Neonatology Flashcards
placental functions
foetal homeostasis gas exchange nutrient transport waste removal acid-base balance hormone production transport of IgG
three shunts in the foetal circulation
- ductus venosus
- foramen ovale
- ductus arteriosus
role of the ductus venosus
passes blood from the placenta to the IVC through the liver
role of the foramen ovale
passes blood through atria from right to left (some blood does still enter the right ventricle)
role of the ductus arteriosus
right ventricle into the aorta
how does waste go back to the placenta?
via the umbilical arteries
resistance in lungs and placenta
high pulmonary resistance
low placental resistance
preparation for birth in the 3rd trimester
surfactant production accumulation of glycogen accumulation of brown fat (between scapulae and internal organs) accumulation of subcutaneous fat swallowing amniotic fluid this is a period of rapid weight gain
preparations for birth during labour and delivery
increased catecholamines/cortisol (stress)
lung fluid synthesis halted and crying absorbs fluid into the lymphatic system
vaginal delivery squeezes the lungs
normal appearance of a baby on delivery
blue (gradually pinkness)
breathing
crying
cord is cut (delayed if premature)
circulatory transitions at birth
pulmonary resistance drops
systemic vascular resistance drops and oxygen tension rises
prostaglandins drop closing ducts
fate of the ductus venosus
ligamentum teres
fate of the foramen ovale
closes (can persist as PFO)
fate of the ductus arteriosus
ligamentum arteriosus (can persist as PDA)
examples of conditions if there is failure of cardiorespiratory adaptation
persistent pulmonary hypertension of the newborn (PPHN)
transient tachypnoea of the new-born (TTPN)
RDS
pneumothorax
meconium aspiration
diaphragmatic hernia
trachea-oesophageal fistula (curled nasogastric tube and no stomach bubble)
causes of PPHN
solid lungs filled with fluid or lack of surfactant
PDA
PFO
diagnosis of PPHN
pre-ductal and post-ductal saturation (positive if more than 3% difference)
management of PPHN
ventilation oxygen nitric oxide (given through ventilator) sedation inotropes ECLS (hypo-coagulable)
cause of transient tachypnoea of the new-born (TTPN)
C-section causes no squeezing of the lungs so fluid is not absorbed fully into the lymphatics
presentation of TTPN
tachypnoea
grunting
first 6 hours of life
management of TTPN
always screen for infection (just in case)
may need respiratory support but often self-limiting
who does RDS occur in and why?
pre-terms due to lack of surfactant and structural immaturity
management of RDS
maternal steroids
surfactant
ventilation
cardiac problems
heart failure (hydrops foetal is e.g. Rhesus disease)
PPHN
congenital
congenital cardiac problems
teratology of Fallot transposition of great arteries coarctation of the aorta TADVD hypoplastic heart
other congenital abnormalities
microcephaly (CMV) spina bifida Potter's syndrome (renal agenesis so no urine so amniotic fluid not swallowed) myotonic dystrophy hypoglycaemia acidosis
three adaptions within the first few hours of life?
thermogenesis
glucose homeostasis
nutrition
ways heat is lost
radiation (large SA to volume ratio, especially head)
convection
conduction
evaporation
how to reduce heat loss
hat dry protect from drafts clothing mother's chest incubator
can babies shiver
no so they breakdown stored adipose tissue in response to catecholamines
other adaptions include peripheral vasoconstriction
can babies use ketones as brain fuel?
yes
hypoglycaemia causes in new-born
increased energy demands e.g. unwell or hypothermic
low glycogen stores due to being small or premature
inappropriate insulin/glucagon (maternal diabetes or hyperinsulinaemia- mother on beta blockers)
role of oxytocin
milk ejection
role of prolactin
milk production
why is foetal Hb disadvantageous when the baby is born?
adapted to a hypoxic state (curve shifted left) so does not release oxygen as easily
cause of physiological jaundice
foetal Hb is broken down faster than adult Hb is made and conjugating pathways are immature leading to rise in unconjugated bilirubin
when does physiological jaundice happen?
2-5 days, outside of this is pathological
risk factors for adaption
hypoxia/asphyxia during delivery small large premature maternal illness medications
define term
37 weeks gestation
post-term
beyond 41 weeks
normal birth weight
2.5-4.0kg
pre-term
before 37 weeks gestation
very pre-term= under 31 weeks
extreme pre-term= under 27 weeks
foetal loss= under 22 weeks
what score is used to asses the new-born’s progression?
APGAR score
appearance, pulse, grimace, activity and respiration
other things to look out for outside the APGAR score?
jaundice low tone (floppy) seizures (eye rolling) poor feeding bilious vomit
management in cerebral palsy
therapeutic cooling
antenatal infection cause
group B strep
perinatal infection cause
herpes
bacterial causes of infection in neonates
group B strep E. coli listeria monocytogenes staph aureus epidermidis
viral causes of infection in neonates
CMV parvovirus herpes enteroviruses toxoplasma gondii HIV syphilis TORCH
management of haemorrhage disease of the new-born
vitamin K IM
oral K
factors that increase the chance of a pre-term birth
multiple pregnancy rupture of membranes hypertension intrauterine growth restrictions smoking alcohol illicit drugs poor nutrition less than 6 month interval IVF
what do premature babies need help with?
- staying warm (reduced brown fat- risk of hypoglycaemia)
- fragile lungs (ribcage not develop)
- breathing (before 34 weeks immature respiratory centres so can forget)
- systemic immaturity (RDS, PDA, IVH, NEC)
- ROP
- nutritional compromise
common problems in pre-terms
RDS PDA IVH NEC ROP hypoglycaemia (immature liver and pancreas) hyponatraemia (immature kidneys) cerebral palsy risk increased
