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
How can IRDS be prevented?
Corticosteroids - prednisone single dose PO - given antenatally to mothers at risk of pre-34wk delivery, considered if between
34-35+6
Be mindful in GDM that this may compromise glycaemic control
How is IRDS managed?
Oxygen - given via CPAP RATES? Or endotracheal tube
Fluids - IV, also to stabilise blood sugar
Exogenous surfactant - e.g. Survanta (bovine origins) - given via ET tube or ‘introducer’ directly into lungs - can be XR’d after as should see very quick resolution of ground glass appearance, will also be able to tell which lungs have not received enough/any surfactant
What is chronic lung disease/bronchopulmonary dysplasia?
Possible consequence of ventilation - either under or over (?) - in premature babies
What is the difference between a pneumothorax and a tension pneumothorax?
Also causes and XR appearance
Tension = progressive and possibly deadly expansion due to increasing pressures in thoracic cavity
If you have no access to an XR, you can transluminate the chest of a premature baby - will glow on the side that the pneumothorax has blown
How do you get vascular access in newborns.
Umbilical cord is a good entry point; easier than a cannula or other lines
Can give central venous drugs e.g. inotropes; also fluids
Can get blood gasses??
What antibiotics do you give a child if they are born unwell? (With sepsis)
You assume pathogens are from the mother:
Benzylpenicillin IV 50mg/kg/12hrly (to cover group B strep) +
Gentamycin IV 5mg/kg/36hrly (to cover gut/vaginal flora) (f/u hearing as ototoxic, though streptomycin is worse)
What are some risk factors for neonatal sepsis?
Spontaneous preterm delivery
Maternal intrapartum pyrexia
Maternal group B strep +ve
Prolonged rupture of membrane (>24hrs between rupture and delivery)
These are all still risk factors for sepsis at 3m postpartum so are relevant in the history of a sick neonate
What is neonatal hypoglycaemia? When is it a problem and how do you manage it?
Low blood sugar is common in the 1st 24hrs in babies born at term but you expect them to correct over this period - after 24hrs should be >2.5mmol - if not then give IV bonus of 10% dextrose 2.5ml/kg or TPN, feed with milk asap but slowly (?NG if needed) and monitor closely
Hypo may be more significant in premature babies - lower glycogen stores and working harder (although this is expected, prolonged hypoglycaemia in term may be more worrying as would expect recovery)
How do you measure growth?
Serial weights and head circumferences - FREQUENCY?
Bloods: Na (necessary for protein production) and phosphate (for bone growth) are good indicators of growing abilities - if low, can’t be growing much
Where else are premature babies liable to bleed from?
Bowel - secondary to NEC
Lungs - surfactant deficiency is a risk factor
What are 4 things to check when assessing why someone with an ET tube might not be achieving optimum stats?
DOPE
Displaced tube? Get an XR (c. T2-4 - 5cm+/-2cm above carina in adults; 1.5cm above in children)
Obstructed tube (blood, secretions)? Suction the tube
Pneumothorax? Hyperresonant chest, uneven expansion, transluminatiom (in prems), XR
Equipment failure?
What is total parentral nutrition?
F
What is hypoxic ischemic encephalopathy?
Intrapartum hypoxia leading to hypoxic brain damage in term infants
Presents with seizures, LoC, respiratory depression/apnoeas, hypotonia
Can lead to PVL and CP
Management: whole-body cooling for 72hrs to slow metabolism and reduce free radical injury (they hate this process)
Who do we give vitamin K to and why?
All babies as they don’t have at birth and can’t get in breast milk
Prevents bleeding - so esp important in any infants born with ventricular haemorrhages - will prevent the ‘haemorrhagic disease of the newborn’ (where babies just bleed from anywhere - bowel, lungs, brain - high risk = prems, mechanical delivery, maternal anticonvulsants etc)
What is meconium?
Infant first poo (of sorts)
Should pass within 24hrs of birth - if not, possible concerns as delay associated with:
Cystic fibrosis
Hirschprungs
Anal atresia
What is meconium ileus?
From a failure to pass meconium
Acts as a blockage, leads to: Abdo distension Bilious vomiting Dilated bowel loops on AXR Possible perforation and septic picture
What is aspiration of meconium?
As it sounds - though will be sterile so not worried about infection, though may present with a pneomonitis picture
What is congenital diaphragmatic hernia and how does it present?
Usually a failure of the pleuroperitoneal canal to close completely - herniation of abdominal viscera into chest cavity due to incomplete closure of the diaphragm; mostly happens on the left side
Presents shortly after birth with:
Pulmonary hypoplasia - respiratory distress, reduced breath sounds, heart sounds displaced medially, tachypnoea
Bowel sounds on auscultation of the chest
Concave abdominal appearance
1/2000 births, 50% survive
What is the Apgar score and it’s components?
Used to assess the health of the newborn baby
Appearance- Colour - pink, body pink/blue extremities, blue all over (cyanosis due to fluid in lungs - give 5 rescue breaths)
Pulse - >100, <100, absent (commence CPR if HR <60)
Reflex irritability - cries on stimulation/sneezes/coughs, grimace, nil
Tone - active movement, limb flexion, flaccid
Resp effort - strong/crying, weak/irregular, nil
Scored at 2, 1, 0 respectively: 0-3 = bad, 7-10 = good
