Neonatology Flashcards
Jaundice
Condition of abnormally high levels of bilirubin in the blood
Physiological jaundice
- high concentration of RBCs in the fetus and neonate which are more fragile than normal RBCs
- have less developed liver function
- fetal RBCs break down more rapidly than normal RBCs, releasing lots of bilirubin
- normally excreted via the placenta
- at birth, no longer have a placenta to excrete bilirubin
- normal rise in bilirubin shortly after birth, causing a mild yellowing of skin & sclera from 2-7 days of age (usually resolves completely by 10 days)
Jaundice causes
- increased production of bilirubin
- haemolytic disease of the newborn
- ABO incompatibility
- haemorrhage
- intraventricular haemorrhage
- cephalo-haematoma
- polycythaemia
- sepsis and disseminated intravascular coagulation
- G6PD deficiency
- decreased clearance of bilirubin
- prematurity
- breast milk jaundice
- neonatal cholestasis
- extrahepatic biliary atresia
- endocrine (hypothyroid and hypopituitary)
- gilbert syndrome
Breast milk jaundice
- babies that are breastfed are most likely to have neonatal jaundice
- components of breast milk inhibit the ability of the liver to process the bilirubin
- breastfed babies are more likely to become dehydrated if not feeding adequately
Jaundice in premature neonates
- physiological jaundice is exaggerated due to the immature liver
- increases risk of complications, particularly kernicterus
- brain damage due to high bilirubin levels
Haemolytic disease of newborn
Caused by the incompatibility between the rhesus antigens on the surface of the red blood cells of the mother and fetus
Jaundice investigations
- FBC and blood for polycythaemia or anaemia
- conjugated bilirubin: increased = hepatobiliary cause
- blood type testing for ABO/rhesus incompatibility
- direct coombs test for haemolysis
- thyroid function
- blood and urine cultures
- G6PD levels for G6PD deficiency
Jaundice mx
- total bilirubin levels are monitored and plotted on treatment threshold charts
- phototherapy
- 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 and eye patches to protect the eyes
- once phototherapy is completes, a rebound bilirubin should be measured 12-18 hours after stopping to ensure the levels do not rise above the treatment threshold again
Kernicterus
- type of brain damage caused by excessive bilirubin levels
- bilirubin can cross the blood brain barrier
- excessive bilirubin causes direct damage to the CNS
- presents with: less responsive, floppy, drowsy baby with poor feeding
- damage to nervous system is permeant, causing cerebral palsy, learning disability and deafness
SIDS
Sudden, unexplained death in an infant (occurs within the first six months of life)
SIDS risk factors
- prematurity
- low birth weight
- smoking during pregnancy
- male baby (slight increased risk)
SIDS minimising risk
- put baby on back when not directly supervised
- keep head uncovered
- place feet at the foot of the bed to prevent sliding down & under the blanket
- keep cot clear of lots of toys and blankets
- maintain a comfortable room temperature (16-20 degrees)
- avoid smoking & handling baby after smoking
- avoid co-sleeping
- if co-sleeping avoid alcohol, drugs, smoking, sleeping tablets/deep sleepers
SIDS care of next infant
- CONI team supports parents with their next infant after a sudden infant death
- extra support & home visits, resuscitation training & access to equipment
- movement monitors that alarm if the baby stops breathing for a prolonged period
Prematurity
- under 28 weeks: extreme preterm
- 28-32 weeks: very preterm
- 32-37 weeks: moderate to late preterm
Prematurity associations
- social deprivation
- smoking
- alcohol
- drugs
- overweight/underweight mother
- maternal co-morbidities
- twins personal/fhx of prematurity
Prematurity management
- in women with a history of preterm birth/ultrasound demonstrating a cervical length of 25mm or less before 24 weeks gestation:
- 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
- prophylactic vaginal progesterone
- where preterm labour is suspected/confirmed there are several options for improving the outcomes:
- tocolysis with nifedipine: CCB that suppresses labour
- maternal corticosteroids: can be offered before 35 weeks gestation to reduce neonatal morbidity/mortality
- IV magnesium sulphate: can be offered before 34 weeks gestation & helps protect baby’s brain
- delayed cord clamping/cold milking: can increase the circulating blood volume and Hb in the baby
Prematurity complications
- issues in early life
- respiratory distress syndrome
- hypothermia
- hypoglycaemia
- poor feeding
- apnoea & bradycardia
- neonatal jaundice
- intraventricular haemorrhage
- retinopathy of prematurity
- NEC
- immature immune system and infection
- long term effects
- chronic lung disease of prematurity
- learning and behavioural difficulties
- susceptibility to infections, particularly respiratory tract infections
- hearing and visual impairment
- cerebral palsy
Apnoea of prematurity
- defined as periods where breathing stops spontaneously > 20 seconds OR
- shorter periods with oxygen desaturation or bradycardia
Apnoea of prematurity causes
- due to immaturity of the autonomic nervous system that controls respiratory and heart rate
- system is more immature in premature neonates
- often a sign of developing illness such as:
- infection
- anaemia
- airway obstruction
- CNS pathology, such as seizures/haemorrhage
- GORD
- neonatal abstinence syndrome
Apnoea of prematurity management
- neonatal units attach apnoea monitors to premature babies
- tactile stimulation is used to prompt the baby to restart breathing
- IV caffeine can be used to prevent apnoea and bradycardia in babies with recurrent episodes
Retinopathy of prematurity
abnormal development of the blood vessels in the retina can lead to scarring, retinal detachment & blindness
Retinopathy of prematurity pathophysiology
- when retina is exposed to higher oxygen concentrations in a preterm baby, particularly with supplementary oxygen during medical care, the stimulant for normal blood vessel development is removed
- hypoxic environment recurs, the retina responds by producing excessive blood vessels, as well as scar tissue
- abnormal blood vessels may regress & leave the retina without a blood supply → scar tissue may cause retinal detachment
Retinopathy of prematurity screening
- babies born < 32 weeks or under 1.5kg should be screened for ROP
- performed by an opthalmologist
- screening starts at:
- 30-31 weeks gestational age in babies born before 27 weeks
- 4-5 weeks of age in babies born after 27 weeks
- should happen at least every 2 weeks & can cease once the retinal vessels enter zone 3, usually at around 36 weeks gestation
Retinopathy of prematurity treatment
- involves systematically targeting areas of the retina to stop new blood vessels developing
- 1st line: transpupillary laser photocoagulation to halt and reverse neovascularisation
- other options: cryotherapy & injections of intravitreal VEGF inhibitors; surgery may be required if retinal detachment occurs
Respiratory distress causes
- respiratory: meconium aspiration, surfactant deficiency, maternal infection, transient tachypnoea of the newborn
- congenital abnormalities
- cardiac issues
RDS
- affects premature neonates, born before the lungs start producing adequate surfactant
- occurs < 32 weeks
- CXR ‘ground-glass’ appearance: bilateral, diffuse small volume lungs with white patches
RDS pathophysiology
- inadequate surfactant leads to high surface tension in alveoli → atelectasis
- leads to inadequate gaseous exchange, resulting in hypoxia, hypercapnia & respiratory distress
RDS prevention
- PERIPREM measures
- antenatal steroids given to mothers with suspected/confirmed preterm labour
- increases production of steroids
- reduces the incidence & severity of respiratory distress syndrome
- volume targeted ventilation +/- hydrocortisone prophylaxis
RDS neonatal management
- premature neonates may need
- intubation and ventilation to assist breathing if respiratory distress is severe
- LISA - less invasive surfactant administration
- endotracheal surfactant → artificial surfactant delivered into the lungs via an ET tube
- CPAP via a nasal mask to help keep the lungs inflated whilst breathing
- supplementary oxygen to maintain oxygen saturations between 91 and 95% in preterm neonates
RDS complications
- short term complications
- pneumothorax
- infection
- apnoea
- intraventricular haemorrhage
- pulmonary haemorrhage
- NEC
- long term complications
- chronic lung disease of prematurity
- retinopathy of prematurity
- neurological, hearing & visual impairment
Neonatal resus principles
- warm the baby
- get baby as dry as possible
- keep baby warm with warm delivery rooms & management under heat lamp
- babies < 28 weeks are placed in plastic bag while still wet & managed under a heat lamp
- calculate the APGAR score
- done at 1, 5 and 10 minutes whilst resuscitation continues
- used as an indicator of the progress over the first minutes after birth
- helps guide neonatal resuscitation efforts
- stimulate breathing
- place head in a neutral position to keep airway open
- if gasping/unable to breathe, check for airway obstruction
- inflation breaths
- given when the neonate is gasping/not breathing despite adequate initial stimulation
- air should be used in term/near term babies & mix of air & oxygen should be used in pre-term babies
- aim for gradual rise in oxygen saturations, not exceeding 95%
- chest compressions
- start chest compressions if HR < 60bpm despite resuscitation & inflation breaths
- performed at a 3:1 ratio with ventilation breaths
APGAR
- appearance (skin colour)
- pulse
- grimmace (respond to stimulation)
- activity (muscle tone)
- respiration
Delayed cord clamping
- also known as placental transfusion
- after birth there is a significant volume of fetal blood in the placenta → provides time for this blood to enter circulation
- in healthy babies:
- improved Hb, iron stores & BP
- reduction in intraventricular haemorrhage & NEC
- increase in neonatal jaundice
- neonates that require resus → umbilical cord clamped sooner to prevent delays in getting the baby to the resuscitation team
Sepsis common organisms
- group B streptococcus
- common bacteria found in the vagina → can be transferred to the baby during labour and cause neonatal sepsis
- e. coli
- listeria
- klebsiella
- staphylococcus aureus
Sepsis risk factors
- vaginal GBS colonisation
- GBS sepsis in a previous baby
- maternal sepsis, chorioamnionitis or fever > 38
- prematurity
- early rupture of membranes
- prolonged rupture of membranes
Sepsis clinical features
- fever
- reduced tone and activity
- poor feeding
- respiratory distress/apnoea
- vomiting
- tachycardia/bradycardia
- hypoxia
- jaundice in first 24 hours
- seizures
- hypoglycaemia
Sepsis red flags
- confirmed/suspected sepsis in the mother
- signs of shock
- seizures
- term baby needing mechanical ventilation
- respiratory distress > 4 hours after birth
- presumed sepsis in another baby in multiple pregnancy
Sepsis management
- 1st line: benzylpenicillin & gentamicin
- 2nd line: 3rd generation cephalosporin may be given as an alternative in lower risk babies
- ongoing
- check CRP at 24 hours & blood cultures results at 36 hours:
- consider stopped abx if baby clinically well, blood cultures are negative 36 hours after taking them & both CRP < 10
- check CRP again at 5 days if they are still on treatment
- consider stopped abx if baby clinically well, lumbar puncture & blood cultures are negative & CRP returned to normal at 5 days
- consider performing a lumbar puncture if any of the CRP results are more than 10
- check CRP at 24 hours & blood cultures results at 36 hours:
HIE
- occurs in neonates as a result of hypoxia during birth
- hypoxia = lack of oxygen, ischaemia = restriction in blood flow, encephalopathy = refers to malfunctioning of the brain
HIE causes
- anything that leads to asphyxia to the brain can cause HIE eg.
- maternal shock
- intrapartum haemorrhage
- prolapsed cord - compression of the cord during birth
- nuchal cord - cord is wrapped around the neck of the baby
HIE general management principles
- coordinated by specialists in neonatology, on the neonatal unit
- involves supportive care with neonatal resuscitation and ongoing optimal ventilation, circulatory support, nutrition, acid base balance
children will need to be followed up by a paediatrician & the multidisciplinary team to assess their development and support any lasting disability
HIE therapeutic hypothermia
- therapeutic hypothermia - option in certain circumstances to help protect the brain from hypoxia injury
- involves actively cooling the core temperature of the baby according to a strict protocol
- baby is transferred to neonatal ICU & actively cooled using cooling blankets and a cooling hat
- temperature is carefully monitored with a target of between 33 and 34 degrees (rectal probe)
- continued for 72 hours, after which the baby is gradually warmed to a normal temperature over 6 hours
- reduced the inflammation & neurone loss after the acute hypoxic injury
- reduces the risk of cerebral palsy, developmental delay, learning disability, blindness & death
NEC
- NEC is a disorder affecting premature neonates, where part of the bowel becomes necrotic
- life threatening emergency
NEC risk factors
- very low birth weight/very premature
- formula feeds
- respiratory distress and assisted ventilation
- sepsis
- patient ductus arteriosus and other congenital heart disease
NEC presentation
- intolerance to feeds
- vomiting, particularly with green bile
- generally unwell
- distended, tender abdomen
- absent bowel sounds
- blood in stools
NEC investigations
- blood tests
- FBC - thrombocytopenia and neutropenia
- CRP - inflammation
- capillary blood gas - metabolic acidosis
- blood culture - sepsis
- abdominal x-ray is the investigation of choice for diagnosis
- dilated loops of bowel
- bowel oedema (thickened bowel walls)
- pneumatosis intestinalis = gas in the bowel wall
- pneumoperitoneum
- gas in the portal veins
NEC management
- NBM with IV fluids, TPN and antibiotics
- NGT can be inserted to drain fluid and gas from the stomach and intestines
- surgical emergency & immediate referral to the neonatal surgical team
NEC complications
- perforation & peritonitis
- sepsis
- death
- strictures
- abscess formation
- recurrence
- long term stoma
- short bowel syndrome after surgery