Neonatology Flashcards
1
Q
Jaundice
A
Condition of abnormally high levels of bilirubin in the blood
2
Q
Physiological jaundice
A
- 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)
3
Q
Jaundice causes
A
- 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
4
Q
Breast milk jaundice
A
- 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
5
Q
Jaundice in premature neonates
A
- physiological jaundice is exaggerated due to the immature liver
- increases risk of complications, particularly kernicterus
- brain damage due to high bilirubin levels
6
Q
Haemolytic disease of newborn
A
Caused by the incompatibility between the rhesus antigens on the surface of the red blood cells of the mother and fetus
7
Q
Jaundice investigations
A
- 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
8
Q
Jaundice mx
A
- 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
9
Q
Kernicterus
A
- 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
10
Q
SIDS
A
Sudden, unexplained death in an infant (occurs within the first six months of life)
11
Q
SIDS risk factors
A
- prematurity
- low birth weight
- smoking during pregnancy
- male baby (slight increased risk)
12
Q
SIDS minimising risk
A
- 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
13
Q
SIDS care of next infant
A
- 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
14
Q
Prematurity
A
- under 28 weeks: extreme preterm
- 28-32 weeks: very preterm
- 32-37 weeks: moderate to late preterm
15
Q
Prematurity associations
A
- social deprivation
- smoking
- alcohol
- drugs
- overweight/underweight mother
- maternal co-morbidities
- twins personal/fhx of prematurity
16
Q
Prematurity management
A
- 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
17
Q
Prematurity complications
A
- 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
18
Q
Apnoea of prematurity
A
- defined as periods where breathing stops spontaneously > 20 seconds OR
- shorter periods with oxygen desaturation or bradycardia
19
Q
Apnoea of prematurity causes
A
- 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
20
Q
Apnoea of prematurity management
A
- 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
21
Q
Retinopathy of prematurity
A
abnormal development of the blood vessels in the retina can lead to scarring, retinal detachment & blindness
22
Q
Retinopathy of prematurity pathophysiology
A
- 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
23
Q
Retinopathy of prematurity screening
A
- 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
24
Q
Retinopathy of prematurity treatment
A
- 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
25
Respiratory distress causes
- respiratory: meconium aspiration, surfactant deficiency, maternal infection, transient tachypnoea of the newborn
- congenital abnormalities
- cardiac issues
26
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
27
RDS pathophysiology
- inadequate surfactant leads to high surface tension in alveoli → atelectasis
- leads to inadequate gaseous exchange, resulting in hypoxia, hypercapnia & respiratory distress
28
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
29
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
30
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
31
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
32
APGAR
- appearance (skin colour)
- pulse
- grimmace (respond to stimulation)
- activity (muscle tone)
- respiration
33
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
34
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
35
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
36
Sepsis clinical features
- fever
- reduced tone and activity
- poor feeding
- respiratory distress/apnoea
- vomiting
- tachycardia/bradycardia
- hypoxia
- jaundice in first 24 hours
- seizures
- hypoglycaemia
37
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
38
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
39
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
40
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
41
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
42
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
43
NEC
- NEC is a disorder affecting premature neonates, where part of the bowel becomes necrotic
- life threatening emergency
44
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
45
NEC presentation
- intolerance to feeds
- vomiting, particularly with green bile
- generally unwell
- distended, tender abdomen
- absent bowel sounds
- blood in stools
46
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
47
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
48
NEC complications
- perforation & peritonitis
- sepsis
- death
- strictures
- abscess formation
- recurrence
- long term stoma
- short bowel syndrome after surgery
