Anoxic/hypoxic brain injury

During initial triage, the patient had cardiac arrest and resuscitation







Five days later







Findings

No significant abnormality is noted on the first non-contrast CT head performed the day of the patient’s cardiac arrest. On the CT head performed five days later, however, there has been interval diffuse loss of gray-white differentiation, decreasing ventricular size, and decreasing sulcal prominence. In addition, at level/window shown, there is now subtle hypodensity of the caudate heads and lentiform nuclei bilaterally.

Differential diagnosis:
- Anoxia/hypoxia
- Toxic exposure
- Metabolic abnormalities


Diagnosis: Anoxic/hypoxic brain injury


Key points

A period of global intracranial hypoxia (hypoperfusion or hypoxemia) tends to affect the most metabolically active areas of the brain preferentially.
These areas include the caudate nuclei, lentiform nuclei, parahippocampal gyri, hippocampi, cerebellar hemispheres, and cerebral white matter.
A similar distribution of injury occurs with exposure to certain toxins like carbon monoxide, methanol, hydrogen sulfide, barbiturates, and Ecstasy.
Metabolic abnormalities like hypoglycemia can also cause injury to these structures and should be included in the differential.
CT findings include hypo densities in the affected areas representing edema, which later resolves leaving residual volume loss with possible calcification and/or hemorrhage.
Evidence of diffuse brain edema (loss of gray-white definition, sulcal effacement, effacement of cisterns, downward herniation, etc.) may be present acutely as well.
MR findings include increased signal on fluid sensitive sequences in the affected areas. Hemorrhagic necrosis (petechial or laminar) may subsequently develop.