Neonatal and newborn Flashcards

1
Q

Define neonate

A

Term: Birth until 4 weeks of age

Pre-term: Birth to 44 post menstrual weeks of age

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2
Q

Define pre-term birth

A

Before 37 weeks

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3
Q

What factors increase the risk of jaundice?

A

Pre-term babies

Low weight

FHx

Maternal DM

Male baby

East Asian

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4
Q

Generally, what is jaundice within the first 24 hours indicative of?

A

Haemolysis or sepsis

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5
Q

When does physiological jaundice present?

A

2 - 3 days of age

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6
Q

Why does physiological jaundice occur?

A

Immature liver function and increased erythrocyte breakdown; the haemoglobin concentration in neonates is much higher than in adults!

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7
Q

When is jaundice always pathological?

A

If less than 24 hours after birth

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8
Q

What are the causes of early jaundice?

A
Haematological: 
ABO/Rh incompatibility 
Haemolytic disease of the newborn
G6PDD
Hereditary spherocytosis
Haematoma
Maternal autoimmune haemolytic anaemia (SLE)
Infection: TORCH or post-natal infection
Toxoplasmosis
Other (syphilis, varicella-zoster, parvovirus B19)
Rubella
Cytomegalovirus (CMV)
Herpes
Other:
Gilberts syndrome
Crigler-Najjar syndrome
Dublin-Johnson syndrome
Brusing
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9
Q

What is prolonged jaundice?

A

> 14 days in term

> 21 days in pre-term

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10
Q

What are the causes of prolonged jaundice?

A

Breast milk jaundice - most common cause

Metabolic:
Galactosaemia
Hypothyroidism
Hypopituitarism

Infection

GI/Conjugated hyperbilirubinaemia:
Biliary atresia
Choledocal cyst
Neonatal hepatitis

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11
Q

Give five causes of conjugated hyperbilirubinaemia

A

Usually due to neonatal liver disease…

GI: Biliary atresia, choledocal cyst, hepatitis

CF

Alpha1 anti-trypsin deficiency

Galactosaemia

Aminoaciduria

Hypothyroidism

Infection

Parenteral nutrition

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12
Q

In cases of jaundice, what other signs should you look for on examination?

A

Neurological: Tone, seizures, altered crying (kernicterus)

Haemolysis/infection: Hepatosplenomegaly, petechiae, microcephaly

Pale stools/dark urine

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13
Q

How should you measure bilirubin?

A

Transcutaneous bilirubinometer if > 35 weeks and >24 hours of age, otherwise serum bilirubin

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14
Q

Give three examples of haemolytic tests used for jaundice

A

Reticulocyte count

Direct Coombs test: looking for ABO/Rh haemolysis

Haemoglobin and haematocrit

Peripheral blood film for erythrocyte morphology

Red cell enzyme assays: GP6DD, pyruvate kinase deficiency

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15
Q

What investigations should you do in cases of prolonged jaundice?

A

Look for pale stools and dark urine

Measure the conjugated bilirubin

FBC

Determine blood group and Coombs test

Urine culture

Routine metabolic screening (incl. for congenital hypothyroidism)

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16
Q

What should you start if bilirubin is rapidly increasing or < 24 hours?

A

Phototherapy

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17
Q

What does phototherapy do?

A

Converts bilirubin to bilverdin

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18
Q

What are the side effects of phototherapy?

A

Dehydration and loose stools

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19
Q

What treatments are there for unconjugated hyperbilirubinaemia?

A

Phototherapy and exchange transfusion

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20
Q

What is kernicterus?

A

Bilirubin encephalopathy: unconjugated bilirubin enters the brain and causes neuronal damage to basal ganglia

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21
Q

What are the clinical features of kernicterus?

A

Irritability

High-pitched cry

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22
Q

What is biliary atresia?

A

Absence of intra/extra-hepatic bile ducts

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23
Q

How does biliary atresia present?

A

Deelops over a few weeks; stools become clay-coloured

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24
Q

What are the complications of biliary atresia?

A

Liver failure - transplant

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25
Q

What procedure can be done to correct biliary atresia?

When is it done?

A

Kasai procedure: hepatopoto-enterostomy

If detected within the first 6 weeks - unconjugated AND conjugated levels must be checked after 2 weeks to check for biliary atresia!

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26
Q

Give three causes of jaundice in older children?

A

Hepatitis A and autoimmune hepatitis

G6PDD

Reye’s syndrome

Paracetamol overdose

Wilson’s disease

Crigler-Najjar disease

Gilbert’s syndrome

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27
Q

What is Reye’s syndrome and what causes it?

A

Metabolic condition causing encephalitis and liver failure

Caused by aspirin, which is contraindicated in kids

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28
Q

Severe birth asphyxia can lead to what?

A

Hypoxic ischaemic encephalopathy

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29
Q

How do foetuses cope with hypoxia?

A

Quite well actually

Cause they’ve got a high Hb (18g/dL) and a high cardiac output

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30
Q

What factors indicate a diagnosis of birth asphyxia?

A

pH < 7.05

APGAR 0 - 5 at 10 mins

Delay in spontaneous respiration (> 10 mins)

HIE (abnormal neuro signs, including convulsion for more than 2 days)

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31
Q

How is birth asphyxia managed?

What is important to avoid?

A

Rapid resuscitation (avoid cerebral oedema)

Treat convulsions

Controlled therapeutic cooling

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32
Q

What does APGAR stand for?

A
Activity (muscle tone)
Pulse
Grimace (reflex irritability)
Appearance (skin colour)
Respiration
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33
Q

What is HIE?

A

Hypoxic ischaemic encephalopathy is abnormal neurological signs, including convulsion for more than 2 days, following birth asphyxia

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34
Q

What are the differences between mild, moderate and severe HIE?

A

Mild: irritable, high-pitched cry, poor feeding

Moderate: lethargic, hypotonic, fits

Severe: diminished consciousness, no movement, multiple seizures, organ failure

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35
Q

What are the complications of HIE?

A

Cerebral palsy

Organ failure

Death

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36
Q

Give three examples of birth marks

A
Pigmented naevi
Cafe au lait spots
Strawberry naevus/superficial haemangioma
Naevus flammeus (salmon patch)
Mongolian blue spots 
Port wine stain
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37
Q

When do pigmented naevi present?

A

About 2 years of age

They very rarely present at birth

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38
Q

In what condition are cafe au lait spots a sign?

A

Neurofibromatosis

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39
Q

What are stork marks?

A

Naevus flammeus/salmon patches

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40
Q

Where do you get salmon pathches?

A

Eyelids neck and forehead

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41
Q

Which type of birth lesion do you get in 75% of black and asian people?

A

Mongolian spots

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42
Q

What are port-wine stains?

A

Mature, dilated dermal capillaires present at birth.

They are macular and appear sharply circumscribed and pink/purple, in different sizes

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43
Q

What should you suspect if port wine stains are localised to the trigeminal area?

A

Sturge-Weber syndrome

There is underlying haemangioma and intracranial calcification, causing seizures

44
Q

What is cephaloheamatoma?

Where does it occur?

A

Subperiosteal bleeding; it cannot cross the midline.

The swelling and amount of blood loss is limited by the periostem attached to the skull margins.

45
Q

Cephalohaematoma can make what worse?

A

Jaundice

Infection of broken skin

46
Q

What are the risk factors for cephalohaematoma?

A

Forceps delivery

Large baby

First pregnancy

Difficult/prolonged labour

47
Q

How does haemolytic disease of the newborn happen?

A

Maternal IgG crosses the placenta and reacts with foetal RBC antigens

When the foetus is Rh+ and the mother is Rh-, the mother will make anti-Rh antibodies

In the 2nd pregnancy, antibodies cross the placenta to destroy foetal RBCs

48
Q

What is the test used to check for haemolytic disease of the newborn?

A

Indirect Coomb’s test - looks for presence of antibodies at first antental visit if mother is Rh-

49
Q

How can babies with HDN appear clinically?

A

Jaundice

Pallor

Hepatosplenomegaly

Hydrops fetalis/polyhydramnios

50
Q

How do you manage HDN in utero?

A

Transfusion with O negative packed red cells cross matched at 18 weeks into umbilical vein

Deliver at 37-38 weeks; 32 if necessary

51
Q

How does the management for HDN differ if after delivery?

A

50% of babies have normal Hb and bilirubin

If moderate disease (25%) then transfusion

If hyperbilirubinaemia - phototherapy to avoid kernicterus

Severe disease - resus, intensive support, transfusion and correction of acidosis

52
Q

When should mothers be given anti-D immunoglobulin?

A

28 and 34 weeks, and soon after delivery

53
Q

How does the gestation at:

  1. 36 weeks…
  2. 33 weeks…
  3. 28 weeks…

…affect neonatal development?

A
  1. 36 weeks - slow to feed
  2. 33 weeks - more serious problem e.g. immature lungs
  3. 28 weeks - very significant problems
54
Q

Give three risk factors for prematurity

A
Young maternal age
Multiple [regnancy
Infection
Maternal illness
Cervical incompetence
Antepartum haemorrhage
Smoking
Alcohol
55
Q

What use are antenatal steroids?

A

These reduce the incidence of respiratory distress syndrome and intraventricular haemorrhage

56
Q

How can prematurity affect the…eyes?

A

Retinopathy due to abnormal vascularisation of the developing retina (increased proliferation with excess oxygen delivery)

Requires laser treatment to prevent retinal detachment and blindness

57
Q

How can prematurity affect the…respiratory system?

A

Respiratory distress syndrome (due to surfactant deficiency)

Apnoea

Pneumothorax

Chronic lung disease (needs oxygen after 28 days of age)

58
Q

How can prematurity affect the…cardiovascular system?

A

Hypotension

Bradycardia

Patent ductus arteriosus

59
Q

How can prematurity affect the…temperature control?

A

Increased SA:volume ratio leads to loss of heat

Immature skin and reduced subcutaneous fat so cannot retain heat and fluid efficiently

60
Q

How can prematurity affect the…metabolism?

A

Hypoglycaemia - treat promptly if symptomatic and maintain above 2.6 to prevent neurological damage

Electrolyte imbalance e.g. hypocalcaemia

Osteopenia

61
Q

How can prematurity affect the…brain?

A

Intraventricular haemorrhage

Post-haemorrhagic hydrocephalus - needs shunt

Periventricular leucomalacia (often result of hypotension) - increased risk of epilepsy and CP (diplegic type)

62
Q

How can prematurity affect the…GI system?

A

Necrotising enterocolitis (life-threatening inflammation of the bowel wall due to ischaemia/infection) - can lead to perforation

GORD

Inguinal hernias (high risk of strangulation)

63
Q

How can prematurity affect the…blood?

A

Anaemia of prematurity

Neonatal jaundice

64
Q

How can prematurity cause infection?

A

Pneumonia

Sepsis (esp. group B strep and coliforms)

Infection of central venous lines for feeding

65
Q

How can prematurity affect feeding?

A

Parenteral nutrition

NG feeds until sucking reflex develops at 32-34 weeks

Difficult to achieve in-utero growth rates

66
Q

What are the clinical features of NEC?

A

Abdominal distension (with increasing gastric aspirates)

Visible intestinal loops (football sign - perforation)

Altered stool pattern

Bloody mucoid stool and bilious vomiting

Decreased bowel sounds

Abdominal erythema

Palpable abdominal mass or ascites

Associated features of bradycardia, lethargy, shock, apnoea, respiratory distress, temperature instability.

67
Q

When does NEC occur?

A

First two weeks of life (3 - 10 days)

68
Q

In which cases do babies require resuscitation?

A

Prematurity

Fetal distress

Thick meconium staining of liquor

Emergency Caesarian section

Instrumental delivery

Known congenital delivery

Multiple births

69
Q

How do different Apgar scores affect prognosis?

A

7 - 10 at 1 minute: normal

4 - 6: moderately ill

0 - 3: severely compromised, needs urgent resuscitation

70
Q

What is done to re-establish cardiac output in neonates requiring resuscitation?

A

Cardiac massage

IV adrenaline

Bicarbonate

71
Q

What are the signs of severe asphyxia?

A

Cord blood pH < 7.0

Apgar < 5 at 10 mins

Delay in spontaneous respiration beyond 10 minutes

Development of HIE (with abnormal neurological signs, including convulsions)

72
Q

Following moderate to severe asphyxia, what can be done to prevent secondary neuronal damage?

A

Therapeutic hypothermia (cooling to 33 degrees) for 72 hours

73
Q

What is the difference between symmetrical and asymmetrical growth restriction?

A

Asymmetrical IUGR is more common (70%). In asymmetrical IUGR, there is restriction of weight followed by length. The head continues to grow at normal or near-normal rates (head sparing) due to selective shunting to the brain.

Symmetrical IUGR is less common (20-25%). It is commonly known as global growth restriction, and indicates that the foetus has developed slowly throughout the duration of the pregnancy and was thus affected from a very early stage.

74
Q

What are the causes of asymmetric and symmetric IUGR?

A
Asymmetric: 
Placental insufficiency
Chronic high blood pressure
Severe malnutrition
Ehlers–Danlos syndrome

Symmetric:
Early intrauterine infections, such as TORCH
Chromosomal abnormalities
Anaemia
Maternal substance abuse (e.g. foetal alcohol syndrome)

75
Q

What are babies with IUGR at risk of in the first few days of life?

A

Hypoglycaemia

Hypothermia

Later: Cognitive impairment (poor head growth)

76
Q

What is Vitamin K deficiency bleeding?

A

Deficiency of Vitamin K or persistent obstructive jaundice, leading to poor synthesis of Vitamin K-dependent clotting factors and therefore bleeding.

Can present as minor bruising or significant intracranial haemorrhage

77
Q

Why and how are Vitamin K supplements given to newborns?

A

Not enough in breast milk

Given either as a single IM injection or orally, at birth, 1 week and 6 weeks.

78
Q

What drugs should be given to the mother of a premature baby antenatally?

A

2 doses of betamethasone 12 mg given intramuscularly 24 hours apart

or

4 doses of dexamethasone 6 mg given
intramuscularly 12 hours apart.

79
Q

What is the postnatal management of premature babies?

A
Paediatrician at birth
Delay cord clamping after 1 minute
Keep warm
NIV (5:20)
ET tube and surfactant if 27 weeks or less
SCBU
Breastfeeding/NG/IV feeds
Benzylpenicillin/gentamicin if septic
80
Q

What is respiratory distress syndrome also known as?

A

Hyaline membrane disease

81
Q

What is RDS caused by?

A

Surfactant deficiency

82
Q

What produces surfactant?

A

Type II alveolar cells

83
Q

Why is RDS self-limiting?

A

The adrenal glands produce endogenous corticosteroids as a response to RDS, which means the condition usually resolves within 7 days.

84
Q

How can RDS be prevented?

A

Antenatal administration of corticostroids between 24 and 34 weeks gestation:

2 doses of betamethasone 12 mg given intramuscularly 24 hours apart

or

4 doses of dexamethasone 6 mg given
intramuscularly 12 hours apart.

85
Q

Give 5 risk factors for RDS

A
Premature delivery
Male infants
Infants delivered via caesarean section without maternal labour
Hypothermia
Perinatal asphyxia
Maternal diabetes
Family history of IRDS
86
Q

What are the clinical features of RDS?

A

Tachypnoea
Intercostal, subcostal and sternal recession
Cyanosis
Expiratory grunting

87
Q

How does RDS appear on CXR?

A

Air bronchiogram - radiolucent air in bronchi against airless lung

Bell-shaped thorax

Ground glass appearance of lung fields - due to alveolar collapse

88
Q

How are neonates with RDS managed?

A

Oxygen

CPAP - if spontaneously breathing
IPPV - if unable to breathe, need to be intubated

Exogenous surfactant via ET tube

89
Q

What is a diagnosis of ‘small for gestational age’ (SGA) based on?

A

An abdominal circumference or estimated foetal weight which is < 10th centile

90
Q

How far apart should measurements be taken?

A

At least 3 weeks apart

91
Q

If a newborn is < 10th centile or has reduced growth velocity, what should they be offered?

A

Serial assessment of foetal size

Umbilical artery doppler scan

92
Q

Give five major risk factors for SGA

A
Maternal age >40 years.
Smoker - ≥11 cigarettes per day.
Paternal or maternal SGA.
Cocaine use.
Daily vigorous exercise.
Previous SGA baby.
Previous stillbirth.
Chronic hypertension.
Diabetes with vascular disease.
Renal impairment.
Antiphospholipid syndrome.
Heavy bleeding similar to menses.
Pregnancy associated plasm protein-A (PAPP-A) <0.4 multiples of the median (MOM).
93
Q

Under what circumstances are mothers reassessed for present SGA risk factors?

What do they look for?

A

If one major risk factor or > 3 minor risk factors, women are reassessed at 20 weeks for abnormal Down’s markers and fetal echogenic bowel

94
Q

What are the criteria for uterine artery doppler scans?

A

Elevated ratio of FL:AC
Elevated ratio of HC:AC
Oligohydramnios

95
Q

What other investigations to suspected IUGR babies undergo?

A

TORCH screening

Karyotyping

96
Q

How does the timing of delivery differ in SGA foetuses with absent or reversed end-diastolic velocity (AREDV) < 32 weeks?

A

Deliver by C-section when ductus venosus doppler becomes abnormal or umbilical vein pulsations appear, provided the foetus is viable and completion of steroids

97
Q

How does the timing of delivery differ in SGA fetuses with a normal doppler before 32 weeks?

A

If doppler is normal, delivery is recommended by 32 weeks

Can off induction of labour, but emergency CS rates are increased

98
Q

When should a baby be delivered if the middle cerebral doppler scan is abnormal?

A

No later than 37 weeks

99
Q

When should a baby be delivered if detected as SGA after 32 weeks, with an abnormal UAD?

A

No later than 37 weeks

100
Q

How can SGA birth be prevented in women with a high risk of pre-eclampsia?

A

Anti-platelets at 16 weeks

101
Q

Why does talipes occur?

A

Fetal foot position in utero

Tight Achilles tendon

102
Q

What other conditions can talipes be associated with?

A

Cerebral palsy
Spina bifida
Arthrogryposis

103
Q

How are talipes diagnosed and graded?

A

Antental US

Graded by the Pirani score (0 - 6)

104
Q

What are the different types of club foot?

A

Talipes equinovalgus
Talipes equinovarus
Talipes calcaneovalgus
Talipes calcaneocavus

105
Q

How are talipes treated?

A

Ponseti technique - stretching and manipulation, before setting in plaster cast

Takes up to 10 weeks to work and must wear special boots afterwards to prevent recurrence

Surgery

106
Q

How often is serum bilirubin checked during phototherapy?

When is treatment stopped?

A

Check very 8 - 10 hours

Stop phototherapy when the value is 50 under the treatment line

107
Q

Clinically, how does GORD differ from just GOR?

A

Irritability

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