Perinatal adaptation Flashcards
Define what the perinatal period is
This is the period from 22+0 wks until 7 days after birth
What is the function of the placenta ?
- Gas exchange - supply O2 & clearance of CO2
- Nutrients supplied to fetus - H2O, glucose, electrolytes (iron,Ca2+), free fatty acids
- Waste product removal
- Acid-base balance
- Hormone production - oestrogen, progesterone, HCG, Human chorionic somatotropin, human placental lactogen, placental growth hormone, relaxin & kisseptin
- Transport of IgG - mainly in the 3rd trimester
When in utero does the fetal lungs carry out gas exchange ?
No, there alveoli are filled with fluid
What is the function of IgG transport during the 3rd trimester ?
To give the baby passive immunity to everything the mother is immune to (passive immunity continued with breastfeeding upto 6 months)
Describe the fetal circulation
- 2 umbilical arteries take deoxygenated blood from the fetus to the placenta, to be reoxygenated
- Oxygenated blood is then transported from the placenta to the fetus via the umbilical vein
- Blood then enters the R side of the fetal heart
- Blood then passes through one of the 2 extra connections in the fetal heart (they close when born)
- Some blood goes through the foramen ovalae travelling from R to L atrium then to L venitrcle & subsequently the aorta & then the rest of the body (blood travelling this route is the most oxygenated
- Blood coming back from the fetus’ body also entres the R atrium (so essentially have oxygenated & deoxygenated blood entering the R atrium, with oxygenated blood passing through the foramen ovalae), deoxygenated blood passes through to pulmonary artery & bypasses lungs through ductus arteriosus
- Some blood then transported to lower half of fetal body but most deoxygenated blood leaves fetus to placenta via the umbilical arteries
What 3 shunts exist in the fetal circulation ?
- Foramen ovalae
- Ductus arteriousus
- Ductus venosus - this shunts a portion of umbilical vein blood flow directly into IVC ==> bypassing the liver
How do the fetal lungs remain perfused ?
7% of the fetal circulation does actually pass into the lungs but this is to just keep them perfused (==> not all the blood actually bypasses the lungs)
What are the main fetal changes which occur during the 3rd trimester in preparation for birth ?
- Surfactant production - produced by type 1 pnuemocytes to aid fetal alveoli/lung patency
- Accumulation of glycogen
- Accumulation of brown fat
- Accumulation of subcutaneous fat
- Swallowing amniotic fluid - this helps drive fetal lung development
What is the importance of the accumulation of fat during the 3rd trimester ?
- It is important because once delivered the baby will no longer have a continuous supply of nutrients from the placenta, so they need to use fat stores in the inital stages for energy following birth (why breastfeeding babies often loose weight first)
- It is also important for insulation/ breakdown for heat production
What changes occur during labour & delivery which help prepare the baby for birth ?
- Increased catecholamines (adrenaline, noradrenaline, dopamine), cortisol & T3 (thyroid hormone) - all required for gluconeogenesis & thermogenesis after birth to help keep the baby fed & warm whilst breastfeeding kicks in
- Sythesis of lung fluid stops
- Vaginal delivery squeezes the babies lungs helping alveolar cells to switch from fluid production to reasorption (so they can inflate & arent filled with fluid)
What is the normal appearance of a baby in the first few seconds after birth ?
- Appears blue initially then gradually goes pink
- Starts to breath & cries
What is the purpose of delayed cord clamping ?
To allow the cord to pulsate for a few mins - this improves iron stores, Hb & transition to life outside the uterus
Describe the transition from fetal to normal circulation after delivery
- There is decreased pulmonary vascular resistance (fluid in alveoli removed within first few breaths)
- Systemic vascular resistance increases (this is resistance to blood flow offered by all the systemic vasculature except pulmonary vasculature)
- O2 tension in blood rises (dilating pulmonary vessels)
- Decreased prostaglandins
- Ducts constrict
- Foramen ovalae closes
What happens to each of the 3 fetal shunts following birth ?
- Foramen ovalae closes (persists in 10% of people = patent foramen ovalae PFO)
- Ductus arteriosus becomes ligamentum arteriosus or persistent ductus arteriosus
- Ductus venosus becomes ligamentum teres
List the risk factors for failure of cardiorespiratory adaptation at birth i.e. PPHN
- Pre-term
- Babies that pass meconium prior to birth
- Babies which get cold during delivery (hypothermia)
- Babies with infections
- Congenital disorders that cause underdeveloped lungs or CHD
Define what persistent pulmonary hypertension of the newborn is (PPHN)
- This is when the babys circulation does not change over from fetal to normal newborn circulation.
- Essentially the pulmonary arteries are narrowed & obstructed (shunts persist) resulting in the R ventricle having to pump harder to properly pump the blood ==> pulmonary HTN
- This can result in R to L intracardiac shunting of blood at the foramen ovalae & ductus arteriosus resulting in hypoxaemia
What are the signs & symptoms of PPHN?
- Asphyxia - O2 deprivation causing unconciousness or death
- Tachypnoea, resp distress
- Resp acidosis
- Loud, single second heart sound or harsh systolic murmur
- Low APGAR score
- Cyanosis due to poor cardiac function
- Systemic hypotension
- Symptoms of shock
How is PPHN diagnosed ?
- Preductal & postductal O2 sats via pulse oximetry show a 5-10% gradient difference, with preductal O2 5-10% higher
- Echocardiography is the gold standard test to establish diagnosis
What is the management of PPHN ?
- Ventilation - O2
- Nitric oxide (pulmonary vasodilator)
- Ionotropes - dopamine 1st line
- Sedation
- ECLS (Extracorporeal membrane oxygenation) used
- Give surfactant - if evidence of parenchhymal lung disease
What is transient tachyponea of the newborn (TTN)?
- This is when extra fluid stays in the lungs or is cleared out too quickly.
- This as a result makes it harder for the baby to breathe
How long does TTN last ?
< 24hrs
What are the risk factors for TTN development ?
- Preterm
- C-section (because fluid not been squeezed out like in SVD)
- Mother has asthma or DM
What are the signs/symptoms of TTN ?
- RR > 60
- Grunting or moaning on exhalation
- Flaring nostrils
- Use of excessory resp muscles (skin pulling between ribs)
- Central cyanosis
How is TTN diagnosed ?
- Physical exammination +/- CXR
- O2 sats monitoring
What does this CXR show ?
TTN - interstitial oedema - predominantly perihilar often seen as perihilar streakiness
What is the management of TTN ?
- Conservative - if O2 sats are low, then give O2
- Ensure adequate nutrition
Following starting to breath and successfully switching to normal circulation, what 3 things does the baby now need to establish ?
- Thermoregulation
- Ensure glucose homeostasis
- Feed/nutrition
Why are babies prone to becoming cold (hypothermia)?
- Because they have:
- A large surface area to volume ratio
- They are wet & naked
- They cannot shiver
- There main source of heat is non-shivering thermogenesis = heat produced by the breakdown of adipose tissue in response to catecholamines which is not efficient
- Peripheral vasocontriction
Why do you want to avoid hypothermia in babies ?
Becuase it predisposes them to other problems
Why are SGA/preterm babies more predisposed to hypothermia ?
- Low stores of brown fat
- Little S/C fat
- Larger surface area to volume ratio
What will SGA/pre-term babies be born into to help keep them warm immediately ?
A plastic bag
What measures are taken to help keep babies warm following birth ?
- Dry
- Hat
- Skin to skin
- Blanket / clothes
- Heated Mattress
- Incubator
Why is maintaining glucose homeostasis for newborns difficult ?
- Because in the early stages following birth there is stoppage of the continual glucose supply & lack of oral intake of milk (mother takes 3-4 days before milk production starts to increase)
- In the first 24hrs the baby only gets roughly 5-10mls of milk
How do babies despite the difficulties, maintain glucose homeostasis in the early stages following birth ?
- To maintain glucose levels, insulin decreases & glucagon increases. This results in mobilisation of glycogen stores (stored in 3rd trimester) for gluconeogensis
- Also newborns are able to utilise ketones as brain fuel
What are the causes of hypoglycaemia in newborns ?
- Increased energy demands due to being unwell or hypothermic
- Low glycogen stores due to being SGA or premature
- Inappropriate insulin / glucagon ratio due to maternal diabetes or hyperinsulinism
- Some drugs e.g. B-blockers
How is hypoglycaemia avoided/treated in newborns ?
- Feed effectively; if preterm may need additional feeding ontop of breast feeding
- Keep warm
- Monitor BG levels
Is it normal for a baby during the first 2 weeks of life to gain very little or usually loose some weight ?
Yes - reassure mothers about this
What is jaundice caused by ?
Raised bilirubin levels
If jaundice is severe what can it result in if untreated ?
Kernicterus which is a permanent form of brain damage
Why do newborns become slightly anaemic following birth and when does this reach its worst ?
- Due to fetal Hb breakdown being faster than adult Hb synthesis
- Hb nadir around 8-10 days
List the causes of jaundice in newborns
- Physiological
- Blood group incompatability (most commonly Rh or ABO incompatability)
- Other haemolytic disorders e.g. GGPD deficiency
- Sepsis
- Liver disease
- Metabolic disorders
When does physiological jaundice develop between and what is it due to ?
Between days 2-14, due to:
- Increased bilirubin production due to breakdown of fetal Hb
- Decreased bilirubin conjugation & subsequent excretion due to hepatic immaturity, causing rise in unconjugated bilirubin
Is physiological jaundice harmful ?
No - unless very high levels
Is jaundice before 24hrs post delivery abnormal ?
Yes - it is always abnormal!
What are the causes of jaundice in newborns before 24hrs post delivery ?
- Rhesus incompatability - main cause
- ABO incompatability
- Sepsis
- Red cell anomalies e.g. GGPD
- If there is substantial increased conjugated bilirubin (>15%) consider hepatitis as the cause
What investigations should be done for jaundice in newborns <24hrs ?
- Total & conjugated serum bilirubin levels
- Maternal blood group & antibody titres if Rh -ve
- Babys blood group, direct antiglobulin (coombs test) which detects antibodies against the babys RBC’s & elution test to detect Anti-A/B antibodies to babys RBC’s
- Full blood exammination looking for evidence of haemolysis, unusually shaped RBC’s or infection
- CRP indicator of infection
Which test is diagnostic of rhesus haemolytic disease i.e. therefore the most important when investigating jaundice < 24hrs ?
Coombs test
Define prolonged jaundice
This is jaundice occuring or lasting after 14days (or >21 days in preterms)
Is prolonged jaundice always pathological ?
No - 10% of babys have jaundice still at 1 month
List the causes of prolonged unconjugated hyperbilirubinaemia
- Breast milk jaundice
- Poor milk intake
- Haemolysis
- Infection esp UTI
- Hypothyroidism
List the causes of prolonged conjugated hyperbilirubinaemia (conjugated is always pathological)
- Hepatitis
- Biliary atresia (usually have pale stools & dark urine)
What is another name given to kernicterus ?
Bilirubin encephalopathy
What are the signs/symptoms of bilirubin encephalopathy ?
- Lethargy
- Poor feeding
- Temp instability
- Hypotonia
- Arching of the head, neck & back
- Spasticity
- Seizures
What levels of unconjugated bilirubin are considered unsafe ?
>340 or > 300 in preterms
What is the treatment of jaundice and when is it initiated ?
- Treat the cause
- Ensure adequate hydration - put to breast 8-12 times per day, supplement with expressed breast milk or formula if needed, but not water. If oral intake inadequate give IV fluids
- Phototherapy if total serum bilirubin ≥ 350
- Exchnage transfusion if total serum bilirubin ≥ 450
- Use IV immunoglobulin for infants with Rh or ABO incompatability which bilirubin levels rise > 8.5 micromol/L/hr or are within 30-50 for exchange transfusion depsite intensive phototherapy
What is resp distress syndrome due to ?
This is due to deficiency of alveolar surfactant, and is a condition mainly confined to premature babies
What are the signs/symptoms of resp distress syndrome ?
- Tachypnoea > 60
- Grunting
- Nasal flaring
- Intercostal recession
- Cyanosis
- CXR - diffuse granular pattern (ground glass appearance)
- Worsens over mins to hrs. Gradual worsening to a nadir at 2-4 days then gradual improvement (this is modified by treatment)
How is resp distress syndrome prevented ?
Steroids for preterm deliveries
What is the treatment of resp distress syndrome ?
- O2
- Pulmonary surfactant
- CPAP if breathing on own
