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2Brain

geneous, low in attenuation, and diusely swollen, with sulcal and cisternal eace-ment. Because the meninges are supplied by branches of the external carotid artery (ECA), which are usually not compromised, they will often appear dense against adja-cent low-attenuation brain and can simu-late diuse subarachnoid hemorrhage.

The basal ganglia, cerebral cortex,thalami, cerebellum, caudate nuclei, andhippocampi are most sensitive to hy-poxic ischemic injury, and patients whosuer less severe hypoxia may show low-attenuation CT changes or high-signal T2-weighted MRI changes in these structures(Fig. 2.22).

◆Anoxic Injury

Anoxic (also known as hypoxic-ischemic) cerebral injury results from global lack of oxygen delivery to the brain for an ex-tended period. It is most frequently the consequence of cardiopulmonary arrest, respiratory failure, carbon monoxide poi-soning, near-drowning, or asphyxia. Pa-tients typically present to the Emergency Department with a history of prolonged resuscitation eorts.

CT findings in adults with prolonged anoxia, hypoxia, or global hypoperfusion include progressive loss of normal gray-white matter dierentiation, generalized cytotoxic edema, and sulcal and ventricu-lar eacement. The brain appears homo-

Fig. 2.22a–fa–d Anoxic injury following prolonged cardiorespiratory arrest. (a,b) Initial NCCT. Diminished gray-white dierentiation with normal ventricles and sulci. (c,d) Follow-up NCCT 24 hours later. Progressive decrease in parenchymal attenuation with complete perimesencephalic cisternal and convexity sulcal eacement. Both lateral ventricles are compressed. Increased apparent density within the subarachnoid space reects maintained meningeal perfusion rather than true subarachnoid hemorrhage.

e,f Less severe anoxic injury following cardiac arrest and resucutation. Immediate post-arrest CT is nor-mal. Four days later, low attenuation changes are limited to the caudate nuclei and lateral putamina.