"Hypoxic-ischaemic encephalopathy in adults and older children (i.e. not neonates), also known as global hypoxic-ischaemic injury, is an acute global brain injury caused by a profound reduction in cerebral oxygen delivery due to hypoxaemia, impaired cerebral perfusion, or both. It often has devastating neurological sequelae1."
"Diffuse white matter involvement in this context refers to a pattern of injury resulting from a global hypoxic-ischaemic event4. It should not be confused with chronic white matter hyperintensities of presumed vascular origin, which are an imaging feature of cerebral small vessel disease5."
"reversal sign: reversal of the normal CT attenuation of grey and white matter, demonstrated within the first 24 hours in a small number of these patients2"
"pseudosubarachnoid haemorrhage: cerebral oedema and a resultant decrease in parenchymal attenuation and swelling and engorgement and dilatation of the superficial venous structures due to an increased intracranial pressure result in the subarachnoid space appearing filled with blood that appears hyperdense."
"Diffusion-weighted MR imaging is the earliest imaging modality to become positive, usually within the first few hours after a hypoxic-ischaemic event due to early cytotoxic oedema. During the first 24 hours, there may be restricted diffusion in the cerebellar hemispheres, basal ganglia, or cerebral cortex (particularly the perirolandic and occipital cortices) 1,3. The thalami, brainstem or hippocampi may also be involved. Diffusion-weighted imaging abnormalities usually pseudo-normalise by the end of the first week 1."
"adults: most commonly follows cardiac arrest; other causes include respiratory arrest, severe systemic hypotension or shock, asphyxiation and near-drowning 1,3"
"adults: most commonly follows cardiac arrest; other causes include respiratory arrest, severe systemic hypotension or shock, asphyxiation and near-drowning 1,3"
"Diffusion-weighted MR imaging is the earliest imaging modality to become positive, usually within the first few hours after a hypoxic-ischaemic event due to early cytotoxic oedema. During the first 24 hours, there may be restricted diffusion in the cerebellar hemispheres, basal ganglia, or cerebral cortex (particularly the perirolandic and occipital cortices) 1,3. The thalami, brainstem or hippocampi may also be involved. Diffusion-weighted imaging abnormalities usually pseudo-normalise by the end of the first week 1."
"Neurologic injury is caused by hypoxia (secondary to carbon monoxide toxicity, near drowning, etc.) or interruption of blood flow (usually from cardiac arrest or hanging). There are often secondary effects of hypoxia on cardiac myocytes, causing reduced cardiac output and further secondary neurological injury. Hypoxia alone rarely causes significant brain damage unless it is profound and prolonged."