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Adult Hypoxic Ischemic Injury


KEY FACTS

Terminology

  • Hypoxic ischemic injury (HII): Global hypoxic ischemic injury, global anoxic injury, cerebral hypoperfusion injury

    • Etiologies: Cardiac arrest, cerebrovascular disease, drowning, asphyxiation

Imaging

  • Injury patterns highly variable depending on brain maturity, severity, and length of insult

    • Mild to moderate: Watershed zone infarcts

    • Severe: Gray matter structures (basal ganglia, thalami, cortex, cerebellum, hippocampi)

  • MR best to assess overall extent of injury within hours after HII event

    • DWI: 1st modality to be positive (within hours)

    • DWI: Restriction in deep nuclei ± cortex

    • T2/FLAIR: ↑ signal in cerebellum, basal ganglia, cortex

    • Acute changes not reliably identified with T2

  • MRS: More sensitive and indicative of severity of injury in first 24 hours after HII

    • ↑ lactate, ↑ glutamine-glutamate

Top Differential Diagnoses

  • Ischemic territorial infarction

  • Traumatic cerebral edema

  • Toxic/metabolic disorder

  • Acute hypertensive encephalopathy, posterior reversible encephalopathy syndrome (PRES)

  • Creutzfeldt-Jakob disease

  • MELAS

Pathology

  • Common underlying process regardless of cause

    • ↓ cerebral blood flow and ↓ blood oxygenation

    • Switch from oxidative phosphorylation to anaerobic metabolism

    • Glutamate-related cytotoxic processes

Axial DTI trace image in a 21-year-old unresponsive man shows extensive hyperintensity related to cytotoxic edema throughout the cortex and subcortical WM
as well as the external capsules
in this patient with severe hypoxic ischemic injury (HII).

Axial T2 MR in the same patient shows hyperintensity throughout the cortex, subcortical WM
and the external capsules
. Complete effacement of the sulci is related to gyral swelling. Involvement of the visual and sensorimotor cortex is common in severe HII.

Axial FLAIR MR shows symmetric hyperintensity of the basal ganglia
and thalami
in this patient status post cardiac arrest. T2 and FLAIR images typically become positive in the early subacute period (> 24 hours to 2 weeks) with increased signal and swelling of the injured GM structures.

Axial DTI trace shows extensive WM hyperintensity
related to cytotoxic edema in this 43-year-old woman with mild to moderate HII. DWI signal abnormalities may pseudonormalize by the end of the 1st week.

TERMINOLOGY

Synonyms

  • Hypoxic ischemic injury (HII), hypoxic ischemic encephalopathy (HIE)

Definitions

  • Includes various etiologies of injury: Global hypoxic ischemic injury, global anoxic injury, cerebral hypoperfusion injury

IMAGING

General Features

  • Best diagnostic clue

    • Symmetric T2/FLAIR hyperintensity in deep gray nuclei ± cortex

  • Location

    • Mild to moderate: Watershed zone infarcts

    • Severe: Gray matter (GM) structures (basal ganglia [BG], thalami, cerebral cortex [sensorimotor and visual], cerebellum, hippocampi)

      • –

        Cerebellar injury tends to be more common in older patients; Purkinje cells are sensitive to ischemia

    • Injury patterns are highly variable depending on brain maturity, severity and length of insult

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