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Paediatrics > Neonatology > Flashcards

Neonatology Flashcards

1
Q

What maternal factors indicate high risk pregnancy?

A

Unbooked
Antepartum bleeding
Maternal comorbidities - eclampsia, GDM, renal disease
Age
Infections
Substance abuse

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2
Q

What fetal factory’s indicate high risk pregnancy?

A

Multiple gestation
Congenital malformation
Prem
Intrauterine growth restriction
Poly/oligohydramios

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3
Q

What labour and delivery factors indicate high risk pregnancy?

A

Abnormal CTG
Prolonged ROM
Cord prolapse
Meconium stained liquor
Emergency c/s
General anaesthesia
Abnormal presentation
Prolonged labour

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4
Q

What temperature should the delivery room be?

A

24-26 degrees celcius

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5
Q

What temperature must a newborn be kept?

A

36,5-37,5 degrees celcius

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6
Q

What position must you place the baby in to maintain the airway and what can help you do this?

A

Sniffing position
Towel under shoulders

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7
Q

Who should be suctioned?

A

ONLY if obvious obstruction to spontaneous breathing - must be under direct vision
NOT routinely done

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8
Q

What methods are used to provide positive pressure ventilation?

A

Bag Mask ventilation
AMBU (artificial breathing manual unit)

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9
Q

When would you intubate a newborn?

A

Ineffective mask ventilation
Chest compressions required
Prolonged ventilation
Special circumstances eg CDH

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10
Q

How do you determine the depth the tube must be inserted?

A

Weight(kg) + 6cm = depth (cm)

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11
Q

How do you verify correct ETT placement?

A

Symmetrical chest rise
Misting of tubes
Auscultation
HR and colour improvement

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12
Q

What are the tube sizes used for neonates?

A

<1000g = 2.5
1000-2000g = 3
2000-3000 = 3,5
3000-4000 = 3.5/4

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13
Q

What is the ratio of compressions to breathes in resus of neonates?

A

3:1

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14
Q

What is the dose and concentration of adrenaline in neonatal resus?

A

IV: 0,1-0,3ml/kg of 1:10000 adrenaline
ETT: 1ml/kg of 1:10000 adrenaline

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15
Q

What and how much fluid is used for volume expansion in newborn?

A

10ml/kg of isotonic crystalloid (NS) /blood IV over 5-10mins

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16
Q

If you have a poor response to volume expansion and adrenaline in resus of newborn, what next?

A

Consider pneumothorax
Check glucose : 2-4ml/kg 10% dextrose solution IVI

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17
Q

What composes post-resus care of the newborn?

A

Maintain normothermia
Consider therapeutic hypothermia in hypoxia ischaemic encephalopathy
Monitor vitals and glucose
Transport to neonatal unit in closed incubator
Document resus
Inform parents

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18
Q

What are the cardiovascular changes that occur after the first breathe?

A

①↓ pulmonary vascular resistance
② No flow through ductus venous
③ ↓ systemic resistance (no more low pressure placenta)
④ reversal of shunt through foreman ovale
⑤ reversal of shunt through ductus arteriosus

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19
Q

What factors are considered in the APGAR score?

A

HR
Respiratory
Colour
Tone
Response to stimulation

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20
Q

What are RF for birth injury?

A

Assisted delivery
Abnormal presentation
Precipitous delivery
Prematurity
Macrosomia

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21
Q

Define birth injury

A

Traumatic event at birth causing structural/functional destruction of the neonates body

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22
Q

Categorise birth injuries

A

Soft tissue
Cranial injuries
Nerve injuries
Fractures
Intra-abdominal injuries
Sub conjunctival haemorrhage

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23
Q

What kind of soft tissue birth injuries occur?

A

Eccymosis and bruising
Petechiae (localised vs generalised)
Subcutaneous fat necrosis
Lacerations
Erythema and abrasions

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24
Q

What kind of cranial brith injures occur?

A

Extracranial
- moulding
- cephalhaematoma
- caput
- subapomeurotic bleed

Intracranial
- subdural haemorrhage
- epidural haemorrhage
- subarachnoid haemorrhage
- intraventricular haemorrhage

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25
Q

Which extracranial injury is a medical emergency and how is it managed?

A

Subaponeurotic haemorrhage.

Monitor haemaglobinuria, serial head circumference, vitals
Supportive management - paracetamol for pain relief
Volume resus if shocked/transfusion
Check for jaundice as bleed is resolved

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26
Q

What nerve injuries occur during birthing?

A

Phrenic
Facial
Brachial

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27
Q

What fractures are common during birth?

A

Clavicle
Cranium
Humerus
Femur

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28
Q

What are some minor abnormalities commonly seen in the first few days of life?

A

Club foot
Vaginal discharge/ hymen tags
Vaginal bleeding
Peripheral cyanosis
Subconjunctival haemorrhage
Epstein pearls
Umbilical hernia
Breast enlargement
Positional talipes vs club foot
Negus simplex
Negus flammeus
Milia and miliaria
Erythema toxicum neonatorum
Transient pustular melanosis
Dermal melanosis
Transient vascular phenomena
Sucking blisters
Neonatal teeth
Gingival cysts
Polydactyly
Preauricular skin tags

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29
Q

Define neonatal hypoglycaemia

A

Glucose measuring <2,6mmol/l

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30
Q

Signs/sx of neonatal hypoglycaemia

A

Jittery/irritable/high-pitched cry
Lethargic/decreased consciousness
Hypotonia
Apnoea
Seizures

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31
Q

Risk factors for neonatal hypoglycaemia

A

Antenatal: maternal diabetes, maternal obesity, maternal B-blocker use

Neonatal: intrauterine growth restriction, prem, large for GA, sepsis, iatrogenic (no feeds/fluids), polycytaemia, HIE, hypothermia, rhesus allo-immune disease

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32
Q

What are the causes for PERSISTENT hypoglycaemia?

A

Hyperinsulinaemia
Endocrine deficiency eg GH deficiency, adrenal insufficiency
Inborn errors of metabolism

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33
Q

What investigations do you do in persistent hypoglycaemia?

A

Serum glucose
Serum insulin
Serum cortisol and GH
Sonar of adrenals

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34
Q

How do you manage neonatal hypoglycaemia?

A

Prevention: early feeding
Asymptomatic/glucose 1,4-2,5: enteral feeds
Symptomatic/glucose <1,4: IV bolus 10% dextrose followed by continuous infusion
Specific management depending on cause

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35
Q

What is neonatal encephalopathy?

A

Disturbed neurological function in the earliest days of life in infants born >/= 35 weeks GA

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36
Q

How does a patient with neonatal encephalopathy present?

A

Abnormal state of consciousness (hyper alert, irritable, lethargic, obtunded)
Decreased spontaneous movements
Poor tone/abnormal posturing
Absent/partial primitive reflexes
Difficulty initiating and maintaining respiration
Feeding difficulties
Seizures

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37
Q

What are the causes of neonatal encephalopathy?

A

Meningitis
Hypoxia ichaemic encephalopathy
Withdrawal from maternal “drugs”
Neonatal epilepsy syndromes
Genetic
Metabolic disorders
Structural brain abnormalities
Intraventricular haemorrhage
Non-accidental injury
Perinatal stroke

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38
Q

What are the abnormal signs consistent with hypoxia ischaemic encephalopathy?

A

Apgar <5/10 at 5 and 10 minutes

Foetal umbilical artery acid acidaemia (pH <7 or base deficit >12 or both)

Presence of multi organ dysfunction (brain, bone marrow, heart, lungs, kidneys, intestine)

Neuroimagining evidence of acute brain injury (deep gray matter and peri-Rolandic motor cortex)

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39
Q

What do you do when a patient has abnormal signs consistent with acute hypoxia encephalopathy?

A

Modified sarnat score
Or
Thompson score

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40
Q

What sentinel events are RF for suspected HIE?

A

Maternal
>cardioresp arrest
> impaired O2 eg asthma/PE
> hypovolaemic shock

Foetal
> exsanguination
• foetal maternal haemorrhage
• twin-twin transfusion syndrome
> cardiac arrhythmias in-utero

Uteroplacental
>abruptio
> cord prolapse
> ruptured placenta
>Hyperstimulation with oxytocin drugs

CTG patterns
>absent variability + recurrent late/variable decal. / Brady
> foetal tachy + recurrent decel

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41
Q

What is jaundice?

A

The yellow discolouration of the skin, sclera and mucus membranes

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42
Q

How do you determine the serum bilirubin?

A

NOT clinical
Non-invasive transcutaneous bilirubin
Or
Total serum bilirubin

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43
Q

Categorise jaundice

A

Unconjugated - indirect (fat soluble)
Conjugated - direct (water soluble)

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44
Q

Categorise the pathological causes of increased RBC destruction in unconjugated jaundice

A

Allo-immune
> Rh incompatibility
> ABO incompatibility
> minor antigen incompatibilities

Non-immune haemolysis
>RBC membrane defects
>RBC haemaglobinuria defects
>RBC enzyme defects

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45
Q

Categorise the non-pathological causes of increased unconjugated bilirubin production

A

Intravascular
>increased RBC breakdown (shorter RBC lifespan)

Extravascular
>bruising
>cephalhematoma
>subaponourotic bleed

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46
Q

What is the exception with regards to blood group antibodies and what problem does this cause?

A

All blood groups have IgM antibodies but group O has IgG antibodies.

If mom is group O, her anti A and anti B IgG antibodies can cross the placenta and cause haemolysis of the fetal blood.

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47
Q

How does Rh incompatibility work?

A

This requires sensitisation unlike ABO incompatibility.
First pregnancy: mom Rh neg and baby Rh pos = mom forms anti Rh IgG antibodies.

Second pregnancy: Moms anti Rh IgG antibodies cross placenta and attack fell Rh positive blood.

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48
Q

What are examples of hereditary RBC membrane defects?

A

Hereditary spherocytosis
Hereditary elliptocytosis

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49
Q

What is an example of RBC haemaglobinuria defects a.

A

Alpha thalassemia.

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50
Q

What are two examples of RBC enzyme defects?

A

Glucose 6 phosphate dehydrogenase deficiency
Pyruvate kinase deficiency

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51
Q

What investigations would diagnose intravascular haemolysis?

A

Haemaglobin decreased
Reticulocyte count increased
LDH increased
Haptoglobin decreased
RBC fragments on smear

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52
Q

What are causes of decreased hepatic uptake and conjugation of bilirubin?

A

Physiological
>immature liver enzymes needed for conjugation
>decreased net hepatic uptake

Pathological
>breast milk jaundice
>hypothyroidism
>Gilbert’s disease
>crigler-Najjar syndromes type 1 and 2

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53
Q

What are causes of increased henterohepatic circulation in unconjugated jaundice?

A

Pathological
>breast feeding failure
>meconium lieu’s
>hirschsprungs disease
>intestinal atresia

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54
Q

Main categories of causes of unconjugated hyperbilirubinaemia

A

Increased RBC destruction
Decreased hepatic uptake
Increased enterohepatic circulation

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55
Q

How do you investigate neonatal jaundice?

A

① total bilirubin+ conjugated bilirubin
= calculate unconjugated
② intravascular haemolysis? (Rh/ABO/non-immune)
• No » extravascular
• yes → direct Coombs test
③ positive direct Coombs = rh/abo incompatibility
negative = membrane /haem/ enzyme defects

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56
Q

How do you decide if it is pathological or physiological jaundice?

A

Refer to table 1

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57
Q

When is phototherapy contraindicated and why?

A

Conjugated hyperbilirubinaemia -> causes bronze baby syndrome

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58
Q

What are the indications for phototherapy?

A

Absolute
>see phototherapy chart
Prophylactic
>ELBW Iinfants
> extravascular bloood collections
>severe bruising, cephalhaematoma, IVH

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59
Q

What are complications of phototherapy?

A

Impaired bonding
Increased insensible water loss (older lights generate heat)
Watery stools
Maculopapular skin rash
Lethargy
Potential for retinal damage

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60
Q

How does phototherapy work?

A

It converts unconjugated bilirubin which is fat solvable into a harmless water solvable molecule which can be excreted in the urine and bile

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61
Q

What are the types of phototherapy?

A

Fluorescent tubes
Halogen bulbs
LED lights

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62
Q

When do you use a lower line for exchange transfusion?

A

If there is sepsis, haemolysis, acidosis or asphyxia

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63
Q

What are the indications for exchange transfusion?

A

① TSB > 85 above exchange threshold at presentation and not expected to fall below within 6hrs
② TSB remains above exchange line despite 6 hrs of intensive phototherapy
③ any acute signs of bilirubin encephalopathy
④ TSB rising quickly despite intensive phototherapy (>17umol/L per hour)

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64
Q

How does exchange transfusion works.

A

Removes maternal antibodies, and replaces87% of newborns blood with new blood. The bilirubin is removed from the plasma.

The blood for exchange is fresh, irradiated and reconstituted whole blood from packed RBC Oneg and FFP (AB)
Exchange double the volume
>160ml/kg term and 180ml/kg preterm
>5ml/kg at a time (max 20ml) with each cycle +- 2 mins
>venous umbilical catheter is ideal

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65
Q

Complications of exchange transfusion

A

Hypocalcaemia
Hypoglycaemia
Hyperkalaemia
Vasospasm and arrhythmias
Bleeding
Infections
Graft vs host disease
Hypothermia
Volume overload

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66
Q

What is the last option to treat unconjugated hyperbilirubinaemia aside from phototherapy and exchange transfusion? Why is it used?

A

IV immunoglobulin

Exchange transfusion has high risk complications. IVIG reduces rate of haemolysis and therefore reduces need for exchange transfusions.

Still needs more evidence

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67
Q

What are complications of prematurity?

A

-RDS
-retinopathy of prematurity
-PDA
-necrotising enterocolitis
-risk for hypothermia
-intraventricular haemorrhage
-apnoea of prematurity
-chronic lung disease of prematurity
-metabolic bone disease of prematurity

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68
Q

What strategies are used to prevent MTCT according to the PMTCT guidelines?

A

1) minimise infant exposure to virus by suppressing maternal VL
2) post exposure prophylaxis of the infant

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69
Q

What are the principles of infant prophylaxis at birth?

A

Principle 1: risk of baby determined by the VL of the mom at birth
Principle 2: infant is high risk until proven low risk
Principle 3: Continue prophylaxis until moms VL is suppressed

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70
Q

What determines high vs low risk neonate?

A

High risk = VL>1000 at birth or in last 12 weeks OR unknown VL
Low risk = VL<1000

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71
Q

What is high risk vs low risk prophylaxis according to PMTCT guidelines?

A

Low risk = Nevirapine once daily x 6 weeks regardless of feeding choice then cotrimoxazole until PCR negative >6 weeks after breastfeeding cessation and infant clinically HIV negative.

High risk = Nevirapine once daily x 12 weeks minimum + AZT twice daily x 6 weeks in the breastfeeding infant
Nevirapine x 6 weeks in the exclusively formula fed infant then cotrimoxazole

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72
Q

What does Breastfeeding Plus refer to?

A

It refers to infant feeding in the context of HIV. Integration of nutrition, nurture and medical intervention.

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73
Q

How long is exclusive breastfeeding recommended for?

A

First 6 months after which introduction of nutritionally adequate complementary feeding initiated.

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74
Q

When is breastfeeding NOT recommended?

A

A mother failing 2nd or 3rd line ART regimen.

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75
Q

What are the explanations for a baby testing positive during breastfeeding period?

A

1) Mom unsupressed (noncompliance/resistance)
2) False negative PCR at birth (birth PCR only tests for intrauterine transmission)
3) maternal seroconversion during breastfeeding
4) baby not fully tested previously

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76
Q

What measures are in place to identify and treat infected children as soon as possible?

A

Birth PCR
10week PCR
6 month PCR for HIV exposed infants
18 month Rapid/Elisa for ALL children (aligned with 18month maternal VL)
Thereafter, when indicated (when symptomatic)

6 weeks post BF cessation

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77
Q

How do we care for HIV exposed, negative children? What are they at risk of?

A

Follow up growth and development
Symptoms of anaemia
Poor birth outcomes
Maternal illness or death
History of hospitalisation

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78
Q

How frequently do pregnant women need to be tested for HIV?

A

At confirmation of pregnancy
At every antenatal visit
At birth

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79
Q

When do breastfeeding women need to be tested for HIV?

A

Every 3 months throughout breastfeeding

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80
Q

When must someone who has been exposed to HIV be tested?

A

Immediately
6 weeks post exposure (window period)
3 months post exposure

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81
Q

What is the 90-90-90 goal?

A

90% of the HIV population should know their status
90% of HIV positive patients who know their status should initiate ARV’s
90% of those who initiated ARV’s should have a suppressed VL

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82
Q

What is the modified sarnat score, what does it consist of and what is it used for?

A

It is a scoring system used to grade HIE (normal, moderate or severe encephalopathy) and decide if the patient qualifies for therapeutic hypothermia.
3 out of 6 categories are required

LOC
Posture
Spontaneous activity
Tone
Rimitive reflexes (Moro and suck)
Autonomic system (pupils, HR, Resp)

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83
Q

What is the Thompson score, what does it consist of and what is it used for?

A

It is used to score a baby to determine its risk of HIE.
Consists of:
1) limb tone
2) LOC
3) visible fits
4) posture
5) Moro
6) grasp
7) suck
8) resp effort
9) fontanel

Each category is given a score of 0-3. You add up the score at the end,
0=normal
1-10 = Mild
11-14 = moderate
15-22 = severe HIE

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84
Q

What are the long term neurodevelopmental sequelae of HIE?

A

Epilepsy
Cognitive impairment and developmental delay or learning difficulty
Blindness/vision defects
Cerebral palsy
Gross motor and coordination problems
Behavioural problems
Hearing loss/deafness

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85
Q

What multi organ involvement is expected in HIE?

A

Respiratory - PPH, Resp failure
Brain - seizures
Cardiac - hypotension, arrhythmias, ischaemia
Hepatic - elevated liver enzymes, coagulopathy
Bone marrow - thrombocytopenia
Renal - acute kidney injury
GIT - necrotising enterocolitis
Metabolic - hyponatraemia, hypocalcaemia, hypoglycaemia, hyperglycaemia

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86
Q

What are the neuroimagining patterns and correlating clinical pathologies in HIE?

A

GA 26 - 36 weeks = ishaemias → p-eriventricular white matter » spastic diplegia

GA > 36weeks =
1) partial asphyxia’s event » parasaggital watershed areas +/- cortex = behavioural problems, language delays, cognitive deficits, possible epilepsy

2) acute total asphyxia → deep gray matter + perirolandic cortex = dyskinetic cp, spastic quad cp, cognitive impairment

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87
Q

How do you identify a baby with hypoxia ischaemic encephalopathy?

A

There is no gold stand diagnosis (most clinical signs/investigations are non-specific)

Abnormal signs consistent with HIE
Contributing events in close proximity to labour and delivery of RF
Long term neurodevelopmental outcome

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88
Q

What contributing events are RF for HIE?

A

Preconception
- advanced maternal age
- family history seizures/neuro disease
- infertility tx
- previous neonatal death

Antepartum
①fetal
- multi gestation.
- genetic abnormality
- congenital malformations
- IUGR
- breech
② maternal
- prothrombotic disease
- thyroid disease
- severe pre-eclampsia /chorioamnionitis
- antepartum haemorrhage
-trauma

Intrapartum
- abnormal fetas HR
- thick meconium
- assisted vag delivery
- emergency c/s
- abnormal lie
- shoulder dystopia
- abruptio
-GA

Postnatal
- 2° to pulm/cardio/ neuro disease

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89
Q

What is the management of HIE?

A

① supportive
- ABC
- glucose nb
- normothermia
- fluid restriction
- monitor for seizures (phenobarbital, phenytoin, lorazepam)

②neuroprotective
- therapeutic hypothermia (decrease progression of injury)

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90
Q

What is the MOA of therapeutic hypothermia?

A

↓ 2° cell damage
- a cerebral metabolism + energy utilisation
- inhibits inflammatory cascade
- suppresses free radical activity

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91
Q

What are the criteria for therapeutic hypothermia?

A

Must be <6hrs of life AND GA >36weeks

Physiological criteria:
-5 + 10 min APGAR <5
Or
-Ph < 7 or base def > 16
Or
Ongoing birth rhesus >10 mins

Neurological criteria:
-Moderate - severe on modified Sarnat +/- abnormal Thompson score

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92
Q

How do you diagnose conjugated jaundice?

A

Conjugated bilirubin >20% of total serum bilirubin

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93
Q

What enzyme converts unconjugated bilirubin to conjugated bilirubin?

A

UGT (glucuronosyltransferase)

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94
Q

What are the pathological causes of conjugated bilirubinaemia?

A

① infections
- torches
- parvovirus B19
- HIV
- sepsis (GBS, staph)
② Metabolic / genetic
- galactosaemia
- cystic fibrosis
- tyrosenaemia
③ endocrine
- hypothyroidism
- hypopituitism
④ Allo immune
- gestational allo immune liver disease (GALD)
⑤toxins
- drugs (inh)
- parental nutrition
⑥ Miscellan
- Idiopathic neonatal hepatitis

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95
Q

What liver enzymes indicate hepatocellular cause of conjugated jaundice and what ratios?

A

Increased ALT and AST
By 2-10 times

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96
Q

What are the cholestatic causes of conjugated hyperbilirubinaemia?

A

Extrahepatic
- biliary atresia
- biliary -cysts
- choledocal stones
- tumor /mass
- Neonatal sclerosing cholangitis

Intrahepatic
- alagille syndrome
-Intrahepatic biliary atresia

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97
Q

What are the clinical findings of conjugated jaundice?

A

Encephalopathy
-raised ammonia
-Hypoglycaemia

Cataracts
-metabolic disease
-congenital infection

Bleeding
-coagulopathy

Failure to thrive
-advanced liver disease
- sepsis
-metabolic disease

Portal hypertension
-dilated abdominal veins
-splenomegaly
-ascites

Acholic stools and dark
-obstructive jaundice

Firm hepatomegaly
-biliary atresia

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98
Q

How do you manage conjugated jaundice?

A
  • Fat solvable vitamin supplementation (AEDK)
  • MCT oil (medium chain triglyceride)
  • Adequate calories
  • Promote bile excretion (urodeoxycholic acid)
  • Galactose is (avoid lactose containing feeds)
  • Surgical - extrahepatic biliary atresia, cholodocal cysts and stones, masses
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99
Q

What are the complications of conjugated jaundice?

A

Increased PT and PTT
Albumin
Ammonia
Glucose

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100
Q

What investigations are done for suspected hepatic cause of conjugated jaundice?

A

LFT = elevated AST and ALT

  • infections
  • GALT
  • A-1-AT
    -thyroid functions
    -serum ferritin
    -sweat test/fecal elastase
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101
Q

What investigations do you do to investigate conjugated/obstructive jaundice?

A

Urine
-dipstix -> bilirubin
-pale stool

Abdo u/s
-presence of gallbladder
-extrahepatic bile ducts
-choledochal cysts or stones
-bile sludge

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102
Q

Which type of PCKD presents in the neonatal period?

A

Autosomal recessive

Dysfunctional kidneys
Multicyctic dysplastic kidneys with cysts in the renal parenchyma

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103
Q

What are examples of CAKUT?

A

Bilateral
-posterior urethral valve
-bladder neck obstruction

Unilateral
-posterior pelvoureteric junction obstruction
-vesicoureteric junction obstruction

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104
Q

How do you detect CAKUT?

A

Kidney sonar antenatally

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105
Q

What is a posterior urethral valve?

A

A mucosal fold that obstructs urine flow leading to hydronephrosis
-key hole appearance
-thickening of bladder wall

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106
Q

How is hypernatraemic dehydration managed?

A

1) calculate fluid losses and replace slowly over 24-48hrs
2) slow rehydration with a reduction in the sodium level by 0,5-1mmol/L per hour
Reduction faster = cerebral oedema

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107
Q

List 4 causes of Hyperkalaemia

A

1)increased administration
2)congenital adrenal hyperplasia
3) kidney injury/Impairment
4) haemolysis tube specimen

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108
Q

What is the most common bacterial infection in the neonate?

A

UTI

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109
Q

RF for UTI in neonates

A

1)prematurity
2) Caucasian
3) congenital abnormalities of the kidney and urinary tract

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110
Q

What is important to investigate when you diagnose a UTI in a neonate?

A

Sonar for exclusion of CAKUT NB

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111
Q

What are the 3 most common organisms that cause UTI in neonates?

A

E.coli
Klebsiella pneumonia
Enterobacter spp

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112
Q

What is optimal nutrition in infants?

A

1) exclusive breastfeeding for 6 months
2) complementary feeding (nutritionally adequate and safe) from 6months of age with continued breastfeeding up to 2 years of age

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113
Q

What is exclusive breastfeeding?

A

Infant receives breast milk only and no other liquids or solids (including water) with the exceptions of oral rehydration solution, vitamin/mineral supplements and medication.

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114
Q

What are the benefits of exclusive breastfeeding for 6 months?

A

-PMTCT
-provides all nutritional needs for first 6 months of life
-benefits increase with amount and duration of breastfeeding
-far lower risk of death from diarrhoea c9mpared to partial BF/formula
-reduces risk of diarrhoea and resp illness compared with exclusive BF 3-4 months only

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115
Q

What beneficial factors are in breast milk?

A

ANTI INFECTIVE FACTORS
-immunoglobulins (IgA)
-white blood cells (lymph, neutrophils, macrophages)
-whey protein (kills pathogens)
-oligosaccharides (prevent bacterial attach,ent to intestinal mucosa)

GROWTH FACTORS
-epidermal GF (intestinal mucosa)
-GF’s for development and maturation of nerves and retina

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116
Q

What are the benefits of breast feeding for the mother?

A

SHORT TERM
-decreases risk PPH
-bonding with baby
-milk is FREE, convenient, readily available
-accelerate recovery pre-pregnancy weight

LONG TERM
-delay return of fertility
-decreases risk of breast and ovarian cancer
-decreased risk DM T2, HT, hyperlipidaemia, CV disease

117
Q

Benefits of breastfeeding for infant?

A

SHORT TERM
-ideal nutrition
-healthy weight gain
-milk easily digested
-maintains GI integrity
-immunity (less severe and common infections)
-decreased risk SIDS
-6-10x less likely to die in first months of life

LONG TERM
-less immunological diseases (asthma, DMT1)
-better cognitive fxn
-less obesity
-less CV risk in adulthood
-lower childhood leukaemia risk

118
Q

What are medical reasons for using breast milk substitutes?

A

Baby
-different nutritional needs eg galactosemia
-in addition to breast milk eg hypoglycaemia
-separation from mother

mom
-maternal illness
-maternal medication eg radioactive iodine
-substance abuse
-HIV with high VL on 2nd line tx

119
Q

What is the target feed volume for infants?

A

Term = 150ml/kg/day
Prem = 160-180ml/kg/day

120
Q

What is the calorie requirements for neonates?

A

Prem = 120-150kcal/kg/day
Term = 100kcal/kg/day

121
Q

Who are supplements given to and what supplements are given?

A

Iron
Vitamin D
Multivitamin

Given to preterm babies once on full feeds as they don’t have adequate iron stores,rapid growth (osteopenia of not supplemented)

122
Q

What factors promote lactation and milk production?

A

-empty breast
-frequent feeding
-calm environment
-medication

123
Q

What factors inhibit lactation/milk production?

A

-engorged breasts
-stressful environment
-pain, illness
-medication

124
Q

What are the consequences of poor breast attachment?

A

-breast engorgement (not enough milk removed) = pain, blocked ducts, mastitis
-cracked and painful. Ipples
-refusal to feed
-insufficient milk intake
-oversupply of milk

125
Q

What are the signs and sx of Candida in the mother and baby?

A

Mom
-painful breasts. It relieved between feeds
-red/flaky rash on areole with itching and depigmentation

Baby
-oral thrush
-refusal to feed or feed for short time

126
Q

How do you treat Candida infection in mom and baby?

A

Nystatin suspension QID after breastfeeds
Nystatin cream to nipples after feeds
No need to tx mom of only baby symptomatic

127
Q

How does a UTI present in a neonate?

A

YOU NEED A HIGH INDEX OF SUSPICION
(Any neonate with sepsis)

-poor weight gain
-vomiting
-pyrexia
-poor feeding
-lethargy
-diarrhoea
-prolonged jaundice (NB)

128
Q

How do you investigate a UTI in a neonate?

A

GOLD STANDARD = single pathogen culture
-in out catheterisation
-suprapubic aspiration

-Blood = infective markers (CRP, high/low White cell count)
Urine dipstix - leukocytes may be negative due to frequent voiding

129
Q

How do you manage a neonatal UTI?

A

-Start antibiotic tx (start B-road spectrum empirically until culture results are out)
-Repeat urine culture after 48hrs of antibiotics
-Renal u/s for every baby to exclude CAKUT

130
Q

Define acute kidney injury

A

An abrupt decline in the ability to clear waste and to maintain fluid and electrolytes homeostasis

131
Q

What parameters do you use to diagnose AKI?

A

-increase serum creatinine by 0,3G/dl
-increase serum creatinine by 1.5times the baseline
-UO <0,5ml/kg/hr for 6hours

132
Q

How is AKI classified?

A

RIFLE

Risk of renal dysfunction (inc creat 150%)
Injury of the kidney (increased creat 200%)
Failure of kidney function (inc creat by 300%)
Loss of kidney fxn (>4weeks)
End stage kidney disease (>3 months)

133
Q

What are the causes of AKI?

A

Prerenal (decreased blood flow to glomeruli)
-hypovolaemia
-blood loss
-decreased CO
-HIE

Renal
-congenital renal abnormality
-vascular insult (Renal vein thrombosis)
-nephrotoxins
-infection
-uncorrected prerenal

Post-renal (obstructive causes
-congenital obstructive uropathy
-neurogenic bladder

134
Q

How do you investigate AKI?

A

-extensive history (underlying cause)
-examination = fluid status, UO, vitals
-Lab = U&E, CMP, urine analysis
-u/s and Doppler

135
Q

How do you manage AKI?

A

Supportive
-fluid balance
-correct electrolytes and acidosis
-treat hypertension
-avoid nephrotoxin agents
-NB nutritional support (avoid high potassium and phosphate foods)

Persistent and severe = refer to nephro

136
Q

When do you worry about undescended testes?

A

If they have still not descended by 6 months and definitely before 2 years = refer to surgery

137
Q

What is the pathology of an inguinal hernia?

A

Continued latency of processes vaginalis = intermittent injuinal swelling
Not reducible = urgent surgical - risk of strangulation and incarceration

138
Q

What is the pathology of a hydrocele and how is it managed?

A

Peritoneal fluid passes through the processes vaginalis and surrounds the tests (often bilateral)

Management
Resolves spontaneously, no management needed.

139
Q

What are the 3 criteria for hypospadia?

A

Dorsal hood
Ventral chordee
ventral opening of urethra

140
Q

What is the pathophysiology of congenital adrenal hyperplasia?

A

Deficiency in 21 hydroxylase enzyme leading to
- increased testosterone production
-decreased cortisol
-decreased aldosterone

141
Q

What are the resulting effects of congenital adrenal hyperplasia? Ie clinically

A

-decreased cortisol = hypoglycaemia, adrenal crisis in periods of increased stress
-decreased aldosterone = Hyperkalaemia, hyponatraemia
-increased testosterone = virilisation of affected females (enlarged clitoris, ambitious genitalia) and males (darkening of scrotal area, enlarged penis)

142
Q

What happens in salt losing adrenal crisis?

A

Vomiting, weight loss = circulatory collapse +/- hypoglycaemia
Hyponatraemia and Hyperkalaemia

143
Q

What is the management of salt losing adrenal crisis?

A

Supportive
-fluids
-correction of electrolytes
-21 hydroxylase levels
-refer to endocrine for steroid replacement

144
Q

How do you classify/approach a vomiting neonate?

A

Bilious vomiting = intestinal obstruction until proven otherwise

Non-bilious =
1) intestinal obstruction
2) non-obstructive

145
Q

What are causes of non-bilious vomiting?

A

Obstructive
-duodenal/pyloric stenosis
-annular pancreas

Non-obstructive
-physiological (over feeding)
-infection
-CNS (ICP)
-endocrine
-drugs
-cows milk protein allergy

146
Q

What are the causes of bilious vomiting?

A

ALWAYS PATHOLOGICAL

Intestinal obstruction
-Functional = Hirschprungs, ileus
-anatomy = small/large bowel atresia, imperforate anus

147
Q

What is the difference between vomiting vs regurgitation?

A

Vomiting = active, involuntary, forceful expulsion

Regurgitation = passive, effortless progress which happens without force

148
Q

What is the management of vomiting neonate?

A

Stabalize and rehydrate (serial weighing to monitor hydration)

Investigate underlying cause
-FBC (infection?)
-X-ray abdo
-electrolytes (hypochlorite is = pyloric stenosis)
-urea and creat
-blood culture

Treat underlying cause

149
Q

How do you approach a neonate with abdominal distension?

A

1) intestinal obstruction (functional or mechanical -upper/lower GIT)
2) Ileus
3) pneumoperitoneum (intestinal perforation)

150
Q

How do you manage an ileus?

A

Check K (hypokalaemia can worsen the paralysis)
Rest bowel - NPO
NG tube with free drainage to decompress
ID and treat underlying cause

151
Q

How do you manage a pneumoperitoneum?

A

NPO
Insert NG tube on free drainage to decompress
General stabalisation (ABC)
Surgical consult for definitive tx (laparotomy/pencil drain)

152
Q

How does an UGIT obstruction present?

A

Hx: polyhydramnios
Early vomiting
May/may not pass meconium
Abdo distension may develop later

153
Q

How does LGIT obstruction present?

A

Abdominal distension
Delayed/absent passing of meconium
Vomiting = late feature

154
Q

What is the most common type of oesophageal atresia?

A

Proximal atresia with distal oesophageal fistula with trachea

155
Q

How would oesophageal atresia present?

A

Polyhydramnios
Increased Frothy secretions
Choking
Cyantoic spells

156
Q

How do you diagnose oesophageal atresia?

A

NG tube. CXR shows coiling of the NG tube
Or barium swallow

157
Q

How does duodenal atresia presents?

A

-bilious/non-bilious vomiting
-feeding intolerance in first 48-72 hours

158
Q

What findings on the X-ray for duodenal atresia?

A

Double bubble sign

159
Q

What syndrome is associated with duodenal atresia?

A

Trisomy 21

160
Q

How does pyloric stenosis present in a neonate?

A

-projectile vomiting 3-8weeks postnatally
-vomit towards the end of feed
-olive-like mass in right upper quadrant with visible peristalsis

161
Q

What investigations would you do and what would the findings be of pyloric stenosis?

A

U&E - hypokalaemic, hypochloraemic metabolic alkalosis
Ultrasound

162
Q

How do you treat pyloric stenosis?

A

Surgical management/referral

163
Q

What would you see on the X-ray in ileal/jejunal atresia?

A

Triple bubble sign

164
Q

What are the differences between gastroschisis and omphalocele?

A

Gatroschisis = defect in abdominal wall with herniation of contents which are not covered by protective layer
Omphalocele = gut doesn’t rotate and failure of gut to return into the abdomen

Gastroschisis = associated abnormalities rare
Omphalocele is associated with other conditions (trisomy 13, 18 and Beckwith Weidemann)

Gatroschisis = right paraumbilical
Omphalocele = central

Gastroschisis = no sac covering
Omphalocele = covering sac

Gatroschisis = free intestinal loops
Omphalocele = liver, bowel, etc

Gastroschisis = excellent prognosis if managed well (and small)
Omphalocele = Varies with associated anomalies

Gastroschisis = immediate management = cover bowel with cellophane to reduce fluid losses, IV fluids, NG tube, antibiotics, urgent surgery
Omphalocoele = bowel covered by sac, semi-urgent surgery unless sac rupture then tx for gastroschisis

165
Q

What history is important to ask in a neonate with respiratory distress?

A

Antenatal
-preterm or poster, delivery
-maternal drugs
-maternal illness
-chorioamnionitis
-oligo/polyhydramnios

Perinatal
-meconium liquor
-PROM
-fetal distress
-difficult delivery
-assisted delivery

Postnatal-excessive drooling
-requiring oxygen
-hypoglycaemia
-coughing/choking when feeding
-resus needed?

166
Q

What is the pathophysiology of cleft lip/palate?

A

Failure of closure of the lateral and medial nasal processes during the 8th week

167
Q

What are complications of cleft lip/palate?

A

Short term
-feeding difficulties (need dental plate and special nipples)

Long term
-middle ear infection
-hearing impairment
-speech difficulties
-facial growth and orthodontic problems

168
Q

How is cleft lip/palate managed?

A

Surgical repair of lip - 3months
Palate repaired 6-12 months

169
Q

What is the inheritance pattern of Pierre Robin syndrome?

A

Single gene defect and is autosomal recessive
(X-linked variant involved cardiac malformations and clubfoot)

170
Q

What is the aetiology of Pierre Robin syndrome?

A

7 and 11th week - mandibular hypoplasia
Tongue kept high in oral cavity causing a cleft and preventing closure
Inverted U-shaped cleft and absence of associated cleft lip.

171
Q

What is the Pierre Robin syndrome triad?

A

Micrognathia
Posterior palate defect
Tongue posterior leg displaced (retroglossoptosis)

172
Q

What is a complication of Pierre Robin syndrome?

A

Resp obstruction = hypoxia = cor-pulmonary = pulmonary HT

173
Q

What is the management of Pierre Robin Syndrome?

A

Prevent obstruction by tongue (prone, may need CPAP via NG tube)
Micrognathia and airway obstruction improve in 2 years
Surgery of palate around 1 year

174
Q

What is choanal atresia?

A

Bony/membraneous blockage between the nasal cavity and nasopharynx which can be uni/bilateral

175
Q

Why is choanal atresia a problem?

A

Newborns are obligatory nose breathers so it can be life threatening causing resp distress and cyanosis, relieved by crying or opening the mouth

176
Q

How do you diagnose Choanal atresia?

A

CT scan
NG tube/nasal airway unable to pass

177
Q

How is choanal atresia treated?

A

Establish airway (oral airway)
Surgical correction by ENT’s ASAP

178
Q

How do you approach respiratory distress?

A

Respiratory
1) pulmonary
-RDS
-TTN
-Congenital pneumonia
-pulmonary haemorrhage
-pneumothorax
-congenital lung disease
2) non-pulmonary
-upper airway problems
-lower airway problems
-diaphragm pathologies
-mediastinal masses
-rib cage abnormalities

Non-respiratory
-cardiac
-metabolic
-neuromuscular
-haemolytic

179
Q

What investigations would you order in Resp distress of the neonate?

A

FBC + diff
CRP
Blood culture

CXR
Cranial and renal u/s
CTscan

180
Q

What are signs of respiratory distress?

A

Tachypnoea >60
Nasal flaring
Grunting (prolonged exp against closed glottis)
Chest retraction
-suprasternal
-sternal
-inter/subcostal
Cyanosis

181
Q

What are the findings on a CXR with RDS?

A

Ground glass appearance
Air bronchograms
Low lung volumes

182
Q

What is important history in a neonate with RDS?

A

Prem?
Gets DM?
Meconium asp? (Decreases surfactant activity)

183
Q

How do you treat RDS?

A

AN steroids (prevention)
CPAP
Surfactant

184
Q

What is the most common cause of resp distress in term infants?

A

Transient tachypnoea of the newborn

185
Q

What is the pathophysiology of TTN?

A

Lower circulation of catecholamines = Na channels not activated in c/s causing delay in the absorption of lung liquid

186
Q

What is the management of TTN?

A

Oxygen
NG feeding
CPAP
Roma
Resolves within 24hrs about

187
Q

When might an infant get meconium aspiration?

A

> 34-36 weeks GA (meconium not present before)

188
Q

What is the pathophysiology of meconium aspiration?

A

Causes inflammatory response (chemical pneumonitis = obstruction and atelectasis = over distension = alveolar rupture, pneumothorax, surfactant deactivation = PPHN

189
Q

What factors promote passage of meconium in utero?

A

Placental insufficiency
Hypoxia
Maternal HT
Preeclampsia
Maternal drug abuse
Oligohydramnios

190
Q

What are complications of meconium aspiration?

A

Airway obstruction
Surfactant dysfunction
Chemical pneumonitis
Pneumothorax
Persistent pulmonary HT of the newborn

191
Q

What are X-ray features of meconium aspiration?

A

Course, widespread patchy infiltrates with hyperinflation

192
Q

What is the management of meconium aspiration?

A

Prevention
Mechanical ventilation with high flow (NO CPAP = worsens hyperinflation)
Surfactant support
Ionotropes

193
Q

What are risk factors for congenital pneumonia?

A

Chorioamnionitis
PROM
Maternal fever/tachy
Hx UTI/vaginitis
Spontaneous ROM

194
Q

What is the most common causative organism of congenital pneumonia?

A

Group B strep

195
Q

What are the X-ray findings of congenital pneumonia?

A

Bilateral opacities,
Focal infiltrates with air bronchograms

196
Q

What is the treatment of congenital pneumonia?

A

Antibiotics (Ampicillin)
Ventilation if signs of resp failure

197
Q

List the causes of persistent pulmonary hypertension of the newborn.

A

Birth asphyxia
Meconium aspiration
Sepsis
Diaphragmatic hernia

198
Q

What is the CXR features of PPHN?

A

Oligaemia (decreased vascularity)
May be normal
may show underlying cause

199
Q

How does a neonate with PPHN present?

A

Cyanosis or difficulty in oxygenation
Reduction between pre and post duct all saturations

200
Q

What is the management of PPHN?

A

Oxygen
Optimise mechanical ventilation
Circulatory support required
Consider surfactant therapy
Pulmonary vasodilator (NO inhaled)/oral or IV sildenafil

201
Q

How is a hyperoxia test conducted?

A

Predictably ABG done on RA
100% O2 given for 10 minutes
PaO2 >110mmHg = unlikely cyanotic heart disease
PaO2<110mmHg = likely cyanotic heart disease

202
Q

What rash is this in picture7?

A

Erythema toxic neonatorum

203
Q

What rash is this (figure 8)?

A

Ache neonatorum

204
Q

What rash is this? Image 9

A

Transient neonatal pustular melanosis

205
Q

What is the rash in image 10?

A

Seborrheic dermatitis

206
Q

What is happening in image 11?

A

Transient vascular phenomena (cutis marmorata)
- transient mottling of the skin symmetrically involving trunk and extremities

207
Q

What is happening in image 12?

A

Transient vascular phenomena (harlequin colour change)
When newborn lies of his sides (blanching of contra lateral side)
Resolves with increased muscle activity or crying

208
Q

What is the distribution of erythema toxicum neonatorum?

A

Palms and soles spared.
Lesions on face, trunk, proximal extremities

209
Q

Describe a typical erythema toxicum neonatorum lesion.

A

2-3mm maculae’s and Paula’s that evolve into pustules and are surrounded by blotchy erythema. =flea-bitten appearance

210
Q

What infections have a similar appearance to erythema toxicum neonatorum and should be kept in mind?

A

Candida
Herpes simplex
Staph infections

211
Q

How do you confirm diagnosis of erythema toxicum neonatorum?

A

Pustular smear
Eosinophilia

212
Q

Describe the appearance of transient neonatal pustular melanosis rash.

A

Lack surrounding erythema
Lesions rupture easily leaving collarette of small and a pigmented macula that fades over a few weeks.

213
Q

Identify the rash in image 13.

A

Milia

214
Q

What’s the difference between miliaria crystallina and miliaria rubra?

A

Miliaria cyrstallina = caused by superficial eccrine gland duct closure, 1-2mm vesicles without erythema

Miliaria rubra = caused by deeper eccrine gland obstruction, erythematous papules and vesicles on portions of the skin

215
Q

How is seborrheic dermatitis treated?

A

White petrolatum
Tar containing shampoo (often on scalp)
Hydrocortisone

216
Q

What is the distribution of seborrheic dermatitis?

A

Scalp “cradle cap”, face, nappy area, ears, neck

217
Q

What lesion is in picture 14?

A

Negus flemmeus/ Port wine stain

218
Q

What is the triad of Sturgeon-Weber syndrome?

A

Seizures
Glaucoma
Port wine stain

219
Q

Port wine stain in the __________ distribution is of the _______ nerve is associated with ______________.

A

Opthalmic
Trigeminal
Ipsilateral glaucoma

220
Q

What is the lesion in image 15?
What is it caused by?

A

Negus simplex
“Stork bites”/ “angel kisses”

Caused by telangiectasis in the dermis

221
Q

What’s the difference between neonatal sepsis and congenital infections?

A

Neonatal sepsis requires rapid and empiric antibiotic treatment and progresses fast, presents early

Congenital infections can be asymptomatic at birth and progress variantly and result in poor long-term outcomes.

222
Q

What are the differences between early onset sepsis and late onset sepsis?

A

Early onset = presents <72hrs of life
Late onset = presents >72hrs of life

Early onset = transplacental, genital tract/PROM transmission
Late onset = nosocomial, HCW, community/environment, nutritional resources, immature immune system

Early onset = GBS, EColi, listeria monocytogenes, staph aureus, h influenzas
Late onset = GBS, Staph aureus, fungal, enterococcus, gram neg organisms

223
Q

Define neonatal sepsis

A

The presence of infections involving bloodstream, urine, CSF, peritoneum/any sterile tissue during the first 28 days of life

224
Q

What are RF for Early onset neonatal sepsis?

A

Maternal factors
-prem labour <37 weeks
-PROM >18hrs
-chorioamnionitis/maternal fever >38
-GBs bacteruria
-colonised with GBS

Neonatal factors
-prem
-male
-low apgar
-hypothermia
-fetal distress

225
Q

What are the RF for late onset sepsis?

A

Inversely related to GA and weight
Catheters
Ventilator tx
Prolonged AB
Damage to skin from tape/skin probes
Gastric acid suppression therapy

226
Q

How does early onset neonatal sepsis present?

A

Non-specific symptoms
-temp irregularity
-change in behaviours
-skin = poor circulation, jaundice, mottling, umbilical redness/discharge
-GIT = vomiting, diarrhoea, abdo distension, jaundice
-Cardio/pulmonary = resp distress, tachypnoea, poor cap refil
-metabolic = hypo/hyperglycaemia
-CNS = irritability, abnormal cry, bulging fontanelle, lethargy, seizures, coma

227
Q

What is the clinical presentation of late onset sepsis?

A

Neonatal meningitis (GabS)
Conjunctivitis
Pneumonia
Umbilical infection
UTI
Osteomyelitis/septic arthritis
Skin = impetigo, staph scalded skin syndrome

228
Q

How do you investigate neonatal sepsis?

A

Thorough history and exam
Blood, urine, CSF, tracheal secretions = gold standard
**CSF for:chemistry, microscopy, culture, latex agglutination
CXR, AXR (NEC, pneumonia)
FBC
-leukopenia/leukocytosis
-neutropenia
-immature neutrophils:total neutrophil ratio >0,2
-platelet count
Acute phase reactants
-CRP
-procalcitonin

229
Q

What is the treatment for neonatal sepsis?

A

1) Prevention (antenatal care, hand washing, infection control, management of catheters, BF, judicious use of AB)
2) Antibiotics (empiric = lifesaving)
-ampicillin and gentamicin for early onset sepsis, length of tx depends on disease progress)
-LOS tx depends on cause (vancomycin, cephalosporins, carbapenems, antifungals)

230
Q

How do you judge how long you should give AB tx for?

A

Judge by clinical picture and by your CRP and other inflam markers

231
Q

What organisms commonly cause congenital infections?

A

Viruses
-Rubella
-CMV
-HSV
-Varicella zoster
-hep B and C
-HIV
-enteroviruses
-papilloma virus

Bacteria, parasites etc
-toxoplasma Gondi
-trop pallidum
-mycobacterium tuberculosis
-plasmodium

232
Q

How does CMV congenital infection present?

A

1) Asymptomatic (90% at birth)

2)Clinical signs:
-prematurity
-rash
-IUGR
-jaundice
-hepatosplenomegaly

Neuro manifestations
-microcephalic
-seizures
-hypotonia
-lethargy
-chorioretinitis
-intracranial calcifications
-sensorineural Hearing loss9

233
Q

How do you diagnose CMV?

A

1) in mother
-seroconversion (neg IgG to pos IgG)
-CMV DNA PCR of amniotic fluid

2) in infant
-IgM (within 3 weeks of age)
-CMV viral DNA of blood, urine, amniotic fluid, saliva of CSF before 3 weeks)

234
Q

How do you treat CMV infection?

A

No vaccine
Hygiene practice
IV ganciclovir 6 weeks 6mg/kg/dose

235
Q

How does congenital rubella present?

A

1) asymptomatic at birth 2/3

2) Rubella syndrome
-sick baby
-jaundiced
-petechiae
-hepatosplenomegaly

-blueberry muffin rash
-thrombocytopaenia
-cataracts
-glaucoma
-hearing loss

236
Q

How do you diagnose congenital rubella?

A

DNA PCR in nasopharyngeal swabs, urine, CSF, blood
Rubella specific IgM before 3%months
Rubella IgG between 6-12 months

237
Q

How do you treat rubella?

A

No treatment available
Vaccination NB

238
Q

How is toxoplasma Gondi transmitted to the baby?

A

Mom primary infection during pregnancy by raw meat/inhalation feline faeces

239
Q

How does toxoplasmosis present?

A

Classic tetrad
-cerebral clarifications
-hydrocephalus
-chorioretinitis
-seizures

75% asymptomatic at birth

-maculopapular rash
-cataracts
-deafness

240
Q

How do you diagnose toxoplasmosis?

A

PCR
IgM in amniotic fluid and newborn

241
Q

How is toxoplasmosis treated?

A

Spiramycin in in 1st/early 2nd trimester
Pyrimethamine/sulfadiazine in late 2nd/3rd trimester and continue 1year post birth

242
Q

How does congenital varicella syndrome present?

A

Varicella is teratogenic
-foetal loss
-IUGR
-skin scarring
-limb deformities
-eye and CNS abnormalities

243
Q

How does the timing of moms infection of varicella influence the neonate?

A

Any stage = IUGR/neonatal infantile zoster
1st 20 weeks = congenital varicella syndrome
>5-6days before delivery = neonatal varicella at age 10-12 days
<4-5 days before to 2 days after delivery = neonatal varicella from birth -12 days after delivery (insufficient t8me for maternal IgG development and passage to fetus

244
Q

How do you treat neonatal varicella? NB

A

Varicella zoster Immune globulin
Aciclovir for I’ll neonates
Vaccinate moms 3months prior to pregnancy

245
Q

How does a mom present with syphillis and why is it important to identify?

A

Primary stage (3-6weeks) = painless, spont resolving petechiae
Secondary stage (6-8weeks) = diffuse inflammation and a disseminated rash often on palms and soles
Latent stage = asymptomatic

Infection occurs in the neonate when the mom is untreated or inadequately treated therefore prenatal care NB
Early infection = hydrous fetal is, stillbirth, prem, LBW, neonatal death

246
Q

How does congenital syphillis present in a child?

A

Early (<2years)
-prem and growth restriction
-hepatosplenomegaly
-nasal chondrites
-skin rash
-osteochondritis
-neurological symptoms including hydrocephalus

Late (>2years)
-craniofacial abnormalities
-dental abnormalities
-deafness
-neuro syphillis
-frontal bossing
-sabre skin
-cognitive disability
-interstitial keratitis

247
Q

How do you investigate congenital syphillis?

A

Screen infant - nontreponemal serologic testing = non-specific but quant and qualitative
-VDRL
-RPR (rapid plasma regain test)

Treponemal tests (positive if past infection)
-enzyme immunoassays
-fluorescent trep antibody absorption = FTA-ABS

248
Q

How do you treat congenital syphillis?

A

Treat mother fully
Treat infant
1)asymptomatic
-benzathine penecillin 50000 u/kg stat IF MOM received less than 3 doses, mom delivers within 4 weeks of tx

2)symptomatic
-procaine penecillin/benzyl penecillin for 10 days

Erythromycin doesn’t cure !!!

249
Q

What are the RF of HIV transmission to child?

A

Maternal Unsuppressed viral load
Prem
Unknown RVD status
Mixed feeding
PROM
Vag delivery

250
Q

What is the fixed dose combination used to treat HIV in pregnant women?

A

TLD

Tenofovir (TDF)
Lamivudine (3TC)
Dolutegravir (DTG)

251
Q

What are the benefits of using dolutegravir?

A

Rapid viral load suppression
High genetic barrier to resistance
No interaction with hormonal contraceptives
SE minimal

252
Q

What are the cons of using dolutegravir?

A

Small risk neural tube defect
Drug interactions (rifampicin, metformin)

253
Q

What are the benefits of using efavirenz?

A

Safe in pregnancy
No interaction TB tx

254
Q

What are the risks of using Efavirenz?

A

Low genetic barrier to resistance
Drug interaction with contraceptives
Neuropsychiatric SE

255
Q

How do you assess a treated patient with a viral load >50?

A

Adherence
Bugs
Correct dose
Drug interactions
E resistance

256
Q

How is prematurity classified?

A

Late preterm = 34-36weeks 6days
Moderate preterm = 32-34weeks
Very preterm = 28-32 weeks
Extreme preterm = <28weeks

257
Q

What factors can you look at to determine the babies age/GA?

A

Birth weight
Skin
Vision
Ears
Hearing
Sucking and swallowing
Cry
Feeding
Taste
Breathing
Breast tissue
Sleep/wake cycle
Posture

258
Q

How do you classify weight at birth?

A

Large birth weight = >4kg
Low birth weight = 1500-2499g
Very low birth weight = 1000-1499g
Extreme low birth weight = <1000g

259
Q

Between what percentiles is “normal” weight for ages? What does it mean if you are above or below?

A

10th-90th percentiles
Below = IUGR
Above = large for date

260
Q

Further classify IUGR

A

Symmetrical
-length, weight and HC small for age

Asymmetrical
-weight small but HC and length normal for age

261
Q

Classify small for GA

A

Constitutionally small (reached genetic potential)

IUGR

262
Q

How is delayed cord clamping beneficial?

A

Fluid bolus (cardiovascular stability)
Reduce Intraventricular haemorrhage
Reduce necrotising enterocolitis
Reduce need for vasopressin’s and blood transfusions

NB not if baby needs resus

263
Q

What are the golden rules of prem delivery

A

Prevent hypothermia
Prevent hyper/hypoxia
Noninvasive ventilation
Early enteral feeding
Delayed cord clamping
Prevent hypoglycaemia
Early admin AB

264
Q

How do you prevent hyperopia in a prem?

A

Titration the oxygen supplementation using pulse oximetry to guide you
Term = infatuate 21%
Preterm = initiate 21-30%
And monitor response

265
Q

What are the complications of prematurity?

A

Intraventricular haemorrhage
Retinopathy of prematurity
RDS
PDA
NEC
Infection

Anaemia
Coagulopathy
Jaundice
Poor weight gain
Electrolyte disturbance
Metabolic bone disease

266
Q

Why are perms susceptible to hypothermia?

A

Unable to shiver
Less subcutaneous fat
Increased skin to volume ratio
Inability to take in enough calories

267
Q

How do you keep a preterm neonate warm?

A

Put in plastic polyethylene bag, hat on head NB
KMC
Warm fluids
Humidified vent basses

268
Q

What is the Pathogenesis of RDS?

A

Incomplete lung development and insufficient endogenous surfactant
No surfactant = collapse of alveoli on expiration and atelectasis = increased work of breathing

269
Q

What is atelectasis?

A

Lung collapse

270
Q

How do you diagnose RDS?

A

Presents within 4 hours after birth (when surfactant is used up

Clinically
-subcostal recessions/intercostal recessions
-tachypnoea
NB sternal recessions
-nasal flaring
-expiratory grunting (collapsed lungs)

CXR
-collapsed lungs
-disuse uniform ground glass appearance
-air bronchograms

271
Q

How do you manage RDS?

A

Antenatal steroid administration

CPAP with supplemental O2
Monitor eats
If not tolerating, exogenous surfactant

272
Q

What are complications of RDS?

A

Infection/lung collapse
Air leaks (pneumothorax/pulm interstitial emphysema)
PDA
Pulm haemorrhage
Intraventricular haemorrhage
Bromchopulmonary dysplasia

273
Q

Define apnoea

A

Cessation of breathing for >20secs with bradycardia or hypoxaemia

274
Q

What is the management of a PDA?

A

Fluid restriction
Diuretics (if signs of heart failure)
Prostaglandin synthase inhibitors (ibuprofen/paracetamol)
Surgical closure

275
Q

What is NEC?

A

Process of inflammation of the bowel wall that may progress to necrosis and perforation

276
Q

How does a patient with NEC presents?

A

Bloody stools (late sign)
Distended abdo wall veins, erythema
Abdo distension
Inability to tolerate feeds: vomiting/Bilious aspirates
Intramural air on X-ray = Intestinal perforation

Systemic signs NB!!!
-CNS - lethargy, irritability
-CVS = decreased peripheral perfusion, hypotension, shock
-resp = resp distress, bradycardia
-renal = oliguria, Andria
-metabolic = acidosis, hypo/hyperglycaemia, electrolyte abnormalities, jaundice, temp instability

277
Q

What are the RF for NEC?

A

Prematurity (»>)
BF is protective
Micro biome pattern of guy

278
Q

How do you investigate NEC?

A

Bloods
-FBC
-Urea, creatinine, electrolytes
-serum bilirubin
-coagulation profile
-blood culture
-Abg

Radiology
-abdo X-ray = pneumatosis intestalis is pathognomonic (intramural air)

279
Q

How do you manage NEC?

A

Stabilise (airway, breathing, circulation)
If resp support required, use invasive (diaphragm splinted)
Correct hypotension and acidosis, bleeding diathesis = vit K and FFP
Keep NPO (insert NG tube on free drainage)
Initiate broad spectrum antibiotics

280
Q

What is the Pathogenesis of IVH?

A

Germinal matrix highly susceptible to damage as a result of alterations in blood flow/coagulation disorders as it is highly vascular

= damage of vascular network with varying degrees of bleeding

281
Q

How does IVH present?

A

Typically asymptomatic
Diagnosed on screening sonar at 72hrs of age (advised in infants less than 32weeks GA)

Or

-abnormal neurological signs
-apnoea and bradycardia
-shock
-acute drop in Hb conc
-hyperglycaemia
-unexplained acidosis
-unexplained increasing vent support

282
Q

How do you manage IVH?

A

Stabalise
Obtain cranial u/s
Refer for further management

283
Q

What is retinopathy of prematurity?

A

Eye disease of prematurity caused by vasculopathy and abnormal proliferation of retinal bv = leaking and scarring and retinal detachment and then blindness.

284
Q

Define chronic lung disease of prematurity

A

O2 requirement at 28 days of life
O2 requirement and characteristic X-ray changes at 28 days of life
O2 requirement at 36weeks postmentrual age

285
Q

What supplementation must the preterm infant receive and for how long?

A

Iron
Vit D
Multivitamin

For 6 months

286
Q

What factors cause delay in onset of respiration at birth?

A

Intrauterine hypoxia
Trauma to the brain
Drugs depressing resp centre

287
Q

What is the effect on the baby if opioids are given to the mom, and how do you treat this?

A

Resp depression
Administration of nalaxone (opioid antagonist)

288
Q

What is depicted in image 16?

A

Mongolian spot

289
Q

What is indicated in image 17?

A

Stork bite/telangiectasic naevi in nape of neck

Disappear in first years of life

Paediatrics (13 decks)

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