Definition
Global hypoxic ischaemia injury can affect the neonates,
older children and adults.
It is secondary to an underlying cause and typically presents with a deterioration in conscious level as scored on the Glasgow Coma Scale.
It can be accompanied by clinical features related to its cause,
typical biochemical derangements ,
often metabolic acidosis,
and imaging.
Pathophysiology
HI-BI occurs when combined low oxygen tensions and limited blood supply are delivered to the brain.
This results in cellular energy failure and neuronal death.
Grey matter ,
basal ganglia and cerebellum are more susceptible to the ischaemic changes in view of their higher metabolic rate and there sensitivity to glutamate excitotoxicity.
The pattern of involvement is characteristically symmetrical.
Glutamate,
an excitatory amino acid,
is released in higher levels in global hypoxic ischaemic injury and its uptake is reduced.
Intracellular calcium increases along with oxygen free- radicals.
Lipid peroxidation follows and these changes cause a disturbance in the autoregulation of cerebral blood flow.
Brain injury is often irreversible in global hypoxic ischaemic injury.
The post- HI-BI sequelae include:
- seizures
- sensory deficits
- motor deficits e.g.
dystonia,
chorea
- cognitive ailments
Clinical presentation
The main clinical feature in HI-BI is a deterioration in the conscious level or sudden death.
This can occur secondary to a wide spectrum of causes.
The main clinical feature in HI-BI is a deterioration in the conscious level or sudden death.
This can occur secondary to a wide spectrum of causes.
Hi-Bi has a trimodal presentation.
Perinatal period: Birth asphyxia leading to hypoxic ischaemic encephalopathy
Older children: Asphyxia
Near-drowning
Adults: Respiratory arrest e.g.
fatal pulmonary embolism
Cardiac arrest or dysrythmias
Ischaemic or haemorrhagic CVA
Metabolic derangements
Toxicity e.g.
CO
Trauma +/- overt/covert bleeds