Neonatology Flashcards

1
Q

What are the affects of hypoxia in neonates?

A

Normal labour will result in hypoxia due to compression of the placenta- reduced gaseous exchange.
Hypoxia can lead to bradycardia which will further the hypoxia.
Further hypoxia can lead to unconsciousness and reduced respiratory effort- further existing hypoxia.
Extended hypoxia can lead to hypoxic-ischaemic-encephalopathy which will present as cerebral palsy.

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2
Q

What are the considerations for neonatal resuscitation?

A

Large SA:V therefore lose heat faster
Born wet so lose heat faster
Can be born through meconium- can get in mouth/airway

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3
Q

What are the steps of neonatal resuscitation?

A

1) Dry the baby- with towel, place in warm room under warm lamp. <28wks place in plastic bag whilst wet and under heat lamp.
2) Calculate APGAR score at 1, 5 and 10 minutes.
3) Stimulate breathing- position and dry the baby. If meconium obstructing the airway then aspirate.
4) If not responding to stimulated breathing then initiate 2 cycles of 5 inflation breaths (3 secs each). If still poor breathing then begin ventilation breaths (30 secs). If still not managing and HR<60 start compressions, co-ordinate with ventilation breaths (3:1 VB:C). Use air for term babies, use mix of air and O2 for preterm).

Some babies may be severe and so to reduce risk of HIE, start IV drugs and intubation. Can also consider therapeutic cooling as a method of managing severe.

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4
Q

What is the APGAR score?

A

Score based on:
Appearance- Blue appearance and pale extremities (0), Blue extremities (1), Pink (2)
Pulse- Absent (0), <100 (1), >100 (2)
Grimace- No response (0), little response (1), good response (2)
Activity- Floppy (0), Flexed arms and legs (1), Active (2)
Respiration- Absent (0), Slow/irregular (1), Strong/crying (2)

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5
Q

What is delayed cord clamping?

A

‘Placental transfusion’.
Shown that delaying the clamping of the cord, even by 1 minute, helps to improve Hb and iron stores, BP, reduces risk of interventricular haemorrhage and necrotising enterocolitis. Can increase risk of jaundice- require phototherapy.

Avoid in neonates in need of resuscitation to avoid HIE.

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6
Q

What is the normal care routine after birth?

A
Skin to skin contact- Allows for better mother-baby interaction, encourages breast feeding, relaxes baby, warms baby.
Cord clamping
Dry baby
Keep baby warm with hats and blankets
Vitamin K injection- Babies usually born with deficiency (therefore increased risk of bleeds i.e. intracranial/gastrointestinal) so given IM shortly after birth- can help to initiate cry to expand the lungs. Can also give orally but will take much longer over several wks. 
Label the baby
Measure and weigh the baby
Heel prick test
New born hearing test
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7
Q

What is the heel prick test?

A

Done at day 5 (latest at day 8), need 4 drops of blood and parents consent.
Results within 6-8wks

Testing for 9 diseases:
CF
Congenital hypothyroidism
Sickle cell disease
Homocysteine
Phenylketonuria
GA-1
IVA
MCADD
Maple Syrup Urine Disease
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8
Q

What is the new born examination?

A

Screening tool.
Within 72 hrs of birth and repetaed by GP at 6-8wks.

Examination of head, shoulders, chest, abdomen, genitalia, legs and reflexes.

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9
Q

What are examples of birth injuries?

A

Caput Succedaneum- Oedema between the scalp and periosteum due to traumatic/prolonged birth or instrumental delivery i.e. ventouse. No/little discolouration, passing over the suture lines and will self resolve within a few days.

Cephalohematoma- Blood between the periosteum and skull, will not pass over the suture lines- can differentiate for caput succedaneum. Also blood collection will lead to discolouration. Will self resolve but need to monitor for jaundice and anaemia.

Erb’s palsy- In macrosomia, traumatic birth. Leads to waiters tip.

Facial nerve palsy- Can occur after forceps delivery. Function will return within a few months, if not then contact neurosurgeons.

Clavicular fracture- Can occur in traumatic birth, macrosomia. Asymmetry of shoulders, lack of movement, distress and pain on movement. Confirm with X-Ray or USS. Manage conservatively with splinting, will self resolve. Complications include brachial plexus injury.

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10
Q

What are the common organisms of neonatal sepsis?

What are the RF?

A

Commonly GBS (Group B Strep). Also E.coli, listeria, Staph.aureus.

RF:
Maternal GBS vaginal colonisation
Previous GBS pregnancy
Prolonged rupture of membranes
Early rupture of membranes
Maternal sepsis
Spontaneous labour
Prematurity
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11
Q

What are the common features of neonatal sepsis?

What are the Red Flags?

A
Features:
Fever
Poor weight gain
Poor feeding
Seizure
Hypoglycaemia 
Jaundice within 24hrs
Vomiting
Respiratory distress
Hypoxia
Tachycardia/bradycardia

Red Flags:
Sibling from same birth with presumed sepsis
Term baby requiring mechanical ventilation
Respiratory distress 4hrs after birth
Confirmed/suspected maternal sepsis
Seizures
Signs of shock

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12
Q

How is presumed neonatal sepsis managed?

A

Commonly due to maternal GBS. Therefore if known vaginal GBS give prophylactic benzylpenicillin in labour.

If one RF/clinical feature then observe for 12hrs.
If ≥ 2 RF/clinical features OR 1 red flag give Abx.
Start Abx within 1hr of deciding.
Ensure blood culture before initiating Abx.
Check baseline FBC and CRP. If ?meningitis then need LP.

First line- benzylpenicillin and gentamycin.
Second line- add cefotaxime

Repeat CRP after 24hrs and repeat blood cultures at 36hrs.
Stop Abx if baby is well and blood cultures are negative after 36hrs and CRP <10.
If need to continue Abx then recheck CRP on day 5.
If any CRP results are >10 consider LP.

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13
Q

What is hypoxic-ischaemic encephalopathy?

What are the causes?

A

Refers to hypoxia which leads to brain injury, this can lead to cerebral palsy.
Suspect if; perinatal/intrapartum hypoxia, umbilical blood gas acidic pH, features of mild/moderate/severe HIE, poor APGAR scores, multi-organ failure etc.

Causes of hypoxia:
Intrapartum haemorrhage
Maternal shock
Prolapsed cord- Compression of cord during labour can lead to hypoxia
Nuchal cord- Cord wraps around the neck of the fetus

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14
Q

What are the features of mild/moderate/severe HIE?

A

Mild- Poor feeding, irritability. Will resolve within 24hrs, prognosis is normal.
Moderate- Poor feeding, hypotonia, seizures, lethargic. Will resolve within weeks. 40% will develop cerebral palsy.
Severe- Flaccid, absent/poor reflexes, reduced consciousness. 50% mortality, 90% cerebral palsy.

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15
Q

How is hypoxic-ischaemic encephalopathy managed?

What is therapeutic hypothermia?

A

Supportive management in the neonatal unit including ventilatory support, cardiovascular support, nutrition, treatment of seizures, therapeutic hypothermia etc.
Children with long lasting disabilities should be followed up by paediatrics to provide support.

Therapeutic hypothermia involves reducing body temperature to 33-34 degrees for 72 hrs to limit brain and neuronal damage. Temperature is measured rectally and is increased back to normal gradually within 6hrs.

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16
Q

What is physiological jaundice?

What is prolonged jaundice?

A

Foetal RBC are more fragile than normal RBC. They breakdown easily and usually bilirubin absorbed by the placenta. After birth there is not placenta but still remaining foetal RBC, therefore commonly get jaundice from day 2-7 (sclera), resolving by 10 days.

NB- PATHALOGICAL TO GET JAUNDICE WITHIN 24HRS OF BIRTH- THINK SEPSIS!

Jaundice longer than physiologically expected.
Term >14 days
Premature >21 days
Consider in biliary atresia, G6PD deficiency and hypothyroidism.

17
Q

What are the causes of neonatal jaundice?

A

Either increased production of bilirubin (i.e. increase RBC breakdown) or decrease clearance.

Increased production:
Haemolytic disease of the new born (Rh group)
Haemorrhage
Cephalohematoma
G6PD deficiency 
ABO incompatibility
Intraventricular haemorrhage
Sepsis

Decreased clearance:
Prematurity- Liver not fully developed therefore increased risk of kernicterus
Breast Milk Jaundice- Breast milk can interfere with livers ability to process bilirubin. Also breastfed babies are more likely to become dehydrated if not fed adequately. Dehydration leads to slow bowel movements and so more time for bilirubin to be absorbed by the gut.
Neonatal cholestasis
Gilbert’s syndrome
Hypothyroidism/Hypopituitary
Biliary atresia

18
Q

How is neonatal jaundice investigated?

How is it managed?

A
Investigate:
FBC and blood film
Conjugated bilirubin levels (high suggest hepatobiliary cause)
Direct-Coombs test for haemolysis
Blood cultures for infection
G6PD levels for deficiency
TFTs
Blood type testing

Management:
Plot the bilirubin levels on a treatment threshold chart. This will indicate the management plan.
- Review
- Phototherapy- Baby stripped down to nappy and eyes covered. Exposed to blue light which converts unconjugated bilirubin into isomers which can be excreted (bypassing the liver). Check bilirubin levels after 12-18hrs.
- Exchange transfusion-n In extreme cases remove the baby’s blood and transfuse with donor blood.

19
Q

What is kernicterus?

A

Bilirubin can pass BBB.
Therefore high bilirubin needs to be reduced as it can cause permanent damage to the CNS.

Results in cerebral palsy, learning difficulties and deafness.

20
Q

What is the WHO classification of prematurity?

What are the RF of prematurity?

A

<28wks- extremely preterm
28-32wks- very preterm
32-37wks- moderate to late preterm

RF:
FHx/Personal Hx of prematurity
Smoking
Drugs
Alcohol
Overweight or underweight mother
Maternal co-morbidities
Twins
21
Q

How is prematurity managed before birth?

A

If there is Hx of giving birth to premature baby OR USS shows cervical length <25mm by 24wks then either:

(a) Prophylactic progesterone suppository to discourage labour
(b) Prophylactic cervical cerclage- suture to keep cervix closed

If confirmed or suspected premature labour-
Tocolysis (nifedipine) to supress contractions
IM corticosteroids to mother if <35wks
IV MgSO4 if <34wks to protect brain
Delayed cord clamping

22
Q

What are the associated issues of prematurity?
In early life?
Long term?

A
RDS
Hypoglycaemia
Hypothermia
Necrotising enterocolitis
Neonatal jaundice
Retinopathy of prematurity
Poor feeding
Bradycardia/apnoea
Immature immune system and infections
Long term?
Chronic lung disease of prematurity
Cerebral palsy
Learning disability
Visual/hearing impairment
Increased succeptibiltiy to infection
23
Q

What is apnoea of prematurity?

How is it managed?

A

Common in babies the more premature they are, due to underdevelopment of the ANS.

Have period of stopping breathing for 20 seconds OR shorter periods but with associated bradycardia and O2 desaturation.

Manage with apnoea monitoring for premature- us tactile stimulation (warming, drying, rubbing back/soles of feet) to restart breathing, can give IV caffeine to prevent the apnoea.

Episodes will settle as the baby grows and develops.

24
Q

What is retinopathy of prematurity? (ROP)

How is it managed?

A

Normal blood vessel development happens in utero at 16wks, in response to hypoxia. Once premature baby born, they are given O2, therefore stop getting new blood vessel formation. Once the O2 is removed this leads to neovascularisation which can then leak, regress etc causing retinal detachment, scarring or blindness.

Screening is done by and ophthalmologist every 2 wks:
From 30-31wks gestational age in babies born <27wks
OR
From 4-5wks of age in babies born >27wks

If there is evidence of neovascularisation; need transpupillary laser photocoagulation. May also benefit from anti-VEGF injections or surgery in the case of retinal detachment.

25
Q

What is respiratory distress syndrome?

How is it managed?

A

Common in preterm babies <32wks.
Not enough surfactant producing, leading to reduce alveoli expansion so lung collapse, reduced gas exchange resulting in hypoxia, hypercapnia and respiratory distress.

CXR- Ground glass appearance, atelectasis.

Management:
If suspect preterm delivery (<35wks) give antenatal dexamethasone.
Intubation and ventilation if severe RDS
CPAP- to keep lungs open whilst breathing
O2- to maintain pO2 between 91-95%
Endotracheal surfactant

26
Q

What are the complications of RDS?

A
Short term:
Pneumothorax
Infection
Apnoea
IVH
NEC

Long term:
Chronic lung disease of prematurity
Visual and hearing impairments
ROP

27
Q

What is necrotising enterocolitis?
What are the RF?
How does it present?

A

Necrosis of part of the bowel- causes is unknown.

RF:
Very LBW or Very premature
RD requiring ventilation
PDA
Sepsis 
Formula feeds
Presents:
Intolerant of feeds
Vomit (green bile mainly)
Distended abdomen
Bloody stools
Unwell 
Absent bowel sounds

If perforated/peritonitis/sepsis- extremely unwell

28
Q

How is necrotising enterocolitis investigated?

How is it managed?

A
Investigation:
FBC- low platelets and low neutrophils
CRP
Blood cultures- sepsis
Capillary BG- Metabolic acidosis
Diagnose with AXR:
Dilated bowel loops
Pneumoperitoneum
Gas in bowel walls- indicative of NEC
Gas in portal veins
Thickened bowel walls
29
Q

How is necrotising enterocolitis managed?

What are the complications?

A

Management:
Stabilise patient- NBM, IV fluids, TPN (total parenteral nutrition), NG tube (‘suck’).
Some can be managed medically, otherwise surgery to remove necrotic bowel. If large resection then temporary stoma.

Complications:
Long term stoma
Surgery- small bowel syndrome
Sepsis
Perforation and peritonitis
Death
Strictures
Abscess
30
Q

What is sudden infant death syndrome (cot death)?
What are the RF?
How can it be prevented?

A

Unexplained death of an infant, occurring within the first 6 months of life.

RF: Male (slight), parental smoking, premature, LMBW.

Prevention:
Avoid smoking around the baby or going to the baby after smoking (stays on clothes)
Lay baby on back if unsupervised
Avoid co-sleeping with baby- if can’t avoid then don’t co-sleep after smoking, drinking, drugs etc
Lay the baby with the feet at the end of the cot- so can’t roll down under the blanket
Keep cot clear i.e. toys
Keep baby face uncovered
Maintain a comfortable room temperature 16-20 degrees.

Lullaby trust- bereavement service.
Care of next infant team (CONI) support with infant born after previous sudden cot death. Providing home visits, resuscitation teaching etc.