Neonatal Medicine Flashcards
What is the epidemiology of prematurity?
Anything under 36+6wks is premature
5-6% of births fall into this category; being really premature - 20-27wks is c.0.5%
What are the laws and ethics of premature resus?
Don’t resus anything <22wks
23-23wks ask parents
Resus anything >23wks
What are the mainstays of foetal wellbeing that we monitor both intrauterine and postpartum?
Foetal HR, size and movement
To add somewhere
24hrs before birth - 2 way comms between baby and mother about readiness (not got if elective decisions)
mum gets a massive hit of adrenaline in order to cope with natural vaginal delivery, babies get this too - babies born by c-section do not get this hit and so may be more likely to experience respiratory distress
What is apnoea of prematurity?
Brainstem is not myelinated until 32-34wks - babies born prem can ‘forget’ to breathe; there are associated bradycardias
Also made worse by sepsis
Treated with caffeine (DOSES??) and CPAP
What are ventricular haemorrhages?
80% babies less than 32wks have a normal scan
C. 14% of them will have small bleeds - poss into ‘non-essential spaces’ e.g. ventricular spaces (although can cause blockages or act as space occupying lesions)
C.5-6% of scans at 32wks will have significant bleeds - lots of blood in intraventricular spaces - shock - cerebral hypoperfusion (CP as a long term outcome)
Damage when born may be a lot less because of plasticity but we don’t know until they have been born and their development is assessed over time
Make sure baby has had its vitamin K to prevent rebleeding
What is cystic periventricular leukomalacia?
Deaths of periventricular oligodendrocytes - characteristic pattern ____ - means you don’t get the plasticity and damage/morbidity is guaranteed in later life
Occurs in 5% of babies born less than 32wks
Risk factors: low maternal BP (? Or foetal?), low O2, low CO2 (?), antenatal or post natal inflammation (from?)
What are the benefits of breast feeding?
Baby:
Fewer ear, respiratory and gastro-intestinal infections and diarrhoea - antibody transmission
Bonding with mother
Energy rich substrate good for growth
Protective of NEC in preterms
Lower risk of sudden infant death syndrome and childhood leukaemias
May reduce the risk of childhood asthma and allergic rhinitis
Increased taste preferences
Maternal:
Reduces risk of obesity and type 2 diabetes
Reduced risk of breast and ovarian (because it delays ovulation) cancer
Cheap
Practical - can do it anywhere theoretically
Good for the planet as less waste
Doesn’t contain Vit K hence supplementation
What is necrotising enterocolitis (NEC) and how is it managed?
Too much food can also put stress on bowel - increased metabolism, free radical production, bowel perforation and subsequent infection
Increases risk: not breast feeding, over feeding/feeding rapidly when very small (term infants have stomachs the size of pennies) - prems are thus at a greater risk; perinatal asphyxia, respiratory distress, congenital heart disease
Presentation:
Abdo distension, change in bowel opening - bloody or mucous stool, bilious vomiting, decreased bowel sounds, features of shock; Dx confirmed on AXR (gas filled loops, bowel wall thickening, ascites)
Management: NBM IV feeding/TPN + fluids IV Abx - cefotaxime + metronidazole NG drainage of stomach contents If unresponsive to above - surgical debridement of necrotic bowel or repair of perforation; possible stoma formation, short bowel syndrome, sepsis, stricture, fistula, adhesions Treat any shock or other complications
What is retinopathy of prematurity?
Retina needs to develop in hypoxic conditions; the hyperoxic conditions of premature incubators mean that babies are at risk of retinopathy
The retina develops between 24wks-term
Assessed by fundoscopy
Checked by 6wks postpartum as part of screening premature infants
Neonatal resus - what’s the process?
Birth - dry the baby - start the clock - assess tone/breathing/HR - if gasping/no breathing then open airway + 5x inflation breaths + SpO2 +/- ECG monitoring - reassess - if chest not moving then recheck head position + repeat as previous - if no increase in HR look for chest movement, when moving (but slow e.g. <60bpm) then ventilate for 30s - if still low, chest chest compressions:ventilation breaths at 3:1 at 100-120bpm - then consider IV access for inotropes e.g. adrenaline
What is infantile respiratory distress syndrome (IRDS)?
Also known as surfactant deficiency syndrome (SDS)
Epidemiology: c.50% of babies born at 26-28wks + 25% born at 30-31wks; more common in males, Caucasians, infants born to diabetic mothers and second born of premature twins; leading cause of death in premature infants
Infants born premature do not have enough pulmonary surfactant - is produced by T2 pneumocytes from 34wks increasingly up until birth - this means that the surface tension of the alveoli is too high and they collapse completely upon exhalation; surfactant decreases the surface tension meaning meaning less collapse and less energy to reopen airspace
What does IRDS looks like histologically and on CXR?
Histo: collapsed airspaces + hyper expanded areas, vascular congestion, possible hyaline membranes (fibrin+cellular debris+RBCs+neutrophils+macrophages - all blocking effective gas exchange
CXR: ground glass appearance - widespread diffuse opacities; decreased lung volumes; possible white-out of cardiac borders in severe
How does IRDS present?
Tachypnoea >60 Tachycardia Increased WOB Cyanosis Apnoeas
Acute phase lasts 2-3 days
What are some complications of IRDS?
Acidosis
Hypoglycaemia
Hypotension
PDA
Chronic lung disease/bronchopulmonary dysplasia
Intracranial haemorrhage
