Locomotor, Nutrition, Developmental problems Flashcards
Kocher criteria for Septic arthritis
WCC>12000
ESR/CRP elevated
Non-Wx bearing
Temp>38
ALL 4= 99% Septic Arthritis
Epidemiology of septic arthritis
50% in first 2 years of life
2x more common in Boys
Underlying joint disease or prosthetic joints or bacteraemia increase risk
Presentation of septic arthritis
Likely < 3 years old 75% Lower limb (Knees>Hip>Ankle) Acute, hot swollen joint Pain on passive movement Pseudoparalysis Cannot weight bear Systemic symptoms
Diagnosis of septic arthritis
Joint aspiration under GA + USS guided
Then Gram stain and culture of synovial fluid
+/- FBC, ESR, CRP, Blood cultures
X-ray findings in septic arthritis
Initially normal +/- Widened joint spaces B/C effusion
Later will have space narrowing, erosive changes, subluxation, dislocation
Management of septic arthritis
Abx after aspiration
-IV up to 3/52 followed by oral for 4-6/52
Surgical involvement if recurrent or affecting hip
Splintage improves pain
Physio to avoid stiffness
Indications for a LP in septic arthritis
If H.Influ then do an LP as there is increased incidence of meningitis
What is developmental dysplasia of the hip
Abnormal formation of the hip joint where there is a shallow acetabulum that doesn’t cover the femoral head sufficiently
Risk Factors for DDH
FEMALE (6X more likely) Breech delivery FHx 1st born Oligohydramnios Other joint problems High birth Wx
Screening for DDH
1st day- Hips examined
6 weeks USS
How are Breech babies screened for DDH
All have USS
Same if 1st degree relative with DDH
Presentation of DDH
From birth or shortly after
Delay in walking
Waddling gait (like a pregnant lady)
Shortened affected leg
Barlow and Ortolani tests
Tests for DDH
Barlow- Press hips posteriorly when flexed to attempt to dislocate
Ortolani- Hips flexed and then abducted to try and relocate the dislocated hip
Management of DDH
Most spontaneously stabilise at 3-6 weeks therefore use double nappies until this point
No success + <6 months= Bracing with Pavlik harness for 3/12
Then consider surgery if above fails
Complications of DDH
OA, Lower back pain
Also a risk of re-dislocation and/or avascular necrosis
Commonest cause of hip pain in 3-10 years
Reactive arthritis/Irritable hip
Presentation of irritable hip/reactive arthritis
Slight limp and hip pain Hx viral infection No systemic symptoms Likely single joint No pain at rest but pain O/E
What features would likely indicate septic arthritis over reactive arthritis in a child with limp
Systemically unwell Fever Night pain and pain on rest Cannot Wx bear > 2 weeks Very elevated inflammatory markers
When would you discharge a child with reactive arthritis?
Non-dramatic physical signs
X-rays and bloods normal
Advise NSAIDS and rest
Reiter’s syndrome
Form of reactive arthritis
“Cant see, can’t wee, can’t climb a tree”
Uveitis, urethritis and arthritis
Classification of JIA
Objective arthritis in >/= 1 joint for at least 6 weeks \+/- Swelling, warmth, reduced movement < 16 years Nil other cause found Most common in girls under 4 years
Oligoarticular/Pauarticular JIA vs Polyarticular JIA vs Still’s disease
Oligo/Pau= Up to 4 joints affected. Most common. Poly= >4 joints affected Still's= Systemic onset JIA
Presentation of JIA
Joints- Painful, swollen, stiff on mornings, cartilage erosion
Walk on toes
Hepato/Splenomegaly
Still’s= + Fever, salmon-pink rash, Uveitis, Wx loss, Anorexia
Likely Blood result changes in Still’s disease
Leukocytes, ESR, CRP and platelets can be raised
HB can be low
Can be similar in non-systemic JIA
Rh and Anti-nuclear factor in JIA
Rh can be -ve or +ve
Anti-nuclear factor +ve in 70% Pauarticular JIA
Management of JIA
Mild exercise alongside rest each day
Physio and splints
NSAIDS and hot baths +/- Steroid injections
Long term: Methotrexate, Sulfasalazine, oral corticosteroids
Surgery to preserve joint function
Osteomyelitis presentation
Fever, Swelling, erythema and severe bony pain
Child will stop using the affected limb
Lucency and periosteal thickening can sometimes be seen on an X-ray
What does a child under 3 years with an acute limp need?
A secondary care assessment
Benign idiopathic nocturnal limb pain of childhood (Growing pains)
Preschool children (~3-5 years) or 8-12 years
Pain at night and no limp by the day
No interference with normal activities
Meeting motor milestones
Most common age range irritable hip is seen
2-8 years
When are Bow legs normal
< 3 years
Surgical referral for Blout’s disease if > 4 years
ALL and limp
ALL can cause pathological fractures and thereby lead to limp/pain/tenderness
Therefore always have malignancy as a differential
Osgood Schlatters
Knee pain in active children
Red flags indicating an organic cause of limp
Day and night pain There on weekends and vacations Interruption of normal activities- ask about play Unilateral Localised to a join Unremitting Refusal to walk Systemic manifestations Wx loss, bruising, night sweats, hepatosplenomegaly Pain on passive internal rotation
Reassuring features indicating a non-organic cause of limp
Painless passive internal rotation Pain only at night/school days No interference with normal activities Bilateral Pain located between joints Not systemic Pain without limp is also reassuring
What is Perthe’s disease
Osteochondritis of the femoral head
Can be caused by or develop into avascular necrosis
Risk factors for Perthe’s disease
MALE
Short
Trisomy 21
Think a child in Primary school
Presentation of Perthe’s disease
Short child 4-8 years who is hyperactive
Progressive hip pain over weeks
Reduced movement, discrepancy in leg length
Limp
Can be bilateral
What gait is classically seen in Perthe’s disease
Trendelenberg gait- Unaffected side rises above affected side
X-ray of perthe’s disease
Sub-chondral linear lucency
Widened joint space early on
Collapsed deformity later on
Management of Perthe’s disease
< 6 years= Observation
If older then try physio and strengthening then callipers (non-wx bearing device) if good imaging
surgery if above fails
What is Slipper upper femoral epiphysis
Femoral head epiphysis displaced postero-inferiorly
Risk factors for SUFE
Secondary school age (10-16 years) Obese Hypothyroidism Trauma Pelvic RT
Presentation of SUFE
Pain, Limp, Reduced movement
Externally rotated hip +/- shorter length
Can be bilateral and thereby look like a ‘normal hip on x-ray’
If Unilateral look for Klein’s line on X-ray- Inferolateral displacement “melting ice cream appearance”
Management of SUFE
Surgical fixation/closure to prevent AVN and chondrolysis
Normal calorie requirements
150mls/kg/day until around 6/12
How many mls per oz
30mls: 1 oz
Maintenance fluids
1st 10kg= 100mls/kg/day
2nd 10kg= 50mls/kg/day
subsequent kgs= 20mls/kg/day
Common causes of malabsorption
GORD Chronic infection CF Immunodeficiency Eating disorder
Definition of malnutrition
BMI<18.5
or
> 10% Wx loss over 3/12
Indicated by falling across two centile lines on serial Hx and Wx (or <3rd centile)
Kwashiokor vs Marasmus malnutrition
Kwashiokor- Severe protein/AA deficiency: Abd distension and growth retardation
Marasmus- Severe calorie deficiency where height is preserved but they have a wasted appearance
(Generally a mix of the two)
Refeeding syndrome
Respiratory and cardiac failure induced by electrolyte imbalance as a consequence of rapid large feeding after a period of minimal feeding
Feeding options for severe malnutrition
Parenteral (IV) or enteral (GI) feeding
What is Ricket’s
Vitamin D deficiency that occurs before fusion of epiphysial plates during growth
Disrupts mineralisation of said plates
What happens to Calcium and Phosphate levels during progression of Vit D deficiency/ Rickets
Initially- Low Ca2+ and normal Phos
Then Normal Ca2+ as compensatory hyperparathyroidism
Finally low Ca2+ and low phosphate
This is advanced bone disease with clinical features
Radiological findings in rickets/Vit D deficiency
Widening at the end of the long bones
Cupped and ragged surfaces
Key features of Rickets
Frontal bossing Ankle and Wrist swelling Delayed closure of fontanelles Harrison's sulcus below ribs Dental hypoplasia Leg bowing Pectus carinatum Craniotabes (bones in cranium collapse under pressure) Rachitic rosary (expansion of the anterior rib ends at the costochondral junctions)
Treatment of Vit D deficiency/Rickets
Colacalciferol- 6 weeks
Then need maintenance
Genetics of vitamin D dependent rickets
Type 1 and 2 are autosomal recessive
Type 1 cannot activate vit D due to enzyme deficiency
Type 2 is end organ resistance to vitamin D
Both present early in life
Strongest RF for Down’s syndrome
High maternal age
Tone features in Down’s syndrome
Hypotonia and marked head lag
Facial features in Down’s syndrome
Small low set ears Upslanting palpebral fissures Prominent epicanthic folds Protuding tongue White Brushfield's spots on iris Flat occiput Short neck
Limb/Motor features in Down’s syndrome
Short broad hands Single palmar crease Wide sandle gap Atlantoaxial instability Short
Most common heart defect associated with Down’s syndrome
AVSD
Conditions associated with Down’s syndrome
Congential HD GI- Pyloric stenosis, Atresia, Hirschsprung's, Umbilical hernias, GORD, Coeliac's DDH Eczema Deafness Cataracts Leukaemia (1%) Infections Hypo/Hyperthyroidism Alzheimer's disease + other dementias
Referrals needed in a newly diagnosed child with Down’s syndrome
Cardiac assessment
Hip USS for DDH (~6 weeks)
Audiology for ?Deafness
Ophthalmic assessment
Median age of death for Down’s syndrome and prognostic information
Mid-50s
Much improved as ,10yrs in 1970s
Majority semi-independent
Big risk of AD in 40+
Amblyopia
Eye fails to achieve visual acuity even with prescription glasses/lenses
Feature of squint when eye has not received clear images in a sensitive period of development
3 key features of squint
Eye misalignment (Stabismus)
Diplopia
Amblyopia
Causes of squint
Number 1 is idiopathic
Also consider: Retinoblastoma, Glaucoma, CN palsy, Retinal disease
Paralytic vs Non-paralytic squint
Non-paralytic= Squint constant in all directions of gaze typically an imbalance of extraocular muscles, convergent or divergent but can be latent where it manifests when tired
Paralytic (Rare)= CN palsy, CN3 is down and out therefore squint varies with direction of gaze
Past what age should a squint always be investigated?
Beyond 12 weeks
How do you investigate a squint?
Full Ophthalmic examination including cover test
What is involved in an ophthalmic examination?
Acuity Colour Fields Pupils + Reflexes Cover test Movements Fundoscopy
Assessing visual acuity
Snellen chart at 6m
Fine print reading
Assessing colour in ophthalmic examination
Ishihara to identify number
Assessing visual fields
Red hot pin
1) Blind spot
2) Peripheral vision
Assessing pupils in an ophthalmic examination
Size, shape, symmetry
Direct and consensual pupillary reflex
Accommodation
RAPD- look for dilatation
Assessing eye movements in an ophthalmic examination
Draw H
Cover test
Shine light in eye- can they see one or multiple sources of light
Cover one eye and observe for movement
Temporal movement in cover test
Esotropia
Convergent squint
Nasal movement in cover test
Exotropia
Divergent squint
Fundoscopy
1% Tropicamide
Red reflex at 30cm
Then look closer
Hypertropia
One eye misaligned superiorly
Management of squint
Correct refractive error with spectacles
Patching good eye prevents ambylopia
Surgery to realign rectus muscle
Features of CN3 palsy
Pupil dilated
Partial ptosis
Eye is “down and out”
Key features of ASD
Abnormal impaired development before 3 years
Poor verbal and non-verbal communication
Obsessive repetitive interests
Reduced imaginative play
Difficulties with reciprocal social interaction
Problems associated with ASD
Epilepsy Visual/Auditory impairment Mental health problems Learning disability PKU, FXS, TS, TORCHES
What does 3/60 mean in term of visual acuity?
Would have to stand 3 metres to see what a normal person would see at 60 metres
Definition of partially sighted and blindness
Partially sighted= <6/60
Blind= <3/60
Causes of blindness
Genetic- Retinoblastoma, cataracts etc Congenital Rubella syndrome Perinatal insult Post-natal insult Vitamin A deficiency
Key signs of blindness in a newborn/infant
Not smiling by 6 weeks
Delayed reaching/Pincer grip (Fine pincer >12 months)
Eye rubbing/irritation
Eyes move and/or look abnormal
Auditory impairment screening
Newborns have otoacoustic emission test
Can also use auditory brainstem response test
Audiology assessment at 7-9 months if abnormal
How does hearing impairment manifest?
Nil response to sound
Delayed speech
Behavioural problems
Associated neurology/pathology like LD or blindness
Most mild-moderate hearing loss is caused by…
Otitis media
Therefore conductive
Causes of sensorineural deafness
Mostly genetic Rubella Perinatal insult Post-natal infections like meningitis Some drugs like Amnioglycosides
Management of sensorineural hearing loss
Sit at front of classroom etc
Hearing aids
Cochlear implants
Makaton if associated learning difficulty
Causes of conductive deafness
Middle ear disease + Glue ear
ET dysfucntion
Management of Conductive deafness
Can try Grommets
Amplification with hearing aids
Cause of FXS
Repeat expansion on the FMR1 gene (>200 CGC repeats)
X-linked and dominant
Features of FXS
LD (IQ<70) therefore delayed milestones
High forehead, large testicles, large jaws/ears, facial asymmetry, prominent ears
Connective tissue problems= MV prolapse
Echolalia and Perseveration
Epilepsy
Causes of developmental delay
Genetic/Syndromes- Down's, Fragile X, ASD etc Perinatal injury Fetal alcohol syndrome TORCHES Congential hypothyroidism PKU Leucomalacia Neurofibromatosis, TS, Sturge-Weber Post-natal insult- Meningitis etc NTDs and Hydrocephalus
Dealing with temper tantrums/aggression
Stay calm Ignore bad behaviour Reward good behaviour- them not doing it initially Avoid precipitants like hunger/tiredness Star chart with child involvement
Managing anxiety in children
CBT is best… hierachial desensitisation and skills acquisition alongside family involvement
Between what ages is normal attachment present
6-36 months
What are the two types of attachment disorder?
Disinhibited
Reactive
Disinhibited attachment disorder
Caused by early institutional style care or care by a variety of carers
Child is unduly friendly with strangers and forms superficial relationships early
Reactive attachment disorder
Caused by abuse
Fearful and hypervigilant, not responsive to reassurance
Does not respond appropriately to social interaction
What are the 4 types of behavioural interaction seen in attachment disorder
A- Insecure avoidant- no reaction to separation/union, suppresses distress
B-Securely attached- distress upon separation, happy upon reunion
C- Insecure ambivalent- stressed upon separation, angry upon reunion
D- Disorganised- mix of A and C
Key features of ADHD
Inattention
Hyperactivity
Impulsivity
Diagnostic features of ADHD
Presents at a young age
Impulsivity, Hyperactivity, Inattention
Pervasive (>1 setting) and excessive vs norm for that age
Management of ADHD
Strict routines Praise concentration Positive reinforcement Mindfullness/CBT Family involvement Ritalin
Ritalin/Methyphenidate in ADHD
Stimulates inhibitory output
Inhibits re-uptake of Dopamine and NorA
Monitor growth 6/12 as it can perturb this and also cause Wx loss
Self-harm red flags
Significant suicidal ideation Hopelessness Violent methods Escalating frequency/severity Disengagement from services No support system
Epidemiology of self harm/suicide
self harm more common in females
Suicide more common in males
Hx of a self-harm event
Explore acute event- Before, During, After Background of self harm Suicidal screen and ongoing intent MSE SHx/DHx etc
Management of ODs/Self-harm in children
Admit all ODs overnight to be seen by CAHMS next day
<16 years + self-harm= Admit overnight
16+= Admit to adult ward
What 3 features typically make up an eating disorder?
Low Wx
Fear of gaining Wx
Desire to be thin
Diagnostic criteria for Anorexia Nervosa
Restriction of energy intake
Intense fear of gaining Wx despite being underweight
Disturbance in the way one’s body shape/Wx is experienced
Common sequela of Anorexia Nervosa
Hypokalaemia Low Sex hormones Impaired Glucose tolerance Hypercholesterolaemia Hypercarotenemia= Yellow Skin Low T3
1st line management for Anorexia Nervosa/ Bulimia Nervosa
Family therapy
Epidemilogy of eating disorders
Bulimia more common than Anorexia
Bulimia rare in <13s
Diagnostic features of Bulimia
Recurrent binges with no control
Recurrent purges to compensate
Above >/=1 time a week for >/=3 months
Self-evaluation entirely based on body shape
Below what age can people not refuse treatment?
<18 years
Although can still consent
Trisomy 18
Edward’s syndrome
2nd most common autosomal trisomy
Trisomy 13
Patau’s syndrome
