Neonatology Flashcards

1
Q

Define neonate

A

From birth to 28 days of age

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2
Q

Admission to neonates

A

Birth - labour ward
PNW - postnatal week
Home - exchange transfer
Transfer from another hospital

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3
Q

Define early onset neonatal sepsis (EONS)

A

Sepsis occuring within the first 48-72 hours of life

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4
Q

Common PC for neonates

A
Prematurity
Respiratory distress - grunting
Cyanosis
Jaundice
Poor feeding
Weight loss
Know congenital abnormalities
Fractures/skull swelling
Concerns about sepsis
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5
Q

Causes of EONS

A

Chorioamnionitis perinatally via direct contact in the birth canal and haematogenous spread

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6
Q

Main organism of EONS

A
Group B streptococcus
- most common
- gram-positive coccus
- present in 25% of pregnant women's genital tract - infection via direct contact
E-coli
Coagulase-negative straphylococcus
H influenzae
Listeria monocytogenes
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7
Q

Risk factors for EONS

A

Invasive group B strep infection in previous baby
Maternal group B strep colonisation, bacteruria or infection in current pregnancy
Prelabour rupture of membranes
Preterm birth following spontaneous labour
Suspected or confirmed rupture of membranes for more than 18 hours in a preterm birth
Intrapartum fever higher than 38
Parental antibiotic treatment for invasive bacterial infection at anytime during labour - red flag
Suspected or confirmed infection in another baby in the case of multiple pregnancy - red flag

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8
Q

Clinical indicators suggestive of infection

A

Altered behaviour or responsiveness
Altered muscle tone (for example, floppiness)
Feeding difficulties (for example, feed refusal)
Feed intolerance, including vomiting, excessive gastric aspirates and abdominal distension
Abnormal heart rate (bradycardia or tachycardia)
Signs of respiratory distress
Respiratory distress starting more than 4 hours after birth (Red Flag)
Hypoxia (for example, central cyanosis or reduced oxygen saturation level)
Jaundice within 24 hours of birth
Apnoea
Signs of neonatal encephalopathy
Seizures (Red Flag)
Need for cardio–pulmonary resuscitation
Need for mechanical ventilation in a preterm baby
Need for mechanical ventilation in a term baby (Red Flag)
Persistent fetal circulation (persistent pulmonary hypertension)
Temperature abnormality (lower than 36°C or higher than 38°C) unexplained by environmental factors
Signs of shock (Red Flag)
Unexplained excessive bleeding, thrombocytopenia, or abnormal coagulation (International Normalised Ratio greater than 2.0)
Oliguria persisting beyond 24 hours after birth
Altered glucose homeostasis (hypoglycaemia or hyperglycaemia)
Metabolic acidosis (base deficit of 10 mmol/litre or greater)
Local signs of infection (for example, affecting the skin or eye

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9
Q

Red flag signs for suggestive neonatal infection

A

Systemic antibiotics given to mother for suspected bacterial infection within 24hr of birth
Seizures
Signs of shock
Resp distress starting more than 4 hours after birth
Need for mechanical ventilation in term baby
Suspected or confirmed infection in co-twin

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10
Q

Differential diagnosis for EONS

A

Transient Tachypnoea of the newborn (TTN) - in term babies, causes tachypnoea and increased work of breathing
Surfactant deficient lung disease / respiratory distress syndrome (RDS) - especially in preterm infants can cause tachypnoea and increased work of breathing
Meconium Aspiration - can cause the baby to be born in poor condition, with respiratory distress, and may require intubation. Meconium aspiration can cause a rise in CRP.
Haemolytic Disease of the Newborn - can present with jaundice within the first 24 hours of life.

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11
Q

Investigations for EONS

A
FBC
CRP
Blood cultures
Relevant swabs/cultures
LP - if suggestive of meningitis
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12
Q

Management of EONS

A

IV benzylpenicillin with gentamicin

  • if cultures + then continue for 7-10 days
  • up to 14 days if CSF also +
  • raised CRP but - cultures 5 days
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13
Q

Define jaundice

A

Yellow colouring of skin and sclera caused by the accumulation of bilirubin

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14
Q

Epidemiology of neonatal jaundice

A

60% of term infants

80% of preterm infants

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15
Q

Physiological causes of jaundice

A

Physiological - jaundice in a healthy baby born at term is normal
Starts at day 2-3, peaks at day 5 and resolved by day 10
- increased RBC breakdown-
- immature liver

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16
Q

Pathological causes of jaundice

A

Onset less than 24 hours = Haemolytic disease
- haemolytic disease of the newborn (rhesus)
- ABO incompatibility
- GPD deficiency
- spherocytosis
Onset after 24 hours
- likely dehydrated
- increased haemolysis due to bruising/cephalohematoma
Unwell neonate = congenital or post-natal infection
Prolonged jaundice - > 14 days in term and 21 days in preterm
- infection
- metabolic - hypothyroid/pituitarism, galactosaemia
- breast milk jaundice - well baby, resolves between 1.5-4 months
- GI - biliary atresia, choledhocal cyst

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17
Q

Define preterm birth

A

Delivery before 37 weeks

  • extreme = before 28 weeks
  • very = 28-32 weeks
  • moderate to late = 32 to 37 weeks
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18
Q

Epidemiology of preterm birth

A

15 million babies born premature each year
- 60,000 in UK
Number one cause of neonatal death globally
number 1 cause of death for under 5s

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19
Q

Risk factors for premature birth

A

Previous preterm delivery
Multiple pregnancy
Smoking and illicit drug use in pregnancy
Being under or overweight in pregnancy
Early pregnancy - within 6 months of previous pregnancy
Problems involving cervix, uterus or placenta - including infection
Certain chronic conditions such as diabetes and hypertension
Physical injury/trauma

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20
Q

Investigations for premature birth

A

Blood gas - assess resp and metabolic state of infant
FBC - high risk of infection, thrombocytopenia and anaemia
U+Es and creatinine - electrolyte and fluid balance
Blood culture
CRP
Blood group and Direct Coombs Test/Direct Antiglobulin Test - blood transfusion and jaundice
CXR - if showing signs of resp distress
AbdoX - central venous and arterial access inserted through umbilical vein and arteries
Cranial USS - assess for signs of haemorrhagic, ischaemic and infective factors

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21
Q

Initial management of preterm birth

A

Planned delivery in hospital with in tertiary level neonatal hospital
Antenatal steroids
Magnesium sulphate - neuroprotective

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22
Q

Guidelines around resuscitation of extreme pre-term infants

A

Less than 23 weeks - resuscitation not performed
23-23+6 weeks - decision not to start resuscitation in best interests of baby especially if parents agree
24 and 24+6 weeks - resuscitation commenced unless baby thought to be severely compromised
After 25 weeks - appropriate to resuscitate and start intensive care

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23
Q

Features of intraventricular haemorrhage

A

Parenchymal bleed due to immature BBB
Bleed during birth due to increased maternal and baby BP
Leads to cerebral palsy - managed by early physiotherapy

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24
Q

Features of surfactant deficiency

A

Difficulty breathing
Cyanosis
Intercostal recession
Increased RR, HR and reduced SaO2

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25
Q

Formation of lungs

A
Type 1 pneumocytes
- needed for gas exchange
- form at 32 wks
Type 2 pneumocytes
- produce surfactant
- form at 24 weeks
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26
Q

Investigations for infant respiratory distress

A

Blood gas - usually type 1 resp failure = low O2 and high CO2
CXR - acute respiratory distress syndrome
- cloudy, speckly = ground-glass sign

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27
Q

Differential diagnosis of respiratory distress in a newborn

A

Surfactant deficiency
Infection
Pneumonia

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28
Q

Management of surfactant deficiency

A

Antenatal steroids if signs of premature labour
Artificial surfactant - 1 per 12 hours
Long term = ventilation

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29
Q

Complications of long term ventilation of newborns

A

Bronchopulmonary dysplasia
- fibrosis of lung
- damage due to barotrauma
Most common in those ventilated from 32-36 weeks +
Increased risk of asthma and chest infections

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30
Q

Features of a patent ductus arteriosus

A

Machinery murmur - loudest at upper left chest
Breathlessness
Poor exercise tolerance
Rapid HR

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31
Q

Define patent ductus arteriosus

A

Unclosed hole in the aorta

- oxygenated blood travels from aorta into pulmonary artery

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32
Q

Management of PDA

A

Ibuprofen - anti-prostaglandin effect

Surgical ligation if unsuccessful

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33
Q

Define NEC

A

Nectrosting Encephalitis

- overgrowth of gut bacteria -> infection

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34
Q

Features of NEC

A
Vomiting + diarrhoea
Feeding intolerance
Abdo distention
Blood in stools
Tachycardia
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35
Q

Ix for NEC

A

Abdo x-ray

- pneumatosis intestinalis = train track sign

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36
Q

Mx for NEC

A

Nil by mouth
IV abx
Total parenteral nutrition
Surgical mx for perforated intestine - removal of affected section

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37
Q

Neurodevelopmental outcomes of premature babies

A

More premature = higher likelihood of neurodevelopmental impairment

  • infants born at 22 weeks, around 1/3 will have no or mild disability
  • increases to 75% at 26 weeks
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38
Q

Risk factors for neonatal jaundice

A
Prematurity, low birth weight or small for dates
Previous siblings requiring phototherapy
Exclusively breast fed
Jaundice < 24 hours
Infant of diabetic mother
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39
Q

Clinical presentation of neonatal jaundice

A

Colour - sclera, gums and blanche the ski
Drowsy - difficult to rouse, not waking for feeds
Neurology - altered muscle tone
Other - signs of infection, poor urine output, abdo mass/organomegaly, stool remains black

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40
Q

Ix for neonatal jaundice

A

Transcutaneous bilirubinometer
- >35/40 gestation and > 24hrs for 1st measurement
Serum bilirubin
- if <35/40 gestation, < 24hrs old or TCB > 250 micromol/L
Only if appear jaundiced to naked eye

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41
Q

Mx for neonatal jaundice

A

Interpret bilirubin using treatment threshold graphs
- gestation specific - the more premature infant the lower level of bilirubin tolerated before neurological impairment
If above live initiated phototherapy and monitor bilirubin
Do not give additional fluids unless indicated
Exchange transfusion
- prevent further bilirubin increase
- via umbilical artery or vein
IV Immunoglobulin
- adjunct to phototherapy in rhesus haemolytic disease of ABO haemolytic disease

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42
Q

Complications of neonatal jaundice

A

Kernicterus

  • bilirubin-induced brain dysfunction
  • irreversible neurological damage to to high bilirubin
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43
Q

Define meconium aspiration syndrome

A

Spectrum of disorders marked by various degrees of respiratory distress in the newborn infant
- follows the aspiration of meconium stained amniotic fluid either antenatally or during birth

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44
Q

Pathophysiology of meconium aspiration syndrome

A

Meconium stained amniotic fluid (MSAF) caused by in-utero peristalsis
- result of foetal hypoxic stress or vagal stimulation due to cord compression
Once aspirated can stimulate the release of vasoactive and cytokine substances
- activate inflammatory pathways
- inhibits effect of surfactant

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45
Q

Common features of MAS-related respiratory distress of the newborn

A

Partial or total airway obstruction - due to thick sticky consistency of meconium
-> atelectasis and ball-valve effect with air trapping
Foetal hypoxia - due to V/Q mismatch, increase of pulmonary vasculature, mechanical obstruction, airway oedema or surfactant inactivation
Pulmonary inflammation
- release of pro-inflammatory cytokines - tumour necrosis factor and interleukins
- contribute to lung tissue, injury, surfactant inactivation and infection
Infection
- inflammation process predisposes lung to increased risk of infection and chemical pneumonitis
Surfactant inactivation
- increases surface tension of alveoli
- reduces efficiency of gas exchange and exacerbates foetal hypoxia
Persistent Pulmonary Hypertension
- due to remodelling of pulmonary vasculature in response to hypoxia, vasoactive mediators and V/A mismatch

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46
Q

Risk factors for MAS

A

Gestational Age > 42 weeks
Foetal distress - tachycardia / bradycardia
Intrapartum hypoxia secondary to placental insufficiency
Thick meconium particles
Apgar Score <7
Chorioamnionitis +/- prolonged pre-rupture
Oligohydramnios
In utero growth restriction Maternal hypertension, diabetes, pre-eclampsia or eclampsia, smoking and drug abuse

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47
Q

Investigations for MAS

A
Diagnosis of exclusion
CXR
- increased lung volumes
- asymmetrical patchy pulmonary opacities
- pleural effusions
- pneumothorax or pneumomediastinum
- multifocal consolidation - due to chemical pneumonitis
Infection markers
- FBC
- CRP
- blood cultures
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48
Q

Ddx of MAS

A
Transient tachypnoea of the newborn
- usually resolves in 24hrs without intervention
- no hypoxia or cyanosis
Surfactant deficiency
- causes resp distress
- more commonly seen in pre-term infants
- no MSAF at delivery
Persistent pulmonary hypertension
- PDA
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49
Q

Management of MAS

A
Observation
Routine care
- infant warmer
- continuous O2 sats
- nutritional support - IV fluids 
Ventilation/O2 therapy
- nasal cannula
- CPAP
- intubation and mechanical ventilation
Antibiotics
- if clinical suspicion of infection
- stopped if negative blood cultures return
Surfactant
Inhaled Nitric Oxide
- pulmonary hypertension
Corticosteroids
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50
Q

Complications of MAS

A
Air leak
- pneumothorax or pneumomediastinum
PPHN
- persistent pulmonary hypertension of the newborn
Cerebral palsy
- due to cerebral hypoxia
Chronic lung disease
- develop from barotrauma and oxygen toxicity
51
Q

Define failure to thrive

A

Poor physical growth and development in a child

  • 1+ centile spaces if birthweight below 9th centile
  • 2+ centile spaces if birthweight between 9th and 91st centile
  • 3+ centile spaces if birthweight above 91st centile
52
Q

Causes of failure to thrive

A
Inadequate nutritional intake
- maternal malabsorption if breastfeeding
- iron deficiency anaemia
- family or parental problems
- neglect
- availability of food
Difficulty feeding
- poor suck
- cleft lip or palate
- pyloric stenosis
Malabsorption
- CF
- coeliac disease
- cow's milk intolerance
- chronic diarrhoea
- IBD
Increased energy 
requirements
- hyperthyroidism
- chronic diseases
- malignancy
- chronic infections
Inability to process nutrition
- inborn errors of metabolism
- DM T1
53
Q

Types of learning disabilities

A

Dyslexia - difficulty reading, writing and spelling
Dysgraphia - difficulty writing
Dyspraxia - developmental co-ordination disorder
Auditory processing disorder
Non-verbal learning disability
Profound and multiple learning disability

54
Q

Define Down’s syndrome

A

Trisomy 21 - 3 copies of chromosome 21

55
Q

Dysmorphic features of Down’s syndrome

A

Hypotonia (reduced muscle tone)
Brachycephaly (small head with a flat back)
Short neck
Short stature
Flattened face and nose
Prominent epicanthic folds - folds of skin over the medial portion of the eye and eyelid
Upward sloping palpable fissures - gaps between lower and upper eyelid
Single palmar crease

56
Q

Complications of Down’s syndrome

A

Learning disability
Recurrent otitis media
Deafness - Eustachian tube abnormalities lead to glue ear and conductive hearing loss
Visual problems - myopia, strabismus and cataracts
Hypothyroidism
Cardiac defects - ASD, VSD, patent ductus arteriosus and tetralogy of Fallot
Atlantoaxial instability
Leukaemia is more common in children with Down’s
Dementia is more common in adults with Down’s

57
Q

Antenatal screening for Down’s sydnrome

A

Combined test
- performed between 11 and 14 weeks
- USS measures nuchal translucency - over 6 mm
- beta-human chorionic gonadotrophin (beta-HCG) - high
- pregnancy-associated plasma protein-A (PAPPA) - low
Triple test
- 14 and 20 weeks gestation
- Beta-HCG
- Alpha-fetoprotein (AFP) - low
- Serum oestriol (female sex hormone) - low

58
Q

Define cerebral palsy

A

Non-progressive, permanent impairment of motor-postural development neurological problems resulting from damage to the immature brain

59
Q

Causes of cerebral palsy

A
Antenatal
- maternal infections
- trauma
Perinatal
- birth asphyxia
- pre-term birth
- intraventricular haemorrhage
Postnatal
- meningitis
- severe neonatal jaundice
- head injury
60
Q

Types of cerebral palsy

A
Spastic 
- hypertonia and reduced function
- upper motor neurons
Dyskinetic
- Athetoid = abnormal, involuntary movements affecting extremities, facial grimacing and drooling, feeding and speech impairment, hypotonia, normal reflexes
- Dystonic - prolonged, slow, repetitive movements, abnormal posturing, hypotonia and normal reflexes
- damage to basal ganglia
Ataxic
- problems with coordinated movement
- damage to cerebellum
Mixed
61
Q

Patterns of Spastic Cerebral palsy

A

Monoplegia - one limb
Hemiplegia - one side on body affected
Diplegia - four limbs affected - mostly legs
Quadriplegia - four limbs affected

62
Q

Presentation of cerebral palsy

A

Failure to meet milestones
Increased or decreased tone, generally or in specific limbs
Hand preference below 18 months
Problems with coordination, speech or walking
Feeding or swallowing problems
Learning difficulties

63
Q

Gait features

A
Hemiplegic / diplegic gait = upper motor neurone lesion
Broad based gait / ataxic gait = cerebellar lesion
High stepping gait = foot drop or a lower motor neurone lesion
Waddling gait = pelvic muscle weakness due to myopathy
Antalgic gait (limp) =  localised pain
64
Q

Features of upper motor neurone lesion

A

Muscle bulk preserved
Hypertonia
Slightly reduce power
Brisk reflexes

65
Q

Features of lower motor neurone lesion

A

Reduced muscle bulk and fasciculations
Hypotonia
Dramatically reduced power
Reduced reflexes

66
Q

Complications/associated conditions of cerebral palsy

A
Learning disability
Epilepsy
Kyphoscoliosis
Muscle contractures
Hearing and visual impairment
Gastro-oesophageal reflux
67
Q

Mx of cerebral palsy

A

MDT approach

  • physio
  • occupational therapy
  • speech and language
  • dieticians
  • orthopaedic surgeons
    • tenotomy
  • paediatrician
    • muscle relaxants
    • anti-epileptic drugs
    • glycopyrronium bromide - excessive drooling
68
Q

Define autsim

A

Spectrum of conditions which affect social and communication skills

69
Q

Rks factors for ASD

A

Male sex
FHx
Fragile X syndrome

70
Q

Clinical features of ASD

A

Social skills
- poor eye contact, difficulty empathizing, social cues being missed, lack of imaginative play
Language
- speech delay, literal interpretation of language, restricted gestures and facial expressions, echolalia
Repetitive behaviour
- hand flapping, tiptoe gait, unusual interests, strict routine adherence

71
Q

Mx of ASD

A

Biological
- co-morbidities
- community paediatrician coordinates
- antipsychotics for aggression - risperidone
- melatonin for severe sleep dysregulation
Psychological
- support groups and counselling for family
- psychological comorbidities common
Social
- applied behavioural analysis
- education support at school

72
Q

Define ADHD

A

Presence of hyperactivity, impulsiveness and inattention

73
Q

Risk factors for ADHD

A

Male
Fhx of ADHD, learning difficulties or substance misuse
In utero exposure to alcohol/nicotine

74
Q

Clinical features of ADHD

A

Inattention
Hyperactivity
Impulsiveness
Usually present with concerns raised by school staff or parents or difficulty with schooling/school refusal

75
Q

Mx of ADHD

A
MDT approach
Social
- behaviour management centred around routines and consistency
- positive reinforcement
- parental training
Biological
- Methylphenidate - CNS stimulant
76
Q

Side effects of methylphenidate

A
Anxiety
Tremors
Hypertension
Insomnia
Anorexia
Hyperhidrosis
77
Q

Method of action of methylphenidate

A

Blocks both dopamine and noradrenaline transporters on synaptic membrane
Inhibits reuptake of dopamine and noradrenaline
Net increase in dopamine and noradrenaline in neuronal synapses
Increased neurotransmission of substances

78
Q

Foetal circulation

A

Oxygenated blood carried through umbilical vein
- enters foetal circulation via ductus venosus into inferior vena cava
IVC drains into the right atrium
- foraeman ovale patent - shunts most blood from right to left
- right sided pressure greater than left
- shunted blood bypasses lungs
Some blood remains on right side leaves via pulmonary artery
- blood flows through patent ductus arteriosus between pulmonary artery and aorta
Deoxygenated blood flows back to placenta via umbilical arteries

79
Q

Circulation changes during birth

A

Removal of placenta
Onset of breathing
Rapid reduction in pulmonary vascular resistance
Closure of shunts - ductus arteriosus, ductus venosus and foramen ovale
Physiology
- amniotic fluid in lungs displaced by squeezing within birth canal
- onset of breathing increases PaP2 and normalises pH and PaCO2 - induce pulmonary vasodilation and reduce pulmonary resistance
- clamping umbilical cord immediately increases systemic vascular resistance
- left atrial pressure now exceeds right atrial pressure -> foramen ovale closes
- Increase in PaO2 triggers closure of ductus arteriosus

80
Q

GI tract changes

A

Develops as a tube from 6 weeks gestation
Foetus swallows amniotic fluid from 16 weeks gestation
- proteins from mother including antibodies transferred to feotus
Nutrients absorbed via gut from 25 weeks gestation
Coordination of suck and swallow develops after 34 weeks gestation

81
Q

Hepatic function changes

A

Neonatal liver has little function
- toxin filtering and metabolism are performed by placenta
After birth liver adjusts but will not reach full capacity for a few months
- neonatal drugs given at low doses because of immaturity in metabolic function

82
Q

Define perinatal mortality rate

A

Number of still births and neonatal deaths within first week of life per 1000 live births

83
Q

Define neonatal mortality rate

A

Total deaths per 1000 live births in first 28 days

84
Q

Risk factors for prematurity/IUGR

A
Multiple pregnancy
Maternal illness
Placental insufficiency
In utero infection
Genetic disorder
85
Q

Types of IUGR

A

Symmetrical
- IU infections and chromosomal abnormalities
- proportionally small head, length and weight
Asymmetrical
- maternal or placental issues - placental insufficiency or pre-eclampsia
- small length and weight, with preserved head size

86
Q

Define prematurity

A

Any birth before 37/40

87
Q

Define IUGR

A

Failure of foetus to achieve genetic growth potential

88
Q

Define SGA

A

Small for gestational age

Newborn below certain centile for particular gestation - usually 10th centile

89
Q

Define LBW

A

Low birth weight

- less than 2500g

90
Q

Define VLBW

A

Very low birth weight

- less than 1500g

91
Q

Define stillbirth

A

Foetus born after 24/40 that never shows signs of life

92
Q

Define neonatal death

A

Death of newborn within 28 days of delivery

93
Q

Define hypoglycaemia

A

Blood sugar < 2.6 mmol/L

94
Q

Causes of hypoglycaemia of the newborn

A
Reduced glucose production
- preterms
- metabolic errors
Increased glucose demands
- sepsis
- hypothermia
Hyperinsulinism
- diabetic mother
Endocrine problems
95
Q

Mx of hypoglycaemia of newborn

A

1.6-2.6 mmol/L and asymptomatic
- feed infant
- consider increasing feed frequency
Severe (<1.6 mmol/L) or symptomatic
- IV dextrose
- admit to neonatal unit and monitor blood sugars hourly till stable
- hypo screen - identify common endocrine and metabolic aetiologies

96
Q

Define RDS

A

Respiratory distress syndrome

  • hyaline membrane disease
  • condition of prematurity caused by insufficient levels of surfactant
  • manifests as a tachypnoeic newborn
97
Q

Pathophysiology of RDS

A

Lack of surfactant in the lungs due to prematurity or effect inhibited by asphyxia

  • surfactant lowers alveolar surface tension
  • loss of surfactant results in alveolar collapse
98
Q

Risk factors for RDS

A
Prematurity
Perinatal asphyxia
- difficult birth
- meconium aspiration
- sepsis
- congenital lung abnormalities
Maternal diabetes - delayed lung maturity
99
Q

Clinical features of RDS

A
Distressed and unwell infant
Poor feeding
Tachypnoea > 60 breaths per minute
Hypoxia
Respiratory distress - intercostal and subcostal recession, head bobbing, tracheal tug and nasal flaring
Grunting
100
Q

Mx of RDS

A

Oxygen - aiming for pO2 6-10
CPAP and mechanical ventilation
Artificial surfactant - increase lung compliance and decrease alveolar surface tension

101
Q

Define IVH

A

Intraventricular hemorrhage

  • alteration in cerebral blood flow results in bleeding in the fragile germinal matrix
  • if severe enough spreads to ventricles
  • most commonly before 32 weeks as germinal matrix disappears in 3rd trimester
102
Q

Define PVL

A

Periventricular leukomalacia

- hypoperfusion and excitotoxic cytokines causes damage to oligodendroglia resulting in white matter injury

103
Q

Risk factors for neonatal brain injury

A
VLBW
Gestation less than 32 weeks
Difficult birth
RDS
Cardiovascular instability
Other prematurity complications
104
Q

Clinical features of IVH

A
Often asymptomatic 
Seizures and apnoeas with big bleeds
Floppy infant with poor feeding
Abnormal movements or tone
Large IVH may present with hypovolaemic neonate - tachycardia, peripherally shut down
105
Q

Mx of IVH

A

ABCDE approach

Maintain good blood pressure and oxygen/CO2 level control

106
Q

Mx of PVL

A

Aim is prevention - avoiding large blood pressure fluctuations and hypoxia

107
Q

Grades of IVH

A

Grade 1 - isolated to germinal matrix
Grade 2 - haemorrhage into ventricles, no dilation
Grade 3 - haemorrhage into ventricle with acute dilation
Grade 4 - parenchymal haemorrhagic infarct

108
Q

Risk factors for neonatal infection

A
Prematurity
Maternal pyrexia in labour
Premature rupture of membranes (PROM)
LBW
Long lines in situ
Chorioamnionitis
Maternal group B strep colonization
109
Q

Clinical features of neonatal infection

A

Clinically deteriorating neonate
Poor feeding
Obs deranged - HR and BP late changes
Crepitations, bowel sounds, organomegaly, rash, abdo distended, fontanelle sunken or bulging

110
Q

Mx of neonatal infection

A

Abx treatment - commenced < 1 hour of suspicion

  • early onset (<72 hours) = IV penicillin + IV aminoglycoside
  • late onset (>72 hours) = IV flucloxacillin + IV aminoglycoside
  • acyclovir to cover potential HSV infection
111
Q

RF for NEC

A
ORal feeding - formula higher risk than breast milk
PRematurity
Concurrent infection
LBW/VLBW
IUGR
Perinatal asphyxia
112
Q

Causes of neonatal jaundice

A
Less than 24 hrs = haemolytic or infection
- haemolytic disease of the newborn - ABO or rhesus incompatibility
- G6PD deficiency
- hereditary spherocytosis
- alpha thalassemia
24 hours - 14 days = physiological
- immature liver
- high haemoglobin levels
Longer than 14 days
- breast milk jaundice
- biliary atresia 
- infection
113
Q

Define kernicterus

A

Bilirubin encephalopathy

114
Q

Pathophysiology of kernicterus

A

Result of excess unconjugated bilirubin crossing the BBB

Any illness causing systemic acidosis disrupts the BBB making kernicterus more likely

115
Q

Risk factors for kernicterus

A

High unconjugated bilirubin
Sepsis
Acidosis

116
Q

Complications of kernicterus

A

Cerebral palsy
Deafness
Intellectual disability

117
Q

Pathophysiology of cleft lip/palate

A

Normal development of facial structures interrupted in utero

  • lip and nose develop between 3rd and 7th week
  • palate forms between th and 12th week
  • interruptions before the 7th week will result in cleft left which will extend into primary (anterior) portion and after 8th week will result in a cleft of larger secondary portion
118
Q

Risk factors of cleft lip/palate

A

Aneuploidy/genetic syndrome
FHx
Maternal drug use, smoking and alcohol

119
Q

Symptoms of cleft lip

A

Difficulty establishing feeds
Recurrent chest infections - from aspirations
Faltering growth

120
Q

Mx of cleft lip/palate

A

Medical
- MDT - paediatrician, SALT, maxillofacial surgeon, orthodontist, ENT, cleft nurse specialist, geneticist
- feeding support
Surgical
- lip repair around 3 months
- palate repair at 6-12 months
- further orthodontic surgery
- long term follow up for ENT - otitis media and Eustachian tube difficulties
Psychological
- reassure that surgical outcomes are good
- support groups - CLAPA and Operation Smile

121
Q

Pathophysiology of spina bifida

A

Brain and spinal cord develop from ectoderm-derived neural tube
Failure of caudal end of tube to close
- normally closes days 17-30 of gestation

122
Q

Types of spina bifida

A

Spina bifida occulta (SBO)
- vertebral arch defect with an intact spinal cord
- clinically apparent as a hairy patch of skin over area
- no neurological defect
Meningocele
- vertebral arch defect with herniation of the meninges but no the spinal cord
- covered with skin
- prognosis following surgery is good - < 10% developing neurological impairment or hydrocephalus
Myelomeningocele
- thoracolumbar defect with herniation of the meninges and spinal cord
- only meninges covering neural tissue - no skin
- prognosis depends on level and extent of lesion

123
Q

Risk factors for spina bifida

A

Maternal folic acid deficiency - up to 50% of cases
Maternal medications - anti-epileptics
Maternal diabetes
Fhx

124
Q

Mx of spina bifida

A

Medical
- for severe defects - MDT management at tertiary centre - neurosurgeons, paediatricians, orthopaedics, urology, child development, psychology
- mx of neuropathic bladder
Surgical
- meningocele and myelomeningocele managed with surgical closure
- close monitoring for development of hydrocephalus
Psychosocial
- specialist nurses and early psychological support