Neonatology Flashcards
What is neonatal sepsis?
- Bacterial or viral infection in the blood that affects babies within the first 28 days of life
How is neonatal sepsis catergorised?
- Early onset- within 72 hours of birth
- Late onset- between 7-28 days of life
Causes of neonatal sepsis?
i.e. bugs
- GBS and E.coli
- Early onset: GBS is most common cause
- Late onset: Staphylococcus epidermis, Pseudomonas, Klebsiella and Enterobacter
- Less common causes incl: Staph aureus, Enterococcus, Listeria, Viruses e.g. herpes and enterovirus
Risk factors for sepsis in the neonate?
- Mother who had previous baby with GBS infection, current GBS colonisation from prenatal screening, current bacteruria, intrapartum temperature greater than or equal to 38 degrees, membrane rupture greater than or equal to 18 hours, or current infection throughout pregancy
- Premature (< 37 weeks)
- Low birth weight (< 2.5kg)
- Evidence of maternal chorioamnionitis
Presentation of neonatal sepsis?
- Respiratory distress (grunting, nasal flaring, use of accessory resp muscles, tachypnoea)
- Tachycardia
- Apnoea
- Apparent changes in mental status/lethargy
- Jaundice
- Seizures- if meningococcal
- Poor/ reduced feeding
- Abdo distension
- Vomitting
Clinical presentation can vary from being very subtle signs of illness to clear septic shock
Frequently, symptoms will be related to source of infection e.g. pneumonia+ resp symptoms
What investigations would you do for neonatal sepsis?
- Blood cultures- ideally 2 to distinguish from contamination
- FBC- associated with abnormal neutrophil count (neutropenia or neutrophilia), but otherwise used to distinguish from healthy neonates
- CRP- usually raised (persistently normal will be used to exclude sepsis)
- Blood gases- metabolic acidosis is concerning, esp with a base deficient of greater than/equal to 10mmol/L
- Urine MC&S- more useful in late onset (rarely positive in early onset), will show signs of infection e.g. raised leukocytes, haematuria,positive culture etc.)
- Lumbar puncture: particularly if worried about meningitis
Management of neonatal sepsis?
- IV benzylpenicillin with gentamicin
- Re-measure CRP 18-24 hours after presentation to monitor progress
- Abx can be ceased at 48 hours in neonated who have CRP of < 10mg/L and a negative blood culture at presentation and at 48 hours
- Other neonates- duration depends on severity etc. usually around 10 days
- Maintain adequate oxygenation status
- Maintain normal fluid and electrolyte status- if v ill may need volume and/or vasopressor support
- Prevention/ management of hypoglycaemia
- Prevention and/or management of metabolic acidosis
What is neonatal hypoglycaemia?
- < 2.6 mmol/L is used in many guidelines
- Transient hypoglycaemia in the first hours after birth is common
What causes persistent/ severe neonatal hypoglycaemia?
- Pre-term birth
- Maternal diabetes mellitus
- IUGR
- Hypothermia
- neonatal sepsis
- Inborn errors of metabolism
- Nesidioblastosis
- Beckwith-Wiedemanna syndrome
Features of neonatal hypoglycaemia?
- May be asymptomatic
- Autonomic
- Jitteriness
- irritable
- tachypnoea
- Pallor
- Neuroglycopenic
- Poor feeding/sucking
- weak cry
- drowsy
- hypotonia
- seizures
- other features
- apnoea
- hypothermia
Management of neonatal hypoglycaemia?
Asymptomatic:
* encourage normal feeding
* monitor blood glucose
Symptomatic or very low blood glucose
* admit to neonatal uni
* IV infusion of 10% dextrose
What is hypoxic ischaemic encephalopathy?
Occurs in neonates
Due to hypoxia during birth
Hypoxia = lack of O2
Ischaemia = restricted blood flow to brain
Encephalopathy = malfunctiong of brain (i.e. brain damage)
What examination/ investigation findings would make you suspect HIE?
- umbilical artery blood gas (ABG) showing acidosis (pH = < 7)
- poor Apgar scores on examination
- evidence of multi organ failure
What are causes of HIE?
Anything that leads to deprivation of oxygen to the brain:
* placental abruption pre partum
* maternal shock
* intrapartum haemorrhage
* prolapsed cord –> causes cord compression during birth
* nuchal cord (cord wrapped around baby’s neck)
* prolonged respiratory arrest post partum
How does HIE present? Group into mild, moderate and severe presentation
Presentation varies on the severity of cerebral hypoxia
Generally - baby will be unwell from birth, need resuscitation
Encephalopathy develops within 24hrs of birth
What investigations are done following suspected HIE?
EEG - monitor brain activity
Multiple MRI brain scans
How is HIE managed?
- specialist management in neonatal unit
- supportive management
- resuscitation and optimal ventilation
- acid base balance
- monitor and treat seizures
- theraputic hypothermia
- follow up by paeds and MDT to assess development and support any lasting disability
Describe theraputic hypothermia in HIE
Describe process and the aim of this therapy
- where you actively cool core temp of baby based on a protocol
- target 33-34 degrees C - measured using a rectal probe
- continue for 72hrs
- then warm baby to a normal temp over 6 hrs.
- Aim = reduce inflamaion and neurone loss after an acute hypoxic injury. Reduces risk of cerebral palsy, developmental delay, learning disability, blindness and death
What is prematurity?
Birth before 37 completed weeks’ gestation (8% of all births).
The WHO classify prematurity as:
* Under 28 weeks: extreme preterm
* 28 – 32 weeks: very preterm
* 32 – 37 weeks: moderate to late preterm
Most problems seen in infants born <32 completed weeks
What are some predisposing factors for prematurity?
- Idiopathic (40%).
- Previous preterm birth.
- Multiple pregnancy.
- Maternal illness, e.g. chorioamnionitis, polyhydramnios, pre-eclampsia, diabetes mellitus.
- Premature rupture of membranes.
- Uterine malformation or cervical incompetence.
- Placental disease, e.g. dysfunction, antepartum haemorrhage (APH).
- Poor maternal health or socio-economic status.
What are some problems / complications that happen with premature neonates early in life?
lots! thing resp, CNS, GI etc.
Respiratory - surfactant deficiency:
* respiratory distress (RDS)
* apnoea of prematurity
* chronic lung disease
CNS:
* intraventricular haemorrhage
* retinopathy of prematurity
GI:
* Necrotizing enterocolitis
* Inability to suck
* poor milk tolerance.
other systems:
* Hypothermia.
* Immunocompromise with ↑ risk/severity of infection.
* Impaired fluid/electrolyte homeostasis (↑ transepidermal water loss, poor renal function).
* Patent ductus arteriosus
* Anaemia of prematurity
* Jaundice (liver enzyme immaturity)
* Birth trauma
* Perinatal hypoxia (Hypoxic–ischaemic encephalopathy)
What are some long term problems that might effect a premature neonate?
- Chronic lung disease of prematurity (CLDP)
- Susceptibility to infections, particularly respiratory tract infections
- adverse neurodevelopmental outcome e.g. cerebral palsy
- hearing and visual impairment e.g squint + retinopathy
- behavioural and learning problems
- sudden infant death syndrome (SIDS),
- non-accidental trauma (NAT), and/or parental marriage break-up.
zero to finals and ox handbook of paeds
What are some associated factors for prematurity ?
e.g. environment, maternal factors (zero to finals)
- Social deprivation
- Smoking
- Alcohol
- Drugs
- Overweight or underweight mother
- Maternal co-morbidities
- Twins
- Personal or family history of prematurity
Antenatal management of prematurity?
Dr Tom if preterm labour is suspected or confirmed what can you do to im
- planned delivery in centre that has preterm care facilities
- Tocolysis with Nifedipine (CCB - suppresses labour)
- IM maternal corticosteroids <34 -35 weeks ( reduced RDS, pervientricular hameorrage and NEC) if given >24 hours before birth
- IM magnesium sulphate - <34 weeks to protect babys brain
- delayed cord clamping or cord milking - increase circulating blood colume and hb in baby
Dr Tom: In women with a history of preterm birth or an ultrasound demonstrating a cervical length of 25mm or less before 24 weeks gestation there are two options of trying to delay birth: what are they?
- Prophylactic vaginal progesterone: putting a progesterone suppository in the vagina to discourage labour
- Prophylactic cervical cerclage: putting a suture in the cervix to hold it closed
Postnatal care of premature infants?
- Stabilisation (or resuscitation if needed)
- senior paediatrician at birth <28 weeks
- delay cord clamping 1 min if not compromised
- immediately place in food grade plastic bag under radiant heater w/ woollen hat
- Resp support NIV, MV as required
- measure weight and temp on NICU admission and monitor
- Nurse in 80% humidity for first 7 days if <30 weeks
- monitor blood glucose with feeds, encouarge mothers to breast express from day 1
- start broad spectrum antibiotics if suspect infection
- treat complications of prematurity e.g. surfactant for RDS
- support parents e.g. www.bliss.org.uk
In additon to immediate post birth resuscitation what 4 things are you trying to reduce to reduce potentatial morbidity of a premature neonate?
reduce excessive oxygen exposure, hyperventilation, hypothermia, and hypoglycaemia
Why is gestational age so important to re-assess with a premature infant, how?
important for:
* designating future care of newborn
* adverse outcome risk varies inversley with gestational age
How measure?
* Maternal last menstrual period
* EDD on 12 week first trimester ultrasound (most accurate) crown-rump length, fetal femur length, head and abdominal circumference, biparietal diameter.
* New Ballard score - measures neuromuscular and physical maturity to complement maternal histoty and US.
If you examined a extremely premature baby (<28 weeks) what would you expect to find?
* weight
* tone / posture
* hair / skin / anatomical features
see BMJ BP ‘premature newborn care’ other premature stages
- weight is typically <1000 g.
- decreased tone, extended rather than flexed extremity posture with a wide range of motion throughout.
- little lanugo hair coverage
- thin transparent/pink skin with visible veins
- limited or no plantar creases
- flat areolae with nearly imperceptible breast tissue
- fused or open eyelids
- folded ear pinna cartilage
- preterm genitalia (male: scrotum empty with faint or no rugae, female: prominent clitoris and small or flat labia minora).
Differencials for prematurity
Small for gestational age
intrauterine growth restriction
What are two main causes (subgroups) of neonatal jaundice?
- increased production of bilirubin
- decreases clearance of bilirubin
What are causes of neonatal jaundice based on increased bilirubin production?
- Haemolytic disease of the newborn
- ABO incompatibility
- Haemorrhage
- Intraventricular haemorrhage
- Cephalo-haematoma
- Polycythaemia
- Sepsis and disseminated intravascular coagulation
- G6PD deficiency
What are causes of neonatal jaundice based on decreased clearance of bilirubin?
- Prematurity
- Breast milk jaundice
- Neonatal cholestasis
- Extrahepatic biliary atresia
- Endocrine disorders (hypothyroid and hypopituitary)
- Gilbert syndrome
in neonates
When is jaundice pathological?
in first 24 hours of life
Note: jaundice in neonate 2-14 days = common, usually physiological
What are RF associated to significant neonatal jaundice?
- preterm delivery
- low birth weight
- having jaundice in first 24hrs of life
- male
- visible bruising
- cephalhaematoma
- maternal age over 25
- maternal DM
- breastfeeding
- having previous babies born with jaundice and needing phototherapy
- ethnicity - asian, european, native american
- dehydration
- neonatal weight loss / poor feeding
Prevalence of neonatal jaundice?
- 60% term and 80% preterm in 1st week of life
- 10% breastfed babies jaundiced at 1month
What is prolonged jaundice in:
1. full term babies
2. preterm babies
- 14 days
- 21 days
What investigations would you do for neonate presenting with prolonged jaundice?
FBC and blood film
* high or low WCC or thrombocytopenia = potential sepsis
* low HB / haematocrit = anaemia (potential haemolytic anaemia)
* increased reticulocytes = haemolysis
* blood film = haemolysis
Blood group - for mum and baby
* ABO incompatibility
* rhesus incompatibiltiy
Direct Coombs test (direct antiglobulin test)
* haemolysis
Bilirubin
* high levels of conjugated bilirubin = hepatobiliary cause of jaundice
LFTs
* hepatobiliary cause
G6PD levels
* G6PD deficiency
Blood cultures and urine for M,S, U
* looking for source of sepsis
Thyroid function test
* hypothyroid
Causes of prolonged jaundice?
- biliary atresia
- hypothyroidism
- galactosaemia
- urinary tract infection
- breast milk jaundice
* jaundice is more common in breastfed babies
* mechanism is not fully understood but thought to be due to high concentrations of beta-glucuronidase → increase in intestinal absorption of unconjugated bilirubin - prematurity
* due to immature liver function
* increased risk of kernicterus - congenital infections e.g. CMV, toxoplasmosis
What causes physiological jaundice?
Elevated bilirubin due to:
* babies being polycythaemic at birth (having lots of RBC at birth so break lots down)
* short RBC life span compared to adults
* hepatic bilirubin metabolism is less efficient in first few days of life
Why are breastfed babies more likely to have jaundice?
Componenets of breast milk inhibit liver to process bilirubin.
Why may premature neonates have jaundice?
Immature liver - so can not process bilirubin.
Why may premature neonates have jaundice?
Immature liver - so can not process bilirubin.
Why may premature neonates have jaundice?
Immature liver - so can not process bilirubin.
Describe pathophysiology of haemolytic disease of the newborn
- caused by incompatibility between rhesus antigens on surface of RBC of mother and fetus.
- woman who is Rh D -ve becomes pregnant. Her child may be Rh D +ve.
- at some point, blood from baby can enter mum’s bloodstream
- baby’s red blood cells (in mum’s blood) display the Rh D antigen
- mum’s immune system recognise this as FOREIGN –> so make antiodies to the antigen = mum become sensitised to Rh D antigens!!
This does not case a problem until second pregnancy, or in antepartum haemorrhage.
Subsequent pregnancies:
* mother’s anti-D antibodies cross the placenta into the fetus
* if this second fetus is RhD +ve = antibodies attach to RBCs of the fetus = immune system of the fetus attacks own RBCs.
* Sooooo…. get haemolysis = anaemia and high bilirubin level.
This is called haemolytic disease of the newborn
What should you ask for Hx and Ex in neonate presenting with jaundice?
- obstetric Hx including mum’s Rhesus status and blood group, baby’s gestational age at birth
- age at onset and duration of jaundice
- feeding history
- number of wet or dirty nappies per day - ask about dark urine and pale stools
- signs of illness - vomiting, fever, lethargy, weight loss, irritability
- family hx of relevant conditions - e.g. G6PD deficiency. Have any siblings or close family needed phototherapy or blood transfusion for neonatal jaundice
On examination:
* signs of illness - fever?
* weight gain
* bruising
* jaundice - usually spreads from head downwards with increasing severity
How is neonatal jaundice initially managed?
i.e when do you send baby in and with what urgency?
Emergency admission (999) if have jaundice with features of bilirubin encephalopathy (atypical sleepiness, poor feeding, vomiting, hypotonia followed by hypertonia)
Urgent admission to neonatal or paeds unit in 2 hours if jaundice appears less than 24hrs of age
Urgent admission to neonates or peads to be seen in 6 hours if:
* jaundice appears after 7 days old
* neonate is unwell
* gestational age < 35 weeks
* prolonged jaundice is suspected
* concerns about weight/ feeding problems
* pale stools or dark urine
- reassure parents and carers and encourage breastfedding mothers to continue
How is neonatal jaundice managed (once baby is in secondary care and has been initially managed)?
Total bilirubin levels are monitored and plotted on a treatment threshold chart. Depending on level, management is decided.
* level below treatment threshold = no treatment needed
* phototherapy
* **exchange transfusion **- usually indicated if baby has signs of bilirubin encephalopathy / jaundice doesn’t respond to phototherapy. (Exchange transfusions involve removing blood from the neonate and replacing it with donor blood.)
* early surgical treatment - if biliary atresia.
* treat any underlying illness, e.g. infection.
What is phototherapy?
for neonatal jaundice
- converts unconjugated bilirubin into isomers that can be excreted in the bile and urine without requiring conjugation in the liver.
- involves removing clothing down to the nappy to expose the skin and eye patches to protect the eyes.
- Blue light is the best at breaking down bilirubin.
- A light-box shines blue light on the baby’s skin. Little or no UV light is used.
- Bilirubin is closely monitored during treatment.
- Once phototherapy is complete, a rebound bilirubin should be measured 12 – 18 hours after stopping to ensure the levels do not rise about the treatment threshold again.
What are complications of neonatal jaundice?
- Kernicterus = rare but serious complication of untreated jaundice. High levels cause brain damage (esp basal ganglia). (on NICE, this is a clinical term to describe both acute and chronic bilirubin encephalopathy - i.e. the features and the long standing effects)
- Acute bilirubin encephalopathy = severe hyperbilirubinaemia
- Chronic bilirubin encephalopathy (features left behind due to acute bilirubin encephalopathy)
Why can high bilirubin levels cause damage to CNS?
Bilirubin can cross blood brain barrier
What are features of kernicterus
complication of neonatal jaundice
less responsive, floppy, drowsy baby with poor feeding.
Note: this complication is rare nowadays
What permenant damage is caused by kernicterus (having v high bilirubin levels)?
Cerebral palsy
Learning disability
Deafness and vision problems
Seizures
What are features of G6PD deficiency?
- neonatal jaundice is often seen
- intravascular haemolysis
- gallstones are common
- splenomegaly may be present
- Heinz bodies on blood films. Bite and blister cells may also be seen
What is inheritence pattern of G6PD deficiency?
X linked recessive
What is pathophysiology of G6PD deficiency?
i.e. how does it cause haemolytic anaemia (presents as neonatal jaundice)
- G6PD is the first step in the pentose phosphate pathway, which converts glucose-6-phosphate→ 6-phosphogluconolactone
- this reaction also results in nicotinamide adenine dinucleotide phosphate (NADP) → NADPH
i.e. glucose-6-phosphate + NADP → 6-phosphogluconolactone + NADPH - NADPH is important for converting oxidizied glutathine back to it’s reduced form
- reduced glutathine protects red blood cells from oxidative damage by oxidants such as superoxide anion (O2-) and hydrogen peroxide
- ↓ G6PD → ↓ reduced NADPH → ↓ reduced glutathione → increased red cell susceptibility to oxidative stress
What are triggers for G6PD deficiency?
Intercurrent illness or infection (often forgotten)
Fava beans: the disease was historically known as favism
Henna
Medications: primaquine (anti-malarial), sulfa-drugs (sulphonamides, sulphasalazine, sulfonylureas), nitrofurantoin, dapsone, and NSAIDs/Aspirin, ciprofloxacin
What investigations would you do for G6PD deficiency?
G6PD enzyme assay = diagnostic test
Blood film = typically shows Heinz bodies and bite cells
Compare and contrast G6PD deficiency and hereditary spherocytosis
* gender and inheritence pattern?
* ethnicity?
* typical Hx features?
* blood film results?
* diagnostic test?
see table:
What is cephaloheamatoma?
- a swelling on the newborns head.
- It typically develops several hours after delivery and is due to bleeding between the periosteum and skull.
- The most common site affected is the parietal region
- takes 3 months to resolve
- main differential = caput succedaneum
What is pathophysiology / cause of neonatal respiratory distress syndrome (NRDS)?
* who does it affect?
* levels of —what?— are low?
- affects premature neonates
- born before lungs start producing adequate surfactant
- Surfactant is a phospholipid-containing fluid produced by type 2 pneumocytes.
- It acts to lower the surface tension in the alveoli helping to keep them open. A lack of surfactant increases surface tension and causes alveoli to collapse, triggering respiratory distress.
- Lungs start to make surfctant at 26 weeks and levels are adequate at ~ 35 weeks gestation.
- This means premature babies are at increased risk of NRDS.
Summary:
* Inadequate surfactant leads to high surface tension within alveoli.
* This leads to atelectasis (lung collapse), as it is more difficult for the alveoli and the lungs to expand.
* This leads to inadequate gaseous exchange, resulting in hypoxia, hypercapnia (high CO2) and respiratory distress.
How is NRDS diagnosed?
Newborn respiratory distress syndrome (NRDS)
- clinical diagnosis usually
- CXR = ground glass appearance
What are steps to do in newborn resuscitation?
Have included pass med 5 step and complex algorithm - resus council
- Dry baby and maintain temperature
- Assess tone, respiratory rate, heart rate
- If gasping or not breathing give 5 inflation breaths*
- Reassess (chest movements)
- If the heart rate is not improving and <60bpm start compressions and ventilation breaths at a rate of 3:1
*Inflation breaths are different from ventilation breaths. The aim is to sustain pressure to open the lungs.
APGAR score:
What points does it look at?
What is the lowest / highest score ?
Describe screening for Down syndrome
* first trimester test
* integrated test
how many weeks? what blood markers?
Thinking about newborn screening timeline, when is:
1. newborn physical exam?
2. newborn blood spot?
3. newborn hearing screen?
4. infant physical examinaton?
i.e. how many hours, days, weeks old are these done?
In NIPE, you find this. What is shown?
Absent red reflex with central opacity in patient with congenital cataract
In NIPE, you find this. What is shown?
Asymmetric red reflex with leukocoria in left eye – unilateral retinoblastoma
Compare and contrast a significant murmer to a benign murmer (in NIPE exam)
In NIPE exam, what are examination findings in baby with congenital hip problem?
Observation
* Differences in leg length.
* Knees at different levels when hips and knees are bilaterally flexed.
* Buttock/posterior thigh skin folds asymmetry on ventral suspension.
* Difficulty in adducting the hip to 90 degrees.
Manipulation
* Palpable ‘clunk’ when undertaking Barlow and Ortolani manouvres.
What conditions are screened for in newborn blood spot screening?
For the following conditions, describe:
* the presentation of them if not detected
* the management
- pheylketonuria
- MCADD
- Isovaleric acidaemia
- GLutaric aciduria T1
- Homocystinuria
- maple syrup urine disease
(unsure how much we need to know but have added from slides)
Describe the aeitology of congenital hypothyroidism
Primary = an issue to do with thyroid gland (e.g. dysgenesis, or inborn error of thyroid hormone)
Secondary = an issue with HPA axis (e.g. TSH deficiency)
What levels of TSH (in a newborn blood spot screen) would prompt you to either repeat bloodspot, refer the newborn or no further action?
How does hypothyroidism present in newborns? (congenital)
How does it presented if acquired (delayed presentation)?
Dr Luyt says can always say as ddx for prolonged jaundice pres
What diagnostic testing would you for cystic fibrosis?
there are three
Describe how the CF sweat test is done, and what is number is abnormal?
How does CF present in
* neonates?
* young children?
* adults?
Describe the pathway in the newborn screening test
After premature infant has been stabilised and taken to neonatal unit. what are some lab tests might be done on them during their stay and why ?
After premature infant has been stabilised and taken to neonatal unit. what are some IMAGING options might be done to them and why?
