Anoxic Brain Injury


Global cerebral ischemia a.k.a. global/diffuse cerebral hypoxia ischemia a.k.a. hypoxic ischemic encephalopathy a.k.a. Postanoxic Encephalopahty


Clinical features with or without MRI

Clinical features:

  • Coma after pulseless cardiac arrest or after significant hypoxia
  • Episode of brain anoxia/global ischemia. Myoclonic status epilepticus may occur (may involve face, trunk, limbs)

Findings on investigations:


  • T2/FLAIR hyperintensity symmetrically both globus pallidi, & caudate nuclei, sometimes cortical.
  • Diffusion: restricted in both globus pallidi symmetrically, sometimes cortical.
  • T1 hyperintensity in the cortex (laminar necrosis), hyperintensity in both globus pallidi,

EEG features suggesting poor prognosis:

  • Burst suppression pattern,
  • Periodic discharges associated with myoclonus
  • Invariant monorhythmic pattern
  • Electrocerebral silence



  • Diffuse swelling (cytotoxic oedema)
  • Softening & discolouration of hippocampus (Somer sector= CA1), watershed areas


  • Hyperacute <12 hours: no changes
  • Acute 12-24 hrs: eosinophilic neurons “ischemic change a.k.a. red-dead a.k.a. acute neuronal cell change” especially pyramidal cells of the hippocampus & cerebellum, hyperchromatic nucleus, pyknosis (shrunken nucleus), pallor of neuropil
  • Subacute 2 days-2 weeks: macrophages, capillary proliferation, astrocytes
  • Chronic months- years: cavitation, macrophages

Investigations to consider:

  • CT: to rule out competing diagnosis
  • MRI: to rule out competing diagnosis
  • EEG: isoelctric pattern, burst-suppression pattern
  • Somatosensory evoked potentials SSEP:Bilateral absence of cortical SSEP (N20 component with median nerve stimulation), within 1st week.


Therapeutic hypothermia if post Ventricular fibrillation arrest & meets other criteria
Supportive care

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