Neonatology Flashcards

1
Q

Jaundice

A

Condition of abnormally high levels of bilirubin in the blood

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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)
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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
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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
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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
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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

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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
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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
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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
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10
Q

SIDS

A

Sudden, unexplained death in an infant (occurs within the first six months of life)

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11
Q

SIDS risk factors

A
  • prematurity
  • low birth weight
  • smoking during pregnancy
  • male baby (slight increased risk)
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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
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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
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14
Q

Prematurity

A
  • under 28 weeks: extreme preterm
  • 28-32 weeks: very preterm
  • 32-37 weeks: moderate to late preterm
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15
Q

Prematurity associations

A
  • social deprivation
  • smoking
  • alcohol
  • drugs
  • overweight/underweight mother
  • maternal co-morbidities
  • twins personal/fhx of prematurity
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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
  • 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
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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
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18
Q

Apnoea of prematurity

A
  • defined as periods where breathing stops spontaneously > 20 seconds OR
  • shorter periods with oxygen desaturation or bradycardia
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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
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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
Q

Respiratory distress causes

A
  • respiratory: meconium aspiration, surfactant deficiency, maternal infection, transient tachypnoea of the newborn
  • congenital abnormalities
  • cardiac issues
26
Q

RDS

A
  • 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
Q

RDS pathophysiology

A
  • inadequate surfactant leads to high surface tension in alveoli → atelectasis
  • leads to inadequate gaseous exchange, resulting in hypoxia, hypercapnia & respiratory distress
28
Q

RDS prevention

A
  • 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
Q

RDS neonatal management

A
  • 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
Q

RDS complications

A
  • 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
Q

Neonatal resus principles

A
  • 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
Q

APGAR

A
  • appearance (skin colour)
  • pulse
  • grimmace (respond to stimulation)
  • activity (muscle tone)
  • respiration
33
Q

Delayed cord clamping

A
  • 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
Q

Sepsis common organisms

A
  • 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
Q

Sepsis risk factors

A
  • 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
Q

Sepsis clinical features

A
  • fever
  • reduced tone and activity
  • poor feeding
  • respiratory distress/apnoea
  • vomiting
  • tachycardia/bradycardia
  • hypoxia
  • jaundice in first 24 hours
  • seizures
  • hypoglycaemia
37
Q

Sepsis red flags

A
  • 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
Q

Sepsis management

A
  • 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
Q

HIE

A
  • 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
Q

HIE causes

A
  • 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
Q

HIE general management principles

A
  • 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
Q

HIE therapeutic hypothermia

A
  • 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
Q

NEC

A
  • NEC is a disorder affecting premature neonates, where part of the bowel becomes necrotic
  • life threatening emergency
44
Q

NEC risk factors

A
  • very low birth weight/very premature
  • formula feeds
  • respiratory distress and assisted ventilation
  • sepsis
  • patient ductus arteriosus and other congenital heart disease
45
Q

NEC presentation

A
  • intolerance to feeds
  • vomiting, particularly with green bile
  • generally unwell
  • distended, tender abdomen
  • absent bowel sounds
  • blood in stools
46
Q

NEC investigations

A
  • 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
Q

NEC management

A
  • 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
Q

NEC complications

A
  • perforation & peritonitis
  • sepsis
  • death
  • strictures
  • abscess formation
  • recurrence
  • long term stoma
  • short bowel syndrome after surgery