Dana C Holl1, Victor Volovici2, Clemens M F Dirven3, Wilco C Peul4, Fop van Kooten5, Korné Jellema6, Niels A van der Gaag4, Ishita P Miah6, Kuan H Kho7, Heleen M den Hertog8, Hester F Lingsma9, Ruben Dammers3. 1. Department of Neurosurgery, Erasmus Medical Center, Erasmus MC Stroke Center, Rotterdam, The Netherlands. Electronic address: d.holl@erasmusmc.nl. 2. Department of Neurosurgery, Erasmus Medical Center, Erasmus MC Stroke Center, Rotterdam, The Netherlands; Department of Public Health and Medical Decision Making, Erasmus Medical Center, Rotterdam, The Netherlands. 3. Department of Neurosurgery, Erasmus Medical Center, Erasmus MC Stroke Center, Rotterdam, The Netherlands. 4. Department of Neurosurgery, Leiden University Medical Center, Leiden, Haaglanden MC and Haga Teaching Hospital, The Hague, The Netherlands. 5. Department of Neurology, Erasmus Medical Center, Erasmus MC Stroke Center, Rotterdam, The Netherlands. 6. Department of Neurology, Haaglanden Medical Center, The Hague, The Netherlands. 7. Department of Neurosurgery, Medisch Spectrum Twente, Enschede, The Netherlands. 8. Department of Neurology, Medisch Spectrum Twente, Enschede, The Netherlands. 9. Department of Public Health and Medical Decision Making, Erasmus Medical Center, Rotterdam, The Netherlands.
Abstract
BACKGROUND: Chronic subdural hematoma (CSDH) is one of the more frequent pathologic entities in daily neurosurgical practice. Historically, CSDH was considered progressive recurrent bleeding with a traumatic cause. However, recent evidence has suggested a complex intertwined pathway of inflammation, angiogenesis, local coagulopathy, recurrent microbleeds, and exudates. The aim of the present review is to collect existing data on pathophysiology of CSDH to direct further research questions aiming to optimize treatment for the individual patient. METHODS: We performed a thorough literature search in PubMed, Ovid, EMBASE, CINAHL, and Google scholar, focusing on any aspect of the pathophysiology and nonsurgical treatment of CSDH. RESULTS: After a (minor) traumatic event, the dural border cell layer tears, which leads to the extravasation of cerebrospinal fluid and blood in the subdural space. A cascade of inflammation, impaired coagulation, fibrinolysis, and angiogenesis is set in motion. The most commonly used treatment is surgical drainage. However, because of the pathophysiologic mechanisms, the mortality and high morbidity associated with surgical drainage, drug therapy (dexamethasone, atorvastatin, tranexamic acid, or angiotensin-converting enzyme inhibitors) might be a beneficial alternative in many patients with CSDH. CONCLUSIONS: Based on pathophysiologic mechanisms, animal experiments, and small patient studies, medical treatment may play a role in the treatment of CSDH. There is a lack of level I evidence in the nonsurgical treatment of CSDH. Therefore, randomized controlled trials, currently lacking, are needed to assess which treatment is most effective in each individual patient.
BACKGROUND:Chronic subdural hematoma (CSDH) is one of the more frequent pathologic entities in daily neurosurgical practice. Historically, CSDH was considered progressive recurrent bleeding with a traumatic cause. However, recent evidence has suggested a complex intertwined pathway of inflammation, angiogenesis, local coagulopathy, recurrent microbleeds, and exudates. The aim of the present review is to collect existing data on pathophysiology of CSDH to direct further research questions aiming to optimize treatment for the individual patient. METHODS: We performed a thorough literature search in PubMed, Ovid, EMBASE, CINAHL, and Google scholar, focusing on any aspect of the pathophysiology and nonsurgical treatment of CSDH. RESULTS: After a (minor) traumatic event, the dural border cell layer tears, which leads to the extravasation of cerebrospinal fluid and blood in the subdural space. A cascade of inflammation, impaired coagulation, fibrinolysis, and angiogenesis is set in motion. The most commonly used treatment is surgical drainage. However, because of the pathophysiologic mechanisms, the mortality and high morbidity associated with surgical drainage, drug therapy (dexamethasone, atorvastatin, tranexamic acid, or angiotensin-converting enzyme inhibitors) might be a beneficial alternative in many patients with CSDH. CONCLUSIONS: Based on pathophysiologic mechanisms, animal experiments, and small patient studies, medical treatment may play a role in the treatment of CSDH. There is a lack of level I evidence in the nonsurgical treatment of CSDH. Therefore, randomized controlled trials, currently lacking, are needed to assess which treatment is most effective in each individual patient.
Authors: Hae-Won Koo; Minkyung Oh; Hyung Koo Kang; Yung Ki Park; Byung-Jou Lee; Seong Rok Han; Sang Won Yoon; Chan Young Choi; Moon-Jun Sohn; Chae Heuck Lee Journal: PLoS One Date: 2019-09-04 Impact factor: 3.240