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4th year Paeds > Neonatal and newborn conditions > Flashcards

Neonatal and newborn conditions Flashcards

1
Q

Is neonatal jaundice common? Esp in who?

A

Yes mild is common esp in pre-term

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2
Q

Which time scales of neonatal jaundice need investigation?

A

First 24hr or lasting beyond 2w

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3
Q

What builds up in neonatal jaundice? What are the two types?

A

Bilirubin Unconjugated Conjugated

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4
Q

What two mechanisms cause unconjugated hyperbilirubinaemia?

A

Excessive haemolysis or impaired conjugation

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5
Q

What are the 8 causes of unconjugated hyperbilirubinaemia?

A

Prematurity (immature liver enzymes)

  • Rh incompatible (haemolytic disease of the newborn (see notes at bottom). Coomb’s test positive.)
  • ABO incompatible (usually milder than Rh)
  • Infection (bacterial)
  • Bruising (traumatic delivery)
  • Hypothyroid (?pituitary disease)
  • Breast milk jaundice
  • Physiological
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6
Q

What is physiological unconj hyperbil. due to? what might it need treatment with?

A
  • low liver enzyme activity (liver immaturity, particularly in pre-term) or breakdown of foetal haemoglobin. Occasionally needs phototherapy.
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7
Q

What is breast milk jaundice?

A

otherwise well baby who is breast-fed develops jaundice day 4-7 until week/month 3. Normal coloured stool and urine. Inhibition of liver conjugation enzymes by breast milk. Diagnosis of exclusion- measure split bilirubin to exclude conjugated hyperbilirubinaemia.

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8
Q

What test would be positive in haemolytic disease of the newborn?

A

Coomb’s test (rhesus)

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9
Q

Why does conjugated hyperbil. occur?

A

Obstruction of drainage of bile ducts

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10
Q

What are the 4 reasons conj, hyperbil. occurs?

A

Hepatitis CF Choledocal cyst Biliary atresia

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11
Q

What are the different types of hepatitis that could cause conj. hyperbil/?

A

A, B, C, CMV Inborn error of metabolism e.g. galactosaemia

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12
Q

Is biliary atresia common?

A

No 1 in 10,000

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13
Q

What is biliary atresia? What are the signs? What would an investigation show? What is the management and what happens if untreated?

A

o Persistent jaundice with rising conjugated fraction over weeks. (>20% after 2 weeks = refer, any jaundice persisting after 2 weeks should have both bilirubins checked.) o Pale, chalky stools o Due to absence of intra/extrahepatic bile ducts. o Undiagnosed- liver failure and may die without transplant. o Urgent referral to paediatric hepatologists for assessment, diagnostic isotope scan and surgical correction.

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14
Q

What is the normal breakdown of bilirubin?

A

RBC breakdown (haem)→ biliverdin→ unconjugated (lipid soluble, can cross BBB) bilirubin → conjugation occurs in liver, conjugated bilirubin is water soluble → enters gut via bile → gut enzymes break it down into urobilinogen → 80% excreted in faeces as stercobilinogen, 2% in urine as urobilin and 18% enter enterohepatic circulation.

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15
Q

Important things to ask in the history of neonatal jaundice?

A

• Age developed (within 24h investigate) • Risk factors for infection • Fhx e.g. CF, spherocytosis • How is baby? Active, alert, feeding well? Lethargic and must be woken for feeds (sig. jaundice) • Breast feeding?

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16
Q

Examination findings of neonatal jaundice?

A

• Extent (spreads head down) • Features of congenital viral infection e.g. petechiae, anaemia, hepatosplenomegaly • Dehydrated? • Pale stool • Baby well in general?

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17
Q

Investigations for neonatal jaundice? What is the justification for each?

A

• Bloods: o FBC (thrombocytopenia = viral infection or IUGR, anaemia = haemolytic disease, neutropenia or neutrophilia in infxn) o CRP (?) o Group and Coombs (ABO and Rh) o TFT o LFT (high ALT suggests hepatitis) o Coag o TORCH screen (for Hep B, CMV) • Urine metabolic screen (inborn errors of metabolism) • Liver USS • Liver isotope scan (r/o biliary atresia in persistent conjugated hyperbilirubinaemia) • ?Urine and CSF infection screen

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18
Q

Management options for neonatal jaundice (5)

A

Identify cause and severity Phototherapy Exchange transfusions Refer to hepatology if biliary atresia Vitamin K supplement depending on coag screen results

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19
Q

What does phototherapy do in neonatal jaundice?

A

Blue light 450nm wavelength converts unconjugated bilirubin to biliverdin (an isomer that can be excreted by the kidneys. In rhesus or ABO incompatibility, if bilirubin levels rise significantly despite phototherapy, may need exchange transfusion.)

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20
Q

When are exchange transfusions needed in neonatal jaundice and why?

A

Severe neonatal jaundice to prevent kernicterus

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21
Q

What is kernicterus?

A

When free bilirubin crosses BBB, deposited in basal ganglia- acute encephalopathy with irritability, high pitched cry or coma. Can lead to deafness and athetiod cerebral palsy.

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22
Q

What is haemolytic disease of the newborn?

A

If ABO or Rh incompatible, Maternal IgG crosses placenta, reacts with foetal RBC antigens.

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23
Q

What happens with haemolytic disease of the newborn in utero?

A

Foetal anaemia can = hydrops (severe oedema)

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24
Q

What is the in-utero management of haemolytic disease of the newborn?

A

Could have intra-uterine blood transfusion if severe Should be delivered before severe haemolysis

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25
Q

In babies with haemolytic disease of the newborn, what happens after birth?

A

Anaemic and quickly become severely jaundiced

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26
Q

Treatment for haemolytic disease of the newborn after birth?

A

o ‘Wash out’ maternal antibodies and bilirubin with exchange transfusions and phototherapy. o Can give IV Ig to block antibody sites.

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27
Q

How long might haemolytic disease of the newborn persist?

A

Several weeks (might still have some Ig around for a bit)

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28
Q

Not obvious reasons a paediatrician should be present at a birth

A

Meconium stained liquor vacuum, mid/high forceps delivery prolonged ROM

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29
Q

The infants condition after birth is described using the ____ score

A

APGAR

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30
Q

what do the bits of apgar stand for?

A

appearance pulse grimace (reflex irritability- suction pharynx to test) activity (muscle tone) RR

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31
Q

What is max apgar score?

A

10

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32
Q

What is a normal APGAR at one minute

A

7-10

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33
Q

At one minute an apgar score of what indicates a moderately depressed baby

A

4-6

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34
Q

At one minute apgar of 0-3 indicates what?

A

Severely depressed baby

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35
Q

Babies who require active resuscitation can be divided into what two groups?

A

Primary apnoea and secondary apnoea

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36
Q

What is primary apnoea

A

Blue colour due to failure to establish spontaneous respiration, but cardio system intact with good circulation Apgar at 1min 4-6

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37
Q

What is secondary apnoea?

A

White colour at birth as failure of circulation as well as respiration. Will die without vigorous resus. Slow or absent HR. Apgar at 1min 0-3

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38
Q

What normally happens to amniotic fluid during delivery?

A

Expelled from lungs by contractions

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39
Q

How can you encourage breathing at birth?

A

Dry with warm towel Gently suck out oropharynx Give to mother to put on breast or cuddle

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40
Q

Apnoiec within the first _____ requires basic resus

A

Minute

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41
Q

Will blue or white babies start to gasp even if nothing is done?

A

Blue

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42
Q

Do blue babies require lung inflation, cardiac support or both?

A

Lung inflation

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43
Q

Do white babies require lung inflation, cardiac support or both?

A

Both

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44
Q

How does tissue hypoxia lead to tissue acidosis?

A

Lactic acid and CO2

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45
Q

What is the accepted clinical definition of asphyxia?

A

N/A doesn’t exist

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46
Q

What are some used definitions of asphyxia?

A

Cord blood gas <7.05 0-5 APGAR at 10mins >10m to establish spont respiration Hypoxic-ischaemic encephalopathy

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47
Q

What is hypoxic ischaemic encephalopathy?

A

Abnormal neuro signs including convulsions lasting >2 days

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48
Q

How do you manage birth asphyxia?

A

Rapid and effective resus at birth Avoid cerebral oedema and treat convulsions

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49
Q

Prognosis of asphyxiated infants?

A

25% severely asphyxiated full term infants die or are severely handicapped Therapeutic cooling can improve neuro outcomes in survivors

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50
Q

What are the 3 categories of HIE?

A

Mild, mod, severe

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51
Q

What is mild HIE like?

A

Increased muscle tone, brisk tendon reflexes, transient behavioural abnorms like poor feeding or excessive crying. Typically resolves in 24h

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52
Q

What is moderate HIE like?

A

Lethargic, hypotonia, diminished reflexes. Grasping/moro/sucking reflexes may be absent. Periods of apnoea. Seizures in first 24h after birth. Full recovery within 1-2w possible

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53
Q

What is severe HIE like?

A

Seizures delayed and severe, may be initially resistant to conventional treatment. Usually generalised, freq may increase in the first 24-48h after onset (reperfusion injury).

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54
Q

What is a cephalohaematoma

A

Haemorrhage of blood between skull and periosteum

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55
Q

Why does cephalohaematoma occur in neonate

A

rupture of blood vessels crossing the periosteum usually due to prolonged second stage of labour or forceps delivery (not ventous)

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56
Q

Does cephalohaematoma pose a risk to brain cells?

A

No, considered a minor injury

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57
Q

How does cephalohaematoma present?

A

soft, fluctuant swelling on head appearing soon after birth

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58
Q

Do cephalohaematomas extend beyond the edges of the bone or cross suture lines?

A

No

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59
Q

Severe cephalohaematoma can cause what 3 things?

A

Jaundice, anaemia, hypotension

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60
Q

What can complications of cephalohaematoma be?

A

It may indicate linear skull fracture, or be at risk of infection (osteomyelitis, meningitis)

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61
Q

How long does it take for cephalohaematoma to resolve

A

Weeks. It calcifies in that time and appears as a depressed fracture

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62
Q

cephalohaematoma should be distinguished from ___?

A

sugaleal haemorrhage- between scalp and skull bone (above periosteum)- this is more extensive and prone to complications (anaemia and bruising)

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63
Q

Management cephalohaematoma

A

Mainly observational IF NEURO Sx- Skull xray or CT IF JAUNDICE- phototherapy IF ANAEMIA- blood transfusion (rare) consider bleeding disorder (unlikely)

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64
Q

Do you need to take bloods for cephalohaematoma?

A

Not usually

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65
Q

Should you aspirate a cephalohaematoma?

A

No risk of infection and abscess formation

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66
Q

Prematurity is defined as what gestation?

A

<37w

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67
Q

‘extremely premature’ is ? gestation

A

<28w

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68
Q

From what premature age can babies survive

A

23w but mortality 60-70% and only 25% disability free

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69
Q

Prognosis is excellent beyond what premature gestation?

A

30-32w

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70
Q

Risk factors for prematurity?

A

Young maternal age Multiple pregnancy Infxn Maternal ‘illness’ (HTN, cervical incompetence, APN, smoking, alcohol, infection)

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71
Q

3 big risks of prematurity?

A

Hypothermia Hypoglycaemia Feeding difficulties

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72
Q

Where are premature babies cared for?

A

SCBU or NICU

73
Q

What is the benefit of incubators?

A

Warmth and humidity

74
Q

When does the suck-swallow pattern develop?

A

34w gestation

75
Q

What respiratory conditions are associated with prematurity?

A

RDS Pneumothorax Pulmonary haemorrhage Bronchopulmonary dysplasia Apnoea Hypoxia-ischaemia

76
Q

What is the most common cause of resp distress in a premature baby?

A

RDS

77
Q

What is RDS?

A

Insufficient surfactant. Neonatal lungs non-compliant (stiff)- leads to hypoxia and acidosis

78
Q

When does surfactant normally develop?

A

35-36w although stress of labour normally stimulates it so RDS can be self limiting to 5-7 days.

79
Q

What can RDS lead to?

A

hypoxia and acidosis, if severe can cause PPHN (persistent pulmonary hypertension of the newborn)

80
Q

What predisposes a baby to RDS?

A

Premature Hypoxia, shock, acidosis, asphyxia Second twin APH Diabetic mother

81
Q

What protects a baby against RDS?

A

Prolonged IU stress as they have endogenous corticosteroid release e.g. in IUGR. Maternal steroids pre-labour

82
Q

How does RDS present?

A

Resp distress from 6 hours Tachypnoea, recessions, cyanosis, grunting

83
Q

What is the course of RDS?

A

worsens over 2-3 days then improves over 1-2 weeks

84
Q

What does a CXR of RDS show?

A

Ground glass appearance Air bronchograms

85
Q

Management of RDS?

A

Surfactant replacement via ETT (porcine) Ventilatory support (O2, CPAP/nasal prongs/PPV) ABx if susp infection Minimal handling

86
Q

Complications RDS

A

Pneumothorax, IV haemorrhage, 20% develop bronchopulmonary dysplasia (late)

87
Q

When should maternal steroids be given to prevent RDS?

A

48h before delivery (or ASAP if that time has passed already)

88
Q

How does pneumothorax present in premature neonate and what is the cause?

A

Mostly asymptomatic, can be idiopathic or sometimes due to ventilation

89
Q

Why does pulmonary haemorrhage happen in premature neonate?

A

elevated pulmonary capillary pressure from an acute LV failure or lung injury (e.g. RDS, pneumonia)

90
Q

How does pulmonary haemorrhage present in premature neonate ?

A

Frothy pink sputum and acutely unwell

91
Q

What is bronchopulmonary dysplasia?

A

Chronic lung damage due to disrupted development in premature neonate.

92
Q

What radiological changes are seen in bronchopulmonary dysplasia?

A

Honeycomb lung (hyperexpanded and diffuse fibrosis)

93
Q

bronchopulmonary dysplasia usually follows ___?

A

Severe RDS

94
Q

bronchopulmonary dysplasia may require what treatment?

A

LTOT for months/years

95
Q

How will bronchopulmonary dysplasia present?

A

Oxygen requirement on day 28 of life or 36w gestation

96
Q

apnoea definition

A

not breathing for >20s ± bradycardia and cyanosis

97
Q

What are the causes of apnoea

A

Many chemoreceptor/resp centre immaturity (poorly developed in neonates) airway obs asipration infection hypoglycaemia PDA

98
Q

How do you treat apnoea

A

Treat underlying cause if poss Stimulate Oropharyngeal suction Bag mask (neonatal resus essentially)

99
Q

Is it ok to have fluctuating O2 levels in premature babies?

A

Not too much- can lead to retinopathy of prematurity

100
Q

Hypoxia-ischaemia after birth can result from what three things? (prematurity)

A

Severe shock Inadequate breathing Severe aneamia

101
Q

What is the effect of hypoxia ischaemia?(prematurity)

A

It can effect all organs e.g. NEC, tubular necrosis, HIE, heart failure, RDS, PPHN, metabolic acidosis, hypoglycaemia…

102
Q

What is the most important factor/body system in long term prognosis of prem baby?

A

Neuro

103
Q

What is intraventricular haemorrhage? (prematurity)

A

Haemorrhage on floor of lateral ventricle and ruptures into the ventricle. Can cause obstructive venous infarct of the surrounding white matter and risks hemiplegic cerebral palsy.

104
Q

Is IVH always symptomatic? (prematurity)

A

No

105
Q

How is IVH diagnosed? (prematurity)

A

USS

106
Q

15% babies get what after IVH? How is this managed? (prematurity)

A

Post haemorrhagic hydrocephalus which may require a ventriculo peritoneal shunt

107
Q

What is the commonest cause of cerebral palsy in surviving premature infants?

A

Periventricular leucomalacia

108
Q

What is periventricular leucomalacia? (prematurity)

A

ischaemic damage to periventricular white matter

109
Q

What is more common IVH or Periventricular leucomalacia? (prematurity)

A

IVH

110
Q

Periventricular leucomalacia is more likely in which three cases? (prematurity)

A

chorioamnionitis, severe hypotension or monozygotic twins

111
Q

What feature of periventricular leucomalacia makes it more likely to progress to cerebral palsy? (prematurity)

A

Cystic changes

112
Q

what is meant by neurodevelopmental consequences of prematurity?

A

Even with normal USS, prem babies have an increased incidence of learning difficulties such as attention difficulties, or subtle problems in higher functioning e.g. maths which may not manifest until school

113
Q

What is the one cardiac condition in prematurity?

A

PDA

114
Q

What are 5 gastro conditions in prematurity?

A

NEC Osteopenia of prematurity GOR Inguinal hernias Nutrition problems

115
Q

What is NEC

A

Bowel wall inflammation, ulceration and perforation, often secondary to ischaemic or hypoxic insult. Mucosal damage leads to bacterial invasion and GI gangrene and perforation.

116
Q

Symptoms NEC

A

Apnoeas lethargy vomiting temp instability acidosis shock

117
Q

Signs NEC

A

Shiny distended abdo Bile aspirates or bilious vomit rectal fresh blood collapse

118
Q

What would AXR NEC show?

A

fixed loops of bowel, pneumatosis intestinalis, portal vein gas, pneumoperitoneum

119
Q

What is the prognosis of NEC?

A

10% mortality (higher if perf) Complications of stricture and short bowel synd

120
Q

What can help NEC?

A

Probiotics and breast milk

121
Q

Why might breast milk help NEC?

A

Lactoferrin

122
Q

Management NEC

A

Stop feeds Support circulation ABx Laparotomy if perf occurs

123
Q

What are two risk factors for NEC

A

PDA and increasing milk feeds (esp formula) too rapidly

124
Q

What is osteopenia of prematurity?

A

Mineral deficiency, esp phosphate. In premature infants and those of low birth weight compared to infants of the same gestation. Classically: immature infant that is solely breast fed.

125
Q

What is the risk of inguinal hernias?

A

Strangulation

126
Q

How should premature infants be fed?

A

NG until develop sucking reflex at 32-34 weeks May require parenteral nutrition

127
Q

Can in-utero growth rates be achieved in premature babies?

A

Unlikely

128
Q

How common is retinopathy of prematurity?

A

35%

129
Q

Does retinopathy of prematurity require rx?

A

Most no.

130
Q

retinopathy of prematurity prognosis

A

1% blind

131
Q

Why does retinopathy of prematurity happen?

A

Proliferation of new blood vessels in an area of relative ischaemia in the developing retina. Can be due to oxygen toxicity (big fluctuations in supplemental o2 conc) May be genetic predisposition

132
Q

What should happen to infants at risk of retinopathy of prematurity?

A

Screen by ophthalmologist

133
Q

What happens if retinopathy of prematurity is detected?

A

laser ablation can prevent retinal detachment and blindness

134
Q

Premature infnats are especially susceptible to which infections?

A

Group B strep and coliforms, pneumonia

135
Q

Why do premature infants have poor thermoregulation

A

High SA:V ratio Immature skin poor at retaining heat and fluid Low SC fat

136
Q

Two haem conditions prem babies can get

A

anaemia of prematurity neonatal jaundice

137
Q

What should be included in a history of a premature baby

A

Maternal risk factors for prem Full obs hx Condition at birth-APGAR, resus? Birth weight Gestation Assoc problems e.g. twin, congenital abnorm, infection e.g. chorioamnionitis may have triggered labour Antenatal steroids given?

138
Q

Survival rates at 24w, 27w and 32w

A

24w- 45% 27w- 80% 32w- excellent NB disabilities likely and more likely the smaller the gestation

139
Q

What are 4 long term problems of prematurity?

A

Chronic lung disease (bronchopulmonary dysplasia) Neuro sequelae (cerebral palsy) Blindness due to RoP (getting rarer) Poor growth (esp if catch up growth not achieved)

140
Q

Small baby is due to what 3 things?

A
  1. prematurity 2. IUGR 3. both
141
Q

What is VLBW?

A

very low birth weight <1500g at birth, would be severely premature

142
Q

What are different ways of calculating gestational age?

A

either from LMP, early dating USS or assessment of gestation after birth- Dubowitz score- physical criteria (skin development, nipple and genitalia appearance, ear form) and neuro criteria (posture, neck and limb tone, joint mobility)

143
Q

What is a premature baby’s tone and joint mobility likely to be like?

A

hypotonic with limbs in extension and increased joint mobility

144
Q

IUGR defined as?

A

Babies SGA below 10th centile on growth chart

145
Q

IUGR is either ___ or _____?

A

Symmetrical or asymmetrical

146
Q

What is symmetrical growth restriction?

A

Wt, head circ and length are ALL below 10th centile in the same proportion. Could be a normal baby that happens to be small (remember 10% normal babies in this centile)

147
Q

Symmetrical IUGR suggests the insult occurred early or late in preg?

A

Early

148
Q

four causes of symmetrical IUGR?

A

Chromosomal abnorms Prenatal infection (TORCH) Maternal disease Maternal alcoholism

149
Q

TORCH stands for?

A

Toxoplasmosis Other (syphilis) Rubella CMV (normally presents with hepatosplenomegaly, purpura (thrombocyt.), and conjugated hyperbil. Rarely causes disabling sequelae) Herpes

150
Q

What are long term sequelae of TORCH?

A

Microcephaly Cerebral palsy mental retardation blindness deafness

151
Q

What does asymmetrical growth restriction look like?

A

weight affected>length>head Infant looks long and thin, little SC fat. Skin dry, cracked, peeling days after birth

152
Q

What is the cause of asymmetrical IUGR?

A

Something late in foetal development, often placental insufficiency Could also be: Toxaemia of pregnancy Multiple pregnancy Maternal smoking

153
Q

Can asymmetrical IUGR be resolved?

A

Yes if adequate nutrition after birth post-natal catch up is often rapid

154
Q

What is the main concern in IUGR?

A

hypoglycaemia- early and effective feeding important

155
Q

How do you estimate expected weight had the IUGR not occurred?

A

Read the expected weight for whatever gestational age they are from growth chart

156
Q

In IUGR do you feed according to expected or actual weight?

A

Expected

157
Q

Small babies are prone to what five things?

A

Hypothermia Hypoglycaemia Feeding problems Infection Apnoea of prematurity

158
Q

Hypoglycaemia is defined as what in a neonate?

A

<2.6mmol/L

159
Q

What is the problem with NG feeding ill premature babies?

A

Risk of NEC contraindicates gastric feed (because asphyxiation could impair blood flow to bowel)

160
Q

How can you minimise risk of infection in small baby?

A

Avoid cross infection and use broad spec antibiotic if susp infection

161
Q

What is apnoea of prematurity? How is it diagnosed and briefly how is it managed?

A

Periods of hyper and hypoventilation alternating, leading to brief apnoeic episodes. Diagnose by excluding other causes of apnoea in otherwise well premature infant. Give xanthine based drugs e.g. caffeine, theophylline.

162
Q

Do IUGR babies have a higher risk of RDS?

A

No reduced due to endogenous steroid production

163
Q

prognosis IUGR?

A

Very severe- can be a cause of short stature in children Severe (esp if brain growth restricted) can = intellectual impairment

164
Q

What is talipes?

A

Neonatal club foot

165
Q

Is talipes normally uni or bi lateral?

A

50/50

166
Q

Cause of talipes?

A

Unknown, possibly genetic Can be due to being squashed in utero- corrects by 3m or some physio

167
Q

Foot appearance in talipes?

A

Inverted Adduction of forefoot relative to hindfoot Equinus (plantar flexion deformity) Foot cannot be passively everted and dorsiflexed through the normal range.

168
Q

What three things is talipes associated with

A

Myelomeningocele Arthrogryposis Prune belly syndrome

169
Q

Treatment of talipes?

A

within a week or two of birth- ponseti method- foot manipulated and placed in long leg plaster cast on repeated occasions for about 5-8 weeks. Done gradually Normally need small op to loosen achilles after the last cast. Then wear special boots full-time first 3m, then overnight until 4/5yo If this does not work- surgery on soft tissues and/or bones from 2yo

170
Q

Talipes prognosis

A

Nearly all treated with Ponseti method have pain-free, normal looking feet. Most learn to walk at normal age and can do sports when older. If unilateral may have one leg shorter than the other, smaller foot on one side. Occasionally recurs- repeat some steps of the treatment.

171
Q

What does this picture show?

When does it normally appear?

Is it bad?

A

Pigmented naevus

Around 2yrs

Risk of malignancy v rare

172
Q

What is this?

How would you describe it?

When is the onset?

What can it indicate?

A

Cafe au Lait spots

Uniformly pigmented, sharply demarcated macules.

Present at birth of develop during childhood

Neurofibromatosis if there are lots

173
Q

What is this?

also known as?

Is it compressible?

What is the prognosis? Should it be treated?

A

Strawberry naevus/superficial haemangioma

compressible

Almost all resolve spontaneously but may get bigger first.

Don’t treate unless interferes with e.g. vision

174
Q

What is this?

AKA?

Where do they often occur?

What happens to them?

A

Naevus flammeus/salmon patch/stork mark

Small pink, flat lesions

Eyelids, neck, forehead

Usually fade and disappear entirely

175
Q

What is this?

where does it often occur?

Which babies does it occur in?

What happens to it?

A

Mongolian blue spot

Sacral area

>80% black and asian babies

Fades in first few years normally

176
Q

What is this?

What is it made up of?

What if it was localised to the trigeminal area?

A

Port-wine stain

mature, dilated, dermal capillaries

Trigeminal= consider sturge-weber syndrome (underlying meninigeal haemangioma and intracranial calcification- assoc with fits)

177
Q
A
178
Q

If mother is colonised with group B strep, no abx prophylaxis and baby is healthy, what needs to be done to baby if anything?

A

Newborns with only one minor risk factor for early onset sepsis should remain in hospital for at least 24 hours with regular observations. Two or more minor risk factor or one red flag warrant empirical antibiotic therapy with Benzylpenicillin and Gentamicin and a full septic screen.

179
Q

What are red flags for sepsis in neonate?

A

Suspected or confirmed infection in another baby in the case of a multiple pregnancy

Parenteral antibiotic treatment given to the woman for confirmed or suspected invasive bacterial infection (such as septicaemia) at any time during labour, or in the 24-hour periods before and after the birth [This does not refer to intrapartum antibiotic prophylaxis]

Respiratory distress starting more than 4 hours after birth

Seizures

Need for mechanical ventilation in a term baby

Signs of shock

4th year Paeds (13 decks)

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