Intracerebral Hemorrhage

2015 ◽  
Author(s):  
Natalie P. Kreitzer ◽  
Opeolu Adeoye

Intracerebral hemorrhage can be classified as either secondary (due to trauma, vascular malformations, aneurysms, tumors, or hemorrhagic transformation of ischemic stroke) or primary (without a clear secondary cause). Intracerebral hemorrhage is a neurologic emergency, and leads to significant death and disability each year; care should be expedited and emergency departments should be equipped to appropriately care for and manage these patients. This review covers the risk factors, natural history, pathophysiology, stabilization and assessment, diagnosis and treatment, and disposition and outcomes for patients with intracerebral hemorrhage. Figures show head computed tomographic scans demonstrating a left basal ganglia intracerebral hemorrhage, and an algorithm of management of intracerebral hemorrhage in the emergency department. Tables list some common causes of intracerebral hemorrhage, Boston criteria for diagnosis of cerebral amyloid angiopathy, mechanism of action of common anticoagulants, and suggested reversal agents. This review contains 2 highly rendered figures, 4 tables, and 79 references.

2018 ◽  
Author(s):  
Natalie P. Kreitzer ◽  
Opeolu Adeoye

Intracerebral hemorrhage can be classified as either secondary (due to trauma, vascular malformations, aneurysms, tumors, or hemorrhagic transformation of ischemic stroke) or primary (without a clear secondary cause). Intracerebral hemorrhage is a neurologic emergency, and leads to significant death and disability each year; care should be expedited and emergency departments should be equipped to appropriately care for and manage these patients. This review covers the risk factors, natural history, pathophysiology, stabilization and assessment, diagnosis and treatment, and disposition and outcomes for patients with intracerebral hemorrhage. Figures show head computed tomographic scans demonstrating a left basal ganglia intracerebral hemorrhage, and an algorithm of management of intracerebral hemorrhage in the emergency department. Tables list some common causes of intracerebral hemorrhage, Boston criteria for diagnosis of cerebral amyloid angiopathy, mechanism of action of common anticoagulants, and suggested reversal agents. This review contains 2 figures, 6 tables, and 59 references. Key words: Intracerebral hemorrhage; intracranial hemorrhage; intraparenchymal hemorrhage; hemorrhagic stroke; hypertensive hemorrhage; spontaneous intracerebral hemorrhage; ICH; cerebral bleeds


2018 ◽  
Author(s):  
Natalie P. Kreitzer ◽  
Opeolu Adeoye

Intracerebral hemorrhage can be classified as either secondary (due to trauma, vascular malformations, aneurysms, tumors, or hemorrhagic transformation of ischemic stroke) or primary (without a clear secondary cause). Intracerebral hemorrhage is a neurologic emergency, and leads to significant death and disability each year; care should be expedited and emergency departments should be equipped to appropriately care for and manage these patients. This review covers the risk factors, natural history, pathophysiology, stabilization and assessment, diagnosis and treatment, and disposition and outcomes for patients with intracerebral hemorrhage. Figures show head computed tomographic scans demonstrating a left basal ganglia intracerebral hemorrhage, and an algorithm of management of intracerebral hemorrhage in the emergency department. Tables list some common causes of intracerebral hemorrhage, Boston criteria for diagnosis of cerebral amyloid angiopathy, mechanism of action of common anticoagulants, and suggested reversal agents. This review contains 2 figures, 6 tables, and 58 references. Key words: Intracerebral hemorrhage; intracranial hemorrhage; intraparenchymal hemorrhage; hemorrhagic stroke; hypertensive hemorrhage; spontaneous intracerebral hemorrhage; ICH; cerebral bleeds


2019 ◽  
Vol 176 ◽  
pp. 110-115
Author(s):  
Taro Yanagawa ◽  
Masaki Takao ◽  
Masami Yasuda ◽  
Tomoya Kamide ◽  
Hiroki Sato ◽  
...  

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Konark MALHOTRA ◽  
Christina Zompola ◽  
Aikaterini Theodorou ◽  
Aristeidis Katsanos ◽  
Ashkan Shoamanesh ◽  
...  

Objective: We sought to determine the prevalence, radiological characteristics, and clinical outcomes of intracerebral hemorrhage (ICH) of undetermined etiology. Methods: Systematic review and meta-analysis of studies involving patients with spontaneous ICH was conducted to assess the prevalence and clinical-radiological characteristics of undetermined ICH. Additionally, we assessed the rates for ICH secondary to hypertensive arteriopathy (HTN-A) and cerebral amyloid angiopathy (CAA). Subgroup analyses were performed based on the use of a) etiology-oriented ICH classification, b) detailed neuroimaging, and c) Boston criteria among CAA-ICH. Results: 24 studies were included (n=15,828; mean age: 64.8 years, males: 60.8%). The pooled prevalence of HTN-A ICH, undetermined ICH and CAA-ICH were 50% (95%CI: 43-58%), 18% (95%CI: 13-23%), and 12% (95%CI: 7-17%; p<0.001 between subgroups). The volume of ICH was largest in CAA-ICH 24.7mL (95%CI: 19.7-29.8mL), followed by HTN-A ICH 16.2mL (95%CI: 10.9-21.5mL) and undetermined ICH 15.4mL (95%CI: 6.2-24.5mL). Among patients with undetermined ICH, the rates of short-term mortality and intraventricular hemorrhage were 33% (95%CI: 25-42%) and 38% (95%CI: 28-48%), respectively. Subgroup analysis demonstrated a higher rate of undetermined ICH among studies that did not use an etiology-oriented classification (22%; 95%CI: 15-29%). No difference was observed between studies based on the completion of detailed neuroimaging to assess the rates of undetermined ICH (p=0.62). Conclusions: The etiology of spontaneous ICH remains undetermined among one in five patients in studies using etiology-oriented classification and among one in four patients in studies that avoid using etiology-oriented classification. The short-term mortality in undetermined ICH is high despite the relatively small ICH volume. Our findings suggest the use of etiology-oriented classification to approach ICH patients (Figure).


Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Andreas Charidimou ◽  
Gregoire Boulouis ◽  
Matthew Frosch ◽  
Jean-Claude Baron ◽  
Marco Pasi ◽  
...  

Introduction: The Boston criteria are used worldwide for in vivo diagnosis of cerebral amyloid angiopathy (CAA). Given substantial advances in CAA research, we aimed to update the Boston criteria and externally validate their diagnostic accuracy across the spectrum of CAA-related presentations and across international sites. Methods: As part of an International CAA Association multicenter study, we identified patients age 50 or older with potential CAA-related clinical presentations (spontaneous intracerebral hemorrhage, cognitive impairment, or transient focal neurological episodes), available brain MRI, and histopathologic assessment for the diagnosis of CAA. We derived Boston criteria v2.0 by selecting MRI features to optimize diagnostic specificity and sensitivity in a pre-specified derivation sample (Boston cases 1994 to 2012, n=159), then externally validated in pre-specified temporal (Boston cases 2012-2018, n=59) and geographical (non-Boston cases 2004-2018; n=123) validation samples and compared their diagnostic accuracy to the currently used modified Boston criteria. Results: Based on exploratory analyses in the derivation sample, we derived provisional criteria for probable CAA requiring presence of at least 2 strictly lobar hemorrhagic lesions (intracerebral hemorrhage, cerebral microbleed, or cortical superficial siderosis focus) or at least 1 strictly lobar hemorrhagic lesion and 1 white matter characteristic (severe degree of visible perivascular spaces in centrum semiovale or white matter hyperintensities multispot pattern). Sensitivity/specificity of the criteria were 74.8/84.6% in the derivation sample, 92.5/89.5% in the temporal validation sample, 80.2/81.5% in the geographic validation sample, and 74.5/95.0% in cases across all samples with autopsy as the diagnostic gold standard. The v2.0 criteria for probable CAA had superior accuracy to the currently modified Boston criteria (p<0.005) in the autopsied cases. Conclusion: The Boston criteria v.2.0 incorporate emerging MRI markers of CAA to enhance sensitivity without compromising their high specificity. Validation of the criteria across independent patient settings firmly supports their adoption into clinical practice and research.


2021 ◽  
pp. 192-194
Author(s):  
Stephen W. English ◽  
James P. Klaas

An 86-year-old woman with a history of hypertension, hyperlipidemia, coronary artery disease, and hypothyroidism sought care for subacute, progressive cognitive decline. Five months earlier, she was hospitalized for a small, left temporal, lobar, intracerebral hemorrhage with associated receptive aphasia. Over the next several months, she had a precipitous cognitive decline. She was prescribed memantine by her primary physician because of concern for dementia. One month before seeking care, she was found unconscious in her bathroom, which was believed to be an unwitnessed seizure. Brain magnetic resonance imaging 1 month before the current evaluation showed a prior, small, left temporal hemorrhage and diffuse lobar microhemorrhages on gradient echo imaging, focal leptomeningeal gadolinium enhancement in the left temporal lobe, and multifocal T2 hyperintensity with mass effect, maximal in the left temporal lobe. Electroencephalography showed multifocal, independent epileptiform discharges. She underwent open biopsy of the left temporal lobe, which indicated focal granulomatous inflammation causing vascular destruction, with β‎-amyloid plaques within the cortical and leptomeningeal vessels. The findings were consistent with a diagnosis of amyloid-β‎-related angiitis in the setting of severe cerebral amyloid angiopathy. Because of concern for subclinical seizures and epileptiform discharges on electroencephalography, the patient was started on levetiracetam without substantial change in her mental status. After the biopsy findings demonstrated inflammatory changes consistent with amyloid-β‎-related angiitis, she was started on intravenous methylprednisolone, followed by transition to prednisone. After 6 months of treatment, she had significant clinical and radiographic improvement. Follow-up magnetic resonance imaging at that time showed interval improvement in the T2 hyperintensity and mass effect in the left temporal lobe. She was again independent with her activities of daily living, and memantine was discontinued. Cerebral amyloid angiopathy encompasses a heterogeneous group of diseases characterized by amyloid-β‎ peptide deposition. The most common clinical manifestation of cerebral amyloid angiopathy is lobar intracerebral hemorrhage, which can be multifocal and recurrent but can also result in cerebral ischemia and ischemic leukoencephalopathy.


Stroke ◽  
2019 ◽  
Vol 50 (9) ◽  
pp. 2562-2564 ◽  
Author(s):  
Lionel Calviere ◽  
Alain Viguier ◽  
Sofia Patsoura ◽  
Vanessa Rousseau ◽  
Jean-François Albucher ◽  
...  

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