Neonatal and Newborn Flashcards
What are the different types of neonatal jaundice
unconjugated - pre-hepatic
conjungated - hepatic and post-hepatic
What is the neonatal jaundice
it is hyperbilirubinaemia in a newborn. It can be a physiological response. but can also be pathological
causes of physiological neonatal jaundice
1) marked physiological release of haemoglobin from the breakdown of RBC due to the high Hb conc. at birth
2) RBC life span is 70 days and adults 120 days
3) hepatic bilirubin metabolism is less efficient in the first few days of life
what can kernicterus cause in infants
acute - lethergy, poor feeding
severe cases - irritability, inc muscle tone leading to acrched back (opisthotonos), seizures, coma
long term - cerebral palsy, LD, sensorineural deafness
signs/symptoms of neonatal jaundice
jaundice - check by blanching of skin (start from head to toe and trunk and limbs last)
dark urine
pale stool
hepatomegaly
poor weight gain
investigation for neonatal jaundince
Blood tests
total and conjugated bilirubin level
FBC
Coomb’s test
transcutaneous bilirubinometer (>35 wks)
Urine sample septic screen if necessary LFT TFT sweat test - CF
management for neonatal jaundice
Support - rehydration, treat underlying causes
phototherapy is the treatment of choice
exchange transfusion in severe cases
differentials for neonatal jaundice
biliary atresia CF hypothyroidism CMV infection duodenal atresia haemolytic disease of newborn Hep B
symptoms of neonatal jaundice
lethergy and poor feeding
dehydration - less intake of feeding
jaundice
clinical findings of neonatal jaundice
jaundice
petechial or purpuric lesions
anaemia
hepatosplenomegaly
what infection can cause neonatal jaundice
rubella HAV HBV CMV herpes syphilis
complication of neonatal jaundice
kernicterus - bilirubin encephalopathy - medical emergency
RF for neonatal jaundice
sibling of neonatal jaundice
East asian
breast fed baby
baby of DM mum
what is birth asphyxia
condition caused by hypoxia in the neonatal period –> hypoxia –> lactate production, acidosis –> tissue/organ damage –> brain could potentially damaged
RF for birth asphyxia
pre-mature baby
aetiology of birth asphyxia
dec BP/blood flow to the placenta of the infant during delivery
could be due to prolapse cord, inadquate circulation or perfusion, inadequat relaxation of uterus due to excess oxytocin, premature seperation of placenta/placental insufficiency
RF for birth asphyxia
older mum prolonger rupture of membranes multiple births lack of antenatal care low birthweight baby
symptoms/clinical findings of birth asphyxia
not breathing when baby born
cyanosis
Ix for birth asphyxia
umbilical cord pH check ABG/VBG –> acidosis (ph < 7.05)
what score is used for birth asphyxia assessment
APGAR score
HR RR muscle tone reflex, irritability colour
what is APGAR score
it is a score used to assess the vital sign of a newborn baby
normal score for APGAR score
7/10
mangement of birth asphyxia
rapid resus
ABCDE
drugs - adrenaline 0.01 to 0.1 solution
hypothermia treatment (reduce body temperature to 3 degree to lessen physiological effect of the body)
prognosis of birth asphyxia
death and severe handicap in 25% of severely asphyxiated full term infants
what is infant respiratory distress syndrome
condition causes by lack of surfactant production –> less surface tension in the alveolar space and so alveolar collapse and respiratory distress
how common is IRDS
5% in full-term baby
> 50% in pre-term babe if 26-28 gestation age
causes of acute respiratory distress in premature infants
IRDS pneumonia (congenital/acquired) pneumothorax diaphragmatic hernia cardiac causes
what can surfactant insufficiency cause to the oxgentation of the blood
less alveolar less air exchange
R to L shunting –> can happen intra-pulmonary (in the lung) or extra-pulmonary (across the ductus arteriosus or foramen ovale)
what are some of the secondary cause of surfactant deficiency
intra-partum asyphyxia
pulmonary infection - eg group B-haemolytic strep. pneumonia
pulmonary haemorrhage
meconium aspiration pneumonia
congenital diaphragmatic hernia and pulmonary hypoplasia
RF to IRDS
premature delivery male Mum is diabetic Caesarian Hypothermia perinatal asphyxia FHx of IRDS
clinical features of IRDS
tachypnoea
recession - intercostal, subcostal, sternal
expiratory grunting
cyanosis
tracheal tug
nasal flaring
heading bobbing
silent chest
SpO2 <85%
investigation for IRDS
Sats to see if hypoxic - aim for 91-95%
CXR - ground glass appearance and air bronchogram
ABG - both resp and metabolic acidosis
what specific CXR findings suggest IRDS
ground glass appearance
air bronchogram
management of IRDS
ABCDE
resp support - O2 aim for 91-95%
CPAP or IPPV or intubation
surfactant - given via an endotracheal tube
treat any underlying conditions eg ABX
what are some preventive management for IRDS
antenatal dexamethasone to encourage rapid maturation of lung tissue of the infant
delay premature birth —> tocolytic agents
complications of IRDS
pneumothorax
pneumonia
intra-ventricular haemorrhage
delayed cognitive impairment
bronchopulmonary dysplasia
retinopathy of prematurity (due to O2 perfusion)
what is a pigmented naevi
a pigmented macular/plaque of lesions of birthmark
start to appear at 2 yrs
low risk of malignancy
what is a cafe-au-lait spot
uniformly pigmented, sharply demarcated, macular lesion
maybe prest at birth or develop in childhood, vary in size
what would be red flag symptoms in the presence of cafe-au-luit spots
extensive spots are features of neurofibromatosis (congenital condition that forms tumours in nerves)
what is strawberry naevus
it is superficial/infantile haemangioma
what is the clniical findings of strawberry naevus
bright red
protuberant
compressible
sharply demaracted (Starwberry for sharplt demaracted)
may vary in size in 12-18 months of baby life before fading, most spontanouesly fade
does strawberry naevus require treatment
no usually unles in sensitive area eg around eye, lips, airway etc and only if interferting with vital function
treatment for strawberry naevus
usually no treatment but if affecting functions then
beta-blocker +/- corticosteriods
surgery if required
what is naevus flammeus
small pink flat lesions commonly on eyelids, neck and forehead
most common between eyebrows and forehead
usually fades and no-harmful
what can Naevus flammeus suggest
Beckwith-Widemann Syndrome - condition of growth regulation leading to overgrowth
what is mongolian blue spots
blue or slate-grey lesions, commonly in sacral area
where can you find most of the mogolian blue spots
in the sacral area of the baby
which population is more commonly born with Mongolian blue spots
> 80% of black and Asian babies
aetiology of Mongolian blue spots
collection of melanocytes in deep dermis
what admin work should you do for Mongolian blue spots
document it in notes to avoid confusion of bruises for later which can relate to abuse issues
will Mongolian blue spots resolve itself
usually within the first few years of life
what is port-wine stain
mature, dilated, dermal capillaries
clinical findings of port-wine stain
macular, sharply circumscribed, pink to purple lesion
can vary in size
will port-wine stain resolve itself
vasuclar lesion whcih will perisist
what is a red flag for port-wine stain
if localised to trigeminal area of ace, sonsider Sturge-Weber Syndrome(seizure. LD. port-wine stain due tp underling meningeal haemangioma + intracranial calcification)
what is cephalhaematoma
it is a collection of blood in the periosteum layer (just under the skin of skull) due to tearing of vessels during birth/at any aged human
RF for cephalhaematoma
pre-term baby
instrumental delivery of babies
symptoms/clinical findings of cephalhaematoma
selling appearing from hours 50 2-3 days post birth
if severe –> jaundice, anaemia or hypotension
takes weeks for blood clots to be absorbed
selling slowly moves towards the centre of head
it will not cross any cranial sutures
management of cephalhaematoma
observation
prognosis of cephalhaematoma
meningitis/osteomyelitis - due to fracture in the skull leading to infection
definition of haemolytic disease of the foetus and newborn
transplacental passage of maternal antibodies reacting to antigen of foetal RBC
what are the 2 main haemolytic diseases of the foetus and newborn
1) . ABO blood group incompatibility
2) . rhesus incompatibility
how does rhesus incompatibility cause HDN
mother rhesus -ve and foetus rhesus +ve and so during pregnancy and delivery, foetal RBC cross the placental barrier to enter the body of mum
mum develops anti-rhesus antibodies which can then cross the placenta to causing haemolysing effect on the foetus
first child might be okay but successive child will defo be affected
wich one of the HDN is most common
ABO blood group incompatility
Rhesus incompatility has now been reduced with Rh immunoglobulin to Rhesus -ve women during prgancy/shorty after birth of a rhesus +ve babe
what other procedure can trigger primary immune response of mum rhesus snesitvity
aminocentesis
how can ABO incompatibility cause HDN
Mother most commonly group O and baby is group A. Mother’s natural anti-A antibodies react with fetal cells haemolysis + jaundice.
can you detect HDN
you can detect Rhesus but not ABO incompatibility
clinical features of HDN
foetal anaemia –> if untreated, severe oedema –> hydrops –> fluid collection in multiple compartments of the bay eg ascites, pleural effusion leading to death
jaundice development within first 24 hours of life –> kernicterus
which type of HDN more likely to cause IRDS
rhesus incompatibility
management of foetus in HDN
deliver before severe haemolysis occur
series of exchange transfusions to remove antibodies + toxic bilirubin
late anaemia can develop –> need top up blood transfusion
management of mum in HDN
rhesus -ve women immunised with anti-D immunoglobulin
prognosis of HDN
kernicterus main worry
can develop IRDS
can develop hydrops
sensorineural hearing impairment
definition of prematurity
birth at <37 wks
how common is prematurity
approx. 7% incidence
1% severe (<1500g)
what are the modifiable factors of prematurity
short inter-pregnancy time (2x risk inc)
lifestyle factor - BMI < or > 35 smoking
psychological stress
intra-uterine/vaginal infection
what are the non- modifiable factors of prematurity
Pace –> black baby have higher risk
previous pre-term birth
chronic medial disease eg DM, astham, thyroid disease
what are the maternal factors of prematurity
pre-eclampsia or related hypertension
management of prematurity
immediate post-birth resuscitation
efforts to reduce excessive o2 exposure
reduce hyperventilation - intubation, surfactant
reduce hypothermia - warming
reduce hypoglycaemia - IV access and detrox
Hypotension - IV fluid bolus of 10ml/kg 0.9% saline then inotropes, dopamine followed by dobutamine, hydrocortisone
how can you determine gestation age?
using the New Ballard Score
USS finding
what is the aim for MAP for a pre-term baby
MAP should equal to the infant’s gestational age eg if gestational age = 28 wks then MAP should be >28
what medication can be used to treat apnoea in infant
methyxanthine (caffeine)
what medication can be used to main ductal patency
prostagladin
which larger group does IUGR belongs to
SGA - Small for Gestational Age
definition of Small for Gestational Age
birth weight < 10th centile/2SD away from the population norm on growth chart
definition of IUGR
only apply to foetus with clinical feature of malnutrition and in–utero growth restriction
irrespective of their weight precentile
what group does IUGR divide into?
symmetrical
asymmetrical
what is the usual cause of symmetrical IUGR
hypoplasia
what is the usual cause of asymmetrical IUGR
malnourishment
most common placental insufficiency
what is the clinical appearance of symmetrical IUGR
both weight and head circumference are below 10th centile
what is the clinical appearance of asymmetrical IUGR
abdo circumference affected
weight and head circumference normal/less affected
what is a maternal factor for IUGR
inter-pregnancy time Maternal lifestyle maternal conditions eg asthma, DM previous SGA babies maternal infectino (TORCH, HIV, syphilis, TB, UTI, bacterial vaginosis
what is a foetual factor for IUGR
chromosomal deficit
major congenital deficit eg trach-oesophageal fistula, congenital heart disease
infection - TORCH, malaria, HIV, syphilis
how do you diagnose SGA/IUGR
foetal abdo circumference and estimated foetal weight < 10 cenile
management of IUGR
similar to prematurity
also effective and encouraging feeding to encourage development
can give endogenous corticosteriod - mature lungs and enhances surfactant production
short term complications for IUGR
IRDS
perinatal asphyxia
meconium aspiration
prematurity
long term complications for IUGR
poor growth and neurodevelopment outcome
general and specific learning difficulties
cerebral palsy
gross motor and minor neurological dysfunction
behaviour problems
what is another name for Talipes
club foots
talipes equinovarus
how common is talipes
1 in 1000 birth in the UK
which gender is more common to have talipes
male > female (2:1)
clinical features of talipes
equinus - foot pointing downwards
varus - foot pointing inwards
middle section of foot usually twisted inwards
achilles tendons is tight
shortening of tendons on medial aspect of leg
what is assoicated with talipes
1/5 associates with
spina bifida
cerebral palsy
arthrogryposis (hooked joint) (curved + joint stiffness + abnor muscle development)
Ix for talipes
antenatal scans can pick it up
neonatal examination
management of talipes
ponseti method (preferred method due to success rate of 8-9/10cases)
manually move foot to correct position
plaster cast for 1 wk
foot mainuplated again then cast 1 wk
repeat for 6 wks
achilles tenotomy recommended after 6 wks
boots with bar for 23 hrs for 3 months
what are the 3 different types of neonatal jaundice
physiological, pathological and prolong jaundice
what constitute a physiological jaundice
occur after 1 day
what constitute a pathological jaundice
occurs within 24 hours
what constitute a prolonged jaundice
over 2 weeks in term baby
over 3 weeks in pre-term baby
and bilirubin > 200 in term baby
what is the difference between unconjugated and conjugated neonatal jaundice
unconjugated - occurs due to haemolysis or pre-hepatic causes
Conjugated - occurs due to hepatic/obstruction ie post-hepatic
what are some of the causes of unconjugated neonatal jaundice which occurs within 24 hours of birth
haemolytic disease
neonatal sepsis
what are some of the causes of conjugated neonatal jaundice which occurs within 24 hours of birth
neonatal hepatitis congenital infections (TORCH syndrome)
what are some of the causes of unconjugated neonatal jaundice which occurs between 24 hours and 2 weeks
physiological
hypothyroidism
haemolysis/sepsis
what are some of the causes of conjugated neonatal jaundice which occurs between 24 hours and 2 weeks
neonatal hepatitis congenital infections (TORCH syndrome)
what are some of the causes of unconjugated neonatal jaundice which occurs after 2 weeks
breast milk jaundice
haemolysis/sepsis
hypothyroidism
what are some of the causes of conjugated neonatal jaundice which occurs after 2 weeks
biliary artresia
choledochal cyst
neonatal hepatitis
Alpha-1 antitrypsin deficiency/TORCH/Glactosaemia/CF)
