Kipyoung Jeon, J. .. Kim, Kijeong Lee, Kyu-Nam Park, B. Kim, Y. Shin, J. Koo
{"title":"血浆因子VIII升高与无颅骨骨折的颅脑损伤后非化脓性脑静脉血栓形成","authors":"Kipyoung Jeon, J. .. Kim, Kijeong Lee, Kyu-Nam Park, B. Kim, Y. Shin, J. Koo","doi":"10.26420/austinjcerebrovascdisstroke.2019.1082","DOIUrl":null,"url":null,"abstract":"Cerebral Venous Thrombosis (CVT) is a relatively uncommon but important cause of stroke that tends to affect young adults, especially women. Head trauma with or without skull fracture was reported to be triggering factors for CVT, but the underlying pathophysiology was not well elucidated. Endothelial injury and coexistent hypercoagulability were supposed to contribute to CVT after head trauma without skull fracture. We report a 49-year-old female patient who presented with headache with vomiting after head trauma and was initially diagnosed as post-traumatic Intracerebral Hemorrhage (ICH), but subsequently, progressed to CVT that resulted in cerebral venous infarction with hemorrhagic transformation. Magnetic Resonance brain Venography (MRV) confirmed CVT in superior sagittal sinus as well as right transverse and sigmoid sinuses. She was treated with endovascular mechanical thrombectomy followed by anticoagulation. The coagulopathy panel was checked both in hospital and in outpatient clinic for evaluating the etiology underlying post-traumatic nonpyogenic CVT. Persistently elevated level of plasma Factor VIII was identified. We should consider that patients with recent head trauma history without skull fracture and coexistent hypercoagulability could develop CVT resulting in cerebral venous infarction with hemorrhagic transformation even when the patient showed no definite focal neurologic deficit or the patient’s initial CT scan revealed no intracranial hemorrhage.","PeriodicalId":90444,"journal":{"name":"Austin journal of cerebrovascular disease & stroke","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2019-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Elevated Plasma Factor VIII in Non-Pyogenic Cerebral Venous Thrombosis after Head Trauma without Skull Fracture\",\"authors\":\"Kipyoung Jeon, J. .. Kim, Kijeong Lee, Kyu-Nam Park, B. Kim, Y. Shin, J. Koo\",\"doi\":\"10.26420/austinjcerebrovascdisstroke.2019.1082\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Cerebral Venous Thrombosis (CVT) is a relatively uncommon but important cause of stroke that tends to affect young adults, especially women. Head trauma with or without skull fracture was reported to be triggering factors for CVT, but the underlying pathophysiology was not well elucidated. Endothelial injury and coexistent hypercoagulability were supposed to contribute to CVT after head trauma without skull fracture. We report a 49-year-old female patient who presented with headache with vomiting after head trauma and was initially diagnosed as post-traumatic Intracerebral Hemorrhage (ICH), but subsequently, progressed to CVT that resulted in cerebral venous infarction with hemorrhagic transformation. Magnetic Resonance brain Venography (MRV) confirmed CVT in superior sagittal sinus as well as right transverse and sigmoid sinuses. She was treated with endovascular mechanical thrombectomy followed by anticoagulation. The coagulopathy panel was checked both in hospital and in outpatient clinic for evaluating the etiology underlying post-traumatic nonpyogenic CVT. Persistently elevated level of plasma Factor VIII was identified. We should consider that patients with recent head trauma history without skull fracture and coexistent hypercoagulability could develop CVT resulting in cerebral venous infarction with hemorrhagic transformation even when the patient showed no definite focal neurologic deficit or the patient’s initial CT scan revealed no intracranial hemorrhage.\",\"PeriodicalId\":90444,\"journal\":{\"name\":\"Austin journal of cerebrovascular disease & stroke\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2019-09-25\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Austin journal of cerebrovascular disease & stroke\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.26420/austinjcerebrovascdisstroke.2019.1082\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Austin journal of cerebrovascular disease & stroke","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.26420/austinjcerebrovascdisstroke.2019.1082","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Elevated Plasma Factor VIII in Non-Pyogenic Cerebral Venous Thrombosis after Head Trauma without Skull Fracture
Cerebral Venous Thrombosis (CVT) is a relatively uncommon but important cause of stroke that tends to affect young adults, especially women. Head trauma with or without skull fracture was reported to be triggering factors for CVT, but the underlying pathophysiology was not well elucidated. Endothelial injury and coexistent hypercoagulability were supposed to contribute to CVT after head trauma without skull fracture. We report a 49-year-old female patient who presented with headache with vomiting after head trauma and was initially diagnosed as post-traumatic Intracerebral Hemorrhage (ICH), but subsequently, progressed to CVT that resulted in cerebral venous infarction with hemorrhagic transformation. Magnetic Resonance brain Venography (MRV) confirmed CVT in superior sagittal sinus as well as right transverse and sigmoid sinuses. She was treated with endovascular mechanical thrombectomy followed by anticoagulation. The coagulopathy panel was checked both in hospital and in outpatient clinic for evaluating the etiology underlying post-traumatic nonpyogenic CVT. Persistently elevated level of plasma Factor VIII was identified. We should consider that patients with recent head trauma history without skull fracture and coexistent hypercoagulability could develop CVT resulting in cerebral venous infarction with hemorrhagic transformation even when the patient showed no definite focal neurologic deficit or the patient’s initial CT scan revealed no intracranial hemorrhage.