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Musculoskeletal MBCHB > Growth and Development Disorders > Flashcards

Growth and Development Disorders Flashcards

1
Q

When do brachial plexus injuries occur?

A

The incidence of brachial plexus injury during vaginal delivery is around 2 in 1000 and most commonly arises in large babies (macrosomia in diabetes), twin deliveries and shoulder dystocia (difficult delivery of the shoulder after the head with compression of the shoulder on the pubic symphysis)

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2
Q

What is the aetiology of Erb’s palsy?

A

Injury to the upper (C5 + C6) nerve roots resulting in loss of motor innervation of the deltoid, supraspinatus, infraspinatus, biceps and brachialis muscles

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3
Q

What is the presentation of Erb’s palsy?

A

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

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4
Q

What is the management of Erb’s palsy?

A
  • Physiotherapy is required to prevent contractures early on and prognosis is predicted by the return of biceps function by 6 months with good outcome in 80‐90% of cases
  • Surgical release of contractures and tendon transfers may be required if no recovery
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5
Q

What is the aetiology of Klumpke’s palsy?

A

Lower brachial plexus injury (C8 + T1 roots) caused by forceful adduction

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6
Q

What is the presentation of Klumpke’s palsy?

A
  • Injury results in paralysis of the intrinsic hand muscles +/‐ finger and wrist flexors and possible Horner’s syndrome (due to disruption of the first sympathetic ganglion from T1)
  • The fingers are typically flexed (due to paralysis of the interossei and lumbricals which assist extension at the PIP joints)
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7
Q

What is the management of Klumpke’s palsy?

A

Prognosis is poorer than for Erb’s palsy with less than 50% recovery and there is no specific treatment

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8
Q

What is valgus deformity?

A

A valgus deformity at the knee will result in a more of a knock kneeappearance with a larger gap than normal between the feet/ankles

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9
Q

What is varus deformity?

A

A varus deformity will result in a larger gap between the knees

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10
Q

What is the management of varus and valgus knee alignment deformity?

A

The majority of cases of bow legs or knock knees will resolve by the age of 10 but genu varum or excessive genu valgum after the age of 10 may require surgery

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11
Q

What are the causes of valgus or varus deformity?

A
  • Many cases are idiopathic, whilst some are familial
  • Some cases may be due to an underlying skeletal disorder (skeletal dysplasia, Blount’s disease), physeal injury with growth arrest (usually unilateral) or biochemical disorder (rickets)
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12
Q

What is in-toeing?

A
  • Referstoachildwho,whenwalkingandstandingwillhavefeetthatpointtowardthemidline
  • Theabnormalityisoftenexaggeratedwhenrunningandchildren are feltbytheirparentstobeclumsyandwearthroughshoesatanalarmingrate
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13
Q

What causes in-toeing?

A

Thereareanumberofcausesofin‐toeing including internal tibial torsion and metatarsus adductus

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14
Q

What is femoral neck anteversion?

A
  • Aspartofnormalanatomythefemoralneckisslightlyanteverted (pointingforwards)
  • Excessfemoralneckanteversioncangivetheappearanceofin-toeing(aswellasknockknees)
  • Howeverthedegreeofapparentintoeingisnotofamagnitudewhichwouldwarrant surgicalintervention
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15
Q

What is the aetiology of flat feet?

A
  • Can be a normal variation affecting up to 20% of the population where the medial arch does not develop in childhood
  • May have a familial tendency
  • Patients with generalized ligamentous laxity are more likely to have flat feet
  • Acquired flat foot may be due to tibialis posterior tendon stretch or rupture, rheumatoid arthritis or diabetes with Charcot foot (neuropathic joint destruction)
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16
Q

What is mobile flat feet?

A

Mobile/flexible flat feet are those where the flattened medial arch forms with dorsiflexion of the great toe (Jack test)/form an arch when patient tip-toes

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17
Q

What are the causes and presentation of mobile flat feet?

A
  • Flexible flat footedness may be related to ligamentous laxity, may be familial or may be idiopathic
  • The flat footedness may only be dynamic (present on weight bearing only)
  • Flexible flat‐footedness in children is a normal variant and medial arch support orthoses are not required
  • In adults mobile flat foot may be related to tibialis posterior tendon dysfunction
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18
Q

What is rigid flat foot?

A
  • In the rigid type of flat footedness the arch remains flat regardless of load or great toe dorsiflexion
  • This implies there is an underlying bony abnormality (tarsal coalitionwhere the bones of the hindfoot have an abnormal bony or cartilaginous connection) which may require surgery
  • May also represent an underlying inflammatory disorder or a neurological disorder
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19
Q

What are the complications of flat footedness?

A

Flat footed people may be at higher risk of tendonitis of the tibialis posterior tendon

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20
Q

What is curly toes?

A

Minor overlapping of the toes and curling of toes is common with the fifth toe is most frequently affected

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21
Q

What is the management of curly toes?

A

Most will correct without intervention but they can occasionally cause discomfort in shoes and persistent cases in adolescence may require surgical correction

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22
Q

What is osteogenesis imperfecta?

A

Rare group of genetic disorders mainly affecting bone; also known as brittle bone disease

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23
Q

What causes osteogenesis imperfecta?

A
  • Defect of the maturation and organization of type 1 collagen (which accounts for most of the organic composition of bone)
  • The majority of cases are autosomal dominant, rarer cases are autosomal recessive
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24
Q

What is the presentation of autosomal dominant osteogenesis imperfecta?

A
  • Multiple fragility fractures of childhood
    • Can be mistaken for child abuse/non-accidental injury
    • Can be mistaken for osteopenia - can result from prematurity
  • Short stature with multiple deformities
  • Blue sclerae
  • Dentinogenesis imperfecta
  • Loss of hearing
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25
Q

What is the presentation of autosomal recessive osteogenesis imperfecta?

A

Either fatal in the perinatal period or associated with spinal deformity

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26
Q

What are the investigations for osteogenesis imperfecta?

A

X-ray

  • Bones tend to be thin (gracile) with thin cortices and osteopenic
  • Mild cases may have relatively normal x-rays with history of low energy fractures
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27
Q

What is the management of osteogenesis imperfecta?

A
  • No cure - only fracture fixation, surgery to correct deformities, bisphosphonates may have benefit in teenage years
  • Fractures tend to heal with abundant but poor quality callus and are treated with splintage, traction or surgical stabilization
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28
Q

What is skeletal dysplasia?

A

Medical term for short stature (dwarfism is no longer used); more than 300 types of skeletal dysplasia have been described

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29
Q

What is the aetiology of skeletal dysplasia?

A

Genetic error (hereditary or sporadic mutation) resulting in abnormal development of bone and connective tissue

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30
Q

What is the pathophysiology of skeletal dysplasia?

A
  • Short stature may be proportionate (limbs andspine proportionally short) or disproportionate (limbs proportionally shorter or longer thanspine)
  • Achondroplasia is the most common type of skeletal dysplasia
    • May be autosomal dominant, however over 80% of cases are sporadic
    • Results in disproportionately short limbs with a prominent forehead and widened nose
    • Joints are lax and mental development is normal
  • Other skeletal dysplasias can 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) and intrauterine or premature death
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31
Q

What are connective tissue disorders?

A

Due to genetic disorders of collagen synthesis, mainly type I - found in bone, tendon and ligaments

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32
Q

What is the pathophysiology of connective tissue disorders?

A
  • Results in joint hypermobility
  • Affect soft tissues more than bone (vs osteogenesis imperfecta which predominantly affects type I collagen of bone)
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33
Q

What is generalised joint laxity?

A
  • Around 5% of normal people have hypermobility of the joints which usually runs in families and is inherited in a dominant manner
  • Patients may describe themselves as ‘double‐jointed’ and be able to perform tricks as a party piece (eg voluntary dislocation of the shoulder)
  • People with generalized ligamentous laxity are more prone to soft tissue injuries (ankle sprains) and recurrent dislocations of joints (especiallyshoulder and patella) which may be painful
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34
Q

What is Marfan’s syndrome?

A
  • Autosomal dominant or sporadic mutation resulting in tall stature with disproportionately long limbs and ligamentous laxity
  • Associated features include a high arched palate, scoliosis, flattening of the chest (pectus excavatum), eye problems (lens dislocation, retinal detachment), aortic aneurysm and cardiac valve incompetence
  • Cardiac abnormalities may result in premature death (aneurysm, dissection, valvular disease)
  • Patients rarely require orthopaedic surgery and soft tissue stabilization of dislocating joints usually has disappointing results as the biological abnormality cannot be corrected
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35
Q

What is Ehlers-Danlos Syndrome?

A
  • Heterogeneous condition which is often autosomal dominantly inherited with abnormal elastin and collagen formation
  • More than 10 types have been described
  • Clinical features include profound joint hypermobility, vascular fragility with ease of bruising, joint instability and scoliosis
  • Bony surgery may be required for dislocating joints however bleeding can be a problem and skin healing can be poor with stretched scars or wound dehiscence common
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36
Q

What is Down Syndrome?

A
  • Musculoskeletal manifestations of Trisomy 21 include short stature and joint laxity with possible recurrent dislocation (especially patella) which may require stabilization
  • Atlanto‐axial instability in the c‐spine can also occur
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37
Q

What is Duchenne Muscular Dystrophy?

A

Rare x-linked disorder (boys only affected) that leads to progressive muscle wasting

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38
Q

What is the aetiology of Duchenne Muscular Dystrophy?

A

A defect in the dystrophin gene involved in calcium transport results in muscle weakness which may only be noticed when the boy starts to walk with difficulty standing (Gower’s sign) and going up stairs

39
Q

What is the presentation of Duchenne Muscular Dystrophy?

A

Progressive muscle weakness follows and by the age of 10 or so he can no longer walk and by age 20 progressive cardiac and respiratory failure develop with death typically in the early 20s

40
Q

What are the investigations of Duchenne Muscular Dystrophy?

A
  • Raised serum creatinine phosphokinase
  • Abnormalities on muscle biopsy
41
Q

What is the management of Duchenne Muscular Dystrophy?

A
  • Physiotherapy, splintage and deformity correction may prolong mobility
  • Severe scoliosis may be corrected by spinal surgery
42
Q

What is developmental dysplasia?

A

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

43
Q

What is the aetiology of developmental dysplasia?

A
  • Congenital
  • Poor positioning after birth
  • Higher incidence in females (8:1)
  • Breech presentations
  • Family history
  • Oliohydramnios
  • First born
  • Moulded baby (feet/neck/head/spine) e.g. twins
  • > 4kg
  • Multiple pregnancy
  • Left hip more commonly involved
44
Q

What is the pathophysiology of developmental dysplasia?

A
  • If left untreated the acetabulum is very shallow and in more 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
45
Q

What is the presentation of developmental dysplasia?

A
  • Neonatal baby checks
  • Selective US screening in Scotland
    • Breech
    • 1st degree family member
    • Moulded
  • 6-8 week GP check
  • Late presentation - any time after 3 months, usually when child starts to walk (12-18 months)
  • Asymmetry
  • Loss of knee height
  • Crease asymmetry
  • Less abduction in flexion
  • Barlow’s test - flex and adduct the hip, sign is positive if hip dislocates posteriorly
  • Ortolani’s test - flexion and abduction reduces femoral head into acetabulum
46
Q

What are the investigations for Developmental Dysplasia?

A
  • USS - preferred
    • Less helpful after 3 months of age as the ossification nucleus begins to develop
  • X-ray - cannot be used for the early diagnosis of DDH as the femoral head epiphysis is unossified until around 4‐6 months but x-rays are the investigation of choice after this age
47
Q

What is the management of developmental dysplasia?

A

Early DDH

  • Pavlik harness 23-24 hrs a day for up to 12 weeks until USS is normal
    • Hip abducted and flexed
    • May need night splints for a few weeks afterwards
  • 95% normal hip

Late DDH

  • Surgery - closed reduction (CR) spica, open reduction (OR) spica
  • For children with persistent dislocation over 18 months old OR is much more likely to be required and the acetabulum is likely to be very shallow by this stage
    • Typically the child will need an open reduction to clear soft tissues and may also need an osteotomy to shorten and rotate the femur and/or pelvic osteotomy to deepen and re‐orientate the acetabulum
  • Persistent or undiagnosed DDH at this stage tends to have a poorer prognosis - unable to construct a normal hip, 30% will require further surgery
48
Q

What is transient synovitis?

A

Self‐limiting inflammation of the synovium of a joint, most commonly the hip

49
Q

What is the aetiology of transient synovitis?

A
  • Commonly occurs shortly after an upper respiratory tract infection (usually viral) although sometimes no cause is found
  • Typical age is between 2 and 10
    • Commonest cause of hip pain in childhood
  • Boys are more commonly affected than girls
50
Q

What is the presentation of transient synovitis?

A
  • Limp/reluctance to weight bear on the affected side
  • Range of motion may be restricted
  • May be low grade fever but child is not systemically unwell
51
Q

What are the investigations for transient synovitis?

A
  • X-ray - to exclude Perthes disease
  • CRP - if normal/near normal can exclude septic arthritis
  • If uncertainty between transient synovitis and septic arthritis - aspiration of the hip or open surgical drainage
  • MRI - rule out osteomyelitis of the proximal femur
52
Q

What is the management for transient synovitis?

A
  • NSAIDs and rest
  • Pain generally resolves within a few weeks but if there is no resolution then another cause for hip pain should be sought
53
Q

What perthes disease?

A

Idiopathic osteochondritis of the femoral head

54
Q

What is the aetiology of Perthes disease?

A
  • Usually occurs between the ages of 4 to 9
  • More common in boys (around 5:1), particularly very active boys of short stature
55
Q

What is the pathophysiology of Perthes disease?

A
  • The femoral head transiently loses its blood supply resulting in necrosis with subsequent abnormal growth
  • The femoral head may fracture and collapse
  • Subsequent remodeling occurs however the shape of the femoral head and congruence of the joint is determined by age of onset (with older children faring worse) and the amount of collapse
  • An incongruent joint will lead to early onset of arthritis and severe cases may require hipreplacement in adolescence or early adulthood
56
Q

What is the presentation of Perthes disease?

A
  • Affected children present with pain and a limp
  • Most cases are unilateral and bilateral cases may represent an underlying skeletal dysplasia or a thrombophilia
  • Loss of internal rotation is usually the first clinical sign followed by loss of abduction and lateron a positive Trendelenburg test from gluteal weakness
57
Q

What is the investigations of Perthes disease?

A
  • X-ray - may be normal
  • MRI or bone scan can be used to identify pathology
58
Q

What is the management of Perthes disease?

A
  • No specific treatment other than regular x-ray observation and avoidance of physical activity
  • Approximately 50% of cases do well
  • In some cases the femoral head becomes aspherical, flattened and widened
    • The lever arm of the abductor muscles is altered resulting in weakness (Trendelenburg positive)
  • Occasionally the femoral head may sublux (partially dislocate) requiring an osteotomy of the femur or acetabulum
59
Q

What is slipped upper femoral epiphysis?

A

Condition mainly affecting overweight pre‐pubertal adolescent boys where the femoral head epiphysis slips inferiorly in relation to the femoral neck

60
Q

What is the aetiology of SUFE?

A
  • Age 8-18
  • Pubertal growth
  • Overweight
  • Mainly affects males
  • Racial differences
  • Endocrine/metabolic - hypothyroidism or renal disease may predispose to SUFE
61
Q

What is the pathophysiology of SUFE?

A
  • The growth plate (physis) is not strong enough to support body weight and the femoral epiphysis slips due to the strain
  • A growth spurt may preclude the onset and puberty may be delayed (idiopathic or hypothyroidism)
62
Q

What is the presentation of SUFE?

A
  • Cases can be acute, chronic or acute-on-chronic
  • Hip, groin, thigh or knee pain with limp
    • Patients can present purely with pain in the knee (due to the obturator nerve supplying both the hip and knee joint) - make sure to examine the hip!
  • 1/3 of cases are bilateral
  • Antalgic gait
  • Loss of internal rotation of the hip
63
Q

What are the investigations for SUFE?

A

X-ray - ensure lateral view is obtained to detect mild degrees of slip

64
Q

What is the management for SUFE?

A
  • Urgent surgery to pin the femoral head to prevent further slippage
  • The greater the degree of slip the worse the prognosis and some cases may require hip replacement in adolescence or early adulthood
  • For severe acute slips gentle manipulation may be attempted but this risks avascular necrosis
  • Chronic severe slips may require an osteotomy
65
Q

What is femoroacetabular impingement syndrome?

A

Altered morphology of femoral neck and/or acetabular causes abutment of the femoral neck on the edge of the acetabulum during movement (usually flexion, adduction, and internal rotation)

66
Q

What is the aetiology of femoroacetabular impingement syndrome?

A

Occurs because the hip bones do not form normally during the childhood growing years

67
Q

What is the pathophysiology of CAM type hip impingement?

A
  • The femoral head is not round and cannot rotate smoothly inside the acetabulum
  • A bump forms on the edge of the femoral head that grinds the cartilage inside the acetabulum
  • Usually young athletic males
  • Can be related to previous SUFE
68
Q

What is the pathophysiology of Pincer type hip impingement?

A
  • Occurs because extra bone extends out over the normal rim of the acetabulum
  • The labrum can be crushed under the prominent rim of the acetabulum
  • Usually seen in females
69
Q

What are the consequences of femoroacetabular impingement syndrome?

A
  • Damage to the labrum and tears
  • Damage to cartilage
  • OA in later life
70
Q

What is the presentation of femoroacetabular impingement syndrome?

A
  • Activity related pain in the groin, particularly in flexion and rotation
  • Difficulty sitting
  • C sign positive
  • FADIR provocation test positive
71
Q

What are the investigations of femoroacetabular impingement syndrome?

A
  • X-ray
  • CT
  • MRI - better for visualising damage to labrum and bony oedema
72
Q

What is the management of femoroacetabular impingement syndrome?

A
  • Observation in asymptomatic patients
  • Try conservative measures before surgery
  • Arthroscopic/open surgery to remove CAM/debride labral tears
  • Peri-acetabular osteotomy/debride labral tears in pincer impingement
  • Arthroplasty/total hip replacement in older patients with secondary OA
73
Q

What is cerebral palsy?

A

A persisting qualitative motor disorder appearing before the age of three years, due to non-progressive damage to the brain occurring before the growth of the central nervous system is complete

74
Q

What is the aetiology of cerebral palsy?

A
  • Insult to the growing brain before, during or after birth
  • Causes include genetic problems, brain malformation, intrauterine infection in early pregnancy, prematurity, intra‐cranial haemorrhage, hypoxia during birth and meningitis
  • Only 1 in 10 cases are due to problems during labour
  • Often no identifiable cause
75
Q

What is the presentation of cerebral palsy?

A
  • The expression of the disease and its severity are variable depending on the area of the brain affected ranging from mild symptoms and signs limited to one limb or total body involvement with profound learning difficulties
  • Developmental milestones may be missed and the ability to ambulate or perform normal tasks may be impaired
76
Q

What is club foot?

A

Condition in which a newborn’s foot or feet appear to be rotated internally at the ankle

77
Q

What is the aetiology of club foot?

A
  • In utero abnormal alignment of the joints between the talus, calcaneus and navicular (7th week of embryo development)
  • Around 50% of cases are bilateral
  • More severe club feet associated with syndromes
78
Q

What are the risk factors of club foot?

A
  • More common in males
  • Family history
  • Breech presentation
  • Oligohydramnios
79
Q

What is the pathophysiology of club foot?

A

The abnormal alignment of the joints between the talus, calcaneus and navicular results in contractures of the soft tissues (ligaments, capsule and tendons) resulting in a deformity consisting of ankle equinus (plantarflexion), supination of the forefoot and varus alignment of the forefoot

80
Q

What is the presentation of club foot?

A
  • Postural talipes - feet turned in at birth but will stretch out with mild physiotherapy
  • Club foot - structural malformation of the bones and muscles of the foot involving resulting in ankle equinus (plantarflexion), supination of the forefoot and varus alignment of the forefoot
81
Q

What is the management of club foot?

A
  • Diagnosis normally obvious, treatment commenced as soon as possible after birth
  • Ponsetti technique - splinting and casting
    • Deformities are corrected progressively in stages and held in plaster casts with 5 or 6 weekly cast changes
  • 80% of children require a tenotomy of the Achilles tendon to maintain full correction
  • Surgery may also be required for cases resistant to splintage
  • Once full correction is achieved the child is then placed in a brace consisting of boots attached to a bar which is worn 23 hours a day for 3 months and used during sleep until the age of 3 to 4 to try to prevent recurrence
  • Late deformity is very difficult to correct and requires extensive surgery with less satisfactory results however delayed presentations are very rare in modern healthcare systems
82
Q

What is the pathophysiology of extensor mechanism problems?

A
  • Knee extensor mechanism pain is a fairly common occurrence during adolescence as body weight increases and sporting activities increase
  • Patellar tendonitis (jumper’s knee) can occur which is self‐limiting and requires rest and possibly physiotherapy
83
Q

What is patellofemoral pain syndrome?

A

Anterior knee pain (patellofemoral dysfunction) is common in adolescence, especially in girls
AKA idiopathic adolescent anterior knee pain, chondromalacia patellae

84
Q

What is the aetiology of patellofemoral pain syndrome?

A
  • Anterior knee pain (patellofemoral dysfunction) AKA idiopathic adolescent anterior knee pain, chondromalacia patellae is common in adolescence, especially in girls
  • Unclear - may be due to muscle imbalance, ligamentous laxity and subtle skeletal predisposition (genu valgum, wide hips, femoral neck anteversion, internal rotation)
  • There may be softening of the hyaline cartilage of the patella (chondromalacia patellae)
  • Some cases have obvious patellar maltracking
85
Q

What is the management of patellofemoral pain syndrome?

A
  • The majority of cases are self‐limiting and the mainstay of treatment is physiotherapy to rebalance the muscles
  • Most patients ‘grow out’ of the condition
  • Occasionally resistant cases may require surgery to shift the forces on the patella (tibial tubercle transfer) - results can be unpredictable
86
Q

What is osteochondritis dissecans?

A

An area of the surface of the knee loses its blood supply and cartilage +/- bone can fragment off

87
Q

What is the aetiology of osteochondritis dissecans?

A

Most common in adolescence

88
Q

What is the presentation of osteochondritis dissecans?

A
  • Knee pain
  • Recurrent effusions of the knee
  • Some asymptomatic
89
Q

What are the investigations of osteochondritis dissecans?

A

X-ray, MRI

90
Q

What is the management of osteochondritis dissecans?

A
  • Can heal or resolve spontaneously
  • Indications for surgery controversial
    • If detaching on MRI can pin in place
    • If detached can fix or remove
    • May consider cartilage regeneration for persistent pain
  • Needs specialist referral
91
Q

What is traction apophysitis?

A

Excessive pull by a large tendon causes damage to the unfused apophysis to which it is attached

92
Q

What is Osgood-Schlatter’s disease?

A
  • Traction apophysitis at tibial tubercle - insertion of patellar tendon into tibial tuberosity
  • Occurs in adolescent active boys
93
Q

What is the presentation of Osgood-Schlatter’s disease?

A
  • Knee pain, swelling
  • Leaves prominent bony lump
94
Q

Where else other than the tibial tubercle can traction apophysitis occur?

A

Can also happen at patella and Achilles

Musculoskeletal MBCHB (21 decks)

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