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Year 4 Paediatrics > Neonatology > Flashcards

Neonatology Flashcards

1
Q

Define ‘Pre-term’

A

Delivery before 37 weeks completed gestation

Extreme - before 28 weeks, Very Preterm - 28 to 32 weeks, Moderate - 32 to 37 weeks

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2
Q

Describe the aetiologies of Preterm Infants

A

25% planned (life threatening pre-eclampsia etc)
30% are due to PPROM
25% are due to emergency (severe infection, placental abruption)

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3
Q

State Naegele’s rule of EDD

A

LMP + 7d -3m +1y

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4
Q

If an EDD wasn’t noted, the age of the baby can be estimated using Dubowitz Scoring. What is it?

A

Uses external physical and neurological features to give a score which then gives a two week window of estimation

Neuromuscular - posture, popliteal angle, heel to ear
Physical - skin, lanugo hair,genitals, eye/ear

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5
Q

After birth the preterm will have a full range of bloods. Describe three other investigations required.

A

CXR (likely to require intubation so looks for any abnormalities which may complicate endotracheal tube)

AXR (check that central line via umbilical artery is in correct place, looks for NE)

Cranial USS (assess for intraventricular haemorrhage or white matter damage)

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6
Q

If a preterm birth is inevitable, what can be done antenatally?

A

Arrange delivery in tertiary centre delivery suite
Antenatal steroids
Magnesium Sulphate (neuroprotective)

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7
Q

At what age are preterm babies rescucitated?

A

<23 weeks ~ not performed

23-23+6 weeks ~ may be a decision not to

24-24+6 weeks ~ commenced unless severely compromised

> 25 weeks ~rescucitation and NICU

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8
Q

Name three things that can aid a newborns thermal regulation after delivery

A

Plastic Wrap
Heated Mattress
Overhead Lamp

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9
Q

What is the long term respiratory management considerations in preterm infants?

A

Surfactant Administration
Intubation and Oxygenation
Caffeine

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10
Q

What is the long term Cardiovascular management considerations in preterm infants?

A

Inotropes
Fluids
Ibuprofen/Indomethacin

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11
Q

What is the long term GI management considerations in preterm infants?

A

TPN
NG
Abx

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12
Q

Survival of preterm babies is rare before 23 weeks. Name four later complications in childhood of prematurity

A

Gross Motor Delay
Fine Motor Impairment
Behavioural Abnormalities
Speech and Language Abnormalities

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13
Q

Name a family support group for premature infants

A

Bliss

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14
Q

What are the five categories of withdrawing Paediatric care?

A
  • The Brain Dead Child
  • The Permanent Vegetative State
  • No Chance (treatment delays death but doesn’t improve life quality or potential, not in best interest of patient)
  • No Purpose (may be able to survive with treatment but it would not be in patients best interest , may leave them in a worse condition)
  • Unbearable Situation (When child or family feel that more treatment is too much to handle)
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15
Q

Jaundice occurs in 60% of term infants and 80% preterm. What is the relevance of conjugation?

A

Unconjugated can be physiological or pathological
Conjugated is always pathological

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16
Q

Physiological jaundice starts at day 2-3 and is resolved by day 10. Give two causes.

A

Increased RBC break down (high concentration required in utero that is no longer needed)

Immature liver (lags behind and unable to conjugate at these high concentrations)

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17
Q

When can Physiological Jaundice become Pathological?

A

If baby is premature
If further extensive breakdown (eg from bruising)

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18
Q

Define Pathological Jaundice

A

A jaundice which requires treatment or further investigation

All jaundice within 24h is pathological

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19
Q

Give three risk factors for pathological jaundice

A

Prematurity
Low Birth Weight
Diabetic Mother

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20
Q

Describe the non physiological jaundice in terms of onset time frame - less than 24 hours

A

Haemolytic Disorders (Rhesus, ABO incompatibility, G6PD, Spherocytosis)

Congenital Infection

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21
Q

Describe the non physiological jaundice in terms of onset time frame - 24 hours to 2 weeks

A

Breast Milk Jaundice
Dehydration
Infection (UTI)
Haemolytic
Bruising
Crigler Najjar Syndrome

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22
Q

Describe the non physiological jaundice in terms of onset time frame - more than 2 weeks

A

Unconjugated: Infection, Hypothyroidism, Haemolytic Anaemia, High GI Obstruction

Conjugated: Bile Duct Obstruction, Neonatal Hepatitis

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23
Q

Describe four possible clinical features of Neonatal Jaundice

A

-Discolouration (examine sclera, gums, skin blanche)
-Drowsy (difficult to rouse, short feeds)
-Altered Muscle Tone
-Seizures

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24
Q

Bilirubin needs to be measured if the Jaundice is not visible to the naked eye. Describe the two methods.

A

Transcutaneous Bilirubinometer (if >35 weeks gestation and >24 hours old, can be used for repeats as long as level is under 250 and no treatment required)

Serum Bilirubin if <35 weeks, <24 hours old or previous level >250

Want to know total and conjugated/unconjugated

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25
Q

Name five further investigations for Neonatal Jaundice

A

Blood Group
Direct Coombs
FBC (haemoglobin and haematocrit)
Infection Screen
LFTs

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26
Q

Phototherapy is a management option for Neonatal Jaundice, how is this decided?

A

Treatment threshold graphs that are gestation specific

If above line - phototherapy initiated and bilirubin monitored
If below line by more that 50, and clinically well don’t repeat
If below line by less than 50 and well, repeat in 18-24 hours

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27
Q

How does Phototherapy work for jaundice?

A

Via Photo- Oxidation

Adds oxygen to bilirubin so it dissolves more easily

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28
Q

When should phototherapy be stopped?

A

6-12 hourly repeats once stable

Stop once more than 50 below threshold

Check for rebound 12-18 hours after stopping

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29
Q

Another option for Jaundice management is Exchange Transfusion. When is this used?

A

If Acute encephalopathy or very high levels (as per graph)

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30
Q

What can you give as an adjunct to pathological jaundice due to ABO/Rhesus incompatibility?

A

IVIG

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31
Q

Kernicterus is the main complication of Neonatal Jaundice, what is it?

A

Bilirubin induced brain dysfunction
Accumulates in CNS grey matter causing irreversible damage

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32
Q

Define Early Onset Neonatal Sepsis

A

Sepsis within the first 48 - 72 hours of life, most commonly due to GBS

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33
Q

State three methods of spread causing Neonatal Sepsis

A

Chorioamnionitis
Birth Canal
Haematogenous

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34
Q

Give two early and two late manifestations of neonatal GBS

A

Early - RDS, Pneumonia
Late - Sepsis, Meningitis

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35
Q

State five red flags of Neonatal Sepsis

A

-RDS starting more than 4hrs after birth
-Seizures
-Signs of Shock
- Abx given to mother around birth
- Suspected in another baby if multiple pregnancy

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36
Q

Give three differentials for Neonatal Sepsis

A

TTN
RDS
Meconium Aspiration

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37
Q

Describe the management of Neonatal Sepsis

A

Initial empirical IV Benzylpenicillin and Gentamicin
If meningitis suspected - Amoxicillin and Cefotaxime

Known GBS - Benzylpenicillin

Continued for 7-10d if positive blood culture, or 14 days if CSF culture positive

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38
Q

How would you manage raised CRP in first 24 hours of life but negative cultures?

A

5 days IV Antibiotics

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39
Q

Define Sudden Infant Death Syndrome

A

Sudden and unexplained death of a child under one (remaining unexplained even after post mortem and history review)

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40
Q

Describe the 1994 triple risk model of SIDS

A

Underlying vulnerability (eg premature)
Critical Development (1-3 months)
Exogenous Stressor (Sleeping Prone)

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41
Q

Give four risk factors for SIDS

A

-Smoking (maternal in pregnancy and passive)
-Alcohol and Substance Abuse
- Preterm Birth (often placed prone to improve resp function so should get used to sleeping on back pre discharge)
- Bed Sharing

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42
Q

Give three protective factors for SIDS

A

Breast Feeding
Dummies
Room Sharing

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43
Q

What is a Life Threatening Event Syndrome?

A

Combination of apnoea/change in colour/change in muscle tone/coughing/gagging

50% underlying condition 50% unknown

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44
Q

Describe a social benefit, and retraction to breast feeding

A

Benefit : It’s free
Detractions: Public Taboo

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45
Q

Give two medical benefits of breast feeding for the mother and the child

A

Child : Increased Immunity, Decreased SIDS risk
Mother: Decreased Breast Cancer, Decreased Ovarian Cancer

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46
Q

Why are feeding difficulties more common in preterm babies?

A

Coordination between suckling/swallowing and breathing is normally developed between 34-36 weeks

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47
Q

Give three broad causes for difficulty feeding in term babies

A

Anatomical Malformations (Cleft Palate, Tongue Tie)

Sleepiness (Hyperbilirubinaemia, Hypoglycaemia, Hypothyroidism)

Neurological (Strokes, Seizures, SAH)

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48
Q

Give four causes for feeding difficulties in infants

A

Cows Milk Protein Allergy
GORD
Colic
Lactose Intolerance

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49
Q

What is Colic?

A

Thought to be a combination of GORD, CMPA and Constipation

Crying more than three hours a day, more than three days a week for more than three weeks.

Drawing up knees and arching back

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50
Q

Give three points of the approach to a Dysmorphic Child

A

-Make an accurate diagnosis
-Recognise associated abnormalities and medical problems
- Optimise QoL

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51
Q

Describe the three types of dysmorphia in a child

A

Normal Spectrum of human variance (no medical significance)

Minor Anomaly (eg flat philtrum, bifid uvula)

Major Anomaly (has medical/surgical/cosmetic significance)

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52
Q

When should you suspect a genetic condition in a child?

A

Multiple minor anomalies (>3)
Or
More than one major anomaly
Or
One major and a few minor anomalies

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53
Q

Give an example of sex limited and sex influences expression

A

Limited - Hereditary Prostate Cancer
Influenced - Hypospadias

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54
Q

Define Malformation

A

Defect of morphogenesis in organ or structure

Can be isolated or part of a chromosomal disorder

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55
Q

Define Deformation

A

Abnormal form/position caused by extrinsic disruptive forces on developing foetus

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56
Q

Define Disruption

A

Destructive breakdown or interference with a normally developing structure

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57
Q

Define Dysplasia

A

Error of morphogenesis due to abnormal cellular organisation in a specific tissue (eg Achondroplasia)

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58
Q

Define Downs Syndrome

A

Genetic disorder caused by Trisomy 21 (non disjunction in maternal oogenesis, or mosaic)

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59
Q

Give 6 features of Downs Syndrome

A

Generalised Hypotonia
Low Set Ears
Upslanting Eyes
Flat Occiput
Single Palmar Crease
Intellectual Impairment (IQ 26-70)

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60
Q

Give four other pathologies associated with Downs

A

Congenital Heart Defects
Deafness
Cataracts
Leukaemia

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61
Q

How is Downs Syndrome diagnosed prenatally?

A

11-14wks - Combined Test (Nuchal Thickness, PAPP- A, bHCG)

15-20wks - Quadruple Test (AFP, Unconjugated Oestriol, bHCG, Inhibin A)

If deemed high risk (>1 in 150 chance) - NIPT (or amniocentesis)

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62
Q

How is Downs Syndrome diagnosed Post Natally?

A

Chromosome analysis via microarray showing Trisomy 21

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63
Q

Give four management points of Downs Syndrome

A

Specialist referrals (audiology, cardiology)

Genetic Counselling

Use of Downs Syndrome Association

Annual TFTs

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64
Q

What is the prognosis of Downs Syndrome?

A

Life expectancy well into adult life although most develop Alzheimer’s by 40 years old

Majority can live semi independent with supervision

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65
Q

What is Patau Syndrome?

A

Trisomy 13

Median survival of 8.5 days

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66
Q

Give 5 features of Patau Syndrome

A

SGA
Microcephaly
Cleft Lip
CHD
Polydactyly

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67
Q

What is Edwards Syndrome?

A

Trisomy 18

Median life expectancy is 74 days

68
Q

Give 5 features of Edwards Syndrome

A

SGA
CHD (particularly VSD)
Short Sternum
Overriding fingers
Rocker Bottom Feet

69
Q

What is Turners Syndrome?

A

Genetic disorder caused by non disjunction characterised by the karyotype 45,X

70
Q

Give 5 features of Turners Syndrome

A

Short Stature
Neck webbing
Ptosis
Wide spread nipples
Puffy hands and feet

71
Q

Give three associated anomalies of Turners Syndrome

A

CHD
Renal Abnormalities
Hypoplastic Ovaries

72
Q

What is Digeorge Syndrome?

A

Genetic disorder caused by micro deletion on Chromosome 22

Characterised by ToF, Wide Nasal Bridge, Hypocalcaemia (Parathyroid Hypoplasia), T Cell Deficiency (Thymus Aplasia)

I.E CATCH 22

73
Q

What is Marfans Syndrome?

A

Autosomal dominant mutation on fibrillin gene

Characterised by tall and slim, pectus malformation, scoliosis, high arched palate, lens dislocation and cardiac abnormalities

74
Q

What is Noonan’s Syndrome?

A

Mutation on chromosome 12

Characterised by Pulmonary Stenosis, Short Stature, Broad Neck, Developmental delay

(‘Male Turners’)

75
Q

What is Williams Syndrome?

A

Micro deletion on chromosome 7

Characterised by periorbital fullness, full cheeks, small spaced teeth, over friendliness

76
Q

State four features of Angelman Syndrome?

A

Severe Developmental delay
Speech impairment
Ataxic Gait
Hand flapping

77
Q

State the features of Fragile X Syndrome

A

Gaze Avoidance
Stereotyped Repetitive Behaviour
Resistance to change of routines

Commonest inherited cause of mental retardation

78
Q

Describe four features of Prader Willi Syndrome

A

Floppy babies with feeding difficulties
Rapid Weight Gain between 1 and 6 years
Learning difficulties
Food foraging and behavioural problems

79
Q

Define Hypoxic Ischaemic Encephalopathy

A

During perinatal asphyxia, gas exchange (placental or pulmonary) ceases resulting in cardio respiratory depression. Compromised cardiac output reduces cerebral perfusion.

80
Q

Give 5 broad aetiologies of HIE

A

-Failure of gas exchange across placenta (placental Abruption)
- Interruption of Umbilical Blood Flow (cord compression)
-Inadequate maternal placental perfusion (hypotension)
- Compromised foetus (IUGR)
- Failure of Cardioresp abnormalities

81
Q

How does HIE present?

A

Encephalopathy + Respiratory Failure + Myocardial Dysfunction + Metabolic Dysfunction + Other Organ Dysfunction

82
Q

Describe mild HIE

A

Irritable, Staring eyes, Hyperventilation, Impaired Feeding

83
Q

Describe moderate HIE

A

Marked abnormalities of tone and movement, cannot feed, may have seizures

84
Q

Describe Severe HIE

A

No spontaneous movement, no response to pain, fluctuating tone, prolonged seizures

85
Q

Describe some management considerations for HIE

A

-Respiratory support
-Treating clinical seizures with anticonvulsants
-Fluid restrict due to transient renal impairment?

Therapeutic Cooling - with blanket for 72h, aiming for 34 degrees (reduces metbaolic demand decreasing the impact of ischaemia

86
Q

What is the prognosis of HIE?

A

If mild then complete recovery

If moderate and appear neurologically normal at two weeks - good

If severe - over 80% have neurodevelopmental disability

87
Q

What is Respiratory Distress Syndrome?

A

Deficiency of surfactant to lower surface tension leading to collapse of alveoli

Common in infants born prior to 28 weeks, or infants of diabetic mothers

88
Q

Give four clinical features of RDS (at delivery or within four hours)

A

-Tachypnoea
-Laboured breathing with chest wall recession
-Expiratory grunting
-Cyanosis if severe

89
Q

What would be seen on a CXR of RDS?

A

Bilateral and diffuse ground glass appearance (generalised atelectasis)
Air bronchograms
Reduced lung volume

90
Q

The level of respiratory support to manage RDS depends on severity of disease. Describe the options.

A

Nasal CPAP/High Flow Oxygen

Endotracheal Intubation and Surfactant (eg Curosurf - first dose as bolus)

91
Q

Other than ventilators support, what managements should be considered in RDS?

A

Antibiotics (Penicillin and Gentamicin until Congenital Pneumonia is ruled out)

IV fluids until baby is stable

Gastric feeds with minimal volume

If preterm delivery is inevitable - maternal corticosteroids

92
Q

What is Necrotising Enterocolitis?

A

Life threatening inflammation of the bowel commonly affecting terminal ileum and proximal colon, 90% premature babies

93
Q

The aetiology of Necrotising Enterocolitis is a multifactorial exaggerated immune response within immature bowel. Give four risk factors

A

Prematurity
Hypoxia
Polycythaemia
Hyperosmolar milk feeds

94
Q

NEC normally presents in the second week after birth, give three early and three late features.

A

Early: Vomiting, Poor Feed Tolerance, Distension

Late: Abdominal Tenderness, Blood/Mucous in stool, Shock

95
Q

As well as a full range of bloods, an AXR will be carried out for NEC. Give three features

A

Gas in the gut wall (Pneumatosis Intestinalis)
Intestinal Distension
Gas outlining falciform (football sign)

96
Q

NEC is staged using examination and radiological features via Bell Staging. Outline stages I-III

A

I - Suspected NEC
II - Proven NEC
III - Advanced NEC

97
Q

How should feeding be managed in NEC?

A

Stop milk feeds for 10-14 days and insert NG tube
Start TPN

98
Q

What is the definitive management of NEC?

A

Antibiotics for 10-14d (Benzylpenicillin, Gentamicin, Metronidazole)

Surgery if perforation/deterioration despite treatment/obstruction secondary to strictures

Surgical repair can be primary if localised disease, if extensive then resection and enterostomy followed by reanastamosis

99
Q

Define Tracheoesophageal Fistula and state it’s associations

A

One or more fistulae communicating between normal trachea and oesophagus

Associated with VACTERL, CHARGE and trisomy 13/18/21

100
Q

Define VACTERL Syndrome

A

Vertebral Defects
Anorectal Malformations
CVS Defects
TOF
Oesophageal Atresia with or without TOF
Renal Abnormalities
Limb Deformities

Defined when >3

101
Q

What is CHARGE Syndrome?

A

Coloboma
Heart Defects
Atresia Chonae
Retarded Development
Genital Hypoplasia
Ear Abnormalities

102
Q

How does TOF present Antenatally?

A

Polyhydramnios
Absent foetal stomach bubble
USS

103
Q

How does TOF present post natally?

A

RDS
Choking
Frothing
Feeding difficulties

104
Q

Name two investigations for TOF

A

AXR - curled NG tube, air in stomach
Fluoroscopy (swallow contrast)

105
Q

Describe the five types of TOF

A

A - Pure Oesophageal Atresia
B - Oesophageal Atresia with proximal TOF
C - Oesophageal Atresia with distal TOF
D - Oesophageal Atresia with proximal and Distal TOF
E - H type (no atresia)

106
Q

How are the non E type TOF repaired?

A

Pre-op bronchoscope followed by open thoracotomy
Fistula ties off
Anastomoses of oesophagus created

107
Q

How are the E type TOF (H) repaired?

A

Surgery formed via neck
Risk of recurrent laryngeal nerve damage

108
Q

Give four causes of Small Bowel Obstruction in Neonates

A

Atresia/Stenosis of Duodenum
Atresia/Stenosis of Jejunum/Ileum
Malrotation with Volvulus
Meconium Ileus

109
Q

Give two causes of Large Bowel Obstruction in Neonates

A

Hirschsprung
Rectal Atresia

110
Q

Define Omphalocoele and its presentation

A

Abdominal contents protrude through umbilical ring covered with transparent sac, often associated with other congenital abnormalities

Presents as a raised maternal AFP and 4-12cm Abdo wall defect

111
Q

What’s the management for Omphalocoele?

A

Replacement of sac into abdominal cavity followed by closure

If the sac ruptures it’s treated the same as Gastroschisis

If larger it is enclosed in silastic sac and contents are gradually returned

Caesarean necessary

112
Q

What is Gastroschisis and how does it present?

A

Abdominal contents herniate into amniotic sac with NO peritoneal covering

Presents as an opening less than 5 cm to the right of the umbilical cord

113
Q

How is Gastroschisis managed?

A

There is a great risk of dehydration and protein loss so the abdomen should be wrapped in several layers of clingfilm

Most sorted with primary closure

If larger it is enclosed in silastic sac and contents are gradually returned

Vaginal delivery may be attempted

114
Q

Define Meconium Aspiration Syndrome

A

Spectrum of disorders characterised by varying degrees of RD following aspiration (occurring either antenatally or during birth)

115
Q

Describe the pathophysiology of MAS

A

Normally post term babies due to hypoxic stress leading to gasping

Results in obstruction (?Atelectasis), Hypoxia, Pulmonary Inflammation, Infection, Surfactant Inactivation, PPH

116
Q

Give three risk factors for MAS

A

Gestational Age >42 weeks
Oligohydramnios
Thick Meconium

117
Q

Describe 5 investigations for MAS

A

Chest a ray (patchy opacity, consolidation, increased lung volumes)
Infection Markers
ABG
Dual Pulse Oximetry (on RUL and LLL to determine shunts)
Cranial USS

118
Q

Give three differentials for MAS

A

Transient Tachypnoea of the Newborn
Persistent Pulmonary Hypertension
Surfactant Deficiency

119
Q

How is MAS is managed?

A

O2 therapy (extent depends on severity)
Antibiotics (stopped after 48 hours if culture is negative, eg ampicillin/gentamicin)

Potentially surfactant, or inhaled NO

120
Q

Give three complications of MAS

A

Air leak (Meconium causes alveolar hyperdistension leading to pneumothorax)

Cerebral palsy

Persistent Pulmonary Hypertension

121
Q

Define Transient Tachypnoea of the Newborn

A

Delayed clearance/absorption of lung fluid after birth, often after caesarean section.

Managed with oxygen and spontaneously resolves within 24 hours

122
Q

Describe the CXR of TToN

A

Streaky perihilar changes
Fluid in horizontal lung fissures

123
Q

Define Bronchopulmonary Dysplasia

A

Form of chronic lung disease affecting infants born preterm with oxygen requirements at 36 weeks
Impaired alveolar development with mechanical/oxidative/inflammatory factors

124
Q

Give three risk factors Bronchopulmonary Dysplasia

A

Gestational Immaturity
FH of Asthma
LBW

125
Q

How does the CXR present for Bronchopulmonary Dysplasia?

A

Hyperextended chest with diffuse patchy collapse and fibrosis interspersed by radiolucent cystic areas

126
Q

Give five managements for Bronchopulmonary Dysplasia

A

Caffeine Citrate for premature
Oxygen
Diuretics
Corticosteroids
Immunisation against RSV

127
Q

Describe the pathophysiology of Persistent Pulmonary Hypertension of the Newborn

A

Failure of the normal circulatory transition occurring after birth, causing R-L shunting and severe hypoxia

Can be Idiopathic, due to Diaphragmatic Hernia, or constricted vasculature due to RDS/MAS

128
Q

How is Persistent Pulmonary Hypertension of the Newborn managed?

A

Treat underlying cause
Oxygen
Dopamine
Inhaled Nitric Oxide

129
Q

Retinopathy of Prematuriy is the leading cause of preventable blindness. Who is most at risk?

A

Infants born at <32 weeks or weighing <1500g

130
Q

Describe the pathophysiology behind Retinopathy of Prematurity

A

In utero retinal development occurs in a relatively hypoxic environment

Incompletely developed if premature and the hyperoxic environment can cause vasoconstriction and retinal ischaemia

131
Q

Retinopathy of Prematurity can be classed by Severity and Location. Describe the stages of Severity

A

1 - Demarcation line visible
2- Ridge evident
3 - Ridge with fibrovascular proliferation
4 - Subtotal retinal detachment
5 - Total Retinal Detachment

132
Q

Retinopathy of Prematurity can be classed by Severity and Location. Describe the stages of Location

A

Zone 1 - 30 degree radius from optic disc
Zone 2 - Nasal Regina periphery in circle
Zone 3 - circumference includes temporal and nasal retina

133
Q

What does ‘+’ disease mean in Retinopathy of Prematurity

A

Engorgement of Posterior Vessels
Iris Rigidity
Vitreous Haze

134
Q

When are infants screened for Retinopathy of Prematurity?

A

<27 weeks - screen at 30 to 31 weeks
27-32 weeks - screened at day 28 to 35 of life

Screen fortnightly unless plus/stage three disease

135
Q

How is Retinopathy of Prematurity managed?

A

Diode Laser Treatment within 72 hours alongside steroid eye drops

Can be retreated if no regression at 10-14d

136
Q

Name three causes of Vitamin K Deficiency (and subsequent HDN)

A

Breast Milk
Maternal Anticonvulsants
Newborn liver disease

137
Q

Describe the presentation of mild and severe HDN

A

Mild - Bruising, Haematemesis, Malaena

Severe - Intracranial Haemorrhage

138
Q

How is HDN prevented?

A

IM Vitamin K immediately after birth

If mother is on anticonvulsants then they receive an extra dose at 36 weeks

139
Q

Describe the pathophysiology behind Intraventricular Haemorrhage

A

Related to rapid alterations in blood flow (eg severe RDS, hypoxia)

Bleeding can dilate ventricles and cause periventricular infarction due to compression

140
Q

How do Intraventricular Haemorrhages present?

A

Most occur within 72 hours and 50% are asymptomatic

Larger bleeds can present with bulging fontanelle, neuro dysfunction, jaundice

141
Q

Intraventricular Haemorrhages are seen on Cranial USS. Who should be screened and when?

A

At risk or pre term infants

At one day, one week and one month

142
Q

The management for Intraventricular Haemorrhage is supportive. How can it be prevented?

A

Antenatal steroids and Indomethacin

143
Q

Give two complications of Intraventricular Haemorrhage

A

Periventricular infarction

Post haemorrhage ventricular dilation (leading to CSF accumulation and raised ICP)

144
Q

Describe the difference between Subgaleal and Cephalohaematoma

A

Subgaleal - boggy swelling all over scalp

Cephalohaematoma - subperiosteal bleed limited by suture lines

145
Q

What is Periventricular Leucomalacia?

A

Softening the white matter associated with extreme prematurity (poor perfusion)

Visible on USS as Periventricular echodensities

Increased risk of cerebral palsy

146
Q

What is Cleft Lip?

A

Failure of fusion of frontonasal and maxillary processes (can be unilateral or bilateral)

147
Q

What is Cleft Palate?

A

Failure of fusion of palatine processes and nasal septum

148
Q

Give two environmental and one syndromic cause of Cleft Palate

A

Foetal Alcohol Syndrome, Folic Acid Deficiency

Pierre Robin Syndrome

149
Q

Apart from an obvious deformity, how could Cleft Lip/Palate present?

A

Difficulty feeding
Upper airway obstruction
Frequent Otitis Media

150
Q

Spina Bifida is failure of midline fusion of dorsal vertebral bodies. What are the three types?

A

Occulta - no herniation, overlying dimple of hair

Meningocoele - herniation of meninges and fluid with a skin covering

Myelomeningocoele - involvement of neural tissue causing paralysis, incontinence etc

151
Q

Milia is an example of benign neonatal dermatology, what are they?

A

<2mm yellow/white spots
Normally on face
Secondary to blocked sweat glands

152
Q

Erythema Toxicum is an example of benign neonatal dermatology, what is it?

A

Discrete erythematous maculopapular lesions often with a white centre

Mostly over knees/elbows/trunk/face

153
Q

Harlequin Colour Change is an example of benign neonatal dermatology, what is it?

A

Marked erythema/pallor in different halves/quadrants due to vasomotor immaturity

154
Q

Superficial Capillary Haemangioma is an example of benign neonatal dermatology, what is it?

A

Also known as Stork Mark

Erythematous Vascular marks on eyelids/face/scalp/nose

155
Q

Mongolian Blue Spots is an example of benign neonatal dermatology, what are they?

A

Bluish black machines often in lumbosacral region

Mostly non Caucasian

156
Q

What is Nappy Rash?

A

Usually contact dermatitis from ammonia in urine

157
Q

How would you manage simple nappy rash

A

Frequent nappy changes

Barrier Cream (Zinc)

158
Q

When would you suspect a secondary infection of nappy rash? How would you manage?

A

Flexural or Satellite lesions

Topical Nystatin

159
Q

What is Infantile Seborrhoeic Eczema? How is it managed?

A

Commonly affecting face/neck/behind ears/scalp

Normally resolves in weeks

Avoid detergents and give mild emollient and steroid

160
Q

State the five parameters of the APGAR score

A

Activity
Pulse
Grimace
Appearance
Respiratory

161
Q

How is ‘Activity’ of APGAR scored?

A

0 - none
1- flexed limbs
2 - active

162
Q

How is ‘Pulse’ of APGAR scored?

A

0 - no pulse
1 - <100
2 - >100

163
Q

How is ‘Grimace’ of APGAR scored?

A

0 - floppy
1 - minimal response
2 - prompt response

164
Q

How is ‘Appearance’ of APGAR scored?

A

0 - Blue
1 - Blue Extremities
2 - Pink

165
Q

How is ‘Respiratory’ of APGAR scored?

A

0- none
1 - slow and irregular
2 - vigorous

Year 4 Paediatrics (15 decks)

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