Neonatology Flashcards
what is a neonate?
infant of 4 weeks (28 days) or less
what is preterm?
gestation less than 37 weeks of pregnancy
define low birth weight?
less than 2.5kg
what monitoring is required for a growth restricted fetus?
monitoring essential to determine optimal time for delivery.
growth parameters-symphysis fundal height (SFH), US measurement of fetal size-will be needed if SFH inaccurate e.g. BMI more than 35, hydramnios, large fibroids.
biophysical profile: amniotic fluid volume
fetal movement
fetal tone
fetal breathing movements
fetal heart activity
and Doppler blood flow velocity-umbilical and middle cerebral artery-if this is absent or reversed during diastole then increased risk of morbidity from hypoxic damage to gut or brain, or of intrauterine death.
umbilical doppler artery scan should be primary surveillence tool in small for gestational age fetus-rpted every 2 wks if indices normal.
patterns of intrauterine growth restriction?
symmetrical and asymmetrical
asymmetrical=more common-weight or abdominal circumference lies on lower centile than that of the head
symmetrical=head circumference equally reduced
aetiology of asymmetrical intrauterine growth restriction?
late in pregnancy, placenta fails to provide adequate nutrition, but brain growth relatively spared receiving preferential nutrition at expense of liver glycogen and skin fat-lack fo storage
assoc. with utero-placental dysfunction secondary to:
maternal smoking
pre-eclampsia
multiple pregnancy
idiopathic
after birth, infants rapidly put on weight-*note normal infants lose weight over 1st 7-10 days due to water weight loss, but should lose no more than 12.5% of their birth weight, and this should be regained by 2 weeks, a rapid increase in weight initially therefore highlights some baby abnormality e.g. asymmetrical IUGR.
aetiology of symmetrical intrauterine growth restriction?
prolonged period of poor intrauterine growth, starting in early pregnancy, OR gestational age is incorrect
usually due to small but normal fetus
other causes: fetal chromosomal disorder or syndrome
congenital infection
maternal drug and alcohol abuse
chronic medical condition
malnutrition
more likely to remain small permanently
risks to fetus of intrauterine growth restriction?
intrauterine hypoxia and ‘unexplained’ intrauterine death
asphyxia during labour and delivery
complications to infant of IUGR?
hypothermia-large SA
hypoglycaemia-poor fat and glycogen stores
hypocalcaemia
polycythaemia-venous haematocrit more than 0.65
impaired neurodevelopment
meconium aspiration
possibly type 2 DM and HTN in adult life
define small for gestational age
birthweight is below the 10th centile for gestational age
major RFs for IUGR?
maternal age greater than 40 years
smoker of 11 cigarettes or more/day
cocaine use
daily vigorous exercise
chronic HTN, DM, vascular disease, renal impairment, antiphospholipid syndrome
previous SGA baby, previous stillbirth-born at 24 or greater weeks of pregnancy with no signs of life
maternal SGA
pre-eclampsia-AP agents should be commenced at or before 16wks of pregnancy if high risk of pre-eclampsia
heavy bleeding
low maternal weight
fetal echogenic bowel
low level of 1st trimester marker pregnancy-associated plasma protein A (PAPP-A)
minor RFs for IUGR?
maternal age 35 years or older nulliparity BMI less than 20, BMI 25-29.9 smokes 1-10 cigarettes/day low fruit intake pre-pregnancy pregnancy interval less than 6 months pregnancy interval 30 months or greater paternal SGA
how does presence of RFs at booking assessment influence re-assessment of pt for IUGR in pregnancy?
if 1 major RF or 3 or more minor, then re-assess at 20 wks for abnormal Down’s syndrome markers and fetal echogenic bowel.
US criteria for IUGR?
elevated ratio of femoral length to abdominal circumference (AC)
elevated ratio of head circumference (HC) to AC
unexplained oligohydramnios
possible intervention for fetuses with IUGR when considering delivery with fetus between 24+0 and 35+6 wks gestation?
single course of antenatal corticosteroids
when is delivery recommended in preterm SGA fetus with umbilical artery absent or reversed end diastolic velocity detected prior to 32 wks gestation?
when ductus venosus doppler scan becomes abnormal or umbilical vein pulsations appear, provided fetus considered viable and after completed course of steroids.
C section recommended
what is the initial screening check of baby in delivery room?
Apgar score-assesses HR, RR, colour, muscle tone, reflex irritability, max score of 10=good.
this is checked at 1 and 5 mins
note any life threatening conditions
obvious dysmorphic features
gross congenital anomalies e.g. NTDs
birth injuries
umbilical cord vessel count-ensure 2 UAs and 1 UV
causes of depressed fontanelles?
dehydration
features of dehydration in neonate?
sunken eye
dry mucous membranes e.g. mouth
poor skin turgor
depressed fontanelles
effect of prematurity on baby’s muscle tone?
very premature (less than 30wks) normally have minimal flexor tone, like a rag doll should appear in LLs by 34 wks, and 36wks in ULs.
when do the fontanelles close?
fontanelles=large membranous unossified gaps that exist between skull bones in early infant life.
anterior=where coronal and sagittal sutures will meet between frontal and parietal bones, closes within 2 years
posterior=where sagittal and lambdoid sutures will meet, between parietal and occipital bones, closes within 6-9 mnths.
what is included in examination of the neonatal head?
initial inspection: dysmorphic features
head examination: fontanelles-assess size, may be widened with raised ICP e.g. hydrocephalus, or narrowed or undetectable and immobile with craniosynostosis. traumatic injuries-abrasions, depressed fractures, haematoma or lacerations. swellings.
measure head circumference-normally 32-37cm at term, average estimation-height/2 + 10.
eyes-red reflex-absence-?congenital cataract, retinoblastoma, enlarged and very hazy corneas-glaucoma.
nose-symmetry, nasal patency.
mouth-lips, tongue-adequate protusion so no tongue tie-tight frenulum, and size-macroglossia may indicate hypothyrodism gums, palate-?cleft, oropharynx.
ears-skin lesions-cysts and skin tags common, symmetry and positioning-low set ears-1/3 of ear should lie above horizontal line from eye, seen in down’s syndrome, noonan syndrome, edward’s syndrome (trisomy 18), patau syndrome (trisomy 13), turner’s syndrome.
neck inspection-? web neck-turner’s and noonan’s syndrome, and palpation-masses or fistulae e.g. branchial-A. to SCM, asymmetry and range of movement-torticollis from SCM fibrosis/tumour.
what are hands inspected for in newborn examination?
single palmar crease-simian line-fusion of 2 palmar creases-down’s syndrome and edward’s syndrome.
extra or missing digits
what are we examining for in heart auscultation during newborn examination?
HR-normal between 120 and 160bpm
S1 and S2-S2 may be loud and single or closely split with pulm HTN
note day 1 murmur may be due to closing DA
coarctation murmur will be present on day 1-look also for RF delay-may be better feeling brachial pulses?
after a few days, VSDs and ASDs become audible as pressures in L heart increase, VSD-pansystolic murmur, ASD*
why is nappy removed during newborn examination?
examine genitalia-ensure in male babies scrotum contains both testes which should be of similar size, may be hydrocele, not urethral orifice position-epi or hypospadias*, females-look for imperforate hymen or vaginal wall cysts, ambiguous genitalia e.g. CAH
anus-patency and position?
groin swelling?-?indirect inguinal hernia
stools-meconium-very dark green
indications in newborn of hip USS at 6 weeks?
following normal hip examination but hx of:
breech presentation OR
FH of DDH (1st degree relative) OR
significant oligohydramnios
difference between ortolani’s and barlow’s tests for DDH?
ortolani-opening out lower limbs, test to reduce a posteriorly dislocated femoral head
barlows-bumps back femoral head, detects whether femoral head can be dislocated.
why might the Moro reflex demonstrate asymmetry of limb movement?
BP injury
or may be asymmetry of facial movement-facial nerve palsy e.g. following forceps delivery and because of small mastoid process.
or may be absent with significant IC pathology.
most common neonatal rash noted in 1st few days of life?
erythema toxicum neonatorum (or toxic erythema of the newborn)-erythematous macules anywhere on body except palms and soles, us. with central white or yellow papule/pustules.
typically presents in 1st few days of life, although onset can be as late as 2 wks, typically waxes and wanes over few days and each individual lesion usually present for no longer than a day.
begins on face, spreads to involve trunk and limbs.
infant otherwise well.
in what syndrome does a ‘port wine stain’ vascular malformation present at birth in trigeminal distribution accompany angiomatous malformation of the brain?
sturge-weber syndrome*
port wine stain (naevus flammeus)-vascular malformation of dermal capillaries, disfiguring lesions can be improved with laser therapy. This does not regress with age.
what are haemangiomata, when are they of a concern?
group of blood vessels appearing as red to purple papules or plaques with a normal epithelial surface
are (usually) NOT present at birth e.g. strawberry naevus (cavernous haemangioma), and grow out of proportion to rest of body for 24 wks, then involute slowly.
of concern if near eyes-can cause amblyopia as vision blocked, ears-auditory amblyopia, ‘beard’ region-may indicate underlying laryngeal involvement-in these cases may need corticosteroid or laser treatment.
when should baby be examined for a second time after initial newborn examination in 1st 72hrs?
at 6-8wks
importantly on second examination, must examine carefully for CVS problems that may not have been apparent on 1st examination e.g. VSD or ASD murmur, or coarctation,
hip examination-DDH can still present late
eyes-congenital cataract and causes of leukocoria
also look for new problems that may have arisen e.g. nappy rashes, haemangiomata, umbilical granulomata.
what hearing screening is carried out in newborns?
all newborns to have hearing test using automated otoacoustic emissions within 1st 4-5wks of birth.
*notes this test will not detect rare auditory neuropathy in child who is deaf as cochlea in these pts normal, this will be detected by automated auditory brainstem response.
if well baby has no clear response to test-lack normal echo from cochlea detected by microphone, then r/f for automated auditory brainstem response screening test.
if baby classified as high risk, having spent more than 48hrs in NICU or SCBU then screened using both tests.
what conditions are screened for using the newborn heel prick blood spot test at 5-8 days following birth?
PKU-test looks for combination of total biopterin and dihydropteridine reductase. essential for early diagnosis so can implement early phenylalanine restriction diet to prevent severe neurocognitive and neuromotor impairment.
congenital hypothyroidism-must rpt test if baby born at less than 32 wks gestation, at 28 days of postnatal age counting original expected birth date as day 0, or date of discharge home, whichever sooner.
sickle cell disease
CF-looking for immunoreactive trypsinogen raised levels-indicates pancreatic duct obstruction, but initial screening can MISS diagnosis
homocystinuria
medium chain acyl-CoA dehydrogenase deficiency (MCADD)-early detection so pt can avoid fasting
maple syrup urine disease
glutaric aciduria type 1
isovaleric acidaemia
which enzyme is deficient in PKU?
PAH: phenylalanine hydroxylase
usual cause of neonatal jaundice?
physiological immaturity of liver-unconjugated hyperbilirubinaemia, self-limiting over 1st week of life as liver function matures.
unconjugated=potentially toxic-kernicterus-brain injury, but can be physiological as well as pathological, conjugated=not toxic, but always pathological.
complication of unconjugated hyperbilirubinaemia on the neonatal brain?
kernicterus-irreversible brain damage from high levels of unconjugated bilirubin
results in nerve deafness, choreoathetoid cerebral palsy (dyskinetic type) and mental retardation.
symptoms in baby of neonatal jaundice?
may feed less well and be lethargic
in those who become dehydrated, there is haemoconcentration causing them to appear more jaundiced and so may feed less well, causing more dehydration.
how does location of neonatal jaundice on examination relate to disease severity?
limited to head and neck=mild
over lower trunk and thighs=moderate
extension to hands and feet=may require treatment.
4 situations in which baby should be investigated rapidly for serious causes of jaundice?
jaundice appearing in 1st 24 hrs of life, suggests underlying haemolysis
clinical evidence of deep jaundice
prolonged conjugated jaundice lasting more than 2 wks, suggests serious underlying cause
increasing levels of conjugated bilirubin, suggests severe hepatic cause of jaundice.
initial treatment of neonatal jaundice?
phototherapy-light degrades unconjugated bilirubin to non-toxic soluble compounds which are excreted in urine.
exchange transfusions necessary if levels continue to rise to potentially toxic level
if conjugated tment depends on cause.
investigations in jaundiced neonate?
FBC: neutrophilia or neutropenia suggests infection, thrombocytpenia suggests TORCH infection-toxoplasma, other-syphilis, rubella, CMV, HSV and VSV.
total serum bilirubin-only test for otherwise well moderately jaundiced baby presenting on 2nd or 3rd day, conjugated bilirubin, transcutaneous bilirubinometer
maternal and neonate blood groups and Coombs’ test-ABO and rhesus incompatability
reticulocyte count
peripheral blood film for red cell morphology
red cell enzyme assays-G6PDD, pyruvate kinase deficiency
LFTs-hepatitis, cholestatic disease
infection screen-must exclude in any unwell baby or presents in 1st 24 hrs or after 3 days-congenital TORCH screen, surface swabs including umbilicus, throat swabs, urince culture, blood culture, CXR, LP
TFTs-hypothyroidism
Hep B antigen-Hep B infection
metabolic screen
sweat test-CF
urine cultures-infection
LP-meningitis
reducing substance in urine-galctosaemia, as long as infant received sufficient milk quantities.
USS-internal haemorrhage, biliary atresia
when is jaundice clinically detectable in newborn?
when bilirubin levels are greater than 85 micromol/L
when does physiological jaundice in neonate present?
this is an unconjugated hyperbilirubinaemia due to liver immaturity and increased red cell b.down presenting in 1st 2-3 days after birth, starting to disappear by end of 1st wk and resolves by day 10.
baby usually remains well.
complications of phototherapy for neonatal unconjugated hyperbilirubinaemia treatment?
separation of baby from mother
dehydration-must increase fluid intake
loose stools
what does use of phototherapy for neonatal jaundice depend on?
level of serum bilirubin gestation of baby rate of rise of bilirubin likely underlying cause baby well-being
indications for immediate phototherapy in neonatal jaundice?
jaundice at less than 24hrs
rapidly rising bilirubin expected e.g. haemolytic disease
features of extrahepatic biliary atresia in jaundiced neonate, and treatment required for good prognosis?
shortly after birth, well child with persistent jaundice, pale stools-but normal meconium passed initially, dark urine in term infant with normal birth weight
failure to thrive
hepatomegaly often present
splenomegaly if late presentation (after 3 mnths)-sign of PH
need surgery before 60 days of life for a better prognosis
how is congenital heart disease detected antenatally?
fetal anomaly US scan at 18-20wks gestation
if abnormality detected, detailed fetal ECHO performed by paediatric cardiologist
this is also performed on any fetus at increased risk e.g. suspected Down syndrome, where parents had previous child with HD or where mother has congenital HD.
why do many newborns with potential cardiac shunts e.g. ASD or VSD, NOT have symptoms or a murmur at birth?
pulmonary vascular resistance still high so lack of pressure difference between R and L sides of the heart
major complication of a L to R cardiac shunt if left untreated?
development of Eisenmenger syndrome: shunt reverses to R to L shunt producing cyanosis as there is increased pulmonary blood flow producing chronically raised pulmonary arterial pressure and flow leading to irreversibly raised pulmonary vascular resistance and subsequent high R sided heart pressures.
presentation of L to R shunts, and give examples?
asymptomatic or breathless NOT cyanotic unless shunt reverses with irreversibly raised pulmonary vascular resistance-Eisenmenger syndrome ASD VSD PDA
differentials for cyanosed newborn with respiratory distress (RR more than 60 breaths/min)?
cardiac-cyanotic congenital HD-R to L shunt-tetralogy of fallot, transposition of great arteries, common mixing-AVSD e.g. Downs syndrome.
resp-surfactant deficient lung disease, meconium aspiration, pulmonary hypoplasia
persistent pulmonary HTN of the newborn-failure of pulmonary vascular resistance to fall after birth
infection-septicaemia from group B streptococcus and other organisms
metabolic disease-metabolic acidosis and shock
RFs for neonatal group B streptococcal infection?
prolonged rupture of membranes (more than 18hrs) preterm maternal fever during labour maternal chorioamnionitis previously infected infant
indications for prophylactic intrapartum antibiotics for neonatal group B streptococcal infection?
high dose IV benzylpenicillin or ampicillin if:
GBS bacteriuria detected in current pregnancy
GBS detected on vaginal swab in current pregnancy
previous baby with neonatal GBS disease
Abx plus immediate inductiomn of labour if prelabour rupture of membranes at 37wks or more and mother known to be colonised with GBS
presentation of group B streptococcal infection in neonates?
early-onset sepsis-resp distress and pneumonia, can be septicaemia and meningitis
late-onset sepsis-usually meningitis, occasionally focal infection e.g. osteomyelitis or septic arthritis
why can a neonate be expected to deteriorate dramatically-collapse with shock, in 1st few days after being born if presence of coarctation of the aorta?
shock develops with left heart outflow tract obstruction following closure of the DA which occurs within the 1st few days.
DA in presence of aortic coarctation maintains the systemic circulation as blood travelling from PA to aorta via DA can pass into the systemic circulation, avoiding the narrowed aorta just proximal to entry of DA into aorta, so with DA closure, massive decrease in CO to systemic circulation, need to maintain ductal patency for early survival with PG E1 infusion before repair-surgery or balloon angioplasty with or without stenting.
why might congenital coarctation of the aorta NOT present in neonates and be diagnosed later in life?
less severe case may go unnoticed with development of collateral circulation of blood to lower body.
