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3A > Paeds- Neonates > Flashcards

Paeds- Neonates Flashcards

1
Q

Important problems with neonatal resuscitation

A

Hypoxia occurs during normal birth, babies have large surface area to volume ratio so loose heat, babies are born wet so loose heat, babies can aspirate Meconium in birth

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2
Q

First stage of neonatal resuscitation

A

Dry and warm the baby- towel, heat lamp, bag if less than 28 weeks

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3
Q

What are APGAR scores and when are they done

A

Appearance, Pulse, Grimmace, Activity, Respiration
Performed at 1, 5 and 10 minutes post birth
Range from 0-10

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4
Q

If neonate is not breathing/gasping despite stimulation what is the first stage of resuscitation

A

Inflation breaths- 5 breaths
Can be repeated

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5
Q

What can be given after inflation breaths if no progress?

A

30 seconds of ventilation breaths

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6
Q

When should chest compressions be given in neonatal resuscitation

A

If heart rate is less than 60 despite inflation and ventilation breaths

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7
Q

Rate of chest compressions in neonates

A

3:1 with inflation breaths

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8
Q

Explain delayed cord clamping

A

If neonate is uncompromised cord clamping should be delayed by at least one minutes to allow all blood to enter baby

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9
Q

What is Meconium aspiration

A

Respiratory distress which is caused by the aspiration of Meconium stained amniotic fluid either antenatally or during birth.

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10
Q

Pathophysiology of Meconium aspiration

A

Meconium usually passes after birth however if in utero peristalsis it can occur earlier
This is usually due to foetal hypoxic stress or vagal stimulation due to cord compression
This leads to Meconium stained amniotic fluid
The neonate can aspirate the Meconium

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11
Q

Consequences of Meconium aspiration

A

Partial or total airway obstruction (due to thick sticky consistency of Meconium, can cause partial collapse)
Foetal hypoxia
Pulmonary inflammation- meconium contains pro-inflammatory cytokines
Infection
Surfactant inactivation - inflammatory reaction can deactivate surfactant
Persistent pulmonary hypertension of the newborn

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12
Q

Presentation of Meconium aspiration

A

Respiratory distress signs:
- Tachypnoea,
- tachycardia
- cyanosis
- grunting
- nasal flaring
- recessions

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13
Q

Differentials of meconium aspiration

A

Transient Tachypnoea of the newborn
Surfactant deficiency
Persistent pulmonary hypertension
Cyanotic congenital heart disease

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14
Q

Diagnosis of meconium aspiration

A

X ray- increased lung volumes, patchy pulmonary infiltrates, may have effusion or pneumothorax
May blood culture to rule out infection

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15
Q

Treatment of Meconium aspiration

A

Depends on the severity of resp distress
- ventilation and oxygen therapy
- antibiotics may be given if concern for infection
- surfactant if severe
- inhaled nitric oxide for hypertension

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16
Q

RF for meconium aspiration

A

Increased gestational age- >42 weeks, foetal distress, intrapartum hypoxia, chorioamnionititsm maternal hypertension, smoking, diabetes

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17
Q

What needs to be considered if bowel sounds can be heard on a respiratory examination of a neonate

A

diaphragmatic hernia

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18
Q

how does a diaphragmatic hernia present in a neonate

A

respiratory distress shortly after birth due to lung hypoplasia

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19
Q

What management can be done to reduce risk of HIE in neonates

A

therapeutic cooling

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20
Q

How does prader willi present in neonates?

A

neonatal hypotonia

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21
Q

What is Epstein’s pearl?

A

a white lesion found on the posterior hard palate- sometiems mistaken for neonatal teeth

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22
Q

features of fetal alcohol syndrome

A

flat philtrum, sunken nasal brdige, small eye openings, small body, low set ears, thin upper lip

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23
Q

x ray findings of meconium aspiration syndrome

A

patchy infiltrations and atelectasis

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24
Q

What investigation is needed for all babies who were breech at or after 36 weeks gestation, regardless of neonatal examination

A

hip ultrasound at 6 weeks

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25
Q

what complication may occur after ventouse delivery

A

cephalohaematoma

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26
Q

How does neonatal hypoglycaemia present

A

jitteriness
irritable
tachypnoeic
poor feeding
drowsy
hypotonia
apnoea

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27
Q

first line treatment of an ASYMPTOMATIC baby with hypoglycaemai

A

encourage normal feeding and monitor

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28
Q

first line treatment of a symptomatic neonate with hypoglycaemia

A

admit to neonatal unit
give IV infusion of 10% dextrose

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29
Q

If a neonate has spO2 of 85% 5 mins after birth what should be done

A

remeasure in 5 mins- suboptimal levels are normal in initial 10 mins

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30
Q

What two prognostic markers can be used to determine the prognosis of a congenital diaphragmatic hernia

A

liver position and lung to head ratio

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31
Q

When do the lungs start producing surfactant

A

after 30 weeks gestation

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32
Q

Pathophysiology of respiratory distress syndrome

A

inadequate surfactant causes alveoli to collapse on expiration which increases the energy needed for breathing.
Inadequate gas exchange leads to subsequent hypoxia and carbon dioxide retention

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33
Q

Presentation of respiratory distress syndrome

A

respiratory distress immediately or within minutes of birth
tachypnoea
nasal flaring
expiratory grunting
subcostal and intercostal recessions
cyanosis
diminished breath sounds

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34
Q

How does respiratory distress syndrome present on X ray/lung USS

A

ground glass appearance

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35
Q

what is oesophageal atresia?

A

a condition where a short section of the top of the oesophagus has not formed properly meaning it is not connected to the stomach.

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36
Q

what is a tracheo-oesophageal fistula and what condition does it usually accompany?

A

it is a connection between the oesophagus and the trachea
can occur alongside oesophageal atresia

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37
Q

What obstetric condition may present with oesophageal atresia

A

polyhydramnios

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38
Q

pathophysiology of oesophageal atresia

A

the oesophagus and the trachea start as a single tube (arising from the common fore gut) in development and then divide into two distinct structures.
Separation usually starts during the 4th week of gestation- failure of this can occur can lead to atresias and fistula formation

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39
Q

How does oesophageal atresia present?

A

baby will not be able to feed - will cough and splutter during feeding
frothy bubble may come out of mouth
baby may choke

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40
Q

How is oesophageal atresia diagnosed?

A

may be identified on USS during pregnancy
May present as failure to pass an NG tube down the babies nose and. into the stomach.
Xrays and endoscopy may be used

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41
Q

How are oesophageal atresias treated?

A

immediate surgical intervention

42
Q

What is cleft lip

A

a congenital condition where there is a split or open section of the upper lip

43
Q

what is a cleft palate

A

a defect exists in the hard or soft palate of the roof of the mouth- leads to an opening between the mouth and the nasal passage

44
Q

what maternal drug may increase the risk of cleft lip and palate

A

epileptic use

45
Q

When are cleft lip and palate surgeries done

A

cleft lip- 3 months
cleft palate- 6-12 months

46
Q

What are the TORCH infections

A

Toxoplasma gondii
Other agents- Treponema pallidum (syphilis), VZV, parvovirus, HIV
Rubella
Cytomegalovirus
Herpes simplex virus

47
Q

Complications of toxoplasmosis gondii infection to the foetus

A

Chorioretinitis
Hydrocephalus
Rash
Intracranial calcifications

48
Q

Complications of Rubella infection in the foetus

A

congenital rubella syndrome- cataracts, rash, heart defects, deafness

49
Q

How does cytomegalovirus present in foetus

A

rashes, deafness, inflammation of the eye, seizures, microcephaly

50
Q

How does congenital syphilis present?

A

death, craniofacial malformations, rash, deafness

51
Q

how does parvovirus B19 present in neonates

A

anaemia of the newborn, fetal hydrops

52
Q

How does meconium aspiration present?

A

signs of respiratory distress in the newborn- tachypnoea, tachycardia, cyanosis, grunting, nasal flaring, recessions, hypotension, barrel shaped chest

born with green stained amniotic fluid
May appear normal straight after birth and then develop respiratory distress hours after

53
Q

Pathophysiology of meconium aspiration

A

in utero massage of meconium leading to meconium-stained amniotic fluid

This usually occurs due to foetal hypoxic stress (e.g. placental insufficiency) or vagal stimulation caused by cord compression

The foetus aspirates the MSAF either antenatally or during birth
Leads to airway obstruction, foetal hypoxia, pulmonary inflammation, infection, surfactant inactivation and persistent pulmonary hypertension.

54
Q

How does meconium aspiration present on x ray

A

increased lung vomules
asymmetrica patchy infiltrations
pleural effusions
pneumothorax

55
Q

How is meconium aspiration treated

A

depends on the severity of respiratory distress:
- suctioning the infant after birth
- warm infant
- oxygen therapy: nasal cannula, CPAP, intubation
-antibiotics if suspicion of infection
- Surfactant
- inhaled nitric oxide - occurs if the infant requires mechanical ventilation and surfactant

56
Q

RF for meconium aspiration

A
  • increased gestational age after 42 weeks
  • foetal distress
  • placental insufficiency
  • chorioamnionitis +/- prolonged pre-rupture
  • oligohydramnios
  • in utero growth restriction
  • maternal hypertension, diabetes, pre-eclampsia, or eclampsia
57
Q

complications of meconium aspiration

A

long term neurological sequale- cerebral palsy
respiratory damage from prolonged ventilator use

58
Q

why may neonates get physiological jaundice

A
  • there is marked release of haemoglobin from the breakdown of RBC as there is high haemoglobin at brith
  • the RBC lifespan in neonates is 70 days (less than 120 in adults)
  • hepatic bilirubin metabolism is less effective in the first days of life
59
Q

what can cause early jaundice (within the first 24 hours of birth)

A

haemolytic disorders (rhesus disease, ABO incompatibility, G6PD deficiency, hereditary spherocytosis)
congenital infection (TORCH)

60
Q

what can cause jaundice in a newborn between 24 hours-2 weeks

A

physiological jaundice
breastmilk jaundice
infection (e.g. UTI)
haemolysis
bruising

61
Q

What is prolonged jaundice

A

jaundice lasting longer than 2 weeks (or 3 weeks if preterm)

62
Q

What can cause prolonged jaundice in infants?

A

unconjugated- physiological, breast milk, infection, congenital hypothyroidism, pyloric stenosis
conjugated- biliary atresia, neonatal hepatitis

63
Q

what is a serious complications of neonatal jaundice

A

kernicterus

64
Q

what is kernicterus

A

encephalopathy that results from deposition of the unconjugated bilirubin in the basal ganglia and brainstem nuclei

65
Q

how does kernicterus present?

A

lethargy, poor feeding, irritability, increased muscle tone
opisthotonos (baby lays with back arched)
seizure and coma

66
Q

what is a long term complication of kernicterus

A

cerebral palsy - choreoathetoid cerebral palsy

67
Q

Investigations that might be used in neonatal jaundice

A

direct coombs test
blood film
infection investigations- cultures, CSF, urine
transcutaneous bilirubinometer and blood bilirubin

68
Q

How does conjugated bilirubinaemia presetn

A

pale stools and dark urine

69
Q

How is neonatal jaundice treated

A
  • treat underlying cause
  • maintain good hydration (poor intake will exacerbate)
  • phototherapy (with blue-green band visible light)
  • exchange transfusion
70
Q

how soon after commencing phototherapy should bilirubin levels be assessed

A

4-6 hours

71
Q

are neonatal inflation breathes given with air or 100% oxygen

A

air

72
Q
A
73
Q

What is raised in physiological jaundice

A

Unconjugated bilirubin

74
Q

What is seen on x ray of a baby with transient tachypnoea of the neonate

A

Hyperinflation and fluid in the horizontal fissure

75
Q

What causes transient tachynpnoea if the newborn

A

Delayed resorption of fluid in the lungs

76
Q

What makes up the TORCH infections

A

Toxoplasmosis
Other- syphillis, VZV, parvovirus
Rubella
Cytomegalovirus
Herpes simple virus

77
Q

How is toxoplasmosis transmitted (2)

A

exposure to undercooked meat
cat faeces

78
Q

How does congential toxoplasmosis present? (5)

A

intracranial calcifications
hydrocephalus
chorioretinitis
retinopathy
cataracts

79
Q

How does congential syphilis present? (6)

A

blunted incisor teeth (Hutchinson teeth)
Rhagades (linear scars at the angles of the mouth)
Keratitis
Saber shins
saddle nose
deafness

80
Q

How does congential varicella zoster present? (5)

A

skin scarring
eye defetcs (microphthalmia)
limb hypoplasia
microcephaly
learning difficulties

81
Q

at what gestation is parvovirus B19 likely to effect the foetus

A

if exposed before 20 weeks gestation

82
Q

How can parvovirus effect the foetus - explain the pathophysiology and how it presents in fetus

A

Parvovirus can cross the placenta and suppress foetal erythropoiesis (as infects erythroid progenitor cells)
- this can cause fetal anaemia and subsequent heart failure
- presents as hydrops fetalis- ascites, pleural effusions, pericardial effusions

83
Q

How is parvovirus infection of foetus treated

A

repeat intrauterine blood transfusions

84
Q

when are foeteses at highest risk for congenital rubella

A

8-10 weeks

85
Q

How does congenital rubella syndrome present? (9)

A

sensorineural deafness
congenital cataracts
congenital heart defects
growth retardation
hepatosplenomegaly
purpuric skin lesions
salt and pepper chorioretinitis
microphthalmia
cerebral palsy

86
Q

How does congenital cytomegalovirus present? (6)

A

growth retardation
pinpoint petechial blueberry muffin rash
microcephaly
sensorineural hearing loss
encephalitis
hepatosplenomegaly

87
Q

How can herpes simplex virus effect a newborn if transmitted in labour

A

blisters and meningioencephalitis

88
Q

if a mother has primary herpes infection after 28 weeks gestation what is the management

A

immedicate course of aciclovir then continuous prophylactic aciclovir until delivery
caesarean recommended

89
Q

if a mother has primary herpes infection before 28 weeks/ pre-existing HSV, what is the treatment?

A

the should be given prophylactic aciclovir from 36 weeks
if no infection at time of birth then vaginal delivery can be done

90
Q

what is biliary atresia?

A

a congenital condition where a section of the bile duct is either narrowed or absent

91
Q

Path of biliary atresia

A

there is a narrowed/ absent section of the bile duct which leads to cholestasis

The baby cannot excrete conjugated bilirubin so it builds up and they become jaundiced

92
Q

How does biliary atresia present ?

A

-significant prolonged jaundice
-dark urine and pale stools
-failure to thrive (poor absorption of long chain fats)
-hepatomegaly
-ascites
-bruising (coagulopathy due to vitamin K deficiency)

93
Q

Differentials of biliary atresia

A

hepatic viral infections
alagille syndrome
alpha-1- antitrypsin deficiency
downs syndrome
cystic fibrosis

94
Q

diagnosis of biliary atresia

A

raised conjugated bilirubin
LFTs- shows disproportionately high GGT
abdominal USS
percutaneous liver biopsy with intraoperative cholangioscopy

95
Q

How is biliary atresia treated ?

A

hepatoportoenterostomy - surgical excision of the obliterated extrahepatic ducts

2nd line- liver transplant

96
Q

Complications of biliary atresia

A

growth failure
cholangitis
portal hypertension
GI bleed
vitamin deficiency

97
Q

what antenatal condition is duodenal atresia associated with?

A

polyhydramnios

98
Q

How does duodenal atresia present?

A

distended abdomen and vomiting within hours of birth

vomiting can be bilious or non-bilious depending on the site of obstruction

99
Q

How is duodenal atresia diagnosed?

A

abdominal x-ray: double bubble sign

100
Q

How is duodenal atresia treated?

A

fluids and surgery (duodenoduodenostomy)

101
Q
A

3A (32 decks)

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