Perinatal Asphyxia and Infection Flashcards

1
Q

Hypoxia-Ischaemia at birth

A

Infants need resuscitations at birth
–> may have absent HR< infant not breathing
–> may require airway, respiratory and haemodynamic support
Infant subsequently encephalopathic

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2
Q

Hypoxia-ischaemia warnings

A

Decreased foetal warnings

Sentinel events- placental abruption, uterine rupture, cord prolapse

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3
Q

HI Preserved blood supply

A

CNS
Myocardium
Adrenals

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4
Q

HI Vulnerable blood supply

A

Kidneys
GI tract
Liver
Muscle

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5
Q

Encephalopathy in newborn

A

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

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6
Q

Sarnat study of perinatal asphyxia

A

Stage 1- less than 24 hrs, hyperalertness, uninhibited Moro and stretch reflexes, symp. effects and normal EEG
Stage 2- obtundation, hypotonia, multifocal seizures, EEG periodic pattern sometimes preceded by continuous delta activity
Stage 3- stuporous, flaccid and brain stem + autonomic functions suppressed

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7
Q

Foetal/perinatal hypoxia +/or ischaemic cerebral insult

A
Leads to primary neuronal injury
Primary energy failure
Derangement of cellular function
Secondary energy failure
Secondary neuronal injury, further necrosis and apoptosis
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8
Q

Energy consequences Hypoxia-Ischaemia

A

Phosphorus spectra normal first few hours after resuscitation
12-24 hours- progressive decline in PCr/Pi ratio
Delayed ATP decline

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9
Q

Secondary energy failure

A

Acute hypoxia ischaemia –> reperfusion (after resuscitation) –> secondary energy failure (several hours after reperfusion)

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10
Q

Cerebral Hypoxic-Ischaemic injury

A

Primary neuronal death

Resuscitation – Reperfusion, Oxygenation

Cerebrovascular dysfunction
Glutamate release
Free radicals
Calcium entry
Apoptosis

Secondary neuronal death

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11
Q

Mechanisms of brain injury in Hypoxia-Ischaemia

A
Glucose + O2 deprivation
Energy depletion – decreased ATP
Glutamate receptor activation
Accumulation of intracellular Ca
Free radicals – NO, superoxide, Fe, H2O2, 
Lipid peroxidation 
Oligodendroglial death
Apoptosis
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12
Q

Neuroprotection targets

A

Decreased energy depletion
Glutamate
Inhibition of leukocyte/microglial/cytokine effects
Blockade of downstream intracellular events

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13
Q

Decreased energy depletion

A

Glucose
Hypothermia
Barbiturates

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14
Q

Glutamate

A

Inhibit glutamate release (Ca channel blockers, magnesium, adenosine, hypothermia)
Fix glutamate uptake impairment - hypothermia
Glutamate receptor blockade- magnesium

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15
Q

Blockade of downstream intracellular events

A
Hypothermia
Free radical synthesis inhibitors (allopurinol, magnesium)
Free radical scavengers (Vit E)
NOS inhibitors
Anti-apoptotic agents
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16
Q

Hypothermia

A
Decreased cerebral metabolism
Decreased energy use
Decreased accumulation of excitotoxic amino acids
Decreased NO synthetase activity 
Decreased free radical activity
17
Q

Early onset sepsis

A
Within 48 hours
Microbes acquired from mother
Before or during passage through birth canal
2-3 per 1000 live births
Fulminating septicaemia --> meningitis, pneumonia
PROM
Maternal UTI
Prematurity
18
Q

Organisms causing early-onset sepsis

A

Group B Strep

E Coli

19
Q

Early Onset GBS

A

Most cases sepsis develop within first few hours
May mimic perinatal hypoxia-ischaemia
–> apnoea, severe hypoxia, cardio-resp failure, hypotension, metabolic acidosis, tachycardia, poor perfusion

20
Q

Early onset GBS predisposing factors

A

1% babies born vaginally to mothers who carry GBS become infected
Evidence chorioamnionitis including maternal fever
Prolonged labour
Prolonged rupture of membranes
Low birthweight

21
Q

Prevention + treatment of GBS sepsis

A

Prevention vertical transmission- intrapartum antibiotic prophylaxis to women who show carriage during pregnancy screening
Treatment- Benzylpenicillin with amikacin or gentamicin

22
Q

Late onset sepsis

A
More than 48 hours after birth
From Postnatal environment
Nosocomial
4-5 per 1000 live births
Mostly preterm infants on neonatal units
23
Q

Late onset sepsis organisms

A

Coagulase-negative staphylococci

Staph Aureus

24
Q

Early onset GBS investigations

A
FBC- neutropenia
CRP- rise may be delayed by 12 hours
Blood cultures
Lumbar puncture
Chest X ray