Diffuse Cerebral Edema

History: status post trauma with severe blood loss. 

Diffuse Cerebral Edema – Axial noncontrast CT scan of the head reveals diffuse effacement of the sulci and lateral ventricles and hypoattenuation of the brain parenchyma. Note also the falx appears hyperattenuating (yellow arrows), although no subdural or subarachnoid hemorrhage was present.

This is a case of diffuse cerebral edema secondary to exsanguination. The pathophysiology of diffuse cerebral edema in the case of exsanguination involves global brain ischemia secondary to hypoperfusion from hypovolemic shock. Brain ischemia leads to anaerobic metabolism that produces less adenosine triphosphate (ATP) and more lactate. This leads to increased release of glutamate, triggering the cytotoxic edema. Cytotoxic edema results from failure of the sodium/potassium (Na/K)  pump to continue pumping sodium out of the cells and into the extracellular space.  Cytotoxic edema appears as diffuse hypoattenuation of the brain parenchyma and effacement of the sulci, as seen above. The prognosis at this point is extremely poor.

The falx in the image above (yellow arrows) appears falsely hyperattenuating, which may mislead one to believe there is subdural or subarachnoid hemorrhage. Read about pseudo-hemorrhage here.

Ball-and-stick model of adenosine triphosphate (ATP), based on x-ray diffraction data from Olga Kennard, N. W. Isaacs, W. D. S. Motherwell, J. C. Coppola, D. L. Wampler, A. C. Larson, D. G. Watson (1971). “The Crystal and Molecular Structure of Adenosine Triphosphate”. Proceedings of the Royal Society of London. Series A, Mathematical and Physical Sciences 325 : 401-436. DOI:10.1098/rspa.1971.0177. (Photo credit: Wikipedia)