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Year 4 - Paediatrics > Neonatology > Flashcards

Neonatology Flashcards

1
Q

What cell produces surfactant?

A

Type II pneumocytes.

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2
Q

What is the role of surfactant?

A

Reduces surface tension of the fluid in the lungs, increasing lung compliance.

This maximises the surface area of the alveoli, by preventing alveolar collapse.

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3
Q

When does surfactant production begin?

A

Between 24 and 34 weeks gestation.

Pre-term babies therefore have problems associated with reduced pulmonary surfactant.

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4
Q

How is neonatal respiratory effort induced after birth?

A

The stress of labour stimulates the release of adrenaline and cortisol, which induces respiratory effort.

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5
Q

Outline the closure of foramen ovale after birth.

A

The first breaths the baby takes expands the alveoli, reducing pulmonary vascular resistance.

This causes a fall in pressure in the right atrium, to below the pressure in the left atrium. This causes a functional closure of the foramen ovale.

The foramen ovale then structurally closes and becomes the fossa ovalis.

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6
Q

Outline the closure of ductus arteriosus after birth.

A

Increased blood oxygenation after birth causes a drop in circulating prostaglandins, causing a closure of ductus arteriosus. This then becomes ligamentum arteriosum.

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7
Q

Outline the closure of ductus venosus after birth.

A

Immediately after birth, the ductus venosus stops functioning because the umbilical cord is clamped and there is no flow in the umbilical veins.

The ductus venosus structurally closes a few days later, becoming the ligamentum venosum.

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8
Q

Outline the consequences of hypoxia in neonates.

A

Normal labour and delivery leads to hypoxia, as powerful contractions disable the placenta from carrying out gaseous exchange.

Extended periods of hypoxia leads to anaerobic respiration and consequent bradycardia.

Further hypoxia leads to reduced consciousness and a drop in respiratory effort, in turn worsening hypoxia.

Extended hypoxia leads to hypoxic-ischaemic encephalopathy (HIE), with life-long consequences in the form of cerebral palsy.

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9
Q

What are the common obstacles to neonatal resuscitation?

A
  • large SA:V ratio, so get cold very easily
  • born wet, so loose heat rapidly
  • babies born through meconium may have this in their mouth or airway
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9
Q

What are the general principles of neonatal resuscitation?

A
  • warm the baby
  • calculate APGAR score
  • stimulate breathing
  • inflation breaths
  • chest compressions
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10
Q

How can a baby be warmed in neonatal resuscitation?

A
  • get baby dry as quickly as possible (vigorous drying)
  • warm delivery rooms and management under a heat lamp
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11
Q

What is the APGAR score?

A

An indicator of progress over the first minutes after birth, helping to guide neonatal resuscitation efforts.

Appearance
Pulse
Grimmace
Activity
Respiration

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12
Q

How can a baby’s breathing be stimulated in neonatal resuscitation?

A
  • virgorously drying with a towel
  • head in a neutral position to keep airway open
  • check for airway obstruction and consider aspiration
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13
Q

Principles of inflation breaths in neonatal resuscitation.

A
  1. Two cycles of five inflation breaths to stimulate breathing and heart rate.
  2. If there is no response and bradycardic, 30 seconds of ventilation breaths are given.
  3. If there is no response, chest compressions can be used, coordinated with the ventilation breaths (3:1).
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14
Q

Principles of chest compressions in neonatal resuscitation.

A
  • start compressions if HR<60bpm despite resuscitation and inflation breaths.
  • chest compressions are performed at a 3:1 ratio with ventilation breaths.
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15
Q

What is the rationale behind delayed umbilical cord clamping?

A

After birth, there is still a significant volume of fetal blood in the placenta. Delayed umbilical cord clamping provides time for this blood to enter the circulation of the baby.

This is known as placental transfusion.

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16
Q

What are the benefits of delayed umbilical cord clamping?

A

Placental transfusion:
- improves haemoglobin
- improves iron stores
- improves blood pressure
- reduces intraventricular haemorrhage
- reduces necrotising enterocolitis

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17
Q

What are the negatives of delayed umbilical cord clamping?

A

Increase in neonatal jaundice, potentially requiring more phototherapy.

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18
Q

Resuscitation Council UK recommends umbilical cord clamping after how long in the following situations?

a) uncompromised neonates

b) neonates requiring resuscitation

A

a) a delay of at least one minute to allow for placental transfusion

b) immediate clamping - priority is resuscitation, not delayed clamping

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19
Q

What actions should be taken immediately after birth of a baby?

A
  • skin to skin contact
  • clamp the umbilical cord (delayed where possible)
  • dry the baby
  • keep the baby warm with a hat and blanket
  • vitamin K
  • label the baby
  • measure the weight and length
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20
Q

Describe the administration of vitamin K to babies following birth.

A

Babies are born with vitamin K deficiency.

IM injection of vitamin K is given in the thigh shortly after birth, which can help to stimulate the baby to cry and expand the lungs.

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21
Q

What is the role of vitamin K in babies?

A

Important co-factor for clotting factors II, VII, IX and X.

Prevents bleeding, particularly intracranial, umbilical stump and gastrointestinal bleeding.

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22
Q

What are the benefits of skin to skin contact?

A
  • helps warm the baby
  • improves mother and baby interaction
  • calms the baby
  • improves breast feeding
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23
Q

Out of the delivery room, how is a baby usually cared for?

A
  • initiate breast feeding or bottle feeding as soon as the baby is alert enough
  • delay first bath until warm and stable
  • newborn examination within 72 hours
  • blood spot test
  • newborn hearing test
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24
Q

What are the conditions screened for on blood spot screening?

A
  • sickle cell disease
  • cystic fibrosis
  • congenital hypothyroidism
  • phenylketonuria
  • medium-chain acyl-CoA dehydrogenase deficiency (MCADD)
  • maple syrup urine disease (MSUD)
  • isovaleric acidaemia (IVA)
  • glutaric aciduria type 1 (GA1)
  • homocystin

A heel prick is used to provide drops of blood on day 5, with results taking 6-8 weeks to come back.

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25
Q

What questions should be asked as part of the newborn examination?

A
  • has the baby passed meconium?
  • is the baby feeding OK?
  • is there a family history of congenital heart, eye or hips problems?
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26
Q

What is the significance of checking pre-ductal and post-ductal oxygen saturations?

A

Duct dependent congenital heart conditions can be screened for by measuring the difference in the pre-ductal and post-ductal saturations.

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27
Q

Where should oxygen saturations be measured on a neonate?

a) pre-ductal

b) post-ductal

A

a) right hand (receives blood from the right subclavian artery)

b) either foot (receives blood from the descending aorta)

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28
Q

What is club foot?

A

Ankles are rolled inwards to a supinated position, either structural or positional in nature.

Positional club foot is where the muscles are tight around the ankle, and can be managed by physiotherapy exercises.

Structural club foot is due to bony irregularities, requiring referral to orthopaedic surgeons.

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29
Q

How are undescended testes managed?

A

Monitoring and referral to urology.

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30
Q

What are port wine stains?

A

Pink patches of skin, often on the face, caused by abnormalities affecting the capillaries.

They don’t fade with time, and typically turn into a darker red or purple colour.

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31
Q

Conditions associated with port wine stains.

A

Sturge-Weber syndrome - associated visual impairment, learning difficulties, headaches, epilepsy and glaucoma.

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32
Q

What is caput succadeneum?

A

Periosteal oedema caused by pressure to the scalp during a traumatic, prolonged or instrumental delivery.

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33
Q

Management of caput succadaneum.

A

No treatment required and will resolve within a few days.

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34
Q

What is a cephalohaematoma?

A

A collection of blood between the skull and the periosteum, caused by damage to blood vessels during traumatic, prolonged or instrumental delivery.

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35
Q

How can caput succedaneum and cephalohaematoma be differentiated?

A

Caput:
- crosses the suture lines
- no skin discolouration

Cephalohaematoma:
- doesn’t cross the suture lines
- skin discolouration

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36
Q

Management of cephalohaematoma.

A

Does not require any intervention usually, resolving without treatment in a few months.

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37
Q

Monitoring of cephalohaematoma.

A

Risk of anaemia and jaundice, secondary to haemolysis of blood within the haematoma.

The baby should be monitored for anaemia, jaundice and resolution of the haematoma.

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38
Q

What nerve injury is commonly associated with forceps delivery?

A

Facial nerve (CN VII) - causing unilateral facial paralysis.

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39
Q

Management of facial nerve palsy.

A

Function usually returns spontaneously within a few months.

If function doesn’t return, neurosurgical input considered.

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40
Q

What nerve roots are affected in Erbs palsy?

A

C5/C6

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41
Q

Causes of Erbs palsy.

A

Injury to the brachial plexus during birth, associated with:
- shoulder dystocia
- traumatic delivery
- instrumental delivery
- large birth weight

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42
Q

Presentation of Erbs palsy.

A

Waiters tip appearance:
- internally rotated shoulder
- extended elbow
- flexed, pronated wrist

This is due to weaknesses in shoulder abduction and external rotation, arm flexion and finger extension.

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43
Q

Management of Erbs palsy.

A

Function usually returns spontaneously within a few months.

Otherwise, neurosurgical input required.

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44
Q

What neonatal fracture is most common during birth?

A

Clavicular fracture - associated with:
- shoulder dystocia
- traumatic delivery
- instrumental delivery
- large birth weight

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45
Q

Presentation of clavicular fracture in neonates.

A
  • lack of movement or asymmetry of movement
  • asymmetry of the shoulders
  • pain and distress on movement of the arm
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46
Q

Diagnostic workup for clavicular fracture in neonates.

A

Ultrasound (first line) or x-ray.

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47
Q

Management of clavicular fracture in neonates.

A

Conservative management, with occasional immobilisation of the affected arm.

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48
Q

Complications of neonatal clavicular fractures.

A

Injury to the brachial plexus, with a subsequent nerve palsy.

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49
Q

Common organisms that cause neonatal sespsis.

A
  • Group B streptococcus (GBS)*
  • E. coli
  • Staphylococcus aureus

*GBS is a common bacteria found in the vagina, and can be transferred to the baby during labour. Prophylactic antibiotics are given during labour for GBS positive mothers.

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50
Q

Risk factors for neonatal sepsis.

A
  • vaginal GBS colonisation
  • GBS sepsis in previous baby
  • maternal sepsis
  • chorioamnionitis
  • maternal fever
  • prematurity
  • PPROM
  • PROM
51
Q

Clinical features of neonatal sepsis.

A
  • fever
  • reduced tone / activity
  • poor feeding
  • respiratory distress
  • vomiting
  • tachy- / bradycardia
  • hypoxia
  • jaundice
  • seizures
  • hypoglycaemia
52
Q

Red flags of neonatal sepsis.

A
  • maternal sepsis
  • signs of shock
  • seizures
  • term baby needing mechanical ventilation
  • respiratory distress starting >4 hours after birth
  • presumed sepsis in another baby in multiple pregnancy
53
Q

Management of presumed sepsis.

A
  • blood culture
  • baseline FBC and CRP
  • lumbar puncture if infection is strongly suspected
  • start abx
54
Q

What antibiotic regime is given in neonatal sepsis?

A

IV amoxicillin and cefotaxime.

Wait for blood culture and take microbiology advice.

55
Q

Ongoing management of neonatal sepsis.

A
  • repeat CRP after 24 hours
  • repeat blood culture after 36 hours
  • check CRP at day 5
56
Q

When can antibiotics be stopped in neonatal sepsis?

A
  • clinically well
  • blood cultures negative
  • CRP <10
57
Q

Pathophysiology of hypoxic ischaemic encephalopathy (HIE).

A

Hypoxia causing restriction in blood flow to the brain, eventually resulting in malfunctioning of the brain.

Some hypoxia is normal during birth, however prolonged or severe hypoxia leads to ischaemic brain damage.

58
Q

HIE aetiology.

A
  • maternal shock
  • intrapartum haemorrhage
  • prolapsed cord (compressed cord)
  • nuchal cord (wrapped around the neck of the baby)
59
Q

When should HIE be suspected?

A
  • hypoxic events
  • umbilical artery blood gas pH <7
  • poor APGAR score
  • evidence of multi-organ failure
60
Q

What grading system is used in HIE?

A

Sarnat Staging

61
Q

What are the features of

a) mild

b) moderate

c) severe

HIE?

A

a) poor feeding, generally irritable, hyper-alert; resolves within 24 hours; normal prognosis.

b) poor feeding, lethargic, hypotonic and seizures; can take weeks to resolve; 40% develop cerebral palsy.

c) reduced consciousness, apnoeas, flaccid and reduced or absent reflexed; up to 50% mortality; 90% develop cerebral palsy.

62
Q

Management of HIE.

A

Managed by MDT:
- neonatal resuscitation
- ongoing ventilation
- circulatory support
- nutrition
- acid base balance
- seizure treatment
- therapeutic hypothermia

63
Q

What are the principles behind therapeutic hypothermia in the treatment of HIE?

A

Active cooling the core body temperature of the baby, with a target between 33 and 34*C.

This reduced inflammation and neurone loss after the acute hypoxic injury, reducing the risk of complications.

64
Q

Complications of HIE.

A
  • death
  • cerebral palsy
  • developmental delay
  • learning disability
  • blindness
65
Q

What are the causes of physiological jaundice?

A

Fetal blood has a high concentration of fragile erythrocytes, and a reduced liver function.

Fetal erythrocytes haemolyse more rapidly, releasing bilirubin. This leads to a normal rise in bilirubin shortly after birth, causing a mild yellowing of the skin and sclera.

66
Q

Timeline of physiological jaundice.

A

Hyperbilirubinaemia evident between 2-7 days of age.

Complete resolution by day 10.

67
Q

In what timeframe is the onset of jaundice considered pathological?

A

Onset within the first 24 hours of life.

68
Q

Causes of pathological neonatal jaundice.

A

Increased production of bilirubin:
- haemolytic disease of the newborn
- ABO incompatability
- haemorrhage
- cephalohaematoma
- sepsis*
- G6PD deficiency

Decreased clearance of bilirubin:
- prematurity
- breast milk jaundice
- neonatal cholestasis
- extrahepatic biliary atresia
- hypothyroidism

*babies with jaundice onset within 24 hours of birth should be managed via a sepsis algorithm until otherwise proven.

69
Q

What are the considerations of jaundice in premature neonates?

A

Physiological jaundice will be more severe due to an immature liver, increasing the risk of kernicterus.

This is brain damage due to hyperbilirubinaemia.

70
Q

Theory of breast milk jaundice.

A

Components of breast milk inhibit the ability of the liver to process the bilirubin.

Breastfed babies are more likely to become dehydrated if not feeding adequately, as this leads to a slow passage of stools. Reabsorption of bilirubin in the small intestine therefore increases.

71
Q

Pathophysiology of haemolytic disease of the newborn.

A

RhD+ve fetus and RhD-ve mother.

RhDAg from fetal blood crosses the placenta, and mother produces RhDAb (sensitisation).

In subsequent pregnancies with a RhD+ve fetus, RhDAb will cross the placenta and haemolyse the fetal erythrocytes. This will cause fetal anaemia and hyperbilirubinaemia.

NB: sensitisation doesn’t usually cause problems during the first pregnancy, unless the sensitisation happens early on (e.g. antepartum haemorrhage).

72
Q

When is jaundice considered prolonged?

a) full term babies

b) pre-term babies

A

a) >14 days

b) >21 days

73
Q

What are the causes of prolonged jaundice?

A
  • biliary atresia
  • hypothyroidism
  • G6PD deficiency
74
Q

Diagnostic workup for neonatal jaundice.

A
  • full blood count
  • serum conjugated bilirubin
  • transcutaneous bilirubinometry
  • blood type testing of the mother and baby
  • Direct Coombs test
  • thyroid function tests
  • blood and urine cultures
  • serum G6PD levels
75
Q

Management of neonatal jaundice.

A

Plot total bilirubin levels on treatment threshold charts.

The tiers of treatment are:
1. Phototherapy
2. Exchange tranfusion

76
Q

How does phototherapy help in neonatal jaundice?

A

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

Bilirubin is closely monitored during and after treatment, to ensure levels do not rise above the treatment threshold again.

77
Q

Pathophysiology of kernicterus.

A

Unconjugated bilirubin can cross the blood brain barrier, causing permanent damage to the central nervous system:
- cerebral palsy
- learning disability
- deafness

78
Q

WHO classification of prematurity:

a) extreme preterm

b) very preterm

c) moderate to late preterm

A

a) less than 28 weeks

b) 28-32 weeks

c) 32-37 weeks

79
Q

Prematurity risk factors.

A
  • social deprivation
  • smoking
  • alcohol
  • drugs
  • overweight or underweight mother
  • maternal comorbidities
  • twins
  • personal or family history of prematurity
80
Q

In women with a history of preterm birth or an ultrasound demonstrating a cervical length of 25mm or less before 24 weeks gestation, what options are there to delay birth?

A
  • prophylactic vaginal progesterone suppository to discourage labour
  • prophylactic cervical cerclage to hold the cervix closed
81
Q

When preterm labour is suspected or confirmed, what options are there to improve outcomes?

A
  • tocolysis with nifedipine (CCB to suppress labour)
  • maternal corticosteroids to reduce neonatal morbidity and mortality
  • IV magnesium sulphate to protect neonatal CNS
  • delayed cord clamping and cord milking to increase circulating blood volume
82
Q

Short-term complications of prematurity.

A
  • respiratory distress syndrome
  • hypothermia
  • hypoglycaemia
  • poor feeding
  • neonatal jaundice
  • retinopathy of prematurity
  • necrotising enterocolitis
  • immature immune system and infection
83
Q

Long-term complications of prematurity.

A
  • chronic lung disease of prematurity (CLDP)
  • learning disability
  • susceptibility to infections, particularly respiratory tract infections
  • hearing and visual impairment
  • cerebral palsy
84
Q

What is apnoea of prematurity?

A

Immaturity of the autonomic nervous system in premature neonates causes periods where breathing stops spontaneously for >20 seconds, accompanied by a period of bradycardia.

85
Q

Management of apnoea of prematurity.

A

Apnoea monitors attached to premature babies, sounding an alarm when an apnoea occurs.

Tactile stimulation is used to prompt the baby to restart breathing.

Intravenous caffeine can be used to prevent apnoeas and bradycardia.

Episodes will settle naturally as the baby matures.

86
Q

What is retinopathy of prematurity?

A

Abnormal development of the blood vessels in the retina leads to scarring, retinal detachment and blindness.

87
Q

Pathophysiology of retinopathy of prematurity.

A

Retinal blood vessel growth is stimulated by hypoxia, which is a normal condition in the retina during pregnancy.

When the retina is exposed to higher oxygen concentrations in a preterm baby, the stimulant for normal retinal blood vessel development is removed.

When the hypoxic environment recurs, the retina responds by excessively producing blood vessels (neovasularisation), as well as scar tissue.

The scar tissue may cause retinal detachment and blindness.

88
Q

What are the zones of the retina?

A

Zone 1 includes the optic nerve and the macula.

Zone 2 is from the edge of zone 1 to the ora serrata.

Zone 3 is outside the ora serrata.

89
Q

When should babies be screened for retinopathy of prematurity?

A

Babies born before 32 weeks or under 1.5kg should be screened for ROP.

Screening should happen at least every 2 weeks and can cease once the retinal vessels enter zone 3.

90
Q

Treatment of retinopathy of prematurity.

A

Systematically targeting areas of the retina to stop new blood vessels developing (neovascularisation).

First line is transpupillary laser photocoagulation.

Other options include cryotherapy and surgery if retinal detachment occurs.

91
Q

Pathophysiology of respiratory distress syndrome.

A

Inadequate surfactant in premature babies leads to a high surface tension within alveoli, leading to atelectasis.

This leads to inadequate gaseous exchange, resulting in:
- hypoxia
- hypercapnia
- respiratory distress

92
Q

How is the risk of respiratory distress syndrome reduced?

A

Administration of antenatal steroids to mothers with suspected or confirmed preterm labour, to increase the production of surfactant.

93
Q

Management of respiratory distress syndrome in neonates.

A
  • intubation and ventilation
  • endotracheal surfactant
  • CPAP
  • supplementary oxygen (91-95%)

Support with breathing is gradually stepped down as the baby develops and is able to maintain their breathing, until they can support themselves in air.

94
Q

Short term complications of neonatal respiratory distress syndrome.

A
  • pneumothorax
  • infection
  • apnoea
  • pulmonary haemorrhage
  • necrotising enterocolitis
95
Q

Long term complications of neonatal respiratory distress syndrome.

A
  • chronic lung disease of prematurity (CLDP)
  • retinopathy of prematurity
  • neurological, hearing and visual impairment
96
Q

What is necrotising enterocolitis?

A

In premature neonates, part of the bowel can become necrotic. This leads to bowel perforation.

Bowel perforation can lead to peritonitis, shock and death.

97
Q

Risk factors for necrotising enterocolitis.

A
  • very low birth weight or very premature
  • formula feeds
  • respiratory distress / assisted ventilation
  • sepsis
  • patent ductus arteriosus
98
Q

Presentation of necrotising enterocolitis.

A
  • feeding intolerance
  • bilious vomiting
  • generally unwell
  • distended, tender abdomen
  • absent bowel sounds
  • blood in stools

When perforation occurs, there will be peritonitis and shock, with the neonate severely unwell.

99
Q

Diagnostic workup for necrotising enterocolitis.

A
  • FBC (thrombocytopenia and neutropenia)
  • CRP (inflammation)
  • capillary blood gas (metabolic acidosis)
  • blood culture (?sepsis)
  • supine AXR
100
Q

Supine AXR findings in necrotising enterocolitis.

A
  • dilated bowel loops
  • bowel wall oedema
  • gas in the bowel wall (pneumatosis intestinalis)
  • pneumoperitoneum
  • gas in the portal veins
101
Q

Management of necrotising enterocolitis.

A
  • NBM
  • IV fluids
  • TPN
  • IV abx
  • NG tube to decompress stomach

Immediate referral to the neonatal surgical team, for removal of dead bowel tissue.

102
Q

Complications of necrotising enterocolitis.

A
  • perforation / peritonitis
  • sepsis
  • strictures
  • abscess formation
  • recurrence
  • long-term stoma
  • short bowel syndrome
  • death
103
Q

What is neonatal abstinence syndrome (NAS)?

A

Withdrawal symptoms that happens in neonates of mothers that used substances during pregnancy.

104
Q

Substances that cause neonatal abstinence syndrome.

A
  • opiates
  • methadone
  • benzodiazepines
  • cocaine
  • amphetamines
  • nicotine
  • cannabis
  • alcohol
  • SSRI antidepressants
105
Q

Signs and symptoms of neonatal abstinence syndrome.

A

CNS: irritability; hypertonia; tremors; seizures.

Vasomotor: yawning; sweating; pyrexia.

Respiratory: tachypnoea.

Metabolic: hypoglycaemia.

Gastrointestinal: poor feeding; regurgitation; vomiting; loose stools.

106
Q

Withdrawal symptoms with onset between 3-72 hours after birth indicates abstinence from which substances?

A
  • opiates
  • diazepam
  • SSRIs
  • alcohol
107
Q

Withdrawal symptoms with onset between 1-21 days after birth indicates abstinence from which substances?

A
  • methadone
  • benzodiazepines
108
Q

Management of NAS.

A

Monitoring on a NAS chart and urine sample sent for toxicology report to identify substances.

Medical treatment options for moderate to severe symptoms:
- oral morphine sulphate (opiate withdrawal)
- oral phenobarbitone (non-opiate withdrawal)

Neonates should be gradually weaned off oral treatment.

109
Q

What is sudden infant death syndrome (SIDS)?

A

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

110
Q

Risk factors for SIDS.

A
  • prematurity
  • low birth weight
  • smoking during pregnancy
  • male sex
111
Q

How can the risk of SIDS be reduced?

A
  • put baby on their back when not directly supervised
  • keep their head uncovered
  • place their feet at the foot of the bed to prevent them sliding down and under the blanket
  • keep the cot clear of lots of toys and blankets
  • maintain a comfortable room temperature (16-20*C)
  • avoid smoking / handling the baby after smoking
  • avoid co-sleeping
112
Q

What support is available for families affected by SIDS?

A

Lullaby trust offers bereavement services and bereavement counselling.

The care of the next infant (CONI) team supports parents with their next infant after a sudden infant death. This provides extra support and home visits, resuscitation training, and apnoea monitoring equipment.

113
Q

What are the effects of alcohol in pregnancy?

A
  • miscarriage
  • small for dates
  • preterm delivery
  • fetal alcohol syndrome
114
Q

Features of fetal alcohol syndrome.

A
  • microcephaly
  • thin upper lip
  • smooth, flat philtrum
  • short palpebral fissure
  • learning disability
  • behavioural difficulties
  • hearing and vision problems
  • cerebral palsy
115
Q

How can congenital rubella syndrome be prevented?

A

Women planning to become pregnant should ensure they have had the MMR vaccine.

As the MMR vaccine is a live vaccine, it cannot be given during pregnancy. Non-immune women should be offered the vaccine after birth.

116
Q

Features of congenital rubella syndrome.

A
  • congenital cataracts
  • congenital heart disease
  • learning disability
  • hearing loss
117
Q

How is exposure to chickenpox managed during pregnancy, if the pregnant woman has previously had chickenpox?

A

No management required - they are safe.

118
Q

How is exposure to chickenpox managed during pregnancy, if the pregnant woman is unsure if she has previously had chickenpox?

A

Measure IgG levels for VZV.

A negative IgG indicates no immunity, and IV varicella immunoglobulins are given within 10 days of exposure.

119
Q

How is exposure to chickenpox, with a chickenpox rash, managed during pregnancy?

A

Treat with oral aciclovir if they present within 24 hours and are more than 20 weeks gestation.

120
Q

Features of congenital varicella syndrome.

A
  • fetal growth restriction
  • microcephaly
  • hydrocephalus
  • learning disability
  • limb hypoplasia
121
Q

What are the features of congenital CMV?

A
  • fetal growth restriction
  • microcephaly
  • hearing loss
  • vision loss
  • learning disability
  • seizures
122
Q

What is the cause of congenital toxoplasmosis?

A

Infection with Toxoplasma gondii parasite, usually causing asymptomatic infection.

It is spread by contamination with faeces from a cat that is a host of the parasite.

123
Q

Triad of congenital toxoplasmosis.

A
  • intracranial calcification
  • hydrocephalus
  • chorioretinitis
124
Q

What is the vector for Zika virus?

A

Aedes mosquitos.

Can also be spread through sexual contact.

125
Q

What are the features of congenital Zika syndrome?

A
  • microcephaly
  • fetal growth restriction
  • ventriculomegaly / cerebellar atrophy
126
Q

What is the treatment of Zika virus in pregnant women?

A

There is no treatment for the virus.

Women with a positive result can be referred to fetal medicine to monitor the pregnancy.

Year 4 - Paediatrics (17 decks)

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