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Specialty Blocks > 3. Paeds [Neonatology + Congenital] > Flashcards

3. Paeds [Neonatology + Congenital] Flashcards

1
Q

Why are preterm infants at an increased risk of infection?

A

IgG is mostly transferred across the placenta in the last trimester, and no IgA or IgM is transferred.

Causes of preterm labour include infection in and around the cervix.

Risk of nosocomial infection due to e.g. indwelling catheters and lines / mechanical vent.

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2
Q

Describe the pathophysiology of Respiratory Distress Syndrome.

A

Deficiency of surfactant.
This lowers surface tension.
This leads to widespread alveolar collapse and inadequate gas exchange.

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3
Q

What is surfactant?

A

Mix of phospholipids and protein secreted by the alveolar epithelium.

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4
Q

Who is at most risk of RDS?

A

<28 weeks very common.
Severity is worse in boys > girls.

Very rare at term, but possible link with diabetic mothers.

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5
Q

If a preterm delivery is anticipated, what should be given to the mother to reduce the risk / severity of RDS?

A

Steroids; to stimulate fetal surfactant production.

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6
Q

What are 3 benefits of giving mothers steroids if preterm delivery is anticipated?

A

Reduces risk of RDS.

Reduced lung damage from bronchodysplasia.

Reduced risk of IVH.

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7
Q

When do signs of RDS typically present?

A

at birth or within 4 hours

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8
Q

4 clinical signs of RDS:

A

Increased work of breathing inc sternal and subcostal recession

RR >60/min

Expiratory grunting (trying to create positive airway pressure)

Cyanosis if severe

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9
Q

CXR of RDS:

A

Ground glass
Air bronchograms

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10
Q

Management of RDS:

A

Oxygen therapy
+/- NIV (CPAP or NC)

Surfactant therapy

Mechanical ventilation if no response

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11
Q

Why is it important to avoid excessively oxygenating a preterm baby?

A

Excess oxygen therapy can damage lungs and brain due to excess free radicals.

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12
Q

RDS causes overextended alveoli, and this can cause air to track into the interstitium. What can this cause, and what is the management?

A

Pulmonary interstitial emphysema.
This can progress to pneumothorax, clinical signs including increased O2 req and reduced breath sounds on affected sides.

Aspirate and chest drain.

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13
Q

Which range of sats are extremely important to avoid in preterms and why?

A

<91% - increased risk of necrotizing enterocolitis and death

> 95% - risk of retinopathy of prematurity

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14
Q

Why are preterms of <32 weeks at risk of apnoeic episodes?

A

Immaturity of central respiratory control.

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15
Q

Management of apnoea in neonates:

A

Physical stimulation
? Caffeine
? CPAP/mechanical vent if frequent

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16
Q
A
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17
Q

4 reasons why preterm infants are vulnerable to hypothermia:

A

Nursed naked

Thin skin

Little subcut fat

Large SA relative to mass so greater heat loss

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18
Q

What is the mortality statistic of necrotizing enterocolitis (NE)?

A

20%

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18
Q
A
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19
Q

What are 3 protective factors against NE?

A

Breast milk
Prebiotics
Probiotics

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20
Q

What are 5 factors that increase the risk of NE?

A

IUGR

Perinatal asphyxia

Formula milk

Antibiotics

Rapid increase in enteral feeds

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21
Q

When is NE most commonly seen?

A

First few weeks of life

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22
Q

Discuss the pathophysiology of NE.

A

Ischaemia injury
OR
Bacterial infection of the bowel wall and altered gut microbiome

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23
Q

Clinical signs of NE:

A

Feed intolerance

Vomiting ?bilious

Blood stained bowel movements

Distended abdomen, discolouration, peritonitis

?Shock due to distension and pain

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24
Q

AXR signs of NE:

A

Distended bowel loops

Thickening of bowel wall

Intramural gas

Pneumoperitoneum if perf; Rigler sign, air under diaphragm

Air outling the falciform ligament

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25
Q

Management of NE:

A

Stop feeding
Parenteral nutrition
Broad spec antibiotics
Vent and circulatory support

If perforation: surgery

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25
Q

3 long term complications of NE:

A

Bowel strictures

Malabsorption if there was a resection

Poor neurodevelopmental outcomes

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26
Q

3 causes of pneumothorax in a neonate:

A

RDS
Meconium aspiration
Complication of mechanical ventilation

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27
Q

Meconium is a lung irritant. What does meconium aspiration cause?

A

Chemical pneumonitis
Mechanical obstruction

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28
Q

8-20% of babies pass meconium before birth. What may this be in response to?

A

Fetal hypoxia

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29
Q

Give 4 features of meconium-aspirated lungs.

A

Patches of consolidation
Patches of collapse
Overinflated
Air leaks can lead to pneumomediastinum / pneumothorax

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30
Q

What may develop as a result of meconium aspiration?

A

PPHN

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31
Q

What is the most common cause of respiratory distress in term infants, and when is it more common?

A

Transient tachypnoea of the newborn

Post c-section

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32
Q

What is transient tachypnoea of the newborn (TTN) caused by, and what is seen on CXR?

A

Delay in absorption of lung liquid.

Fluid in the horizontal fissure.

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33
Q

When does TTN usually settle, and what is the management?

A

It usually settles within the first day of life, but it can take days.

Supplemental O2
Feeding support via NG or IV fluids if unable to feed normally.

34
Q

What does HIE stand for?

A

Hypoxic Ischaemic Encephalopathy

35
Q

Describe the steps that lead to HIE (5).

A
  1. Perinatal asphyxia
  2. Reduced pulmonary and placental gas exchange
  3. Cardiorespiratory depression
  4. Hypoxia, hypercarbia and metabolic acidosis
  5. Compromised cardiac output leading to reduced tissue perfusion and hypoxic / ischaemic injury
36
Q

HIE can present with multiorgan dysfunction. Outline which organ systems (4) can be affected and discuss the symptoms associated with each one.

A

Brain; abnormal neuro signs + seizures

Cardiorespiratory; apnoea + PPHN + hypotension

Metabolic; hypoglycaemia + hyponatraemia + hypocalcaemia

Other; renal failure + DIC

37
Q

HIE usually occurs after a significant hypoxic event immediately before or during labour / delivery. Outline 5 broad causes for this.

A

Compromised fetus

Inadequate maternal placental perfusion

Failure of gas exchange across the placenta

Interruption of umbilical blood flow

Failure of cardiorespiratory adaptation after birth

38
Q

Discuss mechanisms which might contribute to failure of gas exchange across the placenta (3), and state in what time frame this may clinically present:

A

Excessive / prolonged uterine contractions

Placental abruption

Ruptured uterus

Starts immediately or within 48 hours after birth

39
Q

Outline 2 causes of compromised umbilical blood flow.

A

Shoulder dystocia
Cord prolapse

Both are causes of cord compression

40
Q

You can split the clinical features of HIE into mild, moderate and severe. Outline the MILD signs (4).

A

Irritable

Excessive response to stimulation

Staring

Hyperventilation

41
Q

You can split the clinical features of HIE into mild, moderate and severe. Outline the MODERATE signs (5).

A

Marked movement abnormalities

Seizures

Brief apnoeas

Cannot feed and failure to suck

Hypotonic

42
Q

You can split the clinical features of HIE into mild, moderate and severe. Outline the SEVERE signs (4).

A

No spontaneous movements or response to pain

Hypotonic

Prolonged seizures, refractory to treatment

Multiorgan failure

43
Q

Discuss neuronal damage with regards to HIE, including potential management.

A

You can get primary or secondary neuronal damage in HIE.

Secondary is delayed, and is due to reperfusion injury.

The delay offers the chance of neuroprotection via mild therapeutic hypothermia.

44
Q

Fetal growth can be progressively restrictured due to placental insufficiency. What does this cause?

A

Oxygen reduction
Nutrient transfer reduction

45
Q

Babies with identified IUGR must be monitored closely to prevent IU death. What 3 things should be measured to help decide the optimal time of delivery?

A

Growth parameters
Amniotic fluid volume
Doppler blood flow

46
Q

Risk factors for IUGR can be split into maternal, uteroplacental and fetal. Outline the MATERNAL risk factors (4).

A

Substance use e.g. alcohol, drugs, smoking
Teratogens
Previous IUGR pregnancy
Medical conditions

47
Q

List 5 maternal medical conditions that can predispose to IUGR.

A

Hypertension (chronic and gestational)
Diabetes mellitus
Pre-eclampsia
SLE
Antiphospholipid syndrome

48
Q

List 4 teratogenic drugs.

A

Antiepileptics; sodium valproate, carbamazepine, phenytoin

Methotrexate

Isotretinoin

ACEi

49
Q

Risk factors for IUGR can be split into maternal, uteroplacental and fetal. Outline the UTEROPLACENTAL risk factors (5).

A

Umbilical artery thrombosis
Placental insufficiency
Placenta praevia
Uterine fibroids
Multiple gestation

50
Q

Risk factors for IUGR can be split into maternal, uteroplacental and fetal. Outline the FETAL risk factors (3).

A

Congenital infections; CMV, rubella
Genetics; e.g. aneuploidy
Congenital anomalies; e.g. tracheal-oesophageal fistula

51
Q

Complications of biliary atresia (3).

A

Unsuccessful anastamosis

Progressive liver disease

Cirrhosis leading to HCC

52
Q

What is biliary atresia?

A

Progressive fibrosis and obliteration of extra and intrahepatic biliary tree leading to obstruction of bile.

53
Q

Clinical features of biliary atresia (5).

A

Pale stools and dark urine

Jaundice persisting after 2 weeks

Normal birth weight –> faltering growth

Hepatomegaly

Late stage; splenomegaly due to portal hypertension

54
Q

Discuss the investigation process in biliary atresia (indication + 5 tests).

A

If jaundice is persisting after 2 weeks, investigate for liver disease.

Conjugated Br increased
GGT increased
LFTs abnormal

Fasted abdo US; absent or contracted gallbladder

ERCP; can’t outline biliary tree (diagnostic)

55
Q

Types of biliary atresia (3).

A

1) Proximal ducts
2) Cystic duct atresia
3) Atresia of left and right ducts to level of porta hepatis

56
Q

Briefly outline the management of biliary atresia.

A

Kasai operation
Antibiotics
Bile acid enhancer e.g. ursodeoxycholic acid

57
Q

What investigations are important for investigating differential diagnoses of biliary atresia? (4)

A

Serum alpha-1 antitrypsin; can be a cause of neonatal cholestasis.

Sweat chloride test; CF can involve the biliary tract.

US

Liver biopsy

58
Q

Cephalohaematoma and caput succedaneum both present as swelling on a newborn’s head. When are they both more common?

A

Following prolonged, difficult deliveries.

59
Q

What is a complication of cephalohaematoma, and when does it resolve?

A

Jaundice

Resolves in up to 3 months

60
Q

What is a cephalohaematoma?

A

Swelling on newborns head due to bleeding between the periosteum and skull.

61
Q

What are the main differences between cephalohaematoma and caput succedaneum? (4)

A

C is blood between periosteum and skull, whilst CS is localised oedema between the periosteum and scalp.

C does not cross suture lines, whilst CS does.

C most common area is parietal, whilst CS forms over the vertex.

C develops several hours after delivery whilst CS is present at birth.

61
Q

Black race is a risk factor for which specific type of sepsis?

A

Group B Strep

62
Q

Sepsis in neonates can be split into early and late onset (EOS / LOS). What are the time frames for these?

A

Early = <72 hours

Late = >72 hours

63
Q

What are the most common organisms in EOS and LOS respectively?

A

EOS = Group B Strep (75%)

LOS = CoNS (Staph epidermis) and G-ves (Klebsiella, pseudomonas, enterobacter)

64
Q

State 4 routes of infection in neonatal sepsis.

A

Transplacental
Nosocomial
Birth canal
Breast milk

65
Q

Cause of EOS infection (e.g. route).

A

Ascending infection or high bacterial load exposure during birth (after rupture of the membranes).

66
Q

Cause of LOS infection (e.g. route).

A

Source is mainly hospital / community environment.
Nosocomial sources include catheters, invasive procedures and tracheal tubes.

67
Q

List 4 maternal risk factors for neonatal sepsis.

A

Current or previous GBS infection
Current bacteruria
Intrapartum temp >38
Membrane rupture >18 hours

68
Q

State 2 fetal risk factors for neonatal sepsis.

A

Low birth weight (<2.5kg)
Premature (<37 weeks)

69
Q

Initial management of neonatal sepsis (abx) + what if resistant?

A

IV Benzylpenicillin + Gentamicin (to cover staph and g-ves).

If resistant / not responding, then give vanc for CoNS

?Meropenem

70
Q

Discuss the supportive management that you must consider alongside antibiotics in managing neonatal sepsis (4).

A

O2 sats maintenance
Blood glucose monitoring and management
Fluid and electrolyte support
Metabolic acidosis prevention / support

70
Q

Give 2 late signs in neonatal sepsis that may indicate a meningitis.

A

Bulging fontanelle

Opisthotonus (head retraction)

71
Q

Discuss the difference in temperature change in sepsis between preterm and term infants.

A

Preterm = hypothermia

Term = fever

72
Q

Sepsis in neonates vs adults presents with different clinical features. List 12 features of neonatal sepsis.

A

Temp change
Hypo/hyperglycaemia
Shock
Feeding intolerance
Apnoea
Vomiting
Bradycardia
Seizures
Lethargy, drowsiness, irritability
Respiratory distress
Neutropenia
Jaundice

73
Q

When would you do an LP if neonatal sepsis is suspected?

A

BCx positive
OR
<28 days
OR
Any generalized features of neonatal sepsis

74
Q

State 7 medical problems that are associated with Trisomy 21 that would present later on as the child develops.

A

Delayed motor milestones
Learning difficulties
Hearing (glue ear) and visual (cataracts) impairment
Subfertility
Leukaemia and solid tumours (particularly ALL)
Epilepsy
Coeliac disease

75
Q

State 4 cardiac complications of Trisomy 21.

A

VSD
Secundum ASD
Tetralogy of fallot
Isolated PDA

76
Q

State 5 other anomalies that are associated with Trisomy 21 (not craniofacial).

A

Hypotonia
Sngle palmar crease
Sandal gap
Hirschprung’s disease
Duodenal atresia

76
Q

State typical craniofacial appearance of a child born with Trisomy 21.

A

Upslanting palpebral fissures
Small ears
Protruding tongue
3rd fontanelle
Brushfield spots in iris
Round face
Flat nasal bridge

77
Q

Typical screening for Trisomy 21 occurs between 11-13 weeks. What test is offered if a mother books in later than this, and what does it involve?

A

Quadruple test at 15-20 weeks

AFP
Unconjugated oestriol
HCG
Inhibin A

78
Q

Outline the standard testing for trisomy abnormalities including when it is offered and what tests it involves, and what it would show if positive.

A

Combined testing at 11-13 weeks.

Nuchal translucency = thickened
PAPP-A = reduced
Serum beta-HCG = increased

79
Q

Describe how the results of the combined and quadruple tests are reported.

A

They come back with ‘higher chance’ (1/150) or ‘lower chance’ (1/300).

80
Q

What is the preferred further testing for Down’s syndrome, and what does it analyse?

A

NIPT

Analyses cffDNA that circulate in pregnant women’s blood.
cffDNA derives from placental cells and the DNA is identical to fetal DNA.

81
Q
A

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