Neonatology Flashcards
What is jaundice?
What is neonatal jaundice?
The yellow colouring of skin and sclera caused by the accumulation of bilirubin in the skin and mucous membranes.
Neonatal jaundice is caused by hyperbilrubinaemia that is unconjugated (physiological or pathological) or conjugated (pathological).
What is the prevalence of neonatal jaundice in:
a) term infants?
b) preterm infants?
c) breast fed babies at 1 month?
a) 60%
b) 80%
c) 10%
What harmful effect can high levels of bilirubin lead to?
Kernicterus.
What types of jaundice are there?
Which requires treatment?
Physiological jaundice
- jaundice in a healthy baby, born at term, is normal
Pathological jaundice
- jaundice that requires treatment or further investigation
What causes physiological jaundice?
Increased RBC breakdown
- foetal RBC have shorter half lives (90-100 days compared to 120 days in adults)
- in utero, foetus has high Hb concentration that breaks down releasing bilirubin as high Hb is no longer needed
b) Immature liver
- unable to process high bilirubin concentrations
At what time period does physiological jaundice occur?
Starts at day 2-3
Peaks at day 5
Resolved by day 10
Baby remains well and does not require any intervention beyond routine neonatal care.
What can lead physiological jaundice to progress to pathological jaundice?
- If the baby is premature
2. If there is increased RBC breakdown e.g. extensive bruising
What can cause pathological jaundice?
- Haemolytic disease
- e.g. haemolytic disease of the newborn, ABO incompatibility, G6PD deficiency, spherocytosis
- onset <24 hours - Bilirubin above phototherapy threshold
- onset after 24 hours
- likely dehydrated
- increased haemolysis due to bruising/cephalohaematoma - Unwell neonate
- jaundice as a sign of congenital or postnatal infection - Prolonged jaundice
- jaundice for >14 days in term infants OR 21 days in preterm
- consider: infection, metabolic (hypothyroid/pituitarism, galactosaemia), breast milk jaundice, GI (biliary atresia)
What are risk factors for pathological jaundice?
- prematurity, low birth weight, small for dates
- previous sibling required phototherapy
- exclusively breast fed
- jaundice <24 hours
- infant of diabetic mother
How do babies with neonatal jaundice present?
Colour: yellow skin, sclera (determine presence or absence of jaundice)
Drowsy: difficult to rouse, not waking for feeds, very short feeds
Neurologically: altered muscle tone, seizures
Other:
- signs of infection
- poor urine output
- abdominal mass/organomegaly
- stool remains black/not changing colour
What are investigations for neonatal jaundice?
Transcutaneous bilirubinometer (TCB):
- used in >35/40 gestation and >24 hours old for first measurement
- use for all subsequent measurements if level <250umol/L and child has not required treatment
Serum bilirubin:
- if <35/40 gestation, <24 hours old, TCB >250umol/L
- for subsequent levels
Blood group (mother and baby) and DCT
FBC - Hb, haematocrit
As needed:
U&Es - if excessive weight loss/dehydrated
Infection screen - if unwell or <24 hours, cultures if blood, urine, CSF infection suspected, consider TORCH screen
G6PDH - mediterranean or African origin
LFTs - suspected hepatobiliary disorder
TFTs
What is the management for neonatal jaundice?
- Monitor total bilirubin levels and plot on treatment threshold chart
- specific for gestational age of the baby at birth
- age of baby on x-axis
- total bilirubin level on y-axis
- if total bilirubin reaches threshold on the chart, commence treatment to lower bilirubin level - Phototherapy
- Exchange transfusion
- if extremely high levels
- remove blood from neonate and replace with donor blood
1) What is phototherapy?
2) What is double phototherapy?
3) What must be measured once phototherapy is complete and why?
1) Treatment for neonatal jaundice
Converts unconjugated bilirubin into isomers that can be excreted in the bile and urine without requiring conjugation in the liver
Remove clothing down to nappy to expose skin and eye patches to protect the eyes
Light-box shines blue light on to baby’s skin (little or no UV light is used)
2) Double phototherapy involves 2 light boxes
3) Rebound bilirubin measured 12-18 hours after stopping phototherapy to ensure levels do not rise above the treatment threshold again
What is kernicterus?
Brain damage caused by excessive bilirubin levels
Bilirubin can cross the BBB so excessive bilirubin causes direct damage to the CNS
How does kernicterus present?
- less responsive
- floppy
- drowsy
- poor feeding
What complications does Kernicterus cause?
Permanent damage to the nervous system
- cerebral palsy
- deafness
- learning difficulties
Kernicterus is rare now due to effective jaundice treatment
What is hypoxic ischaemia encephalopathy?
Occurs in neonates as a result of hypoxia during birth.
Hypoxia = lack of oxygen Ischaemia = restriction in blood flow to the brain Encephalopathy = malfunctioning of the brain
Some hypoxia during birth is normal but prolonged or severe hypoxia leads to ischaemia brain damage.
What can HIE lead to?
Permanent damage to the brain causing cerebral palsy.
Severe HIE can cause death.
What can cause HIE?
Anything that leads to asphyxia (deprivation of oxygen) to the brain:
- maternal shock
- intrapartum haemorrhage
- prolapsed cord (compression of cord during birth)
- nuchal cord (cord wrapped around neck of baby)
What staging is used to grade hypoxic-ischaemic encephalopathy?
Sarnat staging
What are the grades for Sarnat staging of HIE?
1) Mild - poor feeding, irritable, hyper-alert; resolves within 24 hours; normal prognosis
2) Moderate - poor feeding, lethargic, hypotonic, seizures; can take weeks to resolve; up to 40% develop cerebral palsy
3) Severe - reduced consciousness, apnoeas, flaccid and reduced/absent reflexes; up to 50% mortality; up to 90% develop cerebral palsy
How are patients with HIE managed?
- specialists in neonatology on neonatal unit
- supportive care with neonatal resuscitation and ongoing optimal ventilation, circulatory support, nutrition, acid base balance and treatment of seizures
What are the risk factors for hypoglycaemia in a neonate?
- poor feeding
- infection ie. sepsis
- maternal drugs e.g. labetalol
- diabetes
- prematurity
- preterm
- small baby (low brown fat so use glucose for energy instead)
Who does necrotising enterocolitis affect?
Premature neonates
What is necrotising enterocolitis and what can it lead to?
Where part of the bowel becomes necrotic.
Life-threatening emergency.
Death of bowel tissue can lead to bowel perforation which can lead to peritonitis and shock.
What are risk factors for developing necrotising enterocolitis?
- very low birth weight/very premature
- formula feeds (less common if breast fed)
- respiratory distress/assisted ventiliation
- sepsis
- patent ductus ateriosus/congenital heart disease
How does necrotising enterocolitis present?
- intolerance to feeds
- vomiting (particularly green bile)
- generally unwell
- distended, tender abdomen
- absent bowel sounds
- blood in stools
Severely unwell if perforation, peritonitis and shock
What blood tests should be done for necrotising enterocolitis?
- FBC (thrombocytopenia, neutropenia)
- CRP (inflammation)
- capillary blood gas (metabolic acidosis, high lactate)
- blood culture (sepsis)
What imaging should be done for necrotising enterocolitis?
Abdominal xray
- supine position
- lateral (from side with patient on their back)
- lateral decubitus (side with neonate on their side)
What may an AXR show in necrotising enterocolitis?
- dilated loops of bowel
- bowel wall oedema (thickened)
- pneumatosis intestinalis (gas in bowel wall, sign of NEC)
- pneumoperitoneum (free gas in peritoneal cavity indicating perforation)
- gas in portal veins
How is necrotising enterocolitis managed?
- NBM
- IV fluids
- TPN (total parenteral nutrition)
- antibiotics
- NG tube to drain fluid and gas from stomach and intestines
- immediate referral to neonatal surgical team (surgical emergency)
- some recover with medical treatment
- some require surgery to remove dead bowel tissue
- temporary stoma if significant bowel removed
What are complications of necrotising enterocolitis?
- perforation/peritonitis
- sepsis
- death
- strictures
- abscess formation
- recurrence
- long term stoma
- short bowel syndrome after surgery
Who does respiratory distress syndrome affect and what age?
Premature neonates, commonly occurs below 32 weeks
What is respiratory distress syndrome?
When the neonate is born before the lungs start producing adequate surfactant.
What does respiratory distress syndrome show on CXR?
Ground glass appearance
What is the pathophysiology of respiratory distress syndrome?
Inadequate surfactant leads to high surface tension within the alveoli leading to atelectasis (lung collapse) as it is more difficult for lungs and alveoli to expand.
This leads to inadequate gaseous exchange causing hypoxia, hypercapnia and respiratory distress.
What is the management for respiratory distress syndrome?
Antenatal steroids (dexamethasone) given to mothers of suspected/confirmed preterm labour = increases surfactant production, reduces incidence and severity of RDS in baby
Premature neonates may need:
- intubation/ventilation to fully support breathing if RDS severe
- endotracheal surfactant delivered to lungs via endotracheal tube
- CPAP via nasal mask to help keep lungs inflated whilst breathing
- supplementary oxygen (maintain sats 91-95% in preterm neonates)
Breathing support gradually stepped down as baby develops and able to support themselves on air.
What are short term complications of respiratory distress syndrome?
- pneumothorax
- infection
- apnoea
- intraventricular haemorrhage
- pulmonary haemorrhage
- necrotising enterocolitis
What are long term complications of respiratory distress syndrome?
- chronic lung disease of prematurity
- retinopathy of prematurity
- neurological, hearing, visual impairment
What are signs of respiratory distress?
- nasal flaring
- head bobbing
- tracheal tug
- intercostal/subcostal recession
- tachypnoeic
- dyspnoeic
What is neonatal sepsis?
Caused by infection in the neonatal period potentially resulting in significant morbidity and mortality for the affected infant, especially if treatment is delayed.
What common organisms cause neonatal sepsis?
- Group B streptococcus (GBS)
- E.Coli
- Listeria
- Klebsiella
- S. Aureus
What bacteria is found in the vagina that can be transferred to the baby during labour and cause neonatal sepsis?
How can this risk be reduced?
1) Group B streptococcus (GBS)
Does not cause problems for the mother
2) Prophylactic antibiotics given during labour to reduce the risk of transfer if the mother is found to have GBS during pregnancy.
What are the risk factors for neonatal sepsis?
- vaginal GBS colonisation
- GBS sepsis in a previous baby
- maternal sepsis, chorioamnionitis or fever >38C
- prematurity (<37 weeks)
- Premature rupture of membranes
- Prolonged rupture of membranes
How does neonatal sepsis present?
- fever
- reduced tone/activity
- poor feeding
- respiratory distress/apnoea
- vomiting
- tachycardia/ bradycardia
- hypoxia
- jaundice within 24 hours
- seizures
- hypoglycaemia
What are red flags for neonatal sepsis?
- confirmed/suspected sepsis in the mother
- signs of shock
- seizures
- term baby needing mechanical ventilation
- respiratory distress starting >4 hours after birth
- presumed sepsis in another baby in a multiple pregnancy
If there is one risk factor or clinical feature of neonatal sepsis, what should be done?
Monitor observations and clinical condition for at least 12 hours
When should antibiotics be started in neonatal sepsis?
If 2 or more risk factors or clinical features
If a single red flag
Start within 1 hour of making decision to start them
What should be taken prior to antibiotics starting in neonatal sepsis?
Blood cultures
What other investigations should be done in neonatal sepsis?
Baseline FBC, CRP
Lumbar puncture if infection strongly suspected or features of meningitis (e.g. seizures)
What antibiotics should be used in neonatal sepsis?
- benzylpenicillin
- gentamycin
- third gen cephalosprin e.g. cefotaxime in lower risk babies
When should another set of CRP and blood culture be checkedonce antibiotics for neonatal sepsis has been started?
- CRP at 24 hours
- blood culture at 36 hours
- CRP again at 5 days if still on treatment
When can you consider stopping the antibiotics in neonatal sepsis?
- baby clinically well, blood cultures negative 36 hours after taking them, both CRP <10
- baby is clinically well, LP and blood cultures negative, CRP returned to normal at 5 days
When should you consider performing a LP in neonatal sepsis?
If signs of infection or meningitis (e.g. seizures)
If any CRP results are >10
What can cause early jaundice (<24 hours)?
Always pathological
- haemolysis
- infection
What can cause jaundice >24 hours?
- physiological
- breast feeding
What are the common causes of prolonged jaundice (conjugated form)?
- biliary atresia
- neonatal hepatitis
What is the definition of neonatal hypoglycaemia?
<2.6 mmol/L
Often occurs in the first 24 hours of life without any sequalae as they can use alternate fuels like ketones and lactate
What type of hypoglycaemia is common in first hours after birth?
Transient hypoglycaemia
What can cause persistent/severe neonatal hypoglycaemia?
- preterm birth (<37 weeks)
- maternal DM
- IUGR
- hypothermia
- neonatal sepsis
- inborn errors of metabolism
- DM
- nesidioblastosis
- Beckwith-Wiedemann syndrome
What are the features of neonatal hypoglycaemia?
- asymptomatic
- autonomic features (jitterness, irritable, tachypnoea, pallor)
- neuroglycopenic features (poor feeding/sucking, weak cry, drowsy, hypotonia, seizures)
- apnoea
- hypothermia
What is the management for neonatal hypoglycaemia?
Asymptomatic:
- encourage normal feeding (bottle/breast)
- monitor blood glucose
Symptomatic/very low blood glucose:
- admit to neonatal unit
- IV 10% dextrose
