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Paediatrics > Neonatology > Flashcards

Neonatology Flashcards

1
Q

Prevalence of jaundice in first week of life in neonates

A

60% of full term babies

80% of pre-term babies

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2
Q

Early jaundice (before 24h)

A

Unconjugated bilirubin
ALWAYS PATHOLOGICAL, almost always haemolysis
Haemolysis:
- ABO or Rh factor incompatibility
- Red cell shape abnormalities (e.g. spherocytosis)
- Red cell enzyme pathology (e.g. G6PD)
- Sepsis
- Non-haemolytical red cell destruction (polycythaemia, bruising or cephalhaematoma)

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3
Q

Physiological jaundice

A

Unconjugated
Due to immature liver unable to process and conjugate all the bilirubin
Exaggerated physiological response
Onset >24h
Should resolve within 2 weeks in a term baby (3 weeks in pre-term)

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4
Q

Breast milk jaundice

A

Prolonged unconjugated hyperbilirubinaemia
Jaundice peaks in second week, resolves very slowly and may last up to 3 months
Healthy, thriving infant
Due to factors in breast milk that increase enteric absorption of bilirubin
Can confirm by improvement of jaundice on temporary interruption of breastfeeding, but this is rarely required

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5
Q

Causes of conjugated hyperbilirubinaemia in neonate

A 
ALWAYS PATHOLOGICAL - requires urgent work up
Biliary atresia
Neonatal hepatitis
 - congenital infection
 - alpha-1 antitrypsin deficiency
 - idiopathic
Metabolic
Choledochal cyst
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6
Q

What does yellow sclera indicate

A

unconjugated hyperbilirubinaemia

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7
Q

Likely causes of neonatal jaundice present at birth

A

Severe haemolysis

Hepatitis (unusual)

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8
Q

Likely causes of neonatal jaundice presenting within 48 hours of birth

A

Probably haemolysis

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9
Q

Likely causes of neonatal jaundice presenting after 10 days of life

A

Hypothyroidism

Biliary atresia

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10
Q

At what bilirubin level does jaundice become clinically apparent

A

85-120 micromol/L

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11
Q

Non-haemolytic causes of unconjugated hyperbilirubinaemia

A 
Increased haem load:
 - haemorrhage (e.g. birth trauma)
 - polycythaemia
 - swallowed blood
Increased enterohepatic circulation
 - Bowel obstruction or ileus
 - pyloric stenosis
Impaired hepatic uptake and conjugation
 - Inborn errors of bilirubin metabolism
(e.g. Gilbert's disease, galactosaemia)
 - Endocrine (hypothyroidism, hypopituitarism, drugs)
 - Inhibitors (breast milk)
Mixed
 - asphyxia
 - Prematurity
 - Sepsis
 - Infants of diabetic mothers
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12
Q

Investigations in all jaundiced infants

A

Serum bilirubin ratio
CBE + film
Blood group
Coomb’s test

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13
Q

Investigations in systemically unwell jaundiced infants or those with early jaundice (in addition to general ones)

A 
CRP
Blood cultures
EUC
LFT
VBG
BGL
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14
Q

Investigations in infants with conjugated jaundice

A 
LFT
Clotting
TFT
Septic screen
Viral serology
Alpha-1 Antitrypsin levels 
Abdominal USS
(+Discuss with gastroenterology team)
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15
Q

Treatment options for neonatal jaundice

A

Increase hydration (may reduce enterohepatic circulation of bilirubin)
Frequent breast feeding
Phototherapy (photo-isomerises bilirubin into water-soluble forms excreted directly into bile)
Exchange transfusion if bilirubin >340
IVIG if haemolytic disease and rising bilirubin despite phototherapy

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16
Q

Complications of neonatal juandice

A

Kinicterus:
Unconjugated only - toxic to brain cells - death and yellow staining (particularly grey matter)
Permanent clinical sequelae

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17
Q

Conjugated v unconjugated bilirubin

lipid- v water-soluble

A

Conjugated is water soluble - hence can be excreted in bile, urine, faeces
Unconjugated is lipid soluble - hence cannot be excreted, and is able to cross the blood brain barrier when not bound to albumin

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18
Q

Enzyme responsible for conjugation of bilirubin in the liver

A

Glucuronyl transferase (defective in Gilbert’s Disease)

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19
Q

What is the enzyme defective in Gilbert’s disease?

A

Glucuronyl transferase (responsible for the conjugation of bilirubin in the liver)

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20
Q

Time frame in which biliary atresia must be corrected

A

Must be corrected within 60 days of life`

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21
Q

Glucuronyl Transferase is defective in which disease

A

Gilbert’s disease

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22
Q

Causes of respiratory distress in the newborn (5)

A 
Respiratory distress syndrome (Hyaline Membrane disease)
Transient tachypnoea of the newborn
Pneumonia
Meconium aspiration syndrome
Pneumothorax/Air leak

+other weird shit like diaphragmatic hernias that are rare and low yield

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23
Q

Definition of respiratory distress syndrome

A

When a neonate has difficulty breathing due to surfactant deficiency at birth. It is the dominant clinical problem faced by preterm infants

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24
Q

Risk factors for respiratory distress syndrome

A

Low gestational age
Maternal diabetes
Prenatal asphyxia
Multiple gestation

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25
Q

Clinical presentation of respiratory distress syndrome

A

Symptoms develop within 6 hours of birth

  • grunting
  • intercostal recession
  • nasal flaring
  • cyanosis
  • increased oxygen requirement
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26
Q

Chest x-ray findings in respiratory distress syndrome

A

Diffuse reticulogrannular pattern (ground glass lungs)
Air bronchograms (dark air-filled bronchi made visible by opacification of surrounding alveoli)
Bell-shaped thorax
Hyperinflation excludes RDS unless patient is intubated

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27
Q

Natural history of respiratory distress syndrome

A

Presents within 6 hours of life

Progressive worsening over first 48-72 hours

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28
Q

Management of Respiratory distress syndrome

A 
ABCs:
- Lateral or prone position
- Oxygen (warmed, humidified)
- intubate (cynaosis, recurrent apnoea, resp failure [pH and pCO2)
Thermoregulation
Avoid enteral feeding
Antibiotics (penicillin + gent after initial investigations)
Surfactant administration if intubated
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29
Q

Suction pressure and depth in neonate

A

maximum 100mmHg

Should be limited to a depth of 5cm below lips

30
Q

Signs of adequate inflation and ventilation in neonatal resuscitation

A

increase in HR to 100/minute
Slight rise in chest and upper abdomen with each inflation
Improvement in oxygenation

31
Q

Steps for BREATHING in neonatal resuscitation

A

Attend to adequate ventilation BEFORE oxygenation
60/minute
Positive pressure ventilation started initially in air (21% O2) EXCEPT IF GA less than 32 - should be commenced with 30% O2
Aim for oxygen saturations 91-95% by 5-10 minutes

32
Q

Rate of chest inflation in neonatal resuscitation

A

60/minute

33
Q

Normal oxygen saturation at birth

A

60%, increases to 90% over 5-10 minutes in normal healthy infants

34
Q

Preferred route of drug administration in neonatal resuscitation

A

Umbilical venous catheter

35
Q

Ratio when begin CPR in neonate

A

3:1

Aim for 90 chest compressions and 30 breaths per minute (2 events per second)

36
Q

Indications to begin chest compressions during neonatal resuscitation

A

HR below 60 for over 30 seconds

37
Q

Determining gestational age postnatally

A

Dubowitz Ballard Score:
Neuromuscular maturity
- Posture (more flexion = higher GA)
- Square window (wrist)
- Arm recoil (more flexion = higher GA)
- Popliteal angle (smaller = higher GA)
- Scarf sign (should not be able to pull whole arm across chest)
- Heel to ear (closer to achieving = lower)
PHYSICAL MATURITY:
- skin texture, colour, opacity
- Lanugo
- Plantar surface (size and crease)
- Breast (areola and bud?)
- Eye/ear (lids open/fused, curve of pinna, firmness of cartilage)
- Genitals (male - descent of testes + rugae, female - majora:minora:clitoris ratio)

38
Q

Definition of neonatal hypothermia

A

Neonate with a temperature less than 36.6

39
Q

Causes of neonatal hypothermia

A 
Environmental
Disorders impairing thermoregulation:
- Sepsis
- Intracranial haemorrhage
- Drug withdrawal
40
Q

Neonatal septicaemia presentation

A 
WARM SHOCK: wide pulse pressure, rapid capillary refill
COLD SHOCK: narrow pulse pressure, prolonged capillary refill
\+
fever or hypothermia
Tachycardia
Hypotension
Tachypnoea +/- hypoxia
Altered conscious state
41
Q

Investigations in neonatal septicaemia

A 
Blood cultures
Venous gas
Blood glucose
Lactate
(FBE, EUC, coagulation studies as indicated)
42
Q

Antibiotic therapy to give in neonatal septicaemia

A

Cefotaxime + benzylpenicillin
Give as an IV push

If no IV access by 30 minutes - IM ceftriaxone while achieving IV access

43
Q

Management of neonatal sepsis

A

ABCs
Blood cultures, VBG, BGL (FBE, EUC, coags if easy access)
IV fluids: 20mL/kg bolus push over 10min, consider additional bolus as indicated
IV antibiotics
Inotropes - if no improvement in vital signs/consciousness after fluid boluses
Ventilatory support
Correct any hypoglycaemia, monitor BGL
IF initial lactate higher than 4, repeat after 2 hours, aim for clearance greater than 10%

44
Q

Inotropes to give in neonatal septicaemia

A

Warm shock: noradrenaline

Cold shock: dobutamine

45
Q

Definition of neonatal hypoglyaemia

A

In infant with risk factors but no clinical signs: BGL less than 2.0

In infants with clinical signs of hypoglycaemia: BGL less than 2.6

In infant on SCN/NICU: total blood glucose less than 2.6 (TBG from blood gas analyser or lab, not from bedside glucometer

46
Q

Risk factors for hypoglycaemia

A 
Reduced glycogen stores/increased demands
- Prematurity
- IUGR
- Perinatal asphyxia
- Hypothermia
- Respiratory distress syndrome
- Sepsis
Hyperinsulinaemic states
- maternal DM
- Rh isoimmunisation
- Persistent hyperinsulinaemia hypoglycaemia of infancy
- islet cell hyperplasia
- Beckwith-Wiedemann syndrome
- Pancreatic tumour
Other
- Macrosomic infnats
- CNS depression or encephalopathy at birth
- nil by mouth
47
Q

Presentation of neonatal hypoglycaemia

A 
Majority are asymptomatic!
CNS excitation
- jitteriness
- high pitch cry
- seizures
- irritability
CNS depression
- lethargy
- apnoea
- cyanosis
- poor feeding
- hypotonia
48
Q

Investigations if suspect hyperinsulinism in neonate with hypoglycaemia

A 
Insulin
GH
Cortisol
Free fatty acids
Urinary ketones
49
Q

Prevention of neonatal hypoglycaemia

A

Early prolonged skin-skin contact and breast feeding
Prevent hypothermia
Commence enteral feeds by 1-2 hours of age if able to tolerate
Feed frequently (2-3 hourly if low risk)

50
Q

Treatment of neonatal hypoglycaemia

A

Treat the cause
Feed increased volume of milk if asymptomatic (8-12x per day)
Buccal glucogel
IV glucose - bolus 200-300mg/kg dose, anything higher than 12.5% glucose should be given through umbilical venous catheter
Glucagon for infants with adequate glycogen stores (i.e. hyperinsulinaemic states) with hypoglycaemia despite IV infusion - IM 0.3mg/kg stat

51
Q

Complications of neonatal hypoglycaemia

A 
Short term:
- seizures
- apnoea
- hypoxia
Long term
- neurological damage (CP, mental retardation, recurrent seizure activity, developmental delay, personality disorders)
-?impaired CVS function
52
Q

Definition of transient tachypnoea of the newborn

A

Parenchymal lung disorder characterised by pulmonary oedema resulting from delayed resorption and clearance of foetal alveolar fluid

53
Q

Risk factors for transient tachypnoea of the newborn

A

C-section delivery without labour
Maternal diabetes
Maternal asthma

54
Q

Clinical presentation of transient tachypnoea of the newborn

A 
Immediate onset (within 2 hours, improves within 24 hours)
Tachypnoea (over 60)
Cyanosis
Increased WOB
Expiratory grunting
AP diameter of chest may be increased
Breath sounds typically clear
55
Q

Chest X ray findings in transient tachypnoea of the newborn

A

Alveolar and “fluffy” appearance (alveolar oedema)
Effusion (fluid in fissures, costophrenic angle)
Inc. lung volumes with flat diaphragms
Mild cardiomegaly
Prominent vascular markings in sunburst pattern originating at hilum

56
Q

Management of transient tachypnoea of the newborn

A

Benign, self-limiting condition
Supportive management
- supplemental O2 if required to maintain saturation over 90%
- nasal CPAP may be required if increased WOB or requiring more than 40% inspired O2
- nutrition via IV or NG if oral feeds not tolerated
- Thermal regulation

57
Q

Clinical signs for diagnosis of meconium aspiration syndrome

A
  • Evidence of meconium stained amniotic fluid
  • Respiratory distress at birth or shortly after
  • Characteristic radiographic features
  • presence of meconium in the trachea in the setting of requiring intubation
58
Q

Radiographic features characteristic of meconium aspiration syndrome

A

Progresses from initially global atelectasis to widespread patchy opacification accompanied by areas of hyperinflation and/or atelectasis

Radiologic changes resolve over 7-10 days

59
Q

Risk factors for meconium aspiration syndrome

A

Post-date infants
Small for gestational age
Vaginal breech delivery

60
Q

Incidence of meconium aspiration syndrome

A

0.1% of live births
Occurs in 2-10% of infants born through meconium stained amniotic fluid (which is approx 10% of term babies, more post-term)

61
Q

Prevention of meconium aspiration syndrome

A

Intrapartum:

  • prevent foetal hypoxia
  • prevention of delivery later than 41 weeks gestation
62
Q

Management of meconium aspiration syndrome

A

ABCs
Most infants will only require O2 therapy and general supportive care
Ventilator/CPAP support when refractory hypoxaemia
Intubation indicated with persistent hypoxaemia despite CPAP or respiratory acidosis
+ General supportive care:
- CVS support (volume and inotrope therapy as required)
- fluid restriction
- Antibiotics until primary bacterial infection is excluded
- IV therapy and nil orally until resp distress resolves

63
Q

Characteristics of meconium aspiration syndrome

A 
Early onset (within 2h) of respiratory distress and hypoxaemia in a meconium-stained term or near term infant
Widespread "wet" inspiratory crackles +/- expiratory noises
Tachypnoea, cyanosis and variable hyperinflation
64
Q

Complications of meconium aspiration syndrome

A

Persistent pulmonary hypertension
Air leak (pneumomediastinum, pneumothorax, cystic lung disease)
Pulmonary haemorrhage
Complications of asphyxia (encephalopathy, seizures, oliguria, coagulopathy, thrombocytopaenia)

65
Q

Presence of meconium stained amniotic fluid at preterm delivery raises possibility of which foetal infection in particular

A

Listeria

66
Q

Apgar score correlations for later neurodevelopment

A

At 1 minute does not correlate at all

10 minute apgars between 0-3 much higher risk of cerebral palsy

67
Q

Single palmar crease in an otherwise normal looking baby - what investigations are warranted

A

None

Single palmar creases occur normally in 1/30 healthy people

68
Q

Normal meconium

A

Odour-free, dark, sterile

69
Q

Meconium in baby with CF

A

Thicker, collects in ileum and may present with meconium ileus

70
Q

Cause of meconium aspiration

A

Foetal distress leads to passing of meconium in utero, persistent or worsened foetal distress then leads to gasping efforts by baby and aspiration of the meconium in the liqour

71
Q

Complications in post-term babies

A

Birth asphyxia secondary to traumatic delivery and meconium aspiration
Hypoglycaemia (depleted glycogen stores)

72
Q

APGAR score calculation

A

Appearance: pink = 2, blue peripheries = 1, blue all over= 0
Pulse: more than 100 = 2, less than 100 =1, no HR = 0
Grimace: cough when stimulated = 2, grimace when stimulated = 1
Activity: moving all limbs = 2, some movement = 1, limp = 0
Respiration: Normal, crying = 2, irregular or weak cry = 1 not breathing = 0

Paediatrics (20 decks)

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