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LS YEAR 4 Paediatrics > Neonates > Flashcards

Neonates Flashcards

1
Q

what is neonatal jaundice ?

A

also known as hyperbilirubemia yellowish discolouration of the sclera/conjuctiva of the eye and skin in new borns due to high bilirubin levels typically 2-4 days after birth due to the immaturity of the liver physiologically

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2
Q

do most need treatment?

A

no most resvolve -self-limiting

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3
Q

causes

A

conjugated or unconjugated can be pre-hepatic , hepatic of post hepatic

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4
Q

give examples of each

A

conjugated -neonatal hepatitis, binary atresia, CF unconjugated- prematurity, bacterial infection, excessive bruising, rhesus ABO incompatibility, hypothyroidism pre-hepatic -haemolysis hepatic hepatitis post hepatic- binary atresia, absent bile ductules

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5
Q

two classes of neonatal jaundice

A

physiological and pathological

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6
Q

describe and discuss break milk and breast feeding

A

breastfeeding -inadquate amount, reduced calorie intake unable to stimulate bowel movement for removal so need to hydrate and increase bF breAST MILK -associated with increase b gluctomase within first 2 weeks and can last 3-13 weeks continue bF consider top ups

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7
Q

kerniticus likely when

A

> 8.5micromol/l >340 serum bilirubin

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8
Q

values for pathological and physiological

A

<15 >15 patholoigcal > 20 likely to be due to liver disease

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9
Q

list examples of both classes of neonatal jaundice

A

phsyioloigcal - breast milk and breast feeding pathological conjugated -TORCH, HEP A, B, SEPSIS BILARY ATRESIA, CHOLDECTAL CYST, CF syndromes unconjugated - these are RH, ABO incompatibility, crippler Najjar Gilbert, sepsis, G6pD deficiency

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10
Q

big concern with unconjugated

A

build of bilirubin causing kericterus -irreversible Brain damage caused cause nerve deafness, cerebral palsy and mental retardation

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11
Q

most common cause of prolonged

A

breast feeding

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12
Q

what do u need to rule out with prolonged

A

bilary atresia

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13
Q

presentation in conjugated ??

A

yellow sclera and skin bruising poor feeding hepatomegaly dehydration pale stool, dark urine in conjugated

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14
Q

rf

A

family history cf maternal diabetes male East Asian ethnicity low birth weight pre-term metabolic and liver disorders

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15
Q

chalky poo

A

biliary atresia

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16
Q

investigations

A

transcutaneous bilirubinometer - measure bilirubin in the skin abc - neutrophilic and penny assessment looking for infection throbocytopenia -infection total and unconjugated bilirubin Coombs test- antibodies (in mother) on abc for incompataibility RH positive inborn error of metabolism-met screen urine culture for infection LP for mengitis use FOR BILARY ATRESIA

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17
Q

when exchange transfused done

A

>20mg/DL rapid rise >1mg/l/hour in less than 6 hour excelopathy or haemoltyic via umbilical catheter

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18
Q

how long phototherapy checks

A

4-6 hour monitor if stable, can monitor 6-12 hourly when 50 below treatment line can stop repeat 12 hour after for maintenace

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19
Q

what to do if within 24 hour but below threshold by 50micrommol/litre for phototherapy

A

repeat in 18 hour if suspected in 24 hour without RF

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20
Q

when is intensive therapy photo used

A

50 micromol/litre below exchange, consider intensified >8.5micromol/l per hour no improvement within 6 hour of starting or continuing to increase

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21
Q

what if top end of treatment graph for pho therapy

A

if 50 micromol/litre below exchange, consider intensified

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22
Q

MANAGEMENT

A

self limiting in most aim for treatment is to prevent kernictercus phototherapy to degrade unconjugatred bilirubin excreted via urne followup for neurocomplications hearing assessment exchange transfusions

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23
Q

other tests

A

tft for hypothyrodisim hep b antigen hep b sweat test- cf

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24
Q

four things to classify if haemolysis and or urgent

A

first 24 hour of life-haemolytic >2 weeks or more lasting evidence of deep jaundice severe increased conjugated

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25
Q

Heinz bodies

A

g6pd deficiency

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26
Q

what is birth asphyxia

A

deprivation of oxygen to the newborn resulting in harm usually to the brain

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27
Q

what is primary mechanism

A

hypoxia - build up of lactic acid and co2 - tissue acidosis leading to ischaemia of tissue as result of impaired blood flow

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28
Q

diagnosis is determined by

A

ph < 7.05 and using APGAR score delay in establishing spontaneous respiration (> 10 mins) abnormal neuro signs including convulsions > 2days

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29
Q

what is Apgar score

A

used in newborns and compromised of rest rate, muscle toene, colour, reflect, heart rate to determine physical condition of newborn

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30
Q

causes

A

starvation of oxygen at birth placental abruption - separation from uterine or compression of umbilicaL CORD UTERINE rupture poor placental flow high bloood pressure >42 gestation inadequate oxygen in mothers blood material hypotension drug use multiple pregnancy inadequate relaxation of uterus diabetes maternal

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31
Q

signs and symptoms

A

abnormal heart rate and rhythm acid levels high blueish pale skin weak cry and weak breathing-gasping low heart rate weak muscle tone meconium symptoms can determine if HIE is mild mod or severe

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32
Q

management

A

oxygen to mother at and during delivery and before emergency deliver or c section if needed assested ventilation to assess breathing and bP extrcopeorneal membrane oxygenation treat convulsions

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33
Q

why can inadequate uterine relaxation impact this

A

reduces blood flow thus oxygen flow to placenta

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34
Q

what is biliary atresia?

A

Conjugated hyperbilirubinaemia and is rare (1 in 10000). Absence of intra or extrahepatic bile ducts.

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35
Q

when does biliary atresia occur? how do you manage?

A

evelops over a period of weeks, stools become clay coloured. Can progress to liver failure requiring transplant. If detected within first 6 weeks then carry out hepatoporto-enterostomy (Kasai procedure). Any baby jaundiced after 2 weeks must have unconjugated and conjugated bilirubin levels checked. High conjugated fraction (>20% total) should refer to hepatologist.

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36
Q

percentage of cerebral palsy due to HIE

A

20%

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37
Q

risk factors for birth asphyxiati?

A

maternal low bP maternal diabetes inadequate relaxation of uterus therefore reduced oxygen circulation to placenta uterine rupture 42 weeks > gestation respiratory distress drug use

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38
Q

when do pigmented naevi occur?

A

after 6 months of birth

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39
Q

malignancy risk in pigmented navei?

A

very rare

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40
Q

do they get better with age?

A

yes

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41
Q

appearance of pigmented nave

A

can be flat or elevated

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42
Q

describe cafe au lait

A

latte colour uniform pigmented sharply demarcated macular lesion can be irregular or regular

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43
Q

when do cafe au last spots appear?

A

in infancy or at birth

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44
Q

what are they associated with?

A

neurofibroma

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45
Q

criteria for neurofibroma

A

if six or more by 5 years od age >1cm and if in groin or under arm consider genetic testing and exclude bone tumours

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46
Q

how can they be improved?

A

laser

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47
Q

what is salmon patch

A

also known as stork mark navies flammengus small pink flat lesion on eyelids/neck or forehead

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48
Q

key feature of salmon patch

A

it is flat and it reddens with crying or straining

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49
Q

what is the most common type of vascular birthmark

A

salmon patch

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50
Q

improve how?

A

fade with time few months needed

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51
Q

where does Mongolian blue spot usually present?

A

lower limb, back, buttocks

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52
Q

who?

A

darker skin people very common in black and brown skin

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53
Q

does it improve

A

yes but gradually usually by 4 years of age

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54
Q

what does it look like

A

blueish bruise looking skin

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55
Q

is the Mongolian blue spot harmful?

A

no and it is self limiting

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56
Q

what is a port wine stain?

A

flat purplish mark on skin can be a few mm to cm

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57
Q

key features of port wine stain

A

one sided and usually on face chest back usually present at birth sensitivity to hormones to more prominent in pregnancy puberty and menopause

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58
Q

improve with time

A

no can worsen

59
Q

how to improve it?

A

with lasers

60
Q

what are port wine stain associated with?

A

struge weber syndrome, klippel tranunary syndrome

61
Q

what is a strawberry naevi

A

also known as infantile haemognomia

62
Q

who is it seen in?

A

5% of newborns very common f>m

63
Q

what is a strawberry naevi?

A

red protuberance compressible and may increase in size in first 1-2 years of life but then tends to improve and resolve spontenously monitoring needed

64
Q

what do you need to consider

A

if causing obstruction such as vision if near eye then treat medically ulcerated obstructing airway if near vessels and bleeds alot

65
Q

where are sensitive areas for infantile haemogiomas?

A

napkin area eye lip airway

66
Q

what is cephalhaemtoma

A

traumatic sub peritoneal haemotoma which occurs under the skin in the peritoneum of the skull bone resulting in pooling of blood it cannot occur the midline

67
Q

when does it occur

A

within hours after delivery

68
Q

how does it present

A

bulge on side or posterior of head jaundice sometimes soft flutucant swelling

69
Q

risk factors?

A

head greater then pelvic area first pregnancy large baby use of forceps difficult and prolonged labour

70
Q

management

A

MRI CT scan self limiting itself within 3 months drainage rare and increased infection risk

71
Q

guthrie test

A

Metabolic Screening Programme screens for rare but potentially serious disorders such as phenylketonuria (PKU), cystic fibrosis, and congenital hypothyroidism haemoglobinopathies. A blood sample is taken from your baby’s heel at or as soon as possible after 48 hours of age (the ‘heel prick’ or ‘Guthrie’ test).

72
Q

what is another name for haemolytic disease in the newborn?

A

erythroblastosis fetalis

73
Q

what is erythroblastosis fetalis

A

incompability between maternal and baby blood group causing red blood cell breakdown and immaturity of RBC

74
Q

how does haeoltyic disease in newborn occur

A

it is usually when mother is Rh neg and father is rhesus pos and baby acquires fathers rhesus pos. during delivery there is often exchange of maternal and baby blood during delivery. the maternal body produced antibodies to act against foreign rh POS inducing an immune response. the mother is sensitized once she has produced antibiodies- this poses as a risk for future pregnancies.

75
Q

risk factor

A

2nd or higher pregnancy as mother is sensitised in first pregnancy 3x more common in caucasians

76
Q

mechanism in detail of haemolytic disease

A

the mother antibodies breaks down abc in baaby making baby anaemic and reducing oxygen transportation around the body the baby produced more rbc in the bone marrow spleen and liver causing organomegaly often the abc are immature and not functional as rbc are broken down, bilirubin produced can cause jaundice

77
Q

presentation

A

jaundice pale yellow amniotic fluid organomgaly -can be detected on USS during pregnancy fluid build up breathing difficulity odema

78
Q

diagnosis

A

before birth rhesus pos antibody test in mothers prior USS of foetus during pregnancy aminocestesis can test for bilirubin in amniotic fluid post birth - can test blood from baby via umbilical cord for rh factor, blood group

79
Q

treatment of haemolytic disease

A

throughout pregnancy, intrauterine blood transfusions of rbc into baby circulation via needle into abdominal cavity of mother through to umbilical cord

80
Q

what can trigger early. delivery

A

maturation of the lungs

81
Q

what is given supportively to babies post birth

A

oxygen iv fluids blood transfusion resp distress management surfactant mechanical breathing

82
Q

what other things can be done

A

[1] exchange transfusion to increase abc and reduce bilirubin [2] immunoglobulins IV made from plasma containing antibodies to aid immune system and reduce breakdown of rbc

83
Q

what is a preventative method used in the UK

A

mothers are all undergone testing in the Uk, those identified are given anti-D immunoglobulin to prevent antibodies attacking rhesus Pos cells in the. baby usually given at 28-30 weeks

84
Q

what is the anti d immunoglobulin dose

A

1 at week 28-30 2 doses at week 28 and 34 weeks

85
Q

what can increase still birth in haemolytic disease

A

abnormal accumulation of fluid in two or more fetal compartments, including ascites, pleural effusion, pericardial effusion, and skin oedema causing difficulty breathing and swelling - this can make organs swell due to fluid build up and cause heart failure

86
Q

what is prematurity? what defines term baby

A

a baby with gestation age of less than 37 weeks term baby 37-41 weeks

87
Q

what percentage of births ?

A

8%

88
Q

when does problems occur

A

when less than 32 weeks but this usually affects 2% of births

89
Q

what are the predisposing factors for prematurity

A

idiopathic in 40% of cases multiple pregnancies previous premature pregnancy maternal illness- dm, pre-eclampsia smoking alcohol if under 18 or over 35 (maternal)

90
Q

symptoms for prematurity?

A

full range…. respiratory: surfactant deficiency causing respiratory distress syndrome , apnea anaemia necrotisiing enterocolitis poor milk tolerance inability to suck hypothermia (often kept at warm temps when born) jaundice anaemia increased infection risk if immunocompromised birth trauma patent ductus arteriosis retinopathy of prematurity perinatal hypoxia

91
Q

prognosis is excellent when

A

over 32 weeks

92
Q

management

A

stabilise newborn and provide support if less than 28 weeks need specialist paediatrician there place under heater provide rest support- PEEP start with low pressure intubation if less than 27 weeks ett surfactant monitor o2 sats support parents encourage breast feeding and provide antibiotics - - Benzylpenicillin and gentamycin if septic. monitor weight regularly

93
Q

what is needed if <34 weeks

A

dethametasone to mother need to be given 24 hour before second dose 1 2 hours apart to reduce mortality by 40% as part of antenatal care

94
Q

what is respiratory distress syndrome

A

deficiency in surfactant causing lower surface tension and results in wide spread alveolar collapse and. indaqduate gas exchange

95
Q

risk factors

A

diabetic mothers

96
Q

presentation of RDS

A

grunting nasal flaring tachypnoea cyanosis chest well recession laboured breathing

97
Q

diagnosis of RDS

A

on Xray appears as ground glass diffuse granular on appearance bronchogram monitoring done with blood gases and o2 sats

98
Q

treatment of RDS

A

glucocorticoids , surfactant therapy (curosurf< extracted from pig or calf lung given endotracheally) bolus of ETT intubation artifical ventilation high flow oxygen CPAP

99
Q

what is vitamin k deficiency a risk factor for

A

bleeding and bruising due to lack of clotting factors which dependent on vitamin K

100
Q

what is done to prevent this

A

birth , 1 week and 6 week vitamin k oral or IM injections

101
Q

where is vitamin k found

A

in formula milk but low levels in breast milk

102
Q

what can prevent RDS

A

maternal antenatal corticosteroids

103
Q

what is IUGR and what does it stand for what does it increase risk of

A

intrauterine growth restriction symmetrical or asymmetrical small in utero due to delayed/restricted growth 3 in every 100 pregnancies increased risk of prematurity

104
Q

most common cause of IGUR

A

failure of placenta

105
Q

other causes of IGUR

A

multiple pregnancies infection smoking warfarin alcohol toxaemia in pregnancy TORCH

106
Q

what does torch stand for?

A

toxoplasma other-syphilis rubella cytomegaly herpes

107
Q

how is it diagnosed

A

antenatal appointments through fundal height

108
Q

how is IGUR treated

A

no treatment but managed through regular scans blow flow through placenta is checked via doppler

109
Q

what is the long term sequelae of IGUR

A

microcelaphaly cerebral palsy blindness and deafness mental retardation

110
Q

management of IGUR once baby is born

A

feeding to anticipated weight requirements except hypoglycaemia (and hypothermia

111
Q

what is hypoglycaemia considered to be in these babies

A

< 2.6mmol)

112
Q

how do you treat hypoglycaemia in igur babies

A

dextrose iv and milk feeds

113
Q

what is another concern of IGUR babies with regards to feeding

A

immature GI tract preventing gastric feeding resulting in a need for NG tube

114
Q

when is sucking reflex developed

A

35 weeks (begins 32 weeks, fully developed by 35/36 weeks)

115
Q

what are these children at risk of?

A

poor childhood growth and intellectual impairment

116
Q

define symmetrical and asymmetrical?

A

length and weight proportional to body weight long and thin, lit subcut fat, sparing of head growth (normal head growth)

117
Q

what is another term for talipes what is it who how common

A

club foot when the front half of the foot is inwards and downwards can affect 1 or both feet 2x common in males and 1-2 per 1000 babies usually at birth

118
Q

risk factor

A

family history (if parents had it) 1/3 if both had it

119
Q

what is often seen with babies with talipes

A

1/5 will have another condition such as spina bifida or CF

120
Q

is it painful?

A

no

121
Q

what is problem with talipes

A

likely to impact walking and can cause delay in walking thus needs to be managed

122
Q

when is a diagnosis for talipes made

A

mid pregnancy via USS

123
Q

how is talipes manage

A

PONSETI METHOD of foot maniupulation and then placed in a cast first few months require weekly sessions tenotomy sometimes needed to hot it in place 9boot and bar) where foot is kept in 23 hours daily and then after 2-3 months cut down to just at night until 4-5 years

124
Q

what is acrocyanosis

A

is high Hb marked blue publish colouring of hands and feet normal and harmless common

125
Q

what is erythema toxicum

A

common benign self resolving first48 hours and resolves spontaneously

126
Q

what are milia?

A

keratin filled cyst under epidermis disappear within 2-4 weeks harmless

127
Q

what is transient netonatal pustular melanosis

A

benign self limiting condition common in AAbenign idiopathic skin condition mainly seen in newborns with skin of color, has distinctive features characterized by vesicles, superficial pustules, and pigmented macules.

128
Q

what can talipes be graded with

A

0-6 pirañi score

129
Q

what happens to Achilles in talipes

A

it is tight

130
Q

four positions of the foot

A

equniovalgus calcaneovalgus - cancenocavus equinovarus

131
Q

mmenonic for Guthrie test and tests

A

people can go screen many many infants, how come ? Phenylketouria Cf Gluanic aciduria type 1 Maple syrup urine disease medium chain coA dehydration’s deficiency Isovolemic acidemia Homocysuria Congneitla hypothyoridism

132
Q

criteria for cooling

A

tobys

133
Q

list features of cooling criteria

A

Criteria for therapeutic hypothermia: Infants >36 weeks >1.8kg <6hr old with one of: Apgar <5 at 10 mins or continued need for resuscitation at 10min Acidosis: cord pH (or any blood gas in 1st hr) <7 or BE

134
Q

how long cooling for

A

usuallyy 72 hr

135
Q

when resus needed

A

Apgar score < 5 at 5 mins

136
Q

whats CFAM

A

cerebral function analysis monitoring (CFAM) o Single or 2 channel machines available (2 channel = L and R hemispheres) o Displays ‘raw’ EEG dysmorphism and birth trauma Assess neurological features no seizure activity -goos sign

137
Q
  • Caput succedaneum
A

midline crosses oedema

138
Q

respistry distress symptoms

A

❖ Tachypnoea ❖ Intercostal, subcostal, sternal recession (chest indrawing) ❖ Cyanosis ❖ Expiratory grunting within 4hrs of birth

139
Q

positional and congenital talipes

A

Positional talipes = normal foot that has been held in a deformed position in utero (usually equinovarus or calcaneovalgus) Congenital talipes = fixed structural alteration in morphology of foot – idiopathic in and downwards

140
Q

halo ecchymosis irregular border

A
  1. Disseminated intravascular coagulation (DIC) - Massive ecchymosis with sharp, irregular borders of deep purple colour and an erythematous halo
141
Q

chicken pox exclusion

A

5 days from start of skin eruption/crusted over

142
Q

what can happen post viral infection gastroenteritis

A

lactose intqrolrance lasting 4-6 weeks

143
Q

most common allergie In kiddies

A

cows milk protein allergy

LS YEAR 4 Paediatrics (24 decks)

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