physio to re-balance muscles
resistant cases may need tibial tubercle transfer surgery to shift the forces on the patella
when in dislocation and subluxation of the patella most common
in adolsence
what is patellar instability associated with
trauma with a tear in the medial patellofemoral ligament
predisposed by ligamentous laxity and variations in bony anatomy
what is osteochondritis dissecans
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
can meniscal repair help menisclar tears
yes, younger patients have a higher chance of healing
what are the most common types of meniscal tears
peripheral or bucket handle meniscal tears
what is talipes equnovarus
club foot
congenital deformity of the foot
what causes clubfoot
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)
how many talipes equinovarus cases are bilateral
50%
what deformities make up club foot
ankle equinus (plantarflexion)
supination of the forefoot
varus alignment of the forefoot
which gender is more likely to get club foot
boys 2x more likely
what can increase chances of club foot
male
genetic link
common in breech presentation
oligohydramnios (low amniotic fluid content)
occasionally part of another skeletal dysplasia
how is talipes equinovarus treated
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
describe the ponseti technique
commenced asap after birth
deformities corrected progressively in stages with plaster casts with 5 or 6 weekly cast changes
what is tarsal coalition
abnormal bridge (bony, fibrous or cartilage) between the calcaneus and navicular or between the talus and calcaneus
can cause fixed flat foot deformity
what is scoliosis
lateral curvature of the spine (and rotational deformity)
what can cause scoliosis
idopathic
secondary to neuromusclar disease, tumour (osteo osteoma), skeletal dysplasia or infection
how can severe scoliosis affect the lung
cause a restrictive lung defect
why might surgery be required for scoliosis
in large curves for cosmesis or to improve wheelchair posture
what is spondylolithesis
slippage of one vertebra over another and usually occurs at the L4/5 or L5/S1 level
what can cause spondylolithesis
developmental defect, recurrent stress fracture which fails to heal
true or false: Around the age of 3, children commonely have a valgus knee alignment of around 10-15 degrees?
true
how does polio enter the body
via GI tract with a flu like illness
True or false: Osteogenesis imperfecta is a genetic disorder with both autosomal dominent and recessive models of inheritance
true
(majority dominant, rarer recessive- fatal in perinatal period or associated with spinal deformity
what is internal tibial torsion
bone rotated inwards about its vertical axis- should be ignored
what is the most common form of cerebral palsy and what area of the brain is affected
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
what area of the brain is affected in ataxic CP
cerebellum (reduces coordination and balance)
what area of the brain is affected is athetoid CP
extrapyramidal motor system, pyramidal tract, basal ganglia
(uncontrolled writhing motion, sudden changes in tone and difficulty controlling speech
when and how does spondylolisthesis usually present
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
True or false: ‘Spina bifida occulta’ describes the milder end of the spina bifida spectrum.
true
what are the tell tale signs of spina befida occulta
dimple and tuft of hair on skin overlying the defect
what nerve will a lateral L4/5 disc prolapse afffect
L4 exiting nerve
True or false: Patients with rheumatoid arthritis are at greater risk of atraumatic cervical spine instability.
true (also true for downs syndrome)
