Paeds Flashcards
Risk factors for meconium aspiration syndrome
post-term
maternal HTN
maternal PE
chorioamnionitis
smoking
substance abuse
Is trimethoprim safe during breastfeeding?
Yes
Trimethoprim passes into breast milk in small amounts and is unlikely to cause SE in your baby.
Over long time it may affect your baby’s folic acid levels. If you need to take trimethoprim for longer than a few weeks, talk to your doctor or pharmacist.
Name innocent murmurs found in childhood
Ejection murmurs (turbulent BF at the outflow tract of the heart)
venous hums (due to turbulent BF in the great veins returning to the heart; continuous blowing noise heard just below the clavicles)
Still’s murmur (low-pitched sound heard at the lower left sternal edge)
peak incidence of ALL
2-5 yo
Cyanotic congenital heart disease - when is it TGA and when TOF?
presenting in…
first days of life -> TGA
at 1-2 months -> TOF
What type of medication is dosulepin?
TCA
Which TCAs are more and which ones are less sedative?
More:
- amitriptyline
- clomipramine
- dosulepine
- trazodone (tricyclic related antidepressant)
Less:
- imipramine
- lofepramine
- nortriptyline
causes of increased nuchal translucency?
Down’s syndrome
congenital heart defects
abdominal wall defects
features of foetal alcohol syndrome
flat philtrum
microcephaly
underdeveloped jaw
short palpebral fissure
thin vermillion border/hypoplastic (thin)upper lip
learning difficulties
cardiac malformations
epicanthic folds
growth retardation
when is CVS performed? When is amniocentesisi performed?
CVS: 11w - 13+6
Amnio: 15w +
Features of Edward syndrome
trisomy 18 (second most common autosomal trisomy)
- micrognathia
- low-set ears
- rocker bottom feet
- overlapping of fingers
- heart/lung abnormalities
Mx of meconium aspiraton syndrome
Born @ term with MSAF, clinically well, no hx of GBS -> observations, routine care, no abx needed
Born through MSAF + RFs + tachypnoea in the delivery room
-> can be mild, moderate or severe (latter 2 should be managed in tertiary care)
-> will include observation, monitoring sats, blood gases, FBC, CRP, blood cultures
- if needed abx
mild MAS mx
= <40% oxygen for 48h
monitor blood gas and sats
monitor FBC and CRP, blood culture
nutritional support
abx only if RFs present
does not need to be in tertiary care centre
moderate MAS mx
manage in tertiary care centre
= >40% oxygen for > 48h
CPAP
monitor ABG, dual O2 sats
FBC, CRP, blood culture
IV fluids
abx (IV ampicillin and gentamicin)
vent support if O2 requirement >60%
severe MAS mx
= need for assisted ventilaion
manage in tertiary care centre
PPHN +/-
monitor ABG, BP, dual o2 sat
FBC, CRP, blood culture
cardiac echo
work up for sepsis
start abx
nutritional support
inhaled NO for PPHN
What is PPHN?
persistent pulmonary HTN of newborn
Which abx would you give in MAS?
IV ampicillin AND gentamicin
Form or resp support in MAS
O2 therapy and non-invasive ventilation (e.g. CPAP) may be used in more severe cases
boluses of surfactant and inotropes given in moderate cases
Timing of onset of IgE and non-IgE cow’s milk protein allergy
IgE: within minutes (up to 2h) of ingestion
Non-IgE: 2-72h of ingestion
how common is cow’s milk protein allergy
affects 5-15% infants
Mx of cow’s milk protein allergy
breastfeeding: mum should avoid cow’s milk products (note it takes 2-3 weeks to eliminate cow’s milk from breastmilk)
formula: switch to hypoallergenic formula
consider calcium + vit D supplementation
how long does it take to eliminate cow’s milk from breastmilk?
2-3w
When should you refer a child with cows milk protein allergy to A&E?
if CVS / respiratory signs are present
anaphylaxis
Where should you refer children with CMA?
allergy testing and paediatric dietician (if IgE mediated is suspected or if non-IgE is severe)
What is severe non-IgE CMPA?
if measures taken for mild/moderate have not been effective and are severe
Sx to look out for:
- Skin: pruritus, erythema, atopic eczema
- GI: GORD, vomiting, loose stools, bloor or mucous in stools, abdominal pain or discomfort, infantile colic, food refusal or aversion, constipation, perianal redness, pallor or tenderness, faltering growth
- Resp: cough, wheeze, SoB
Mx of IgE mediated CMPA
mild:
- excl BFing: mum to exclude milk products, take caclium and vit D
- if formula/mixed feeding, try extensively hydrolysed formula
- refer to allergy testing at specialist and a paediatric dietician
severe:
as above plus: consider elemental (amino acid) formula if extensively hydrolysed not effective
- ref to A&E is resp/CVS sx present as there is a risk of anaphylaxis
Mx of non-IgE mediated CMPA
Mild:
- exclusively BFing:
exclude milk products from mum’s diet for 2-4w followed by home reintroduction to confirm dx (mum to take calcium and vit D supplementation)
-mixed/formula feeding: trial of extensively hydrolysed formula
(be wary of making this diagnosis as vomiting and diarrhoea are quite common)
severe:
Mx of non-IgE mediated CMPA
Mild:
- exclusively BFing:
exclude milk products from mum’s diet for 2-4w followed by home reintroduction to confirm dx (mum to take calcium and vit D supplementation)
-mixed/formula feeding: trial of extensively hydrolysed formula
(be wary of making this diagnosis as vomiting and diarrhoea are quite common)
severe: sx not improving despite measures and are severe.
-> continue mx as per non severe
-> urgent referral to local paeds allergy service
-> urgent referral to dietician
ADVISE COW’S MILK FREE DIET UNTIL CHILD IS 9-12 MONTHS AND FOR AT LEAST 6 MONTHS IF NON-IgE MEDIATED ALLERGY IS CONFIRMED.
-> then commence milk ladder (available from allergy UK) to see if tolerance is acquired.
Another term for non-IgE CMPA?
delayed CMPA
Summarise the milk ladder
1) starts with wellcooked (baked) milk products (form of milk least likely to cause an allergic reaction; also flour binding with the baked milk makes it less allergenic. heating -> protein is changed into a less allergenic form)
2) then lightly cooked milk products (less baked) or heated milk products without flour are given
3) uncooked fresh milk can be tried when recommended.
How should you monitor children (weaned infants/older children) affected by CMPA?
exclude CMP from their diet
offer nutritional counselling and paediatric dietician
regularly monitor growth
re-evaluate child every 6-12 months (incl. re-intorduction of milk using the milk ladder)
How should you monitor children (weaned infants/older children) affected by CMPA?
exclude CMP from their diet
offer nutritional counselling and paediatric dietician
regularly monitor growth
re-evaluate child every 6-12 months (incl. re-intorduction of milk using the milk ladder)
What can be heard in PDA?
continous machniery like murmur
left subclavicular thrill
What are the symptoms of Rheumatic Fever>
remember: JONES criteria
J = Joints (migratory polyarthritis)
♥ = Pancarditis
N = Nodules
E = Erythema marginatum
S = Sydenham chorea
What is rheumatic fever?
two to four weeks after an untreated infection with group A Streptococcus (GAS)
The pathogenic mechanisms that cause RF are not completely understood, but molecular mimicry between streptococcal M protein and human cardiac myosin proteins is thought to play a role.
1st and 2nd line management of croup
- single dose oral dexamethasone 0.15 mg / kg
If oral not possible:
- IM dexamethasone 0.6 mg / kg
-inhaled beclomethasone 2 mg
Supportive management in croup
analgesia and antipyretics (paracetamol/ibuprofen)
advice fluid intake
supplement oxygen if needed
nebulised adrenaline 1:1000 1 mg/ml if severe
Intubation rarely needed
What are indications for admission in croup
- oxygen requirement
- features of moderate or severe illness
- impending resp failure
- RR > 60/min
- toxic appearance
- also consider admission in children with mild illness who have a lower threshold for admission (e.g CLD, hemodynamically significant heart disease, immunodeficiency, age under 3 months, inadequate fluid intake, factors affecting carer’s abilities and longer distance to healthcare in case of deterioration)
find out abo
What virus causes croup and at what time of the year
Parainfluenza virus is responsible for 75% cases
most common in fall and winter.
What is the abnormality in osteogenesis imperfecta?
-> brittle bone disease, increased risk of fractures (type of skeletal dysplasia)
mutations in type I collagen lead to impaired osteogenesis (various genetic defects can lead to OI)
there are 2 types:
- type I is more common and milder
- type II is more severe and usually fatal in the 1st year of life
How is osteogenesis imperfecta diagnosed?
DNA test
USS before birth and radiographic skeletal survey afterwards (to visualise fractures, causes, deformities)
Bone or skin biopsy to examine collagen
Mx of osteogenesis imperfecta
no definitive treatment available
supportive measures: walking aids, wheelchairs, devices to improve mobility and function
bisphosphonates to increase cortical thickness and decrease # risk
surgery to improve mobility and correct associated skeletal defects
Prevalence of osteogenesis imperfecta
1/10.000-20.000
1:1 m:f
what is the life expectancy with osteogenesis imperfecta?
with mild forms -> normal
with very severe form (type 2) usually lethal in the first year of life
Inheritance pattern of osteogenesis imperfecta
AD is most common but cam also be AR
What are the features of osteogenesis imperfecta?
short stature
triangular face appearance
blue sclera
deafness (affected ossicles)
dentinogenesis imperfecta
scoliosis
frequent fractures
bone deformities
tendon instability
ligamentous laxity and joint hyper mobility
remember BITE: bones, I (eye - blue sclerae), teeth (dental abnormalities), Ears (hearing loss)
How common is achondroplasia?
1:15.000 - 40.000
what mutation is responsible for achondroplasia?
gain of function mutation in fibroblast growth factor receptor 3 gene on Chr 4
-> new sporadic mutations in ~80% (probability increases with the father’s age at the time of conception)
What is the underlying pathophysiology in achondroplasia?
defective FGFR3 mutation -> inhibited chondrocyte proliferation -> endochondral ossification -> impaired longitudinal bone growth
Outline the P-GALS assessment
- screening Qs
- Inspection
- Gait
- arms
- legs
- spine
also TMJ
What Cobb angle is seen in scoliosis?
> 10 degrees
what is scoliosis?
deformity of the spine
occurring during growth
characterised by a lateral curvature and simultaneous rotation of the vertebrae
what gender is more affected by scoliosis?
females > male in idiopathic adolescent scoliosis
juvenile and infantile idiopathic scoliosis is more common in males.
What is the management of SA in children?
2 weeks of IV flucloxacillin
followed by 4 weeks oral flucloxacillin
review by orthodontist, may need washout of the joint
Causes of septic arthritis
haematogenous spread (most common)
direct contamination (iatrogenic, trauma)
Contiguous spread (septic bursitis, osteomyelitis)
Management of scoliosis
referral to paeds ortho
- back brace
- PT
- surgery may be indicated in some severe, rapidly progressing cases
What is calculated in ?scoliosis?
Cobb’s angle
What investigation for scoliosis?
X-ray spine
What antibodies could be seen in someone with coeliac disease and IgA deficiency?
IgG
anti-tTG and anti-endomysial
Antibiotiv options in whooping cough
ACE
azithromycin used if >1 month (for 21d)
Clarithromycin used if <1month
Erythromycin used if pregnant
can use co-trimoxazole if macrolides are contraindicated (but not in pregnancy or if <6 weeks old)
What is the full name of GTN?
glyceryl trinitrate
