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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

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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17
Q

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

A

20%

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17
Q

What are 3 protective factors against NE?

A

Breast milk
Prebiotics
Probiotics

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18
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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19
Q

When is NE most commonly seen?

A

First few weeks of life

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20
Q

Discuss the pathophysiology of NE.

A

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

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21
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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22
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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23
Q

Management of NE:

A

Stop feeding
Parenteral nutrition
Broad spec antibiotics
Vent and circulatory support

If perforation: surgery

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23
3 long term complications of NE:
Bowel strictures Malabsorption if there was a resection Poor neurodevelopmental outcomes
24
3 causes of pneumothorax in a neonate:
RDS Meconium aspiration Complication of mechanical ventilation
25
Meconium is a lung irritant. What does meconium aspiration cause?
Chemical pneumonitis Mechanical obstruction
26
8-20% of babies pass meconium before birth. What may this be in response to?
Fetal hypoxia
27
Give 4 features of meconium-aspirated lungs.
Patches of consolidation Patches of collapse Overinflated Air leaks can lead to pneumomediastinum / pneumothorax
28
What may develop as a result of meconium aspiration?
PPHN Post-term delivery is a risk factors for meconium aspiration
29
What is the most common cause of respiratory distress in term infants, and when is it more common?
Transient tachypnoea of the newborn Post c-section
30
What is transient tachypnoea of the newborn (TTN) caused by, and what is seen on CXR?
Delay in absorption of lung liquid. Fluid in the horizontal fissure.
31
When does TTN usually settle, and what is the management?
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.
32
What does HIE stand for?
Hypoxic Ischaemic Encephalopathy
33
Describe the steps that lead to HIE (5).
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
34
HIE can present with multiorgan dysfunction. Outline which organ systems (4) can be affected and discuss the symptoms associated with each one.
Brain; abnormal neuro signs + seizures Cardiorespiratory; apnoea + PPHN + hypotension Metabolic; hypoglycaemia + hyponatraemia + hypocalcaemia Other; renal failure + DIC
35
HIE usually occurs after a significant hypoxic event immediately before or during labour / delivery. Outline 5 broad causes for this.
Compromised fetus Inadequate maternal placental perfusion Failure of gas exchange across the placenta Interruption of umbilical blood flow Failure of cardiorespiratory adaptation after birth
36
Discuss mechanisms which might contribute to failure of gas exchange across the placenta (3), and state in what time frame this may clinically present:
Excessive / prolonged uterine contractions Placental abruption Ruptured uterus Starts immediately or within 48 hours after birth
37
Outline 2 causes of compromised umbilical blood flow.
Shoulder dystocia Cord prolapse Both are causes of cord compression
38
You can split the clinical features of HIE into mild, moderate and severe. Outline the MILD signs (4).
Irritable Excessive response to stimulation Staring Hyperventilation
39
You can split the clinical features of HIE into mild, moderate and severe. Outline the MODERATE signs (5).
Marked movement abnormalities Seizures Brief apnoeas Cannot feed and failure to suck Hypotonic
40
You can split the clinical features of HIE into mild, moderate and severe. Outline the SEVERE signs (4).
No spontaneous movements or response to pain Hypotonic Prolonged seizures, refractory to treatment Multiorgan failure
41
Discuss neuronal damage with regards to HIE, including potential management.
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.
42
Fetal growth can be progressively restrictured due to placental insufficiency. What does this cause?
Oxygen reduction Nutrient transfer reduction
43
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?
Growth parameters Amniotic fluid volume Doppler blood flow
44
Risk factors for IUGR can be split into maternal, uteroplacental and fetal. Outline the MATERNAL risk factors (4).
Substance use e.g. alcohol, drugs, smoking Teratogens Previous IUGR pregnancy Medical conditions
45
List 5 maternal medical conditions that can predispose to IUGR.
Hypertension (chronic and gestational) Diabetes mellitus Pre-eclampsia SLE Antiphospholipid syndrome
46
List 4 teratogenic drugs.
Antiepileptics; sodium valproate, carbamazepine, phenytoin Methotrexate Isotretinoin ACEi
47
Risk factors for IUGR can be split into maternal, uteroplacental and fetal. Outline the UTEROPLACENTAL risk factors (5).
Umbilical artery thrombosis Placental insufficiency Placenta praevia Uterine fibroids Multiple gestation
48
Risk factors for IUGR can be split into maternal, uteroplacental and fetal. Outline the FETAL risk factors (3).
Congenital infections; CMV, rubella Genetics; e.g. aneuploidy Congenital anomalies; e.g. tracheal-oesophageal fistula
49
Complications of biliary atresia (3).
Unsuccessful anastamosis Progressive liver disease Cirrhosis leading to HCC
50
What is biliary atresia?
Progressive fibrosis and obliteration of extra and intrahepatic biliary tree leading to obstruction of bile.
51
Clinical features of biliary atresia (5).
Pale stools and dark urine Jaundice persisting after 2 weeks Normal birth weight --> faltering growth Hepatomegaly Late stage; splenomegaly due to portal hypertension
52
Discuss the investigation process in biliary atresia (indication + 5 tests).
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)
53
Types of biliary atresia (3).
1) Proximal ducts 2) Cystic duct atresia 3) Atresia of left and right ducts to level of porta hepatis
54
Briefly outline the management of biliary atresia.
Kasai operation Antibiotics Bile acid enhancer e.g. ursodeoxycholic acid
55
What investigations are important for investigating differential diagnoses of biliary atresia? (4)
Serum alpha-1 antitrypsin; can be a cause of neonatal cholestasis. Sweat chloride test; CF can involve the biliary tract. US Liver biopsy
56
Cephalohaematoma and caput succedaneum both present as swelling on a newborn's head. When are they both more common?
Following prolonged, difficult deliveries.
57
What is a complication of cephalohaematoma, and when does it resolve?
Jaundice Resolves in up to 3 months
58
What is a cephalohaematoma?
Swelling on newborns head due to bleeding between the periosteum and skull.
59
What are the main differences between cephalohaematoma and caput succedaneum? (4)
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.
59
Black race is a risk factor for which specific type of sepsis?
Group B Strep
60
Sepsis in neonates can be split into early and late onset (EOS / LOS). What are the time frames for these?
Early = <72 hours Late = >72 hours
61
What are the most common organisms in EOS and LOS respectively?
EOS = Group B Strep (75%) LOS = CoNS (Staph epidermis) and G-ves (Klebsiella, pseudomonas, enterobacter)
62
State 4 routes of infection in neonatal sepsis.
Transplacental Nosocomial Birth canal Breast milk
63
Cause of EOS infection (e.g. route).
Ascending infection or high bacterial load exposure during birth (after rupture of the membranes).
64
Cause of LOS infection (e.g. route).
Source is mainly hospital / community environment. Nosocomial sources include catheters, invasive procedures and tracheal tubes.
65
List 4 maternal risk factors for neonatal sepsis.
Current or previous GBS infection Current bacteruria Intrapartum temp >38 Membrane rupture >18 hours
66
State 2 fetal risk factors for neonatal sepsis.
Low birth weight (<2.5kg) Premature (<37 weeks)
67
Initial management of neonatal sepsis (abx) + what if resistant?
IV Benzylpenicillin + Gentamicin (to cover staph and g-ves). If resistant / not responding, then give vanc for CoNS ?Meropenem
68
Discuss the supportive management that you must consider alongside antibiotics in managing neonatal sepsis (4).
O2 sats maintenance Blood glucose monitoring and management Fluid and electrolyte support Metabolic acidosis prevention / support
68
Give 2 late signs in neonatal sepsis that may indicate a meningitis.
Bulging fontanelle Opisthotonus (head retraction)
69
Discuss the difference in temperature change in sepsis between preterm and term infants.
Preterm = hypothermia Term = fever
70
Sepsis in neonates vs adults presents with different clinical features. List 12 features of neonatal sepsis.
Temp change Hypo/hyperglycaemia Shock Feeding intolerance Apnoea Vomiting Bradycardia Seizures Lethargy, drowsiness, irritability Respiratory distress Neutropenia Jaundice
71
When would you do an LP if neonatal sepsis is suspected?
BCx positive OR <28 days OR Any generalized features of neonatal sepsis
72
State 7 medical problems that are associated with Trisomy 21 that would present later on as the child develops.
Delayed motor milestones Learning difficulties Hearing (glue ear) and visual (cataracts) impairment Subfertility Leukaemia and solid tumours (particularly ALL) Epilepsy Coeliac disease
73
State 4 cardiac complications of Trisomy 21.
VSD Secundum ASD Tetralogy of fallot Isolated PDA
74
State 5 other anomalies that are associated with Trisomy 21 (not craniofacial).
Hypotonia Sngle palmar crease Sandal gap Hirschprung's disease Duodenal atresia
74
State typical craniofacial appearance of a child born with Trisomy 21.
Upslanting palpebral fissures Small ears Protruding tongue 3rd fontanelle Brushfield spots in iris Round face Flat nasal bridge
75
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?
Quadruple test at 15-20 weeks AFP Unconjugated oestriol HCG Inhibin A
76
Outline the standard testing for trisomy abnormalities including when it is offered and what tests it involves, and what it would show if positive.
Combined testing at 11-13 weeks. Nuchal translucency = thickened PAPP-A = reduced Serum beta-HCG = increased
77
Describe how the results of the combined and quadruple tests are reported.
They come back with 'higher chance' (1/150) or 'lower chance' (1/300).
78
What is the preferred further testing for Down's syndrome, and what does it analyse?
NIPT Analyses cffDNA that circulate in pregnant women's blood. cffDNA derives from placental cells and the DNA is identical to fetal DNA.
79

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