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Paeds > Neonate > Flashcards

Neonate Flashcards

1
Q

ROP

A

Screening - <30 weeks - < 1250g

Other RF: TTTS, PPHN ON NO, grade 3/4 IVH, hydrops, severe sepsis

Plus disease - tortuousity of retinal vessels

Treatment

Zone 1 - any stage with plus; stage 3 w/o plus

zone 2- stage 2/3 with plus

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2
Q

LEOPARD Syndrome (noonan with multiple lentigenes)

A

Lentigenes (multiple brown black spots) ECG conduction Ocular hypertelorism Pulmonary stenosis Abnormal genitals Retarded growth (short stature) Deafness or inner ear malfunction Mutation PTPN11 mutation, AD you inheritance

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3
Q

HIE Cooling

A

Aim to decrease apoptosis and reduce glutamate/lactate/NO/free radicals causing damage

  • Ideal within 6 hours
  • Reduce core temp 33.5
  • Whole body best
  • For 72 hours

Reduced mortality and improves outcome at 18/12

Seizures managed with phenobarb

Prognosis: Ph < 6.7 90% death or severe impairment

Other High risk, low Apgar 5 mins Base deficit >22, decerebrate posture, seizures beyond 72hrs, severe lesions on imaging

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4
Q

Omphalocoele

A

60% associated other anomalies CHD BWS BWS Foetal overgrowth syndrome Imprinting defect Ch11 (IGF2 gene) Macroglossia Abdominal wall defect Hypoglycemia (hyperinsulinism) Ear lobe creases Hemi hypertrophy Facial nevus flammeus

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5
Q

Fetal NAIT Fetal platelets have antigens inherited from father, that not present on mum, maternal immune system recognised it as foreign and mounts immune response

A

Often occurs first pregnancy 2 most common antigens are 1. HPA 1a 2. HPA 5a Low platelets, risk bleeding, rare ICH ROLE IVIG, platelet transfusion

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6
Q

Fetal alcohol syndrome

A

IUGR Facial features - short palpebral fissures, epicanthic folds, smooth philtrum, thin upper lip Cardiac defects - ASD OR VSD Limb anomalies Developmental delay / ID

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7
Q

Infant diabetic mother’s Maternal hyperglycaemia causes fetal hyperglycaemia which causes fetal hyperinsulinism

A

Hypoglycemia Hyperinsulinism - LGA - cardiomyopathy (HOCM) - birth asphyxia - surfactant deficiency : RDS Mortality 5x increase INCREAsed risk still birth chromosomal abnormalities (3x risk) Fetal hypoxia and elevated haematocrit Jaundice Diazoxide for hyperinsulinism - Opens K ATP channel, beta cells pancreas, inhibits insulin release from pancreas SE sodium and water retention

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8
Q

HFOV Improve ventilation by

A

Decreasing frequency Increasing amplitude Improve oxygenation (increase MAP)

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9
Q

Tidal volume

A

4-7 ml/kg

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10
Q

Increase MAP

A

Increase PIP Increase PEEP (May increase CO2) Increase Ti / reduce Te

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11
Q

Oxygenation increase

A

Fio2 Map

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12
Q

Minute ventilation

A

VT X rr (200-300ml/kg)

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13
Q

Infantile Haemangiomas

A

1-3% newborns ; 3:1 Female to male

Preterm 30%, LBW 25%

Present at 2 weeks usually, rapid growth in first year (80%growth by 6/12), stabilise and involute from 12months (3-10years gone by)

GLUT1+ve

PHACES (9:1 F:M) - screen if segmental IH of head >5x5cm or if other anomalies

Alternative types: -RICH(rapid involute) -NICH(non involute)

  • older, glut1-ve, non response propranolol

Rx propranolol if needed SE

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14
Q

PHACES

A

9:1 F:M screen if segmental IH of head >5x5cm or if other anomalies - Posterior fossa ; - Haemangioma (segmental IH of face) - Arterial anomalies (AV malform, cerebral infarct) - Cardiac - Endocrine anomaly - thyroid, pituitary ; Eye abnormal Risk stroke, airway obstruction, SNHL, dysphagia, endocrine Rx Propranolol

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15
Q

Audiology tests and ages

A

Birth - ABR

Visual reinforcement test 6-12mo

Play audiometry 2-4 years

Pure tone audiometry 4 years

Tympanometry only measures middle ear pressures

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16
Q

Prelingual hearing loss

A

20% environmental

80% genetic

  • Syndromic 20%
  • Non syndromic 80%

80%recessive, 20% dominant

Connexin26 (GJB2 mutation most common non syndromic genetic cause

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17
Q

Syndromic hearing loss

A
  • Goldenhar (Oculo-Auricular-Vertenral syndrome) - Hemifacial microsomia, spinal problems, cardiac, hearing loss (SNHL + CHL)
  • Wardenburg - AD, 1:40,000, hearing loss from birth, SNHL ; white forelock, iris heterochromia
  • Brachio-Oto-Renal - AD, Branchial cleft anomalies, Ear problems-pits, hearing loss ; renal dysplasia (60%)
  • PENDRED -AR severe profound SNHL and goitre with normal TFTs(7% CHL)
  • NF
  • CHARGE
  • Treacher collins
  • Ushers
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18
Q

Tympanograms

A

A - Normal

B - Flat - OME, Cholesteatoma, Otosclerosis

C- high negative pressure w/o effusion (Eustachian tube dysfunction)

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19
Q

Subgaleal bleed

A

Occurs 1/200 vacuum delivery (1/2000 NVD) RF - 3+ pulls, >20mins effort, cup comes off ; contraindicated to do vacuum under 36weeks Fluctuating mass. Diffuse, crosses suture lines Can cause shock, can lose up 20-40% circulating volume Baby has 80ml/kg circulating volume 35ml blood needed to increase HC by 1 cm

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20
Q

Craniosynostosis

A

Craniosynostosis is premature closure of the cranial sutures, and is associated with varying skull shapes. ◾Primary craniosynostosis results from closure of one or more sutures owing to abnormalities of skull development. ◾Secondary craniosynostosis results from failure of brain growth and expansion. Primary craniosynostosis: ◾Occurs 1:2000 births. ◾Cause is unknown in the majority. ◾Deformational forces are important in occipital and frontal plagiocephaly. ◾Early detection of posterior skull shape is critical to allow successful intervention (e.g. physical therapy for torticollis.) Sagittal craniosynostosis: ◾Most common CSO affecting a single suture ◾~80% male ◾Results in scaphocepahly (boat-shaped head) ◾Frontal bossing, prominent occiput, normal occipto-frontal circumference, reduced biparietal diameter, small or absent anterior fontanelle ◾Nil hydrocephalus/normal ICP/normal neurology Metopic craniosynostosis: ◾Association with 19p chromosome abnormality ◾Results in trigoncephaly ◾Pointed forehead and midline ridge, hypertelorism Coronal Craniosynostosis: ◾18% of craniosynostosis ◾More common in females ◾Associated with Apert syndrome (with syndactyly) and Crouzon disease (with hypoplasia of the midface) ◾Unilateral - plagiocepahly, bilateral - brachycephaly, acrocephaly ◾Elevation of the eye socket, flattening of the ridge of the eye and displacement of the nose on the affected side, flat cheeks Lamboid craniosynostosis: ◾10-20% ◾More common in males ◾Right side affected in 70% cases ◾Flattening of occiput, bulging of ipsilateral forehead, ipsilateral ear is anterior and inferior Multiple craniosynostosis ◾Oxycephaly - tower skull with undeveloped sinuses and shallow orbits, elevated ICP Treatment: ◾Most cases are evident at birth as a result of premature suture fusion ◾Palpation of the suture reveals a prominent bony ridge ◾Fusion of the suture can be confirmed on skull x-ray ◾Premature fusion of only one suture rarely causes a neurological deficit ◾Sole indication for surgery is the child’s cosmetic appearance - prognosis depends on the suture involved and the degree of disfigurement ◾In general craniosynostosis can be surgically corrected with good outcomes and relatively low morbidity and mortality, especially for non-syndromic infants

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21
Q

Lung embryology

A

There are four stages of in utero lung development.

• Embryonic – up to 5 weeks

Pseudoglandular – weeks 6 – 16.

• Airways grow via branching out to terminal bronchioles

Canalicular – weeks 17 – 24.

  • More conventional architecture of lungs with initial development of alveolar acini, thinning out of distal cells, development of arterial and venous circulation.
  • Fluid in lungs.
  • Surfactant first starts to be produced.

Saccular stage – weeks 24 – 40.

• Respiratory bronchioles, alveolar ducts, alveoli develop and cells differentiate into type 1 (gas exchange) and type 2 (make surfactant) pneumocytes.

Alveolar stage – 36 weeks gestation until 24 months postnatal.

  • Further alveolar formation and maturation, secondary alveolar septa, cell proliferation and maturation.
  • 20-50 million alveoli by birth, 300 million alveoli by adulthood.

Development of lung contributed to by

  • Fetal / neonatal growth (nutrition)
  • Antenatal steroid exposure,
  • Transcription and growth factors,
  • Sufficient lung fluid,
  • Muscle tone and fetal breathing,
  • Toxicity (e.g. from oxygen, barotrauma, infection/ inflammation)
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22
Q

Craniosynostosis 2

A

Scaphocephaly – fusion of sagittal suture, resulting in elongation of anteroposterior axis of cranium. • It accounts for 50% of craniosynostosis cases, at a rate of 1 in 2000

Trigonocephaly – premature closure of metopic suture, resulting in a triangular shaped forehead. • It accounts for 10% of craniosynostosis cases

Plagiocephaly – premature closure of unilateral coronal or lambdoid sutures, resulting in a asymmetric or twisted skull. Incidence of 1 in 10,000. • Not to be confused with positional plagiocephaly

Acrocephaly – premature closure of combined sagittal, coronal and lambdoid sutures, resulting in elevation of anterior cranium. • Seen in Crouzon or Apert syndromes

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23
Q

Survival in preterm 23/40, 24, 25, 27, >30

A

23: 15% 24: 66% 25: 80% 27: 90-95% 30: 97-99%

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24
Q

Severe neurological disability ELBW

A

10-20%

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25
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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26
Q

HFOV under ventilated and under oxygenated change what settings

A

To improve ventilation (increase amplitude and then decrease Hz) AF To improve oxygenation (increase MAP)

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27
Q

Most common type oesophageal atresia

A

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

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28
Q

Hearing screen NZ and Aus use

A

Automated auditory brainstem response (aABR

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29
Q

Antigen in neonatal alloimmune thrombocytopenia

A

Human platelet antigens (HPA-1a)

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30
Q

Fetal haematopoeisis

A

Yolk sac from 2weeks – 2 months; liver 2-7 months; bone marrow starts at 3 months and predominates from 7th month

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31
Q

Which drug exposure in utero causes broad low nasal bridge epicanthal folds, wide spaced eyes, microcephaly, cleft lip and palate with hypoplasia distal phalanges

A

Fetal hydantoin syndrome from phenytoin

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32
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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33
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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34
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) Syndrome with cleft palate - Stickler syndrome - 22q11 deletion - Treacher-Collins syndrome

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35
Q

Describe neonatal lupus

A
  • Symptoms: 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)

Recurrence risk future pregnancies approx 20%

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36
Q

What develops from the endoderm?

A
  • Internal layer - Alveolar/lung cells, thyroid, GI, pancreas
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37
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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38
Q

What develops from the ectoderm?

A
  • Outer layer - Skin, pigment cells, central nervous system
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39
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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40
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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41
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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42
Q

Risks of hypertension/pre-eclampsia for neonate

A
  • SGA - Polycythaemia - Neutropenia, thrombocytopenia - Hypoglycaemia
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43
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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44
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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45
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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46
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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47
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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48
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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49
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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50
Q

Teratogenic effects of isotretinoin and high dose Vit A?

A

Cleft palate, hydrocephalus, CHD

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51
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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52
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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53
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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54
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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55
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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56
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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57
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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58
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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59
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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60
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)
  • Decreased Surfactant: prematurity, males, sepsis, diabetes, 2nd twin, elec C/S, FHx
  • Increased surfactant: females, PROM, maternal opiate use, IUGR, AN steroids
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61
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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62
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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63
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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64
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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65
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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66
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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67
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
68
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)
69
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 surger
70
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
71
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
72
Q

What reduces the risk of NEC?

A

AN steroids, probiotics, breast milk

73
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
74
Q

What are the complications of TPN?

A

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

75
Q

What anomalies are associated with duodenal atresia?

A

70% are associated with other abnormalities: T21 (1/3 of pt with DA have T21), CHD, malrotation

76
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 - Tx: resp support, suction catheter in oesophageal pouch, surgery

77
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
78
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
79
Q

Describe omphalocele + treatment

A
  • Failure of gut to return into abdominal cavity during development. Covered with peritoneum, may rupture at birth - 75% associated other anomalies - Beckwith-Wiedemann, trisomies, CHD - Tx: primary or staged surgical repair. If delayed then can use topical silver sulfadiazine to promote granulation of the peritoneal covering
80
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
81
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 Risk factors 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
82
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% Presentation >50% in first 24 hours, 10-20% day 2-3, 20-30% day 4-7
83
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 RD
84
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
85
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

86
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 RF: severe IVH, chorioamnionitis, hypoxia, ischaemia
87
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
88
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

89
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
90
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 Plus disease - 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
91
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 nephropath
92
Q

What are the investigations for ambiguous genitalia in a neonate?

A

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

93
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
94
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
95
Q

What is the definition of a micropenis?

A

Stretched penile length of <2.5cm

96
Q

Describe signs and treatment of neonatal GBS infection

A
  • 20-40% 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
97
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
98
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
99
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)

100
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
101
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)
102
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
103
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
104
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.
105
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
106
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
107
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
108
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
109
Q

What are the risk factors for RDS?

A

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

110
Q

What are the effect of prophylactic caffeine? CAP trial

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

111
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.
112
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)
113
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)
114
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
115
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
116
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
117
Q

Early vs late use of postnatal corticosteroids for CLD

A

arly (< 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

118
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
119
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
120
Q

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

A

Pneumomediastinum - air is displacing the lobes of the thymus upwards

121
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
122
Q

Lung lesion with systemic arterial connection?

A

Pulmonary sequestration

123
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
124
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
125
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

126
Q

Describe congenital diaphragmatic hernia

A
  • L sided, posterolateral most common (Bochdalek) - R sided (Morgagni) 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
127
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
128
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
129
Q

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

A

Occipital lobe

130
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
131
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
132
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
133
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
134
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)
135
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
136
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)
137
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
138
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
139
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
140
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
141
Q

What cells are found in pustular melanosis and erythema toxicum?

A
  • Pustular melanosis - neutrophils - Erythema toxicum - eosinophils and neutrophils
142
Q

High frequency oscillation can increase the risk of…

A
  • Pneumothorax - Hyperinflation - Airway damage - possibly IVH Decrease risk of CLD
143
Q

What area is most commonly affected in neonatal stroke?

A

Left MCA territory

144
Q

What tidal volume are you likely to ventilate a baby at?

A

4-6mL/kg

145
Q

What is the most important indicator of effective neonatal resuscitation?

A

Rise in heart rate

146
Q

What is the most likely cause of Horner syndrome in the neonate?

A
  • Birth trauma with shoulder dystocia - brachial plexus injury. - Klumpke palsy (C8, T1) - “claw hand” where the forearm is supinated and the wrist and fingers are hyperextended. - Horner’s secondary to injury of stellate ganglion. - unequal pupils
147
Q

If maternal blood is present on an APT test then what happens?

A
  • Akalised sample goes yellow after 2mins - If it stays pink, there is HbF
148
Q

What are the possible causes of hyponatremia in a 12 hour old term neonate?

A
  • SIADH secondary to maternal oxytocin administration (similarity to ADH, stimulates renal Na excretion) - Could be from excessive maternal fluid administration - Could be from excessive fluids for baby (usually okay as long as <90mL/kg/day)
149
Q

If you see a large facial port-wine stain think…

A
  • Sturge-Weber - opthalmology (as get glaucoma in that eye) - brain MRI second (get vascular brain problems)
150
Q

How do you calculate oxygenation index?

A

(FiO2 X MAP) / PaO2 (all in mmHg NOT kPa)

151
Q

What renal disease would you associate with congenital cataracts?

A

Lowe Disease (oculocerebrorenal)

152
Q

What drug teratogens are most associated with cleft palate and palate?

A
  • AEDS such as phenytoin, sodium valproate, and topiramate - methotrexate - folic acid may be protective
153
Q

What blood group combinations give you MORE risk of haemolytic disease of the newborn?

A

Rh incompatible WITHOUT blood group incompatibility is highest risk. Rhesus disease is more common than ABO disease BUT if mother and fetus are rhesus incompatible, the additional ABO incompitability decreases the risk of maternal sensitisation to Rh (because maternal anti-A or anti-B antibodies kill foetal RBC in maternal circulation prior to Rh antibody production)

154
Q

How much blood can a baby lose into a subgaleal?

A
  • 50-100mL (20-40%)
155
Q

Congenital gonorrhoea

A

-Neisseria gonorrhoeae -Delivery of the baby until 5 days after birth (early onset) - marked bilateral purulent discharge and local inflammation. Inflammation more marked than Chlamydia - Discharge re accumulates quickly when wiped - RX with Ceftriaxone 7 days - Prophylaxis if known to be at risk with topical ointment within 1 hour of birth

156
Q

Chlamydia trachomatis infection

A

– C. trachomatis is primarily transmitted to newborns via exposure to an infected mother’s genital flora during vaginal birth. - 5 days after birth to 2 weeks -The most frequent clinical manifestation of C. trachomatis infection in the newborn is conjunctivitis. - Clinical findings of conjunctivitis range from mild swelling with a watery eye discharge, which becomes mucopurulent, to marked swelling of the eyelids with red and thickened conjunctivae (chemosis). - A pseudomembrane may form as the exudate adheres to conjunctiva. The conjunctivae may also be very friable resulting in bloody discharge -Babies infected with chlamydia may develop pneumonitis (chest infection) at a later stage (range 2–19 weeks after delivery). Infants with chlamydia pneumonitis should be treated with oral erythromycin

157
Q

5 phases of neonatal lug development

A
  1. embryonic = 26 days to 6 weeks gestation 2. Pseudoglandular = 6-16 weeks 3. Canniculare = 16-28 weeks 4. Saccular = 28-36 weeks 5. Alveola = 36 weeks to infancy
158
Q

Bronchopulmonary dysplasia

A
  • babies <28 week gestation - more susceptible to lung injury -disruption of 3rd phase of lung development (16-28 weeks) = cannilicular and early saccular phase –> caused by medical treatments to babies <28 weeks resulting in dysmorphic growth and interrupted maturation
159
Q

Gastroschisis

A

-Separation in the abdominal wall, and evisceration of gastrointestinal contents (intestines) through a right paraumbilical defect, NOT covered by peritoneum. -Herniation can occur antenatally or perinatally. -Concurrent chromosomal anomalies in less than 5%, but bowel scarring, strictures/adhesions and atresias can be associated. Complications: FTT, short gut syndrome. RX: -Resuscitation and replacement of hypoalbuminaemia -Gastric decompression and wrap gastrointestinal contents initially -Cover with IVABx -TPN for nutrition -Primary closure for small lesions, staged surgical repair for larger lesions.

160
Q

Omphalocele

A

-Opening in the abdominal wall at site of umbilicus with herniation of the midgut, covered by peritoneum and amniotic membrane. -Due to embryological failure of the midgut to re-enter the abdomen -Incidence of 1:5000 -35-80% incidence of other clinical problems: trisomy 13, 18; Beckwith-Weidemann syndrome; renal malformations (bladder extrophy, Wilms tumour (40%)); congenital heart disease Other: cleft palate, and musculoskeletal and dental occlusion abnormalities. RX: -Resuscitation and replacement of hypoalbuminaemia -Gastric decompression and wrap gastrointestinal contents initially -Cover with IVABx -TPN for nutrition -Primary closure for small lesions, staged surgical repair for larger lesion

161
Q

Persistent hyperinsulinaemic hypoglycemia

A
  • if persistent often genetic component –> especially ATP gated K channel K channel at baseline normally should be OPEN Defect results in K channel being CLOSED Normally: Glucose –> B cell via Glut2 receptor –> glucokinase phosphorylates into Glucose-6-phosphate releasing ATP —> ATP binds to K channel –> K channel CLOSES –> intracellular K RISES –> membrane of cells DEPOLARISE –> voltage gated calcium channels OPEN –> calcium floods INTO cells–> insulin released into blood by exocytosis In PHH: K channel remains CLOSED the whole time –> high K+ ALL the time –> cell membrane depolarised ALL the time –> calcium influx ALL the time –> Insulin secreted ALL the time = high circulating insulin Rx: Diazoxide –> forces ATP dependent K channels to open
162
Q

Indications HFOV

A

At present HFOV is only indicated as a rescue therapy Failure of conventional ventilation in the term infant (Persistent Pulmonary Hypertension of the Newborn [PPHN], Meconium Aspiration Syndrome [MAS]). NB: The evidence for HFOV in term infants with severe pulmonary dysfunction is not strong. Air leak syndromes (pneumothorax, pulmonary interstitial emphysema [PIE]) Failure of conventional ventilation in the preterm infant (severe RDS, PIE, pulmonary hypoplasia) or to reduce barotrauma when conventional ventilator settings are high. HFOV is not as yet proven to be of benefit in the elective or rescue treatment of preterm infants with respiratory dysfunction and may be associated with an increase in intraventricular haemorrhage. Furthermore, caution is needed when HFOV is used as high airway pressures may result in impaired cardiac output causing hypotension requiring inotropic support or volume expansion. Some infants poorly tolerate the extra handling involved in switching ventilators or may not respond to HFOV. If there is no improvement with HFOV, consider reverting to conventional ventilation.

163
Q

Adjusting settings on HFOV

Increase Oxygenation

Increase Ventilation

A
164
Q

Aortic arches

A
165
Q

Layers skull

A
166
Q

Energy content of breastmilk

A

60-70kcal/100ml

Energy requirements for preterm 120kcal/kg/day (180ml/kg/day)

Paeds (25 decks)

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