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Neonatology Flashcards

1
Q

Which congenital heart lesions are cyanotic? (3)

A

Those that involve R–>L shunts (blue)

  • Tetralogy of Fallot (5%)
  • Transposition of great arteries (5%)

Common mixing
- AVSD complete (breathless and blue) – 2%

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2
Q

Which congenital heart lesions are acyanotic? (5)

A

Generally those with L–>R shunt (breathless)

  • VSD (30%)
  • ASD (7%)
  • Persistent arterial duct (12%)

→ Outflow obstruction if not severe (asymptomatic with murmur)

  • PS (7%)
  • AS (5%)
  • Severe outflow obstruction will present with collapse and shock
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3
Q

Common heart conditions associated with Down syndrome? (2)

A
  • AVSD
  • VSD

30% incidence

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4
Q

Common heart conditions associated with Turner syndrome? (2)

A
  • Aortic valve stenosis
  • Coarctation of the aorta

15% incidence

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5
Q

RFs for neonatal infection? (6)

A
  • Maternal pyrexia
  • PROM
  • Prematurity
  • Evidence of chorioamnionitis
  • Maternal GBS colonization
  • Foul smelling liquor
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6
Q

RFs for neonatal GBS infection? (4)

A
  • PPROM
  • Maternal fever in labour >38
  • Maternal chorioamnionitis
  • Previously infected infant
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7
Q

Management for mums and babies if GBS positive mum?

A

Mums:

  • UK → Mothers with RFs for infection offered IV intrapartum abx
  • USA/AUS → universal screening at 35-38w to identify carriers then those given IV abx

Babies:

  • Usually appears as pneumonia/ sepsis/ meningitis
  • Resp distress, apnoea,  temp
  • Ix → Septic screen: CXR, FBC, cultures, CRP, ?LP
  • Rx → Abx immediately – amoxicillin/ benzylpenicillin
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8
Q

What does a septic screen consist of? (6)

A 
FBC
CRP
Cultures
CXR
Urinalysis
?LP
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9
Q

Common viral (5) and bacterial (7) pathogens causing infection in newborn?

A

Viral:

  • HSV
  • CMV
  • HIV
  • HBV, HCV
  • Rubella

Bacterial:

  • GBS
  • E Coli
  • Gonorrhoea
  • Treponema
  • Listeria
  • Other gram neg
  • Atypical → chlamydia, ureaplasma
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10
Q

Most common congenital infection?

A

CMV

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11
Q

3 types of presentation of congenital CMV?

A

CID - 5%

  • Most severe
  • IUGR, hepatosplenomegaly, thrombocytopenia
  • 90% neurological sequalae

‘Asymptomatic’ 90%
- Subtle IUGR

Present later in life with neurological sequalae - 5%
- Eg hearing loss

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12
Q

Features of congenital rubella infection?

A
  • Rarely seen now
  • Antenatal surveillance – must be confirmed serologically – clinical diagnosis unreliable
  • Risk and extent of fetal damage determined by gestational age at onset of maternal infection
  • Infection <8w gestation → deafness, congenital heart disease + cataracts in >80%
  • 30% of fetuses of mothers infected at 13-16w have impaired hearing
  • > 18w – risk to fetus minimal
  • Congenital rubella = preventable due to MMR
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13
Q

Management with known maternal HIV?

A

If undetectable viral load:

  • IV ZDV 4h before LSCSS, till cord clamped
  • Neonatal ZDV monotherapy for 4w
  • Viral PCR at birth, 1m, 3m, 12m

Detectable viral load:

  • HAART/ Regimens for mother
  • Triple therapy (ZDV + LZMU + NVP)
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14
Q

Clinical features of neonatal sepsis? (many)

A
  • Fever or temp instability or hypothermia
  • Poor feeding
  • Vomiting
  • Apnoea and bradycardia
  • Respiratory distress
  • Abdo distension
  • Jaundice
  • Neutropenia
  • Hypo­/hyperglycaemia
  • Shock
  • Irritability
  • Seizures
  • Lethargy, drowsiness
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15
Q

Causes of sticky eyes in neonatal period? (4)

A

Sticky eyes common in neonatal period – starts day 3, cleaning with saline/water works

Staph/strep - more troublesome discharge with redness
–> abx eye ointment e.g. neomycin

Gonococcal infection - purulent discharge & eyelid swelling in 1st 24h (can lead to blindness)
–> gram stain & culture –> 3rd gen IV cephalosporin

Chlamydia - purulent discharge & eyelid swelling at 1-2w
–> immunofluorescent staining –> oral erythromycin for 2w

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16
Q

Features and management of neonatal HSV?

A
  • Uncommon
  • Risk to infant with primary genital infection = 40%
  • Risk to infant with recurrent maternal infection <3%
  • Most infants infected unexpected as mother asymptomatic
  • RF = preterm
  • Presentation at any age ≤4w → localized herpetic lesions on skin or eye, or with encephalitis or disseminated disease
  • Mortality with localized disease = low
  • Disseminated disease mortality = high even with acyclovir
  • -> If mother has primary or active recurrent disease at time of delivery → LSCS
  • If mother has had in past but not active → acyclovir + vaginal delivery
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17
Q

Define SGA and IUGR?

A

SGA = birth weight <10th centile

IUGR = fails to meet genetically determined growth potential

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18
Q

What is asymmetrical IUGR?

A
  • Asymmetrical (more common) – abdo circumeference lies on lower centile than head
  • Due to placenta failing to provide adequate nutrition late in pregnancy
  • Asymmetrical associated with utero-placental dysfunction due to: pre-eclampsia, multiple pregnancy, smoking, idiopathic
  • These infants rapidly put on weight after birth
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19
Q

Features/ causes of symmetrical IUGR?

A
  • Symmetrical → prolonged period of IUGR
  • Usually small but normal fetes
  • May be fetal chromosomal disorder or syndrome, congenital infection, maternal drug/ alcohol use, chronic medical condition or malnutrition
  • More likely to remain small permanently
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20
Q

Common causes of asymmetrical IUGR? (4)

A
  • Pre-eclampsia
  • Multiple pregnancy
  • Smoking
  • Idiopathic
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21
Q

Common causes of symmetrical IUGR? (6)

A
  • Normal but small fetus
  • Fetal chromosomal disorder/syndrome
  • Congenital infection
  • Maternal drug/ alcohol use
  • Chronic medical condition
  • Malnutrition
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22
Q

Short-term complications from IUGR?

A
  • Intrauterine hypoxia
  • ‘Unexplained’ intrauterine death
  • Asphyxia during labour/ delivery
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23
Q

After birth complications of IUGR? (4)

A
  • Hypothermia as large SA
  • Hypoglycaemia from poor fat and glycogen stores
  • Hypocalcaemia
  • Polycythaemia (venous haematocrit >0.65)
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24
Q

Name the pulmonary causes of neonatal respiratory distress?
Common (1)
Less common (6)
Rare (5)

A

Common:
- Transient tachypnoea of newborn

Less common:

  • Meconium aspiration
  • Pneumonia
  • Respiratory distress syndrome
  • Pneumothorax
  • Persistent pulmonary HTN of newborn
  • Milk aspiration

Rare:

  • Diaphragmatic hernia
  • Tracheo-oesophageal fistula (TOF)
  • Pulmonary hypoplasia
  • Airways obstruction eg choanal atresia
  • Pulmonary haemorrhage
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25
Q

Signs of newborn respiratory distress? (4)

A
  • Tachypnoea (>60 breaths/min)
  • Laboured breathing – chest wall recession (esp sternal and subcostal) and nasal flaring
  • Expiratory grunting
  • Cyanosis if severe
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26
Q

Non-pulmonary causes of respiratory distress in the newborn? (4)

A
  • Congenital heart disease
  • Intracranial birth trauma/ encephalopathy
  • Severe anaemia
  • Metabolic acidosis
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27
Q

What is transient tachypnoea of the newborn?

A
  • By far commonest cause of neonatal resp distress
  • Caused by delay in resorption of lung liquid
  • More common after C-section
  • CXR may show fluid in horizontal fissure
  • Additional ambient O2 may be required
  • Usually settles within 1d but can take several to resolve completely
  • Diagnosis made after consideration and exclusion of other causes
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28
Q

In what % is meconium passed before birth?

A

8-20%

- Rarely in preterm

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29
Q

Predispositions to neonatal pneumonia? (3)

A
  • PROM
  • Chorioamnionitis
  • Low birth weight
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30
Q

What is persistent pulmonary HTN of newborn associated with? (4)

A

Birth asphyxia
Meconium aspiration
Septicaemia
RDS

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31
Q

Management of persistent pulmonary HTN of newborn?

A
  • Most need mechanical ventilation/circulatory support
  • Inhaled NO (potent vasodilator) often beneficial
  • High frequency or oscillatory ventilation sometimes helpful
  • Extracorporeal membrane oxygenation (ECMO) – placed on heart and lung bypass for several days – indicated for severe but reversible cases
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32
Q

Management of diaphragmatic hernia in newborn?

A
  • Large NG tube passed and suction applied to prevent distension of intrathoracic bowel
  • After stabilization, hernia repaired surgically
  • Most infants with this condition main problem = pulmonary hypoplasia – compression by herniated viscera prevented development of lung
  • If lungs hypoplastic → high mortality
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33
Q

2 things to look for on examination for heart failure?

A

Femoral pulses - coarctation/interruption of arch important causes

Hepatomegaly - due to venous congestion - useful sign

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34
Q

Common medical problems of preterm infants? (many)

A
  • Need for resus at birth
  • Resp - RDS, pneumothorax, apnoea + bradycardia
  • Hypotension
  • PDA
  • Temp control
  • Metabolic - hypoglycaemia/calcaemia, osteopenia
  • Nutrition
  • Infection
  • Jaundice
  • IVH/ periventricular leukomalacia
  • NEC
  • Retinopathy of prem
  • Anaemia of prem
  • Bronchopulmonary dysplasia
  • Inguinal hernias
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35
Q

What 3 factors largely determine a premature neonates course and outcome?

A
  • Gestational age at delivery
  • Severity of respiratory disease
  • Episodes of infection
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36
Q

What is respiratory distress syndrome?

A

Deficiency of surfactant, which lowers surface tension

  • Deficiency → widespread alveolar collapse and inadequate gas exchange
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37
Q

Clinical signs of RDS? (4)

A

Within 4h of birth

  • Tachypnoea >60
  • Chest wall recessions (sternal and subcostal) + nasal flaring
  • Expiratory grunting
  • Cyanosis if severe
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38
Q

Diagnosis of RDS?

A

CXR –> characteristic

  • Diffuse granular/ground glass appearance of lungs
  • Air bronchogram
  • Indistinct heart border or obscured completely if severe
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39
Q

Management of RDS? (4)

A
  • Prophylactic glucocorticoids given antenatally if preterm delivery anticipated
  • Raised ambient O2 +/- CPAP via nasal cannulae or artificial ventilation via tracheal tube
  • High-flow humidified O2 therapy to wean babies from added O2 therapy
  • Surfactant therapy derived from calf/pig lung instilled directly to lung via tracheal tube – reduces mortality by 40%
40
Q

Presentation of NEC? (5)

A
  • Infant stops tolerating feeds
  • Milk aspirated from stomach and may be vomiting –pos bile-stained
  • Abdo distension
  • Stool sometimes contains fresh blood
  • Infant may rapidly become shocked → require artificial ventilation because of abdo distension + pain
41
Q

Management fo NEC?

A
  • Stop oral feeding
  • Broad spectrum abx
  • Parenteral nutrition always needed
  • Artificial ventilation and circulatory support often needed
  • Surgery performed for bowel perforation
  • Long-term sequalae = development of strictures and malabsorption if extensive bowel resection has been necessary
42
Q

Mortality of NEC?

A

20%

43
Q

RFs for hypoglycaemia in neonates? (7)

A 
IUGR
Preterm
Maternal DM
Large-for-dates
Hypothermic
Polycythaemic
Ill for any reason
44
Q

What level of glucose is hypoglycaemic in newborn?

A

<2.6mmol/L (no confirmed definition)

45
Q

Sx of hypoglycaemia in neonates? (5)

A
  • Jitteryness
  • Irritability
  • Apnoea
  • Lethargy/ drowsiness
  • Seizures
46
Q

Management of hypoglycaemia in neonate?

A
  • Often preventable by early & frequent milk feeding
  • In high risk → monitor blood glucose reg
  • IV 10% glucose if symptomatic or 2 low values + adequate feeding, or 1 v low value
  • High conc IV glucose via central venous catheter to avoid extravasation into tissues – may cause skin necrosis and reactive hypoglycaemia
  • If difficulty/delay in infusion - give glucagon or hydrocortisone
47
Q

Treatment of apnoea of prematurity? (3)

A
  • Physical stim often triggers breathing to be restarted
  • Can use respiratory stimulant e.g. theophylline or caffine
  • Sometimes CPAP required
48
Q

Leading cause of preventable blindness?

A

Retinopathy of prematurity

- Raised risk if uncontrolled use of high conc O2

49
Q

What % of infants <32w have an IVH?

A

10%

- Raised risk the smaller/earlier they are

50
Q

Presentation of IVH in neonate?

A
  • Most within 72h of birth
  • 50% asymptomatic –> small and harmless

Larger bleeds may present as:

  • Circulatory collapse
  • Bulging fontanelle (↑ICP)
  • Neurological (seizures)
  • Anaemia
  • Jaundice (↑ breakdown of bleed)
  • Apnoea
  • Lethargy
  • Poor muscle tone
51
Q

How is IVH confirmed?

A

Cranial USS

52
Q

Management of IVH in neonate? (2)

A
  • Supportive treatment- correct acidosis, anaemia, hypotension
  • May need ventriculoperitoneal shunt
53
Q

At what gestational age can infants swallow and suck?

A

35-36w

–> <35w NG feeds

54
Q

Why are mothers encouraged to breast feed esp in preterms? (2)

A
  • NEC with formula

- Septicaemia with parenteral feeds

55
Q

What is bronchopulmonary dysplasia?

A
  • When infants have O2 requirement at post-menstrual age of 36w
  • Lung damage comes from pressure and volume trauma from artificial ventilation, oxygen toxicity and infection
56
Q

What % of v low birthweight infants develop CP?

A

5-10%

57
Q

What is classed as a very low birthweight?

A

<1.5kg

58
Q

How is lung liquid reabsorbed when baby is born?

A

Chest compression during birth squeezes out 1/3

Release of adrenaline promotes reabsorption of 2/3

59
Q

Timeframes for baby to

a) open bowels
b) pass urine
c) regain birth weight?

A

Bowels – usually within 6h or before birth but up to 24h


Bladder – up to 24h


Weight – newborns lose 7-10% weight but should regain it in 2w

60
Q

2 RFs for baby vitamin K deficiency after birth?

A
  • Mum on anti-epileptics

- Liver disease of baby

61
Q

What can vitamin K deficiency lead to?

A

Haemorrhagic disease of newborn

  • ↓ vitamin K dependent clotting factors
  • Occurs either early (during 1st week) or late (1-8w)
  • Haemorrhage can be mild e.g. bruising/ haematemesis/ melaena/ prolonged bleeding from umbilical stump/ after circumcision
  • If severe can be intercranial haemorrhage (1/2 permanently disabled or die)
  • Breast milk has ↓ vit K, formula milk much higher
62
Q

When is the Guthrie test carried out?

A

Day 5-9

63
Q

What is tested for on the Guthrie test? (9)

A
  • CF
  • Hypothyroidism
  • Sickle cell
  • Thalassaemia
  • PKU
  • MCADD (medium-chain acyl-CoA dehydrogenase deficiency)
  • MSUD (maple syrup urine disease)
  • IVA (isovaleric acidaemia)
  • GA1 (glutaric aciduria type 1)
  • HCU (homocystinuria (pyridoxine unresponsive)
64
Q

What is checked for antenatally with maternal blood sample? (7)

A

Infections

  • Hepatitis B
  • Syphilis
  • Rubella
  • HIV infection

Rhesus group

NTDs risk

Downs risk

65
Q

What is checked for at antenatal USS? (5)

A
  • Gestational age
  • Multiple pregnancies
  • Structural malformation
  • Fetal growth
  • Amniotic fluid volume
66
Q

What may lead to oligohydramnios? (3)

A

Reduced urine production - kidney problem

PROM

Severe IUGR

67
Q

What is polyhydramnios associated with? (2)

A

Maternal DM

GI atresia in fetus

68
Q

RFs for serious jaundice in newborn? (6)

A
  • Low birth weight
  • Breastfed
  • Prev sibling with neonatal jaundice
  • Visible jaundice in 24h
  • Diabetic mum
  • East Asian
69
Q

Name 8 common newborn problems?

A 
Erythema toxicum
Mongolian blue spots
Capillary haemangiomas
Physiological jaundice
Feeding difficulties
Small for gestational age
Birth trauma - cephalohaematoma, brachial plexus injury
Sticky eye
70
Q

What is erythema toxicum?

A
  • Also called neonatal urticaria
  • Common rash appearing at 2-3d of age
  • White pinpoint papules at centre of erythematous base
  • This fluid contains eosinophils and lesions are concentrated on trunk
  • Come and go at different sites
71
Q

What are capillary haemangiomas?

A
  • Pink macules on upper eyelids, mid-forehead and nape of neck are common and arise from distension of the dermal capillaries
  • Those on eyelids gradually fade over first year
  • Those on neck become covered in hair
72
Q

What is a cephalohaematoma?

A
  • = Haematoma from bleeding below periosteum, confined within margins of skull sutures
  • Usually involves parietal bone
  • Centre of the haematoma feels soft
  • Resolves over several weeks
73
Q

Name some possible sensitising events in rhesus disease of newborn? (8)

A 
Labour (86%)
C section
Miscarraige
Abortion
Amniocentesis
Ectopic pregnancy
Abdo trauma
ECV
74
Q

Sx of rhesus disease? (4)

A

Anaemia
Hydrops
Hepatosplenomegaly
Jaundice

75
Q

What is ABO incompatability?

A
  • More common than rhesus haemolytic disease
  • Most ABO antibodies = IgM and do not cross placenta
  • Some group O women have IgG anti­-A ­haemolysin in blood which can cross placenta and haemolyse RBCs of group A infant
  • Occasionally, group B infants affected by anti-­B haemolysins
  • Haemolysis can cause severe jaundice but usually less severe than rhesus disease
  • Infant’s Hb level usually normal or slightly reduced and, in contrast to rhesus disease, hepatosplenomegaly absent
  • Direct antibody test (Coombs’ test), which demonstrates antibody on surface of red cells, is positive
  • Jaundice usually peaks in first 12–72h
76
Q

Management of ABO incompatibility?

A

Antenatal

  • Intrauterine transfusion
  • Early induction of labour when pulmonary maturity has been obtained
  • Mothers may also undergo plasma exchange to lower circulating antibodies by 75%

Post-natal

  • Depends on severity of condition
  • May simply involve treating jaundice with phototherapy
  • May be cause for transfusion with RBCs and also bicarbonate to correct an acidosis
77
Q

RFs for congenital abnormalities? (4)

A
  • Maternal and paternal age

  • Infections (TORCH – toxoplasmosis, others, rubella, CMV and HSV)
  • Toxins e.g. alcohol, smoking, mercury or prescription drugs
  • Dietary deficiencies e.g. folic acid

MANY more, these are important ones

78
Q

What is CHARGE syndrome?

A

Genetic syndrome that is an acronym to describe a set of unusual congenital features seen in many newborn children

  • Coloboma of eye (a hole in one of the eyes structures e.g. the iris, retina, choroid or optic disc)
  • Heart defects
  • Atresia of nasal choanae
  • Retardation of growth and/or development
  • Genital and/or urinary abnormalities
  • Ear abnormalities and deafness

This syndrome = leading cause of congenital deaf-blindness

79
Q

What is VACTERL syndrome?

A

Syndrome (or an association) of birth defects
Thought to be genetic and associated with trisomy 18 or more frequently with diabetic mothers

  • Vertebral defects (hypoplastic vertebrae and scoliosis)
  • Anal atresia
  • CV abnormalities (ASD, VSD and Tetralogy of fallot)
  • Tracheoesophageal fistula
  • Esophageal atresia
  • Renal anomalies (usually one umbilical vein instead of two which causes problems – outflow obstruction, reflux and kidney failure)
  • Limb defects (hypoplastic thumbs, extra digits, fusion of digits etc)

Most will have normal development and intelligence but can be quite small

80
Q

What is Patau syndrome and clinical features (6)?

A

Trisomy 13

  • Least common and most severe of trisomies
  • Much more likely to affect females
  • RFs: affected close family, maternal age
  • Most affected babies die in infancy – median survival = 2.5d

Clinical features

  • Structural defect of brain
  • Scalp defects
  • Small eyes and other eye defects
  • Cleft lip and palate
  • Polydactyly
  • Cardiac and renal malformations
81
Q

What is Edward’s syndrome and clinical features?

A

Trisomy 18
- Poor prognosis – mean life expectancy 4d, 5-10% survive beyond 1y

Clinical features

  • Low birth weight
  • Prominent occiput
  • Small mouth and chin
  • Short sternum
  • Flexed, overlapping fingers
  • ‘Rocker­bottom’ feet
  • Cardiac and renal 
malformations
82
Q

Types of NTDs? (5)

A

Anencephaly

Encephalocele

Spina Biffida

  • Occulta
  • Cystica (meningocele, myelomeningocele)
83
Q

What is anencephaly?

A
  • Failure of development of most of cranium and brain
  • Affected infants stillborn or die shortly after birth
  • Detected on antenatal USS and TOP usually performed
84
Q

What is encephalocele?

A
  • Extrusion of brain and meninges through midline skull defect
  • Can be corrected surgically
  • However, often underlying associated cerebral malformations
85
Q

What does spina bifida mean?

A
  • Failure of fusion of vertebral arch
86
Q

What is a meningocele?

A

Type of NTD

  • Skin and meninges form out-pouching
  • Unlikely to suffer long-term health problems
  • May be underlying tethering of cord - with growth, may cause neurological deficits of bladder function and lower limbs
  • Extent of underlying disease can be delineated using USS +/or MRI scans
  • Neurosurgical relief of tethering usually indicated
87
Q

What is a myelomeningocele?

A

Type of NTD

  • Communication b/w surface and meninges, along with some neural tissue (a neural plaque)
  • Associated with many complications such as paralysis, sensory loss, muscle imbalance, neuropathic bladder and bowel, scoliosis and hydrocephalus
  • Most severe have lesions above L3
  • → Unable to walk, have scoliosis, neuropathic bladder and bowel, hydronephrosis and frequently develop hydrocephalus
88
Q

What may a disorder of sexual differentiation be secondary to? (4)

A

XS androgens producing virilisation in a female
- Mostly due to congenital adrenal hyperplasia

Inadequate androgen action, producing under­ virilisation in a male

Gonadotrophin insufficiency
–> small penis and cryptochidism

Ovotesticular disorder of sex development (DSD)
- XY and XX cells

89
Q

What is congenital adrenal hyperplasia?

A
  • Number of autosomal recessive disorders of adrenal steroid biosynthesis result in congenital adrenal hyperplasia
  • RF = consanguineous marriages
  • > 90% have deficiency of enzyme 21­hydroxylase→ needed for cortisol biosynthesis
  • 80% also unable to produce aldosterone→ salt loss (low Na and high K+)
  • In fetus, resulting cortisol deficiency stims pituitary to produce ACTH, which drives overproduction of adrenal androgens
90
Q

Clinical features of congenital adrenal hyperplasia? (4)

A
  • Virilisation of external genitalia
  • Salt ­losing adrenal crisis (1-3weeks old) in 80% males –> vomiting, wt loss, floppiness, circulatory collapse
  • Tall stature in 20% non-salt losing males
  • M+F non-salt losers –> muscular build, adult body odour, pubic hair (i.e. precocious pubarche)
91
Q

Diagnosis of congenital adrenal hyperplasia?

A
  • Finding markedly raised levels of metabolic precursor 17α­hydroxyprogesterone in blood
92
Q

Management of congenital adrenal hyperplasia?

A

Females may need corrective surgery

Males in salt-losing crises need saline, dextrose and hydrocortisone IV

Long term:

  • Lifelong glucocorticoids to suppress ACTH (+ hence testosterone) - allow normal growth/development
  • Mineralocorticoids if salt loss (fludrocortisone)
  • Monitoring of growth, skeletal maturity and plasma androgens and 17α­hydroxyprogesterone
  • Additional hormone replacement to cover illness/surgery, as unable to mount cortisol response
93
Q

Causes of haemolytic diseases of the newborn? (4)

A
  • Rhesus haemolytic disease
  • ABO incompatibility
  • G6PD deficiency
  • Spherocytosis
94
Q

Causes of significant hypoxic event that may lead to HIE? (5)

A
  • Failure of gas exchange across placenta – XS or prolonged uterine contractions, placental abruption, ruptured uterus
  • Interruption of umbilical blood flow – cord compression inc shoulder dystocia, cord prolapse
  • Inadequate maternal placental perfusion, maternal hypotension or HTN – often with IUGR
  • Compromised fetus – anemia, IUGR
  • Failure of cardiorespiratory adaptation at birth – failure to breathe
95
Q

Classification of HIE?

A
  • Mild → infant irritable, responds XS to stimulation, may have staring of eyes and hyperventilation and impaired feeding
  • Moderate → marked abnormalities of tone and movement, cannot feed and may have seizures
  • Severe → no normal spontaneous movements or response to pain; tone in limbs may fluctuate between hypotonia and hypertonia; seizures prolonged and often refractory to treatment; multi­organ failure present
96
Q

Prognosis of HIE?

A

Mild HIE
- Complete recovery expected

Moderate HIE

  • If recovered fully on clinical neurological examination and feeding normally by 2w → excellent long­-term prognosis
  • If clinical abnormalities persist beyond 2w→ full recovery unlikely

Severe HIE

  • Mortality = 30–40%
  • Of survivors, >80% have neurodevelopmental disabilities, esp CP
  • If MRI at 4–14d in term infant shows sig abnormalities (bilat abnormalities in basal ganglia and thalamus and lack of myelin in posterior limb of internal capsule) →v high risk of later CP
97
Q

What can HIE present with if there is multi-organ dysfunction?

A 
Encephalopathy
Respiratory failure
Myocardial dysfunction
Metabolic --> Hypo-glycaemia, calcaemia, natraemia
Renal failure
DIC

Paeds (15 decks)

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