Brain edema from intracerebral hemorrhage.
Sequential changes in brain parenchyma surrounding an intracerebral hemorrhage are described here. Re-bleeding occurs within the first several hours after the initial hemorrhage in about 30%, of cases. The coagulation cascade is activated as soon as blood encounters tissue. Perihematomal brain edema develops in response to clot retraction, thrombin formation, erythrocyte lysis, hemoglobin toxicity, complement activation, mass effect, and blood-brain barrier disruption. Early hematoma evacuation interrupts edema formation. The toxicity ofextravasated blood in brain parenchyma has not been studied well in traumatic injury or in hemorrhagic tumor models yet, but similar mechanisms of edema formation are likely to occur in these conditions.
Hoff
J T
JT
Department of Neurosurgery, University of Michigan Health System, Ann Arbor, Michigan 48109-0338, USA. jhoff@umich.edu
Xi
G
G
D000818:Animals; D001777:Blood Coagulation; D001812:Blood-Brain Barrier; D001929:Brain Edema / Q000097:blood / Q000209:etiology* / Q000503:physiopathology; D002545:Brain Ischemia / Q000150:complications; D002543:Cerebral Hemorrhage / Q000150:complications*; D003167:Complement Activation; D004912:Erythrocytes; D006454:Hemoglobins / Q000378:metabolism; D006801:Humans; D013917:Thrombin / Q000096:biosynthesis
D006454:Hemoglobins; D013917:Thrombin