Neonatology Flashcards

1
Q

DDH affects 1-3% newborns, what are risk factors and which hip is most affected?

A

Anything causing crowding in uterus eg. large birth weight, oligohydramnios
-female, first born babies,
-breech position, sibling(s) affected
Left hip most affected.

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2
Q

When should babies have their hips examined? (NB: if high risk US is done at 2-4weeks)

A

in first days of life and at 6weeks

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3
Q

If neonatal exam suggests hip instability what should you and in what timeframe? If hips still unstable at x weeks=requires rx.

A
  • arrange an US by 2-4weeks

- x = 6weeks

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4
Q

What is the treatment for DDH that hasn’t resolved by 6 weeks?

A

-long-term splinting in flexion abduction in a Pavlik harness

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5
Q

If DDH is detected from 6-18months how is it treated? And if after 18months?

A

6-18mnths: exam under anaesthesia, arthrography and closed reduction
18mnths+: open reduction with corrective osteotomies to maintain joint stability

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6
Q

What Test and Manoeuvre are used to examine the neonates hip?

A
  • The Ortolani Test: clunk as femoral head relocated

- The Barlow Manoeuvre: attempt to dislocate an unstable hip with pressure on femoral head w thumb

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7
Q

What is the main risk with a Pavlik harness to treat DDH? How can you monitor this? What age are these contraindicated in?

A
  • AVN of fem head from excess abduction
  • US and making sure fit is good
  • CI >4.5 months (or if hips are irreducible)
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8
Q

Talipes equinovarus is club foot, most idiopathic but 20% associated with genetic conditions. What is the 3 abnormalities of foot?

A
  • inversion
  • adduction of forefoot relative to hindfoot
  • equinus=plantarflexion deformity
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9
Q

What is the preferred treatment of talipes equinovarus, starting ASAP but changing gradually.

A

-Ponseti method: foot manipulated in a long leg plaster cast

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10
Q

If ponseti method fails to correct talipes, what surgery is carried out?

A

-soft tissue release

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11
Q

Neonatal jaundice is divided into: early, jaundice and prolonged jaundice, describe each in terms of mostly pathological or physiological and time frames

A

Early - <24hrs, most pathological (!) action needed
Jaundice - 24hr-14days mostly physiological
Prolonged - 14days+ (>21 if preterm) can be phys or pathological

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12
Q

Name 2 ways in which bilirubin can me measured in suspected neonatal jaundice:

A
  • transcutaneous bilirubinometres

- serum bilirubin measurements

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13
Q

Name 3 pathological causes of early neonatal jaundice (!)

A
  • sepsis
  • rhesus incompatibility
  • ABO incompatibility
  • red cell anomalies: spherocytosis, eliptocytosis, G6PD def.
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14
Q

In ABO incompatibility in neonate, what IgG antibody is always present?

A

Maternal anti-A or anti-B haemolysin

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15
Q

Based on differentials, what tests are important when investigating early neonatal jaundice?

A
  • septic screen: FBC, CRP, blood culture
  • packed cell vol, blood film
  • group and save
  • DAT, maternal blood group, G6PD level
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16
Q

For what reasons does neonatal jaundice often occur between 24hrs-2weeks?

A
  • shorter RBC lifespan so more bilirubin produced
  • less bilirubin conjugated (hepatic immaturity)
  • absence of gut flora impedes bile pigment elimination
  • breastfeeding w difficulties -> dehydration and less elimination of bilirubin (more enterohepatic circulated)
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17
Q

In physiological neonatal jaundice the bilirubin is __ and rises in first few days then resolves over 2weeks, levels should be monitored to prevent___

A
  • unconjugated

- kernicterus

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18
Q

What pathological causes of neonatal jaundice (24hr-2wks ) exist (name 2+)

A
  • polycythaemia
  • cephalohaematoma resorption
  • hypothyroidism
  • haemoglobinopathies
  • viral hepatitis
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19
Q

What is kernicterus? Levels of unconjugated bilirubin >350umol high risk(!)

A

Permanent neurological sequelae of severe hyperbilirubinaemia and acute bilirubin encephalopathy (deposited in basal ganglia and brainstem nuclei)
e.g. cerebral palsy, deafness, low IQ

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20
Q

How is kernicterus prevented?

A
  • phototherapy
  • exchange transfusion
  • IV Ig (if cause is isoimmune haemolytic disease)
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21
Q

What are signs of ABE (acute bilirubin encephalopathy) in neonates.

A
  • lethargy, poor feeding
  • hypotonia, shrill cry -> irritability, hypertonicity
  • then apnoea, seizures, coma, death
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22
Q

Phototherapy works by using light energy to convert __ to __ products (lumirubin etc) that can be excreted without __.

A
  • bilirubin
  • soluble
  • conjugation
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23
Q

Side effects of phototherapy for jaundice:

A
  • high/low temperature
  • eye damage (give protection)
  • diarrhoea, fluid loss
  • separation from mother
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24
Q

Exchange transfusion to treat jaundice uses __ blood, xml/kg given via __ vein and removed via the __ artery. Aim is to removed bilirubin.

A
  • warmed (37degrees)

- umbilical vein, umbilical artery

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25
Q

Prolonged jaundice is often physiological/breastmilk jaundice, what red flags alert a more serious pathology?

A
  • pale stool
  • hepatosplenomegaly, ascites
  • bruising/bleeding
  • neurological signs
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26
Q

Crigler-Najjar and Gilbert S. are unconjugated bilirubin causes of prolonged jaundice, name some conjugated causes:
clues: gland related, chole-related, aemia/blood related and deficiency

A
  • hypothyroidism, CF
  • biliary atresia
  • choledochal abnormalities
  • galactosaemia
  • a1 anti-trypsin def
  • neonatal haemochromatosis
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27
Q

Biliary atresia = biliary tree occlusion due to progressive cholangiopathy, it is rare but serious and earlier identified better prognosis, what signs?

A
  • jaundice, dark urine, pale stools
  • spleen palpable by ~4wks
  • liver may become hard and enlarged
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28
Q

RDS (Resp. distress S.) is when a deficiency of __ leads to lower __ causing widespread __ __ and inadequate __

A
  • surfactant
  • surface tension
  • alveolar collapse
  • gas exchange
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29
Q

Surfactant is a mixture of ___ and proteins excreted by the __ of the alveolar epithelium

A
  • phospholipids

- type II pneumocytes

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30
Q

The more preterm the infant the higher chance of RDS, if preterm is anticipated what can be done? What does this trigger? timeframe -24-34wks

A
  • give antenatal glucocorticoids to mother

- stimulates fetal surfactant production

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31
Q

At delivery/within 4hrs, what signs will be present in a baby with RDS? and when severe?
NB: atelectasis then re-inflation w each breath exhausts the baby..

A
  • tachypnea (>60breaths/min)
  • laboured breathing, chest wall recession, subcostal indrawing and nasal flaring
  • expiratory grunting (trys to create a positive airway pressure)
  • (severe ->cyanosis, hypoxia, low co, low BP, acidosis & renal failure)
32
Q

How is RDS treated?

A
  • delay clamping cord to promote placenta-fetal circulation
  • oxygen via 02-air blender start at 30% and increase
  • surfactant therapy
  • CPAP, NIPPV or mechanical ventilation
33
Q

Name 3 ddx of increased work of breathing within hours of birth other than RDS.

A
  • sepsis, meconium aspiration, congenital pneumonia
  • tracheo-oesophageal fistula
  • TTN
34
Q

Describe an RDS typical CXR appearance:

A

-X-ray: ground glass diffuse granular lungs +/- air bronchograms (large airways outlined), heart border indistinct

35
Q

Based on preterm gestation weeks and FiO2 %, you can intubate and give RDS prophylactic .. via..

A
surfactant
ET (endotrachal) tube
36
Q

Bronchopulmonary dysplasia (BPS) complicates ventilation in some __ baby’s especially with a birth weight

A
  • RDS, <1kg
  • ante and postnatal steroids
  • surfactant
37
Q

Pulmonary hypoplasia is rare, suspect in infants with persisting __ +/- feeding difficulties. Some degree occurs with an early elective delivery for early spontaneous ROMs

A

-neonatal tachypnoea

38
Q

Define : preterm, low birthweight (LBW), very LBW, extremely LBW and small for gest. age (SGA).`12

A

Preterm: neonate <37weeks gestational age (GA)
LBW: <2500g regardless of GA
VLBW: <1500g regardless of GA
ELBW: <1000g “”
SGA: birthweight below the 10th percentile for GA

39
Q

IUGR = a reduction of expected fetal growth in utero, most commonly is __ when weight centile is __ compared to length and head circumference -ie. __. (usually due to an insult __ in pregnancy e.g. __)

A
  • asymmetrical
  • reduced
  • head sparing
  • later in pregnancy e.g. pre-eclampsia
40
Q

Less common symmetrical IUGR suggest foetus was affected from __ pregnancy, seen in babies with __ or constitutionally small and are more likely to remain __

A
  • early
  • chromosomal abnormalities
  • small permanently
41
Q

Poverty accounts largely for variance in birthweights, what other factors can cause IUGR?

A
  • malformation, twins, congenital infection

- placental insufficiency (maternal HD, high BP, smoking, diabetes, sickle cell..)

42
Q

Other than shorter adult stature and possibly health, what are major complications of IUGR? -risks from infection/malformation if present..

A
  • hypogylcaemia (poor fat/glycogen stores)
  • hypothermia (larger SA)
  • polycythaemia 2dry to chronic hypoxia
  • NEC
  • meconium aspiration
43
Q

~40% prematurity causes are unknown, what are some possible causes?

A
  • smoking, malnutrition, poverty
  • PMH of prematurity, GU infectio/chorioamnionitis
  • PT, DM, polyhydramnios, multiple pregnancy
  • uterine malformation
  • placenta disorders, premature ROM
44
Q

What are pre-term babies likely to require support with after birth?

A
  • thermoregulation

- nutrition

45
Q

In RDS air from overdistended alveoli can track into the interstitium -> pulmonary interstitial __ .
In 10% ventilated infants, air leaks into pleural cavity causing a _

A
  • emphysema

- pneumothorax

46
Q

How can you thermoregulate a pre-term baby?

A
  • put in plastic bag at birth
  • stabilise under a radiant warmer +/- heated matress
  • humidified incubator
47
Q

What can stimulate respiration for a preterm with periods of bradycardia/apnnoea?

A

Caffeine

48
Q

Patent ductus arteriosus with shunting of blood from left to right is common in preterm infants with__ and can cause difficulty __

A

RDS

-difficulty weaning the infant from artificial ventilation

49
Q

If symptomatic how can a patent DA be closed medically in a pre-term?

A

-a prostaglandin sythetase inhibitor, indomethacin or ibroprofen

50
Q

Why are preterm babys at risk of iron deficiency? (same reason they are at increased risk of infection) and 2 other reasons..

A
  • iron is mostly transferred in the last trimester and from loss of blood from sampling and inadequate EPO response
  • iron supplements are started at several weeks
51
Q

NEC (Necrotising Enterocolitis) is higher in preterms due to the bowel being vulnerable to _, what is beneficial in preventing this disease?

A
  • ischaemic injury and bacterial invasion

- breast milk = (can add pre+probiotics too)

52
Q

what are signs of NEC in the infant? What can NEC progress to?

A
  • feed intolerance, vomiting, bile may be stained
  • distended abdomen, stool +/- blood
  • pain
  • can –> bowel perforation
53
Q

NEC treatment? NB: mechanical ventilation and circulatory support may be needed

A
  • stop oral feeding
  • give broad-spec Abx vs aerobic and anerobes
  • parenteral nutrition
54
Q

20% VLBW infants have haemorrhages in the brain, these can be detected with _. RFs include:

A

US scans of craium

-asphyxia, severe RDS, pneumothorax

55
Q

Retinopathy of prematurity affects developing blood vessels at the junction of the __& __ __. There is vascular __ which can progress to retinal __ , fibrosis and __.

A

vascularised and non-vascularised retina
proliferation
retinal detatchment
blindness

56
Q

Retinopathy of prematurity affects 35% VLBW infants so infants at risk (

A

<1500g or <32 weeks GA

57
Q

Laser therapy reduces visual impairment in retinopathy of prematurity, what injections may prove beneficial?

A

-intravitreal anti-VEGF

58
Q

At birth name 3 things the growth-restricted infant is at risk of:

  • hypo
  • hypo
  • hypo
  • p____
A
  • hypothermia (large SA:V ratio esp w large head)
  • hypoglycaemia (from poor fat and glycogen stores)
  • hypocalcaemia
  • polycythaemia Ht > 0.65
59
Q

name 3 problems associated w being large for gestational age infants (>90th centile) (most = normal but may be from mother T1/gest.DM or congenital disease)

  • birth ___ e.g. from ___ ___, or birth ____
  • hypo___ due to _____
  • p____
A
  • birth trauma e.g. shoulder dystocia, birth asphyxia
  • hypoglycaemia due to hyperinsulinemia
  • polycythaemia
60
Q

Give 5 scenarios in which hypoglycaemia is more likely in first 24hrs of life:
..babies:

A
  • with IUGR
  • who are pre-term
  • who are born to mothers with DM
  • who are large-for-dates
  • hypothermic, polycythaemic, or ill for any reason
61
Q

Preterm/IUGR babies may have hypoglycaemia due to: ___?

vs. infants of a DM mother –> hypoglycaemia due to: ___?

A
  • IUGR: poor glycogen stores

- DM: sufficient stores but hyperplasia of the islet cells -> high insulin levels

62
Q

Name 3 sx of hypoglycaemia in the newborn:

A
  • jitteriness
  • irritability
  • apnoea
  • lethargy
  • drowsiness
  • seizures
63
Q
  • how is hypoglycaemia usually prevented?

- if BMs are low on 2 occasions despite this, what/how do we give?

A
  • prevent by early and frequent milk feeding

- if still low, give IV dextrose infusion (aim maintain BM > 2.6mmol/l)

64
Q

NB: to correct hypoglycaemia in a new born dextrose is usually given IV infusion, if v high conc e.g. 20% is needed, how should it be given due to what risk?

A

-high concs give via central venous catheter (avoids extravasation into tissues can -> tissue necrosis)

65
Q

If in a hypoglycaemic neonate there has been a significant difficulty or delay in starting IV dextrose what can be given instead?

A

-Glucagon

66
Q

Explain what birth asphyxia is? Risk?

A
  • lack of oxygen in labour/delivery

- risk of brain injury and death

67
Q

What gasping is seen in birth asphyxia and what do we call it? and how does HR change?

A
  • fetus O2 deprived in utero -> gasps, primary apnoea (HR maintained)
  • if lack of O2 continues, –> irregular gasping then 2nd period of apnoea (secondary) with this HR and BP falls
68
Q

In secondary apnoea from birth asphyxia (-if lack of O2 continues, –> irregular gasping then 2nd period of apnoea), what is the only way infant can recover upon delivery?

A

-needs help with lung expansion upon delivery: positive pressure ventilation or tracheal tube to lungs directly

69
Q

Name 2 causes of a continuous asphyxia insult (rare)

and 1 v common cause of intermittent birth asphyxia:

A
  • continuous: after placental abruption, or cord prolapse

- intermittent: during labour from prolonged and frequent contractions

70
Q

HIE (Hypoxic-Ischaemic Encephalopathy) clinical manifests ~48hrs post asphyxia, state a ft of:

  • mild
  • moderate
  • severe
A

mild: irritable infant, +/- hyperventilation, hypertonia, impaired feeding, stary eyes
mod: abnormal movements, hypotonic, can’t feed, +/- seizures
severe: no normal spontaneous movement/response to pain, fluctuating limb tone, multi-organ failure, seizures

71
Q

Name 4 ways you can manage infants with HIE (different aspects of their care)

A

-respiratory support
-rx clinical seizures w anti-convulsant
-fluid restrict due to transient renal impairment
-rx hypotension by volume and inotrope support
-monitor and rx hypoglycaemia, electrolyte imbalance esp low Ca2+
-

72
Q

What is the standard therapy for mod-severe HIE?

Neuroprotection achieved how?

A
  • inducing mild therapeutic hypothermia (cool to 33-34 rectal temperature for 72hrs by wrapping in a cooling blanket)
  • reduces brain damage if started within 6hrs of birth in an infant >36weeks’ gestation
73
Q

Trisomy 18: small babies, short sternum (resp problems), small chin and rockerbottom feet, heart and renal abnormalities
What syndrome and prognosis?

A
  • Edward’s Syndrome

- 90% die within first year

74
Q

Polydactyly, severe developmental malformations, heart, renal, midlife defects, rarely survive >1 month, what is this rarer trisomy syndrome?

A

-trisomy 13: Patau Syndrome

75
Q

What would the karyotype be for a female child with Turner’s Syndrome?

A

45X

76
Q

Williams syndrome is a 7q11.23 deletion that often presents with congenital heart defects (AS, PS) with bulbous tipped nose, wide mouth and widely spaced teeth, developmental delay…

  • what is the personality?
  • 15% have a what electrolyte abnormality
A
  • overfriendly personality

- hypercalcaemia