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Paediatrics RACP written exam > Neonatology > Flashcards

Neonatology Flashcards

1
Q

In HFOV changing what setting has the highest effect on oxygenation?

A

Mean airway pressure has the most important effect on oxygenation, as altering to optimal levels will change lung volume, improve VP matching, and decrease shunting.

PaO2 is dependent on Paw (MAP) and FiO2.
PaCO2 is dependent on delta P and frequency.

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2
Q

What is the major component of both naturally occurring surfactant and purified animal derived surfactant for exogenous use?

A

Dipalmitoylphosphatidylcholine (DPPC), also known as Lecithin

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3
Q

What factors are required to calculate the oxygenation index (OI)?

A

[FiO2 (%) x Mean airway pressure (mmHg)] / PaO2 (mmHg)

Oxygenation index is useful for objectifying the intensity of ventilation required and the severity of hypoxaemia. >25 is “high” and correlates with severe type 1 respiratory failure, ECMO required

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4
Q

Persistent pulmonary hypertension of the newborn (PPHN)

A
  • Tachypnoea, possible pansystolic murmur (tricuspid regurg), prominent 2nd heart sound
  • If significant then >10% pre and post ductal sats discrepancy (pre>post) resulting from R-L shunting via the ductus
  • Often idiopathic, but can be due to sepsis, birth asphyxia meconium aspiration, pulmonary hypoplasia, and maternal medications (SSRI+NSAIDs)
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5
Q

What is the most common type of oesophageal atresia?

A

Type C - oesophageal atresia with a distal TOF (85% of cases)

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6
Q

What proportion of cleft lip and palates are not associated with a syndrome (i.e. non-syndromic)?

A

70% (in contrast, 50% of isolated cleft palate are not associated with a syndrome, and 90% of isolated cleft lips)

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7
Q

Syndromes associated with cleft palate?

A
  • Stickler syndrome
  • 22q11 deletion
  • Treacher-Collins syndrome
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8
Q

Signs of congenital zika?

A
  • Microcephaly, intracranial calcifications
  • Seizures, spasticity
  • Feeding issues, developmental delay
  • Contractures and limb abnormalities
  • Visual abnormalities
  • NOT hepatosplenomegaly
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9
Q

Describe neonatal lupus

A
  • Symptoms: SGA, congenital heart block, cutaneous lesions after UV exposure, hepatitis, thrombocytopenia, neutropenia, pulmonary and neurological disease
  • Maternal transfer of SLE IgG autoantibodies, usually anti Ro/SSA or anti La/SSB, between 12-16/40
  • Most manifestations resolve, apart from heart block (can use AN and PN steroids)
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10
Q

What develops from the endoderm?

A
  • Internal layer

- Alveolar/lung cells, thyroid, GI, pancreas

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11
Q

What develops from the mesoderm?

A
  • Middle layer

- Cardiac, smooth muscle cells (gut), skeletal muscle, RBC/circulatory system, tubules of kidney

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12
Q

What develops from the ectoderm?

A
  • Outer layer

- Skin, pigment cells, central nervous system

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13
Q

Describe the process of gut formation in the fetus?

A
  • Extra-abdominal gut rotates 270 degrees anticlockwise around the mesentery (containing SMA)
  • Failure to complete this results in malrotation and risk of volvulus
  • Gut returns to abdomen at 12/40. Errors in this result in gastroschisis and exomphalos
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14
Q

What is a meckel’s diverticulum?

A

A remnant of the vitelline duct (yolk sac stalk)

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15
Q

Describe the process of neural tube development

A
  • Neural tube forms by 3/40
  • Neural groove closes in cranial to caudal direction at end of 4/40
  • Myelination of Schwann cells begins at 12/40, increases from 24/40, not complete until age 2
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16
Q

Describe the process of gonadal development

A
  • Y chromosome (SRY gene) influences the development of the gonads after 6/40
  • Testes secrete Mullerian inhibiting factor which results in regression of the uterus/vagina/fallopian tubes
  • Testosterone influences development of Wolfian structures (prostate, seminiferous tubules, vas deferens)
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17
Q

Risks of maternal diabetes for neonate

A
  • 3 x inc congenital malformations (CHD, sacral agenesis, NTD, microcolon)
  • SGA (due to small vessel disease) or LGA (hyperglycaemia)
  • Hypoglycaemia, low Ca + Mg
  • Surfactant deficiency, polycythaemia, jaundice, transient septal hypertrophic cardiomyopathy
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18
Q

Risks of hypertension/pre-eclampsia for neonate

A
  • SGA
  • Polycythaemia
  • Neutropenia, thrombocytopenia
  • Hypoglycaemia
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19
Q

Risks of maternal thyroid disease for neonate

A
  • Maternal Grave’s causing thyrotoxicosis

- Neonatal hypothyroidism due to maternal anti-thyroid medications

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20
Q

Describe neonatal thyrotoxicosis

A
  • Due to transplacental passage of thyroid-stimulating antibodies from mother with Grave’s disease
  • Rare, only 1/70 mothers with thyrotoxicosis
  • Can cause goitre, low birth weight, failure to gain weight, tachycardia, restlessness, jitteriness
  • Check cord TSH + TSH/T4 at 10-14 days age
  • Severe cases treat with beta-blocker and carbimazole
  • Self resolves as antibody levels fall
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21
Q

Neonatal thrombocytopenia

A
  • Autoimmune: maternal ITP, mother also has low platelets. If <50 treat IVIG and plt transfusion due to risk ICH. Can’t use Mum’s platelets
  • Alloimmune: NAIT, maternal antibodies against father’s platelet antigen, IgG antibodies cross placenta. Risk ICH, treatment IVIG, irradiated maternal platelets/random donor
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22
Q

Risk of maternal myasthenia gravis on neonate

A
  • 10% risk - transplacental passage of ACh receptor antibodies
  • Weakness, poor suck, resp distress, ptosis
  • Maternal severity doesn’t correlate with baby’s severity
  • Diagnosis via antibody assay, EMG, neostigmine test
  • Usually presents early, resolves by 2 months of age. May require physio if contractures
  • If antibodies absent or symptoms persist then consider congenital myasthenia gravis (AR)
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23
Q

Describe the features of foetal alcohol syndrome

A
  • SGA, IUGR, postnatal growth failure
  • Microcephaly, CHD
  • Facies: long and smooth philtrum, thin upper lip, micrognathia, ear abnormalities, flat nasal bridge, epicanthic folds, short palpebral fissures
  • Intellectual impairment
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24
Q

Describe neonatal abstinence syndrome

A
  • Within 1-2 days, but up to 7-10 days age
  • Persists longer with methadone
  • Wakefulness, irritability, jitteriness, sneezing, apnoea, tachypnoea, diarrhoea, weight loss, seizures,
    high pitched cry
  • Inc risk SIDS, decr risk surfactant deficiency
  • <50% require treatment. Tx PO morphine
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25
Q

Teratogenic effects of phenytoin?

A
  • Fetal hydantoin syndrome

- Broad nasal bridge, hypertelorism, ptosis, ear abnormalities

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26
Q

Teratogenic effects of sodium valproate?

A

Neural tube defects, fused metopic suture, mid-face hypoplasia, CHD, hypospadius, talipes, GDD, finger/toe abnormalities

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27
Q

Teratogenic effects of isotretinoin and high dose Vit A?

A

Cleft palate, hydrocephalus, CHD

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28
Q

Teratogenic effects of cocaine?

A

SGA, prune belly, renal anomalies, cardiac/skeletal/eye abnormalities

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29
Q

What are the causes of oligohydramnios?

A
  • Placental insufficiency + IUGR
  • Urinary tract abnormalities
  • PROM
  • Chromosomal abnormalities, eg trisomies
  • Infections
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30
Q

What are the causes of polyhydramnios?

A
  • Maternal diabetes
  • Oesophageal atresia
  • Abnormal karyotype
  • Neuromuscular disease (congenital myotonic dystrophy, SMA, congenital myopathy, Moebius syndrome)
  • Congenital diaphragmatic hernia
  • Idiopathic
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31
Q

Small salmon pink papules and sepsis is likely due to which organism?

A

Listeria monocytogenes infection - not susceptible to cephalosporins
(GBS and E. coli are most common cause early-onset sepsis, responsible for 60–70% of cases).

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32
Q

10% of neonates with galactosaemia present with?

A

E.Coli sepsis

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33
Q

Discuss the role of oestrogen during pregnancy

A

Comes from placenta, increases as pregnancy progresses. Causes proliferation of uterine smooth muscle, breast development, change in pelvic musculature and ligaments

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34
Q

Discuss the role of progesterone during pregnancy

A

Increased amount after first trimester, comes from placenta. Relaxes uterine smooth muscle, decreases in final few weeks of pregnancy, triggering onset of labour. Also helps with glandular development of breasts.

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35
Q

Discuss the role of oxytocin during pregnancy

A

Secreted by the posterior pituitary, released by stimulation of the cervix. Causes contraction of the uterine smooth muscle, and milk secretion/ejection (via contraction of the breast myoepithelial cells)

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36
Q

Discuss the role of prolactin during pregnancy

A

Secreted by the anterior pituitary, inhibited by oestrogen and progesterone. These decrease post-partum, causes increase in prolactin, causes milk production. Inhibits FSH post-partum, preventing ovulation

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37
Q

When does the ductus arteriosus close?

A

Functional closure within 15 hours (due to inc PO2, decr prostaglandin E2, decr pulm vascular resistance)

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38
Q

When does the ductus venosus close?

A

Functional closure within hours, anatomical closure 3/52

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39
Q

Discuss the circulatory changes that occur after delivery

A
  • Expansion of the lungs + inc arterial PO2 causes rapid decrease in pulmonary vascular resistance
  • Removal of low-resistance placental circulation causes inc systemic vascular resistance
  • Output from RV flows entirely into the pulmonary circulation and shunt through ductus reverses L-R (pulm resistance < systemic resistance)
  • High arterial PO2 constricts ductus arteriosus
  • Inc volume of pulmonary blood flow returning to the left atrium causes inc LA pressure > RA pressure, functionally closing flap of foramen ovale
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40
Q

What keeps the ductus open during fetal life?

A

Prostaglandin E2 + I2 (prostacyclin) (note: use prostaglandin E1 infusion to keep ductus open post-natally)

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41
Q

How does nitric oxide work?

A

In vascular smooth muscle nitric oxide causes inc intracellular cGMP. This leads to smooth muscle relaxation and vasodilation by stimulating cGMP-dependant protein kinase which reduces intracellular calcium

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42
Q

What is the definition of a stillbirth?

A

In utero death >20/40

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43
Q

How do you calculate the perinatal mortality rate?

A

Death from 20/40 to 6 days/ per 1000 live and stillbirths

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44
Q

How do you calculate the neonatal mortality rate?

A

Death of liveborn infants <28 days old/ per 1000 live births

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45
Q

How do you calculate the perinatal mortality rate?

A

Stillbirth + death <6 days of age per 1000 live and stillbirths

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46
Q

What are the early and late complications of IUGR?

A
  • Early: hypothermia, hypoglycaemia, hypoxia, HIE, polycythaemia, neutropenia, thrombocytopenia, NEC
  • Late: metabolic syndrome, HTN, diabetes, increased neurodevelopmental issues, short stature (if severe IUGR)
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47
Q

What are the causes of SGA?

A
  • Maternal - smoking, diabetes, HTN, PET, lupus, altitude
  • Placental - insufficiency
  • Neonatal - multiple gestation, infection, congenital malformations
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48
Q

What are the early and late complicaitons of IUGR?

A
  • Early: hypothermia, hypoglycaemia, hypoxia, HIE, polycythaemia, neutropenia, thrombocytopenia, NEC
  • Late: metabolic syndrome, HTN, diabetes, increased neurodevelopmental issues, short stature (if severe IUGR)
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49
Q

Role of T1 and T2 pneumocytes

A
  • T1 pneumocytes responsible for gas exchange

- T2 pneumocytes produce surfactant after 26/40, line 5-10% of alveolar surfaces

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50
Q

What is the role of surfactant, and what is it made of?

A
  • Lowers surface tension at the air-alveolar interface, preventing end-expiratory alveolar collapse, stimulates lung-host defence mechanisms
  • Made of phospholipids (85%), other lipids (10%, help with immune function and absorption) and platelet-activating factor (increases surfactant secretion)
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51
Q

What increases and decreases surfactant levels?

A
  • Decreased: prematurity, males, sepsis, diabetes, 2nd twin, elec C/S, FHx
  • Increased: females, PROM, maternal opiate use, IUGR, AN steroids
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52
Q

What are the benefits of maternal antenatal steroids?

A
  • Decrease in: mortality (by 31%), IVH (by 46%), NEC, RDS, requirement for resp support, NICU admission, early onset sepsis
  • Give if likely preterm birth 24-34+6/40, also elec C/S up to 38+6/40
  • Repeated doses after 7 days. No benefit after 34+6/40
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53
Q

What are the benefits of exogenous surfactant administration?

A
  • Decreased mortality, pneumothoraces, and possibly CLD.
  • No effect on IVH
  • Give early to those who need it - early but selective (FiO2 >30% and worsening, 200mg/kg for initial dose)
  • Benefit with multiple doses
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54
Q

Describe CLD/BPD

A
  • Requirement for resp support >28d or >36/40
  • Risk factors: prem, prolonged I+V, barotrauma, O2 toxicity, pneumothoraces, GOR, PIE, PDA, chorioamnionitis, infection (esp CMV)
  • Only a few require home O2, weaned by age 1-2y
  • Inc risk infection and hospitalisation
  • Usually normal exercise tolerance in childhood
  • No treatment. Good nutrition important
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55
Q

Describe risks and treatment for meconium aspiration

A
  • RFs: term or post-term, SGA, perinatal asphyxia
  • Leads to airway blockage (inc airway resistance, gas trapping, pneumo), chemical pneumonitis, infection (E.Coli), surfactant deficiency/PPHN (lipid content of meconium displaces surfactant from alveolar surface)
  • Tx: resp support, surfactant replacement shows benefit but require large doses, ECMO if severe
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56
Q

Risk factors for pneumothoraces in neonates

A

Prematurity, surfactant deficiency, MAS, pneumonia, pulmonary hypoplasia, 1% of healthy infants

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57
Q

Ventilator adjustments to decrease risk of pneumothroaces

A

Volume guarantee, lower ventilation pressures, faster rate ventilation with short iTime, surfactant, paralysis of infants fighting ventilator

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58
Q

Describe pulmonary interstitial emphysema (PIE)

A
  • Up to 25% of VLBW infants
  • Rupture of overdistended alveoli causes cysts in pulmonary interstitium
  • Increased risk if chorioamnionitis
  • Ventilation is difficult
  • Increased risk of CLD and mortality
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59
Q

What are the causes of pulmonary hypoplasia?

A
  • Primary: rare
  • Secondary causes:
  • Oligohydramnios (renal agenesis/Potter’s syndrome, PCKD, PUV, renal dysplasia)
  • PROM <26/40
  • Amniocentesis
  • Lung compression (thoracic dystrophy, diaphragmatic hernia, CCAM, pleural effusions)
  • Reduced fetal movements (myotonic dystrophy, SMA, congenital myopathy)
  • Outcome depends on severity and underlying cause
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60
Q

What are the causes and management of chylothorax?

A
  • Lymph into pleural space - either congenital abnormality of pulmonary lymphatics, or iatrogenic post-op
  • Can do AN drainage via intercostal drains - decrease risk of pulmonary hypoplasia, facilitate resus post-delivery
  • Reduce chyle volume by using MCFA triglyceride milk formula and octreotide
  • May need a period of NBM + TPN to help underlying problem resolve
  • Subsequent protein and lymphocyte depletion can cause hydrops and infection
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61
Q

Describe the causes, risk factors, symptoms, and treatment of subglottic stenosis

A
  • Congenital or acquired
  • RFs: prem, recurrent intubations/traumatic, GOR, infection, Keloid-forming (black babies), incorrect ET tube size
  • Sx: stridor, wheeze, SOB, recurrent croup
  • Tx: systemic steroids may help facilitate extubation. Laser or cryotherapy to granulomatous tissue. In severe cases tracheostomy or laryngotracheal reconstruction
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62
Q

What are the benefits of patient-trigger mode ventilation?

A
  • Improves synchronisation with baby’s breathing
  • Improves oxygenation
  • Decreased risk pneumothorax
  • Facilitates weaning from ventilator
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63
Q

What are the benefits of volume guarantee ventilation?

A
  • Reduced mortality
  • Decreased BPD, pneumothorax, hypocapnia
  • Decreased PVL and ICH
  • Reduced time on ventilator
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64
Q

When would you use ECMO?

A
  • In severe resp failure, membrane “lung” used so lungs can rest and recover
  • Consider in severe resp failure if: reversible lung disease, >35/40, >2kg, no IVH > grade 1, normal coags
  • Use if oxygenation index >40 (mean airway pressure x FiO2 x 100 / PO2)
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65
Q

Describe the presentation and treatment of PDA

A
  • Uncommon in term infants >2/7
  • VLBW infants present day 3 life as pulm resistance decreases, increased L-R shunt
  • Systolic or continuous murmur, bounding pulses, wide pulse pressure (due to runoff of blood into the pulmonary artery during diastole), active precordium, cardiac failure, apnoea
  • CXR: may shoe cardiomegaly, pulmonary plethora
  • Tx: indomethacin (decr NEC and CLD). Ibuprofen as effective, and decr SEs (NEC, transient renal failure). Coil/ligation surgery
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66
Q

Causes of hypertension in a neonate?

A
  • Vascular: renal artery or aortic thrombosis (UAC), renal vein thrombosis (mat diabetes), coarctation aorta
  • Renal: obstructive uropathy (PUV), dysplastic kidney, PCKD, tumour
  • Intracranial hypertension
  • Endocrine: CAH, hyperthyroid, neuroblastoma, pheochromocytoma
  • Meds: steroids, inotropes, mat. cocaine
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67
Q

What are the risk factors for NEC?

A
  • Prematurity, IUGR, enteral feeding (early high volumes increase risk, no benefit of delayed feeding)
  • Hypoperfusion/gut ischaemia
  • APH, perinatal asphyxia, polycythaemia, PDA, PROM, CHD, Hirschsprung’s, formula, microbiome altered by antibiotics, lack of antenatal steroid
  • Most commonly 2-3rd week of life but in term infants can present within days
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68
Q

Complications and treatment of NEC

A
  • Perforation (20-30%), sepsis, DIC, strictures, recurrence (consider Hirschsprung’s), short gut, lactose intolerance
  • Tx: NBM 7-14/7, NGT free drainage, IVF/TPN, triple IV ABs, serial AXR to r/o perforation, surgical - peritoneal drain, laparotomy, resection, ileostomy/colostomy
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69
Q

Describe the NEC triad

A

Abdominal distension, bloody stools, bile-stained aspirates

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70
Q

What reduces the risk of NEC?

A

AN steroids, probiotics, breast milk

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71
Q

What are the complications of TPN?

A

Sepsis (line-related), extravasation, venous thrombosis, fluid/elec imbalance, high lipids, cholestatic jaundice

72
Q

What is the most common type of oesophageal atresia?

A

85%: oesophageal blind pouch with distal oesophagus to trachea fistula. 10% OA without fistula. H-type (no atresia) uncommon.

73
Q

What anomalies are associated with duodenal atresia?

A

70% are associated with other abnormalities: T21, CHD, malrotation

74
Q

Presentation of oesophageal atresia/ToF?

A

Polyhydramnios, salivation, respiratory distress, abdo distension, vomiting/choking with feeds, cannot pass NGT, other abnormalities in 30-50% e.g. VACTERL, absence of gastric gas if no ToF

75
Q

Presentation + treatment of oesophageal atresia/ToF?

A
  • Polyhydramnios, salivation, respiratory distress, abdo distension, vomiting/choking with feeds, cannot pass NGT, other abnormalities in 30-50% e.g. VACTERL, absence of gastric gas if no ToF
  • Tx: resp support, suction catheter in oesophageal pouch, surgery
76
Q

What associations might you find with malrotation?

A

Diaphragmatic hernia, duodenal atresia, situs inversus

77
Q

Signs, investigations, and treatment of malrotation

A
  • Bilious vomiting, abdominal distension
  • Upper GI contrast study: duodenal-jejunal flexure on right side abdomen with high caecum
  • Tx: surgical repair
78
Q

What are the symptoms and treatment for meconium ileus?

A
  • Antenatal perforation, peritonitis, intra-abdominal calcification, postnatal obstruction
  • Tx: water soluble contrast enema can lead to resolution
79
Q

What is the most common presentation of CF in infants?

A
  • Meconium ileus, in 10-15% of CF cases
  • 90% of those with meconium ileus have CF, so require genetic testing
  • Meconium plug is not associated with CF + symptoms resolve with passage of plug
80
Q

Describe anorectal atresia causes, investigations, and treatment

A
  • May be associated with VACTERL features
  • High atresias have issues with faecal incontinence later, require colostomy
  • Low atresias more common in females
  • Need renal USS and MCUG to rule out fistulas (caginal, vesical)
  • Tx: surgical repair/reconstruction
81
Q

What percentage of omphalocele are associated with other congenital abnormalities?

A
  • 75%

- Beckwith-Wiedemann, trisomies, CHD

82
Q

Describe omphalocele + treatment

A
  • Failure of gut to return into abdominal cavity during development. Covered with peritoneum, may rupture at birth
  • Tx: primary or staged surgical repair. If delayed then can use topical silver sulfadiazine to promote granulation of the peritoneal covering
83
Q

What are the risks of gastroschisis?

A

Adhesions, functional atresia, intestinal motility issues

84
Q

Describe gastroschisis

A
  • Increasing incidence, 5 x more common than omphalocele
  • Not covered by peritoneum, not associated with other congenital anomalies
  • Up to 10-15% have intestinal atresias
  • RF: teenage pregnancy, possibly smoking + recreational drugs
85
Q

Describe the pathogenesis of neonatal IVH

A
  • Germinal matrix is located in the floor of the lateral ventricle and is the site of migrating neuroblasts
  • By 24-26/40 it is highly cellular and vascularised, then involutes rapidly by 34/40
  • Susceptible to haemorrhage, decreased autoregulation of cerebral blood flow
  • In term infants, IVH may originate from the choroid plexus (4th ventricle or inferior horn of lateral ventricle)
  • Brain can become replaced by porencephalic cyst
86
Q

What are the risk factors for developing neonatal IVH?

A

Prematurity (28% at 25/40), lack of AN steroids, I+V, hypercarbia, metabolic acidosis, pneumothoraces, coagulopathy, rapid change in volume or pressures (transfusions, inotropes), perinatal asphyxia, hypotension, PDA

87
Q

When do neonatal IVH occur?

A

> 50% in first 24 hours, 10-20% day 2-3, 20-30% day 4-7

88
Q

Describe the grades of IVH

A
  • G1: isolated to germinal matrix
  • G2: IVH without dilation of ventricle
  • G3: IVH with dilation ventricle. Can present as shock due to blood loss
  • G4: echogenic intraparenchymal lesions with IVH (extension of bleed vs infarct). Can present with shock, seizures, poor tone, bulging fontanelle. High mortality up to 60%
89
Q

What factors can decrease risk of IVH?

A
  • Prenatally: AN steroids, maternal Vit K, delayed cord clamping
  • Postnatally: avoid fluctuations in cerebral blood flow, surfactant (no effect on IVH but reduces mortality), indomethacin (reduces IVH but no change in long-term neurodisability), volume controlled ventilation reduces IVH by providing more stability in RDS
90
Q

Outcomes of IVH

A
  • Depends on stage
  • CP most common adverse neurodevelopmental outcome
  • Can develop post-haemorrhagic ventricular dilation. Communicating > non communicating. Due to malfunction of the arachnoid villi, may require shunt
91
Q

Describe the process of periventricular leucomalacia

A
  • Hemorrhagic necrosis in PV white matter, progresses to cystic degeneration and cerebral atrophy
  • The corticospinal tracts descend through the periventricular white matter, hence the association between cerebral white matter injury/PVL and motor abnormalities, including cerebral palsy.
  • Associated with spastic diplegia or tetraplegia (>90%), learning difficulties, seizures (inc infantile spasms), blindness
  • USS: initial echogenicity/flare - may resolve or become cystic after 1-4/52. Usually bilateral neurological effects
  • Worse outcomes with subcortical PVL. If transient but >1-2 weeks old then 5-10% risk of spastic diplegia
92
Q

What are the risk factors for PVL?

A

Often associated with severe IVH, chorioamnionitis, hypoxia, ischaemia

93
Q

Describe the pathophysiology of neonatal encephalopathy

A
  • Can be AN, perinatal, PN causes. Usually due to placental insufficiency
  • Primary neuronal injury: energy failure due to inefficiency of anaerobic respiratory causing ion pump failure, neuronal death, cerebral oedema
  • Secondary (delayed) neuronal injury: hypoperfusion with subsequent reperfusion injury after resuscitation, leading to neutrophil/prostaglandin/free radical release. Necrosis and apoptosis of cells
94
Q

Describe the Sarnat staging

A

Staging of HIE:

  • Stage 1: hyperalert, irritable, poor suck, normal neuro. Resolve <24 hours. 99% good outcome
  • Stage 2: lethargic, obtunded, poor tone and reflexes, seizures. 75-80% good outcome
  • Stage 3: comatose, resp failure, severe hypotonia and hyporeflexia, seizures less common but EEG flat with burst suppression. >50% death, remainder severe disability
95
Q

What is the treatment of HIE?

A
  • Therapeutic hypothermia if >35/40. 33-35 degrees. From <6 hrs post delivery until 72 hours age. Decreases risk of death and severe disability
  • Can get renal/liver/coagulation derangement, fat necrosis
96
Q

Describe pathogenesis and risks of ROP

A
  • Vascular proliferation due to retinal vasoconstriction
  • VEGF plays an important role. Inc risk with hyperoxia and EPO, IUGR, prem, male
  • Can lead to fibrosis, scarring, retinal detachment
  • If < 32/40 or <1500g then screening from 30/40
  • Stage 1-5, zones 1-3
  • If > stage 3 with plus disease then treatment via cryotherapy or laser
97
Q

Describe the stages and zones of ROP

A
  • Stage 1 +2: resolve without risk
  • Stage 3: inc risk visual impairment
  • Stage 4 (subtotal) + 5 (total retinal detachment) - visual impairment
  • Zone 1 = greatest risk as most central/posterior around optic disc
98
Q

What does “plus” disease refer to?

A
  • Tortuosity of retinal vessels, pupil rigidity, vitreous haze, iris vessel engorgement
  • If > stage 3 with plus disease then treatment via cryotherapy or laser
  • Plus disease associated with severe disease and worse outcomes
99
Q

What are the antenatal signs of urinary abnormalities?

A
  • Oligohydramnios (Potter’s if severe)
  • Urinary ascites (result of obstructive uropathy)
  • Dilated renal tracts
  • Cystic dysplasia/ polycystic disease
  • Renal agenesis
100
Q

Describe the changes in urine concentrating ability post delivery

A
  • Preterms have immature tubular function leading to a high FeNa + high Na intake requirements
  • 90% of infants PU within 24 hours of delivery
  • Collecting ducts have increased sensitivity to ADH after birth + the urine-concentrating ability increases rapidly
101
Q

Describe presentation and treatment of posterior urethral valves

A
  • Mucosal folds in the posterior urethra in males, leading to urinary obstruction and bladder hypertrophy
  • May have palpable abdominal mass
  • Diagnosis via MCUG
  • Tx: suprapubic catheter insertion, then surgical resection via cystoscopy, or vesicostomy with delayed resection
102
Q

What are causes of haematuria in the neonate?

A

UTI, obstructive uropathy, renal artery/vein thrombosis, stones, trauma, tumour, cystic dysplasia, coagulopathy

103
Q

Describe prune-belly syndrome

A
  • Megacystitis-megaureter
  • Lax abdominal musculature, dilated bladder and ureters, undescended testes, neurogenic bladder
  • Usually due to abnormalities of the lumbosacral spine
  • 97% male
104
Q

What are the causes of AKI in the neonate?

A
  • Pre-renal: hypotension, dehydration, indomethacin
  • Renal: cystic dysplasia, PCKD, renal artery/vein thrombosis, congenital nephrotic syndrome, DIC, nephrotoxins e.g. gentamicin
  • Post-renal: PUV/ obstructive nephropathy
105
Q

What are the investigations for ambiguous genitalia in a neonate?

A

Karyotype, electrolytes, BP + BSL, abdo USS, 17-OH, 11- deoxycortisol, testosterone/oestrogen/progesterone/LH/FSH, urine steroid profile, MCUG

106
Q

What are the differential diagnoses for ambiguous genitalia in a neonate?

A
  • True hermaphroditism (ovotesticular disorder of sexual development)
  • Male under-virilisation: androgen insensitivity, CAH, panhypopituitarism, 5a reductase deficiency (become virilised at puberty) , testosterone synthesis defect
  • Female virilisation: CAH, aromatase deficiency
  • Chromosomal abnormality e.g. 45X/46XY mosaicism
107
Q

Describe 5a reductase deficiency

A
  • Under-virilised males at birth (more female-appearing) but at puberty have amenorrhea and virilization
  • 5α-Reductase converts testosterone to 5α-dihydrotestosterone (DHT) in peripheral tissues
  • DHT is a potent androgen, and is necessary for the development of male external genitalia in utero
  • Fertility: may have viable sperm for extraction. May have blind-ended vagina, but no ovaries or uterus
108
Q

What is the definition of a micropenis?

A

Stretched penile length of <2.5cm

109
Q

Describe signs and treatment of neonatal GBS infection

A
  • 20% pregnant women are carriers, can have transient carriage
  • Early GBS <7 days, usually septicaemia, resp distress (pneumonia, PPHN)
  • Late GBS >7 days, septicaemia, meningitis (vertical or nosocomial). Serotype 3 more common in late-onset disease or meningitis
  • Intrapartum antibiotics decreases early GBS sepsis. No effect on late sepsis, stillbirth, or GBS-related prematurity
  • Treatment: penicillin
110
Q

What are the risk factors for neonatal GBS infection?

A
  • Positive GBS vaginal swab after 35-37/40
  • Positive GBS urine anytime during pregnancy
  • Previous baby with GBS infection
  • ROM >18 hours
  • Prematurity <37 weeks
  • Fever in labour >37.8 degrees
111
Q

Describe signs and treatment of neonatal E.Coli infection

A
  • Usually vertical transmission, often associated with pre-term birth
  • Septicaemia, meningitis, UTI, NEC
  • Tx: gentamicin
112
Q

Describe signs and treatment of neonatal Listeria infection

A
  • Gram +ve rod, outbreaks associated with dairy products, coleslaw, pate, undercooked meats
  • Flu-like in pregnancy
  • Can present with stillbirth or severe neonatal sepsis and meningitis. Early and late onset, similar to GBS
  • Associated with pre-term birth and “meconium” or pus-stained amniotic fluid
  • Maculopapular or pustular rash is typical
  • Tx: amox and gent
113
Q

What are the genes associated with congenital nephrotic syndrome?

A 
NPHS1 (encodes nephrin)
NPHS2 (encodes podocin)
NPHS3 (encodes phospholipase C epsilon)
WT1 (encodes transcription tumour suppressor)
LAMB2 (encodes laminin beta 2)
114
Q

What are the causes of neonatal hypoglycaemia?

A
  • Demand/supply - preterm, IUGR, hypothermia, infection, asphyxia, polycythaemia
  • Hyperinsulinism - maternal diabetes, Beckwith-Wiedemann, haemolytic disease newborn, transient neonatal hyperinsulinism, islet cell adenoma
  • Endocrine - CAH, pituitary (GH def, septo-optic dysplasia)
  • Metabolic - glycogen storage disease, galactosaemia, aminoacidopathy, organic acidaemia, MCAD, VLCAD
115
Q

Describe the presentation and blood results of a neonate with panhypopituitarism

A
  • Persistent hypoglycemia, poor feeding, micropenis, conjugated jaundice (hypothyroid), midline facial defect, optic atrophy
  • Low GH/cortisol/TSH, hyponatraemia (decr cortisol)
116
Q

What are the causes and treatment of adrenal insufficiency in a neonate?

A
  • Causes: CAH, Smith-Lemli-Opitz syndrome, Wolman syndrome, adrenal haemorrhage, secondary (panhypopit, withdrawal from steroid treatment)
  • Tx: management of salt loss, hydrocortisone + fludrocortisone replacement
117
Q

How does phototherapy work, and what are the side effects?

A
  • Photo-oxidises and isomerises bilirubin, facilitating excretion via urine and bile
  • Complications: diarrhoea, rash, transcutaneous fluid loss
118
Q

How does exchange transfusion work in severe jaundice?

A
  • Dilutes bilirubin, removes sensitised RBC, corrects anaemia.
  • Can use IVIG as adjunct if severe/rapid rise in SBR.
119
Q

What are the causes of conjugated hyperbilirubinemia?

A
  • TPN cholestasis, IFALD
  • Viral hepatitis, TORCH
  • Metabolic (CF, a1aT def, galactosaemia)
  • Biliary atresia, Alagille’s, choledochal cyst, tumour/haemangioma causing bile duct obstruction
120
Q

Management of haemolytic rhesus disease

A
  • Anti-D should be given to mother after any event leading to sensitisation: labour, APH, trauma, antenatal procedure
  • Test Abs at booking + 28 + 36/40
  • If above threshold then require serial USS to detect hydrops, amnio/fetal blood sampling +/- fetal transfusion if severe anaemia
  • Require pre-term delivery if complicated
121
Q

Definition, causes, and treatment of neonatal polycythaemia

A
  • Hct >65%
  • Causes: IUGR, maternal diabetes, delayed cord clamping, TTTS, trisomies, CAH, thyrotoxicosis, Beckwith-Wiedemann
  • Complications: hypoglycaemia, jaundice, NEC, venous thrombosis, stroke, PPHN
  • Tx if Hct>65% and symptomatic - partial exchange transfusion using N. saline
122
Q

What are the causes of DIC in a neonate?

A
  • Sepsis, placental abruption, NEC, meconium aspiration syndrome
  • Thrombocytopenia, consumptive coagulopathy, fibrinolysis (leading to accumulation of fibrin degradation products)
  • Tx underlying causes, plt transfusion, FFP, cryoprecipitate if fibrinogen low
123
Q

What is the benefit of antenatal magnesium sulphate administration?

A
  • Neuroprotection for preterm infant, associated with a reduction in long-term gross motor dysfunction
124
Q

Describe the ideal location of UVC, UAC, ETT on x-ray

A

ETT - above carina
UVC - above diaphragm
UAC - T6-T7

125
Q

What are the risk factors for RDS?

A

Prematurity (80% of <28/40), M>F, birth depression, hypothermia, maternal diabetes

126
Q

What are the effect of prophylactic caffeine?

A

Decreased apnoea of prematurity, decr CLD, decr PDA requiring medication or surgery, decr severe ROP, decr CP + cognitive delay, inc disability-free survival, reduced risk motor impairment aged 11

127
Q

Describe apnoea of prematurity

A
  • Pause in breathing >20 seconds, or <20 seconds but associated with cyanosis, marked pallor, hypotonia, or bradycardia
  • 80% central, 10% obstructive, 10% mixed
  • Develop at end of first week of life, resolve by 36/40
  • R/o: sepsis, IVH, esp in older babies
  • Tx: caffeine (inc HR, BP, cardiac output). Doxapram in resistant cases.
128
Q

What are the risks of indomethacin?

A

Renal impairment, GI dysfunction, platelet dysfunction

129
Q

What are the sequelae of a PDA?

A
  • Due to “ductal steal”
  • Pulm haemorrhage (engorged lung capillaries), CLD (inc resp support), IVH (swinging pressures), NEC and renal hypoperfusion (decr perfusion)
130
Q

What are the differences between a term and pre-term infant with PDA?

A
  • Term infant: wall of the ductus is deficient in mucoid endothelial layer and the muscular media
  • Premature infant: PDA has a normal structure but is less responsive to high PO2 stimulus
  • Thus, a PDA persisting beyond the 1st few weeks of life in a term infant rarely closes spontaneously or with indomethacin (c.f. preterm)
131
Q

How does indomethacin work?

A
  • Cyclooxygenase 1 and 2 inhibitor (c.f. ibuprofen co2 inhibitor)
  • Limits production prostaglandins
  • Induces a significant reduction in blood flow velocities (cerebral, mesenteric, renal), decr platelet function, decr GFR and urine output
132
Q

What are the components of breast milk?

A

IgA, lactoferrin, epidermal growth factors

133
Q

What are the symptoms of early congenital syphilis?

A
  • Stillbirth, rhinorrhoea/snuffles, bony lesions, hepatosplenomegaly, and a bullous skin disease
  • Treponema pallidum is a spirochaete
  • Tx: IV penicillin
134
Q

Signs of hypermagnesemia in a neonate secondary to maternal magnesium sulphate?

A
  • CNS depression featuring lethargy, hypotonia, hyporeflexia, poor feeding and respiratory depression
  • Delayed passage of meconium
  • Management is generally supportive, such as ventilatory support, however in extreme cases IV calcium and diuresis can be used to reduce serum magnesium levels
135
Q

Describe intestinal lymphangiectasia

A
  • Dilatation of intestinal lymphatics and loss of lymph fluid into the gut
  • Present in childhood with oedema and non-bloody diarrhoea
  • Steatorrhea (stool fat globules), malabsorption, lymphocytopenia, and hypoalbuminemia
  • Ascites and chylous pleural effusions in long-standing lymphangiectasia
136
Q

Describe the development of ROP

A
  • Hyperoxia leads to delayed vascularisation
  • Due to deficient vascularisation, peripheral retina becomes hypoxic
  • VGEF release leads to abnormal angiogenesis
  • Normally vasculogenesis occurs from 14-15 weeks, angiogenesis from 17-18 weeks (drive by relative tissue hypoxia and stimulated by VEGF)
137
Q

Early vs late use of postnatal corticosteroids for CLD

A
  • Early (< 8 days) - decr CLD but inc CP, adverse neurodevelopmental outcome, GI bleeds, GI perforation.
  • Late (>7 days) - decr CLD, no inc CP, but inc ROP but not blindness
138
Q

RDS appearance on CXR?

A
  • Granular due to surfactant deficiency
  • Small lung volumes, air bronchograms
  • If lung is more granular-appearing than axilla = bad = RDS
139
Q

Pulmonary haemorrhage appearance on CXR?

A
  • Diffuse white-out on x-ray
  • Often seen post surfactant administration, or with PDA
  • Due to increased pulmonary blood flow with pressure changes
140
Q

Appearance of CLD on CXR?

A
  • Coarse areas of dilated air spaces and bands of scarring due to alveolar breakdown
141
Q

Appearance of meconium aspiration on CXR?

A
  • Coarse opacity with hyperexpansion

- Can look similar to CLD patients

142
Q

Appearance of PIE of CXR?

A
  • Initially mimics air bronchograms but is actually interstitial air
  • Starts peripherally and works its way back towards hilum
  • Interstitial air in vessels and airways
  • Severe PIE can lead to hyperexpansion due to air trapping
  • Tx with HFOV and nursing with affected side down
143
Q

What is the significance of a “figure of 8 mediastinum”?

A

Bilateral pneumothoraces - air is outlining the cardiac and thymic borders

144
Q

What is the significance of an “angel wing sign”?

A

Pneumomediastinum - air is displacing the lobes of the thymus upwards

145
Q

Lucent vs dense appearances on neonate x-rays

A
  • Lucent: pneumothorax, PIE, pneumatocele
  • Dense: collapse, consolidation, cyst, sequestration (extra-lobar)
  • Mixed: CPAM, bronchopulmonary cyst
146
Q

Lung lesion with systemic arterial connection?

A

Pulmonary sequestration

147
Q

Outcome of delayed vs immediate cord clamping in preterm infants trial

A
  • No difference in death + major morbidity combined
  • Decrease in death with delayed cord clamping. Same outcome seen in both <37w and <28w gestations
  • Reduction in need for subsequent blood transfusions
  • Increase in jaundice but no inc in exchange transfusion
  • Trials still needed about delayed clamping + resus
148
Q

Outcomes of research about meconium aspiration syndrome

A
  • No benefit to suctioning meconium in either vigorous or non vigorous babies
  • No difference in outcome of MAS but some improvement in NICU admission/O2/ventilation outcomes?
149
Q

What is the most important indicator of successful IPPV?

A

Rise in neonatal HR

150
Q

Oxygen vs air for resus trials

A
  • Resus with room air: no apparent harm, reduction in mortality, spontaneous respirations established faster
  • BUT preterm <29w, inc mortality with room air vs O2 but trial not completed due to loss of equipoise. Need further trials
151
Q

Outcome of trials with CPAP vs HFNC for primary support and post extubation

A
  • Favours CPAP as primary support for preterm infants
  • No significant difference post extubation or primary support
  • Less nasal trauma with HFNC
  • HFNC had higher failure rate post extubation but could be rescued with CPAP, therefore no inc rate of intubation
152
Q

Outcomes of probiotics + NEC trials

A
  • Decreased incidence of NEC and all cause mortality in those given probiotics, but only with multi-species, no difference in culture +ve sepsis rates, possibly decr late onset sepsis rates with lactoferrin
153
Q

Outcomes of trials looking at cooling in HIE

A
  • Cooling targets latent phase of 6-15 hours before delayed neuronal death due to cytotoxic mechanisms (primary death has already occurred)
  • Cooling reduces death and severe disability in both mod and severe HIE
  • Does not make babies survive to have severe disability that would otherwise have died
  • Aim 33-34 degrees, cool ASAP, duration 72 hours, only >35/40
  • Additional treatments trialled: xenon, topiramate, clonidine, EPO
  • May be benefit of still starting cooling >6 hrs age, no harm
154
Q

Oxygen saturation targets in NICU for preterms

A
  • Aim 91-95%
  • Higher O2 lead to increased ROP, but reduced mortality/morbidity
  • Higher O2 after 32 weeks no increased risk of ROP
155
Q

Outcomes of misting surfactant trials

A
  • Decreased need for mechanical ventilation

- Decr BPD due to ventilation

156
Q

Describe congenital diaphragmatic hernia

A
  • L sided, posterolateral most common
  • R sided inc risk mortality, esp if liver in chest
  • 30% of CDH are stillborn
  • Risk is from associated pulmonary hypoplasia. Initial ventilation should be standard I+V, not HFOV. May require this later.
  • Up to 30% associated with other malform: oesophageal atresia, omphalocele, trisomies
  • Intubation, NGT, surgical repair
157
Q

Adjusting HFOV settings

A
  • Decreasing the frequency allows more time for volume to be displaced, which will decrease CO2 level
  • The higher the frequency, the smaller the volume displaced (decreased tidal volume) due to decreased time
  • HFOV waveform is dampened down the further down the airway you go
158
Q

What are risk factors for cerebral palsy?

A
  • Chorioamnionitis, maternal thyroid disease, low birth weight, multiple birth, elevated cord levels or IL1,6,8, TNF-a, maternal thrombophilia, other congenital abnormalities
159
Q

Which part of the brain is most vulnerable to the effects of hypoglycaemia in the newborn period?

A

Occipital lobe

160
Q

Risks associated with late-preterm birth (34-36/40)

A
  • Inc cerebral palsy (>3 x term babies) cognitive impairment, behavioural disorders
  • Inc morbidity and mortality
  • Early term infants (37+38/40) have higher mortality rates, post-neonatal mortality, and CP than term infants
161
Q

Goals of ventilation: what is oxygenation influenced by?

A
  • Appropriate oxygenation: PaO2
  • Influenced by:
    • FiO2
    • MAP (mean airway pressure). To increase MAP:
      • Inc PEEP: direct 1:1 relationship with increasing MAP
      • Inc PIP: lesser extent than PEEP
      • Inc iTime: increased duration of positive pressure
      • Inc rate: increased number of cycles
162
Q

Goals of ventilation: what is ventilation influenced by?

A
  • Appropriate ventilation: PaCO2
  • Influenced by: tidal volume (difference between PIP and PEEP aka amplitude), ventilation rate, the gas exchange surface area and diffusion
163
Q

What is the mechanism CPAP?

A
  • Reduced airway resistance (stenting airway)
  • Chest wall more stabilised
  • Reduced obstructive apnoeas
  • Increased FRC (less V/Q mismatch, better oxygenation)
  • Reduced lung trauma, conserves surfactant
  • Note: too high pressures can cause decreased venous return
164
Q

What is the mechanism of HiFlow?

A
  • Generation of pharyngeal pressure (ie CPAP)
  • Supports inspiration
  • Washout of dead space (mouth, nasopharynx)
165
Q

What are the benefits of NIPPV?

A
  • CPAP with superimposed inflations to a set peak pressure
  • Reduces extubation failure (more effectively than CPAP), but no effect on BPD or mortality
  • May be of benefit in severe apnoea
  • Increases MAP, improves recruitment and maintains FRC, reduced inspiratory effort (if synchronised)
166
Q

Discuss pressure-volume loops and compliance

A
  • Lower line = inspiratory cycle, vol inc as pressure inc
  • Upper line = expiratory cycle, vol decr as pressure decr
  • Compliance: connects the points of minimum and maximum inflation.
  • Compliance= change in volume/change in pressure
  • Poor compliance (eg surfactant deficiency, meconium asp): need increased ++ pressures to a achieve increased volumes
167
Q

What are the benefits of volume-targeted ventilation?

A
  • Decr death or BPD at 36/40
  • Decr pneumothorax
  • Decr duration of ventilation
  • Decr hypocarbia
  • Decr PVL +/- grade 3-4 IVH
  • And not associated with any increased adverse outcomes
  • Not good for large leaks >60%, BPD (different areas of lung fill differently)
168
Q

Describe the mechanism of HFOV?

A
  • Small tidal volumes (1-3ml/kg) with high frequencies (8-15Hz). Note 10Hz = 10 oscillations/sec = 600/min
  • Optimal lung volume strategy - recruits lung
  • Good for rescue, esp for recruitable lung disease
169
Q

In HFOV, increasing MAP and increasing amplitude does..?

A
  • Inc MAP: incr lung recruitment, lung volume, oxygenation

- Inc amplitude: inc tidal volume and CO2 removal, inc ventilation

170
Q

Adjusting HFOV settings: oxygenation and ventilation

A
  • Low O2: inc FiO2 or MAP (1-2cmH20)
  • High O2: decr FiO2 or MAP
  • High CO2: inc amplitude, decrease Hz frequency (if amplitude maximal), or inc tidal volume if on VG
  • Low CO2: decr amplitude, increase Hz (1-2Hz) if amplitude minimal, or decr TV if on VG
171
Q

What are the risk factors, investigations and treatment for metabolic bone disease of prematurity?

A
  • 30 weeks gestation, <1000g birthweight, male gender
  • Delayed establishment of full enteral feeds, fluid restriction
  • Prolonged TPN
  • Enteral feeds with low mineral content or bioavailability (unfortified EBM, term formula)
  • Short gut syndrome
  • Vitamin D deficiency
  • Ix: Ca, ALP, phosphate
  • Tx: preterm formula, HMF, Ca and phos supplements
172
Q

What are the expected saturations for a healthy newborn at 2, 3, 4, 5, and 10 minutes?

A

2 min = 60, 3 min = 70, 4 min = 80, 5 min = 85, 10 min = 90

173
Q

What cells are found in pustular melanosis and erythema toxicum?

A
  • Pustular melanosis - neutrophils

- Erythema toxicum - eosinophils and neutrophils

174
Q

What is the formula for calculating CO2 removal?

A

CO2 removal = f (rate) x Vt (diff between PIP and PEEP), aka amplitude

175
Q

The use of HFOV benefits…. and worsens…?

A
  • Benefit in air leak syndromes (pneumothorax, PIE)

- Small evidence could increase IVH

Paediatrics RACP written exam (18 decks)

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