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3a paeds > Neonatology > Flashcards

Neonatology Flashcards

1
Q

What is neonatal sepsis

A

infection in the neonatal period (first 28 days) results in significant morbidity and mortality (10%)

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2
Q

what are common causative organism of neonatal sepsis

A

** Group B streptococcus (GBS) **
Escherichia coli (e. coli)
Listeria
Klebsiella
Staphylococcus aureus

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3
Q

what are RF for neonate sepsis

A
  • Vaginal GBS colonisation
  • GBS sepsis in a previous baby
  • Maternal sepsis, chorioamnionitis or fever > 38ºC
  • Prematurity (less than 37 weeks)
  • Early (premature) rupture of membrane
  • Prolonged rupture of membranes (PROM)
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4
Q

how does neonatal sepsis present

A

Respiratory distress
fever
tachycardia
Apnoea
Reduced tone and activity
jaundice
Vomiting
poor feeding

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5
Q

what are red flag symptoms of neonatal sepsis

A
  • Confirmed or suspected sepsis in the mother
  • Signs of shock
  • Seizures
  • Term baby needing mechanical ventilation
  • Respiratory distress starting more than 4 hours after birth
  • Presumed sepsis in another baby in a multiple pregnancy
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6
Q

what is the management for suspected neonatal sepsis if there is ONE risk factor or clinical feature

A

monitor the observations and clinical condition for at least 12 hours

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7
Q

what is the management for suspected neonatal sepsis if there is TWO or more risk factor or clinical feature

A

start antibiotics

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8
Q

what is the management for suspected neonatal sepsis if there is ONE red flag sign

A

start Abx

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9
Q

how soon should Abx be started in neonatal sepsis

A

within 1 hr of decsion

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10
Q

when should blood cultures be taken in neonatal sepsis

A

before antibiotics are given
also baseline FBC and CRP

LP if meningitis suspected

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11
Q

what is 1st line Abx of neonatal sepsis and the alterantive

A

benzylpenicillin with gentamycin

alt = third generation cephalosporin (e.g. cefotaxime)

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12
Q

What is the ongoing management of neonatal sepsis

A
  • Check the CRP again at 24 hours
  • Check the blood culture results at 36 hours
  • Check the CRP again at 5 days if they are still on treatment
  • Consider performing a LP if any of the CRP results are more than 10.
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13
Q

When can Abx be considered being stopped in neonatal sepsis

A
  • at 48 hours if clinically well, the blood cultures are negative and both CRP results are less than 10

or

  • at 5/10 day if clinically well, the lumbar puncture and blood cultures are negative and the CRP has returned to normal
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14
Q

what are steps of neonatal resuscitation

A
  1. Dry baby and maintain temperature
  2. Assess tone, respiratory rate, heart rate
  3. If gasping or not breathing give 5 inflation breaths*
  4. Reassess (chest movements)
  5. If the heart rate is not improving and <60bpm start compressions and ventilation breaths at a rate of 3:1
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15
Q

what score is used to assess newborns health after birth

A

APGAR Score

appearance:
pulse
grimace = reflex irritability
activity = tone
respiration

taken at 1 min and 5 mins

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16
Q

what can prolonged hypoxia lead to

A

hypoxic-ischaemic encephalopathy (HIE)

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17
Q

in severe hypoxia situations what management can be considered

A

IV drugs and intubation
therapeutic hypothermia with active cooling.

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18
Q

what is benefit of delayed cord clmaping

A

improved haemoglobin, iron stores and blood pressure and a reduction in intraventricular haemorrhage and necrotising enterocolitis.

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19
Q

what is downside to delayed cord clamping

A

increase in neonatal jaundice, potentially requiring more phototherapy

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20
Q

how long should cord clamping be delayed in uncompromised neonates

A

at least 1 min

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21
Q

what is respiratory distress syndrome

A

affects premature neonates, born before the lungs start producing adequate surfactant

common <32 weeks

mortality ~40%

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22
Q

what is pathophysiology of RDS

A

Inadequate surfactant leads to high surface tension within alveoli.

= lung collapse = more difficult for lungs and alveoli to expand

= inadequate gaseous exchange

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23
Q

what are blood gas results of RDS

A

hypoxia, hypercapnia (high CO2)

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24
Q

what are chest XRay results of RDS

A

“ground-glass” appearance

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25
Q

what are features of RDS

A

tachypnoea, intercostal recession, expiratory grunting and cyanosis

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26
Q

how is RDS managed before labor

A

mother given antenatal steroids (dexamethasone) to increase production of surfactant with suspect or confirmed preterm labour

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27
Q

how is a neonate with RDS managed

A
  • intubation and ventilation
  • Endotracheal surfactant (artificial surfactant by trach tube
  • Continuous positive airway pressure (CPAP
  • Supplementary oxygen 91-95% o2 stat
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28
Q

what are short term complications of RDS

A
  • Pneumothorax
  • Infection
  • Apnoea
  • Intraventricular haemorrhage
  • Pulmonary haemorrhage
  • Necrotising enterocolitis
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29
Q

what are long term complications of RDS

A
  • Chronic lung disease of prematurity
  • Retinopathy of prematurity
  • Neurological, hearing and visual impairment
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30
Q

what is Hypoxic-Ischaemic Encephalopathy

A

occurs in neonates as a result of hypoxia during birth.

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31
Q

When should HIE be suspected in neonates

A
  • when there are events that could lead to hypoxia during the perinatal or intrapartum period
  • acidosis (pH < 7) on the umbilical artery blood gas
  • poor Apgar scores
  • features of mild, moderate or severe HIE (see below)
  • evidence of multi organ failure.
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32
Q

what causes HIE

A
  • Maternal shock
  • Intrapartum haemorrhage
  • Prolapsed cord, causing compression of the cord during birth
  • Nuchal cord, where the cord is wrapped around the neck of the baby
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33
Q

what is the grading system of HIE

A

Sarnat Staging

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34
Q

what is mild in Sarnat Staging

A

Poor feeding, generally irritability and hyper-alert
Resolves within 24 hours
Normal prognosis

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35
Q

what is moderate in Sarnat Staging

A
  • Poor feeding, lethargic, hypotonic and seizures
  • Can take weeks to resolve
  • Up to 40% develop cerebral palsy
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36
Q

what is severe in Sarnat Staging

A
  • Reduced consciousness, apnoeas, flaccid and reduced or absent reflexes
  • Up to 50% mortality
  • Up to 90% develop cerebral palsy
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37
Q

how is HIE managed

A

supportive care with neonatal resuscitation
ventilation
circulatory support
nutrition
acid base balance
treatment of seizures.
Therapeutic hypothermia

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38
Q

what is Therapeutic hypothermia

A

actively cooling the core temperature of the baby to reduce the inflammation and neurone loss after the acute hypoxic injury

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39
Q

what is the temperate aim of Therapeutic hypothermia and for how long

A

between 33 and 34°C, measured using a rectal probe for 72 hours

baby is gradually warmed to a normal temperature over 6 hours

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40
Q

What is Jaundice

A

abnormally high levels of bilirubin in the blood

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41
Q

what do RBC contain

A

unconjugated bilirubin

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42
Q

where is unconjugated bilirubin conjugated

A

liver

43
Q

how is conjugated bilirubin excreted

A
  • via the biliary system into the gastrointestinal tract
  • via the urine.
44
Q

what is the physiology of neonatal jaundice

A

high concentration of red blood cells in the neonate

more fragile than normal + less developed liver function

= break down more rapidly = releasing lots of bilirubin

usually excreted via placenta, after birth - rise in bilirubin shortly after birth

45
Q

how does neonatal jaundice present

A

mild yellowing of skin and sclera from 2 – 7 days of age

46
Q

what are increased production of bilirubin causes of neonatal jaundice

A

Haemolytic disease of the newborn
ABO incompatibility
Haemorrhage
Intraventricular haemorrhage
Cephalo-haematoma
Polycythaemia
Sepsis and disseminated intravascular coagulation
G6PD deficiency

47
Q

what are decreased clearance of bilirubin causes of neonatal jaundice

A

Prematurity
Breast milk jaundice
Neonatal cholestasis
Extrahepatic biliary atresia
Endocrine disorders (hypothyroid and hypopituitary)
Gilbert syndrome

48
Q

when is neonatal jaundice pathological

A

Jaundice in the first 24 hours of life

= urgent investigations and management

common cause = sepsis

49
Q

what are causes of jaundice in first 24hrs

A

rhesus haemolytic disease
ABO haemolytic disease
hereditary spherocytosis
glucose-6-phosphodehydrogenase

50
Q

what is kernicterus

A

brain damage due to high bilirubin levels.

51
Q

when is jaundice prolonged

A

More than 14 days in full term babies
More than 21 days in premature babies

52
Q

what are causes of prolonged jaundice in newborns

A

biliary atresia
hypothyroidism
galactosaemia
urinary tract infection
prematurity

53
Q

how is newborn jaundice investigared

A

FBC and Blood film
conjugated bilirubin
blood type testing
direct coombs test
thyroid function
blood and urine cultures
G6PD levels

54
Q

how is the decision to start treatment for neonatal jaundice decided

A

total bilirubin levels are monitored and plotted on treatment threshold charts

x axis = age of the baby (hours)
y axis = total bilirubin level

if bilirubin reaches threshold = commence treatment

55
Q

what is the treatment for neonatal jaundice

A

Phototherapy

Extremely high = exchange transfusion

56
Q

how does phototherapy work

A

converts unconjugated bilirubin into isomers that can be excreted in the bile and urine without requiring conjugation in the live

blue light is best

Once phototherapy is complete, a rebound bilirubin should be measured 12 – 18 hours after stoppin

57
Q

how does Kernicterus present

A

less responsive, floppy, drowsy baby with poor feeding

permeant damage –> cerebral palsy, learning disability + deafness

58
Q

What is Necrotising enterocolitis

A

part of the bowel becomes necrotic

in premature neonates

life threatening

59
Q

what can untreated Necrotising enterocolitis lead to

A

lead to bowel perforation. Bowel perforation leads to peritonitis and shock.

60
Q

what are risk factors for Necrotising enterocolitis

A

Very low birth weight or very premature
Formula feeds
Respiratory distress and assisted ventilation
Sepsis
Patient ductus arteriosus and other congenital heart disease

61
Q

how does Necrotising enterocolitis present

A

feeding intolerance
abdominal distension
bloody stools
Absent bowel sounds
vomiting

62
Q

what is investigation of choice for Necrotising enterocolitis

A

Abdo Xray

63
Q

what are blood tests for Necrotising enterocolitis

A

Full blood count for thrombocytopenia and neutropenia
CRP for inflammation
Capillary blood gas will show a metabolic acidosis
Blood culture for sepsis

64
Q

what would XRay show for Necrotising enterocolitis

A
  • Dilated loops of bowel
  • Bowel wall oedema (thickened bowel walls)
  • Pneumatosis intestinalis is gas in the bowel wall and is a sign of NEC
  • Pneumoperitoneum is free gas in the peritoneal cavity and indicates perforation
  • Gas in the portal veins
65
Q

what is the management for Necrotising enterocolitis

A

stabilize = nil by mouth with IV fluids, total parenteral nutrition (TPN) and antibiotics

Ng tube to drain fluid and gas from stomach and inesteine

surgical emergency = remove the dead bowel tissue

66
Q

what are complications of Necrotising enterocolitis

A

Perforation and peritonitis
Sepsis
Death
Strictures
Abscess formation
Recurrence
Long term stoma
Short bowel syndrome after surgery

67
Q

what is neonatal hypoglycaemia

A

< 2.6 mmol/L

68
Q

what can cause persistent/severe hypoglycaemia after birth

A

preterm birth (< 37 weeks)
maternal diabetes mellitus
IUGR
hypothermia
neonatal sepsis
inborn errors of metabolism
nesidioblastosis
Beckwith-Wiedemann syndrome

69
Q

how does hypoglycaemia present in neonates

A

may be asymptomatic
‘jitteriness’
irritable
tachypnoea
pallor
poor feeding/sucking
weak cry
drowsy
hypotonia
seizures

70
Q

how is asymptomatic hypoglycaemia managed in neonates

A

encourage normal feeding (breast or bottle)
monitor blood glucose

71
Q

how is symptomatic hypoglycaemia managed in neonates

A

admit to the neonatal unit
intravenous infusion of 10% dextrose

72
Q

when is Meconium aspiration syndrome most common

A

post-term deliveries, with rates of up to 44% reported in babies born after 42 weeks.

73
Q

What are RF for Meconium aspiration syndrome

A

maternal hypertension, pre-eclampsia, chorioamnionitis, smoking or substance abuse.

74
Q

how common is cleft lip and palate

A

1 in every 1,000 babies

75
Q

what fails to fuse in cleft lip

A

fronto-nasal and maxillary processes

76
Q

what dails to fuse in cleft palate

A

palatine processes and the nasal septum

77
Q

what are problems associated with having Cleft lip and palate

A

feeding: orthodontic devices may be helpful
speech: with speech therapy 75% of children develop normal speech
increased risk of otitis media for cleft palate babies

78
Q

how is Cleft lip and palate managed

A

lip repaired first before 3 months
then palate in 6-12 months

79
Q

what are TORCH infections

A

Toxoplasmosis
Others (syphilis, hepatitis B)
Rubella
Cytomegalovirus
Herpes simplex

80
Q

what is Gastroschisis

A

birth defect where there is a hole in the abdominal (belly) wall beside the belly button.

This results in the baby’s intestines extending outside of the baby’s body

81
Q

in pregnancy what thryoid hormone increases

A

thyroxine-binding globulin (TBG).
= increase in total thyroxine but not free thyroxine

82
Q

what can Untreated thyrotoxicosis cause

A

increases the risk of fetal loss, maternal heart failure and premature labour

83
Q

how is maternal hyperthyroid managed

A

1st trimester = Propylthiouracil
2nd trimester = carbimazole

84
Q

what is checked in pregnancy at 30-36 weeks to help determine the risk of neonatal thyroid problem

A

thyrotrophin receptor stimulating antibodies

85
Q

what is Abx of choice for GBS prophylaxis

A

benzylpenicillin

86
Q

when are swabs for GBS offered

A

35-37 weeks or 3-5 weeks before delivery date

87
Q

what are fluid requirements for children for the first 10kg

A

100ml/kg

88
Q

what are fluid requirements for children 10-20kg

A

100ml/kg for first 10kg

+ 50ml/kg for each addition 1kg of weight between 10kg - 20kg

89
Q

what are fluid requirements for children over 20kg

A

100ml/kg for each kg for first 10kg

+ 50ml/kg for each addition 1kg of weight between 10kg - 20kg

+ 20ml/kg for each 1kg of body weight over 20kg

90
Q

what is max fluid requirment

A

2L for girls 2.5 L for boys

91
Q

what is school exclusion for scarlet fever

A

24 hours after commencing antibiotics

92
Q

what is school exclusion for whooping cough

A

2 days after commencing antibiotics (or 21 days from onset of symptoms if no antibiotics )

93
Q

what is school exclusion for measles

A

4 days from onset of rash

94
Q

what is school exclusion for rubella

A

5 days from onset of rash

95
Q

what is school exclusion for chickenpox

A

All lesions crusted over

96
Q

what is school exclusion for mumps

A

5 days from onset of swollen glands

97
Q

what is school exclusion for D&V

A

Until symptoms have settled for 48 hours

98
Q

what is school exclusion for impetigo

A

Until lesions are crusted and healed, or 48 hours
after commencing antibiotic treatment

99
Q

what is school exclusion for scabies

A

Until treated

100
Q

what is school exclusion for influenza

A

Until recovered

101
Q

how does Oesophageal atresia present

A

choking and cyanotic spells following aspiration

102
Q

what are characteristic features of congenital Rubella

A

Sensorineural deafness
Congenital cataracts
Congenital heart disease (e.g. patent ductus arteriosus)
Glaucoma

103
Q

what are characteristic features of congenital Toxoplasmosis

A

Cerebral calcification
Chorioretinitis
Hydrocephalus

104
Q

what are characteristic features of congenital Cytomegalovirus

A

Low birth weight
Purpuric skin lesions
Sensorineural deafness
Microcephaly

3a paeds (12 decks)

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