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Year 4 Paeds Conditions > Neonatal and Newborn > Flashcards

Neonatal and Newborn Flashcards

1
Q

What are the different types of neonatal jaundice

A

unconjugated - pre-hepatic

conjungated - hepatic and post-hepatic

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2
Q

What is the neonatal jaundice

A

it is hyperbilirubinaemia in a newborn. It can be a physiological response. but can also be pathological

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3
Q

causes of physiological neonatal jaundice

A

1) marked physiological release of haemoglobin from the breakdown of RBC due to the high Hb conc. at birth
2) RBC life span is 70 days and adults 120 days
3) hepatic bilirubin metabolism is less efficient in the first few days of life

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4
Q

what can kernicterus cause in infants

A

acute - lethergy, poor feeding

severe cases - irritability, inc muscle tone leading to acrched back (opisthotonos), seizures, coma

long term - cerebral palsy, LD, sensorineural deafness

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5
Q

signs/symptoms of neonatal jaundice

A

jaundice - check by blanching of skin (start from head to toe and trunk and limbs last)

dark urine

pale stool

hepatomegaly

poor weight gain

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6
Q

investigation for neonatal jaundince

A

Blood tests
total and conjugated bilirubin level
FBC
Coomb’s test

transcutaneous bilirubinometer (>35 wks)

Urine sample 
septic screen if necessary 
LFT
TFT
sweat test - CF
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7
Q

management for neonatal jaundice

A

Support - rehydration, treat underlying causes

phototherapy is the treatment of choice

exchange transfusion in severe cases

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8
Q

differentials for neonatal jaundice

A 
biliary atresia 
CF 
hypothyroidism
CMV infection 
duodenal atresia 
haemolytic disease of newborn
Hep B
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9
Q

symptoms of neonatal jaundice

A

lethergy and poor feeding

dehydration - less intake of feeding

jaundice

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10
Q

clinical findings of neonatal jaundice

A

jaundice

petechial or purpuric lesions

anaemia

hepatosplenomegaly

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11
Q

what infection can cause neonatal jaundice

A 
rubella
HAV 
HBV 
CMV 
herpes syphilis
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12
Q

complication of neonatal jaundice

A

kernicterus - bilirubin encephalopathy - medical emergency

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13
Q

RF for neonatal jaundice

A

sibling of neonatal jaundice
East asian
breast fed baby
baby of DM mum

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14
Q

what is birth asphyxia

A

condition caused by hypoxia in the neonatal period –> hypoxia –> lactate production, acidosis –> tissue/organ damage –> brain could potentially damaged

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15
Q

RF for birth asphyxia

A

pre-mature baby

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16
Q

aetiology of birth asphyxia

A

dec BP/blood flow to the placenta of the infant during delivery

could be due to prolapse cord, inadquate circulation or perfusion, inadequat relaxation of uterus due to excess oxytocin, premature seperation of placenta/placental insufficiency

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17
Q

RF for birth asphyxia

A 
older mum 
prolonger rupture of membranes 
multiple births 
lack of antenatal care 
low birthweight baby
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18
Q

symptoms/clinical findings of birth asphyxia

A

not breathing when baby born

cyanosis

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19
Q

Ix for birth asphyxia

A

umbilical cord pH check ABG/VBG –> acidosis (ph < 7.05)

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20
Q

what score is used for birth asphyxia assessment

A

APGAR score

HR 
RR 
muscle tone 
reflex, irritability 
colour
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21
Q

what is APGAR score

A

it is a score used to assess the vital sign of a newborn baby

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22
Q

normal score for APGAR score

A

7/10

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23
Q

mangement of birth asphyxia

A

rapid resus
ABCDE

drugs - adrenaline 0.01 to 0.1 solution

hypothermia treatment (reduce body temperature to 3 degree to lessen physiological effect of the body)

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24
Q

prognosis of birth asphyxia

A

death and severe handicap in 25% of severely asphyxiated full term infants

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25
Q

what is infant respiratory distress syndrome

A

condition causes by lack of surfactant production –> less surface tension in the alveolar space and so alveolar collapse and respiratory distress

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26
Q

how common is IRDS

A

5% in full-term baby

> 50% in pre-term babe if 26-28 gestation age

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27
Q

causes of acute respiratory distress in premature infants

A 
IRDS 
pneumonia (congenital/acquired) 
pneumothorax 
diaphragmatic hernia 
cardiac causes
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28
Q

what can surfactant insufficiency cause to the oxgentation of the blood

A

less alveolar less air exchange

R to L shunting –> can happen intra-pulmonary (in the lung) or extra-pulmonary (across the ductus arteriosus or foramen ovale)

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29
Q

what are some of the secondary cause of surfactant deficiency

A

intra-partum asyphyxia
pulmonary infection - eg group B-haemolytic strep. pneumonia
pulmonary haemorrhage
meconium aspiration pneumonia
congenital diaphragmatic hernia and pulmonary hypoplasia

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30
Q

RF to IRDS

A 
premature delivery 
male 
Mum is diabetic 
Caesarian 
Hypothermia 
perinatal asphyxia 
FHx of IRDS
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31
Q

clinical features of IRDS

A

tachypnoea

recession - intercostal, subcostal, sternal

expiratory grunting

cyanosis

tracheal tug

nasal flaring
heading bobbing

silent chest

SpO2 <85%

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32
Q

investigation for IRDS

A

Sats to see if hypoxic - aim for 91-95%
CXR - ground glass appearance and air bronchogram
ABG - both resp and metabolic acidosis

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33
Q

what specific CXR findings suggest IRDS

A

ground glass appearance

air bronchogram

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34
Q

management of IRDS

A

ABCDE

resp support - O2 aim for 91-95%
CPAP or IPPV or intubation

surfactant - given via an endotracheal tube

treat any underlying conditions eg ABX

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35
Q

what are some preventive management for IRDS

A

antenatal dexamethasone to encourage rapid maturation of lung tissue of the infant

delay premature birth —> tocolytic agents

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36
Q

complications of IRDS

A

pneumothorax

pneumonia

intra-ventricular haemorrhage

delayed cognitive impairment

bronchopulmonary dysplasia

retinopathy of prematurity (due to O2 perfusion)

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37
Q

what is a pigmented naevi

A

a pigmented macular/plaque of lesions of birthmark

start to appear at 2 yrs

low risk of malignancy

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38
Q

what is a cafe-au-lait spot

A

uniformly pigmented, sharply demarcated, macular lesion

maybe prest at birth or develop in childhood, vary in size

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39
Q

what would be red flag symptoms in the presence of cafe-au-luit spots

A

extensive spots are features of neurofibromatosis (congenital condition that forms tumours in nerves)

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40
Q

what is strawberry naevus

A

it is superficial/infantile haemangioma

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41
Q

what is the clniical findings of strawberry naevus

A

bright red
protuberant
compressible
sharply demaracted (Starwberry for sharplt demaracted)

may vary in size in 12-18 months of baby life before fading, most spontanouesly fade

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42
Q

does strawberry naevus require treatment

A

no usually unles in sensitive area eg around eye, lips, airway etc and only if interferting with vital function

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43
Q

treatment for strawberry naevus

A

usually no treatment but if affecting functions then

beta-blocker +/- corticosteriods

surgery if required

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44
Q

what is naevus flammeus

A

small pink flat lesions commonly on eyelids, neck and forehead

most common between eyebrows and forehead

usually fades and no-harmful

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45
Q

what can Naevus flammeus suggest

A

Beckwith-Widemann Syndrome - condition of growth regulation leading to overgrowth

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46
Q

what is mongolian blue spots

A

blue or slate-grey lesions, commonly in sacral area

47
Q

where can you find most of the mogolian blue spots

A

in the sacral area of the baby

48
Q

which population is more commonly born with Mongolian blue spots

A

> 80% of black and Asian babies

49
Q

aetiology of Mongolian blue spots

A

collection of melanocytes in deep dermis

50
Q

what admin work should you do for Mongolian blue spots

A

document it in notes to avoid confusion of bruises for later which can relate to abuse issues

51
Q

will Mongolian blue spots resolve itself

A

usually within the first few years of life

52
Q

what is port-wine stain

A

mature, dilated, dermal capillaries

53
Q

clinical findings of port-wine stain

A

macular, sharply circumscribed, pink to purple lesion

can vary in size

54
Q

will port-wine stain resolve itself

A

vasuclar lesion whcih will perisist

55
Q

what is a red flag for port-wine stain

A

if localised to trigeminal area of ace, sonsider Sturge-Weber Syndrome(seizure. LD. port-wine stain due tp underling meningeal haemangioma + intracranial calcification)

56
Q

what is cephalhaematoma

A

it is a collection of blood in the periosteum layer (just under the skin of skull) due to tearing of vessels during birth/at any aged human

57
Q

RF for cephalhaematoma

A

pre-term baby

instrumental delivery of babies

58
Q

symptoms/clinical findings of cephalhaematoma

A

selling appearing from hours 50 2-3 days post birth

if severe –> jaundice, anaemia or hypotension

takes weeks for blood clots to be absorbed

selling slowly moves towards the centre of head

it will not cross any cranial sutures

59
Q

management of cephalhaematoma

A

observation

60
Q

prognosis of cephalhaematoma

A

meningitis/osteomyelitis - due to fracture in the skull leading to infection

61
Q

definition of haemolytic disease of the foetus and newborn

A

transplacental passage of maternal antibodies reacting to antigen of foetal RBC

62
Q

what are the 2 main haemolytic diseases of the foetus and newborn

A

1) . ABO blood group incompatibility

2) . rhesus incompatibility

63
Q

how does rhesus incompatibility cause HDN

A

mother rhesus -ve and foetus rhesus +ve and so during pregnancy and delivery, foetal RBC cross the placental barrier to enter the body of mum

mum develops anti-rhesus antibodies which can then cross the placenta to causing haemolysing effect on the foetus

first child might be okay but successive child will defo be affected

64
Q

wich one of the HDN is most common

A

ABO blood group incompatility

Rhesus incompatility has now been reduced with Rh immunoglobulin to Rhesus -ve women during prgancy/shorty after birth of a rhesus +ve babe

65
Q

what other procedure can trigger primary immune response of mum rhesus snesitvity

A

aminocentesis

66
Q

how can ABO incompatibility cause HDN

A

 Mother most commonly group O and baby is group A. Mother’s natural anti-A antibodies react with fetal cells  haemolysis + jaundice.

67
Q

can you detect HDN

A

you can detect Rhesus but not ABO incompatibility

68
Q

clinical features of HDN

A

foetal anaemia –> if untreated, severe oedema –> hydrops –> fluid collection in multiple compartments of the bay eg ascites, pleural effusion leading to death

jaundice development within first 24 hours of life –> kernicterus

69
Q

which type of HDN more likely to cause IRDS

A

rhesus incompatibility

70
Q

management of foetus in HDN

A

deliver before severe haemolysis occur

series of exchange transfusions to remove antibodies + toxic bilirubin

late anaemia can develop –> need top up blood transfusion

71
Q

management of mum in HDN

A

rhesus -ve women immunised with anti-D immunoglobulin

72
Q

prognosis of HDN

A

kernicterus main worry
can develop IRDS
can develop hydrops
sensorineural hearing impairment

73
Q

definition of prematurity

A

birth at <37 wks

74
Q

how common is prematurity

A

approx. 7% incidence

1% severe (<1500g)

75
Q

what are the modifiable factors of prematurity

A

short inter-pregnancy time (2x risk inc)

lifestyle factor - BMI < or > 35 smoking

psychological stress

intra-uterine/vaginal infection

76
Q

what are the non- modifiable factors of prematurity

A

Pace –> black baby have higher risk

previous pre-term birth

chronic medial disease eg DM, astham, thyroid disease

77
Q

what are the maternal factors of prematurity

A

pre-eclampsia or related hypertension

78
Q

management of prematurity

A

immediate post-birth resuscitation

efforts to reduce excessive o2 exposure

reduce hyperventilation - intubation, surfactant

reduce hypothermia - warming

reduce hypoglycaemia - IV access and detrox

Hypotension - IV fluid bolus of 10ml/kg 0.9% saline then inotropes, dopamine followed by dobutamine, hydrocortisone

79
Q

how can you determine gestation age?

A

using the New Ballard Score

USS finding

80
Q

what is the aim for MAP for a pre-term baby

A

MAP should equal to the infant’s gestational age eg if gestational age = 28 wks then MAP should be >28

81
Q

what medication can be used to treat apnoea in infant

A

methyxanthine (caffeine)

82
Q

what medication can be used to main ductal patency

A

prostagladin

83
Q

which larger group does IUGR belongs to

A

SGA - Small for Gestational Age

84
Q

definition of Small for Gestational Age

A

birth weight < 10th centile/2SD away from the population norm on growth chart

85
Q

definition of IUGR

A

only apply to foetus with clinical feature of malnutrition and in–utero growth restriction

irrespective of their weight precentile

86
Q

what group does IUGR divide into?

A

symmetrical

asymmetrical

87
Q

what is the usual cause of symmetrical IUGR

A

hypoplasia

88
Q

what is the usual cause of asymmetrical IUGR

A

malnourishment

most common placental insufficiency

89
Q

what is the clinical appearance of symmetrical IUGR

A

both weight and head circumference are below 10th centile

90
Q

what is the clinical appearance of asymmetrical IUGR

A

abdo circumference affected

weight and head circumference normal/less affected

91
Q

what is a maternal factor for IUGR

A 
inter-pregnancy time 
Maternal lifestyle 
maternal conditions eg asthma, DM
previous SGA babies 
maternal infectino (TORCH, HIV, syphilis, TB, UTI, bacterial vaginosis
92
Q

what is a foetual factor for IUGR

A

chromosomal deficit
major congenital deficit eg trach-oesophageal fistula, congenital heart disease

infection - TORCH, malaria, HIV, syphilis

93
Q

how do you diagnose SGA/IUGR

A

foetal abdo circumference and estimated foetal weight < 10 cenile

94
Q

management of IUGR

A

similar to prematurity
also effective and encouraging feeding to encourage development

can give endogenous corticosteriod - mature lungs and enhances surfactant production

95
Q

short term complications for IUGR

A

IRDS
perinatal asphyxia
meconium aspiration
prematurity

96
Q

long term complications for IUGR

A

poor growth and neurodevelopment outcome

general and specific learning difficulties
cerebral palsy
gross motor and minor neurological dysfunction
behaviour problems

97
Q

what is another name for Talipes

A

club foots

talipes equinovarus

98
Q

how common is talipes

A

1 in 1000 birth in the UK

99
Q

which gender is more common to have talipes

A

male > female (2:1)

100
Q

clinical features of talipes

A

equinus - foot pointing downwards

varus - foot pointing inwards

middle section of foot usually twisted inwards

achilles tendons is tight

shortening of tendons on medial aspect of leg

101
Q

what is assoicated with talipes

A

1/5 associates with

spina bifida

cerebral palsy

arthrogryposis (hooked joint) (curved + joint stiffness + abnor muscle development)

102
Q

Ix for talipes

A

antenatal scans can pick it up

neonatal examination

103
Q

management of talipes

A

ponseti method (preferred method due to success rate of 8-9/10cases)

manually move foot to correct position

plaster cast for 1 wk

foot mainuplated again then cast 1 wk

repeat for 6 wks

achilles tenotomy recommended after 6 wks

boots with bar for 23 hrs for 3 months

104
Q

what are the 3 different types of neonatal jaundice

A

physiological, pathological and prolong jaundice

105
Q

what constitute a physiological jaundice

A

occur after 1 day

106
Q

what constitute a pathological jaundice

A

occurs within 24 hours

107
Q

what constitute a prolonged jaundice

A

over 2 weeks in term baby

over 3 weeks in pre-term baby

and bilirubin > 200 in term baby

108
Q

what is the difference between unconjugated and conjugated neonatal jaundice

A

unconjugated - occurs due to haemolysis or pre-hepatic causes

Conjugated - occurs due to hepatic/obstruction ie post-hepatic

109
Q

what are some of the causes of unconjugated neonatal jaundice which occurs within 24 hours of birth

A

haemolytic disease

neonatal sepsis

110
Q

what are some of the causes of conjugated neonatal jaundice which occurs within 24 hours of birth

A 
neonatal hepatitis
congenital infections (TORCH syndrome)
111
Q

what are some of the causes of unconjugated neonatal jaundice which occurs between 24 hours and 2 weeks

A

physiological
hypothyroidism
haemolysis/sepsis

112
Q

what are some of the causes of conjugated neonatal jaundice which occurs between 24 hours and 2 weeks

A 
neonatal hepatitis
congenital infections (TORCH syndrome)
113
Q

what are some of the causes of unconjugated neonatal jaundice which occurs after 2 weeks

A

breast milk jaundice
haemolysis/sepsis
hypothyroidism

114
Q

what are some of the causes of conjugated neonatal jaundice which occurs after 2 weeks

A

biliary artresia
choledochal cyst
neonatal hepatitis
Alpha-1 antitrypsin deficiency/TORCH/Glactosaemia/CF)

Year 4 Paeds Conditions (10 decks)

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