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Peadiatrics > Neonatology > Flashcards

Neonatology Flashcards

1
Q

What are causes of polyhydramnios?

A

(Severe)

  1. Fetal anomalies - Decreased swallowing (GI obstruction) or increased amniotic fluid production (renal hyperperfusion)
  2. Aneuploidies (T21, T18)

(Milder)

  1. Maternal diabetes
  2. Multiple gestation
  3. Idiopathic - Fetal anaemia, Bartter syndrome, infection (TORCH), neuromuscular disorders
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2
Q

What are the parameters for AFI?

A

AFI 8-18 = Normal
AFI <5-6 = Oligohydramnios
AFI >24-25 = Polyhydramnios

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3
Q

What are the energy requirements of infants?

A

Infants with chronic illness = 150 kcal/kg/day
Premature infant = 120 kcal/kg/day (enterally fed)
= 80-100 kcal/kg/day (parenterally fed)
Term neonate = 100-120 kcal/kg/day
1-12 months = 90-100 kcal/kg/day
1-6 years = 75-100 kcal/kg/day

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4
Q

How much protein do infants require?

A

Premature = 2.5-3g/kg/day
Infants (0-1 years) = 2.5g/kg/day
Children (2-13 years) = 1.5-2g/kg/day
Adolescents/adult =

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5
Q

What are the insensible fluid losses in a neonate?

A 
<750g = 4ml/kg/hr 
750-1000g = 3ml/kg/hr 
1000-1500g = 2ml/kg/hr 
>1500g = 1ml/kg/hr
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6
Q

What are causes of increased insensible fluid losses?

A

Increased RR, surgical malformations, increased ambient temperature, increased motor activity

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7
Q

What are the causes of decreased insensible fluid losses?

A

Use of incubators, humidification of inspired gas, increased ambient humidity, thin plastic barriers.

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8
Q

What is the most common aneuploidal cause of non-immune fetal hydrops?

A

Turner syndrome

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9
Q

What is the most common group cause of non-immune hydrops fetalis?

A

Cardiovascular - Accounts for around 40% of cases

  1. Structural
  2. Arrhythmias
  3. Vascular
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10
Q

What is the most common cause of non-immune fetal hydrops in Southeast Asians?

A

Alpha-thalassaemia.

Fetal hydrops develops early mid-trimester.

AR condition, with mutation/deletion of haemoglobin alpha gene. Gamma chains accumulate to form haemoglobin Barts (which bind oxygen but cannot release). Can see using high-performance liquid chromatography or electrophoresis.

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11
Q

What is the most common intrathoracic mass cause of non-immune hydrops fetalis?

A

Congenital pulmonary malformation

Bronchopulmonary sequestration

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12
Q

What are the broad categorical causes of non-immune hydrops fetalis?

A

Cardiovascular (40%) - Structural, arrhythmias, vascular
Anaemia (10-27%) - Alpha thalassaemia (SEA)
Aneuploidy (7-16%) - Turner
Syndromes (5-10%) - e.g. Noonan
Infection (5-10%) - Parvovirus B19
Thoracic and lymphatic abnormalities (10%)
Twin gestation
Genitourinary and gastrointestinal abnormalities
Inborn errors of metabolism - e.g. Lysosomal storage
Skeletal dysplasias

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13
Q

Where do neonates lose their insensible fluids?

A

2/3 skin

1/3 respiratory tract

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14
Q

What is the difference in body water composition in neonates compared with adults?

A 
Neonates = 70% water 
Adult = 60% water

Preterm neonates have proportionally more water than term (e.g. 90% at 23/40)

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15
Q

What is the definition of ‘extremely low birth weight’ and ‘extremely preterm’?

A

Extremely preterm = GA <28 weeks
Very preterm = GA 28-31+6
Moderate preterm = GA 32-33+6
Late preterm = GA 34-36+6

Extremely low birth weight = <1000g
Very low birth weight = <1500g
Low birth weight = <2500g

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16
Q

What conditions are associated with preterm births?

A

Bronchopulmonary dysplasia
Perinatal infections (NEC, sepsis, meningitis)
ROP
IVH
Poor growth
Congenital anomalies
Surgical procedures during birth hospitalisation

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17
Q

What is the commonest cause of oligohydramnios?

A

Rupture of membranes

Usually occurs in third trimester

  1. First trimester - Aetiology often unclear, poor prognosis.
  2. Second trimester -Related to renal/urinary disorders. Also maternal and placental factors (PPROM, placental abruption, FGR)
  3. Third trimester - PPROM, uteroplacental insufficiency
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18
Q

What maternal drugs affected metabolism of vitamin K in the neonate?

A
  1. Warfarin
  2. Anti-tuberculosis drugs
    e. g. rifampin, isoniazid)
  3. Antiseizure drugs
    e. g. phenytoin, barbiturates, carbamazepine
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19
Q

What are the causes of DIC in the newborn?

A 
Hypoxia
Hypotension 
Asphyxia 
Sepsis (bacterial or viral) 
NEC 
Neonatal cold injury 
Neonatal neoplasm 
Hepatic disease 
Death of twin in utero
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20
Q

What are the haematological markers of DIC?

A 
Increased aPTT and PT ++ 
Decreased platelets 
Microangiopathic haemolytic anaemia 
Decreased fibrinogen 
Increased fibrin degradation products
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21
Q

Which maternal drugs cause thrombocytopenia in the newborn?

A

Quinine, quinidine, thiazide diuretics, sulfonamides

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22
Q

Apart from maternal drugs and syndromic causes, what are non-syndromic causes of thrombocytopenia in a well neonate?

A
  1. Transient ISOIMMMUNE thrombocytopenia
    Antiplatelet antibodies produced by HPLA-1 negative mother to paternal platelet antigen (HPA-1a and HPA-5b). Crosses placenta to baby.
  2. Transient NEONATAL thrombocytopenia
    Transfer of maternal IgG antibodies across placenta directed against all palatelet antigens (BOTH mother and baby have decreased platelets)
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23
Q

What is the leading cause of non-hereditary sensorineural hearing loss?

A

Congenital CMV infection

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24
Q

What are the symptoms of congenital CMV infection?

A
  1. Sensorineural hearing loss (33-50%)
    Can be delayed and bilateral.
  2. Chorioretinitis
    Other ocular: Retinal scars, optic atrophy, central vision loss)
  3. Somatic menifestations
    (Jaundice, petechiae, microcephaly)
  4. Ascites, myocarditis, cardiomyopathy, ventricular trebeculations

(Can present as fulminant disease with viral-associated haemophagocytic syndrome or severe end-organ disease.

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25
Q

What is the most common ocular abnormality in congenital CMV?

A

Chorioretinitis

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26
Q

What is the transmission rate to infant in primary vs. secondary congenital CMV?

A

Primary - 50% risk transmission; symptomatic in 10% cases, and carry 90% risk of sequelae.

Non-primary - <1% risk transmission; >99% will have asymptomatic congenital CMV (of these, 5% SNHL, 2% chorioretinitis)

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27
Q

What are in utero ultrasound findings suggestive of CMV disease?

A 
Periventricular calcifications 
Ventriculomegaly 
Migrational abnormalities of brain
Microcephaly 
FGR
Ascites/pleural effusion
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28
Q

Apart from SNLH, choriorenitis and microcephaly, what are other common signs seen in congenital CMV?

A 
Petechiae 
Jaundice at birth 
Hepatosplenomegaly 
SGA 
Poor suck
Lethargy and/or hypotonia
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29
Q

What are the lab findings in congenital CMV?

A 
Increased LFTs (transaminases) 
Thrombocytopenia
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30
Q

Within what timeframe does diagnosing virologically proven CMV differ from possible CMV?

A

Less than 3 weeks.

If results positive after 3 weeks, can be either congenital or acquired postnatally.

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31
Q

When do you commence antiviral therapy in congenital CMV infection?

A

For symptomatic infants (>/=1 symptoms at birth), with virologically-proven CMV infection and at least one end organ system

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32
Q

What is the difference between valgangiclovir and ganciclovir?

A

Ganciclovir (IV)

Valganciclovir (PO - prodrug to ganciclovir)

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33
Q

What is the definition of avidity and what is its use in congenital CMV?

A

Avidity = The aggregate strength with which a mixture of polyclonal IgG molecules bind to multiple antigenic epitope of proteins

LOW avidity = Recent primary infection
HIGH avidity = Past infection

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34
Q

What blood type (of both mother and neonate) is most common seen in ABO haemolysis of the newborn?

A

Mother - O type
Neonate - A type

Naturally occurring antibodies in type A or B mothers are IgM (does not cross placenta as too large). 1% blood O mothers produce IgG

Haemolysis due to anti-A is more common than anti-B

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35
Q

What factors affect drug placental transfer?

A
  1. Size - Molecular weight < 600 cross placenta. Most >1000 Da do not (heparin, protamine, insulin)
  2. Charge - Non-ionised drugs tend to cross more easily
  3. Protein binding - Generally taught that protein-bound less easily crosses planceta
  4. Lipiphilicity - Generally advantageous with regards to placental transfer (unless extreme lipophilic as can accumulate in placenta)
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36
Q

How much glucose per minute does a neonate require?

A

6-8mg/kg/min - Neonate

4-6mg/kg/min - Infant/child

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37
Q

What are drugs that do not cross the placenta?

A

Insulin
Heparin
All paralytics
Glycopyrrolate

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38
Q

Which site of the placenta is involved in the exchange of nutrients and gases between maternal bloodstream and fetus?

A

Synctiotrophoblast

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39
Q

What is the most common infectious agent causing neonatal conjunctivitis?

A

Chlamydia trachomatis

Weakly Gram negative
Obligate intracellular parasites

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40
Q

What is the treatment for chlamydial conjunctivitis?

A

Oral erythromycin (not topical)

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41
Q

What is the incubation period of neonatal conjunctivitis depending on microbial cause?

A

N. gonorrhoea = Appears 2-5 days after birth
C. trachomatis = 5-14 days
Non-gonorrheal, non-chlamydia cause= 5-14 days
HSV = Presentation within 2 weeks

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42
Q

What is the treatment for gonorrhea conjunctivitis?

A

Ceftriaxone (IV/IM)

Gram-negative diplococci (kidney-shaped)

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43
Q

What are the clinical findings in neonatal brachial plexus injuries?

A

C5. C6 (Erb’s) = Upper arm adducted, IR, forearm extended, hand and wrist normal

C5, C6, C7 (Erb’s plus) = Waiter’s tip posture - As above with flexion of wrist and fingers

C5 to T1 = Arm paralysis with some sparing of finger flexion. Flail arm and Horner if severe

C8, T1 (Klumpke) = Isolated hand paralysis and Horner

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44
Q

Where are brachial cleft cysts found in relation to the sternocleidomastoid muscle?

A

Anterior

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45
Q

What are some causes of asymmetric vs symmetric IUGR?

A

Asymmetrical: (70%)

  1. Chronic high blood pressure
  2. Severe malnutrition
  3. Some genetic mutations (Ehler-Danlos, Russell-Silver)
  4. Multiple gestation
  5. Abnormal placental structure
  6. High altitude
  7. Uteroplacental insufficiency

Symmetrical: (30%)

  1. Early intrauterine infections
  2. Chromosomal abnormalities
  3. Anaemia
  4. Maternal substance abuse
  5. Cigarette smoking
  6. Maternal SLE
  7. Chromosomal deletions, inborn errors of metabolism
46
Q

What is the most common bone fracture in neonatal delivery?

A

Clavicle

Reduced movement and Moro of affected. Usually conservative, rarely requires immobilisation

47
Q

What is the clinical course of neonatal hepatitis B and how is it prevented?

A

Usually asymptomatic

  • Mild, often persistent raised LFTs at 2-6 months. Small number develop acute hepatitis by 2 months age.
  • Most develop chronic infection, which may progress to cirrhosis and hepatocellular carcinoma

Infants with HbsAg positive mothers:

  1. Universal hepatitis B vaccination
  2. HBIg (immunoprophylaxis)
48
Q

Is hepatitis B transferred through breastmilk?

A

No, breastfeeding not contraindicated. Does not increase transmission

Infection rate 90% in neonates who do not receive prophylaxis who are born to HBV-infected mother

49
Q

What are the major causes of neonatal mortality?

A
  1. Prematurity/low birth weight
  2. Congenital anomalies

Accounts for 2/3 of all infant deaths

50
Q

What factors reduce risk of neurodevelopmental impairment or death?

A
  1. Higher birthweight
  2. Female
  3. Singleton birth
  4. Antenatal steroids
51
Q

What are risk factors for subgaleal haemorrhage?

A
  1. Prolonged second stage
  2. Large infants
  3. Cephalopelvic disproportion
  4. Neonatal coagulopathy
52
Q

What are the anatomical boundaries of extracranial injuries?

A

Caput = Oedematous swelling of soft tissues of the scalp

Cephalohaematoma = Subperiosteal haemorrhage

Subgaleal = Bleed beneath the aponeurosis (serves as insertion for occipitofrontalis muscle)

53
Q

What is the most serious complication of chronic oligohydramnios?

A

Pulmonary hypoplasia

54
Q

How do you interpret maternal serum alpha-fetoprotein?

A 
Elevated MSAFP: 
'RAIN' - umbrella 
R - renal anomalies 
A - abdominal wall defects 
I - incorrect dating (most common); multiples (twins) 
N - neural tube defects

Low MSAFP:

  1. Trisomies - 13, 18 and 21 (MSAFP is down with Downs)
  2. IUGR
  3. Incorrect dating

**Note that incorrect dating can either raise or lower MSAFP depending on whether too early vs. late

55
Q

What are complications associated with IUGR in the perinatal period?

A 
Preterm delivery 
Perinatal asphyxia 
Impaired thermoregulation 
Hypoglycaemia 
Polycythaemia and hypervisciosity 
Impaired immune function 
Mortality
56
Q

What factors of the oxygen dissociation curve affect neonatal cyanosis?

A

Shift to the LEFT:

  1. Alkalosis (increased pH)
  2. Hyperventilation (decreased PCO2)
  3. Cold (decreased temp)
  4. Decreased 2,3 diphosphoglycerate (DPG)

Shit to the RIGHT:

  1. Acidosis
  2. Fever
  3. Increase in adult Hb
57
Q

What are the broad pathophysiological causes of central cyanosis in a neonate?

A

Alveolar hypoventilation
Ventilation-perfusion mismatch
Right-to-left shunting
Diffusion impairment

58
Q

How do you differentiate a central nervous system disorder vs. neuromuscular disease?

A

Generally:

CNS disorder = Reduced tone > reduced muscle strength
Neuromuscular disorder = Absent or very reduced antigravity movement

59
Q

In a neonate with facial nerve palsy, what is the other cranial nerve commonly affected in intracranial injury?

A

6th nerve palsy

60
Q

What is the best measure of neonate’s response to heat and cold stress and at what temperature should it be maintained at?

A

Skin temperature > rectal/core
- Reflects alterations of skin blood flow as initial response before any change in heat production

Aim for abdominal temperature 36 degrees (36.1-36.8)

61
Q

What are the clinical features of neonatal cold injury?

A

(Initial)
Apathy, food refusal, oliguria, coldness to touch.
Body temperature 29/5-35.5
Immobility, oedema, redness to extremities, erythema of face
Associated with haemorrhagic manifestations (e.g. pulmonary haemorrhage)

Hypoglycaemia and acidosis common
10% mortality
Treat by warming

62
Q

What are complications in infants of diabetic mothers?

A
  1. Increased risk congenital anomalies (poor metabolic control during periconception and organogenesis; cardiac malformations and lumbosacral agenesis most common; also NTD, hydronephrosis, renal agesis; small left colon syndrome)
  2. Pre-term delivery
  3. Perinatal asphyxia (macrosomnia and cardiomyopathy)
  4. Macrosomnia (excessive nutrients)
  5. Birth injury (macrosomnia)
  6. RDS occurs more frequently (delay surfactant production, more likely pre-term)
  7. Polycythaemia and hyperviscosity (increased EPO) -> renal vein thrombosis
  8. Low iron stores (inverse to degree of polycythaemia)
  9. Hyperbilirubinaemia
  10. Cardiomyopathy (thickening IV septum; usually transient)
  11. Hypoglycaemia, hypocalcaemia, hypomagnesaemia
63
Q

What are causes of neonatal cholestasis?

A
  1. Biliary atresia (most common; = progressive idiopathic disease of extrahepatic biliary tree)
  2. Infections (TORCH, UTI)
  3. Alagille syndrome (= paucity of interlobular ducts; AD)
  4. Inborn errors of metabolism
  5. Cystic fibrosis
  6. Parenteral nutrition
64
Q

Which maternal immunologic diseases adversely affect the newborn and why?

A

IgG antibodies.

ITP, SLE, myasthenia and Graves disease

65
Q

What are available chemical indices for fetal maturity of lungs and kidneys?

A

Amniotic fluid creatinine (kidney) and lecithin (lung) functions.

Lecithin is produced by alveolar type II cells. Until middle of T3, concentration nearly equals that of sphingomyelin; thereafter sphingomyelin constant while lecithin increases. Thus at 35/40, L:S ratio around 2:1 = mature lung. If < 2:1 = immature

66
Q

What are significant findings on fetal antenatal USS?

A
  1. Dilated cerebral ventricles (hydrocephalus, hydraencepahlous, Dandy-Walker cyst, agenesis corpus callosum)
  2. Choroid plexus cyst (T21/18, aneuploidy)
  3. Nuchal pad thickening (T21/18, Turner)
  4. Dilated renal pelvis (uteropelvic junction obstruction, VUR, PUV, entopic ureterocele)
  5. Echogenic bowel (CF, aneuploidy)
  6. Small or absent stomach, or with double bubble (upper GI obstruction, duodenal atresia; >30% with double bubble have T21)
67
Q

What are the maternal effects of smoking on the neonate/pregnancy?

A

PREGNANCY
Placental abruption, placenta praevia, preterm labour, LBW, ectopic pregnancy

NEONATE
SIDS, respiratory infections (bronchitis, pneumonia), asthma, atopy, otitis media, infantile colic, short stature, shorter attention spans, childhood obesity, decreased school performance

68
Q

What is the most serious complication of neonatal lupus?

A

Complete heart block

2% of newborns of mothers with anti-Ro or La antibodies.

69
Q

What are the clinical findings of hypermagnesaemia in the newborn?

A

Usually in neonates whose mothers treated with magnesium sulfate for pregnancy-induced hypertension or tocolysis.

Associated with: 
1. Respiratory depression
2. Apnoea 
3. Generalised hypotonia 
Additional complications: 
1. GI hypomotility 
2. Meconium plug syndrome (mimicking intestinal obstruction)

Typically self limited; levels normalise within several days.
Severe cases = IV calcium and diuretics

70
Q

What are the fetal effects of intrahepatic cholestasis of pregnancy?

A

ICP = c/b pruritus and elevation of serum bile acids; typically develops in T2/3; rapidly resolve after delivery. Pruritus predominantly palms and soles, worse at night.

Fetal effects:

  1. Increased risk intrauterine demise
  2. Meconium-stained amniotic fluid
  3. Preterm delivery
  4. Respiratory distress syndrome (a/w bile acids entering lungs)

Tx (maternal) = ursodeoxycholic acid, given before term
No fetal/neonatal toxicity

71
Q

What are the features of fetal alcohol syndrome?

A

= Most common known cause of preventable intellectual disability

Risk factors = alcohol during pregnancy, older maternal age, women of higher parity, poor maternal nutritional status

FEATURES
1. IUGR, microcephaly with growth failure persisting throughout childhood and adolescence
2. Dysmorphic facial features - 3 in DIAGNOSTIC CRIETRIA = small palpebral fissure, thin vermilion border, smooth philtrum
Also: small, upturned nose, broad nasal bridge, hypoplastic midface
3. Increased risk cleft lip +/- cleft palate; micrognathia
4. Septal defects - esp. ASD
5. Renal anomalies
6. Visual and auditory defects
7. MSK findings - 5th finger clinodactyly, fixed flexion of digits, hypoplastic nails
8. Developmental delay, learning disorders, lower IQ (almost all universally present with varying severity)
9. Behaviour disorders (ADHD, poor socialisation)

72
Q

What is a neonate most at risk of with maternal lithium use?

A

Cardiac malformations
- Especially Ebstein anomaly = apical displacement of septal leaflet of tricuspid valve and a displace, elongated anterior leaflet

73
Q

What are the features of fetal hydantoin syndrome?

A

= use of PHENYTOIN during pregnancy (phenytoin embryopathy)
Category D drug

FEATURES

  1. Microcephaly, brachycephaly, midface hypoplasia, low-set ears, mild hypertelorism, depressed nasal bridge, cleft lip and palate.
  2. Digits of hands and feet often hypoplastic
  3. Cardiac defects - coarctation of aortia, endocardial cushion defect, septal defects
  4. Increased risk of coagulation defects
  5. Genitourinary defects
  6. Increased risk of certain neoplasms - neuroblastoma, mesenchymoma, Wilms tumour
74
Q

What are neonatal effects of maternal ACEI use?

A

ACEI contraindicated THROUGHOUT pregnancy - cross placenta and inhibit renin-angiotensin system -> decrease GFR and urine production -
oligohydramnios

FIRST TRIMESTER
Congenital cardiovascular and CNS anomalies = most common
e.g. septal defects, PDA, neural tube defect

SECOND/THIRD TRIMESTER
Renal anomalies = most common
Also fetal growth restriction, oligohydramnios (due to decrease urine production), in utero fetal demise, neonatal renal failure

Surviving infants often have limb and hand anomalies, widely spaced eyes, low-set ears, posteriorly rotated ears, and facial deformities (small chin, beaked nose, unusual facial creases) resulting from compression of fetus in uterus (Potter syndrome)

75
Q

What is the recommended delivery room temperature for newborns?

A

23-25 degrees Celsius

as per AAP Committee

76
Q

What are the teratogenic effects of warfarin?

A

Nasal hypoplasia

Also more prone to bleeding due to vitamin K antagonism

77
Q

What drug is associated with neural tube defects?

A

Antiepileptics
e.g. valproic acid, carbamazepine

NTD = result from failure of neural tube to close spontaneously between 3rd and 4th week in utero development

78
Q

What drugs are thought to be associated with gastroschisis?

A

Vasoactive drugs

e.g. cocaine, nicotine, pseudoephidrine

79
Q

What are the neonatal effects of maternal propanolol use?

A

Decreased placental perfusion
Fetal bradycardia
Hypoglycaemia
Thrombocytopenia

80
Q

What is associated with small left colon syndrome?

A

Maternal diabetes

Seen in infants of diabetic mothers.
= Colonic obstruction involving significant caliber reduction in the sigmoid and descending colon that is unrelated to meconium inspissation or aganglionosis.

Associated with transient inability to pass meconium.

Resolves spontaneously

81
Q

What are IUGR neonates at risk of later on in (adult) life?

A

NEURODEVELOPMENT

  1. Intellectual and neurologic deficit
  2. Neurodevelopmental impairment (mental retardation, CP, blindness, deafness)
ADULT CHRONIC DISORDERS
(Barker hypothesis = Fetal undernutrition results in changes in vascular development)
1. Coronary heart disease 
2. Hyperlipidaemia 
3. Hypertension 
4. Chronic kidney disease
5. Type II DM 
6. Obesity 
7. Fatty liver disease
8. ?Growth abnormalities
82
Q

What is the follow-up regimen for infants of HBsAg-positive mothers?

A

HBIg and HepB vaccine within 12 hours of birth

Completion of HepB vaccine: 1-2 months of age; and 6 months (unless weigh <2000g as birth dose not counted thuerefore 3 additional doses needed beginning at 1-2 months)

Infant tested for anti-HBs and HBsAg at 9-12 months

  • > If anti-HBsAg levels >/= 10 mIU/mL: immune; no follow-up
  • > If <10 mIU/mL + HBsAg-negative: reimmunised HepB at 2 month intervals; retested for anti-HBsAg 1-2 months after third dose
83
Q

What are the indications of surgery for an umbilical hernia?

A

Often associated with diastasis recti.

Most appear before 6 months; disappear by 1 year

INDICATIONS FOR SURGERY

  1. Persists to age 4-5 years
  2. Causes symptoms
  3. Strangulated
  4. Progressively larger after 1-2 years age
84
Q

What is the triad for renal vein thrombosis?

A

TRIAD

  1. Sudden onset gross haematuria
  2. Unilateral (usually)/bilateral (results in renal failure) flank mass
  3. Thrombocytopenia

OTHER SYMPTOMS
Hypertension, microangiopathic haemolytic anaemia, oliguria

CAUSES IN NEWBORNS
Asphyxia, dehydration, shock, sepsis, hypercoagulable states, maternal diabetes

INVESTIGATIONS

  1. USS - renal enlargement
  2. Radionuclide studies - little or no renal function
  3. Doppler flow of IVC and renal vein to confirm diagnosis

Avoid contrast studies

85
Q

What are causes of craniotabes in a neonate?

A

= Softened, thinned, flexible area of the cranial bones, usually over the parietal or occipital region
(pressing down sensation like ‘ping-pong’ ball)

CAUSES
Syphillis
Intrauterine crowding

If PERSISTENT >6-9 months, can be: 
Rickets 
Hypervitaminosis A 
Vitamin D deficiency in utero 
Osteogenesis imperfecta 
Hydrocephalus
86
Q

How do you test for congenital syphilis?

A

SCREENING
(Nontreponemal tests)
- Titers increase with active disease and decline with adequate treatment
1. Veneral Disease Research Laboratory (VDRL)
2. Rapid plasma reagin (RPR)

CONFIRMATORY TESTS
(Treponemal tests)
- Measure specific T. pallidum antibodies (IgG/M/A) which appear earlier than nontreponemal antibodies
- Do not correlate with disease activity
- Usually remain positive for life
1. T. pallidum haemagglutination assay
2. Fluorescent treponemal antibody absorption test

87
Q

Which types of twins are at risk for twin-to-twin transfusion?

A

Monozygotic twins with same placenta (i.e. monochorionic)

  • Monozygotic twins with dichorionic placentation NOT at risk
  • Both can have hydrops fetalis

DIZYGOTIC TWINS
70% twin pregnancies
Always have separate placentas (dichorionic)
Most reliable sign of dizygosity is different sex fetuses
Risk factors: IVF, advanced maternal/paternal age, family history, ethnicity (Nigerian)

MONOZYGOTIC TWINS
30% twin pregnancies
No maternal/paternal age or ethnic predisposition
Time at which separation occurs determines chorionicity and amnionicity

88
Q

What are two distinguishing features between Apert and Crouzon syndrome?

A

Both are syndromic carniosynonstosis

Syndactyly in Apert - ‘mitten hand’ fusion of 2nd, 3rd, 4th and sometimes 5th fingers

Ocular proptosis more prominent in Crouzon

89
Q

What is the associated risk of macrolide antibiotics (erythromycin, azithromycin)?

A

Pyloric stenosis

90
Q

What maternal infections are contraindications to breastfeeding?

A

HIV
Active tuberculosis
Human T-cell lymphotrophic virus types 1 and 2
Herpes virus infection on breast
Maternal treatment with some radioactive compounds

91
Q

What are the indications for therapeutic hypothermia in HIE?

A

= 72 hours of hypothermia at 33-35 degrees celsius; started within the first 6 hours after delivery
(only proven neuroprotective therapy for treatment of neonatal encephalopathy)

  1. GA >/= 36 weeks and = 6 hours age
  2. pH = 7.0 OR base deficit >/= 16 mmol/L in a sample of umbilical cord blood or any blood obtained within the first hour after birth
  3. One of the following:
    i) a 10-minute Apgar of <5
    ii) ongoing resuscitation (assisted ventilation, chest compressions, cardiac medication) initiated at birth and continued for at least 10 minutes
  4. Moderate to severe encephalopathy on clinical examination (Sarnat examination)
92
Q

What are the indications for mechanical ventilation in neonates?

A
  1. Respiratory acidosis (arterial pH <7.2 and PaCO2 >60-65 mmHg)
  2. Hypoxia (arterial PaO2 < 50mmHg) OR when FiO2 >40% on nCPAP
  3. Severe apnoea
93
Q

What are the benefits of providing mechanical ventilation?

A

Improved gas exchange
Decreased WOB
Provide adequate minute ventilation

94
Q

What are the XR changes seen with meconium aspiration?

A
  1. Increased lung volumes
    = hyperinflated with flattened diaphragm; secondary to distal small airway obstruction and gas trapping
  2. Asymmetric patchy pulmonary infiltrate
    = due to subsegmental atelectasis; may be ‘ROPE-LIKE’
  3. Pleural effusion
  4. Pneumothorax or pneumomediastinum (20-40%)
    = due to increased alveolar tension from obstructed airways
  5. Multifocal consolidation
    = due to chemical pneumonitis
95
Q

What conditions are a single umbilical artery associated with?

A

T18
Cardiac and urogenital abnormalities

In general -> think congenital abnormalities

96
Q

What is placenta accreta spectrum?

A

= term to describe abnormal trophoblast invasion into the myometrium of the uterine wall

Results from placental implantation at an area of defective decidualisation typically caused by secondary damage to the endometrial-myometrial surface

PLACENTA ACCRETA
Anchoring placental villi attach to the myometrium (rather than decidua)

PLACENTA INCRETA
Anchoring placental villi penetrate into the myometrium

PLACENTA PERCRETA
Anchoring placental villi penetrate through the myometrium to the uterine serosa or adjacent organs

97
Q

What is the highest risk factor for preterm delivery?

A

History of previous preterm delivery

98
Q

The incidence of congenital malformations in diabetic mothers is related to what?

A

Degree of maternal hyperglycaemia PRIOR to conception

99
Q

What is the HbA1c aim both before and during pregnancy?

A

< 6%

100
Q

What are the causes of nasal stuffiness in the neonatal period?

A

Mucus in nostrils
Trauma
Opiate withdrawal
Congenital syphillis (haemorrhagic, thick, purulent)

101
Q

What are causes of a protruding tongue in a neonate?

A 
Down syndrome 
Beckwith-Wiedemann syndrome 
Hypothyroidism 
Isolated macroglossia 
Haemangioma
102
Q

What syndromes are associated with cystic hygroma?

A

Turner syndrome
Klinefelter syndrome
T13, 18, 21

= lymphangioma caused by abnormal development of the lymphatic system -> obstruction of lymphatic flow and sequestration of lymphatic fluid

Associated karyotypic abnormalities seen in 70%

103
Q

Oedema/webbing of the neck and widely spaced nipples are seen in what 2 syndromes?

A

Turner syndrome

Noonan syndrome

104
Q

What is hemihypertrophy of the limbs associated with?

A

Wilms tumour
Hepatoblastoma
Adrenal carcinoma

105
Q

In what syndrome are overriding fingers (index over 3rd; 4th over 5th) seen?

A

Trisomy 18

106
Q

In what disease in thumb hypoplasia seen in?

A

Fanconi anaemia

107
Q

What are causes of a high-pitch cry in a neonate?

A 
CNS abnormalities (e.g. HIE) 
Neonatal abstinence syndrome
108
Q

What syndromes is clinodactyly seen in?

A

Down syndrome (T21) (5th finger with hypoplastic mid-phalynx)
Fetal alcohol syndrome (5th finger)
Russell-Silver syndrome (5th finger)

109
Q

In what congenital infection do you see haemorrhagic rhinitis ‘sniffles’?

A

Congenital syphilis

110
Q

What is Hutchinson’s triad and what is it a sign of?

A

Congenital syphilis

Think ‘eye, ear, mouth’

  1. Malformed teeth (Hutchinson’s incisors, mulberry molar)
  2. CN VIII deafness
  3. Interstitial keratitis (corneal scarring due to chronic inflammation of corneal stroma)

Peadiatrics (13 decks)

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