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Yr4: Child Health > Neonatology > Flashcards

Neonatology Flashcards

1
Q

Remind yourself:

  • Which cells produce surfactant
  • When these cells start producing surfactant
  • Consequences of reduced surfactant
A
  • Type II alveolar cells
  • Start maturing and producing surfactant around 24 weeks. Keep maturing, and increasing surfactant producing abilities, up until week 34
  • Pre-term babies may have reduced surfactant which means there is increased surface tension in the alveoli which decreases lung compliance and can result in unequal pressures in alveoli
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2
Q

State some factors which contribute to clearing fluid from baby’s lungs during birth

A
  • Baby’s thorax is squeezed through vagina
  • First breath (expands the previously collapsed alveoli)
  • Adrenaline & cortisol released in response to stress of labour stimulating respiratory effort
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3
Q

Hypoxia during birth is normal; true or false?

A

True, during contractions placenta unable to carry out normal gaseous exchange so hypoxia occurs

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4
Q

State some differences between a baby and adult that are relevant to resuscitation/must be considered

A
  • Babies have large SA to volume ratio so get cold easily
  • Born wet so loose heat quickly
  • If born through meconium may have this in mouth or airway
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5
Q

What happens to fetal heart rate during hypoxia?

A

Bradycardia

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6
Q

Explain the APGAR score, including:

  • 5 different categories
  • Scores for each
A
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7
Q

Five principles of neonatal resuscitation include: warming the baby, APGAR score, stimulating breathing, inflation breaths & chest compressions.

Discuss how we keep babies warm

A
  • Vigorous drying (also stimulates breathing)
  • If <28 weeks, place in a plastic bag whilst still wet then put under heat lamp
  • Keep babies warm under heat lamps
  • Ensure delivery rooms are warm
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8
Q

Five principles of neonatal resuscitation include: warming the baby, APGAR score, stimulating breathing, inflation breaths & chest compressions.

How often should APGAR score be calculated?

A
  • Do at 1, 5 and 10 minutes
  • Indicates progress over first few minutes & helps guide resuscitation

*Lecturer said they don’t use APGAR in clinical practice

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9
Q

Five principles of neonatal resuscitation include: warming the baby, APGAR score, stimulating breathing, inflation breaths & chest compressions.

Discuss how we can stimulate and aid a baby’s breathing (excluding inflation breaths)

A
  • Stimulate baby (e.g. dry vigorously with towel)
  • Place head in neutral position (towel under shoulders can help)
  • Check for airway obstruction (e.g. meconium) and consider aspiration if can visualise
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10
Q

Five principles of neonatal resuscitation include: warming the baby, APGAR score, stimulating breathing, inflation breaths & chest compressions.

Discuss the process/protocol for giving inflation breaths (i.e. when you give them and how many you give)

A

Give inflation breaths when gasping or not breathing

  • 2 cycles of 5 inflation breaths (each lasting 3 seconds) can be given to stimulate breathing & HR
  • If there is no response and HR is low, can give 30 secs of ventilation breaths
  • If still no response, chest compressions coordinated with ventilation breaths should be used

**Use** **air in term or near term babies, can use mix of air & oxygen in pre-term babies.** **Monitor O2 sats throughout, do not exceed 95%.

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11
Q

Five principles of neonatal resuscitation include: warming the baby, APGAR score, stimulating breathing, inflation breaths & chest compressions.

Below what HR do we start chest compressions in neonates and at what ratio

A
  • Start chest compressions if HR still <60bpm after inflation & ventilation breaths
  • 3:1 with ventilation breaths
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12
Q

When do the current resuscitation council guidelines say you should cut the umbilical cord in uncompromised neonates?

What happens when you delay clamping of the cord?

What are advantages of delaying cord clamping?

What are disadvantages of delaying cord clamping?

A
  • Uncompromised neonates should have delay of at least 1 minute. Neonates requiring resuscitation should have umbilical cord clamped sooner to prevent delays in resuscitation.
  • At birth still a significant volume of blood in placenta and by delaying clamping of cord allow time for this blood to enter baby’s circulation ‘placental transfusion.’
  • Advantages:
    • Improved Hb stores
    • Improved Fe stores
    • Improved BP
    • Reduction in intraventricular haemorrhage
    • Reduction in NEC
  • Disadvantages:
    • Increase in neonatal jaundice (requiring more phototherapy)
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13
Q

Summary of neonatal life support

A
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14
Q

Talk through this graph regarding neonatal resuscitation

A
  • Blood supply to baby is cut off
  • Baby is stimulated to start breathing
  • Lungs are filled with fluid… breathes, breathes and breathes but no oxygen can get into lungs so PaO2 falls
  • Respiratory centre stops responding and they stop breathing so go into primary apnoea
  • Spinal reflex kicks in and they start to gasp (if still in utero then still can’t get oxygen in lungs so PaO2 continues to fall and PaCO2 and acid continues to rise)
  • Will stop gasping and go into terminal apnoea
  • Whilst been hypoxic, HR has fallen and continues to fall
  • If we then delivered them, inflated their lungs they would then start to gasp
  • We would ventilate through gasping

*NOTE: when born you can’t tell if in primary or terminal apnoea. You will only know when they start to respond. When you do resuscitation, you move them backwards/left along the graph. Hence if they started breathing they were in primary apnoea and if they started gasping they were in terminal apnoea

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15
Q

State some important things that should happen immediately after birth

A
  • Skin to skin
  • Clamp the umbilical cord
  • Dry the baby
  • Keep the baby warm with a hat and blankets
  • Vitamin K
  • Label the baby
  • Measure the weight and length
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16
Q

Why are babies given vitamin K?

A
  • Babies born with vit K deficiency
  • Helps prevent bleeding (particularly intracranial, umbilical stump & GI bleeding)
  • Standard practice go give as IM injection in thigh (can also help to stimulate cry which helps expand lungs). Can also give PO but takes longer to act and is required at birth, day 7 and week 6
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17
Q

What are benefits of skin to skin contact?

A
  • Helps warm baby
  • Improves mother and baby interaction
  • Calms baby
  • Improves breastfeeding
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18
Q

What 3 tests/investigations should happen in first week of life? If relevant, state when they should be done.

A
  • Newborn examination (within 72hrs)
  • Newborn hearing test
  • Blood spot test (taken on day 5, day 8 at latest)
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19
Q

How many drops is required from heel prick for blood spot screening test?

It tests for 9 congenital conditions; state some

A
  • 4 drops
  • Conditions it tests for:
    • Sickle cell disease
    • Cystic fibrosis
    • Congenital hypothyroidism
    • Phenylketonuria
    • Homocystin
    • Medium-chain acyl-CoA dehydrogenase deficiency (MCADD)
    • Maple syrup urine disease (MSUD)
    • Isovaleric acidaemia (IVA)
    • Glutaric aciduria type 1 (GA1)

*Results take 6-8 weeks to come back

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20
Q

State some common causative organisms of neonatal sepsis- highlight two most common

A
  • Group B streptococcus (GBS)
  • Escherichia coli
  • Listeria
  • Klebsiella
  • Staphylococcus aureus
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21
Q

Do we routinely screen pregnant women for GBS in UK?

A
  • Don’t do routine screening but do opportunistic screening
  • If mother is found to have GBS in vagina (a normal commensal in women’s vaginas) then they are given prophylactic abx during labour; these must be given at least 2hrs before birth
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22
Q

State some risk factors for neonatal sepsis

A
  • Vaginal GBS colonisation
  • GBS sepsis in previous baby
  • Maternal infection (sepsis, chorioamnionitis, fever >38)
  • Prematurity
  • Early/premature rupture of membrane
  • Prolonged rupture of membranes
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23
Q

State some clinical features of neonatal sepsis

A

Presents with non-specific signs:

  • Fever
  • Reduced tone and activity
  • Poor feeding
  • Respiratory distress or apnoea
  • Vomiting
  • Tachycardia or bradycardia
  • Hypoxia
  • Jaundice within 24 hours
  • Seizures
  • Hypoglycaemia
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24
Q

State some red flags for neonatal sepsis

A
  • Confirmed or suspected sepsis in the mother
  • Signs of shock
  • Seizures
  • Term baby needing mechanical ventilation
  • Respiratory distress starting more than 4 hours after birth
  • Presumed sepsis in another baby in a multiple pregnancy
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25
Q

When deciding whether to treat a baby for suspected neonatal sepsis there are clear NICE guidelines to follow; in summary, what would you do if:

  • 1 risk factor or clinical feature indicating sepsis
  • 2 or more risk factors or clinical features
  • 1 or more red flags
A
  • 1 risk factor or clinical feature indicating sepsis: moniroe observations & clinical features for at least 12hrs and use clinical judgement
  • 2 or more risk factors or clinical features: start antibiotics
  • 1 or more red flags: start antibiotics

*Just like with adult sepsis, abx should be given within 1hr

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26
Q

What investigations should be performed if you suspect neonatal sepsis?

A

Full sepsis screen:

  • FBC
  • CRP
  • Blood cultures
  • Lumbar puncutre
  • CXR
  • Urine dipstick/culture not usually done as urinary tract sterile at birth
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27
Q

What are the first line abx for neonatal sepsis?

A
  • First line= benzylpenicillin and gentamycin
  • Second line/alternative in lower risk: cefotaxime
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28
Q

Discuss how to decide when to stop abx in neonatal sepsis

A
  • Check CRP at 24hrs and blood cultures at 36hrs; if baby is clinically well and blood cultures -ve at 36hrs and CRP <10 then consider stopping
  • If still on treatment, check CRP, blood cultures +/- lumbar puncture on day 5 and stop abx if all are -ve and baby is clinically well
  • Review baby regularly (at least every 24hrs)
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29
Q

What is hypoxic ischaemic encephalopathy?

What condition can it cause?

A

Brain damage (encephalopathy) due to oxygen deprivation (hypoxia) and decreased blood flow (ischaemia). Hypoxia in birth is normal but prolonged or severe hypoxia can lead to permanent brain damage resulting in cerebral palsy or even death.

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30
Q

State some potential causes of hypoxic ischaemic encephalopathy

A

Anything that leads to asphyxia (deprivation of oxygen) to the brain:

  • Maternal shock
  • Intrapartum haemorrhage
  • Prolapsed cord, (causing compression of the cord during birth)
  • Nuchal cord (cord is wrapped around baby’s neck)
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31
Q

What staging can be used to grade HIE? Describe each of the 3 stages (mild, moderate and severe) in terms of:

  • Presentation/clinical features
  • How long it takes to resolve/mortality
  • Prognosis/risk of cerebral palsy
A

Sarnat staging

*In mild pupils are dilated & reactive, in moderate constricted & reactive, in severe variable & fixed

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32
Q

Discuss the management of hypoxic ischaemic encephalopathy

A
  • Supportive care in neonatal unit
    • Ventilatory support
    • Circulatory support
    • Nutrition
    • Acid base balance
    • Seizure management
  • Therapeutic hypothermia (option in certain cases)
  • Follow up by MDT to assess development and any lasting disability
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33
Q

Therapeutic cooling may be used in some neonates with HIE. Discuss:

  • Principles behind therapeutic cooling
  • How baby is cooled and targets
  • How long they are cooled for
  • Aims
  • Criteria
A
  • Idea that primary neuronal death occurs at time of severe hypoxic & ischaemic insult. Secondary neuronal death occurs after period of at least 6hrs. Means there is a window to prevent the secondary neuronal death.
  • In NICU, actively cool using cooling blankets and cooling hat. Target between 33 and 34 degrees C (measure using rectal probe)
  • Cooled for 72hrs then gradually warmed to normal temp over 6hrs
  • Aims to reduce inflammation & neurone loss to reduce risk of cerebral palsy, developmental delay, learning disability, blindness & death.
  • Extensive criteria (so would look up) but key ones: gestation age >/=36 weeks, severe metabolic acidosis, history of event associated with hypoxia, evidence of moderate to severe HIE
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34
Q

There are lots of potential complications of therapeutic cooling (too many to list them all); state a few

A
  • Arrhythmias (most commonly sinus brady)
  • Reduced CO and hypotension
  • Reduced surfactant production
  • Increased pulmonary vascular resistance (which can lead to PPH)
  • Anaemia
  • Coagulopathy
  • Renal impairment
  • Liver impairment (most commonly hyperbilirubinaemia)
  • Hypoglycaemia
  • Hypocalaemia
  • Seizures
  • Skin breakdown
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35
Q

Remind yourself of the excretion of bilirubin

A
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36
Q

What is physiological jaundice?

Explain pathophysiology of physiological jaundice

A
  • Jaundice that occurs in first few days of life (usually within first 2-7 days of life- pathological if in first 24hrs and lasts no longer than 10 days; due to normal physiology and not a pathological cause
  • There is a high concentration of RBCs (high haematocrit) in fetus and neonate but these RBCs are more fragile and break down more rapidly than normal RBCs releasing lots of bilirubin. In utero, this bilirubin was excreted by placenta but once born the neonate’s liver must excrete the bilirubin; liver is not less developed/not fully developed hence there is a normal rise in bilirubin shortly after birth. Most babies remain otherwise healthy & well.
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37
Q

Jaundice in the first _____ is pathological. It needs urgent investigation & management as ______ is a common cause.

A

24hrs

Neonatal sepsis

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38
Q

Pathological causes of neonatal jaundice can be divided into:

  • Increased bilirubin production
  • Decreased bilirubin clearance

… state some examples for each

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 disorders (hypothyroid and hypopituitary)
  • Gilbert syndrome
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39
Q

Aswell as classifying causes of neonatal jaundice based on increased production and decreased clearance of bilirubin we can also classify based on when it presents. State some causes of jaundice in first 24hrs

A
  • Rhesus haemolytic disease of newborn
  • ABO haemolytic disease of newborn
  • Hereditary spherocytosis
  • G6PD deficiency
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40
Q

Aswell as classifying causes of neonatal jaundice based on increased production and decreased clearance of bilirubin we can also classify based on when it presents. State some causes of prolonged jaundice

A

Causes of prolonged jaundice

  • biliary atresia
  • hypothyroidism
  • galactosaemia
  • urinary tract infection
  • breast milk jaundice
  • prematurity
  • congenital infections e.g. CMV, toxoplasmosis
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41
Q

Explain why breast milk jaundice can occur/why babies who are breastfed are more likely to develop neonatal jaundice

A

Several reasons:

  • Components of breast milk inhibit livers ability to process bilirubin
  • Breastfed babies more likely to become dehydrated if not feeding adequately and dehydration may lead to slowing of passage of stools and subsequent increased absorption of bilirubin in intestines
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42
Q

What is meant by premature jaundice/why does prematurity lead to jaundice?

A

In premature babies, the process of physiological jaundice is exaggerated due to the immature liver.

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43
Q

What is meant by prolonged jaundice? *Think about differences for full term & premature babies

A
  • Jaundice >14 days in full term
  • Jaundice >21 days in premature babies

Prolonged jaundice should prompt further investigations for an underlying cause (see previous flashcards for possible causes)

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44
Q

What investigations would you consider in a baby with prolonged jaundice?

A
  • FBC: anaemia, polycthamia
  • Blood film: may show Heinz bodies in G6PD
  • Conjugated & unconjugated bilirubin
  • Direct Coombs test: for haemolysis
  • TFTS: for hypothyroidism
  • Blood cultures, urine cultures, LP: if infection suspected
  • Glucose-6-phosphate dehydrogenase levels: G6PD deficiency
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45
Q

Discuss the management of neonatal jaundice

A
  • Phototherapy
    • Plot age (x axis) and total bilirubin level (y axis) on treatment threshold chart to see if they should be started on phototherapy
  • If don’t meet treatment threshold, monitor baby & bilirubin levels (may be physiological) or treat underlying cause if one suspected (e.g. sepsis)
  • If extremely high bilirubin levels, exchange transfusion (remove blood from neonate & replace with donor blood) may be needed

*NOTE: thresholds decrease with decrease in gestational age

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46
Q

Explain how phototherapy works

Explain how it is done/given

When must you recheck bilirubin after stopping phototherapy

A
  • Phototherapy converts unconjugated bilirubin into isomers that can be excreted in the bile without requiring conjugation
  • Remove all clothing except nappy, put eye patches on to protect eyes. Blue light is shone on baby’s skin (little or no UV used). Double phototherapy involves 2 light boxes.
  • Measure bilirubin 12-18hrs after stopping (rebound bilirubin) to ensure levels have not risen above treatment threshold again
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47
Q

Kernicterus is a potential complication of neonatal jaundice; explain:

  • What it is
  • Presentation
  • Potential complications
A
  • Brain damage due to excess bilirubin levels (unconjugated bilirubin can cross BBB)
  • Presentation:
    • Less responsive
    • Floppy
    • Drowsy
    • Poor feeding
  • Complications:
    • Cerebral palsy
    • Learning disabilty
    • Deafness
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48
Q

Define:

  • Premature
  • Moderate to late preterm
  • Very preterm
  • Extreme preterm
A
  • Premature: birth before 37 weeks
  • Moderate to late preterm: 32-37 weeks
  • Very preterm: 28-32 weeks
  • Extreme preterm: <28 weeks
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49
Q

State some associations/risk factors for prematurity

A
  • Twins
  • Personal of FH of prematurity
  • Smoking
  • Alcohol
  • Drugs
  • Over- or underweight mother
  • Maternal comorbidities
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50
Q

During pregnancy, we can identify women who may be at risk of preterm delivery; state 2 categories of women we say are at risk

A
  • History of preterm birth
  • US shows cervical length of 25mm or less before 24 weeks gestation
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51
Q

State two options for trying to delay birth

A
  • Prophylactic vaginal progesterone: putting progesterone suppository into vagina thought to work by preventing contractions that lead to preterm birth
  • Prophylactic cervical cerclage: putting suture in cervix to hold it
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52
Q

When preterm labour is suspected or confirmed there are a few things we can try to help improve outcomes; state 4 options

A
  • Tocolysis with nifedipine: CCB that suppresses labour
  • Maternal corticosteroids: can be offered <35 weeks to reduce neonatal morbidity & mortality as it can increase surfactant production in baby
  • IV magnesium sulphate: can be offered <34 weeks and helps to protect baby’s brain
  • Delayed cord clamping or cord milking: increase circulating blood volume and Hb to baby
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53
Q

State some potential issues/complications a preterm baby may have in early life

A
  • Respiratory distress syndrome
  • Hypothermia
  • Hypoglycaemia
  • Poor feeding
  • Apnoea
  • Bradycardia
  • Neonatal jaundice
  • Intraventricular haemorrhage
  • Retinopathy of prematurity
  • Necrotising enterocolitis
  • Immature immune system and infection
54
Q

State some potential long term effects/consequences of being born prematurely

A
  • Chronic lung disease of prematurity (CLDP)
  • Learning and behavioural difficulties
  • Susceptibility to infections, particularly respiratory tract infections
  • Hearing and visual impairment
  • Cerebral palsy
55
Q

Define apnoea

A

Periods in which breathing stops spontaneously

Often accompanied by period of bradycardia

56
Q

Apnoea is very common in premature neonates; true or false?

A

True; occur in almost all babies <28 weeks and incidence decreases with increased gestational age. Apnoea in term neonates usually indicates underlying pathology.

57
Q

Why does apnoea occur in neonates? Why is it more common in premature neonates?

A
  • Occurs due to immaturity of autonomic nervous system
  • System is more immature in premature neonates
58
Q

Apnoeas may indicate neonate is developing underlying illness; state some examples of illnesses that may present with apnoeas

A
  • Infection
  • Anaemia
  • Airway obstruction (may be positional)
  • CNS pathology (seizure, haemorrhage)
  • GORD
  • Neonatal abstinence syndrome
59
Q

Discuss the management of apnoeas

A
  • In neonatal until, apnoea monitors will be attached to premature babies and these make sound when apnoea’s occurring. Can then use tactile stimulation to prompt breathing
  • IV caffeine can be used as preventative measure in neonates with recurrent apnoeas

*Episodes usually settle as baby grows & develops

60
Q

What is retinopathy of prematurity?

A

Condition that affects preterm & low birth weight babies (typically affects babies <32 weeks); there is abnormal development of blood vessels in retina which can lead to scarring, retinal detachment & blindness.

61
Q

Explain the pathophysiology of retinopathy of prematurity

A
  • Retinal blood vessel development starts ~16 weeks and is complete by 37-40 weeks gestation
  • Blood vessels grow from middle of retina to outer area
  • Vessel formation stimulated by hypoxia (normal condition during pregnancy)
  • Hence, when retina exposed to higher O2 concentrations in preterm baby (in which development of retinal vessels is incomplete) the stimulant for retinal blood vessels development is removed
  • When hypoxic environment recurs, retina responds by producing excessive blood vessels (neovascularisation) and scar tissue
  • Consequences:
    • Abnormal vessels may regress & leave retina without blood supply
    • Scar tissue may cause retinal detachment
    • … both of which can lead to blindness
62
Q

When assessing the retina we divide it into zones & areas, stages and ‘plus’ disease. Explain:

  • 3 different zones
  • How we describe which area is affected
  • Staging
  • What ‘plus’ disease is
A
  • Zones:
    • Zone 1= optic nerve & macula
    • Zone 2= edge of zone 1 to ora serrata (pigmented border between retina and ciliary body)
    • Zone 3= outside ora serrata
  • Describe areas as a clock face (e.g. disease from 1 to 4 o’clock)
  • Stages:
    • Stage 1: slightly abnormal vessel growth
    • … to stage 5: complete retinal detachment
  • Plus disease= additional findings e.g. tortuous vessels, hazy vitreous humour
63
Q

Which babies should be screened for retinopathy of prematurity?

A
  • Born <32 weeks
    • If born <27 weeks, start screening at 30-31 weeks gestational age
    • If born after 27 weeks, start screening at 4-5 weeks of age
  • Babies <1.5kg
64
Q

Discuss the management of retinopathy of prematurity

A
  • Monitoring/screening in those at risk
  • Treatments are centred around systematically targeting areas of retina to stop new blood vessel development; options include:
    • Transpupillary laser photocoagulation
    • Cyrotherapy
    • Injections of intravitreal VEGF inhibitors
    • Surgery
65
Q

For respiratory distress syndrome, discuss:

  • Who common in
  • Cause
  • What it presents with/leads to
A
  • Occurs in premature neonates (commonly below 32 weeks)
  • Lack of surfactant (as lungs aren’t producing adequate amount since type II alveolar cells only fully mature at around 34 weeks) leads to high surface tension and atelectasis and consequently inadequate gas exchange
  • Hypoxia, hypercapnia, respiratory distress
66
Q

What would you see on CXR in respiratory distress syndrome?

A

Ground glass appearance

67
Q

Discuss the management of respiratory distress syndrome; include antenatal management and management of premature neonate

A

Antenatal management

  • Antenatal steroids (e.g. dexamethasone) to mothers with suspected or confirmed preterm labour (increase production of surfactant)

Premature neonate management

  • Endotracheal surfactant
  • CPAP (to help keep lungs inflated whilst breathing)
  • Oxygen (aim sats 91-95%)
  • Intubation & ventilation (if severe)

Support with breathing can be gradually stepped down as baby improves.

68
Q

State some potential short term complications of respiratory distress syndrome

A
  • Pneumothorax
  • Infection
  • Apnoea
  • Intraventricular haemorrhage
  • Pulmonary haemorrhage
  • Necrotising enterocolitis
69
Q

State some potential long term complications of respiratory distress syndrome

A
  • Chronic lung disease of prematurity
  • Retinopathy of prematurity (occurs more often & more severely n in neonates with RDS)
  • Neurological impairment
  • Visual impairment
  • Hearing impairment
70
Q

What is necrotising enterocolitis?

What is the cause?

A
  • NEC is a disorder affecting premature neonates where part of bowel becomes necrotic. Can lead to perforation, peritonitis & shock. Life threatening paediatric surgical emergency.
  • Cause is unclear
71
Q

Cause of NEC is unclear however there are some risk factors; state some

A
  • Very premature
  • Very low birth weight
  • Formula fed
  • Respiratory distress syndrome & assisted ventilation
  • Sepsis
  • PDA & other congenital heart diseases
72
Q

Describe presentation of NEC

A
  • Intolerance to feeds
  • Vomiting (may be green bile)
  • Generally unwell
  • Blood in stool
  • Distended abdo
  • Tender abdo
  • Absent bowel sounds
  • Evidence of peritonitis & shcck
73
Q

What investigations would you do if you suspect NEC?

A

Bedside

  • Capillary blood gas: show metabolic acidosis

Bloods

  • FBC: thrombocytopenia, neutropenia
  • CRP: raised
  • Blood culture: sepsis?

Imaging

  • Abdo x-ray (SUPINE +/- lateral, +/- lateral decubitus): evidence of NEC
74
Q

What might you see on AXR of neonate with NEC?

A
  • Dilated bowel loops
  • Bowel oedema/thickened bowel wall
  • Pneumatosis intestinalis (gas in bowel wall)
  • Pneumoperitoneum (indicates perforation)
  • Gas in portal veins
75
Q

Discuss the management of NEC

A

Surgical emergency so refer to paediatric surgical team:

  • NBM
  • IV fluids
  • TPN
  • Abx
  • NG tube (drain fluid & gas from stomach & intestines)
  • Surgery to remove dead bowel +/- temporary stoma formation

Some neonates recover with medical treatment alone but others may require surgery.

76
Q

State some potential complications of NEC; divide into short and long term complications

A

Short Term

  • Perforation & peritonitis
  • Sepsis
  • Death
  • Abscess formation

Long term

  • Recurrence
  • Strictures
  • Long term stoma
  • Short bowel syndrome (after surgery)
77
Q

What is neonatal abstinence syndrome?

State some substances that cause it

A
  • Withdrawal symptoms that happen in neonates of mothers that used substances during pregnancy
  • Substances that can cause it:
    • Opiates
    • Methadone
    • Cocaine
    • Amphetamines
    • Nicotine
    • Cannabis
    • Alcohol
    • SSRIs
78
Q

When do withdrawal symptoms in neonate typically occur?

A
  • Most opiates, diazepam, SSRIs, alcohol: 3-72hrs after birth
  • Methadone & other benzo’s: 24hrs-21 days
79
Q

Symptoms of NAS can vary dependent on substance used in pregnancy; however, symptoms can be broadly classified into:

  • CNS
  • Vasomotor & respiratory
  • Metabolic & GI

… state examples of each

A

CNS:

  • Irritability
  • Increased tone
  • High pitched cry
  • Not settling
  • Tremors
  • Seizures

Vasomotor and respiratory:

  • Yawning
  • Sweating
  • Unstable temperature and pyrexia
  • Tachypnoea (fast breathing)

Metabolic and gastrointestinal:

  • Poor feeding
  • Regurgitation or vomiting
  • Hypoglycaemia
  • Loose stools with a sore nappy area
80
Q

Discuss the management of NAS in regards to treating the withdrawal (separate flashcard to ask about other considerations)

A
  • Should have an alert on their notes
  • Be kept in hospital with monitoring on a NAS chart for at least 3/7 (48hrs for SSRIs) to monitor for withdrawal symptoms
  • Keep in quiet, dim environment with gentle handling & comforting
  • Urine sample from neonate (to test for substances)
  • If moderate-severe may use:
    • PO morphine sulphate for opiate withdrawal
    • PO phenobarbitone for non-opiate withdrawal
  • Safety net advice upon discharge (regarding signs & symptoms of withdrawal)
  • Follow up (pediatricians, GP, health visitor etc…)

*NOTE: SSRI withdrawal doesn’t typically require or benefit from medical treatment

81
Q

Alongside managing the withdrawal in NAC there are additional aspects of management to consider; state some

A
  • Testing for Hep B, C and HIV
  • Safeguarding concerns & social services involvement
  • Support for mother to stop using substances
  • Check suitability for breastfeeding in mothers with substance use
82
Q

For fetal alcohol syndrome, discuss:

  • Which trimester alcohol consumption has greatest effect/implications
  • Other risks associated with alcohol use in pregnancy
  • What fetal alcohol syndrome is
  • Characteristic signs & symptoms of fetal alcohol syndrome
A
  • Effects greatest in 1st trimester (but no safe level at any point in pregnancy)
  • Other risks:
    • Miscarriage
    • Preterm delivery
    • Small for dates
  • Fetal alcohol syndrome refers to certain characteristics and other physical, intellectual, cognitive disabilities due to significant alcohol consumption during pregnancy
  • Characteristic signs & symptoms:
    • Microcephaly
    • Thin upper lip
    • Smooth flat philtrum
    • Short palpebral fissure
    • Learning disability
    • Behavioural difficulties
    • Hearing problems
    • Visual problems
    • Cerebral palsy
83
Q

For congenital rubella syndrome, discuss:

  • Cause
  • When risk is highest
  • Precautions/preventative measures
  • Features of congenital rubella syndrome
A
  • Infection with rubella during pregnancy
  • Risk highest in 1st trimester
  • Precuations:
    • If planning to get pregnant, should ensure have had MMR vaccine (can test for rubella antibodies if not sure and if not immune can have 2 doses of MMR 3/12 apart)
    • If pregnant & non-immune, cannot have MMR vaccine as it’s live. Should be offered after giving birth
  • Features:
    • Congenital catarcts
    • Congenital heart disease (PDA, pulmonary stenosis)
    • Learning disability
    • Hearing loss
84
Q

For congenital varicella syndrome, discuss:

  • What it is
  • Why varicella infection is dangerous in pregnancy
  • In what % of varicella infections in pregnancy does congenital varicella syndrome occur
  • Typical features of congenital varicella syndrome
A
  • Syndrome due to varicella/chickenpox infection in first 28 weeks of gestation
  • Varicella infection in pregnancy can cause:
    • Varicella pneumonitis, hepatitis or encephalitis in mother
    • Fetal varicella syndrome
    • Severe neonatal varicella infection (if mum infected around delivery)
  • 1%
  • Features:
    • Fetal growth restriction
    • Microcephaly
    • Limb hypoplasia
    • Scars & skin changes following dermatomes
    • Cataracts & inflammation in eye (chorioretinitis)
    • Hydrocephaly
    • Learning disability
85
Q

If a pregnant lady is not immune and is exposed to chicken pox, what can be given?

If pregnant lady develops chickenpox rash whilst pregnant what may they be given?

A
  • IV varicella immunoglobulins (within 10 days of exposure)
  • May be given PO aciclovir if present within 24hrs and >20 weeks gestation
86
Q

For congenital ctyomegalovirus, discuss:

  • How CMV is spread
  • Whether CMV in pregnancy is likely to cause congenital CMV
  • Features
A
  • Spread via infected saliva or urine of asymptomatic children
  • Most cases don’t cause congenital CMV (risk higher later in pregnancy)
  • Features:
    • Fetal growth restriction
    • Microcephaly
    • Hearing loss
    • Vision loss
    • Learning disabilities
    • Seizures
87
Q

For congenital toxoplasmosis, discuss:

  • How usually spread
  • When risk is higher
  • Classic triad
A
  • Contamination with faeces from infected cat
  • Risk higher in later pregnancy
  • Classic triad:
    • Intracranial calcification
    • Hydrocephalus
    • Chorioretinitis
88
Q

For congenital Zika syndrome, discuss:

  • Spread
  • Features
A
  • Ade mosquitos in areas of world where virus prevalent or by sex with infected person
  • In mother can cause no symptoms or minimal/mild flu-like symptoms. In neonate triad of:
    • Microcephaly
    • Fetal growth restriction
    • Other intracranial abnormalities
89
Q

What is sudden infant death syndrome (also known as cot death)?

A

Sudden, unexplained death of an infant (usually occurs in first 6 months of life)

90
Q

State some risk factors for sudden infant death syndrome

A
  • Prematurity
  • Low birth weight
  • Smoking in pregnancy
  • Male (slight increased risk)
91
Q

State some measures that can be used to reduce risk of sudden infant death syndrome

A
  • Put baby on back when not directly supervised
  • Keep head uncovered
  • Place feet at foot of bed to stop them sliding down and under blanket
  • Keep cot clear of lots of toys & blankets
  • Maintain comfortable room temp (16-20)
  • Avoid smoking & handling baby after smoking (as it stays on clothes)
  • Avoid co-sleeping
  • If co-sleeping, avoid alcohol, drugs, smoking, sleep tablets or deep sleepers

*Common OSCE station. Make sure don’t blame or judge parent, “lots of things we can do to reduce the risk & make it less likely to happen”

92
Q

What charity can help families affected by sudden infant death syndrome?

What team supports parents with their next infant after sudden infant death syndrome?

A
  • Lullaby trust
  • CONI team (provide extra support, resuscitation training, access to monitors/equipment)
93
Q

What charity can help families affected by sudden infant death syndrome?

What team supports parents with their next infant after sudden infant death syndrome?

A
  • Lullaby trust
  • CONI team (provide extra support, resuscitation training, access to monitors/equipment)
94
Q

What are intraventricular haemorrhages?

A
  • Haemorrhage into ventricles in brain
  • Occurs almost always in premature babies or those with low birth weight (<1000g) as blood vessels are more fragile
95
Q

How is intraventricular haemorrhage diagnosed?

A

Based on clinical features and ultrasound of head (all babies <32 weeks should have one in first few days of life)

96
Q

State some clinical features of intraventricular haemorrhages in neonates

A
  • tense anterior fontanelle
  • apnoeas
  • pallor and associated drop in haematocrit
  • limp, unresponsive infant
  • seizures
97
Q

Describe different grades of IVH in neonate

A
98
Q

Discuss the management of intraventricular haemorrhages

A
  • Mostly supportive care (circulatory, respiratory & coagulopathy support)
  • May need blood transfusion
  • Hydrocephalus and rising ICP may need ventriculoperitoneal shunt

*Corticosteroids can be given to mother to reduce risk of IVH if at risk of premature delivery

99
Q

Discuss the prognosis of IVH in neonates

A
  • Hydrocephalus
  • Developmental delay
  • Hearing loss
  • Vision loss
  • Brain damage
  • Death
100
Q

What is chronic lung disease of prematurity also known as?

Which babies does it occur in?

A

Bronchopulmonary dysplasia

Born <28 weeks gestation

101
Q

Describe clinical features of chronic lung disease of prematurity

A

Suffered respiratory distress syndrome at birth and have:

  • Low oxygen sats
  • Increased work of breathing
  • Poor feeding & weight gain
  • Crackles & wheeze on auscultation
  • Increased susceptibility to infection
102
Q

How is chronic lung disease of prematurity diagnosed?

A

Diagnoses based on CXR changes (ground glass appearance) when infant requires oxygen therapy after 36 weeks gestational age

103
Q

Discuss prevention of chronic lung disease of prematurity

A
  • Corticosteroids to mother showing signs of premature labour at <36 weeks gestation
  • Once neonate born:
    • CPAP rather than intubation & ventilation where possible
    • Use caffeine to stimulate respiratory effort
    • Not over-oxygenating with supplementary oxygen
104
Q

Discuss management of chronic lung disease of prematurity

A
  • May be sent home with low dose oxygen via NC (e.g. 0.01L/min. Do formal sleep study to help guide management). Wean off over 1st year of life.
  • Protection against RSV with palivizumab monthly injections
105
Q

Neonatal hypoglycaemia is common especially in first 24hrs of life; true or false?

A

True (only problem when it is persistent

106
Q

Define hypoglycaemia in a neonate

A

=2.6mmol/L

107
Q

State signs & symptoms of hypoglycaemia in neonates

A
  • Altered level of consciousness (coma, lethargy, hypotonia, stupor, irritability)
  • Hypothermia
  • Apnoea
  • High pitched cry
  • Cyanosis
  • Pallor
  • Abnormal feeding behaviour after previously feeding well
  • Seizures
  • Tremor and jitteriness (jitteriness - excessive repetitive movements of one or more limbs, which is unprovoked and not in response to a stimulus)
  • Abnormal feeding behaviour (not waking for feeds, not sucking effectively, appearing unsettled and demanding very frequent feeds), especially after a period of feeding well may be indicative of hypoglycaemia.
108
Q

State some potential causes of neonatal hypoglycaemia

A
109
Q

Discuss the management of neonatal hypoglycaemia

A

Asymptomatic

  • Encourage normal feeding (breast or bottle)- aim 10-15ml/kg in 3hrly feed volumes
  • Monitor blood glucose
  • Consider administration of 40% buccal dextrose as 200mg/kg as part of feeding plan

Symptomatic or very low

  • Admit to neonatal unit (<1mmol/L)
  • IV infusion 10% dextrose or if unable to get IV access 40% buccal dextrose as 200mg/kg as part of feeding plan
110
Q

State some potential complications of neonatal hypoglycaemia

A
  • Neurologic damage that results in mental retardation
  • Developmental delay
  • Recurrent seizure activity
111
Q

State some common birth injuries

A
  • Caput succedaneum
  • Cephalohaematoma
  • Fractured clavicle
  • Erbs palsy
  • Facial paralysis
112
Q

For caput succedaneum, discuss:

  • What it is
  • Cause
  • Presentation
A
  • Oedematous swelling on scalp outside/external to periosteal layer of scalp
  • Caused by pressure to specific area of scalp during traumatic, prolonged or instrumental delivery
  • Presentation:
    • Soft, puff swelling
    • Crosses suture lines
113
Q

For cephalohaematoma, discuss:

  • What it is
  • Cause
  • Presentation
  • Increased risk of….?
A
  • Collection of blood between skull and periosteum
  • Due to damage to blood vessels during traumatic, prolonged or instrumental delivery “traumatic subperiosteal haematoma”
  • Presentation:
    • Lump that does not cross suture lines
    • May have discolouration of skin in affected area
    • Most commonly affects parietal area
  • Increased risk of anaemia and jaundice (hence monitor)
114
Q

Compare caput succedaneum and cephalohaematomas, consider:

  • Time of presentation
  • Presentation itself
  • Resolution
A
115
Q

For facial paralysis (as a complication of birth), discuss:

  • What kind of delivery typically associated with
  • Prognosis
A
  • Forceps delivery
  • Usually spontaneously returns in a few months but it not then may require surgical input
116
Q

For Erb’s palsy, discuss:

  • Pathophysiology
  • What associated with
  • Presentation
  • Prognosis
A
  • Injury to C5/C6 nerves of brachial plexus
  • Associated with shoulder dystocia, large birth weight, traumatic or instrumental delivery
  • Presentation is ‘waiter’s tip appearance’:
    • Internally rotated shoulder
    • Extended elbow
    • Flexed wrist
    • Pronated wrist
    • Lack of movement in affected arm
  • Function normally returns in a few months but it doesn’t may require neurosurgical input
117
Q

For a fractured clavicle (due to birth), discuss:

  • What it is associated with
  • Presentation
  • Investigations
  • Management
  • Complications
A
  • Associated with shoulder dystocia, large birth weight, traumatic or instrumental delivery
  • Presentation:
    • Noticeable lack of movement in affected arm
    • Asymmetry of shoulders (affected shoulder lower)
    • Pain & distress on movement of arm
  • Confirm via ultrasound or x-ray
  • Conservative management occasionally with immobilisation of arm; usually heals well
  • Main complication is damage to brachial plexus leading to nerve palsy
118
Q

How much milk should a baby have per day?

A
  • 60mls/kg/day on day 1
  • 90mls/kg/day on day 2
  • 120mls/kg/day on day 3
  • 150mls/kg/day on day 4 and onwards
119
Q

What is responsive feedings?

Give some examples of hunger cues

A

Responsive feeding involves recognising baby’s hunger and fullness cues and feeding in response to these

120
Q

If a baby presents with feeding problems what investigations may you consider?

A
  • Blood gas (will give glucose, also others e.g. Na+)
  • U&Es
  • CRP
  • FBC
  • Split bilirubin
121
Q

What kinds of questions should you ask in history if infant presents with feeding problems?

A
  • Feeding questions
    • Breast or bottle
    • How much (bottle) and how often
    • How long (breast) and how often
    • Latching well (breast)
    • Does mum hear them sucking and swallowing (breast)
    • Does mum feel relief after feeding (breast)
    • Behaviour of baby (e.g. irritable around feeding, comfortable)
    • Associated symptoms
  • Baby’s health
    • Wet nappies (from day 6 onwards expect 6-8)
    • Dirty nappys (at least 3 by from day 3 onwards)
    • Colour of poo (should have changed from green to seedy yellow by day 3)
  • Mum’s health
    • Any issues with her health
  • Birth history
    • C-section or vaginal delivery
    • Complications in pregnancy
    • Complications in baby
122
Q

What is meconium aspiration syndrome?

A
  • Respiratory distress in newborn as a result of meconium in trachea
  • Risk factors:
    • Post-term baby (>42 weeks)
    • Maternal hypertension
    • Pre-eclampsia
    • Smoking
    • Substance abuse
    • Chorioamnionitis
123
Q

Describe presentation/clinical features of meconium aspiration

A

Often neonates present soon after birth with respiratory distress but some may be asymptomatic initially and develop respiratory distress later

124
Q

How is meconium aspiration syndrome diagnosed?

A
  • CXR: may see consolidation atelectasis, hyperexpanded lungs, pneumothorax
  • FBC: rule out infection
  • CRP: rule out infection
  • Blood culture: rule out infection
125
Q

Discuss the management of meconium aspiration syndrome

A
  • If no risk factors for infection and vigorous at birth allow to stay with mum and observe
  • If risk factors for infection or lab findings suggestive of infections then broad spec abx (e.g. ampicillin & gentamycin)
  • If mild respiratory distress, give oxygen to maintain sats 92-97%, nutritional support if needed, abx only if risk factors or lab findings suggestive of infeciton
  • If moderate to severe reps distress: CPAP (may need intubation & ventilation), abx regardless, nutritional support,
126
Q

State some potential complications of meconium aspiration syndrome- highlighting common ones

A
  • Pneumothorax (thick meconium get stuck and allows air to move into lungs during inspiration but obstructs flow of air out of lungs in expiration)
  • Persistent pulmonary hypertension
  • Pneumomediastinum
  • Seizure (secondary to hypoxic ischaemia)
  • Cerebral palsy (secondary to hypoxic ischaemia)

*NOTE: risk of infection low as meconium is sterile

127
Q

What is transient tachypnoea of newborn?

What might you see on CXR?

Discuss the management

A

Transient tachypnoea of the newborn (TTN) is the commonest cause of respiratory distress in the newborn period. It is caused by delayed resorption of fluid in the lungs

It is more common following Caesarean sections, possibly due to the lung fluid not being ‘squeezed out’ during the passage through the birth canal

Chest x-ray may show hyperinflation of the lungs and fluid in the horizontal fissure

Supplementary oxygen may be required to maintain oxygen saturations. Transient tachypnoea of the newborn usually settles within 1-2 days

128
Q

Put the following in order of most common to least common: isolated cleft palate, isolated cleft lip, combined cleft lip & palate

A
  • Combined cleft lip & palate (45%)
  • Isolated cleft palate (40%)
  • Isolated cleft lip (15%)
129
Q

Briefly, in one line, describe pathophysiology behind:

  • Cleft lip
  • Cleft palate
A
  • Cleft lip: failure of fronto-nasal and maxillary processes to fuse
  • Cleft palate: failure of palatine processes and nasal septum to fuse
130
Q

Use of what medications during pregnancy increases risk of cleft lip and cleft palate

A

Anti-epileptics

131
Q

State some problems associated with cleft lip & palate

A
  • Feeding (orthodontic devices can help)
  • Speech (with therapy 75% develop normal speech)
  • Increased risk of otitis media (cleft palate)
132
Q

Discuss the management of:

  • Cleft lip
  • Cleft palate
A
  • Cleft lip: repair within fist week to first 3 months of life
  • Cleft palate: repaired between 6-12 months of age

Yr4: Child Health (21 decks)

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