Neonatology Flashcards

1
Q

Define an extremely, very and moderatly preterm birth

A

extreme: before 28 weeks
very: 28-32 weeks
moderate: 32-37 weeks

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2
Q

Give 4 risk factors for preterm birth

A
  • previous prem deliveries
  • multiple pregnancy
  • cervical incompetence
  • placental insufficiency
  • smoking and drug use in pregnancy
  • being underweight or overweight in pregnancy
  • early pregnancy (within 6 months of previous pregnancy)
  • cervix, uterus or placental problems inc infection
  • certain chronic conditions such as diabetes or HTN
  • physical injury/ trauma
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3
Q

What imaging may be needed to be carried out on a prem baby?

A
  • CXR- check no infection or ards and position of ET tube
  • AXR- risk of necrotising enterocolitis and check position of umbelical artery lines
  • cranial US- check for intraventricular haemorrhage or ischaemic periventricular white matter damage
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4
Q

Generally, how should prem births be managed?

A
  • if extreme, need to go to tertiary level neonatal unit
  • antenatal steroids to reduce risk of ARDS of newborn
  • magnesium sulphate- neuroprotective to baby
  • resus for almost all over 24 weeks and some over 23 weeks
  • will likely need TPN feed initially, then slowly introducing NG feeds
  • reduce infection risk
  • keep walk in intubation
  • respiratory support
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5
Q

Give 3 respiratory complications of prem birth

A
  • resp distress syndrome
  • surfactant deficient lung disease
  • chronic lung disease
  • recurrent apnoea
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6
Q

Give 2 cardio complications of prem birth and briefly describe how they’re managed

A
  • poor contracility and hypotension: dopamine, adrenaline infusions/ inotrope support, fluid resus, NSAID administration
  • PDA: NSAIDs and indomethacin, if fail surgical ligation
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7
Q

Give 3 neuro complications of prem brith

A
  • intravascular haemorrhage
  • seizures
  • post haemorrhagic ventricular dilation
  • developmental delay
  • cerebral palsy
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8
Q

Give 2 GI complications of prem birth

A
  • immature gut causing feeding intolerance

- necrotising enterocolitis

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9
Q

Give 5 benefits to breast feeding

A
  • bonding with baby
  • antibodies protect from URTIs, influenza, otitis media, asthma and eczema
  • hormones for development
  • reduced risk of sudden infant death syndrome
  • reduced obesity and type 2 diabetes risk
  • long chain poly unsaturated fatty acids are good for brain development
  • environmental and financial benefits
  • suckling promotes uterine contractions so reduced post partum haemorrhage risk
  • visual acuity is higher
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10
Q

give 3 common problems with breast feeding

A
  • its hard work, and somtimes never works
  • weening can be challenging
  • can make nipples sore and cracked
  • breast engorgement can be painful
  • mastitis is common
  • can get thrush on nipples
  • break milk supply can be low
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11
Q

How is mastitis managed?

A
  • flucloxacillin for 7-10 days
  • continue breast feeing
  • Ibuprofen
  • hot and cold compress
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12
Q

Give 3 contraindications to breast feeding

A
  • HIV
  • amiodarone
  • antimetabolites
  • carbimazole
  • opiates
  • many other drugs- check bnf
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13
Q

how much formula is needed and for how long

A
  • after 7 days they need 150mls/kg/day
  • 200g if prem and 100g if large for age
  • feed 4-6 times per day
  • wean at 6 months
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14
Q

What are the different types of formula milk

A
  • standard: cows milk with modified fat, protein and vitamin content
  • follow on: casein based protein component, delays stomach emptying so less frequent feeds
  • hydrolysed formulas: if cows milk allergy
  • specialist milks: for gord, malabsorbtion or metabolic diseases
  • soya products arnt recommended as they have oestrogen in which could affect immune and thyroid function
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15
Q

What is involved in a newborn screening examination

A
  • eyes: red reflex absent= cateracts and white= retinoplastoma
  • heart: listen for CHD and resp distress signs
  • hips: for DDH which barlow and ortolani manoeuvers
  • testes: check descent
  • general examination- blue spots, spina bifida, downs and other trisomy characteristics etc
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16
Q

State as many of the 9 things screened for on the blood spot screening test as you can

A
  • congenital hypothyroid (TSH)
  • cystic fibrosis (immunoreactive trysinogen)
  • phenylketonuria
  • sickle cell disease and B thalassaemia major
  • MCADD
  • isovaleric acidaemia
  • glutaric aciduria type 1
  • homocystinuria
  • maple syrup urine disease
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17
Q

when are hearing tests done?

A
  • after 4 weeks if hospital based
  • after 5 if in community
  • and at 5 yrs (also get sight done)
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18
Q

Describe the screening tests that take place during pregnancy

A
  • HIV, Hep B and syphilis at 8-12 weeks
  • combined test at 10-14 weeks - blood test for trisomies 13,18 and 21 + nuchal translucency on USS
  • rhesus disease screening
  • anaemia screen at 28 weeks
  • chorionic villus sampling at 11-14 weeks or amniocentesis at 15 weeks for definitive diagnosis if combined test suspicious
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19
Q

How is gestational diabetes screened for and who gets screened?

A
  • oral glucose tolerance test at 24-28 weeks
    if:
  • overweight
  • diabetes in pregnancy before
  • had a baby weighing 4.5kg or more before
  • close relative with diabetes
  • SE asian, black caribbean or middle eastern origin
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20
Q

Describe the foetal circulation

A
  • Blood oxygenated at placenta, enters IVC via ductus venosus on umbilical vein
  • IVC-> RA -> RV -> PA
  • most blood in PA goes to aorta via PDA, some goes to lungs
  • lungs -> LA-> LV -> Aorta
  • aorta -> body-> umbilical arteries -> placenta
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21
Q

What is vaccinated against?

A
Diptheria
tetanus
pertussis
polio
h. influenza
meningitis (Hib/MenC and ACWY)
rotavirus
rubella
measles
mumps
VZV
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22
Q

What is diphtheria?

A

gram +ve bacteria releases toxin causing upper airway swelling and lymphadenopathy which can result in resp failure, circulatory collapse, coma and death

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23
Q

What is tetanus?

A

toxin from clostridium tetani (found in soil/ manure and enters through broken skin) causes local muscle spasm (lockjaw, back spasms etc) and then generalised spasm-> painful and can affect respiratory effort

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24
Q

What is pertussis

A

Droplet spread bacteria with 3 phases:
1. catarrhal phase (1-2 weeks)- like viral URTO
2. paroxysmal phase (100 day cough)- intense coughing fits for several mins with loud inspiratory whoop
3. convalescent phase- chronic cough lasting weeks
Complications inc . pneumonia, bronchicetasis, vomiting, brain hypoxia.
Need deep nasophayngeal swab to diagnose

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25
Q

What is poliomyelitis

A

Enterovirus spread by faecal oral transmission.
Usually affects children <5 yrs, many will get subclinical corzyal symptoms, some flu like headache, fever, sore throat etc and 5% get sudden onset paralysis which is often fatal

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26
Q

What is haemophilus infuenza

A

Common resp spread bacterial infection causing pneumonia, bacteraemia, pericarditis, osteomyelitis and epiglottitis inparticular.

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27
Q

When are the Hib/ MenC and MenACWY vaccines given?

A

Hib/ menC at 12 months and menACWY at 14 yrs

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28
Q

what is rotavirus

A

common cause of gastroenteritis, vaccine protects against 5 serotypes

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29
Q

What are the differences between live and attenuated vaccines?

A
  • live carry infection risk and rely on functioning immune system
  • live are longer lasting
  • inactivated often require boosters
  • live vaccines can often be oral, inactivated cant
  • live vaccines tend to be better at protecting from other strains
  • live vaccines often cheaper
30
Q

What is the difference in time and cause of early vs late onset neonatal sepsis?

A
Early= within 72 hrs- usually group B strep or E coli
Late= after 72 hrs- usually coagulase neg staph, enterobacteria or staph a
31
Q

Antibiotics in the first few days of life increase risk of what conditions?

A

atopic conditions - eczema, asthma etc

32
Q

Give 6 risk factors for neonatal sepsis

A
  • invasive group b strep infection in previous baby
  • maternal group b step colonisation, bacteriuria or infection in current pregnancy
  • pre-labour rupture of membranes
  • low birth weight baby (<2500g)
  • prem birth (<37 weeks)
  • intrapartum fever >38degrees
  • chorioamnionitis
  • parenteral abx gievn to woman for confirmed or suspected invasive bacterial infection at any time 24 hrs before, during and after labour
  • suspected or confirmed infection in another baby in the case of multiple pregnancies
33
Q

Give the 6 red flag signs for neonatal infection

A
  • seizures
  • apnoea in a term baby
  • shock
  • resp distress starting more than 4 hrs after birth
  • need for ventilation in a term baby
  • suspected or confirmed infection in twin
  • systemic abx given to mother 24hrs around birth
34
Q

Describe the possible clinical features of neonatal infection, other than the red flags

A
  • altered behaviour or responsiveness
  • altered muscle one (floppy)
  • feeding difficulties
  • feeding intolerance (vomiting, abdo distension etc)
  • abnormal heart rate
  • signs of resp distress
  • hypoxia and cyanosis
  • jaundice within 24hrs of birth
  • apnoea
  • encephalopathic signs
  • need for resus
  • persistent pulmonary HTN
  • hypo/ hyperthermia
  • unexplained bleeding
  • oliguria persisting beyond 24 hrs of birth
  • hypo/hyperglycaemia
  • metabolic acidosis
  • local signs of infection
35
Q

How should a baby with suspected neonatal sepsis be investigated?

A
  • swabs- eye discharge, wounds, umbilical discharges etc
  • cultures- blood, urine, stool etc
  • bloods- crp, lactate, fbc, u&e, capillary gas
  • lumbar puncture
  • cxr
36
Q

Give 3 differentials for neonatal sepsis

A
  • transient tachypnoea of newborn
  • surfactant deficient lung disease/ ARDS
  • meconium aspiration
  • haemolytic disease of newborn (cause of jaundice before 24hrs)
37
Q

How is neonatal sepsis managed?

A
  • intrapartum abx prophylaxis if mother has had previous baby with neonatal sepsis or had has significant group b strep infection in current pregnancy
  • IV benzylpenicillin and gent is empiric abx
  • other sepsis management as adults (fluids, inotropes, oxygen etc)
38
Q

Describe the cause and course of physiological jaundice

A
  • in normal baby it starts at day 2-3 and peaks at day 5 and resolved by day 10
  • due to increased RBC turn over (doesnt need foetal Hb anymore) and immature liver which cant process the high conc of bilirubin
39
Q

What could cause early jaundice? (within 24hrs)

A
  • sepsis
  • haemolytic disease of newborn
  • G6PD
  • TORCH infection
40
Q

What causes intermediate jaundice? (day 2-21)

A
  • physiological
  • breast milk jaundice (inadequate intake)
  • sepsis
  • biliary atresia
  • haemolysis
  • hypothyroidism
  • haemoglobinaemia
  • polycythaemia
  • dehydration
41
Q

What can cause prolonged jaundice? (split into conjugated and unconjugated) - after 21 days

A

Conjugated (dark urine, pale stools): biliary atresia, intra/ post hepatic obstruction, hepatitis, hypothyroid, gilberts
Unconjugated: hypothyroidism, physiological, breast milk jaundice, infection,

42
Q

What signs and symptoms should be assessed for in neonatal jaundice?

A
  • level of jaundice
  • level of consciousness
  • feeding
  • neurological symptoms- muscle tone, seizures
  • infective signs (UTI, resp, GI)
  • urine output
  • abdomass/ organomegaly
  • stool and urine colour
43
Q

How should neonatal jaundice be investigated?

A
  • transcutaneous bilirubinometer if >35 week gestation and >24 hrs old
  • serum bilirubin if <35 weeks gestation, <24 hrs old or TCB value is >250
  • blood grouping of baby and mother
  • FBC, U&E, LFT, TFT
  • infection screening
  • G6PD levels
  • coombs test and other haemolysis screen- retics, LDH, film, haptoglobin
  • later, viral screens and imaging of biliary tract may be needed
44
Q

How is neonatal jaundice managed?

A
  • Phototherapy: use treatment threshold graphs. Repeat bilirubin 4-6hrs after starting to ensure not still rising and 6-12 hrly once stable. Stop when >50umol below line and check again after 12 hrs to check not risen again. If <50 below level and clinically well, continue and repeat in 18hrs if risk factors present and 24 hrs if not.
  • fluids- expressed maternal milk is preffered, NG feeding may be needed.
  • exchange transfusions- performed via umbilical artery/ vein
  • IV immunoglobulins- used with phototherapy in rhesus haemolytic disease
45
Q

What is the main complication of neonatal jaundice and what are the signs of it?

A
High levels of bilirubin lead to accumulation in CNS grey matter causing irreversible neurological damage. Permanent brain damage due to acute bilirubin encephalopathy is called kernicterus. 
Signs:
- difficulty walking
- high pitched cry
- poor sucking or feeding
- backward arching of neck and body
- fever
46
Q

What can kernicterus result in?

A
  • involuntary and uncontrolled movements (athetoid CP)
  • permanent upward gaze
  • hearing loss
  • improper develoment of tooth enamel
  • high cortical brain dysfunction
47
Q

Give 3 risk factors for neonatal jaundice

A
  • prem
  • low birth weight
  • fhx
  • exclusively breast fed
  • maternal diabetes
48
Q

What are the TORCH infections? (common congenital infections)

A
  • taxoplasmosis
  • Other (syphilis, VZV, parovirus)
  • Rubella
  • CMV
  • Herpes virus
49
Q

What is meconium aspiration syndrome?

A

where the meconium is passed in utero (usually due to prolonged pregnancy or fetal distress) and the baby aspirated it, leading to respiratory distress

50
Q

Describe how meconium aspiration leads to respiratory distress

A
  • partial or total obstruction due to thick and sticky consistency of meconium
  • pulmonary inflammation due to cytokines in the meconium
  • infection
  • surfactant inactivation due to inflammation
  • persistent pulmonary hypertension also due to inflammation
51
Q

Give 3 differentials for meconium aspiration syndrome

A
  • transient tachypnoea of newborn (resolves after 24hrs)
  • surfactant deficiency
  • persistent pulmonary htn
52
Q

Give 4 risk factors for meconium aspiration

A
  • gestational age >42 weeks
  • foetal distress
  • intrapartum hypoxia secondary to placental insufficiency
  • apgar score <7
  • chorioamnionitis
  • prolonged pre rupture of membranes
  • oligohydramnios
  • in- utero growth restriction
  • maternal hypertension, diabetes, preeclampsia, smoking, drug abuse
53
Q

Give 3 complications of meconium aspiration

A
  • pneumothorax or pneumomediastinum due to alveolar hyperdistension
  • cerebral palsy due to hypoxia
  • chronic lung disease due to barotrauma and oxygen toxicity with ventiliation
54
Q

How is meconium aspiration managed?

A
  • incubator as hypothermia inhibits surfactant production
  • nutritional support and IV fluids
  • antibiotics if ?infection
  • surfactant bolus
  • inhaled nitric oxide if mechanical ventilation and surfactant needed due to pulmonary HTN
  • corticosteroids: reduces lung inflammation
  • ventilation/ oxygen therapy/ CPAP
55
Q

How does biliary atresia present?

A
prolonged jaundice: (14days if term, 21 if prem)
dark yellow urine
pale stools
spleen palpable be 3-4 weeks
liver hard and enlarged
56
Q

How is biliary atresia managed?

A

kasia procedure performed within 60 days- connects bile duct to bowel, needs to be done quickly to avoid liver damage and cirrhosis or may need transplant

57
Q

What is retinopathy of prematurity?

A

Abnormal blood vessel development in retina of eye. Premature blood vessels are also fragile so can leak and cause bleeding in eye, scar tissue may develop and pull retina loose from inner surface of eye- retinal detachment. in severe cases this can result in vision loss.

58
Q

Give 4 risk factors for retinopathy of prematurity

A
  • prematurity
  • apnoeas
  • heart disease
  • hypercapnia
  • infection
  • acidosis
  • resp distress
  • bradycardia
  • transfusions
59
Q

How is retinopathy of prematurity managed?

A
  • laser treatments (photocoagulation)- stops abnormal blood vessels from growing
  • injecting antibody that blocks VEG- F into eye
60
Q

what can be long term consequences of bronchopulmonary dysplasia/ neonatal chronic lung disease

A
  • decreased IQ
  • cerebral palsy
  • asthma and exercise limitation
61
Q

What causes respiratory distress syndrome in neonates?

A
  • deficiency in surfactant
  • leads to difficulty inflating alveoli
  • and atelectasis
  • hypoxia causes reduced cardiac output, hypotension, acidosis and renal failure
62
Q

give 3 risk factors for respiratory distress syndrome of neonate

A
  • prem
  • male
  • maternal diabetes
  • 2nd twin
  • c section
63
Q

How is respiratory distress of prem neonate prevented and managed?

A

prevented- betamethasone or dexamethasone given to mum if high risk of prem birth
managed:
- delay clamping of cord to promote placento- feotal transfusion
- give o2 via oxygen air blender
- stabilise with CPAP if not improveing
- <26 weeks- intubate and give surfactant via ET tube
- sats of 85-93% to reduce risk of chronic lung disease and retinopathy
- warm in intubatory
- give 10% dextrose
- parenteral nutrition may help

64
Q

When does rhesus haemolytic disease occur?

A
  • when a rhD -ve mum delivers a rhD +ve baby, she may be exposed (due to leak such as mild trauma, threatened miscarriage, APH, amniocentesis, chorionic villous sampling etc) and mated anti- rhD IgG antibodies
  • so if next baby is rhD +ve, it will receive the antibodies from the mother and and mount an immune response against its own antibodies
65
Q

Describe the clinical features of rhesus haemolytic disease

A
  • early jaundice (day 1)
  • yellow vernix
  • CCF - odema and ascites
  • hepatosplenomegaly
  • bleeding
  • CNS signs
  • kernicterus
66
Q

How is rhesus haemolytic disease managed?

A

Give Anti- D immunoglobulins, phototherapy and exchange tranfusions useful also

67
Q

What is necrotising entercolitis

A

inflammatory bowl necrosis, maybe due to infection, premature bowel, hypoxia or often unknown

68
Q

Describe the clinical features of necrotising enterocolitis and what is AXR sign

A
  • abdo distension
  • little blood/ mucus passed PR
  • tenderness/ perforation
  • shock
  • DIC
  • mucousal sloughing
  • pneumatosis intestinalis- gas in gut wall seen on xray
69
Q

Give 3 risk factors for necrotising enterocolitis

A
  • prem
  • VLBW
  • enteral feeds
  • bacterial colonisation
  • mucosal injury
70
Q

How is necrotising enterocolitis managed?

A
  • stop oral feeds
  • give cefotaxime and vanc// ?gent and met + fluclox if >72 hrs old and benzyl pen if <72hrs
  • liase with surgeons
  • laparotomy indications inc progressive distension and perforation
71
Q

Describe the process of resus of a newborn

A
  1. dry baby
  2. if gasping or not breathing, open airway and give 5 inflation breaths
  3. reassess- if no increase in heart rate, check that chest is moving during inflation
  4. if chest not moving- recheck head position, airway manoeuvres etc
  5. if chest moving- ventilate for 30 s
  6. if heart rate still <60, start chest compressions and cooredinate with ventilation breaths in 3:1 ratio
  7. reassess heart rate every 30 seconds, eventually start to consider venous access or drugs
72
Q

how should neonatal hypoglycaemia be managed?

A

BM1-2 and well= buccal dextrose gel and suppor breast feed/ formula feeding, if twice investigate further
BM<1 or unwell= 2.5 mg/kg 10% dextrose IV bolus and 75ml/kg/day therafter