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FRACP > Neonates > Flashcards

Neonates Flashcards

1
Q

NEC Clinical features Radiological features

A

General early clinical signs

  • temp instability
  • apnoea
  • bradycardia
  • lethargy

Abdo signs

  • bile-stained aspirates
  • abdominal distension, tenderness
  • feed intolerance
  • positive faecal occult blood/fresh PR blood

Radiological

  • pneumatosis (gas within bowel wall)
  • pneumoperitoneum (if perf)
  • portal venous gas or bubbles in portal vein on ultrasound
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2
Q

Risk factors or causative factors for NEC

A

Prematurity

  • Premature immunen system
  • Impaired intestinal barrier function
  • VLBW (poor blood supply to gut)

Exogenous RF

  • Formula feeding (carb and protein excess leads to bacterial overgrowth) –> Mx: Breast milk
  • infx -> inflammation
  • hypoxia -> incr ROS
  • anaemia -> incr ROS

Microbial dysbiosis

  • Decr beneficial microflora
  • Incr pathogenic bacteria

–> Mx: probiotics

Other RF

  • PDA (treating PDA doesn’t reduce NEC however)
  • Incr gut pH (H2 blockers are assoc w NEC however ?cause/effect)
  • Fortification in PT infants
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3
Q

Routine prophylaxis against NEC

A

Probiotics Breast milk (mother’s own or donor)

Early (day 2) commencement of enteral feeds

Antenatal steroids in premature infants reduce risk of NEC

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4
Q

Microbiome in term babies

A

Pick up the flora of mother’s vaginal canal as they are born: Term babies ‘good’ bacteria - Lactobacilli and bifidobacteria Formula-fed Coliforms, enterococci, bacteroids

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5
Q

Microbiome in preterm babies

A

Often from nursery environment rather than from mother’s vaginal canal and skin surface Use of abx can reduce the bacterial diversity (prolonged duration of initial abx course in preterm babies is assoc w risk of NEC and death) Hence give probiotics to give them ‘good bacteria’ normally found in the gut of healthy term bugs (lactobacillus etc) - shown to reduce risk of NEC

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6
Q

Indications for surgical mx of NEC

A

Perforation Abdo mass Not responding to medical management Via Formation of ileostomy then closure after 4-6 weeks (contrast study pre closure to ensure no stricture)

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7
Q

What is the strongest stimulant for the closure of ductus arteriosus

A

Increased systemic oxygen supply is most important (from initial breaths Also - Decr circ Prostaglandin - Decr pulm vasc res - incr pulm blood flow (due o foramen ovale closure and reduced shunting across DA)

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8
Q

Ix for prolonged jaundice (and what is considered ‘prolonged’)

A

2 weeks or 3 weeks in preterm babies FBC Direct/conjugated bilirubin TFTs

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9
Q

Congenital hypothyroid features

A

Early signs - prolonged jaundice - poor suck/feeding - bradycardia - constipation - poor tone - FTT - umbi hernia - large anterior fontanelle

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10
Q

Definition of hypoglycaemia in newborn

A

<2.6

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11
Q

Causes of transient hypoglycaemia in newborn

A

ketotic (low substrate availability ) - IUGR - prematurity - asphyxia - hypothermia - sepsis - malformation Hyperinsulinism (non-ketotic) - diabetic mother - GDM - rhesus isoimmunisation

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12
Q

Clinical features of hypoglycemia

A

Apnoea Jitteriness Seizure lethargy Hypotonia

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13
Q

Causes of persistent hypoglycaemia in newborn

A

Hyperinsulinism: - Persistent hyperinsulinaemic hypoglycaemia of infancy - Beckwith-Wiedemann syndrome - Insulinoma Metabolic: Carbohydrte metabolism disorder - Galactosaemia - Hereditary fructose intolerance Organic academia - Maple syrup urine disease

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14
Q

Mx of hypoglycaemia in nweboern

A

If can feed - Oral glucose (BM or formula then hourly feeds with monitoring if blood glucose levels If cannot feed - IV 10% dextrose (5mg/kg bolus then infusion with TFI 60-90ml/kg/d) - If remains low, may need to escalate to 15-20% glucose infusion

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15
Q

What part of brain is most vulnerable to effects of hypoglycaemia?

A

Occipital lobe

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16
Q

Effect of caffeine when used to treat AOP

A

Decr ventilation Decr CLD decr need for PDA ligation decr incidence of severe ROP Incr disability free survival Decr cerbral palsy Decr cognitive delay

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17
Q

What are the target sats in a preterm baby and why?

A

aim spO2 91-95% reduce risk of ROP reduce need for ongoing O2 at 36 weeks

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18
Q

What is late preterm?

A

34 to 36 weeks gestation Incr morbidity and mortality Worse neurodev outcomes at 2 years of age Incr risk of CP

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19
Q

Risks of mid trimester oligohydramnios

A

Pulmonary hypoplasia

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20
Q

Mx of neonatal abstinence syndrome

A

Morphine -weaning regime

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21
Q

Mx of congenital diaphragmatic hernia

A

Intubate at birth then use conventional mechanical ventilation (over oscillation)

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22
Q

What does this ultrasound series show?

A

grade IV bleed (arrow in a), which developed into a porencephalic cyst (arrow in b).

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23
Q

Maternal antenatal screening ix (not including imaging)

A

Blood group and Ab (Rh)

RBC

Rubella, syphilis and hep B serology

HIV status

Sickle/thal haemoglobinopathy screening

Rhesus Ab if negative

OGTT

Urine dips

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24
Q

Maternal antenatal screening ultrasounds

A

1) 8-12 week dating scan
2) 11-14 week nuchal scan
- > nuchal fold thickness measured, is increased in down syndrome (77% sensitivity, 5% risk of false +)
- > presence/absence of nasal bone can give up to 97% risk of down syndrome (when combined with nuchal fold thickness)
- > gives risk for down, trisomy 13 and 18
- > can detect early anomalies and diagnosis of twins and onset twin-twin transfusion syndrome
3) 20-24 week anomaly scan
- > more detailed look at getal growth and looking for major congenital abnormalities and neural tube defects
4) +/- >20 weeks - growth scans (only done if concern for fetal growth or wellbeing)

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25
Q

Invasive tests for downs syndrome

How early can they be done and what is the risk of miscarriage with each?

A

1) Chorionic villous sampling
- Can be done as early as 11 weeks GA.
- overall 3-4% risk miscarriage
2) Amniocentesis
- Can be done as early as 16 weeks GA
- overall 1.5-2% risk of miscarriage

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26
Q

What is ‘the triple test’ ?

A

It is 3 maternal serum tests used to predict risk for down and other trisomies at 14-22 weeks GA if nuchal scanning is not available

Tests for:

  • free beta-hcg - incr in downs
  • unconjugated oestradiol - decr
  • alpha fetoprotein (AFP) - decr

62% sensitivitity w 5% risk of false positives

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27
Q

Indications for the following things in pregnancy:

  • folic acid
  • oily fish/omega 3
A

FOlic acid

  • reduces incidence of neural tube defects

Oily fish

  • neonatal brain development
  • reduce risk of preterm labour
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28
Q

Definition of twin-twin transfusion syndrome

what sort of twins does it affect?

Which twin is at higher risk?

A

Monochorionic twins

Share the same placenta

Difference in Hb >5 between the twins due to one twin hogging the majority of placental blood flow and nutrients -> becomes large and plethoric vs the othertwin becoming small and anaemic

Larger twin is at higher risk due to reduced

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29
Q

Do antenatal steroids reduce rate of IVH?

A

Yes

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30
Q

egg on a string xray = ?

A

TGA

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31
Q

boot shaped heart xray = ?

A

TOF

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32
Q

What is this image of?

What is the pathophys and clinical significance of this condition?

A

Periventricular leukomalacia

Pathophys:

It likely occurs as a result of hypoxic-ischaemic lesions resulting from impaired perfusion at the watershed areas, which in premature infants are located in a periventricular location. It is likely that infection or vasculitis also play a role in pathogenesis.

early: periventricular white matter necrosis
subacute: cyst formation
late: parenchymal loss and enlargement of the ventricles

Clinical significance:

  • PVL may manifest as cerebral palsy (>50% in the setting of cystic PVL), intellectual disability or visual disturbance
  • when cystic PVL is present, it is considered the most predictive sonographic marker for cerebral palsy
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33
Q

Indication for methenele blue in cyanosed newborns?

A

Methaemoglobinaemia

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34
Q

What do u give cyanosed babies to keep duct open?

A

Prostaglandin E1 (note - prostaglandin E2 has opposite effect- cuases closure of duct)

PGE1 MOA - prevents the ductus arteriosus from closing, creating an intentional shunt to allow mixing of deoxygenated with oxygenated blood

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35
Q

Case

  • cyanosed newborn
  • cxr showing large heart, oligaemic lung fields

?diagnosis

A

Pulmonary atresia with intact VSD

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36
Q

what sort of blood gas will long-term or high dose furosemide cause?

what medication should be paired with it to reduce risk of this

A

metabolic alkalosis with low Na and low K, high bicarb

Pair with K sparing diuretic (spironolactone)

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37
Q

Effect of antenatal steroids in women at risk of preterm labour?

A

reduced risk of serious resp illness and death

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38
Q

What gut condition is associated with beckwith wiedemann syndrome

A

Omphalocoele

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39
Q

Omphalocele VS gastroschesis.

What is the difference and which is associated with orther organ system anomalies?

A

Both result of abdominal wall defect. Can be detected antenatally.

In contrast to omphalocele, there is no sac covering the intestines in gastroschisis

Gastroschesis - no membrane covering intestines , isolated anomaly

vs omphalocele - membrane covered. associated with particularly renal, cardiac defects.

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40
Q

If you’ve got a high Co2, what change do you make to the freqyency on HFOV?

A

Reduce the frequency (greater volume of air displaced)

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41
Q

What is this CXR of and what is the appx survival of live births and what side has higher mortality?

is this condition assoc w other chromosomal abnormalities?

A

CDH

60-70% survival

R sided lesions have higher mortality rate (if liver in chest)

not assoc w chromosomal abnormalities. usually isolated defet.

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42
Q

Mec stained liquor in a preterm baby - what infection are you most concerned about and what is the gram stain appearance of this?

What might the sources of this be?

A

Listeria infection - GP bacilli

Sources - Unpasturised milk, soft cheese

Uncooked raw fruis/veg

Chicken

Over counter reheated foods

Uncooked, smoked meats

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43
Q

Blueberry muffin rash is consistent with what neonatal infection?

how is this condition diagnosed and what other clinical features are there?

A

CMV

Diagnosed on urien or serum PCR

Other clin ft

  • Brain - cerebral periventricular calcifications, sensorineural deafness, dev delay, microcephaly, encephalitis

Skin: petechial rash (see above)

Liver: hepatosplenomegaly, jaundice

Lungs: pneumonitis

Eyes: Chorioretinitis, optic atrophy

Ears: SNHL!!

Teeth: dental defects

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44
Q

What is maternal lupus disease assoc with in the neonate?

A

Neonatal lupus

Congenital heart block

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45
Q

What is maternal diabetes assoc w in hte baby?

A

Macrosomia

Neonatal hypoglycaemia from hyperinsulinism

RDS

Polycythaemia

x2 risk congenital anomaly

Renal vein thrombosis

CHD (VSD, coarct, TGA, hypertrophic subaortic stenosis, hypertrophic obstructive cardiomyopathy)

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46
Q

Risk of hyperthyroidism in mother to baby and why does it occur?

What investigations would you do to diagnose this condition in the baby

WHat is the treatment?

A

Transient neonatal thyrotoxicosis

Mothers - generally on anti-thyroid meds, pmhx Graves

  • Occurs secondary to transplacental Ab (TRAb) transfer in maternal graves disease (lasts 6-12 weeks)
  • Neonate will have elevated T3, T4 and low TSH + anti-thyroid receptor Ab

Tx - beta blocker for sx control; carbimazole (PTU 2nd line) or radioactive iodine

47
Q
A
48
Q

Source of toxoplasmosis

A

Is an intracellular parasite

Vertical transmission from infected mother antenatally

Acquired from

  • raw meat
  • unwashed fresh fruit/veg
  • cat faeces

Clinical features

  • Brain: cerebral calcifications, round lesions, seizures, microchaly, dev delay, encephalitis
  • Eyes: chorioretinitis, cataracts
  • Liver: hepatosplenomegaly, jaundice
  • Haem: anaemia
  • Lungs: pneumonitis
49
Q

What are the TORCH infections?

Common sx/signs

A

Toxoplasmosis

Other - Varicella

Rubella

CMV

HSV

Sx

  • Fever
  • Feeding difficulty
  • Petechial rash (CMV, rubella)
  • Hepatsplenomegaly
  • Jaundice
  • Sensorineural deafness (CMV, rubella)
  • Chorioretinitis (CMV, toxo)
  • Cataracts (Rubella)
  • Meningitis/encephalitis
  • Brain calcifications (CMV, toxo)
50
Q

What is the highest risk period (to baby) for motehrs to acquire maternal chicken pox

What is the treatment?

A

Maternal chickenpox around delivery (last 4 weeks but especially <5 days before delivery or <2 days after delivery) can cause severe infection in infant due to high viral titres without maternal Ab yet to protect infant

Clnical features

BRAIN - microcephaly, brain aplasia, hydrocephaly

EYS - cataracts, chorioretinitis, microphtalmia

SKIN - zigzag scarring (cicatrix)

LIMBS - limb malformation, shortening, paresis

Tx

  • babies are given VZIG (anti-varicella zoster IgG) IM as post-exposure prophylaxis
  • IV aciclovir if any vesicles develop
51
Q

Advantages of breast feeding

A
  • Nutrition: improved neonatal brain development
  • Immune protection, particularly maternal IgA (protects against resp and GI disease)
  • Uterine involution and maternal weight loss expedited
  • Contraceptive (lactation amenorrhoea) - as effective as OCP in first 6 months
  • Cheap!
  • Decr risk of breast cancer x4.3% per year of breast feeding
  • Reduced incidence of atopy in childhood and teenage years
  • Maternal-infant bonding
52
Q

Risk factors for group B strep sepsis in neonate

A

Maternal fever

PROM

Preterm infant

Inadequate labour prophylaxis given (penicillin or clindamycin to vaginally colonised mothers)

53
Q

what is this photo of, how is it aquired?

A
  1. Erb palsy ie damage to upper roots C5 +/- 6, 7 -> often from shoulder dystocia -> presents with arm/wrist/hand in ‘waiters tip’ position
54
Q

What is this photo of, how is it typically acquired?

A

Klumpke palsy

damage to lower nerve roots (C7, 8, T1) of brachial plexus during delivery

Wrist drop and paralysis of small muscles of hand (‘claw’ hand)

May be assoc w horner’s syndrome

55
Q

cephalohaematoma

  • what is it?
  • mx
  • complications
A

Should self resolve over several weeks

Does NOT cross suture lines

  • Is due to bleed beneath periosteum due to torn veins)

Cx

  • jaundice
  • calcification -> permanent bump on head
  • Assoc IVH
  • underlying skull # (20% of cases but rarely needs treatment)
56
Q

What is the most risky time period for acquisition of fetal varicella infection frmo mother?

A

Acquired from maternal genital tract during delivery (thus C/S has been proven to be effective in limiting transmission in mothers who are actively shedding viral particles)

  • Primary maternal infection during pregnancy is most risky - up to 50% babies affected
  • Recurrent maternal infection during pregnancy - only 3% babies affected
57
Q

Fetal varicella infection clinical presentation

A
  1. Skin/eyes/mouth - limitation of rash/vesicles to these areas.
  2. CNS - encephalitis +/- skin
  3. Disseminated disease - multi-organ failure. viral sepsis with resp, hepatic failure and DIC +/- CNS, skin, eye, mouth
58
Q

Conjunctivitis in the newborn period

  • ddx and how to distinguish clinically
A

Chlaymdia vs gonococcal

Both purulent

Chalmydia presents in 2nd week of life

Gonococcal presents days 1-2 of life

59
Q

Definition and Treatment of Omphalitis

Complications

A

Definition: infection of umbilical stump

Treatment: MCS swab of umbi

Gentle cleansing

IV abx if signs of cellulitis around umbi

Cx - portal vein infection and subsequent portal HTN

60
Q

Metabolic acidosis/alkalosis picture

vs Respiratory

A

Met acidosis - low pH, low bicarb (sick infant)

Met alkalosis - high pH, high bicarb (GI losses/vom/diarr, diuretics, renal/Bartters/Gitelmans)

Resp acidosis - low pH, high Co2 (underventilated)

Resp alkalosis - high pH, low Co2 (overventilated)

61
Q

What is continuous mandatory ventilation?

A

Form of IPPV - full ventilation to baby

62
Q

What is IMV (intermittent mandatory ventilation)?

A

Form of IPPV

Only occasional breaths gienv by ventilator

USed to wean babies who are making some resp effort off the ventilator

63
Q

What is patient triggered ventilation (PTV)?

A

Form of IPPV

Ventilator assists breaths after they are triggered by baby - used to wean babies off ventilator

64
Q

Indication for nitic oxide and MOA

SE

A

MOA - vasodilator that acts on pulmonary artery smooth muscle via increasing cGMP levels

Indication: PPHN to decrease pulm artery hypertension

SE - methaemoglobinaemia and can alter plt function

65
Q

IUGR

  • Causes of asymmetrical growth failure
A

IUGR: growth <3rd centile for dates

Asymmetrical: weight < HC centile due to relative sparing of brain

  • Cause: placental failure LATE in pregancy -> growth post birth accelerates
  • > pre-eclampsia, multi gestation, maternal cardiac/renal disease affecting blood supply to placenta, uterine malformation
66
Q

IUGR - causes of symmetrical growth failure.

A

Symmetrical: HC, weight, length all equally affected

  • Cause: CHRONIC intrauterine growth failure -> growth post birth continues to be poor
  • Cause: smoking, malnutrition, chornic disse; chromosomal disorder, congenital infection
67
Q

Definition of large for gestational age and causes

A

LGA weight > 90th centile

Causes

  • diabetic mother
  • Familial (large parents)
  • Beckwith-wiedemann syndrome
68
Q

Problems associated with prematurity

A

Temperature instability

Brain - HIE, intracranial haemmhorage, lack of primitive reflexes (suck)

Lungs - apnoeas, RDS, pneumothorax, haemmhorage, BPD

Heart - PDA, PPHN

GI - feeding intolerance, GORD, NEC

Liver - Jaundice

Kidneys - impaired concentration ability, impaired acid excretion

Immunity - impaired immune system, susceptible to infx

Eyes - ROP

Metabolic - low sugars, low Ca, osteopaenia of prematurity

Haem - anaemia

Surgial - hernias

69
Q

What is RDS?

Definition

RF

Protective

Clinical features

CXR findings

Mx

A

Defintion: Resp distress caused by insufficient surfactant

=> Non-compliant/stiff lungs -> hypoxia and resp aciodis -> severe cases can lead to PPHN

RF - prem, hypoxia, acidosis, shock, asphyxia, diabetic mother, APH, second twin, male

Protective - maternal steroids (given to mohers 48hrs before delivery if prem delivery expected)

Clnical ft

  • Resp distress from 6 hours of age
  • Worsens over 2-3 days then improves over 1-2 weeks

CXR: ground glass apperaance, air bronchograms

Mx:

  • surfactant via ETT or MIST
  • resp support: O2, CPAP or positive pressure ventilation

+/- abx

  • Minimal handling
70
Q

Surfactant - what is it produced by and what is its role?

At what age does it begin to be produced?

A

Lowers surface tension and increases compliance in alveoli -> decreased pressure required to open alvoeli

Produced by type II pneumocytes

Produced around 24 weeks of age

71
Q

What is bronchopulmonary dysplasia?

Definition

Clinical features

CXR

Mx

A

Now known as CLD

Chronic lung damage with persistent Xray changes secondary to severe RDS or other neonatal lung disease

Persisting O2 requirement on day 28 of life or at 36 weeks gestation

Clinical features:

  • Chest hyperinflation, WOB (IC and SC recession)
  • Lung Creps

CXR: honeycomb lung (cystic pulm infiltrates in reticular pattern), areas of emphysema, collapse and fibrosis and thickening of pulonary arterioles

Mx

  • Steroids and diuretics if vnetilator dependent
  • Bronchodilators if wheezy

+/- home O2

72
Q

Wilson MIkity Syndrome

A

A form of BPD

  • Respiratory distress (WOB, hypoxia, apnoea) that develops SLOWLY over the first month in PREMATURE/LWB (<1.5kg) babies who have no history of severe resp distress earlier in life

Characteristic CXR findings: streaky infiltrates and cysts

73
Q

TTN:

Definition

Cause

RF

CXR

Tx

A

Definition: resp distress at birth resolving over FIRST 24HRS

Due to excess retained fetal lung fluid -> self-limiting cdtn

RF: LUSCS, diabetic mother, heavy maternal analgesia

CXR: streaky, fluid in fissures, pleural effusions

Tx - supportive (O2) +/- abx

74
Q

Common causative agents for neonatal pneumonia

A

Group B haemolytic strep

GNB ( e coli, klebsiella, pseudomonas, serratia)

Staph saprophyticus

Rarer - lysteria, chlamydia, mycoplasma, CMV, coxsackie, RSV

75
Q

What can inhaled meconium result in

A

Airway plugging with distal atelectasis, air leaks

Secondary pneumonia

Chemical pneumonitis (toxic to lung tissue)

Hypoxia, resp/metabolic acidosis

PPHN if severe

76
Q

CXR features of Mec aspiration syndrome

A

Hyperinflation

Diffuse patchy opacification

77
Q

Causes of neonatal cyanosis

A

Cardiac - cyanotic CHD (tof, ta, pa, ebstein anomaly, tga, tapvd, hypoplastic l heart, double inlet ventricle)

Respiratory - severe lung disease, PPHN

  • airway obstruction

Brain - asphyxia, seizures, neuromuscular

Haem - methaemoglobinaemia

78
Q

PPHN - Definition/Cause

Clinical features

Gas finding

CXR findings

ECho findings

Mx

A

IE ‘Persistent foetal circulation’ - failure of pulmonary vascular resistance to fall after birth

Results in blood continuing to be shunted AWAY from lungs (high pressure -> lower pressure systemic) via ductus arterius and foramen ovale (R -> L shunt)

Clinical features:

  • Central cyanosis
  • LOUD P2
  • Little impr in sats with 100% O2
  • Preductal paO2 > 5mmHg than postductal paO2

Gas: low pO2, relaitvely normal pCO2

CXR: NORMAL heart size, oligaemic lung fields

Echo: structurally NORMAL heart (not CHD), high pulmonary art pressures

Mx - resp support, NO

79
Q

Signs of fetal distress inutero

A

Fetal bradycardia with reduced variability

Late decelerations

Reduced fetal movements

Meconium

80
Q

What is HIE?

Clinical features

Prognosis

A

Hypoxic ischaemic encephalopathy

  • results from ischaemic injury to brain
  • affects WATERSHED zones between major arteries as these are most susceptible to hypoperfusion

Clinical features: develops over a few days - low apgars, floppy, seizures and irreg breathing

Incr risk of ID, seizures, cerberal palsy and death in severe disease.

81
Q

Causes of HIE

A

Maternal - pre-eclampsia, eclampsia, hypotension

Palcental - abruption, cord prolapse, insufficiency

Foetal - prem, post-dates, obstructed labour (breech, shoulder dystocia)

82
Q

Commonest type of intracranial haemorrhage in neonates?

Cause and location of these bleeds?

Timing

Risk factors

A

Name: Periventricular haemorrhage (PVH)

Location :The highly vascularised subependymal germinal matrix (at head of caudate nucleus)

Cause: Unstable cerebtral circulation (blood vessels of the germinal matrix are weak-walled and predisposed to haemorrhage). Significant stress experienced by a premature infant after birth may cause these vessels to rupture into periventricular areas and may progress to IVH (grades 2-4).

Timing: Usually occur within 1st week of life (90% in first 4 days) in premature/LBW infants

Other RF:

    • RDS*
    • IPPV*
    • Metabolic acidosis*
    • Hypercapnoea*
    • Coagulation disorder*
83
Q

Grading/classification of Perivenricular haemorrhage

  • Grade 1 -4
A

Grade 1: periventricular/subependymal bleed (confined to seminal matrix)

GRade 2: IVH (extension into lateral ventricle WITHOUT ventriculomegaly)

Grade 3: IVH with ventriculomegaly

Grade 4: Bleeding into brain parenchyma

84
Q

Treatment and Complications of intracranial bleeds

A

Tx - supportive

Cx

  • Hydrocephalus (may require supportive shunt)
  • Porencephaly (cyst or cavity filled with cerebrospinal fluid develops in the brain - see image)
  • Cerebral palsy
85
Q

Causes of jitteriness

A
  • Hypoglycaemia
  • Hypocalcaemia
  • Sepsis
  • Drug withdrawal (opiates, benzos in particular; also SSRIs eg sertraline)
86
Q

How to distinguish between seizures and jitteriness clinically?

A

Jitteriness - Rhythmic movements

Can occur when baby is alert or asleep

Normal eye movements

Movement stops when limb is held.

Seizures - Can be multifocal, w tone alteration +/- apnoea

Altered conscious state

Eye deviation

Movements do NOT stop when limb is held

87
Q

Causes of neonatal seizures

A

Congenital brain anomaly

Other brain stuff- CVA, subarachnoid haemorrhage

Asphyxia/respiratory

Infection/sepsis/meningitis

Metabolic/electrolyte disturbance (low glucose, low Ca, low Mg)

Inborn error of metabolism (pyridoxine deficiency etc)

88
Q

Management of opiate withdrawal in neonates

A

Opiates - morphine weaning regime (sometimes use other sedatives such as diazepam, chlorpromazine) over several weeks

Do NOT give naloxone - can induce immediate withdrawal which can be life threatening

89
Q

Short and long term complications of NEC

A

Short - perforation, obstruction, gangrenous bowl, intrahepatic cholestasis, sepsis, DIC

Long - stricture, short bowel syndrome (resection of diseased bowel), lactose intolerance

90
Q

Meconium ileus - clinical presentation and significance

A

Intestinal obstruction of terminal ileum due to THICK INSPISSATED MEC

Failure to pass mec within 48hrs of birth

Clinical features of obstruction - bilious vomiting, abdo distension

AXR: dilated loops of bowel centrally (small intenstine) WITHOUT air fluid levels. Bubbly appearance of intestinal contents in the right lower quadrant.

COntrast enema for diagnosis - microcolon; contast unable to get past point of transverse colon

10% of CF cases present with this

91
Q

What is osteopaenia of prematurity caused by and what investigations support its diagnosis?

A

Premature and IUGR/VLBW kids are susceptible:

  • Mineral deficiency (particularly phosphate) due to
  • Placental insufficiency
  • Inadequate Ph levels in breast milk or feeds
  • Meds: Long-term steroids or diuretics

Ix =

  • Phosphate L
  • PTH H (response to low Ph)
  • ALP H (released from resorbing bone w high bone turnover)
  • Note: Ca can be N/L/H

Mx

  • Vitamin D
  • Low BW formula (contains more Ph)
  • Ph supplements if breast feeding
92
Q
A

Hydrops - Severe oedema, ascites and pleural effusions at birth

Causes

  1. Intrauterine anaemia due to
    - > severe haemolytic disease of newborn (Rh, blood group incompatibilities)
    - > twin-twin transfusion syndrome
    - > fetomaternal haemorrhage
    - > Hb barts
  2. Congenital infection (parvovirus B19)
  3. Cardiac failure
  4. Hypoproteinaemia (congenital nephropathy Finnish, Maternal pre-eclampsia)
  5. Congenital malformations such as obstructive uropathy
93
Q

What is the kleihauer test used for?

A

Used to diagnose and quantitate a fetomaternal hemorrhage

Looks for foetal cells (HbF) in maternal circulation

May be done in case of hydros foetalis or in case of foetal anaemia (if mother is Rh neg and baby Rh positive as these are incompatible)

94
Q

5Ts of cyanotic CHD

A

Tetralogy of Fallot

Transposition of the great vessels

Tricuspid valve anomalies

Total anomalous pulmonary venous return

persistent Truncus arteriosus

Also

Hypoplastic L heart

Ebstein anomaly

95
Q

What is this condition?

A

Boot shaped heart

= TOF

RVOTO

Right ventricular hypertrophy

Ventricular septal defect

Overriding aorta are the characteristics of

Tetralogy of FallOt.

96
Q

What is this condition?

A

Transposition of the great arteries

‘egg on a string’

Narrow mediastinum (due to stress induced mediastinal atrophy)

globar large heart on its side

97
Q

SIMV

A

Delivers SET amount of breaths to neonate that are supported by ventilator

Synchronised w pt’s own breaths

If pt breaths ABOVE set rate, those breaths are not supported by ventilator (useful when weaning ventilation)

98
Q

SIPPV/PCAC

A

Supports every breath the infant makes (even if breaths above set number of delivered breaths)

The set ventilator respiratory rate is the backup number of breaths that will be mechanically administered if the infant makes no spontaneous breaths

99
Q

Volume guarantee

A

This mode of ventilation can be used with SIMV or SIPPV.

The ventilator aims to deliver tidal volumes (VT) [=volume guarantee) set by the clinician. A maximum peak inspiratory pressure (Pmax) is set, the ventilator’s PIP will vary to reach the target volume

VG = Usually around 4-5ml/kg

Pmax: In the volume-controlled mode this is the maximum peak inspiratory pressure you wish the ventilator to administer to reach target tidal volumes. Usually set 5 cmH2O higher than the average PIP used to achieve the set tidal volume.

Benefits are that it reduces the:

  • Duration of ventilation
  • Risk of pneumothorax
  • Risk of grade 3/4 intraventricular haemorrhage,
  • Risk of chronic neonatal lung disease.
100
Q

INdications for surfactant administration

A

Reccomended in:

  • Neonates with clinical and radiographic evidence of RDS
  • neonates at risk of developing RDS (e.g. <32 weeks or low birth weight <1300g)
  • neonates who are intubated, regardless of gestation, and requiring FiO2 >40%

Considered in:

  • Severe meconium aspiration syndrome with severe respiratory failure – may improve oxygenation and reduce the need for extracorporeal membrane oxygenation (ECMO)
  • Pulmonary haemorrhage with clinical deterioration
  • Severe RSV-induced respiratory failure - may improve gas exchange and respiratory mechanics and shorten the duration of invasive mechanical ventilation
101
Q

projectile vomiting in 6-8 week old hungry infant ?diagnosis

?picture on gas

A

Pyloric stenosis

Hypocl hypoK metabolic alkalosis

102
Q

Bilious vomiting in baby with trisomy 21

?diagnosis

?AXR finding

A

Duodenal atresia

See double bubble on AXR

103
Q

Sudden bilious vomiting in neonate with abdominal distension and tenderness and followed by haematemesis

?diagnosis and how to you diagnose this

?mgmt

A

Malrotation and volvulus

UGI contrast study is diagnosistic

Surgical emergency - ischaemia can lead to small bowel infarction req surgical resection -> extensive resection = poor prognosis

104
Q

BIlious vomiting, abdo distension and failure to pass mec in a neonate

?diagnosis

?what do you need to check for in these pts

A

Mec ileus

CHeck for CF (95% of infants with mec ileus have underlying CF)

ABdo xray findings - dialted loops of bowel, air fluid levels, ground glass soap-appearance of mec. may see intraabdominal calcification

105
Q

Causes of Cerebral palsy

A

Prematurity (80%) - Periventricular leukomalacia

IUGR (34%)

Intrauterine infection (30%)

Antepartum haemorrhage (27%)

Severe placental pathology (21%)

Multiple pregnancy (20%)

106
Q

Most likely outcome of PVL at 18 months

A

Unable to walk independently -> progression to spastic diplegia or quadriplegia

107
Q

Renal function in preterm vs term infant

A
  • preterms have lower GFR (10 vs 30). Reach adult GFR (120) in first 2 years of age.
  • renal function is optomised for RETENTION of dietary solutes for growth, not for excretion
  • reduced urine concentration ability in preterms
  • preterm kidney LOSES Na (prone to hypoNa) whereas the term kidney conserves N
  • Preterms have reduced ability to RESORB bicarb (therefore prone to low bicarb/met acidosis due to bicarb wasting)
  • Reduced ability to EXCRETE K (prone to hyperK)
108
Q

Causes of HTN in the neonate

A
  1. Renovascular
    - UAC assoc thrombus (forms on tip of catheter)
    - REnal vein thrombosis (flank mass, gross haematuria, thrombocytopaenia)
    - Renal artery stenosis (Fibromuscular dusplasia msot common; NF and Williams syndr)
  2. Renal parenchymal
    - PCKD (ARPKD and ADPK)
    - AKD
    - Nephrocalcinosis (if obstructive calculus forms)
    - Obstructive uropathy
  3. Cardiovascular (coarctation of aorta)
  4. Bronchopulmonary dysplasia (mechanism unclear)
  5. Endocrine (hyperthyroid)
109
Q

Pierre Robin Sequence

What is it

Mgmt

A

Due to mandibular hypoplasia (occurs < 9 weeks of development)

Features include:

  • Micrognathia
  • Cleft palate
  • Posteriorly displaced tongue -> can lead to airway obstruction and feeding difficulties

Management

  • Prone positioning
  • NPA
  • May need CPAP
  • Need palatal surgery by 1 year of age
  • Feeding can be problematic - can feed with special teats/bottle tops but may require NG feeding initially
110
Q

Infant of hyperparathyroid mother

-What to expect postnatally?

A

Mother with hypoparathyroidism -> hypercalcaemia if not poorly controlled

Transplacental transport of calcium -> foetal hypercalcaemia

Foetal hypercalcaemia -> suppression of PTH secretion

Postnatally, hypocalcaemia ensues

111
Q

Infant of mother with Graves, what to expect post-natally?

A

Transplacental passage of TSHR-Ab causing hyperthyroidism

112
Q

Acute prognosis - at risk of:

  • birth asphyxia
  • hypoglycaemia
  • hypothermia
  • polycythaemia
  • mortality

Chronic prognosis

  • Most show catch yp growth but some will remain short and thin
  • Incr risk of learning difficulties
  • incr risk of chronic diseases DMT2, CHD, HTN, stroke

-

A
113
Q

Causes of IUGR

A

Fetal

  • chromosomal abnorlities (T21, 18 etc)
  • structural malformations
  • congenital infx (CMV, toxoplasmosis, rubella)

Maternal

  • Malnutrition
  • Maternal hypoxia (CHD, chronic resp disease, altitude)
  • Drugs, alchohol, smoking etc

Placental

  • Compromised vascular supply - Pre-eclampsia, HTN, DM, renal disease
  • Thrombosis, infarction - maternal SLE, anti-PLD syndrome, sickle cell anaemia
  • Sharing of uterine vasculatiy (multi-gestation)
114
Q

HFOV vs PCOC in terms of outcomes/prognosis

A

No effect on mortality at 28-30 days of life, or at term equivalent age

Significant reduction in CLD in survivors at term equivalent GA in the HFOV group, however to an inconsistent degree

Increased risk of pulmonary air leaks (pneumothorax, pneumediastinum, pulmonary interstitial emphysema, pneumopericardium) in the HFOV group

Reduced risk of severe retinopathy of prematurity

No difference in severe grade intracranial haemorrhage or periventricular leukomalacia

Potential reduction in the risk of cerebral palsy and poor mental development

FRACP (21 decks)

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