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Paediatrics > Neonatology > Flashcards

Neonatology Flashcards

1
Q

Define neonate, low birth weight, very low birth weight, and extremely low birth weight

A

First 28 days of age
<2.5kg
<1.5kg
<1 kg

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2
Q

What are appearance and maturational differences of very preterm infants?

A

Gestation 23-27 weeks
Birthweight: 600-700g
Skin: very thin, dark red colour all over body
Ears: Pinna soft, no recoil
Breast: no breast tissue palpable
Genitalia:
Male - scrotum smooth, no testes in scrotum (no rugae)
Female - Clitoris and labia minora protruding (not covered), labia Majora separated
Breathing: needs respiratory support, apnoea common
Sucking and swallowing: no coordinated sucking
Feeding: needs parenteral nutrition andntuve feedinf
Cry: faint
Vision: eyelids fused, infrequent eye movements, no eye contact/interaction
Hearing: startles to loud noise
Posture: limbs extended, jerky movements

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3
Q

Complications of prematurity

A 
Resuscitation 
Respiratory distress syndrome
Pneumothorax
Apnoea and bradycardia
Hypotension
Patent ductus arteriosus
Temperature control
Metabolic: hypoglycaemia, hypocalcaemia, electrolyte imbalance, osteopenia of prematurity
Nutrition
Infection
Jaundice
Intraventricular haemorrhage/periventricular leukomalacia 
Necrotising enterocolitis
Retinopathy of prematurity 
Anaemia of prematurity
Iatrogenic
Bronchopulmonary dysplasia
Inguinal hernia
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4
Q

What are the interventions in Resuscitation and stabilisation of preterm infants

A

A + B: clear airway, oxygen, CPAP or high flow nasal cannula, mechanical ventilation

C: 
Peripheral intravenous line
Umbilical venous line
Arterial line - if frequent blood gas or continuous BP monitoring 
PIC line for parenteral nutrition

Temperature:
Place in plastic bag
Stabilisation under radiant warmer, heated mattress, or humidified incubator (evaporative heat loss)

CXR
Broad spectrum antibiotics
Minimal handling (affects oxygenation and circulation)

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5
Q

Pathophysiology of respiratory distress syndrome

A

Surfactant is mixture of phospholipid/protein produced by T2 pneumoncytes that lowers surface tension
Deficient in surfactant
Alveolar collapse and impaired gas exchange

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6
Q

Clinical and radiographic features of respiratory distress syndrome

A

Tacypnoea >60/min
Laboured breathing: chest wall recession, nasal flaring
Expiratory grunting (to create positive pressure during expiration)
Cyanosis
CXR: granular, ‘ground glass’ appearance

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7
Q

Management of RDS

A

Raised ambient Oxygen therapy
Surfactant therapy via tracheal tube/catheter
Non-invasive ventilation: CPAP, High-flow nasal cannula
Mechanical ventilation

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8
Q

What are the features of oxygen therapy in preterm infants

A

21-30% oxygen used
91-95% O2 sats maintained
Because hyperoxia is damaging from excess free radicals, increased risk of retinopathy of prematurity
And low saturations increase risk of necrotising enterocolitis/death

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9
Q

Pathophysiology of pneumothorax in preterm infant

A

In RDS, air from alveoli may track into interstitium and cause pulmonary interstitial emphysema (air outside alveolar air space)
When ventilated, air leaks into pleural cavity and cause pneumothorax
Occurs in 10% infants ventilated for RDS

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10
Q

How can you detect pneumothorax in preterm infants

A

Transillumination with fibre optic light applied to chest wall
CXR

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11
Q

How can you prevent pneumothorax in preterm infants

A

Ventilated with lowest pressures that provide adequate chest movement and satisfactory blood gases

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12
Q

What are causes of bradycardia and apnoea in preterm infants

A 
Bradycardia: infant stops breathing for 20-30 seconds or against closed glottis
Immaturity of central respiratory control
Hypoxia
Infection
Anaemia
Electrolyte disturbance
Hypoglycaemia
Seizures
Heart failure
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13
Q

Management of apnoea in preterm infants

A

Physical stimulation

Caffeine

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14
Q

Why are preterm infants vulnerable to hypothermia

A

Large SA:Mass ratio - heat loss > heat generation
Skin thin and permeable - greater evaporative water loss
Little subcutaneous fat for insulation
Cannot conserve heat by curling up
Cannot generate heat by shivering

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15
Q

Why is it important to avoid hypothermia in preterm infants

A

Increased energy consumption
Hypoxia
Hypoglycaemia
Failure to gain weight

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16
Q

Measures for temperature control in newborn infants

A

Convection:
Raise temperature of air in incubator
Clothing
Avoid draughts

Radiation:
Cover baby
Double walled incubator

Evaporation:
Plastic bag at birth without drying
Humidify incubator

Conduction:
Heated mattress

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17
Q

What are clinical features of patent ductus arteriosus

A

Asymptomatic
Apnoea and bradycardia
Difficulty weaning from artificial ventilation (Respiratory problems from increased flow)

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18
Q

Management of patent ductus arteriosus

A

Diuretics + fluid restriction
Ibuprofen
Prostaglandin synthase inhibitor
Surgical ligation

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19
Q

Management of nutrition in preterm infants

A

NGT feeding: until 35-36 weeks gestational age, cannot suck and swallow milk

Fortified Breast milk:
introduced as soon as possible
Maternal, donor, formula
Phosphate, vitamin D, calcium supplements added (prevent osteopenia of prematurity)

Parenteral nutrition: PIC line or umbilical venous Catheter
Increased risk of sepsis or thrombosis in major vein

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20
Q

Pathophysiology of necrotising enterocolitis

A

Due to GI prematurity, bowel is vulnerable to ischaemic injury and bacterial infection

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21
Q

Risk factors for necrotising pancreatitis

A

Increasing prematurity
Cows milk formula feed
Rapid increase in feed

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22
Q

Clinical features of necrotising enterocolitis

A

Feed intolerance
Bilious vomiting
Abdominal distension, tense and shiny skin of abdomen
Blood stained stool
Shock
X Ray: intramural air, distended bowel loops, air in portal tract

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23
Q

Management of anaemia of prematurity

A

Nutrition

Iron supplements

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24
Q

What are the types of brain injuries in preterm infants

A

Haemorrhage: germinal layer, intraventricular, parenchymal (+infarction)

Ventricular dilatation: due to large IVH, can resolve or progress
Tx with LP, ventriculoperironeal shunt

Periventricular white matter injury:
Ischaemic white matter injury
Periventricular leukomalacia - bilateral multiple cysts on cranial USS

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25
Q

Risk factors for brain injuries in infants

A

Perinatal asphyxia
RDS
Pneumothorax

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26
Q

Consequences of brain injuries in preterm infants

A

Hemiplegia
Hydrocephalus
Cerebral palsy

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27
Q

What is bronchopulmonary dysplasia

A

Need for supplemental oxygen for at least 28 days after birth
Aka chronic lung disease

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28
Q

Cause of BPD

A

Delay in lung maturation
Trauma from mechanical ventilation
Oxygen toxicity
Infection

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29
Q

Management of BPD

A

Early extubation: wean to CPAP or high flow nasal cannula

Caffeine therapy: for apnoea

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30
Q

Prognosis of BPD

A

Need for home oxygen therapy

No other long term lung complications

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31
Q

Prevalence of neonatal jaundice

A

50% neonates

80% preterm infants

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32
Q

Classification of neonatal jaundice

A

Physiological: appears 2-4 days after birth and resolves 1-2 weeks later
Pathological: any jaundice in first 24 hours of life
Prolonged: jaundice for > 2 weeks or >3 weeks in premature neonate

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33
Q

Physiology of neonatal jaundice

A

Physiological:
Increased RBC turnover and Increased Hb lysis due to increased adult Hb synthesis and breakdown of fetal Hb
Less efficient hepatic bilirubin metabolism

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34
Q

Causes of pathological neonatal jaundice

A

<24hours:
Haemolytic anaemia - Rhesus/ABO incompatibility, G6PD deficiency, spherocytosis
Congenital infection - TORCH

24hrs - 2 weeks: 
Physiological 
Breast milk jaundice
Infection
Haemolysis
Bruising
Polycythaemia
Inborn errors of metabolism (Crigler-Najjar Syndrome ) 
>2weeks: 
Unconjugated - 
Physiological, Breast milk jaundice
Infection (UTI) 
Hypothyroidism 
Haemolytic anaemia
Upper GI obstruction 
Conjugated - 
Bile duct obstruction 
Neonatal hepatitis 
TPN
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35
Q

What is breast milk jaundice

A

Unconjugated jaundice, Jaundice more prolonged and common in breastfed infants

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36
Q

What is Crigler-Najjar Syndrome

A

Rare syndrome of glucuronyl transferase deficiency causing defective conjugation and unconjugated jaundice

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37
Q

Investigations for neonatal jaundice

A

Transcutaneous bilirubinometer: screening test for all babies in first 72hrs of life
Total serum bilirubin: confirms diagnosis, pathological >205

Direct Coombs test
Direct serum bilirubin 
FBC 
Peripheral blood smear
Blood groups
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38
Q

Assessment of neonatal jaundice

A

Severity: blanching skin (starts at head and spreads down), transcutaneous bilirubinometer, total serum bilirubin
Gestation: lowers threshold for intervention
Age: <24hrs haemolytic anaemia likely, >2wks need to check conjugated or unconjugated
Well or unwell: evidence of sepsis, dehydration
Investigations

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39
Q

Management of neonatal jaundice

A

Unconjugated:
Phototherapy
Hydration
Exchange transfusion

Kernicterus:
Immediate exchange transfusion

Conjugated:
Treat underlying cause

Breast milk jaundice:
Temporary cessation of breast feeding and supplemental feeding

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40
Q

What is phototherapy

A

Blue-green light delivered, to convert unconjugated bilirubin into harmless water soluble pigment excreted in urine
Contraindicated in conjugated jaundice: bronze discolouration of skin

41
Q

What is exchange transfusion

A

Blood removed from baby in small aliquots and replaced with donor blood
Indicated if bilirubin Levels rise to dangerous levels
Immediate transfusion required If signs of kernicterus

42
Q

What is kernicterus

A

Encephalopathy from deposition of unconjugated bilirubin in basal ganglia and brainstem nuclei
Bilirubin is neurotoxic (impairs mitochondrial function and metabolism) and preferentially taken up by basal ganglia, caudate nuclei, putamen, globus pallidus
Hyperbilirubinaemia high risk in neonates - developing BBB allows for bilirubin to enter CNS

43
Q

Clinical features of kernicterus

A

Early: lethargy, hypotonia, poor sucking, high pitched cry
Intermediate: irritable, variable tone, high pitched cry
Advanced: hypertonia - opisthotonos (arched back), deep stupor or coma

44
Q

Long term consequences of kernicterus

A

Choreathetoid cerebral palsy
Learning difficulties
Sensorineural deafness

45
Q

Management of necrotising enterocolitis

A

Prevention: antenatal steroids, human breast milk feed, probiotic supplementation
Stop oral feed
Broad spectrum antibiotics
Parenteral nutrition
Ventilation and circulatory support
Surgery: complications - short gut syndrome, TPN dependence, chronic cholestasis

46
Q

Define hypoxic-ischaemic encephalopathy

A

Hypoxic-ischaemic injury to brain due to perinatal asphyxia

47
Q

Pathophysiology of HIE

A

Perinatal hypoxia-ischaemic event
Cardiorespiratory depression
Hypoxaemia, Hypercarbia -> Respiratory acidosis
Reduced cardiac output -> Reduced tissue perfusion -> Metabolic acidosis
Encephalopathy + multi-organ dysfunction

Reperfusion injury and secondary neuronal damage

48
Q

Clinical features of HIE

A 
Mild: 
Irritable
Responds excessively
Hyperventilation
Hypertonia
Impaired feeding
Moderate: 
Abnormal response/movement 
Hypotonia
Cannot feed
Seizures

Severe:
No spontaneous movement, no response to pain
Fluctuating tone
Seizures - prolonged and refractory to treatment
Multi-organ failure

49
Q

Management of HIE

A 
Resuscitation and stabilisation:
Respiratory support
Tx Hypotension with fluid and inotropes
Fluid restriction for renal impairment 
Anticonvulsants for seizures 
Tx hypoglycaemia, electrolyte imbalance

Amplitude-integrated EEG:
To confirm encephalopathy and detect seizures

Mild therapeutic hypothermia:
Cooling with cooling blanket within 6hrs of birth to temp 33
For mod-severe HIE: improve survival wo disability
Neuroprotection from reperfusion injury

50
Q

Prognosis of HIE

A

Mild: complete recovery
Clinical abnormalities persist >2 weeks: poor
Severe: high mortality, high risk of CP

51
Q

Define perinatal/birth asphyxia

A

Evidence of hypoxia antenatally or during labour
Resuscitation needed at birth
Features of encephalopathy
Evidence of hypoxic damage to other organs
No other cause identified (e.g. kernicterus)

52
Q

Classification of neonatal infection

A

Early onset: <48hrs after birth

Late onset: >48hrs after birth

53
Q

What are the red flag risk factors for neonatal sepsis

A

Invasive GBS infection in previous baby
Maternal GBS colonisation/bacteriuria/infection current pregnancy
PROM
Preterm birth Following spontaneous labour
Rupture of membranes >18hrs in a preterm birth
Intrapartum Fever >38, suspected/confirmed chorioamnionitis

54
Q

What are the red flag clinical features of neonatal sepsis

A

Jaundice within 24 hrs
Altered behaviour or responsiveness
Altered muscle tone
Feeding difficulties
Feed intolerance - vomiting, excessive gastric aspirates, abd distension
Abnormal HR
Signs of respiratory distress
Hypoxia
Apnoea
Signs of neonatal encephalopathy
Need for cardio-pulmonary resuscitation
Need for mechanical ventilation in term baby
Persistent fetal circulation (persistent pulm hypertension)
Temperature abnormality (<36, >38) unexplained by enviro factors
Unexplained excessive bleeding, thrombocytopenia, abnormal coagulation
Oliguria persisting beyond 24hrs after birth
Hypo/hyperglycaemia
Metabolic acidosis
Local signs of infection

55
Q

Causative organisms of early onset infection

A

GBS
E. Coli
Listeria monocytogenes

56
Q

Clinical features of neonatal meningitis

A 
Tense or bulging fontanelle 
Head retraction (opisthotonos)
57
Q

Investigations for neonatal sepsis

A 
Blood culture
FBC
CRP
Swabs/urine If signs of local infection present 
Lumbar puncture
58
Q

Antibiotics for neonatal infection

A

IV benzylpenicillin + gentamicin

Cover gram +ve and -ves

59
Q

What types of infections does GBS cause and how do they present

A

Early onset: pneumonia, sepsis, meningitis

Late onset: meningitis, osteomyelitis, septic arthritis

60
Q

How is Listeria monocytogenes transmitted

A

To mother In food - unpasteurised milk, soft cheese, undercooked poultry
Causes bacteraemia and transmission to baby via placenta

61
Q

Clinical features of neonatal L monocytogenes infection

A 
Meconium stained liquor 
Wide spread rash 
Pneumonia
Sepsis
Meningitis
62
Q

How is HSV transmitted and what is the risk of transmission

A

During passage through birth canal
Ascending infection of amniotic fluid

High if primary infection in late pregnancy
Low if recurrent maternal infection

63
Q

Consequences of neonatal herpes

A

Localised herpetic lesions on skin, eye
Encephalitis
Sepsis

64
Q

Management of umbilical infection

A

Systemic antibiotics
Silver nitrate
Ligature around base of stump

65
Q

Causes of sticky eyes in neonates

A

Physiological
Staph/strep infection
Gonoccocal incecfion
Chlamydia trachomatis

66
Q

Clinical features for each cause of sticky eyes

A

Physiological: washes off with saline/water
Staph/strep: troublesome discharge, redness of eye
Gonococcal: purulent discharge, conjunctival injection, lid swelling, within 48 hrs
Chlamydia: purulent discharge, lid swelling, at 1-2 weeks

67
Q

Management of hepatitis B infection

A

Infants of mothers HBsAg positive - hepatitis B vaccination

68
Q

Clinical features of respiratory distress in term infants

A

Tachypnoea (>60)
Dyspnoea - recession, nasal flaring
Expiratory grunting
Cyanosis

69
Q

Causes of respiratory distress in term infants

A 
Transient tachypnoea of newborn
Pneumonia
Meconium aspiration 
Milk aspiration 
Persistent pulmonary hypertension of newborn 
Diaphragmatic hernia 
Non-pulmonary: CHD, anaemia, HIE
70
Q

What is transient tachypnoea of newborn

A

Respiratory distress due to delay in resorption of pulmonary fluid

71
Q

Clinical features of transient tachypnoea of newborns

A

More common in birth by Caesarian
Self limiting - resolves in first 3 days
CXR - fluid in horizontal fissure

72
Q

What is meconium aspiration syndrome

A

Respiratory distress due to meconium aspiration

Meconium causes mechanical obstruction, chemical irritation and predisposes to infection

73
Q

Clinical features of meconium aspiration syndrome

A

Post term infants

CXR - hyperinflated, patchy consolidation and collapse

74
Q

Causes of pneumothorax in newborns

A

Spontaneous
Meconium aspiration
RDS
Mechanical ventilation

75
Q

Causes of milk aspiration

A

Premature infants
Neurological damage
Bronchopulmonary dysplasia
Cleft palate

76
Q

What is persistent pulmonary hypertension of newborn

A

Life threatening condition of multiple causes, which leads to right-to-left shunting at lungs, atria and ductus arteriosus

77
Q

What is persistent pulmonary hypertension of newborn

A

Life threatening condition of persisting high pulmonary vascular pressures, leading to right-to-left shunting

79
Q

Risk factors for persistent pulmonary hypertension of newborn

A

Birth asphyxia
Meconium aspiration
Sepsis
RDS

80
Q

Management of persistent pulmonary hypertension of newborn

A 
Mechanical ventilation 
Circulatory support 
Inhaled nitric oxide (vasodilator) 
High-frequency ventilation 
ECMO (heart and lung bypass)
81
Q

What is diaphragmatic hernia

A

Left-sided Herniation of abdominal contents through posterolateral Foramen of diaphragm

82
Q

Clinical features of diaphragmatic hernia

A 
Antenatal diagnosis
Failure to respond to resuscitation
Respiratory distress 
Cyanosis at birth 
Apex beat and heart sounds displaced to right 
Poor air entry on left
83
Q

Risk factors for respiratory distress syndrome

A 
Extreme pre-term (23-25wks) 
Chorioamnionitis
Birth weight 
Antpartum haemorrhage - blood inhibits surfactant 
GDM 
IUGR favourable - due to stress hormones
84
Q

Clinical importance of birth size

A

Common - 7%
Influences medical conditions encountered in neonatal life
Accounts for 70% of neonatal deaths

85
Q

Define SGA

A

Birth weight <10th centile for gestational age
Can be benign or pathological
If <2nd centile - Increased risk of congenital anomalies and neonatal problems

86
Q

Define IUGR

A

Failure to reach genetically determined growth potential

87
Q

Patterns of growth restriction

A

Asymmetrical

Symmetrical

88
Q

Pathophysiology and Causes of asymmetrical growth restriction

A

Uteroplacental dysfunction in late pregnancy - head growth spared in expense of glycogen and fat :
Pre eclampsia
Multiple pregnancy
Smoking

89
Q

Pathophysiology and causes of symmetrical growth restriction

A

Prolonged poor growth:
Chromosomal disorder, syndromes
Maternal medical conditions
Malnutrition

90
Q

Fetus and infant Risks from growth restriction

A

Fetus:
Stillbirth
Perinatal asphyxia

Infant: 
Hypothermia 
Hypoglycaemia - Low glycogen and fat stores 
Hypocalcaemia
Polycythaemia
91
Q

Recommended duration of breastfeeding

A

6 months

92
Q

Advantages of breastfeeding

A

Ideal nutrition for first 6 months
Reduced risk of GI/Resp infections, otitis media
Reduced risk of NEC in preterm infants
Reduced risk of Obesity, DM, HTN in later life
Improved mother-child relationship

93
Q

Breast milk components

A

Colostrum: higher protein + immunoglobulin content

Humoral immunity: IgA, Lactoferrin (inhibit e Coli), Bifidus factor (promote lactobacillus), lysozyme (bacteriolytic), interferon (antiviral)
Cellular immunity: macrophages, lymphocytes

Nutrition: protein, lipid, lipase, iron, vitamins, low solute load, long chain polyunsaturated fatty acids

94
Q

Complications of breastfeeding

A

Unknown intake - monitor growth on growth centile chart
Transmission of infection - cmv, hiv, Hep b
Transmission of drugs
Transmission of environmental contaminants - alcohol, nicotine, caffeine
Vitamin K deficiency
Breast milk jaundice
Nutrient inadequacies beyond 6 months

95
Q

What is formula feeding and how long do you recommend this for

A

Modified Cows milk

12 months

96
Q

When can you start cows milk

Why not earlier

A

After 12 months

Low iron and vitamin A, C, D content

97
Q

What is specialised formula

A

Non cows milk based formula

98
Q

Indications for specialised formula

A 
Cows milk protein allergy
Preterm 
Lactose intolerance
Cystic fibrosis
Neonatal cholestatic liver disease
Neonatal intestinal resection 
Reflux
99
Q

Differences in specialised formula milk

A

Higher calorie and mineral content
Hydrolysed cows milk protein
No lactose
Fat from medium chain FA - no need for lipase/bile salts
Anti reflux milk - rice starch causes milk to become viscous in stomach

100
Q

When do you start weaning

A

6 months

Paediatrics (15 decks)

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