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Paediatrics > Neonates > Flashcards

Neonates Flashcards

1
Q

What type of cerebral palsy is associated with an intraventricular haemorrhage?

A

spastic diplegic cerebral palsy due to the anatomical proximity of the corticospinal tracts.

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2
Q

What are the four causes of jaundice in the first 24 hours of life?

A

rhesus haemolytic disease
ABO haemolytic disease
hereditary spherocytosis
glucose-6-phosphodehydrogenase

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3
Q

What percentage of infants born at 26-28 weeks will have SDLD?

A

50%

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4
Q

What percentage of infants born at 30-31 weeks will have SDLD?

A

25%

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5
Q

What other risk factors are there for SDLD?

A

Male sex
Diabetic mothers
C-section
Second born of pre-term twins

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6
Q

What appearance is seen on a chest x-ray with a neonate with `SDLD?

A

Ground glass appearance with an indistinct heart border

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7
Q

How do you manage SDLD?

A

prevention during pregnancy: maternal corticosteroids to induce fetal lung maturation
oxygen
assisted ventilation
exogenous surfactant given via endotracheal tube

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8
Q

When is the neonatal blood spot screening performed? (heel-prick/guthrie test)

A

5-9 days of life

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9
Q

Which conditions are screened for with the heel prick test?

A 
congenital hypothyroidism
cystic fibrosis
sickle cell disease
phenylketonuria
medium chain acyl-CoA dehydrogenase deficiency (MCADD)
maple syrup urine disease (MSUD)
isovaleric acidaemia (IVA)
glutaric aciduria type 1 (GA1)
homocystinuria (pyridoxine unresponsive) (HCU)
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10
Q

What might a jittery hypotonic neonate represent?

A

Neonatal Hypoglycaemia

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11
Q

What are the risk factors for neonatal hypoglycaemia?

A 
maternal diabetes mellitus
prematurity
IUGR
hypothermia
neonatal sepsis
inborn errors of metabolism
nesidioblastosis
Use of maternal labetalol
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12
Q

What is galactosaemia?

A

Galactosemia is a rare genetic metabolic disorder that affects an individual’s ability to metabolize the sugar galactose properly. Galactosemia follows an autosomal recessive mode of inheritance that confers a deficiency in an enzyme responsible for adequate galactose degradation.

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13
Q

What is PKU?

A

Our bodies break down protein in foods like meat and fish into amino acids, which are the “building blocks” of protein. These amino acids are then used to make our own proteins. Any amino acids that aren’t needed are broken down further and removed from the body.
People with PKU can’t break down the amino acid phenylalanine, which then builds up in the blood and brain. So can’t have breast milk.

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14
Q

What is classified as prolonged ROM?

A

> 18 hours

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15
Q

How is bilirubin excreted in the womb?

A

Bilirubin is not conjugated by the fetus, so it is excreted by placental transfer but after birth conjugation and hepatic excretion of bilirubin must take over.

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16
Q

Which enzyme conjugates bilirubin which doesn’t develop until after birth?

A

Gluconyl transferase

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17
Q

What percentage of infants are visibly jaundice in the fist week of life?

A

60%

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18
Q

If jaundice is present in the first 24hours, what is it?

A

Always pathological

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19
Q

What are the rules of physiological jaundice?

A

Not apparent in the first 24 hours, the infant remains well, the serum bilirubin does not reach treatment level, the jaundice fades by 14 days.

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20
Q

What are the causes of pathological jaundice?

A

Rhesus haemolytic disease, ABO haemolytic disease, hereditary spherocytosis, glucose-6-phosphodehydrogenase.

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21
Q

Is jaundice more common in bottle or breast fed babies?

A

Breast fed

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22
Q

What is breast milk jaundice?

A

Breast milk jaundice is a type of neonatal jaundice associated with breastfeeding. It is characterized by indirect hyperbilirubinemia in a breastfed newborn that develops after the first 4-7 days of life, persists longer than physiologic jaundice, and has no other identifiable cause.

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23
Q

What is the most important blood test in a baby with jaundice?

A

Test for raised CONJUGATED BILIRUBIN level because if its conjugated then it is probably BILIARY ATRESIA because the liver is still able to conjugate the bilirubin so this would be a post-hepatic cause of jaundice.

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24
Q

How many days is it normal to have jaundice?

A

Day 2-14

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25
Q

Which blood tests must be performed in the newborn with jaundice?

A

Look for maternal antibodies on antenatal blood tests and check the babys bilirubin, haemoglobin and Coombs test. (direct anti-body test)

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26
Q

What is the most common cause of haemolytic jaundice?

A

ABO incompatibility

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27
Q

What is involved in the jaundice screening?

A

Coombs test, TFTs, FBC and blood film, urine for MC&S and reducing sugars, U&E’s and LFTs

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28
Q

What is kernicterus?

A

This is when unconjugated bilirubin can enter the brain and cause neuronal damage. High serum bilirubin, preterm birth, acidosis or hypoxia

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29
Q

What does phototherapy do?

A

When serum bilirubin is high, treatment with phototherapy through the light of a wavelength converts unconjugated bilirubin to non-toxic isomers and this allows bilirubin excretion without conjugation.

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30
Q

What are the haemolytic causes of neonatal jaundice?

A

ABO incompatibility, rhesus or other isoimmunisation, red cell defects eg G6PD deficiency..

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31
Q

What are more physiological causes of neonatal jaundice?

A

Prematurity, bruising, polycythaemia, dehydration, sepsis.

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32
Q

What are the causes of prolonged jaundice?

A

Breast milk, biliary atresia, neonatal hepatitis, hypothyroidism, inborn errors of metabolism (galactosaemia).

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33
Q

What happens in ABO incompatibility and how is it treated?

A

Usually the mother in O and the baby is A or B and the maternal anti-A cross over to the baby. The treatment is exchange transfusion.

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34
Q

What 4 things happen in exchange transfusion?

A

Removes bilirubin, removes haemolysing red cells, corrects anaemia and removes antibody.

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35
Q

What is the treatment for Rhesus disease in babies?

A

May need in-utero transfusion and exchange transfusion.

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36
Q

How does Coombs test work?

A

You basically want to see if there are antibodies attached to the red cells so you add an antiglobulin (an antibody against antibodies). This will then cause clumping if they are present.

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37
Q

How is therapy for jaundice decided?

A

Serum bilirubin is plotted against age (in hours) to decide upon therapy

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38
Q

When is the guthrie test carried out and what does it test for?

A

One week, sickle cell & other haemoglobinopathies, congenital hypothyroidism, cystic fibrosis, phenylketonuria (PKA) and acyllcarnitine.

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39
Q

What is tested within 72 hours?

A

Eyes, heart, hips, testes (for males) and automated hearing screen

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40
Q

What happens at 8 weeks?

A

Thorough physical for eyes, heart, hips and testes.

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41
Q

What happens at 9-12 months?

A

Language & learning, safety, diet & behaviour assessment.

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42
Q

What happens at 2-2.5 years?

A

General development, including movement, speech, social skills and behaviour, dentist, sleeping habits, healthy eating etc etc.

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43
Q

What is the life span of a RBC or an infant?

A

70 days

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44
Q

How does jaundice appear on the body?

A

Cephalic to caudal direction.

45
Q

What is opisthotonos?

A

Arched back resulting from increased muscle tone maybe due to kernicterus.

46
Q

At which levels do babies become clinically jaundice?

A

When levels reach more than 80umol/L.

47
Q

What are the main, non-harmful causes of prolonged jaundice?

A

Breast milk (disappears by 4-5 weeks), congenital hypothyroidism, infection (particularly UTI).

48
Q

Why does hypothyroidism cause jaundice in the newborn?

A

It causes a decrease in rate in the conjugation of bilirubin and it also slows down gut motility contributing to jaundice.

49
Q

What is GP6 deficiency?

A

GPD6 is an enzyme which ensures that RBCs live their full life span, so without this there is a quicker breakdown of RBCs due to the shorter half life.

50
Q

What is Gilbert’s syndrome?

A

Mildly reduced activity of UDP-glucoronyltransferase

51
Q

What are the clinical features if there is pulmonary depression in a neonate?

A

Hypoxia, hypercapnia and respiratory acidosis

52
Q

What are the CFs if there is cardiac depression in a neonate?

A

Hypocapnia, decreased perfusion and metabolic acidosis

53
Q

How might birth asphyxia be treated?

A

Therapeutic hypothermia- involves ctive treatment that tries to achieve and maintain a specific body temperature in a person for a specific duration of time in an effort to improve health outcomes during recovery after a period of stopped blood flow to the brain.. done to reduce brain injury following hypo perfusion.

54
Q

How do you treat seizures in neonates?

A

Benzos/anti-convulsants

55
Q

What is Dyskinetic cerebral?

A

Athetoid cerebral palsy or dyskinetic cerebral palsy (sometimes abbreviated ADCP) is a type of cerebral palsy primarily associated with damage, like other forms of CP, to the basal ganglia in the form of lesions that occur during brain development due to bilirubin encephalopathy and hypoxic-ischemic brain injury.

56
Q

What is a salmon patch/stork mark?

A

Telangiectactic nevus appearing pink or tanned, commonly on knee, back of neck or forehead. Its present in 50% of babies and normally disappears within a few months. smooth like rest of body

57
Q

What is a strawberry mark/haemangioma?

A

Benign self-involating tumour that occurs in 5% of babies, increases in size before decreasing by age of 5.

58
Q

What is a port wine stain/capillary malformation/nevus flammeus?

A

Vascular birthmark caused by abnormal BV formation int he skin. Usually on head or neck and tend to be permanent. sensitive to hormones so mat become deeper during pregnancy/puberty

59
Q

What is a cephalhaematoma?

A

Collection of blood between the skull and the periosteum, caused by a rupture of blood vessels crossing the periosteum. Confined within the two bones (skull sutures)

60
Q

What causes a cephalhaematoma?

A

Prolonged 2nd stage of labour, instrumental delivery (ventouse)

61
Q

What are the clinical features in severe cases of cephalhaematomas?

A

Infants may develop jaundice, anaemia or hypotension.

62
Q

How long does the swelling take to go down in a cephalhaem?

A

Weeks to resolve as blood clot is slowly absorbed. Should distinguish from subgleal/subpeneurotic haemorrhage as this takes longer to heal and is more prone to infection.

63
Q

In rhesus iso-immunisation, what does trans-placental passage of anti D cause?

A

Foetal RBC haemolysis

64
Q

What are the clinical features antenatally of rhesus disease?

A

Foetal anaemia, IMMUNE hydrops foetalis

65
Q

What is immune/non-immune hydrous foetalis?

A

Hydrops fetalis usually stems from fetal anemia, when the heart needs to pump a much greater volume of blood to deliver the same amount of oxygen. This anemia can have either an immune or non-immune cause. Non-immune hydrops can also be unrelated to anemia, for example if a fetal tumor or congenital cystic adenomatoid malformation increases the demand for blood flow. The increased demand for cardiac output leads to heart failure, and corresponding edema in amniotic sack.

66
Q

What are the clinical features of rhesus disease pst-natally?

A

Hydrops fetalis, early jaundice and kernicterus (result of hemolysis) (due to antibody and antigen on RBC coming together and causing haemolysis. So would be pre hepatic jaundice!! Also hepatosplenomegaly, coagulopathy, thrombocytopenia and leucopenia.

67
Q

How do you manage rhesus disease?

A

Check serum bilirubin and Hb and start intensive phototherapy, may need exchange transfusion. Also give anti-D bla bla.

68
Q

What is RDS?

A

Lung disease caused by surfactant deficiency. Largely seen in preterm infants and rare in babies born after 32/40.

69
Q

What does surfactant deficiency cause?

A

Alveolar collapse (in alveolar type 2 cells), increased woB and hypoxia due to intrapulmonary shunting of blood.

70
Q

What are the risk factors for RDS?

A

Premature, c-section, hypothermia, maternal DM, perinatal hypoxia, meconium aspiration, congential pneumonia, FH of RDS

71
Q

What is the chest X-ray appearance in RDS?

A

Bilateral diffuse ground glass appearance (fine reticular granularity of the parenchyma), reduced lung volume, air bronchogram, white lung.

72
Q

What are the clinical features of RDS?

A

Tachypnoea (>60bpm), cyanosis, grunting within 4hours of birth, use of accessory muscles.

73
Q

How do you manage RDS?

A

Betamethasone/dexamethasone steroids given IM antenatally

74
Q

What causes positional talipes?

A

Caused by muscle tightness/uterine compression rather than a structural abnormality . The foot isa normal size and can be fully corrected to the neutral position with passive manipulation.

75
Q

What is talipes equinovarus (structural)?

A

(club foot) Complex abnormality in which the entire foot is inverted and supinated causing forefoot adduction. Heel is rotated inwards (varus) and in plantar flexion (equinus). The affected foot is shorter and has thinner calf muscles.

76
Q

What is the cause of talipes equinovarus?

A

Oligohydraminos

77
Q

What is the management for talipes equino?

A

Treatment started immediately to take advantage of pliable infant bones, splint is applied for 3 months.

78
Q

What is talipes calcaneovalgus?

A

Foot is dorsiflexed and everted

79
Q

What causes talipes calcaneo?

A

Intrauterine moulding and self-corrects via passive foot exercises. Associated with developmental dysplasia of the hips.

80
Q

What is prematurity?

A

When a baby is delivered before 37/40. (1 in 10 pregnancies)

81
Q

Which respiratory problems are seen in prem infants?

A

RDS, Bronchopulmonary dysplasia, recurrent apnoea

82
Q

What is bronchopulmonary dysplasia?

A

Chronic lung disease found in infants who have been ventilated due to RDS, high oxygen concentrations and partial pressures cause lung damage.

83
Q

What is recurrent apnoea and how is it treated?

A

Preterm infants who do not breathe regularly- prone to apnoeas (prolonged apnoeas can cause cyanosis and bradycardia). Caffeine is given to stimulate regular breathing.

84
Q

Why do preterm infants have poor temp regulation?

A

Large surface area relative to body mass & very little subcut fat means heat is lost very quickly. Severely preterm babies are placed in a polythene bag straight from the uterus (without drying/washing), incubators &heaters also used.

85
Q

How is the renal function of preterm babies affected?

A

They have poor renal function and high water loss via their permeable skin- high risk of dehydration and electrolyte imbalances.

86
Q

When does the baby develop the sucking reflex?

A

This reflex does not begin until about the 32nd week of pregnancy and is not fully developed until about 36 weeks. Premature babies may have a weak or immature sucking ability because of this. So NG feeding is needed with breast milk (better tolerated, induces gut maturation and reduces risk of NEC). Very low birth weight babies have protein and calories added to their milk.

87
Q

Concerning the heart, what is a preterm at risk of?

A

Patent ductos arteriosus and therefore left to right shunting of blood.

88
Q

Why are pre terms at more risk of intraventricular haemorrhages?

A

Lateral ventricle walls have fragile capillaries which can bleed easily leading to brain damage/hydrocephalus.

89
Q

Anaemia in preterms?

A

Anemia of prematurity (AOP) is an exaggerated, pathologic response of the preterm infant to this transition. AOP is a normocytic, normochromic, hyporegenerative anemia characterized by a low serum EPO level, often despite a remarkably reduced hemoglobin concentration. RBC breakdown means anaemia is common.

90
Q

What is the most common surgical emergency in neonatal medicine?

A

NEC- portion of bowel undergoes ischaemia- inflammation- necrosis- perforation. It is associated with bacterial invasion of the gut milk and more common in pre terms who don’t have breast milk (protective).

91
Q

What are the clinical features of NEC?

A

Distended abdomen, bile stained vomiting, irritable with feeds, bloody stool.

92
Q

What is seen on an x-ray with NEC?

A

Air in intestinal wall & free gas- football sign

93
Q

What is the criteria for resuscitation of babies in the UK?

A

24/40 or weigh more than 500g

94
Q

How is surfactant administered?

A

Endotracheal tube

95
Q

What are risk factors for nec?

A

Prematurity and formula feeding

96
Q

What is a choanal atresia and how would it present?

A

Episodes of cyanosis worse during feeding, happens when the posterior nasal airway is occluded by bone or soft tissue. Babies with unilateral disease will go unnoticed. Treatment is with fenestration measures to restore patency.

97
Q

If born before 37 weeks, how long does jaundice have to be present for, for it to be prolonged?

A

21 days
so perm baby- 21 days
term baby- 14 days

98
Q

What percentage of pre term babies will be jaundice in the first week?

A

80%

99
Q

Where does bilirubin deposit in babies brain if it crosses?

A

Basal ganglia

100
Q

What are the chronic outcomes of bilirubin crossing into the brain?

A

Athetoid cerebral palsy (a form of dyskinetic cerebral palsy), learning difficulties, sensorineural deafness.

101
Q

What other metabolic conditions can cause pathological jaundice?

A

crigler-najjar syndrome, gilberts, hypothyroidism.

102
Q

NB

A

Polycythaemia- diabetic mothers (pathological jaundice)

INFECTION can cause pathological jaundice

103
Q

When would you keep a baby in hospital with jaundice?

A

<24 hours, appears after 7 days, unwell neonate, gestational age <35 weeks, prolonged, pale stool/dark urine

104
Q

What do you plot bilirubin against in the neonatal ward?

A

Level of bilirubin against age.

105
Q

What investigations would you do in order to find out the cause of jaundice?

A

FBC, BLOOD FILM, blood group (mother & baby), coomb’s test, LFTs, Blood GPDD, micro cultures of blood, urine, CSF (excludes infection).

106
Q

NB

A

Hepatomegaly can be seen in an infant with biliary atresia. (kiasi procedure to correct biliary atresia)

107
Q

Blood tests to do in a baby with suspected pathological jaundice

A

Split bilirubin, fbc, blood group, direct coombs test and urine (dip and culture to test for UTI).

108
Q

What are the genetics for G6PD deficiency?

A

X-linked recessive (males).

109
Q

Which drugs can precipitate haemolysis in G6PD deficiency?

A

anti-malarials: primaquine
ciprofloxacin
sulph- group drugs: sulphonamides, sulphasalazine, sulfonylureas

Paediatrics (23 decks)

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