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Sarah Paeds > Neonatalogy > Flashcards

Neonatalogy Flashcards

1
Q

What are three severeties of HIE? What characterises them?

A

Mild - irritable neonate, increased response to stimulation. Staring. Impaired feeding. Most recover.
Moderate - abnormal tone/movement. Reduced feeding. Seizures
Severe - no normal spontaneous movements to pain. Hypo/hypertonia. Seizures prolonged and refractory to treatment. Multi-organ failure

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2
Q

What is the mortality rate in severe HIE?

A

30-40%

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3
Q

Management for HIE

A

Hypothermic cooking shown to reduce brain damage

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4
Q

What is the prognosis of HIE features persisting beyond 2 weeks

A

Poor prognosis

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5
Q

What may bilateral abnormalities in the basal ganglia/thalamus suggest in suspected HIE?

A

HIGH risk of later cerebral palsy

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6
Q

Causes of HIE

A 
Uterine rupture 
Plaental abruption 
IUGR 
Failure to breathe 
Cord compression
Cord prolapse
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7
Q

Jaundice <24 hours causes

A

SEPSIS until proven otherwise
Haemolysis (ABO incompatibility, Rhesus disease, G6PD deficiency)
Physiological

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8
Q

Jaundice 24h-2 weeks causes

A

Physiological (breakdown product of excess Hct)
Breastfeeding
Haemolysis (ABO incompatibility, Rhesus disease, G6PD deficiency)
Polycythaemia
Infection

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9
Q

Jaundice >2 weeks high unconjugated causes

A

Haemolysis
GI obstruction
Hypothyroid

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10
Q

Jaundice >2 weeks high conjugated causes

A

Obstructive picture

  • Biliary atresia
  • Choledochal cyst

Hepatitis

  • Infection
  • a1 antitrypsin
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11
Q

What is the commonest indication for a paediatric liver transplant?

A

Biliary atresia

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12
Q

What is biliary atresia?

A

Destruction/absence of extrahepatic biliary tree and intrahepatic ducts

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13
Q

Clinical features of biliary atresia

A

Normal birth weight but FTT
Pale stools, dark urine
Jaundice
Hepatomegaly (then splenomegaly)

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14
Q

Ix for biliary atresia

A 
USS abdomen 
TIBIDA scan (good uptake but no excretion into bowel)
Liver biopsy
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15
Q

Management of biliary atresia

A

Surgical bypass hepatoportoenterostomy (Kasai)
Ursodeoxycholic acid (bile movement)
Nutritional supplementation incl vitamins ADEK
Prophylactic abx to reduce risk of cholangitis

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16
Q

Signs of resp distress in a neonate

A 
Tachypnoea 
Increased WOB 
Grunting 
Recessions 
Cyanosis
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17
Q

What is the primary cause of transient tachypnoea of the newborn?

A

Delay in lung liquid reabsorption

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18
Q

In which type of birth is TTotN more common?

A

CS

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19
Q

CXR TTotN

A

Fluid line in horizontal fissure

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20
Q

What percentage of babies pass meconium before birth?

A

8-20%

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21
Q

Three severities of meconium aspiration

A

Mild
Moderate
Severe

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22
Q

What other resp disorder are babies who aspirate meconium more likely to suffer from?

A

Pneumothorax

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23
Q

CXR features of meconium aspiration

A

Features of sepsis - unstable temperatures, resp distress, jaundice, slow CRT, apnoea
Overinflated lungs
Collapse
Consolidation

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24
Q

Treatment of meconium aspiration

A

IF RFFS:

- IV ampicillin and gentamicin

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25
Q

Risk factors for sepsis

A 
Chorioamnionitis 
PROM
PPROM 
Maternal fever during labour 
FHR abnormalities 
Oligohydramnios
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26
Q

What are the risk factors for pHTN?

A

RDS
Pneumothorax
Meconium aspiration

L to R shunt

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27
Q

Ix for pHTN

A

Urgent ECHO (congenital lesions)

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28
Q

Mx of pHTN

A

Mechanical ventilation and circulatory support

Inhaled nitric oxide and sildenafil (viagra) - both vasodilators

To consider ECMO

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29
Q

Complications of pHTN (with patent duct)

A

Eisenmenger’s syndrome - L to R shunt becomes R to L shunt

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30
Q

What is a diaphragmatic hernia?

A

L sided herniation of abdo contents through posterolateral foramen of diaphragm

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31
Q

Disaphragmatic hernia signs

A

Apex beat and HS displaced to R – pulmonary hypoplasia

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32
Q

Ix for suspected diaphragmatic hernia

A

CXR/AXR

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33
Q

Mx diaphragmatic hernia

A

Large NGT w/ suction applied (to prevent dilatation)

Surgical repair once normal pulmonary pressures are maintained

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34
Q

Management of infant born to HbsAg positive mother

A

Vaccinaton shortly after birth

AND HepB Ig if at risk

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35
Q

Management of infant with active HepB

A

Supportive therapy

Immune active phase - treat with interferon/tenofovir disoproxil

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36
Q

Management of pregnant mother HbsAg positive

A

Antiviral monotherapy (tenofovir disoproxil) if viral load >200,000

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37
Q

Treatment/advice for rubella

A

Rest, fluids, paracetamol
AVOID other pregnant women for 6 days after rash onset
IM immunoglobulin

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38
Q

When is the highest risk of rubella transmission?

A

EARLY pregnancy (<20 weeks) - 8-10 weeks worst

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39
Q

Symptoms of rubella (in mother)

A

Rash (starting on face, spreading to body)

Post-auricular lymphadenopathy

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40
Q

Three primary features congenital rubella syndrome

A

Deafness
Cataracts
Cardiac problems - PDA common

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41
Q

Which cardiac issue is common in congenital rubella syndrome?

A

PDA

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42
Q

Which neonates are at highest risk of hypoglycaemia?

A

IUGR
GDM
Prem
Hypothermic

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43
Q

Features hypoglycaemia neonate

A

Jittery, irritable, apnoea, lethargy, drowsy, seizures

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44
Q

What blood glucose is desirable for neonates to ensure normal neurodevelopmental outcome

A

> 2.6

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45
Q

What is a complication of prolonged and symptomatic hypoglycaemia in the neonate?

A

Neurodisability

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46
Q

How is neonatal hypoglycaemia managed?

A

Glucose IV infusion (until BM >2.6)
Early/more frequent feeding
Glucagon/steroids if necessary

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47
Q

What blood glucose is desirable for neonates to ensure normal neurodevelopmental outcome

A

> 2.0 pre feed

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48
Q

What is early onset sepsis?

A

Within 48 hours of birth

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49
Q

How is neonatal hypoglycaemia managed?

A

Glucose IV infusion (until BM >2.0)
Early/more frequent feeding
Glucagon/steroids if necessary

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50
Q

What is late onset sepsis?

A

After 48 hours of birth

51
Q

Primary causes late onset sepsis

A

Nosocomial - lines, catheters, ventilation

52
Q

Commonest early onset sepsis causative organisms

A

GBS
Listeria
E.coli

53
Q

Commonest late onset sepsis causative organisms

A

Coagulase negative staph.

E.g. staph epidermis

54
Q

Abx for early onset sepsis organisms (+ve and -ve)

A

+ve benpen, amoxicillin

-ve gentamicin

55
Q

Abx for late onset sepsis organisms (+ve and -ve)

A

vanc/gent/fluclox

56
Q

% of pregnant women with GBS (vaginal/faecal)

A

30%

57
Q

When are abx appropriate (for mum and baby) in GBS positive mothers?

A

IF:

  • Suspected sepsis in mother (intrapartum abx once labour starts)
  • Previous baby with GBS (intrapartum abx)

For baby if increased risk and/or abx not started within 4 hours before birth

58
Q

Treatment for listeria

A

Amoxicillin/cotrimoxazole

59
Q

Features of listeria infection

A

Mec in a preterm baby (unusual).
Rash
Septicaemia

60
Q

Conjunctivitis in newborn

A

Troublesome discharge,
Red
Itchy eyes

61
Q

Commonest causative agent in conjunctivitis <48hr after birth

A

Gonococcal

62
Q

Conjunctivitis causative agent

A

Chlamydia trachomatic

63
Q

Ix/Mx for conjunctivitis

A

Swab

Abx - erythromycin

64
Q

Treatment of omphalitis

A

Aim to prevent involution by granuloma

AgNo3

65
Q

Highest risk for transmitting HSV

A

Mother with primary genital herpes infection within 6 weeks of birth

66
Q

What is the risk of a mother with primary genital herpes infection transmitting to infant in vaginal delivery?

A

40%

67
Q

Management of mother with primary genital herpes infection within 6 weeks of delivery

A

ELCS
IV aciclovir for mother
IV aciclovir for baby on delivery

68
Q

Treatment for congenital CMV

A

Ganciclovir

69
Q

When does necrotising enterocolitis present?

A

First few weeks of life

70
Q

What is necrotising enterocolitis?

A

Bacterial invasion of ischaemic bowel wall

71
Q

Which group of neonates are more likely to develop necrotising enterocolitis?

A

Those drinking cow’s mil formula

72
Q

Clinical features of necrotising enterocolitis

A 
Reduced feeding 
Milk aspiration 
Bile stained vomit 
Abdominal distension (tense, shiny skin)
PR bleed 
BOWEL PERFORATION - SHOCK
73
Q

AXR features of necrotising enterocolitis

A

Distended bowel loops, thickened bowel wall, intramural gas

74
Q

Mx necrotising enterocolitis

A

STOP oral feed
Broad spec abx - vanc/cefotaxime
TPN
Surgery

75
Q

Commonest cardia lesion in preterm babies

A

PDA

76
Q

Management of PDA

A

Medical

  • Prostacyclin synthetase inhibitor
  • IV indomethacin
  • Ibuprofen

Surgery - balloon

77
Q

How much should a preterm baby be feeding?

A

60-90ml/kg/day

78
Q

How much should a term baby be feeding?

A

90-120ml/kg/day

79
Q

Baby with poor feeding maintenance fluids

A

2/3

80
Q

Why is haemorrhage common (25%) in vLBW naeonates?

A

Fragile blood vessels around the germinal matrix above the caudate nucleus

81
Q

Name one (resp) risk factor for neonatal naemorrhage?

A

Pneumothorax

82
Q

Three types of brain injury in preterms

A
  • Haemorrhage
  • Ventricular dilatation (blockage of CSF drainage) –> hydrocephaly
  • Periventricular leukomalacia
83
Q

What clinical features does periventricular leukomalacia later present with?

A

Spastic diplegia

84
Q

What % of vLBW babies have retinopathy of prematurity

A

35%

85
Q

What is the pathophysiology of retinopathy of prematurity?

A

Vacular proliferation = detachment, fibrosis and blindness

86
Q

Mx of ventricular dilation

A

Ventriculo-peritoneal shunt

87
Q

Mx of retinopathy of prematurity

A

R/f to ophthalmology

Laser therapy

88
Q

Pathophysiology of respiratory distress syndrome

A

Reduced lung surfactant (type II pneumocytes) = reduced surface tension = alveolar collapse = impaired gas exchange

89
Q

Is RDS more severe in male or female preterms?

A

Male

90
Q

How can RDS be prevented?

A

Antenatal steroids (within 7 days of delivery)

91
Q

Features of RDS

A

All within 4 hours of birth:

  • Tachypnoea
  • Cyanosis
  • Increased WOB
  • Expiratory grunt
92
Q

CXR features of RDS

A

Granular/ground glass appearance

Air bronchograms

93
Q

Management of RDS

A

O2 ventilation (CPAP)
Exogenous surfactant via an ET tube
Supportive preterm therapy

94
Q

Pathophysiology of pneumothorax in preterm

A

Air from overdistended alveoli tracks into interstitium

95
Q

Risk factors for pneumothorax

A

Ventilation
RDS
Infection (mec aspiration)

96
Q

Ix for pneumothorax

A

Transillumination

CXR

97
Q

Mx of pneumothorax in preterm

A

O2
Decompression
Chest drain

98
Q

How can pneumothoraces be prevented in preterm babies?

A

Ventilate at lowest possible pressure

99
Q

What is apnoea in the neonate?

A

Cessation of breathing for >20 seconds

100
Q

What is the commonest cause of apnoea/bradycardia in preterm baby?

A

Immaturity of respiratory control

101
Q

How is apnoea/bradycardia in preterm baby managed?

A

Physical stimulation
Caffeine
CPAP

102
Q

What is bronchopulmonary dysplasia?

A

Chronic lung disease - continued O2 requirement beyond 36/40

103
Q

CXR features of bronchopulmonary dysplasia

A

Widespread opacification

104
Q

Management of bronchopulmonary dysplasia

A

Weaning from ventilation –> CPAP –> ambient O2

Management of GORD - common comorbidity

105
Q

What are infants with bronchopulmonary dysplasia more likely to suffer from?

A

GORD

Increased risk pertussis/RSV infection

106
Q

Management of bronchopulmonary dysplasia

A

Weaning from ventilation –> CPAP –> ambient O2
- Steroids after 7/7 if still on ventilator
- Diuretics if on ventilator
- Caffeine
- Nitric oxide
(Management of GORD - common comorbidity)

107
Q

Cause of cleft lip

A

Failure of fusion of frontonasal and maxillary processes in embryogenesis

108
Q

Cause of cleft palate

A

Failure of fusion of the palatine processes and the nasal septum

109
Q

What are cleft lip/palate associated with?

A

Maternal anti-convulsants

Chromosomal abnormalities

110
Q

Management of cleft lip/palate

A

Specialised feeding advice
Observe for airway problems (Pierre Robin sequence)
SLT/orthodontists

Surgery = definitive

111
Q

Clinical features of Pierre-Robin sequence

A

Micrognathia, posterior displacement of the tongue and midline cleft of the soft palate

112
Q

Presentation of Pierre-Robin sequence

A 
Feeding difficulty --> FTT 
Airway difficulty (cyanotic episodes)

– as tongue falls back

113
Q

Mx of Pierre-Robin sequence

A

Nasopharyngeal airway

Maintaining prone position

114
Q

Abx for GBS

A

Benpen and gent

115
Q

Mx haemolytic disease of the newborn

A

Anti D Ig at 28 weeks and birth

  • Exchange transfusion if severe
  • Phototherapy
  • IVIG
116
Q

Mx toxoplasmosis in newborn

A

Pyrimethamine, sufadiazine, calcium folinate

+ prednisolone

117
Q

RFs for RDS

A

Prematurity, male, CS, GDM, multiple pregnancy

118
Q

Complications of mec aspiration

A

Infection (sepsis)

Persistent pHTN of newborn

119
Q

Most common cardiac defect in T21?

A

AVSD

120
Q

When is benpen and gent coverage for suspected sepsis switched over to cefotaxime?

A

Once they have been out of the hospital and been exposed to a broader range of pathogens

121
Q

Why do neonates have cefotaxime rather than ceftriaxone? When?

A

Ceftriaxone can cause biliary sludging

After 1 month

122
Q

Why do you need an anaesthetist if giving prostin (prostaglandin) for a duct-dependent circulatory problem?

A

Respiratory depression (apnoea)

123
Q

Investigations for suspected metabolic problems

A

Gas - LDH (mitochondrial)

Ammonia (urea cycle)

124
Q

What might a raised ammonia indicate?

A

Urea cycle disorder

Sarah Paeds (20 decks)

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