Neonatology 3

Question 1

What is the treatment for early-onset sepsis?

Answer 1

• IV antibiotics are given to cover certain infection (penicillins)- combined with cover for Gram –ve organisms (aminoglycosides)
o Group B streptococci
o Listeria monocytogenes
o Other Gram +ve organisms (penicillins)

Question 2

What is the treatment for late-onset sepsis?

Answer 2

• Initial therapy is aimed to cover most staphylococci and Gram –ve bacilli- flucloxacillin & gentamicin
• If organism is resistant to these antibiotics or the infant’s condition does not improve, specific antibiotics or
broad-spectrum  eg. vancomycin for coagulase-negative staphylococci or enterococci

Question 3

What is the treatment for meningitis?

Answer 3

ampicillin or penicillin and a third-generation cephalosporin (eg. Cefotaxime, which has CSF penetration) are given

Question 4

What are the clinical features of neonatal sepsis?

Answer 4

o	Fever or temperature instability or hypothermia
o	Poor feeding
o	Vomiting
o	Apnoea & bradycardia
o	Respiratory distress
o	Abdominal distension
o	Jaundice
o	Neutropenia
o	Hypo-/hyperglycamemia
o	Shock
o	Irritability
o	Seizures
o	Lethargy & drowsiness

Question 5

What is included in a sepsis screen?

Answer 5

o	FBC
o	U&E’s with glucose
o	Blood culture
o	Chest radiograph
o	Lumbar puncture
o	Urine culture and dip
o	CRP
o	CT or MRI (if suspected meningitis)

Question 6

How is hepatitis B/C transmitted?

Answer 6

o Perinatal transmission from carrier mothers
o Transfusion of infected blood or blood products
o Needlestick injuries with infected blood
o Renal dialysis
o Horizontal spread within families
o Among adults it can also be transmitted sexually

Question 7

What happens when children get HBV?

Answer 7

• Infants who contract HBV perinatally are asymptomatic- but at least 90% become chronic carriers
• Older children who contract HBV may be asymptomatic or have classical features of acute hepatitis
• The majority resolve spontaneously, but 1-2% develop fulminant hepatic failure, while 5-10% become chronic carriers

Question 8

How is HBV diagnosed?

Answer 8

o IgM antibodies to the core antigen (anti-HBc) are positive in acute infections
o Positivity to hepatitis B surface antigen (HBsAg) denotes ongoing infectivity
• There is no treatment for acute HBV infection

Question 9

What is the management for chronic hepatitis B?

Answer 9

approx. 30-50% of carrier children will develop chronic HBV liver disease, which may progress to cirrhosis in 10%
Interferon treatment for chronic HBV is successful in 50% of children infected horizontally and 30% of children infected perinatally
• Oral anti-viral therapy is effective in 23%, but is limited by the development of resistance- such as lamivudine
• Newer drugs may be more effective- such as adefovir or long-acting interferon

Question 10

How is hepatitis B prevented?

Answer 10

• All pregnant women should have antenatal screening for HbsAg- babies with all HBsAg-positive mothers should receive a course of hepatitis B vaccination with hepatitis B immunoglobulin also being given if the mother is also hepatitis B e antigen (HbeAg)-positive

• Antibody response to the vaccination course should be checked in high-risk infants as 5% require further vaccination, other members of the family should also be vaccinated
• There is evidence that effective neonatal vaccination reduces the incidence of HBV-related cancer (HCC)

Question 11

What is intrauterine growth retardation (IUGR)?

Answer 11

reduction and restriction in expected foetal growth pattern
it affects 3-10% of pregnancies and 20% of still-born infants are thought to have evidence of IUGR
• Perinatal mortality rates are 4-8 times higher for growth-retarded infants, and morbidity is present in 50% of surviving infants
• IUGR is failure of growth in utero that may or may not result in SGA- infants have been asymmetrically restricted, so are less than their genetically predetermined size

Question 12

What is small for gestational age (SGA)?

Answer 12

Birth weight <10th centile for gestational age, often normal, but small
incidence of congenital abnormalities and neonatal problems is higher in those whose birth weight falls below 2nd centiles, generally genetically programmed to be small, but does also include children who have failed to meet their genetic size (eg. IUGR)

Question 13

What are the placental causes of IUGR?

Answer 13

o A small placenta- cannot supply the needed nutrients
o Cell death of the placenta
o Pre-eclampsia

Question 14

What are the foetal causes of IUGR?

Answer 14

o Multiple pregnancies- 15-20% of twins
o Chromosomal abnormalities- eg. Down/Edward/Turner/Patau’s syndrome
o Congenital defects- associated with SGA
o Intrauterine infection- eg. CMV, toxoplasmosis, rubella or syphilis

Question 15

What are the maternal factors for IUGR?

Answer 15

o	Increased maternal age
o	Hypertension or heart disease
o	Diabetes
o	Alcohol abuse
o	Use of drugs- include cannabis
o	Maternal smoking- 30-40% of cases
o	Renal disease
o	Untreated Coeliac disease
o	Thrombophilia
o	Drugs- including warfarin, steroids and phenytoin

Question 16

What are the long term affects of IUGR?

Answer 16

adult onset of HTN & CHD, and in early onset obesity, PCOS and T2DM
• If there was slow head growth before 26 weeks, then they may show significant development delays at 4yrs
• An extremely low birth weight confers a high risk of perinatal mortality and neonatal morbidity- studies have shown an infant <2.5kg birth weight have x3 increased risk of coronary artery disease later in life, there is also an increased risk of hypertension, T2DM and autoimmune thyroid disease

Question 17

What are the signs of respiratory distress?

Answer 17

• Tachypnoea >60 breaths/min
• Laboured breathing, with chest wall recession and nasal flaring
• Expiratory grunting
• Cyanosis if severe

Question 18

What is transient tachypnoea?

Answer 18

Commonest cause of respiratory distress in term infants
Delay in the resorption of lung liquid and is more common after birth by C-section
CXR- fluid in the horizontal fissure
Ambient oxygen may be required
usually settles down in first day of life

Question 19

What is respiratory distress syndrome?

Answer 19

• Ground glass appearance-often pre-term (<28wks)
Deficiency in surfactant and an immature respiratory centre in the brain
May have a genetic cause, diabetic mothers or meconium aspiration
Develop signs 4hrs postpartum- characterised by grunting, which is breathing out against a closed epiglottis in order to maintain positive pressure in the airways

Question 20

What is the treatment for respiratory distress syndrome?

Answer 20

antenatal steroids in 2 doses within 48hrs before delivery when the labour is <34 weeks gestation-this leads to lung maturation and surfactant production
the 2nd therapy is artificial surfactant that can reduce deaths by over 40%

Question 21

What is congenital pneumonia?

Answer 21

• It can be caused by a virus or bacteria
Predisposing factors- prolonged rupture of membranes, chorioamnioitis, low birthweight
• Broad-spectrum antibiotics are started early until the results of the infection screen are available

Question 22

What is meconium aspiration?

Answer 22

• Meconium is passed before birth by 8-20% of babies
• May be passed in response to foetal hypoxia- asphyxiated infants may start gasping and aspirate meconium before delivery- meconium is a lung irritant and results in both mechanical obstruction and a chemical pneumonitis, as well as predisposing to other infection
CXR- lungs are over-inflated, accompanied by patches of consolidation & collapse
High incidence of air leak leading to pneumothorax and pneumomediatrinum

Question 23

What is the management for meconium aspiration?

Answer 23

• Artificial venitliation is often required- may also develop perisistent pulmonary hypertension of the newborn, which may make it difficult to achieve adequate oxygenation despite high pressure ventilation
• Severe meconium aspiration is associated with significant morbidity & mortality