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Child Health > Neonatology > Flashcards

Neonatology Flashcards

1
Q

What are some RFs for neonatal infections (4)

A 
Preterm (no IgG across placenta until 3rdT)
Cervical infection
Hosp derived: 
PROM (>18hrs) 
Indwelling lines/catheters
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2
Q

What % of women are GrpB Strep carriers?

What are the RFs for neonatal infection in a colonised mother? (5)

A

10-30% pregnant women
Faecal/vaginal carriage

Preterm
PROM
Previously infected infant 
Maternal pyrexia
Maternal chorioamnionitis
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3
Q

What are some complications of neonatal GrpB Strep infection? (5)

A

Early onset sepsis (48hrs):
Newbon resp distress
Pneumonia
Septicaemia

Late onset (48hrs - 3m):
Meningitis
Focal infection (osteomyelitis, septic arthritis)
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4
Q

What 3 general features would make you suspect neonatal sepsis?

A

Resp distress
Apnoea
Temp instability

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5
Q

If suspect neonatal sepsis, how is this managed? (Ix (5) + Tx)

A 
Septic screen: 
CXR
LP
Blood cultures
FBC (detects neutropenia)
CRP (helpful but takes 12-24hrs to rise)

Broad spec Abx

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6
Q

What is the regime in neonatal sepsis if cultures come back +ve / -ve ?

A

-ve and clinical signs return to normal → stop Abx after 48hrs

+ve → continue Abx, check for neuro signs + culture CSF

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7
Q

What is the regime for prophylactic intrapartum IV Abx for neonatal sepsis?

A

Either:
Screen at 35-38wks to identify carriers
Or:
Abx given to high-risk mums

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8
Q

What is the incidence of congenital CMV infection?

How is it transmitted?

A

4 in 1000 live births (0.4%) (commonest congenital inf)
(1% women have primary infection during preg + 40% those infants get infected)

Transmitted via saliva / genital secretions / breast milk

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9
Q

What is the presentation of CMV infection in mothers + in babies?

A

Mums (healthy): mild non-specific infection
But more significant infection in immunocompromised + foetuses

90% babies normal + norm devel
5% birth features: hepatosplenomegaly, petechiae, neurodevelopment (sensorineural loss/ CP/ LDs etc)
5% features later (e.g. sensorineural loss)

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10
Q

How is maternal/neonatal CMV infection managed?

A

Antivirals + ganciclovir (potential treatment)

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11
Q

What type of pathogen is toxoplasmosis?
What is the incidence of neonatal toxoplasmosis infection??
How is it transmitted normally + mum-baby?

A

Protozoan (food contamination + faecal-oral)
0.1 in 1000 live births
If mum in primary infection (parasitaemia) → transplacentally 40% infants get infected

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12
Q

What are the clinical features / presentation of neonatal toxoplasmosis infection? (4)

How is it treated in the neonate?

A

Retinopathy
Hydrocephalus
Cerebral calcification
Long-term neuro disabilities

1yr pyrimethamine + sulfadiazine

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13
Q

What are the neonatal effects of maternal rubella infection at different gestations?

A

<8/40 → deafness, congenital heart disease + cataracts (80%)
13-16/40 → impaired hearing
>18/40 → minimal effects

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14
Q

List some clinical features of HIV in an untreated child? (6)

A 
Lymohadenopathy
Parotid swelling
Hepatosplenomegaly
Thrombocytopenia
Recurrent fever
Serious recurrent infections (→ AIDS)
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15
Q

What are the main principles of HIV management in children / young people? (6)

A

Anti-retrovirals
PCP prophylaxis
Immunisations (Hep A/B, VZV, influenza)
Do NOT give BCG (live vaccine)
Regular FU in family clinic (wt, neurodevel)
Education of safe sex etc for adolescents

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16
Q

What measures can be taken to avoid vertical transmission of HIV? (4)

What is the change in transmission risk if these measures are taken?

A

Get viral load as low as poss around time of delivery
Active labour management (avoid PROM / unnecessary instrumentation)
Pre-labour C-Section
Avoidance of breast feeding

Risk from 25-40% reduces to 1%

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17
Q

What are the effects of neonatal Hep B/C infection?

How is it treated?

A

Increased risk of chronic hepatitis (+ assoc probs)

Tx by passive immunisation within 24hrs

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18
Q

How does neonatal herpes infection present? (3)

A 
Commoner in preterms
Presents upto 4wks:
Localised herpetic skin/eye lesions
Encephalitis
Disseminated disease (v high mortality)
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19
Q

How is maternal/neonatal herpes managed?

A

C-Section at delivery

Antivirals

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20
Q

List the symptoms of neonatal syphilis infection (7)

A

Failure to thrive
Irritability
Fever

Hepatosplenomegaly
Bone inflammation

Nose (no bridge + discharge)
Rash (mouth/anus/genitalia)

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21
Q

What are some complications of neonatal syphilis infection? (4)

How is it treated?

A

Blindness
Deafness
Face deformities
Neurological probs

Treated with penicillin

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22
Q

How may neonatal chlamydia infection present? (2)

How is it treated

A

Conjunctivitis + eyelid swelling after birth / 1-2wks old
Possibly pneumonia at 4-6wks

Tx: oral erythromycin

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23
Q

What are the maternal antenatal complications of gonorrhoea infection?
+ Neonatal effects?
+ Neonatal treatment

A

Maternal: chorioamnionitis + higher risk premature labour

Neonate: opthalmia neonatorum (purulent discharge, lid swelling + corneal haze)

Urgent penicillin / 3rd gen cephalo (prevent blindness)

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24
Q

How is SGA / IUGR officially determined?

A 
SGA = <10th centile
IUGR = wt + abdo circumference on lower centile than head (asymmetrical)
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25
Q

List some maternal RFs for IUGR? (9) (opposed to placental + fetal)

A

Smoking
Alc / drug abuse
Older mums

HT/Heart disease
DM
Renal 
Coeliac (untreated)
Thrombophilia

Drugs (warfarin/steroids/phenytoin)

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26
Q

List some placental RFs for IUGR? (3)

List some fetal RFs? (4)

A

Pre-Eclampsia
Small placenta
Placenta cell death

Multiple pregnancy
Csome abns (Downs/Turners/Edwards/Patau's)
Congenital defects assoc w. SGA
Intrauterine infection (Rubella, CMV, toxo, syphilis)
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27
Q

What further Ix are done in IUGR/SGA? (2)

A 
Detailed USS (assess risk csome defect)
Umb aa Doppler (assess placental insufficiency)
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28
Q

What are the 4 main clinical signs of neonatal respiratory distress?

A

Tachypnoea
Laboured breathing (recession/flaring/tug)
Expiratory grunting
Cyanosis (if severe)

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29
Q

What are the causes of neonatal respiratory distress? (7)

Tasty Roll-ups Can Damage the Heart Some May say

A 
Transient tachypnoea of the newborn
Respiratory distress syndrome
Congenital pneumonia
Heart disease
Septicaemia
Diaphragmatic hernia
Meconium aspiration
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30
Q

What is the commonest cause of respiratory distress
in term babies?
in premature babies?
in Prolonged pregnancies?

A 
Term = transient tachypnoea of newborn
Preterm = respiratory distress syndrome
Post-term = meconium aspiration
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31
Q

What causes transient tachypnoea of the newborn?
How is Dx made?
How is it managed?

A

Due to delay in resorption of lung fluid (commoner in C-Section babies)
Dx (after exclusion of other causes) - CXR shows fluid in horizontal fissures
Usually settles within a day but poss require atmospheric O2

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32
Q

What is respiratory distress syndrome due to in preterms? What could it be due to in term babies?

A

Defc in surfactant + immature respiratory centre in brain

Term babies - genetic / maternal DM / meconium aspiration

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33
Q

How is respiratory distress syndrome managed? (2)

A

Antenatal steroids 48hrs before delivery if <34wks (→ lung maturation)
Artificial surfactant

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34
Q

What are the RFs for congenital pneumonia? (3)

How is it managed?

A

PROM
Chorioamnionitis
Low birth wt

Managed with broad spec Abx (early until microscopy back)

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35
Q

What effects does meconium aspiration have on the lungs? (3)

What is a further complication?

A 
Mechanical obstruction
Chemical pneumonitis (destroys surfactant)
Predispo to infection

Lungs overinflate + causes patches of collapse/consolidation

Can → air leak (pneumothorax + pneumomediastinum)

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36
Q

How is meconium aspiration managed?

What is a complication of the management?

A

Require artificial ventilation
May → persistent pulmonary HT of newborn (where difficult to achieve adequate oxygenation despite high pressure ventilation)

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37
Q

What are some common problems with prematurity? (11)

A 
Respiratory distress
Necrotising enterocolitis (NEC)
Infection (no IgG until 3rdT)
Hypoglycaemia
Temperature control
Apnoea of prematurity
Retinopathy of prematurity
Intraventricular haemorrhage
Bronchopulmonary dysplasia
Neurodevelopment complications
Nutrition problems
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38
Q

What are some RFs for NEC

A

Preterm (in 1st week of life)

Cows milk fed (not breast)

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39
Q

What are the features of NEC (4)

What Ix can be done

A

Stops tolerating feeds
Abdomen distends
Stool contains fresh blood
(can progress to) shock / bowel perf

Seen on AXR

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40
Q

How is NEC managed? (4)

A

Stop oral feeds + parenteral
Broad spec Abx
Artificial ventilation often required
Surgery for perforations

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41
Q

What are some features of neonatal hypoglycaemia?

A

Apnoea
Seizures

Jitteriness
Irritability
Lethargy
Drowsiness

42
Q

How is neonatal hypoglycaemia prevented / managed?

A

Early/frequent feeding with breast milk
Regular monitoring if at risk

IV infusion if 2 levels <2.6 or one <1.6 (high concs given to avoid peripheral skin necrosis)

43
Q

Why are preterm infants particularly vulnerable to hypothermia?

A 
Large SA:V
Thin skin / heat permeable
Little subcut fat
Nursed naked
Cannot curl up / shiver
Higher neutral temp range of minimal energy consumption
44
Q

What happens in apnoea of prematurity? 3 features

What gestational age babies does it occur in?

A

Episodes of apnoea, bradycardia + desaturation

Common in very low birth wt babies <32wks gestational age

45
Q

What is the main cause of apnoea of prematurity?

List some other underlying causes for apnoea of prematurity? (8)

A

Mostly due to central resp control

Infection
Anaemia
Electrolyte disturbance
Hypoglycaemia
Hypoxia
Seizures 
Heart failure
Aspiration
46
Q

How are the apnoeic episodes in apnoea of prematurity managed?

A

Usually restarts after gentle physical stimulation
Caffeine
Potentially CPAP

47
Q

How does retinopathy of prematurity occur?
What is the main RF?
What is the incidence?

A

Vascular proliferation at developing vessel junction of vasc/non-vasc → retinal detachment / fibrosis / blindness
RF: uncontrolled use of high conc O2

35% very low birth wt + 1% → severe bilateral visual impairment

48
Q

How is retinopathy of prematurity treated?

A

Laser therapy

Weekly FU with ophthalmologist

49
Q

What is the incidence of IVH in pre terms?

How does it present? (6)

A

60-70% extremely low birth wt (500-750g)

Apnoea
Poor muscle tone
Poss bulging fontanelle (raised ICP)
Lethargy
Sleepiness
May progress to coma
50
Q

How is IVH managed? (3)

A 
SUPPORTIVE
Correct acidosis / anaemia / hypotension
Fluids 
Meds to reduce ICP
Ventriculoperitoneal shunt
51
Q

Give the definition of bronchopulmonary dysplasia
How does it occur (3)
What are the CXR characteristics? (2)

A

= infants with O2 requirement at post-conception age 36wks
Trauma (Lung damage from pressure/volume)
Toxicity - oxygen toxicity
Infection

CXR: widespread opacification + poss cystic changes

52
Q

What are the main complications of artificial ventilation in neonates? (2)

A 
Bronchopulmonary dysplasia (from long-term)
Pneumothorax (10%)
53
Q

How is ventilation weaning done in bronchopulmonary dysplasia?

A

CPAP → additional ambient O2

Use corticosteroids in early weaning

54
Q

How can pneumothorax occur as a complication of RDS/ventilation

A

Air from over-distended alveoli tracks into interstitum → pulmonary interstitial emphysema → air leaks into pleural cavity

55
Q

What is seen O/E in pneumothorax in neonates? (3)

A

O2 requirements increase
Reduced breath sounds
Reduced chest movement

56
Q

How is pneumothorax prevented/managed in ventilated babies?

A

Given at lowest pressure to achieve good oxygenation
CXR
Chest drain

57
Q

What is the growth rate in preterm babies vs term?

A

Preterm: double wt in 6wks + triple in 12wks

Term: double wt in 4.5m + triple in 1yr

Therefore v high nutritional requirement

58
Q

How is nutrition administered depending on maturity/gestational age in pre terms?

A

35-36wks → suck/swallow
Less → NG
V premature → enteral
V immature / sick → parenteral via central vv catheter

59
Q

How is lung fluid resorbed during the respiratory changes at birth?
How exactly does pulmonary resistance decrease so much after birth?

A

Chest compression during birth squeezes out 1/3rd
Adrenaline promotes resorption of rest

O2’s vasodilatory effect + alveolar expansion reduces capillary pressure in lungs

60
Q

How is surfactant released during the respiratory changes at birth?

A

Triggered by adrenaline + steroids (+ synth)

61
Q

What are the normal timeframes after birth for:
Bowels opening
Passing urine
Wt loss

A

BO - before birth / within 6yrs / before 24hrs
PU - up to 24hrs
Wt - lose 10% but regain in 2wks

62
Q

What are some RFs for haemorrhagic disease of the newborn (3)

A

Occurs with Vit K defc so:
Wholly breast fed (little VitK)
Maternal anticonvulsants (impair clotting factor synth)
Infant liver disease

63
Q

What are some clinical signs of haemorrhagic disease of newborn? (4) + a complication
How long can it take to present?

A 
Mild:
Bruising
Haematemesis
Malaena
Prolonged umbilical stump bleeding
Severe may → Intracranial haemorrhage

Early (1st wk) or late (1-8wks)

64
Q

How is haemorrhagic disease of the newborn prevented? (2)

A

IM Vit K at birth

Mums on anticonvulsants need prophylaxis from 36wks+

65
Q

What is screened for in a Guthrie test? (5)

When is it done

A 
CF
Hypothyroidism
Haemoglobinopathies (sickle + thalass)
Phenylketonuria
MCAD (mitochondrial)

Done on day 5-9 (when estab feeding)

66
Q

What does a newborn baby check consist of?

A 
Birth wt / gestation / centile
Posture / movement
Head circumference
Fontanelle
Face - any syndromes
Pale / excess blood (check haematocrit)
Jaundice - any within 24hrs req Ix
Eyes - red reflex
Palate - cleft (visually + physically)
Breathing + chest wall movement
Heart auscultation
Palpate abdo 
Femoral pulses (reduced in CoarcAo + raised in PDA)
Genital/anus - check latency 
Scrotum - check presence 
Muscle tone
Back + spine (bifida)
Hips - DHH
67
Q

What are some methods of hearing tests in the newborn? (2)
How done in 7-9m
10m-3yrs
4yrs+

A

Evoked otoacoustic emission
OR
Automated auditory brainstem response + EEG analysis

7-9m: Distraction testing
10m-3yrs: Visual reinforced audiometry
4yrs+: Audiometry

68
Q

Why is a newborns acuity so poor (2)? + what is the usual acuity in a newborn

A

Fovea immature
Optic nn unmyelinated
(but peripheral retina well developed)
(any obstrn eg cataract will interfere with pathway devel)

Normal 6/200 in newborn

69
Q

List some common newborn problems (8)

EM Can Poo / Fart Sloppy Big Shits

A

Mongolian blue spot
Erythema toxicum
Capillary haemangiomas

Physiological jaundice
Feeding problems
SGA
Birth trauma
Sticky eye
70
Q

When does erythema toxicum (neonatorum) usually appear?

How would you describe this rash? (3)

A

2-3d after birth

White papules (eosinophils)
Erythematous base
Lesions mainly on trunk

71
Q

How would you describe a Mongolian blue spot?
What is a RF
How is it treated?

A

Blue/black discolouration
At base of spine/buttocks (/legs)

Occurs in Afro-Caribbean / Asian

Fades after few yrs

72
Q

How would you describe a capillary haemangioma?

Where on the body do they occur?

A

Pink macules

Upper eyelid / mid-forehead / neck

73
Q

List some possible reasons for feeding difficulties? (4)

A

Cleft palate/lip
Gastro-oesophageal reflux
Premature + unable to suck/swallow
Poor technique / nipple attachment

74
Q

What types (2) of birth trauma injuries can occur? + How

A

Cephalohaematoma = haematoma from bleeding below periosteum

Brachial plexus injury = from traction of brachial nerve roots

75
Q

What are the RFs for brachial plexus injury ? (2)

What kind of palsy can it result in?

A

Shoulder dystocia
Breech

→ Erb palsy (C5+6): usually recover

76
Q

What is sticky eye and why does it occur in newborns?

A

Yellow discharge + crust formation occurring in 1st 48hrs after birth

Due to blockage of tear ducts

77
Q

What types of antibody involved in ABO incompatibility?

A

Most ABOs are IgM + don’t cross placenta

Some GrpO have IgG anti-A-haemolysin in blood → crosses placenta + haemolyses RBCs of GrpA baby

78
Q

What are the clinical features of ABO incompatibility?

A

Haemolysis → Severe jaundice (less severe than Rh disease) which peaks at 12-72hrs
No hepatosplenomegaly

79
Q

How is ABO incompatibility managed? (Dx / before birth / after)

A

Dx: +ve sAb on RBCs in bloods + high bilirubin

Before birth: intrauterine transfusion / early IoL at term / maternal plasma exchange

After birth: Phototherapy for jaundice / transfuse with RBCs + HCO3- to correct acidosis

80
Q

What are the main RFs for congenital abnormalities? (4)

A

Maternal/paternal age
Infections (TORCH - toxo, other, rubella, cmv, hsv)
Toxins (alc, smok, medications)
Dietary defc e.g. folic acid

81
Q

What is the prevalence of CHARGE syndrome

What are the different abnormalities?

A

1 in 10,000
Leading cause of congenital deafblindness

Coloboma of eye (hole in 1 eye structure)
Heart defects
Atresia of nasal choanae
Retarded growth/devel
Genito-urinary abns
Ear abns + deafness
82
Q

What is the incidence of VACTERL syndrome?

What are the different abnormalities?

A

16 in 100,000 live births

Vertebral (hypoplastic + scoliosis)
Ano(-rectal) atresia
Cardiac
Tracheo-oesophageal fistula
Esophageal atresia
Renal anomalies
Limb defects (extra/fused digits etc)
83
Q

What is Patau syndrome due to?

What is the incidence

A

Trisomy 13

1 in 20,000

84
Q

What is Edwards syndrome due to?

What is the incidence?

A

Trisomy 18

1 in 6000 (2nd commonest trisomy after Downs)

85
Q

What are the features of Patau syndrome (9)

A 
Those who survive (few):
Low birth wt
IUGR
Congenital heart defects (ASD, VSD, PDA, dextro)
Neural tube /Brain structural 
Cleft / scalp defects
Small eyes
GI malformations
Urogenital malformations
Polydactyly
86
Q

What are the antenatal features of Edwards syndrome? (5)

A 
Poly/oligo hydramnios
IUGR
Small placenta
1 umb aa
Fetal distress
87
Q

What are the postnatal features of Edward syndrome? (8)

A 
Low birth wt
Craniofacial abns - sim to Patau
Skeleton abns - sim to Patau
GI - T-O fistula / pyloric stenosis / imperf anus / inguinal
Cardiac 
Urogenital - hydronephrosis, cystic, cryptochordism
Neuro - hydrocephaly / severe LDs
Pulmonary - hypoplasia
88
Q

What are the diff types of neural tube defects? (5) + what are they

A

Anencephaly
Spina bifida occulta (failed vertebral arch fusion)

Encephalocele - brain/meninges extrusion thru midline skull
Meningocele - skin/meninges form out-pouch (cord stays within so fewer probs)
Myelomeningocele - communication b/wn neural tissue / meninges / surface (a neural plaque)

89
Q

What are some associated complications with myelomeningocele? (6)

A

Paralysis
Sensory loss
Muscle imbalance

Hydrocephalus

Neuropathic bladder/bowel
Scoliosis

90
Q

What features of ambiguous genitalia may be seen in (apparently) males? (3)
+ in (apparently) females? (3)

A 
Male:
Severe hypospadia 
Bifid scrotum
Undescended testis/es
Bilateral non-palpable testes

Female:
Clitoral hypertrophy
Non-palpable gonads
Vulva w. single opening

91
Q

List some gonad/endocrine causes of sexual differentiation disorder (4)

A

*Excess androgens (congenital adrenal hyperplasia)
Gonadotrophin insufficiency (e.g. prader-willi)
Inadequate androgen actions
Ovotesticular disorder of sex development (DSD) (XX + Y cells in fetus)

92
Q

What is the aetiology of congenital adrenal hyperplasia?
What is the incidence?
What group of people is it common in?

A

Many autosomal recessive disorders of adrenal steroid synthesis
1 in 5000 births
Common in consanguineous offsprings

93
Q

How does congenital adrenal hyperplasia present? (3)

A

Ambiguous genitalia
Salt losing crises
Poss other androgenic features (boys tall / hirsutism)

94
Q

What is Potters syndrome?

What causes it? (4)

A

Oligohydramnios → pressure in utero effects

Bilateral renal agenesis (usually)
Renal hypoplasia
Polycystic kidneys
Obstructive uropathy

95
Q

Describe the physiology behind Hypoxic Ischaemic Encephalopathy

A

Perinatal asphyxia
→ compromised/no gas exchange (placental/pulm)
→ cardioresp depression
→ hypoxia + hypercapnia + metab acidosis

Compromised CO = reduced tissue perfusion → HIE

96
Q

What are some of the antenatal/intrapartum causes of hypoxic ischaemic injury (6)

A

Interrupted umb aa blood flow (cord prolapse/shoulder dystocia)
Inadequate maternal placental perfusion (hypotension / major abruption)
IUGR (compromised fetus)
Anaemia (compromised fetus)
Failure of cardioresp adaptation at birth (failure to breathe)

97
Q

What are some features of mild HIE seen within 48hrs of birth? (5)

A 
Mild 
Irritable
Excessive response to stimulation
Staring eyes
Hyperventilation
Impaired feeding
98
Q

What are some features of moderate HIE seen within 48hrs of birth? (3)

A

Marked abnormal tone / movement
Cannot feed
Poss seizures

99
Q

What are some features of severe HIE seen within 48hrs of birth? (4)

A

No spontaneous movements / response to pain
Fluctuating hyper/hypotonia
Prolonged seizures
Multi-organ failure

100
Q

How is HIE managed? (6)

A 
Resp suppot
EEG
Fluid restriction
Treat hypotension + seizures
Monitor hypogly / elec imbalance
Cool baby to 33/34 (prevent repercussion injury)
101
Q

What is the prognosis like in mild/moderate/severe HIE?

A

Mild: v good prognosis + expect full recovery
Moderate: recovery only likely if normal neuro Ex + feeding by 2wks
Severe: 30-40% mortality or severe neurodisabilities eg CP

102
Q

What are the characteristic facies in Potters syndrome? (4)

Where else may there be deformities (5)

A

Parrot beaked nose
Prominent epicanthal folds
Low set ears
Recessed chin

Cardiac / Neuro / MSK / Opthalmic
+ Pulm hypoplasia (from oligohydramnios)

Child Health (14 decks)

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