Acute brain swelling often occurs following external decompression but only rarely following drainage of cerebrospinal fluid (CSF). How can we predict acute brain swelling before external decompression or CSF drainage? It has been suggested that the mechanism of acute brain swelling involves an increase in cerebral blood volume (CBV) but this remains uncertain. A patient with acute brain swelling following head injury in whom intracranial pressure (ICP), jugular venous oxygen saturation (SjO2), and transcranial Doppler sonography (TCD) were serially monitored is presented, and the mechanism is discussed. A 17-year-old man was admitted to the emergency room following a traffic accident on a motorcycle. He was comatose with a score of 6 on the Glasgow coma scale. Pupils were anisocoric, and brain stem reflexes were absent except for the cough reflex. Computed tomography showed traumatic subarachnoid hemorrhage and acute hydrocephalus. Initial TCD showed that the brain was hyperemic. The ICP had increased to 50mmHg, despite barbiturate therapy. Therefore ventricular drainage was implemented via the anterior lateral ventricle to decrease ICP. Ventricular drainage was opened while ICP, SjO2, TCD were being serially monitored. At 4 minutes 30 seconds after opening the drainage, ICP suddenly increased, and SjO2 simultaneously decreased rapidly. There were no changes in TCD waveform during the first 4 minutes, change, indicating the absence of any significant increase in CBV. At that point ICP suddenly increased to 60mmHg, and the TCD waveform changed to systolic flow. Subsequent CT clearly revealed brain swelling. After that the ICP continued at 60∼70mmHg, but the SjO2 increased from 20% to 80%, and then decreased to 20% again. During the next stage, the SjO2 continued at 80∼90%. These changes were explained in terms of alternating periods of relative brain ischemia and brain hyperemia. Hyperemia and intracrnial hypertension were suspected prior to drainage, based on serial monitoring of TCD, ICP, and SjO2 upon admission. Presumably the sudden increase in cerebral perfusion pressure under these conditions caused the acute brain swelling. When brain hyperemia is suspected, it is important to control ICP gradually.
