Paediatric FC from ppt Flashcards
what are the 4 fields of development
- gross motor
- fine motor and vision
- speech, hearing and language
- social, emotional and behavioural
what is the difference between age and limit age for developmental milestones
median age - when half of a standard population of children reach that level of development
limit age - the age a child is expected to have acquired a particular skill/reached a particular milestone
limit age is usually 2 standard deviations from the mean
what are the median and limit ages for walking
median - 12 months
limit - 18 months
how should you adjust developmental milestones for prematurity
age correct up to 2 years of age
i.e. a 9 monht old baby who was 2 months early - only expected to be at a developmental stage of a 7 month ond
should vaccinations be adjusted for prematurity
no
vaccines must be given according to chronological age
babies born <28 weeks should receive their first set of immunisations in hospital due to apnoea risk
what are the primitive reflexes
moro - startle - symmetrical extenstion and flexion of the limbs if you suddenly lower them backwards
grasp - grabbing an object placed in their hand
rooting - turning head towards stimulus placed near mouth
stepping
positive supporting reflex (legs push up against gravity when placed)
atonic neck reflex
when should the primitive reflexes have diminished by
4-6 months
if they haven’t - could be a sign of cerebral palsy
when should a baby be able to sit unsupported
6 months
when should a child be able to make a mature pincer grip
10 months
when should a child be able to draw a line, circle, cross, square and triangle
line - 2 years
circle - 3 years
cross - 4 years
square - 4.5 years
triangle - <5 years
*these drawing skills are being able to draw without being shown how it is done, they can copy (after being shown) 6 months earlier
when should a child start to express 2-3 words in addition to mama and dada
12 months
when should a child be able to talk in sentences
2.5-3 years
at what age should a child start smiling
6 weeks
at what age should a child be toilet trained during the day
2 years
at what age do children start playing with someone else interactively
3 years
before 3 - normal for a child to play by themselves
after 3 you would expect them to start sharing/interacting, so may worry if they struggle to play with others >3 years
when do children have their hearing checked
newborn hearing screening
hearing screening when they start school
if parents concerned about hearing
up to what age is it normal to be able to see a squint in a child
newborns may appear to squint when looking at near obejcts
by 12 weeks - NO SQUINT should be present at all
when is vision screening performed
pre-school children
school entry
what are some causes of developmental delay
genetic - chromosomal abnormality, brain malformation
congenital hypothyroidism
teratogenic medications during pregnancy
hypoxic brain injury during birth
history of meningitis
head trauma (accidental or non-accidental)
brain hypoxia due to near drowing, seizures
unknown
what are some genetic causes of severe visual impairment
congenital cataracts
albinism
retinal dystrophy
retinoblastoma
define strabismus
misalignment of the visual axes
also known as squint
what is the most common cause of squint
failure to develop binocular vision due to REFRACTIVE ERRORS of the eyes
(can also be caused by cataracts, retinoblastoma and other intra-occular problems that must be excluded)
what are the 2 divisions of squints
non-paralytic (concomintant, common) - usually due to refractive error, often treated by glasses but may need surgery
paralytic (rare) - due to paralysis of the motor nerves. When rapid onset, can be sinister - due to underlying SOL
what tests can be done to detect squint
corneal light reflex test - shine pen torch in eyes, reflection of light should appear in same position in both eyes. If not, there may be squint
cover test - cover good eye and the squinting eye will move. Perform close (33cm) and distant (6m) as some squints are only present at one distance
what are the refractive errors seen in childhood
- hypermetropia
- myopia
- amblyopia
what are hypermetropia and myopia, and why are they important to correct early
hypermetropia - long sightedness (MC)
myopia - short sightedness (uncommon and less likely to elad to permenant visual changes)
correct early to avoid amblyopia - irreversible damage to vision
what is amblyopia
also known as lazy eye
potentially permanent loss of visual acuity in an eye that has not received a clear image
usually affects one eye
what causes amblyopia
any interferemce with visual development:
squint
refractive erros
ptosis
cataract
how is amblyopia treated
glasses to correct visual impairment
patching of good eye to force lazy eye to work
early treatment essential - after 7 years unlikely to improve
considerable support to children and parent - children do not like having eye patched
name some of the ways in which visual impairment can present in childhood
loss of red reflex (from cataract)
white reflex in the pupil (retinoblastoma, cataract, ROP)
not smiling responsivley by 6 weeks
lack of eye contact with parents
random eye movements
failure to fix and follow
nystagmus
squint
photophobia
how can you treat strabismus
conservative - glasses, orthoptic exercises to improve eye muscle control
surgery:
strengthen procedure - resection
weakening procedure - recession of muscle on side the eye goes towards
esotropia (eye pointing inwards) - strengthen lateral rectus by resection, recession of the medial rectus
exotropia - opposite
botox injections - paralyse muscle that is pulling the eye in a certain direction
describe some possible behavioural changes that may present as a result of hearing loss
appears to daydream
sits near the TV and turns the volume really loud
watches the speaker’s face closely for clues
misunderstands/slow in responding
answers questions incorrectly
soft/fuzzy speech
doesn’t turn immediately when name called
aggressive
alowly schoolwork/grades start to get worse
what are the 2 categories of hearing loss and the underlying pathology behind them
conductive hearing loss - an obstruction in the ear canal preventing sound from getting through (often reversible)
sensorineural hearing loss - nerve damage (progressive, never reversible)
what are the causes for conductive hearing loss in children
most common - congestion behind the eardrums (with a cold)
glue ear
ear wax
middle ear infection
peforated ear drum
structural abnormality of the outer ear - certain syndromes
what are some risk factors conductive hearing loss
Down’s syndrome
craniofacial syndromes
cleft palate
if you performed a test with a vibrating tuning fork in someone with conductive hearing loss, what would you find
better hearing through bone conduction
how do you manage conductive hearing loss
most are self-limiting (inner ear infection/cold)
ENT referral - insertion of grommets to help drain excess fluid out of the middle ear
hearing aids if they have a permanent cause for the hearing loss
what are some causes of sensorineural hearing loss
unknown in many cases
genetic / syndromal
perinatal cause - trauma, infection, hypoxia at birth
congenital infections - rubella, CMV
meningitis - pneumococcus can cause ossification of the cochlear
premature babies - increased risk
if you were to perform a vibrating tuning fork test on someone with sensorineural hearing loss, what would you find
hearing is not better through bone
on audiology - hearing loss worse in higher frequencies
how do you manage sensorineural hearing loss
hearing aids
cochlear implants
aim = raise the level of hearing so that as much speech is audible as possible
which cases are cochlear implants reserved for
profound hearing loss (>90 decibles)
high frequency
bilateral hearing loss
meningitis hearing loss
what are some long term effects of hearing loss
developmental delay - particularly in speech and language
behavioural problems - too loud or too quiet
impact on education
impact on friendship and social life
impact on emotions/psychosocial impact
name some members of the MDT involved in child development services
paediatrician
PT
OT
SALT
dietician
nurses
health visitor
psychologist
family therapist
social worker
key worker
teachers and school nurses may also be involved
what is the role of the MDT service for child development
help liaise between home and school and the childs care needs
assess the child’s functional ability and need
to provide therapy where needed
to provide psychosocial support to the family
to ensure health needs of the child are met
what is down’s syndrome
trisomy 21
chromosomal abnormality in which there are three copies of T21, rather than 2 copies
leads to specific learning difficulties and dysmorphic features
what is the main risk factor for down’s syndrome
increasing maternal age
what are the 3 causes/mechanisms by which Down’s syndrome can arise
- non-dysjunction - 94%
- unbalanced Robertsonian translocation - 4%
- gonadal mosaicism - 1% (milder phenotype)
what is non-dysjunction
an error in meiosis 1
pair of chromosomes 21s fail to seperate - one gamete has 2 21s and other has none
fertilisation of gamete w/ 2 = zygote with trisomy 21
parents chromosome do not need to be examined
related to maternal age
47 chromosomes in karyotype
what is translocation and which chromosome is often involved in trisomy 21
extra copy of chromosome 21 joined onto another chromosome - usually C.14
these children will have 46 chromosomes on a karyotype - but 3 copies of 21 material (one portion tacked onto 14)
parental chromosomes analysis is needed - one parent is a carrier in 25% of cases
translocation carriers have 45 chromosomes on karyotype (one of the 21s is in wrong place)
what are some classic appearance features seen in someone with Down’s syndrome
flat bridge of nose
flat occiput
wide space between the eyes
small mouth and hence apparently large tongue (pseudo macroglossia)
single palmar crease
eyes slanting down and inwards
what are some medical conditions that people with down’s syndrome are more at risk of
complete atrioventricular septal defect - ECHO all T21 babies
hypothyroidism
duodenal atresia
hypotonia
later in life - Alzheimer’s
how is Down’s syndrome screened for antenatally
risk score - serum markers and nuchal translucency
diagnostic testing if high risk score - amniocentesis or chorionic villus sampling
how do you manage a child with down’s syndrome
MDT team involvement
cardiology
endocrinology
childhood disability services
SALT
physio
special education needs school
liasion between school, healthcare and family imperative
what are some clincal features associated with Edward’s syndrome (T18)
low birthweight
prominent occiput
small mouth and chin
short sternum
flexed, overlapping fingers
rocker-bottom feet
cardiac and renal malformation
microcephaly
90% die in first year
what are some clinical features of Patau syndrome (T13)
structural defect of brain (single lobed)
scalp defects
small eyes (microopthalmia)
cleft lip and palate
polydactyly
cardiac and renal malformations
not compatible with life
how are Patau’s and Edwards syndrome diagnosed
often antenatally - abnormalities detected on USS, risk score comes back high for trisomy
prenatal diagnosis - amnio or CVS
karyotype genetic analysis confirms diagnosis at birth
what is Turner’s syndrome
a chromosomal condition in which females only inherit one copy of the X chromosomes, rather than 2 copies
should be 46, XX
Turner’s = 45, X or 45 XO
what are some clinical features of Turner’s syndrome
female
short stature
webbed neck
infertility/primary amenorrhoea
delayed puberty
wide spaced nipples
what congenital heart defects is associated with Turner’s syndrome
coarctation of the aorta
how is Turner’s syndrome diagnosed
clinical suspicion
diagnosis confirmed on karyotypin (45, XO)
how is Turner’s syndrome managed
growth hormone therapy
oestrogen replacement - develop secondary sexual characteristics at time of puberty
infertility - IVF
what is Klinefelter’s
a genetic condition in which males inherit an extra copy of the X chromosome - karyotype = 47, XXY (should be 46, XY)
what are some clinical features of Kleinfelter’s syndrome
male
Tall stature
infertility - adult life
delayed puberty - lack of pubic hair
gynaecomastia in adolescence
how do you treat Kleinfelter’s syndrome
testosterone replacement - 1 injection/month for life
promotes development of sexual characteristics
what is fragile X syndrome
an inherited form of learning disability due to a trinucleotide repeat expansion on the X chromosome
affects males more thna females as they have protection from their other X chromosome
females have a milder phenotype
what are the clinical features of Fragile X syndrome
‘cocktail personality’ - happy, bouncy children
macrocephaly
large ears
learning difficulties/autism
joint laxity
large testes
hypotonia
mitral valve prolapse
how would a diagnosis of Fragile X syndrome be confirmed
FISH testing (fluorescence in situ hybridisation) - to look at the content of the cells
what is DiGeorge syndrome
abnormal branchial arch development
leading to problems with the heart, thymus and palate
what are the clinical features of DiGeorge syndrome
CATCH 22:
cardiac
abnormalities
thymus hypoplasia (T-cell dysfunction => primary immune def.)
cleft palate
hypocalcaemia
22 - defect - chromosome 22 material deletion
which type of cardiac abnromalities are seen in DiGeorge syndrome
truncus arteriosus
tatralogy of fallot
interrupted aortic arch
coarctation
vascular ring around trachea => stridor
what investigation should be done in someone with suspected DiGeorge syndrome
T-cell count
CXR - any pt with recurrent infections to look for thymus
anyone with congenital cardiac disease - test for diGeorge
what is Noonan’s syndrome
look like the boy version of Turner’s
short stature
webbed neck
ptosis
hypothyroidism
pulmonary stenosis
hypogonadism
what is Marfan’s syndrome
a connective tissue disorder
caused by fibrillin deficiency
what are some clinical features of Marfan’s syndrome
arachnodactyly
aortic dilatation => aneurysm => dissection
lens dislocation
long arms and legs
high arched palate
lax/hypermobile joints
what regular investigation is important in someone with Marfan’s syndrome
ECG - check for aortic dilatation - fix to prevent dissection
which type of connective tissue abnormality is associated with Ehler-Danlos syndrome
Elastin defect
so affects collagen - skin etc
what are the signs and symptoms of Ehlers-Danlos syndrome
stretchy skin
able to touch thumb to radius side of their arm
excessive bruising (weak collagen in blood vessels)
tissue fragility
brain aneurysms
‘cigarette paper scars’ - shiny thin scars on the skin
poor healing
what are the types of mendelian inheritance
auto dom
auto rec
X-linked
Y-linked
what is the chance of inheriting an autosomal dom condition from an affected parent
50%
give some examples of auto dom conditions
adult polycystic kidney disease
familial hypercholesterolaemia
Marfan’s syndrome
Huntington’s disease
some cancers - BRCA
give three reasons why someone may have an auto dom condition but a negative family history
MC = non-paternity
new mutation
gonadal mosaicism
what is the risk of inheriting an autosomal recessive condition from 2 carrier parents
1 in 4 (25%)
what is the risk of that a sibling of a child affected with an auto rec condition is a carrier
2 in 3 carrier risk for unaffected siblings
(take away possibility of them being affected)
what is the population carrier risk for CF
1 in 25
what is a big risk factor for auto rec conditions, particularly in people with an Asian origin
consanguinous parents
especially in families with many generation of consanguinity - can look like an auto dom pedigree for a rec condition
general rule for auto dom vs rec conditions
dom = structural protein defects
rec - affects metabolic pathway
what transmission pattersn (i.e male to male/male to female) would be seen in an X-linked rec condition
NO male to male transmission (2 consecutive generational males squares shaded on a pedigree, it is not X linked)
every affected male will produce a female carrier
if mothercarrier:
- 50% sons affected
- 50% daughters carriers
give some examples of X-linked rec conditions
Duchenne’s and Becker’s
haemophilia A
some types of albinism
Fragile X syndrome
what are the types of non-mendelian inheritance
multi-factorial/polygenic inheritance
imprinting and uniparental disomy
mitochondrial inheritance
give an example of a disease which has multifactorial inheritance
combinaton between the pre-disposing genes and the lived environment
spina bifida
folic acid deficiency linked to SB and you have a higher risk if you had a sibling with it
explain what imprinting and uniparental disomy is
for most genes both copies are expressed
some genes only are maternal or paternal expressed - IMPRINTING
Prader-willi and Angleman’s syndrome - cytogenic deletions of same region of C.15q or by uniparental disomy of C.15 (both copies of 15 come from same parent)
what is the chromosomal abnormality in Prader-Willi syndrome
Chromosome 15
occurs when failure to inherit the active paternal gene occurs
so either inherit 2 copies from mum or an abnormal copy from dad
what are the clinical features of Prader-Willi syndrome
hypotonia (even from neonate)
learning difficulties
obesity (due to hyperphagia)
small genitalia
what is Angleman’s syndrome
Chromosome 15 abnormality
failure to inherit active maternal gene
2 copies from dad
Or abnormal copy from mum
what are some clinical features of Angleman’s syndrome
severe learning difficulty
ataxia
broad based gait
characteristic facial appearance
epilepsy
‘happy puppet’ - unprovoked laughing and clapping
microcephalyb
how is DNA analysis performed
DNA PCR
what are the main roles of DNA analysis in genetic counselling
- confirmation of a clinical diagnosis
- detect female carriers for X-linked disorders
- detect carriers in auto rec disorders (siblings of CF patients)
- pre-symptomatic diagnosis of auto dom disorders (Huntington’s disease)
woul you test a child from a parent with known Huntington’s if the parent asked, to see if child with have disease
Sorry not an option
Not performed on healthy children, wait until old enough until informed consent
what is the role of a clinical geneticist
- involved in making diagnoses
- to explain the diagnosis to the family
- discuss prognosis
- discuss options available - genetic testing, screening, prenatal diagnosis
- refer to appropriate specialists for management
what are the main reasons for a referral to genetic counselling
preconception advice for someone with a FHx of a genetic disorder
antenatal
from paeds - development delayed, dysmorphic features
carrier testing for known family history
adult onset conditions - advice whether they should have test if parents did
post-mortem - unexplained death to look for genetic cause
what are the congential infections to be aware of
TORCHS
toxoplasmosis
other (HIV)
Rubella
CMV
HSV
Syphillis
what treatment do yu give a pregnant woman with syphillis
IM BenPen
what treatment do you give to a pregnant woman with toxoplasmosis
catch from cat poo
treatment - spiromycin
what are some complications of measles
encephalitis
subacute sclerosing pan-encephalitis
febrile convulsions
giant cell pneumonia
diarrhoea
appendicitis
myocarditis
what is Perthe’s disease and how does it present
degenertive condition of the hip joint due to avascular necrosis of the femoral head
more common in boys
features - hip pain (may present as knee pain), limp, shortening of affected leg, pain on int and ext rotation of hip
imaging - flattening of the femoral head
what is the clinical presentation of Hirshprung’s disease
failure to pass meconium
symptoms of bowel obstruction - abdo distension, bilious vomiting
failure to thrive, low birthweight, size
PR exam = stool ejection
more common in boys
what is the definitive diagnosis for Hirschprung’s disease
rectal biopsy
what complications can occur to the fetus if the mother is infected with rubella during the pregnancy
congential cataracts
congenital heart disease
sensorineural deafness
how are these complications prevented
MMR vaccine
if you see a pregnant lady - check they have MMR vaccine
what is the main complication to worry about if a pregnant woman has CMV
90% babies normal at birth
5% may develop sensorineural hearing loss later in life
are prenant women screened for CMV
no
no vaccine or antiviral therapy for CMV so screening no appropriate
how is toxoplasmosis typically caught
eating infected meat
contact with infected cat faeces
pregnant women not screened
what are the consequences of infection with toxoplasmosis during pregnancy
most infants born asymptomatic
other:
retinopathy
cerebral calcification
hydrocephalus
long term neuro disability
what are the risks of chickenpox (varicella zoster) to the fetus during pregnancy
<20 weeks - risk of skin scarring and neuro damage
2 days before or 5 days after delivery - high viral load (fetus unprotected by maternal ABs) - mortality 30%
how should a pregnant woman who has been exposed to chickenpox be treated
varicella zoster immunoglobulin
acyclovir
is maternal syphilis screened for during pregnancy
YES
So is HIV and hep B
how is maternal syphilis treated during pregnancy and what are the long term complications for the baby
penicillin
if fully treated a month or more before delivery - infant does not require treatment and has a good prognosis
if any doubt adequate maternal treatment - infant also treated with penicillin
how much is an Apgar score out of
10
normal = between 7 and 10
what factors are considered when giving an Apgar score
cardio
resp
colour
reflexes
tone
what is the purpose of teh NIPE examination
detect congential abnormalities not already identified at birth - heart disease, DDH
check for potential problems that could arise due to family history
provide an opportunity for parents to ask questions about baby
what are some common findings on a NIPE exam
congenital heart disease development dysplasia of hip (DDH)
Talipes (clubfeet) - positional or true
T21
cleft lip and palate
urogenital - hypospadias, undescended testes
spina bifida
what are some common cardiac issues affecting premature babies
structural heart defect
patent ductus arteriosus
anaemia of prematurity
what are some common resp problems affecting premature infants
surfactant deficiency - risk of resp distress syndrome
chronic lung disease of prematurity (bronchopullmonary dysplasia) - more prone to pneumonia and viruses - give palivizumab to protect against RSV
pneumothorax
apnoea, bradycardia and desaturations
what are some common GI problems in premature babies
necrotising enterocolitis - underdeveloped gut bacteria = swollen gut and pedematous and risk of perforation (red, shiny, tender abdo in babies) - breast milk protective
feeding problems / nutrition - slower establishment of feeding, unable to suck and swallow until 33-34 weeks so will need IV - build feeds up slowly to reduce risk of NEC
what are some common metabolic issues in preterm babies
hypoglycaemia - lack of glycogen stores developed
hypocalcaemia - kidneys and parathyroid not fully developed
electrolyte and fluid imbalance and hypothermia - excess losses through thin skin
osteopenia or prematurity
what are some neurological problems that preterm babies are at risk of
long term neuro issues
apnoea of prematurity - brain stem not fully myelinated until 32-34 weeks so the pontine resp centre is not fully developed
intraventricular haemorrhage - diagnose with cranial USS
what are the main infections that affect babies
preterm babies in general more prone to infections
Group B strep
E.coli and other gram neg
fungal infections - candida
viral infections - herpes from genital tract during delivery
what eye problems affect premature infants and what is thought to be the cause of this
retinopathy of prematurity
occurs due to hyperoxic insult whilst the blood given vessels are still developing (premies baby giving O2 as they are struggling to breathe and end up damaging their eyesight)
what is normally the cause of neonatal infection <48 hours and >72 hours
<48 hours - infection generally from the birth canal
> 72 hours - source of infection usually from the environment (catheters for nutrition, tracheal tubes, skin breaking procedures - drawing blood) - most common coagulase negative strep (epidemrins)
what are some risk factors for early onset infection in neonates
prolonged ROM
if mother has fever during labour or develops one shortly after birth
if infant is pre-term
if mother is GBS+ve or has another genital tract infection
whats the main risk factor for developing late onset neonatal infections
being on ICU or NICU - possibility of exposure t patogens and cross contamination
what are the clinical features of neonatal sepsis
fever/hypothermia/temp instability
poor feeding
vomiting
apnoea and bradycardia
resp distress
abdo distension
jaundice
irritabilit
seizures
lethargy/drowsiness
how does GBS infection tend to present
pneumonia
septicaemia
occasional meningitis
mortality - 10%
which women are considered high risk for GBS infection and are therefore screened selectively (not everyone is screened)
pre-term babies
prev baby with GBS infection
prolonged ROM
fever > 38 degree during labour
intrapartum ABs given to these high risk ladies if possible
where can listeria monocytogenes infection be caught from
unpasturised milk
soft cheese
undercooked poultry
can cause miscarriage, pre-term delivery and fetal infection
how to manage conjunctivitis and sticky eyes in newborns
common - clean with water or saline
more troublsome discharge - maybe due to staph or strep - neomycin eye ointment
gonococcal infection - purulent discharge, 48 hours after birth, gram stain, treat with penicillin or 3rd gen cephalosporin - cleanse frequently
chlamydia trachomatis eye infection - purulent, 1-2 weeks of age, identify with immunofluroscent staining, treat with oral erythromycin for 2 weeks
how should an infant born HBsAg positive mother be treated
Hep B vaccine shortly after birth to prevent vertical transmission
complete vaccine course during infancy and check antibody response
what is in the septic screen done for infants presenting with signs of sepsis
- CXR
- urine sample
- LP - CSF sample
- blood cultures
- FBC
- U&E’s
what should your immediate action be in child presenting with signs of sepsis
perform a septic screen
commence treatment without waitng for culture results
which antibiotics would you prescribe
IV broad spec gram +ve and -ve cover
BETA LACTAM (amoxicillin) for gram +ve
aminoglycoside (gentamycin) for gram -ve
if cultures negative and child clinically well after 48 hours then ABx can be stopped
why is it important to treat jaundice win neonates
to prevent kernicterus
this is billirubin induced encephalopathy caused by unconjugated bilirubin being deposited in the brain
this happens because babies blood brain barriers are not well developed so allow billirubin to cross the BBB
what may cause neonatal jaundice
physiological jaundice
infection
haemolysis/haemolytic anaemia
metabolic disease
how common is neonatal jaundice
60% of neonates experience it
what are the causes of jaundice starting <24 hours of age
congenital infection
haemolytic disorders:
- Rhesus incompatibility
- ABO compatibility
- G6PD deficiency
- spherocytosis
- pyruvate deficiency
what are the causes of jaundice between 24 hours and 2 weeks of age
physiological
breast milk jaundice
infection - UTI
haemolysis - G6PD deficiency, ABO compatibility
bruising
polycythaemia
Crigler-Najjar syndrome
what are the causes of jaundice at >2 weeks of age
unconjugated:
- physiological or breast milk jaundice
- infection (UTI)
- hypothyroidism
- haemolytic anaemia (G6PD def)
- high GI obstruction
conjugated
- bile duct obstruction (biliary atresia)
- neonatal hepatitis
what is physiological jaundice
no underlying cause behind mild or moderately jaundiced babies
bilirubin rises as infant adapts from fetal life - babies RBC have shorter lifespan (70), compared to adult (120), so increased destruction leads to higher amount of circulating bilirubin
hepatic bilirubin metabolism is less efficient in the first few days of life
can only be called physiologicla after other causes have been considered and ruled out
which type of infection in particular tends to presenta as neonatal jaundice
UTI
(investigate - urine sample, blood culture, CXR, FBC)
which type of jaundice is most worrying
persisten/prolonged jaundice
most jaundice between 2days-3weeks is physiological
however, prolonged is more likely to be sinister
what would the parents complain of in a jaundiced infant
looks slightly yellow on skin or eyes
often only visible when outside in sunlight
if prolonged jaundice was caused by biliary atresia or another type of cholestasis, what other associate symptoms would there be
pale stools
dark urine
probably off feeds and generally unwell in themselves
possible itching/scratch marks on their skin
what investigations should be done on a child presenting with jaundice
serum bilirubin level
transcutaneous billirubin measurement
if suspicious biliary atresia - USS liver is gold standard diagnosis
what factors need to be taken into consideration when assessing a jaundiced baby
age of onset (prolonged more worrying)
severity of jaundice
rate of change
gestation - pretemr infants more susceptible
clinical condition - pyrexia, hypothermia
how can jaundice be treated
PHOTOTHERAPY
- blue-green (450nm wavelength)
- converts unconjugated bilirubin into harmless water-soluble pigment by photodegeneration
- no long term sequeale
- cover infants eyes
- side effects - temp, instability, rash, bronze discolouration
EXCHANGE TRANSFUSION
- if bilirubin levels are too high to be treated with phototherapy
what are some risks for neonatal hypoglycaemia
preterm infants - lack of glycogen stores
IUGR infants - lack of glycogen stores
babies born to diabetic mothers - have hyperinsulinaemia in response to maternal hyperglycaemia
large for dates
polycythaemia
unwell for any reason
how does neonatal hypoglycaemia present
jitteriness
irratibility
apnoea
lethargy
drowsiness
seizures
what precautions need to be taken in babies at risk of neonatal hypoglycaemia
regular blood glucose monitoring at bedside
prevent by early and frequent milk feeding
if needs treating - IVI dextrose via central venous catheter
what is the role of growth chart in paeds
assess whether a childs overall height is abnormal - below 2nd or above 98th centile
ass whether a child is failing to grow to their potential - drop below centile line
assess whether a child i losing or gaining weight to quickly - could be a sign of pathology
how is mid-parental height calculated
for boys ((Dad + mum height in cm)/2)+7
for girls ((Dad + mum height in cm)/2)-7
what is the first sign of puberty in gilrs
breast development (thelarche)
usually occurs between 8.5-12.5 years
menarche occurs on average 2.5 years after the start of puberty
what is the first sign of puberty in males
testicular enlargement >4ml in volume (measured using a Prader Orchidometer)
usually occurs between 10-14 years of age
what are the normal ages of onset of puberty for girls and boys
girls - between 8-12
boys - between 9-13
what is considered early puberty in boys and girls - which are you more worried about
early in girls <8y/o
early in boys <9y/o
more worried about early puberty in boys - most commonly a brain tumour (pituitary adenoma)
in girls, early puberty more common
what is considered late puberty in boys and girls - which is more worrying
girls >13 y/o
boys >14y/o
more worrying in gilrs - can be sign of abnormal karyotype such as Turner’s or primary ovarian failure
what is the definition of short stature
height below the 2nd centile
what are the causes of short stature
familial - parental shortness, fall in mid-parental range height
IUGR and extreme prematurity
constitutional delay of growth and pubery
endocrine - GH deficiency, steroid excess (Cushing’s), hypothyroidism
syndromes - Turner, Noonan, Downs
Chronic illness and failure to thrive
psychosocial deprivation
skeletal dysplasias - disproportionate limb and back length
how do you investigate a child with short stature
serial measurements on growth chart
calculate mid-parental height
bone age scan - wrist X-ray
FBC and U&E
pituitary function test (GH)
dexamethasone suppression test (Cushing’s)
TFT
karyotype
coeliac antibodies (endomysial and ant-TTG)
what is the definiton of tall stature
height above the 98th centile
what are some causes of Tall stature
familial
obesity
syndrome - Marfan’s
hyperthyroidism
precocious puberty
congenital adrenal hyperplasia
excess GH secretion - true gigantism (then after puberty => acromegaly)
what are some causes of precocious puberty in females
breast development before 8 y/o
usually idiopathic/familial
can occasionally be late presenting CAH
what are some causes of precocious puberty in males
secondary sexual characteristics before 9 y/o
uncommon
usually brain tumour
CAH
gonadal tumour
how could you investigate precocious puberty
full history + ages parents hit puberty
USS of uterus and ovaries
boys - MRI brain
how do you treat precocious puberty
boys - treat cause
girls - if they okay, leave them. if not GnRH analogues to stop puberty progression until ready
what are some causes of delayed puberty in females
absence of pubertal development by 14 years
constituional delay (mum and sisters also did)
systemic disease - Crohn’s, organ failure, CF
hypothalamic causes - stress, anorexia, excessive athletic training
what is the most common cause of delayed puberty in boys
absence of pubertal development by 15 y/o
usually familial/constituional - may give testosterone if really bugging them
may be due to chronic disease - Crohn’s Cf, Coeliac
how to treat delatyed puberty
identify and treat underlying pathology
reassure
testosterone for boys
oestradiol for girls
what is the role of anti-mullerian hormone
produced by the sex-determining region of the Y chromosome
Role = prevent mullerian duct from persisting and instead encourage development of Wolffian ducts - stops fetus from being females and instead makes them male
what is congenital adrenal hyperplasia
a condition where there is reduced production of cortisol (+/- aldosterone)
most commonly due to 21 hydroxylase deficiency
the cortisol and aldosterone pre-cursors are instead converted into testosterone (which in gilrs causes virillisation of the external genitalia)
the reduced amount of circulating cortisol triggers a negative feedback response causing more ACTH to be released from the anterior pituitary
this then stimulates the adrenal gland to grow - hence hyperplasia
what mode of inheritanve os CAH
autosomal recessive
what is a large risk factor for CAH
consanguinous parents
how does CAH present
femal babies - ambiguous genitalia (clitoral engorgement, fusion of labia)
male babies - salt losers - slat-losing adrenal crisis - vomiting, weight loss, floppiness, circulatory collapse
non salt-losing male babies - precocious puberty, tall stature, large muscles
females may also have preociouc puberty (if they have not already present with ambiguous genitalia)
what would the biochemical abnormalities be in a salt-losing CAH baby
low plasma sodium
high plasma potassium
metabolic acidosis
hypoglycaemia
how do you treat a baby in a CAH salt-losing crisis
IV saline
IV dextrose
IV hydrocortisone
how is CAH treated
affected females - corrective surgery for external genitalia
internal genitalia not corrected until puberty/sexually active as they will need to use vaginal dilators to keeps passage patent
medical treatment - lifelong hydrocortisone (glucocorticoid) and in salt-losers lifelong fludrocortisone (mineralcorticoid)
NaCl may also need added before weaning
sick day adjustment of cortisol
what investigations need to be done in babies born with ambiguous genitalia
determine karyotype
adrenal and sex hormone levels
USS of internal structure and gonads
difference between glucocorticoid and mineralcorticoid
glucocorticoid = cortisol, control glucose
mineralocorticoid = aldosterone, controls salt, which is a mineral
what are the advantages of breastfeeding
has the optimum macronutrients needed for baby
contains maternal ABs to protect against infection
free
helps mum lose the baby weight
‘breast feeding contraception’
helps maternal and baby bonding
reduced the risk of NEC in preterm infants
can help reduce the risk of post-menopausal breast cancers
what are the disadvantages of breast feeding
mum has to do all feeds unless shes expressed milk
unknown intake so hard to quantify baby feeding amount
breast milk jaundice
transmission of drugs/infections from mum to baby
can be painful for mum
can be upsetting if baby doesn’t want to feed
insufficient vitamin D and K in breast milk - introduce solids at 6 months (for vit D) and Vit K - injection at birth
define failure to thrive
failure to gain adequate weight or achieve adequate growth at a normal rate for age OR suboptimal weight gain in infants and toddlers
can also be weight/growth faltering
serial measurements on growth charts is needed for the diagnosis to be made
how can mild and severe failure to thrive be quantified/classified
mild - fall across 2 centiles lines on growth chart
severe = fall across 3
how can you differentiate a child who is constitutionally small from a child who is failing to thrive
consider overall clinical picture - normal child will have:
- no symptoms - happy, alert, responsive, normal milestones
- parents also short
- may have been extremely premature
what are some non-organic causes of failure to thrive
MOST CHILDREN failing to thrive will be due to non-organic causes
any form of socioeconomic deprivation
maternal factors - depression, poor understanding of baby’s needs
poor housing
poverty
inadequate social support/lack of extended family
neglect/abuse
inadequate calorie intake (under-nutrition)
what are some organic causes of failure to thrive
impaired suck/swallow - inadequate intake - cleft palate, neuro-motor dysfunction, CP
cardiac disease - breathlessness during feeding
malabsorption - Coeliac, CF, food intolerance, short gut syndrome
chronic illness - renal, liver, cardiac disease
excessive calorie loss - vomiting, protein enteropathy
increased caloried requirement - malignancy, throtoxicosis, CF
chromosomal abnormalities - Down’s
how would you manage a child who is failing to thrive
full history - social factor focus
Examine - heart murmur, abdo distension, cough
bloods - FBC, U&E, CRP/ESRm, Coeliac screen, TFT
CXR and swab - CF
how do you approach treating failure to thrive
increase parental support
paediatric dietician
SALT
specialist for paediatric problem (CF - resp)
social services
nursery placement
hospital admission
organic - identify and treat cause
what is the most common surgical cause of acute abdo pain
appendicitis
uncommon under the age of 3
what is the most common cause of intestinal obstruction in neonatal period
intussusception
between 2 months-2 years
usually at ileocaecal valve
what are the causes of acute abdo pain in children
acute appendicitis
non-specific and mesenteric adenitis
intussusception
Meckel’s
malrotation
Medical cause - Lower lobe pneumonia, DKA, hepatitis, pyelonephritis
Boys - testicular torsion or strangulated hernia
what are the symptosm of acute appendicitis
abdo pain - intially central colicky and then localise to RIF
anorexia
vomiting (normally only a few times)
what are the signs of acute appendicitis
flushed face with bad breath
low grade fever
abdo pain aggravted by movement
persistent tenderness with guarding at RIF (McBurney’s)
Rebound tenderness
Rosving’s signs - LIF pressure = RIF pain
what is the clinical presentation of non-specific abdominal pain and mesenteric adenitis
non specific abdo pain = pain resolves in 24-48 hours
pain less severe than appendicitis
tenderness (and position) variable
often accompanied by URTI and cervical lymphadenopathy
what is the clinical presentation of intussusception
paroxsymal, severe, colicky pain
child become pale and draws up legs during pain
sausage shaped mass on abdo palpation
inconsolable crying
passage of RED CURRANT JELLY STOOLS
abdo distension
shock
vomiting
what is the clinical presentation of Meckel’s diverticulum
severe rectal bleeding - neither bright red or true melena
can present as intussusception
can present as volvulus (bowel obsturction)
can present as diverticulitits which mimics appendicitis
how does malrotation present
usually presents in first 1-3 days of life with intestinal obstruction
may present at any age with volvulus causing obsruction and ischaemic bowel
clinical features:
- bile or blood stained vomit
- abdo pain
- tenderness - from peritonitis or ischaemic bowel
often associated with exopthalmous and congenital diaphragmatic hernia
what is the gold standard diagnosis for appendicitis
CT abdo
how is a deifinitive diagnosis of mesenteric adenitis made
laparotomy or laparoscopy showing normal appendix and large mesenteric lymph nodes
what is the gold standard diagnosis for intussusception
USS - target sign
others - AXR - distended small bowel and no gas distally
how would you investigate suspected malrotation
urgent upper GI contrast study
need to do whenever there is blood or bile stain vomiting
how do you treat appendicitis
appendicetomy
how do you treat NSAP and mesenteric adenitis
leave alone
in some - appendicetomy may be done is symptoms persist and mesenteric adenitis can be definitley diagnosed
how do you treat intussusception
aggressive fluid resus
reduction via air enema - USS guidance
laparotomy if above does not work
how do you treat Meckel’s diverticulum
fluid resus
surgical resection
how do you treat malrotation
urgent surgical correction
how do you define recurrent abdo pain
recurrent pain, sufficient to interrupt normal activities
lasting for at least 3 months
what are the causes of recurrent abdo pain in paediatrics
GI - IBS, constipation, non-ulcer dyspepsia, abdo migraine, gastritis, PUD, IBD, malrotation, coeliacs
gynae - dysmenorrhoea, ovarian cysts, PID, pregnancy
liver - hepatitis
pancreatitis
UTI
psychological - bullying, abuse, stress
what is the clinical presentation of IBS
change of bowel habit
sensation of intra-abdo events (bloating)
pain - often worse before and relieved by defecation
mucousy stools
bloating
feeling incomplete defecation
constipation/diarrhoea/mixed
how does non-ulcer dyspepsia present
epigastric pain
postprandial vomiting
belching
bloating
early satiety
heartburn
what are the symptoms of abdominal migraine
(classic cranial migraines associated with abdo pain along with headaches)
pain is:
- midline
- paroxysmal
- associated with facial pallor
family history of migraine
what are some worrying sign/symptoms that may occur alongside recurrent abdo pain that may indicate organic disease
epigastric pain at night - haematemesis - duodenal ulcer
diarrhoea, weight loss, growth failure, blood in stools - IBD
vomiting - pancreatitis
dysuria, secondary enuresis - UTI
Vomiting and abdo distension - malrotation
How should recurrent abdominal pain be investigated?
Guided by clinical features
Essential to do urine MC&S as UTI can cause abdo pain
Endoscopy if dyspeptic symptoms
Colonoscopy if any rectal bleeding or lower abdominal symptoms
IBS – diagnosis of exclusion
How is IBS treated
Can talk to a dietician about possible exclusion diets to see if any particular food aggrevates symptoms
Manage stress
Antispasmodics (for the pain) – i.e. mebeverine
Anti-diarrhoea – loperamide
Laxatives if they are suffering constipation
How is non-ulcer dyspepsia treated?
If H. pylori - needs eradicating with triple therapy
How is abdominal migraine treated?
Pizotifen – a serotonin receptor antagonist
Used as prophylaxis in children with frequent, severe symptoms
What is the definition of posseting?
Non-forceful return of small amounts of milk
Usually accompanied by wind
Occurs normally in nearly all babies
What is regurgitation?
Non-forceful return of milk
Larger, more frequent losses than possetting
Usually indicates gastro-oesophageal reflux
what is the definition of vomiting
Forceful ejection of gastric contents
What are the causes of vomiting in infants?
Reflux (very common)
Feeding problems
Infection (gastroenteritis, whooping cought, UTI, meningitis)
Dietary protein intolerances
Intestinal obstruction (pyloric stenosis, atresia, Hirshprung’s, malrotation, intussusception etc.)
Inborn errors of metabolism
CAH
Renal failure
What are the causes of vomiting in pre-school children?
Gastroenteritis
Other infections (kidneys, septicaemia, meningitis)
Appendicitis
Intestinal obstruction (intussusception, maloration, volvulus, adhesions)
Raised ICP
Coeliac disease
Renal failure
Inborn errors of metabolism
Torsion of testis
What are the causes of vomiting in school age children/adolescents?
Gastroenteritis
Other infection – kidneys, septicaemia, meningitis
Peptic ulcers
Appendicitis
Migraine
Raised ICP
Coeliac
DKA
Alcohol/drugs
Cyclical vomiting syndrome
Bulimia
Pregnancy
Testicular torsion
What are some diagnostic clues in the vomiting infant?
Bile stained – exclude intestinal obstruction
Blood in the vomit – oesophagitis, peptic ulcer, oral/nasal bleeding, malrotation
Projectile vomiting in the first few weeks of life – exclude pyloric stenosis
Associated symptoms – CNS, GI, UT infections
Vomiting after paroxysmal cough – whooping cough (Pertussis)
Dehydration or shock – could be an obstruction – 3rd spacing 🡪 shock
Abdominal distention – exclude lower intestinal obstruction and strangulated inguinal hernia
How do you manage a vomiting infant?
VITAL SIGNS
ASSESS FOR DEHYDRATION AND SHOCK
Rehydrate and support
Find and treat underlying cause
Reflux is common in infants, but can progress to GORD. What features are associated to class it as a disease?
Faltering growth/failure to thrive
Oesophagtis +/- stricture
Apnoea
Aspiratation, wheezing, hoarseness – often comes as referrals from respiratory
IDA
Seizure like events/opsthotonos (acid causes arching of the back to adjust position)
What is the gold standard diagnosis for GORD?
pH study
What other investigations might you do for GORD?
Barium swallow and meal
Endoscopy
PPI trial
How to manage a baby with GORD?
Position of their feeds - on their left, hold them upright
Thicken feeds - gaviscon
Drugs - antacid, H2 blocker (ranitidine), PPI
Surgery – fundoplication
What is the definition of diarrhoea?
Change in the consistency of stools (loose/liquid)
And/or increase in the frequency of passing stools
Acute – less than 2 weeks
What are some causes of acute diarrhoea?
Viruses – rotavirus, norovisu, enterovirus, many more
Bacteria – C.diff, E.coli, salmonella
Parasites – giardia
Other infections – otitis media, tonsillitis
Food allergies and other diseases
What is hypernatraemia dehydration?
Complication of diarrhoea
Happens because the water loss exceeds the sodium loss
Difficult to detect – blood test shows serum sodium > 145
Unusual and serious
Irritable with doughy skin
Water shifts from intracellular to extracellular
Rehydration should be slow
What are the features of hypernatraemic dehydration?
Jittery movements
Increased muscle tone
Hyperreflexia
Convulsions
Drowsiness/coma
Doughy skin
Irritable
How do you investigate a child with diarrhoea?
Firstly – ASSESS FOR DEHYDRATION – cap refill, pinch test, sunken eyes, mucous membranes
Look for an underlying cause
How do you manage a child with acute diarrhoea?
Encourage normal diet
Assess and treat dehydration – either oral or IV/NG if severe
Supportive therapy
Treat underlying cause if possible – antibiotics, probiotics
What is the most common GI related food allergy?
Cow’s milk protein allergy
This is NON IgE mediated
How does cow’s milk protein allergy present?
Loose stool
Vomiting
Failure to thrive
Reflux
Mouth ulcers
Atopic history (eczema, asthma, hayfever)
Bloody stools
Constipation
Very rarely – anaphylaxis
How does lactose intolerance present?
Explosive watery stools
Abdominal distention
Flatulence
Audible bowel sounds
How is cow’s milk protein allergy diagnosed?
Elimination damage
How is cow’s milk protein allergy treated?
Change feeds – hydrolysed or powdered milk feeds
Hope that the child will “grow out of it” eventually
What are the main causes of malabsorption?
Small intestine disease – coeliac
Exocrine pancreatic dysfunction – i.e. in CF (absence of lipase, proteases and amylase lead to defective digestion)
Cholestatic liver disease/biliary atresia – malabsorption of fat due to lack of bile salts
Short bowel syndrome – resection due to congenital abnormalities/NEC. Nutrient, water and electrolyte malabsorption
Loss of terminal ileum function – resection, Crohn’s. absent bile acid and vitamin B12 absorption
How does malabsorption present?
Abnormal stools – difficult to flush, extremely offensive odour
Failure to thrive/poor growth
Specific nutrient deficiencies e.g. iron deficiency anaemia, B12 deficiency
What is the classic coeliac disease history?
Present in the first few years of life after introduction of gluten in cereals
Generally irritable
Abnormal stools (smelly, diarrhoea, floating)
Abdominal distention
Buttock wasting
Failure to thrive/poor growth
What investigations do you do for coeliac disease?
Antibodies – endomysial antibodies and tissue transglutaminase antibodies
Gold standard diagnosis – intestinal (jejunal) biopsy showing villous atrophy and crypt hyperplasia
How is coeliac disease treated?
Lifelong gluten free diet
Define constipation and encopresis
Constipation = painful passage of hard, infrequent stools
Encopresis = involuntary soiling
What causes constipation in young children?
Child may avoid defecating due to pain (i.e. they have a transient superficial anal fissue)
Occasionally follows – forceful potty training, use of uncomfortable toilets (on holiday/at school) or psychological family stress
How does constipation cause soiling?
Child avoids toileting due to pain
Prolonged faecal status = resorption of fluids = increase in size and constistency
Can lead to stretching of the rectum (stools withheld for a long time due to not wanting to defecate)
This leads to reduced sensation
Which can lead to overflow and soiling
What are some red flags to be aware of in a constipated child?
Delayed passage of meconium – Hirshprung’s, CF
Fever, vomiting, bloody diarrhoea
Failure to thrive
Tight empty rectum and palpable abdo mass – Hirshprung’s
Ejection of stools on PR – Hirshprung’s
Abnormal neuro examination – abdo exam in children should include SPINAL EXAMINATION due to close proximity of the rectum
What are the long term complications of constipation?
Acquired megacolon
Anal fissues
Overflow incontinence (soiling)
Behavioural problems
What are some differential diagnoses for constipation in children?
Hirschsprung’s
Anorectal malformations
Spina bifida
Neuromuscular disease
Hypothyroidism
Hypercalcaemia
Coeliac
Food allergy/intolerance
CF
Sexual abuse
Poor diet
What investigations need to be done for constipation?
Clinical diagnosis
Abdo exam – hard stools palpable
Further Ix only if organic cause suspected
How is constipation treated?
Diet, fluids, exercise
Toilet training – sit after breakfast/lunch/dinner
Star charts – simple reward scheme
Medications
Softener – lactulose
Movicol
Stimulant – senna, dulcolax
Bulking agent – fybogel
What are the pathological features of Crohn’s disease?
Affects the mouth to anus
Transmural inflammation
Discontinuous with skip lesions
GRANULOMATOUS
Rectal sparing
Fissures, fistulae, abscesses and strictures
Perianal disease
What causes Crohn’s disease?
Unknown
How does Crohn’s disease present in paediatrics?
FAILURE TO THRIVE – poor growth, delayed puberty
Abdominal pain
Diarrhoea
Rectal bleeding
Tiredness/malaise
Extra GI symptoms – fever, arthritis, uveitis
Can present identical to anorexia nervosa – important to think about this
What is the main differential diagnosis for Crohn’s?
Ulcerative colitis
How is Crohn’s investigated?
Clinical examination
Endoscopy
Histology – look for granulomas
Biochemistry – inflammatory markers
How is Crohn’s treated in paeds?
Exclusive enteral nutrition – feed them loads of milk for 7-8 weeks and they get better
Corticosteroids – prednisolone, budenoside
Aminosalicylates – sulfasalazine, mesalazine
Antibiotics
Immunomodulators – MTX, azathioprine, 6-mecaptopurine
Biologics – infliximab, adalimumab
Surgery
What are the pathological features of UC?
Affects ONLY the colon
And ONLY the mucosa
No granulomas
No skip lesions – the whole colon is affected
Ulcers
Increased risk of adenocarcinoma in adulthood
How does ulcerative colitis present in paeds?
Failure to thrive/weight loss
Rectal bleeding
Diarrhoea
Colicky pain
Extra GI – mouth ulcers, arthritis, erythema nodosum, spondylitis
What are some differential diagnoses for UC?
Crohn’s disease
Infective causes of colitis e.g. C. Diff
How is UC diagnosed?
Colonoscopy – friable membranes (bleeding), visible ulcers
How to treat ulcerative colitis?
Mild attacks – topical steroids when confined to rectum/sigmoid colon, sulfasalazine for more extensive disease
Severe disease –systemic steroids
1/3 patients – colectomy (curative)
What is the first step of asthma management?
Very low dose inhaled corticosteroid
Plus salbutamol PRN
What are the Fraser guidelines?
Used to assess if a patient who has not yet reached age is competent to consent to treatment.
Criteria:
Understands the professional’s advice
Cannot be persuaded to inform their parents
Likely to begin or continue sexual intercourse without contraception
Physical and mental health will suffer if they don’t get the contraceptive treatment
The young person’s best interests require them to receive contraceptive treatment with or without parental consent
What is the main risk factor for neonatal respiratory distress syndrome?
Prematurity
What is the main risk factor for transient tachypnoea of the newborn?
Caesarean section
What are the features of a severe asthma attack?
SpO2 < 92%
PEF 33-50%
Too breathless to talk or feed
Heart rate - >125 (>5 years), >140 (1-5 years)
Resp. rate > 30/min (> 5 years), > 40 (1-5 years)
Use of accessory neck muscles
What are the criteria for a life threatening asthma attack?
SpO2 < 92%
PEF < 33%
Silent chest
Poor respiratory effort
Agitation
Altered consciousness
Cyanosis
What causes measles?
Infection with the measles virus
Droplet infection is the method of transmission
Highly contagious
What is the main risk factor for contracting measles?
Avoidance of the MMR vaccination
What are the symptoms of measles?`
PRODROMAL SYMPTOMS - CCCK:
Cough
Coryza (runny nose/cold like symptoms)
Conjunctivitis
Koplick spots (white spots on the buccal mucosa – pathognomonic)
RASH – maculopapular, spreads downwards from behind the ears to the whole of the body
Fever
Marked malaise
What are some complications of measles?
Respiratory – pneumonia, otitis media, tracheitis
Neurological – febrile convulsions, encephalitis
Diarrhoea
Hepatitis
Corneal ulceratoin
Appendicits
Myocarditis
How is measles diagnosed?
Clinical diagnosis
Can confirm with serological testing of blood or saliva
How is measles treated?
VIRAL ILLNESS so supportive treatment only (symptomatic, fluids If needed, isolate if in hospital)
Antivirals in immune compromised
School exclusion for 5 days from onset of rash
Best treatment – preventative vaccine
What are the risk factors for developing mumps?
Unvaccinated children
What are the clinical features of mumps?
Fever
Malaise
Parotitis (swollen parotid gland)
May complain of pain eating and drinking
May complain of earache
Hearing loss can occur – usually unilateral and transient
What are some complications of mumps?
Viral meningitis and encephalitis
Orchitis – reduced sperm count in males
Oophoritis
Mastitis
Arthritis
How is measles diagnosed and managed?
Clinical diagnosis
Management – symptomatic (viral illness)
School exclusion for 7 days from onset of parotitis
What time of year do you expect to see rubella virus?
Winter and spring months (could be a hint in questions)
Describe the rash seen in Rubella
Maculopapular rash starting on the face and spreading across the entire body
NOT itchy in children (but is in adults)
Rubella is a diagnosis made clinically. In which situation would you need to perform serological testing to confirm your diagnosis?
When there is a risk of exposure to non-immune pregnant lady
Congenital Rubella – cataracts and sensorineural deafness
How is rubella treated?
No effective anti-viral treatment
Usually resolves in 3-5 days
Prevention lies in immunisation
How are the human herpes viruses transmitted?
Through mucous membranes of skin
Kissing
Genital contact
Vertical transmission at birth
How do herpes simplex viruses present?
Gingiostomatitis – sores on the lips, gums, tongue and hard palate – can lead to ulceration and bleeding, common reason why child may refuse to eat or drink
Cold sores
Herpetic whitlows – in thumb suckers
Conjunctivitis and inflammation of the eyelids
CNS infection – aseptic meningitis (self-resolving), encephalitis
How is herpes simplex diagnosed and treated?
Clinical diagnosis
Acyclovir
Give during pregnancy especially to stop transmission to baby
Which infecting organism causes chickenpox and what other infection may it cause?
Varicella zoster virus
(human herpes virus 3)
May also cause shingles virus later in life – reactivation and then a rash appears in a dermatomal distribution
How is chickenpox spread?
Droplet infection via the respiratory route
Highly infectious – contagious from 2 days before the rash appears and until it disappears
Describe the rash seen in chickenpox?
Vesicular rash
Very itchy
Starts on the head and trunk and progresses to the peripheries
What is the typical prodrome of chickenpox?
High fever – 38-39*C
Usually stops when the rash appears
What are some complications of chickenpox in the immunocompromised?
Haemorrhagic lesions
Pneumonitis
Progressive and widespread infection
DIC
How is chickenpox managed?
Camomile lotion to stop the itching
Keep away from high risk individuals – i.e. don’t put them anywhere near a clinical area in which there are immune suppressed patients
How do you protect immune compromised individuals who have been exposed to chickenpox?
Human varicella zoster immunoglobulin (HVZIG)
(bone marrow transplant patients, congenital or aquired immune deficiency, steroids, neonates)
What are the clinical features of glandular fever and which organism causes it?
Fever
Malaise and extreme lethargy
Tonsillopharyngitis
Prominent cervical lymphadenopathy
Petechiae on soft palate
Splenomegaly
Hepatomegaly
Maculopapular rash
Jaundice
Caused by Epstein Barr virus
What investigations can be done for EBV?
Positive monospot test
Seroconversion – IgG to Epstein-Barr virus antigens
Treatment = symptomatic
What childhood rash is caused by HHV6?
Roseola infantum
Generalised macular rash which appears after the prodromal fever wanes
Common cause of febrile convulsions
What is the presentation of “slapped cheek syndrome” and which infecting organism causes it?
Most common during spring
Fever, malaise, headache, myalgia – prodromal
Characteristic cheek rash – looks like they have been slapped on the cheeks
Progresses to maculopapular rash on the trunk and limbs
Caused by parvovirus b19
What is the pathology of parvovirus B19 and which group of children is this dangerous for?
Infects the red cell precursors in the bone marrow
Can lead to aplastic crisis in children with chronic haemolytic anaemias (sickle cell, thalassaemia) and immunocompromised children
What infection is caused by coxsackie virus?
Hand, foot and mouth disease
What are the symptoms of hand, foot and mouth disease?
Painful vesicular lesions on the hands and feet
Painful ulcers in the mouth and on the tongue
Systemic features are mild
Subsides in a few days
Which ways can staph aureus cause disease?
Direct effect – abscess, cellulitis, oesteomyeltitis, impetigo, septic arthritis, septicaemia
Toxin-mediated (indirect) – TSS, food poisoning
Toxin-mediated (direct) – scalded skin syndrome
Which infecting organism causes scarlet fever?
Strep. Pyogenes (group A beta haemolytic strep)
Same bacteria that causes strep throat
