Neonatology Flashcards

1
Q

What is the most common cause of neonatal jaundice?

A

Physiological jaundice

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2
Q

When should we be concerned about neonatal jaundice?

A

If it appears within the first 24 hours of life, or if it persists past day 14.

Equally if it is over the threshold for treatment.

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3
Q

How common is neonatal jaundice?

A

Very - 60% of neonates get it at some point.

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4
Q

A neonate is 6 hours old and the mother notices she is jaundiced.

What are the differentials in this case?

A
  • Haemolysis

- Infection

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5
Q

What causes of haemolysis can cause jaundice in a neonate under 24 hours old?

A
  • ABO incompatibility
  • Rhesus disease of the newborn
  • Hereditary spherocytosis
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6
Q

What infections can cause jaundice in a neonate under 24 hours old?

What is the acronym to remember them?

A
TORCH:
  Toxoplasmosis
  Other
  Rubella
  CMV
  Hepatitis/Herpes
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7
Q

What 4 things should we assess in the brand new new-born?

A
  • Muscle tone
  • Colour
  • Breathing/Airway
  • Heart rate
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8
Q

A newborn is different from an adult how? (3)

A

It’s all wet (so its cold), it’s smaller so SA:V is higher so gets cold quicker, and…………………

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9
Q

If a newborn has an obstructed airway, what might be in there?

A
  • Meconium

- Blood

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10
Q

How long can a newborn be blue for? Why?

A

Can be ok up to 10 minutes after birth as takes that much time to adjust to its own air supply to bring sats from ~60% up to “adult” saturations

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11
Q

If a newborn looks like it needs resusitation, what method should we use?

A

ABC

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12
Q

What is the A of newborn resus?

A

Airway!!

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13
Q

What is the very first thing you do with a baby (while assessing tone/colour/breathing/HR)?

A

Warm it up!!

“You’re not dead until you’re warm and dead.”

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14
Q

How do you assess tone in the newborn?

A

Are they floppy? That’s not good.

Are they moving their limbs? Or holding their arms and legs close to their body? That IS good.

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15
Q

How do you assess breathing in the newborn?

A

Have they cried/screamed? That IS good.
Are they visibly breathing? Clearly, that would be good too.
Is their breathing easy? i.e. are they gasping/do they have a weak cry? Not good.

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16
Q

How do you assess the colour of the newborn?

A

Pink? Great.
Pink body but blue extremities? Ok but keep an eye on it.
Blue or pale all over? May resolve in the first 10 minutes of life, but keep an eye on it.

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17
Q

How do you assess the HR of the newborn?

A

Listen to the chest and count!
No heart beats? Thats bad.
HR less than 100 bpm? That’s also bad.
HR over 100 bpm? Grand.

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18
Q

When assessing a newborns airway, what do you do?

A
  1. Put the child’s head in neutral position to open airway fully.
  2. Look in airway with laryngoscope (left hand, right hand open mouth with one finger in mouth to open from top).
  3. Apply some suction if something visible blocking airway.
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19
Q

What is the B of newborn resus?

A

Breathing!!

You knew that. Easy win.

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20
Q

What do we do for breathing in newborn resus?

A
  1. Check for chest movements
  2. If none, apply an ETT or laryngeal mask.
  3. Give some inflation breaths.
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21
Q

What do we need to know for inflation breaths?

A

They help increase pressure in the lung to force fluid out of the air space.

In a term neonate, the air pressure should be 30cm of water.

Each breath should be given over 3 seconds.

5 breaths should be given over 30 seconds.

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22
Q

If the term newborn doesn’t respond to inflation breaths, what is the next step?

A

Chest compressions and inflation breaths at a certain ratio.

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23
Q

What ratio should chest compressions and inflation breaths be done at in the C part of newborn resus?

A

5 chest compressions to 2 breaths

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24
Q

If the neonate doesn’t respond to chest compressions, what should we try next?

A

Drugs - IV adrenaline

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25
Q

How fast should chest compressions be done at for a newborn?

A

Roughly 100 bpm

1-2 beats per second, so 5 should take 3 seconds

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26
Q

How do you measure up an endotracheal tube for a newborn?

A

Length of tube should go from middle of mouth to angle of mandible/tragus of ear.

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27
Q

What can cause potentially 10% of newborns to have feeding difficulties?

A

Tongue tie

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28
Q

An infant presents to GP with feeding problems.

From this skint history, build a list of differentials.

A
GORD
Cow's milk allergy
Colic
Lactose intolerance
Overgrowth syndromes
URTI/blocked nose
Teething
Neurological (swallowing difficulties)
Overfeeding with bottle feeding
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29
Q

WRT nutrition, what is important to note about preterm babies?

A

They have a very high nutritional requirement as growth and weight gain is the aim in the 3rd trimester.

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30
Q

When does a baby’s suckling reflex kick in?

A

Around 34-36 weeks

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31
Q

How do we need to feed preterm infants who have not developed a suckling relfex yet?

A

NG tube or parenteral feeding

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32
Q

What is better for a baby - breast milk or formula milk?

Why?

A

Breast milk - breast feeding encourages bonding, helps build the child’s immune system, reduces the risk of necrotising enterocolitis, and has a demand-lead pattern of feeding.

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33
Q

What can we do to breast milk for preterm infants to help it meet their requirements?

A

Use breast milk fortifier to increase calorie, protein, phosphate, and calcium intake.

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34
Q

How can we give parenteral nutrition to very immature or sick infants?

A

Central line (PIC) or vie an umbilical venous catheter.

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35
Q

What are the risks of parenteral feeding?

A

Infection
Extravasation
Skin damage/scarring
Necrotizing enterocolitis

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36
Q

What is necrotizing enterocolitis?

A

Ischaemic injury to or bacterial infection of the bowel in infants causing a portion of bowel to die.

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37
Q

What are the risk factors for necrotising enterocolitis?

A
Preterm birth
Cows-milk formula feeding
Ischaemic bowel injury
Bacterial bowel infection
Low birth weight
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38
Q

How does NEC present?

A
  • Feed intolerance
  • Tender abdomen
  • Blood in stool
  • Bilious vomiting
  • Generally unwell (PEWSing)
  • Abdo distension
  • Collapse
  • Shock
  • Sepsis
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39
Q

How does NEC look on an abdo xray?

A
  • Distended loops of bowel
  • Intramural gas
  • May be perforated (free gas under diaphragm/Rig;er’s sign (double wall sign)/football sign)
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40
Q

How should NEC be managed?

A
  • Stop oral feeds
  • Broad spec abx
  • Parenteral nutrition
  • Cardio/resp support often needed
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41
Q

A newborn who is 10 hours old is jaundiced.

What investigations should be done?

A
  • Bilirubin - get conjugated and unconjugated as separate levels.
  • Blood film
  • G6PD enzyme assay
  • Coombs’ test
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42
Q

When is knowing if jaundice is caused by conjugated or unconjugated bilirubin most important?

Why?

A

In prolonged jaundice (past 14 days of life)

Raised conjugated bilirubin suggests biliary atresia.

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43
Q

How do we decide how to manage neonatal jaundice?

A

Based on severity and rate of change - bilirubin levels plotted on a chart adjusted for gestational age.

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44
Q

How does jaundice spread?

A

From head to toes (so sclera should be a good place to look for it).

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45
Q

Why do we adjust for gestational age when deciding on jaundice treatment?

A

Preterm infants have a less well developed BBB so are at a higher risk of kernicterus compared to older/term babies.

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46
Q

What treatment can we do for neonatal jaundice?

A
  • Supportive (hydration and nutrition)
  • Phototherapy
  • Exchange transfusion in severe cases
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47
Q

What are the main causes of prolonged/persistent neonatal jaundice?

A
  • Biliary atresia
  • Infection (often a UTI)
  • Breast milk jaundice
  • Congenital hypothyroidism
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48
Q

What are the 2 categories of neonatal infection?

A

Early-onset and late-onset sepsis

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49
Q

What is the cut off for early-onset sepsis?

A

Less than 48 hours after birth

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50
Q

What are the features of neonatal sepsis?

A
  • Fever/hypothermia
  • Poor feeding
  • Vomiting
  • Apnoea & bradycardia
  • Jaundice
  • Neutropenia
  • Hypo/hyper-glycaemia
  • Shock
  • Seizures
  • Lethargy/drowsiness/irritability
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51
Q

By what mechanism can early-onset sepsis occur in a neonate?

A

Bacteria ascend the birth canal and invade the amniotic fluid -> fluid into lungs -> pneumonia and secondary septicaemia.

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52
Q

When do most metabolic conditions get picked up?

A

At the blood spot/Guthrie test done on day 5-8 of life.

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53
Q

What conditions does the guthrie test look for?

A
PKU
HCU
Congenital Hypothyroidism
CF
MSUD
Sickle cell anaemia
Beta thalassaemia major
MCADD
Glutaric aciduria type 1
Isovaleric acidaemia
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54
Q

A child has a rare metabolic condition that isn’t picked up at birth.

How might they present chronically?

A
  • Failure to thrive
  • Developmental delay
  • Chronic episodic illness
  • System specific, generalised symptoms e.g. cardiomyopathy, D&V, muscle weakness etc.
  • Decompensation after minor illness
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55
Q

A child has a rare metabolic condition that isn’t picked up at birth.

How might they present acutely?

A
  • Metabolic acidosis
  • Hypoglycaemia
  • Non-specific symptoms e.g. hypotonia, seizures, lethargy, poor sucking reflex, respiratory distress
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56
Q

What inheritance pattern do most inherited metabolic disorders demonstrate?

A

Autosommal recessive

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57
Q

What inheritance pattern do mitochondrial disorders demonstrate?

A

Maternal inheritance

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58
Q

What is the most common cause of early-onset severe infection in the neonatal period?

A

Group B Strep

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59
Q

When might a neonate be exposed to Group B strep?

A

During labour as many mothers are carriers in their bowel flora.

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60
Q

Which neonates are at increased risk of Group B strep infections?

A
  • Premature infants
  • Prolonged labour/rupture of membranes
  • Previous sibling GBS infection
  • Maternal pyrexia
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61
Q

What are the main culprits in congenital cyanotic heart disease?

A
Tetralogy of Fallot
Transposition of the great arteries
Coarctation of the aorta
Pulmonary atresia
Pulmonary stenosis
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62
Q

When might cyanosis worsen, and why?

A

Day 1-2 as the PDA closes so there is no blood mixing/flow from left to right.

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63
Q

How would coarctation of the aorta present O/E?

A

Upper limb hypertension
Weak/absent femoral pulses
Cyanosis after day 2/3

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64
Q

How is congenital heart disease detected?

A

Antenatal scans
NIPE
Presentation with heart murmur, heart failure, or cyanosis.

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65
Q

How do we diagnose congenital heart disease?

A

Echocardiography

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66
Q

How do we manage cyanotic congenital heart disease?

A

Keep the PDA open with prostaglandins as immediate management, along with airway stabilisation and A to E assessment.

Definitive Rx is usually surgery.

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67
Q

When can a neonate contract an infection?

A

At any time - in utero, during delivery, or post-natally.

68
Q

When is early onset neonatal sepsis defined as?

A

Sepsis occuring within the first 48-72 hours of life.

69
Q

What is important once early onset neonatal sepsis is identified?

A

Starting treatment immediately! Reduces risk of death :)

70
Q

What is the most common cause of EONS? (Organism)

A

Group B Streptococcus

71
Q

Other than group B strep, what organisms are often responsible for EONS?

A

E. coli
Coagulase negative staph
H. influenzae
Listeria monocytogenes

72
Q

How do neonatal infections that lead to EONS present?

A

Respiratory distress
Pneumonia
Septicaemia

73
Q

What are the factors that predispose neonates to EONS?

A

Previous baby or current pregnancy having invasive GBS
Prelabour rupture of membranes
Preterm birth
Infrapartum fever

74
Q

What are the RED FLAGS for EONS?

A

Respiratory distress starting more than 4 hours after birth
Seizure
Signs of shock
Need for mechanical ventilation in a term baby
Suspected/confirmed infection in a co-twin

75
Q

What differentials can there be for respiratory distress in a neonate?

A
Early onset neonatal sepsis
Transient tachypnoea of the newborn
IRDS
Meconium aspiration
Haemolytic disease of the newborn
76
Q

What antibiotics do we use for EONS?

A

IV benzylpenicillin and Gentamicin

Unless micro say use something else, or local guidelines say something else.

77
Q

What is the overall mortality rate for sepsis in late-preterm/term neonates?

A

2-4%

78
Q

A newborn has respiratory distress. During the birth, the amniotic fluid was stained with meconium, and the mother bled heavily (but she’s ok now, dw).

What might be causing the respiratory distress in this case?

A

Aspiration of meconium or blood would be my top 2 differentials.

79
Q

What are the 3 main risk factors for meconium aspiration?

A

Post-term infant
Thick meconium at birth
Birth asphyxia

80
Q

What are the main effects that meconium has once it has been aspirated?

A
  • Degree of airway obstruction
  • Foetal hypoxia
  • Pulmonary inflammation
  • Infection
  • Surfactant inactivation
  • Persistent pulmonary hypertension
81
Q

How is meconium aspiration diagnosed?

A

Clinically:

  • Tachypnoea/cardia
  • Cyanosis
  • Grunting/nasal flaring/recessions
82
Q

What investigations would support a diagnosis of meconium aspiration syndorme?

A

Chest x-ray
Infection markers
ABG

83
Q

A child has meconium aspiration syndrome. You think the degree of hypoxia could have been severe. What extra scans might you want to order?

A

Cranial ultrasound - assess for hypoxic damage to the brain

84
Q

How should a newborn with meconium aspiration syndrome be managed?

A
Observation of vitals
Routine care (incubator, continuous obs, assess haem, nutritional support)
Ventilation/Oxygen
Antibiotics
Surfactant
Inhaled nitric oxide
85
Q

Why would we use inhaled nitric oxide as a therapy in meconium aspiration syndrome?

A

For pulmonary hypertension as it is a vasodilator

86
Q

A newborn with meconium aspiration syndrome gets a chest xray. On it you notice a pneumothorax.

How might this have happened?

A

Meconium -> obstruction of airway outflow -> alveolar hyperinflation -> air leak into pleural space, or into mediastinum -> pneumomediastinum.

87
Q

A newborn with meconium aspiration syndrome has been ventilated with CPAP, then with intubation as he didn’t respond to CPAP.

Despite intubation, he is still in respiratory failure. What else can we try?

A

ECMO

88
Q

A newborn with meconium aspiration syndrome has been ventilated with CPAP, then with intubation as he didn’t respond to CPAP. You are fortunate because the Glenfield can take him for ECMO.

How do you explain to parents what ECMO is?

A

It is a way of oxygenating the blood without using the lungs.

Insert a tube into a vein, which takes blood out into a machine that pumps oxygen into it. The blood is then returned to the body ready for tissues to use.

This allows the lungs to rest and recover. Not a long term solution.

89
Q

What are the risks associated with ECMO? How do we manage them?

A

Risks - bleeding (blood products, care of any wounds, monitor), clots (heparin), infection (antibiotics), neurological damage (regular checks), renal damage (monitor, dialysis), failure to recover.

90
Q

What does ECMO stand for?

A

Extracorporeal membrane oxygenation

91
Q

What are the acyanotic congenital heart problems?

A
VSD
ASD
PDA
Aortic stenosis
Pulmonary stenosis
Coarctation of the aorta (initially)
Atrioventricular canal defect
92
Q

How common are congenital heart defects?

A

8.2 per thousand live births in Europe.

Accounts for 1/3 all major congenital anomalies.

93
Q

What are the risk factors for congenital heart disease?

A
  • 1st degree relative with congenital her disease
  • Consanguineous union of parents
  • Infection during pregnancy
  • Drugs/alcohol during pregnancy
  • Genetic conditions
  • Maternal Diabetes mellitus
94
Q

In which group of newborns might we particularly see transient congenital heart defects?

A

Premature babies

95
Q

How are the majority of congenital heart defects diagnosed in the UK?

A

Detailed antenatal scans.

If not them, picked up during the NIPE

96
Q

How might a baby present with a significant L->R shunt if it is not picked up on antenatal screening or the NIPE?

A

Signs of heart failure and faltering growth early in infancy.

97
Q

What hx do we need to take when an infant/child present with a heart murmur?

A
  • Full SQITARS esp. are they symptomatic with it?
  • Developmental hx
  • Hx of pregnancy
  • Mothers health in pregnancy inc. infections
  • Drug/alcohol/medication use in pregnancy
  • FHx
98
Q

What is the first line investigation for heart murmurs in secondary care?

A

Echocardiography

99
Q

Some children with congenital heart disease may not require any specific treatments, but may need something else. What is this “something else”?

A

Prevention for infective endocarditis

100
Q

What can we give to neonates with ducuts-dependant congenital heart defects?

A

Prostaglandin infusion to keep the ductus arteriosus open.

101
Q

What tends to be the definitive treatment for congenital heart defects?

A

Surgery

102
Q

What are the complications associated with congenital heart defects?

A
  • Risk of infective endocarditis
  • Failure to thrive
  • Paradoxical embolism -> systemic embolism.
  • Pulmonary hypertension
  • Cyanosis -> polycythaemia
103
Q

What is IUGR?

A

A condition where a baby’s growth slows or ceases when it is in the uterus. It is part of a wider group called small for gestational age foetuses.

104
Q

What maternal factors can cause IUGR?

A
  • Age of mother (under 16, over 35)
  • Inter-pregnancy interval being less than 6 or more than 120 months
  • Maternal illhealth
  • Maternal lifestyle (smoking, alcohol, substance abuse)
  • Maternal infections
  • Placental dysfunction or abruption
105
Q

What foetal factors can cause IUGR?

A
  • Chromosomal abnormalities
  • Genetic syndromes
  • Major congenital anomalies
  • Multiple gestation
  • Congenital infections
  • Metabolic disorders
106
Q

What are the 3 types of IUGR and what are they caused by?

A

Symmetrical (i.e. all proportions reduced) - early onset, hypoplasia.

Asymmetrical (abdo circ reduced, other measurements normal) - malnourishment.

Mixed - early IUGR augmented by placental causes later in pregnancy.

107
Q

What are the short term complications of IUGR?

A

Neonates are more prone to asphyxia, meconium aspiration, persistent pulmonary HTN, hypothermia, hypo/hyperglycaemia, hypocalcaemia, jaundice, feeding problems, NEC, late onset sepsis…

It’s just not good.

108
Q

What are the long term complications of IUGR?

A
  • Lower scores on cognitive testing.
  • Learning difficulties
  • Cerebral palsy, gross motor and minor neurological dysfunction.
  • Behavioural problems
  • Poor perceptual performance, poor visuo-motor perception.

They are also more susceptible to develop adult-onset diseases in their infancy and adolescence - eg, diabetes, hypertension, obesity, metabolic syndrome, coronary heart disease.

109
Q

How can we try and prevent IUGR/SGA foetuses?

A
  • Give antiplatelet therapy to mother if at risk of pre-eclampsia
  • Smoking cessation
110
Q

At what gestational age is a baby defined as being premature?

A

Before 37 weeks.

111
Q

What affects prognosis when it comes to premature babies?

A

Birth weight as well as gestational age at birth.

112
Q

Why is a premature baby at increased risk of hypothermia?

A

They have little subcutaneous fat, they are less able to shiver, and less able to maintain homeostasis.

113
Q

Which metabolic abnormalities are premature babies at risk of, and what can that predispose them to?

A

Hypoglycaemia and hypocalcaemia.

This predisposes them to convulsions -> long term brain damage.

114
Q

What respiratory problem are premature babies at risk of, and why?

A

Respiratory distress syndrome.

Surfactant production from type 2 pneumocytes may not have started/be sufficient and the lungs may not be structurally mature.

115
Q

Which GI disorders are premature babies more at risk of developing?

A

Jaundice

NEC

116
Q

Which neurological and sensory disorders are premature babies more at risk of developing?

A

Kernicterus (due to jaundice)
Intraventricular brain haemorrhage
Retinopathy of prematurity
Hearing impairment

117
Q

Other than neonatal sepsis, what neonatal infections can occur?

A

Meningitis
Pneumonia
UTI

118
Q

If menningitis is suspected in a noentae, what should the first Ix be?

A

Lumbar puncture

119
Q

Which organisms are implicated in neonatal meningitis?

A

Group B strep. and E. coli are responible 2/3 of the time.

120
Q

What is neonatal pneumonia thought to be due to?

A

Aspiration of micro-organisms during delivery

121
Q

What can neonatal pneumonia be similar to in presentation?

A

IRDS

122
Q

What is the pathophysiology of pneumonia in a neonate?

A

Infection -> pulmonary changes with infiltration and bronchopulomnary tissue destruction.
Pulmonary surfactant function is inhibited.

123
Q

How should a neonatal UTI be managed?

A

Treat immediately in the ill child. Use IV cefotaxime or an aminoglycoside with careful monitoring.

124
Q

What might a neonatal UTI suggest?

A

Congenital structural abnormality.

125
Q

What is the most common organism in neonatal skin infections?

A

Staph. aureus

126
Q

Where on the skin is a neonatal skin inection most concerning?

A

Periumbilical

127
Q

Why is a periumbilical skin infection in neonates worrying?

A

There is a possibility of bacteria passing up umbilical vein -> thrombophlebitis/hepatic abscess.

128
Q

How can oral thrush in a baby be distinguished from milk curds?

A

If scraped with a tongue spatula, the milk curds will move but thrush will be adherent.

129
Q

How does a neonatal oral thrush infection present?

A
  • D+V
  • Firmly adherent small white plaques
  • Sore mouth -> feeding difficulties
130
Q

How should neonatal oral thrush infection be managed?

A

Topical antifungal like miconazole

131
Q

How might a neonatal TB infection present?

A
At around 6 weeks of life (if acquired at birth).
Unwilling to feed
Excessive weight loss
Slight fever
Hepatosplenomegaly
132
Q

How should neonatal TB be investigated?

A

CXR

133
Q

How is neonatal TB treated?

A

If FHx of TB in prev. 6 months, BCG is given at 3 days.

Rx is with standard antituberculous drugs.

134
Q

What is conjunctivitis within the first 28 days of life called?

A

Ophthalmia neonatorum

135
Q

What used to be the most common cause of neonatal conjunctivitis?

A

Neisseria gonorrhoeae, then Chlamydia thrachomatis overtook it.

Neither of them are the most common any more.

136
Q

What organisms cause most cases of neonatal conjunctivitis?

A

Non-sexually transmitted bacteria like S. aureus, Strep. pneumonia, Pseudomonas, and Haemophilus species.

137
Q

Is neonatal conjunctivitis usually severe or mild?

A

Mild

138
Q

Is neonatal conjunctivitis a notifiable condition?

A

Not any more

139
Q

How does neonatal conunctivitis present?

A

Sticky eyes i.e. purulent, mucopurulent, or mucoid discharge from one or both eyes.
Conjunctiva are typcally injected and lid is swollen.

140
Q

A neonate has a crusty, sticky eye. What are the differentials?

A
  • Ophthalmia neonatorum

- Blocked nasolacrimal duct

141
Q

How does presentation of blocked nasolacrimal duct differ to neonatal conjunctivitis?

A

Block nasolacrimal duct will not cause red conjunctiva or swollen eyelids, and the dischareg may be intermittent.

142
Q

If a neonate is taken to the GP with red and sticky eyes, what should happen?

A

They should be referred, always.

143
Q

What is erythema toxicum?

A

A common benign rash in neonates characterised by blotchy erythematous papules with pustules and vesicles.

144
Q

Is the cause of erythema toxicum known?

A

No, although it is thought to be an immune reaction due to high levels of eosinophils within the lesions.

145
Q

How common is erythema toxicum?

A

Very, especially in caucasian neonates.

146
Q

When does erythema toxicum typically present?

A

3 days to 2 weeks

147
Q

What is the characteristic behaviour of erythema toxicum lesions?

A

They appear and disappear within minutes to hours.

148
Q

Does ?erythema toxicum need to be investigated?

A

If the hx is clear, then no. If the picture is atypical, swab a pustule for infection.
If sepsis suspected, manage accordingly.

149
Q

Does erythema toxicum need treatment?

A

No it is self-limiting

150
Q

Are there any complications associated ith erythema toxicum?

A

Nope, not even an increased risk of atopy. Full resolution occurs within 2 weeks.

151
Q

What is haemolytic disease of the newborn?

A

A condition which results from transplacental passage of maternal antibodies which cause immune haemolysis of fetal/neonatal red blood cells.

152
Q

Which pathogenesis for haemolytic disease of the newborn is most commonly recongised?

A

Rhesus D alloimmunisation

153
Q

What iatrogenic causes are there for foetal-maternal transfusion which can precipitate haemolytic disease of the newborn?

A

Amniocentesis, chorionic villus sampling, cordocentesis.

154
Q

What blood groups do the parents need to be in order for rhesus snsitisation to occur?

A

Mother need to be rhesus negative, and father resus positive.

155
Q

What has reduced the incidence of haemolytic disease of the newborn in the estern world?

A

Use of Anti-D (rhesus D immunoglobulin administration to 1) Rh-neg pregnant women and 2) Rh-neg women post-natally from Rh-pos baby.

156
Q

Does rhesus alloimmunisation cause more serious issues during the primary exposure, or subsequent pregnancies?

A

Subsequent pregnancies because arge amounts of maternal anti-D antibodies are produced.

157
Q

How does rhesus alloimmunisation cause haemolytic disease of the newborn?

A

After a sensitising event, maternal anti-D antibodies cross the placenta and bind to foetal red cell. These are then recognised as “foreign” by the foetal immune system which subsequently recruits macrophages and lymphocytes to destroy its own red cells.

158
Q

How can haemolytic disease of foetus cause hydrops fetalis?

A

Rate of red cell destruction is greater than production, causing foetal anaemia, which leads to foetal heart failure, fluid retention, and swelling, causing foetal death.

159
Q

Why is moderate haemolytic disease of the newborn not a problem for the foetal liver?

A

RBC breakdown produces bilirubin which is cleared by the placenta when the foetus is in-utero.

160
Q

Why do newborns become jaundiced after birth due to haemolytic disease of the newborn?

A

Bilirubin is no longer cleared by placenta, and neonate liver is not capable of handling this amount of bilirubin, so unconjugated bilirubin enters circulation and causes jaundice.

161
Q

How do we screen to prevent haemolytic disease of the newborn?

A

Indirect Coomb’s test on mother at first antenatal booking for all rhesus negative women. Routine scans to pick up hydrops or foetal anaemia.

162
Q

How is foetal anaemia picked up antenatally?

A

Doppler scan of MCA vessel blood flow increased as metabolic demand of growing brain is not met. Performed if blood flow is abnormal or signs of heart failure (secondary to aneamia)

163
Q

When is a Direct Coomb’s test done?

A

Immediately after any birth to a rhesus negative mother - blood taken from cord or baby, as well as tested for blood groups, and Hb and bilirubin at baseline.

164
Q

How does management of haemolytic disease of the foetus differ from haemolytic disease of the newborn?

A

HDoF should be traeted with blood transfusion to foetus as soon as anaemia is confirmed, usually at 18 weeks. HDoN usually means there was no sensitisation until birth, management in-utero is not normally needed.

165
Q

What are the complications of haemolytic disease of foetus and newborn?

A

Kernicterus late onset anaemia, other concurrent metabolic disorders, hydrops.

166
Q

When is anti-D prophylaxis given?

A

Either 2 dose at 28 and 34 weeks, or one larger dose at 28 weeks.

167
Q

Under what circumstances is anti-d prophylaxis given?

A

All rh-neg women who have not been sensitised, and following abortion/miscarriage/amniocentesis/ectopic pregnancy/bdominal trauma.