Illness in the Full-term Baby Flashcards
What major complication can perinatal asphyxia cause?
Hypoxic ischaemic encephalopathy
How may a neonate with asphyxia present? (3)
Not breathing
HR<60 (bradycardia)
Floppy
What is given to treat seizures that may result due to HIE? (3)
Phenobarbitone, phenytoin and clonazepam infusion
What does asphyxia/HIE mean for the tissue? (4)
Tissue suffers hypoxaemia, ischaemia, hypercarbia, metabolic acidosis.
What are the warning signs for hypoxia-ischaemia? (5)
Decreased foetal movements Sentinel events Placental abruption Uterine rupture Cord prolapse
In HI, the blood supply is redistributed. What is preserved? (3)
Central nervous system
Myocardium
Adrenals
In HI, the blood supply is redistributed. What is vulnerable? (4)
Kidneys
GI tract
Liver
Muscle
What does encephalopathy of the newborn refer to? (4)
Abnormal neurologic function and consciousness level
Abnormalities of tone and reflexes
Autonomic dysfunction
Seizures
Sarnat and Sarnat grading - describe stage 1.
Lasts < 24 hours
Hyper-alertness
Uninhibited stretch reflexes
Normal EEG
Sarnat and Sarnat grading - describe stage 2.
Obtundation (altered level of consciousness)
Hypotonia
Multifocal seizures
The EEG - periodic pattern sometimes preceded by continuous delta activity
Sarnat and Sarnat grading - describe stage 3.
Stuporous
Flaccid
Brain stem and autonomic functions suppressed
EEG isopotential or infrequent periodic discharges
What neurological deficit does HIE cause?
Cerebral palsy
How many live births have HIE in the West?
1-2 per 1000
How does hypoxia lead to necrosis and apoptosis?
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
What are the energy consequences of HI?
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.
What are the mechanisms of brain injury in HI? (8)
- 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
How is hypothermia neuroprotective? (5)
↓ cerebral metabolism ↓ energy use ↓ accumulation of excitotoxic amino acids ↓NO synthetase activity ↓free radical activity
A potential target for neuroprotection is decreasing energy depletion. What can be given? (3)
Glucose, Hypothermia, Barbiturates
A potential target for neuroprotection is inhibition of glutamate release. What can be given? (7)
Ca channel blockers Magnesium (glutamate receptor blcoker) Adenosine Hypothermia (fix uptake impairment) Free radical scavengers Lamotrigine Phenytoin
A potential target for neuroprotection is blockade of downstream intracellular events. What can be given? (6)
Hypothermia Free radical synthesis inhibitors (allopurinol, indomethacin, iron chelators, magnesium) Free radical scavengers Vitamin E NOS inhibitors/scavengers Anti-apoptotic agents
What are the two main infections do newborns suffer?
GBS
E. coli
Which groups of newborns have higher rates of infections and mortality from infection? (3)
Infants requiring intensive care
Preterm infants
Newborns in developing world
What is the incidence of neonatal sepsis in the USA? Is early (within 48 hours) or late onset more common?
0.7% in the USA
Late onset
With early onset sepsis, where are the microbes acquired from?
From the mother, before or during passage through the birth canal (vertical/perinatal transmission)
