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HD 2 > Illness in the Full-term Baby > Flashcards

Illness in the Full-term Baby Flashcards

1
Q

What major complication can perinatal asphyxia cause?

A

Hypoxic ischaemic encephalopathy

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2
Q

How may a neonate with asphyxia present? (3)

A

Not breathing
HR<60 (bradycardia)
Floppy

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3
Q

What is given to treat seizures that may result due to HIE? (3)

A

Phenobarbitone, phenytoin and clonazepam infusion

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4
Q

What does asphyxia/HIE mean for the tissue? (4)

A

Tissue suffers hypoxaemia, ischaemia, hypercarbia, metabolic acidosis.

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5
Q

What are the warning signs for hypoxia-ischaemia? (5)

A 
Decreased foetal movements
Sentinel events
Placental abruption
Uterine rupture
Cord prolapse
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6
Q

In HI, the blood supply is redistributed. What is preserved? (3)

A

Central nervous system
Myocardium
Adrenals

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7
Q

In HI, the blood supply is redistributed. What is vulnerable? (4)

A

Kidneys
GI tract
Liver
Muscle

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8
Q

What does encephalopathy of the newborn refer to? (4)

A

Abnormal neurologic function and consciousness level
Abnormalities of tone and reflexes
Autonomic dysfunction
Seizures

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9
Q

Sarnat and Sarnat grading - describe stage 1.

A

Lasts < 24 hours
Hyper-alertness
Uninhibited stretch reflexes
Normal EEG

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10
Q

Sarnat and Sarnat grading - describe stage 2.

A

Obtundation (altered level of consciousness)
Hypotonia
Multifocal seizures
The EEG - periodic pattern sometimes preceded by continuous delta activity

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11
Q

Sarnat and Sarnat grading - describe stage 3.

A

Stuporous
Flaccid
Brain stem and autonomic functions suppressed
EEG isopotential or infrequent periodic discharges

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12
Q

What neurological deficit does HIE cause?

A

Cerebral palsy

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13
Q

How many live births have HIE in the West?

A

1-2 per 1000

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14
Q

How does hypoxia lead to necrosis and apoptosis?

A

Hypoxia:

  • -> primary neuronal injury
  • -> primary energy failure
  • -> derangement of cellular function (excitotoxicity, inflammatory, oxidative stress)
  • -> secondary energy failure (several hours after reperfusion)
  • -> secondary neuronal injury, further necrosis and apoptosis
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15
Q

What are the energy consequences of HI?

A

Although the phosphorus spectra is “normal” in first few hours after resuscitation (as mitochondrial oxidative phosphorylation has been restored), 12-24 hours after there is a progressive decline in PCr/Pi ratio and a decline in ATP.

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16
Q

What are the mechanisms of brain injury in HI? (8)

A
  • Glucose and oxygen deprivation
  • Decreased ATP and energy depletion
  • Glutamate release (and receptor activation)
  • Free radicals (NO, superoxide, Fe, H2O2)
  • Calcium entry and intracellular accumulation
  • Lipid peroxidation
  • Oligodendroglial death
  • Apoptosis
17
Q

How is hypothermia neuroprotective? (5)

A 
↓ cerebral metabolism
↓ energy use
↓ accumulation of excitotoxic amino acids
↓NO synthetase activity
↓free radical activity
18
Q

A potential target for neuroprotection is decreasing energy depletion. What can be given? (3)

A

Glucose, Hypothermia, Barbiturates

19
Q

A potential target for neuroprotection is inhibition of glutamate release. What can be given? (7)

A 
Ca channel blockers
Magnesium (glutamate receptor blcoker)
Adenosine
Hypothermia (fix uptake impairment)
Free radical scavengers
Lamotrigine
Phenytoin
20
Q

A potential target for neuroprotection is blockade of downstream intracellular events. What can be given? (6)

A 
Hypothermia
Free radical synthesis inhibitors (allopurinol, indomethacin, iron chelators, magnesium)
Free radical scavengers
Vitamin E
NOS inhibitors/scavengers
Anti-apoptotic agents
21
Q

What are the two main infections do newborns suffer?

A

GBS

E. coli

22
Q

Which groups of newborns have higher rates of infections and mortality from infection? (3)

A

Infants requiring intensive care
Preterm infants
Newborns in developing world

23
Q 
What is the incidence of neonatal sepsis in the USA?
Is early (within 48 hours) or late onset more common?
A

0.7% in the USA

Late onset

24
Q

With early onset sepsis, where are the microbes acquired from?

A

From the mother, before or during passage through the birth canal (vertical/perinatal transmission)

25
Q

Name some organisms that cause early neonatal sepsis. (7)

A 
Group B Strep (Strept. Agalactiae) and other strepts
E. coli
H. Influenezae
L. Monocytogenes
Gram negative anaerobes
Fungi
Chlamydia trachomatis
26
Q

What are the signs/symptoms of early onset GBS? (7)

A 
Apnea
Severe hypoxia
Cardio-respiratory failure
Hypotension
Metabolic acidosis
Tachycardia
Poor perfusion
27
Q

What may be seen on a FBC of a neonate who has early onset GBS?

A

Neutropenia (low neutrophils)

28
Q

How many % of babies born vaginally to mothers who carry GBS become infected?

A

1%

29
Q

What are the predisposing factors to neonatal GBS? (4)

A

Evidence of chorioamnionitis including maternal fever
Prolonged labour
Prolonged rupture of membranes
Low birthweight

30
Q

How is GBS vertical transmission prevented?

A

Intrapartum antibiotic prophylaxis

31
Q

How is GBS treated?

A

Benzylpenicillin with amikacin or gentamicin

32
Q

What does nosocomial mean?

A

Means the infection was caught in hospital

33
Q

What organisms cause late onset sepsis? (2)

A

Coagulase-negative staphylococci

Staph Aureus

HD 2 (25 decks)

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