Approximately 15% of strokes are haemorrhagic.
Computed tomography (CT) or magnetic resonance imaging (MRI) scans, with high sensitivity for intracerebral haemorrhage, are essential in diagnosis.
Treatments for intracerebral haemorrhage (ICH) and ischaemic stroke differ radically.
The primary treatment of haemorrhagic stroke involves supportive care and optimisation of intracranial haemodynamics.
Surgical resection of intracerebral haematomas may be of benefit in select cases, but has yet to be demonstrated as effective in clinical trials. Newer minimally invasive surgical techniques are currently being investigated.
Study results show that patients in dedicated stroke units have improved survival and reduced disability at 1 year.
Stroke is an acute neurological deficit caused by cerebrovascular aetiology. It is further subdivided into ischaemic stroke and haemorrhagic stroke. Ischaemic stroke is lack of blood perfusion due to occlusion or critical stenosis of a cerebrospinal artery, and haemorrhagic stroke is due to rupture of a cerebrospinal artery, resulting in intraparenchymal, subarachnoid, and intraventricular haemorrhage. Intracerebral haemorrhage is further subdivided into primary and secondary aetiology. Primary spontaneous intracerebral haemorrhage is defined as haemorrhage in the absence of vascular malformations or associated diseases. Secondary intracerebral haemorrhage is from an identifiable vascular malformation or as a complication of other medical or neurological diseases that either impair coagulation or promote vascular rupture.
History and exam
- neck stiffness
- history of atrial fibrillation
- history of liver disease
- visual changes
- sudden onset
- altered sensation
- sensory loss
- history of haematological disorder
- altered level of consciousness/coma
- gaze paresis
- advanced age
- male sex
- Asian, black and/or Hispanic
- family history of haemorrhagic stroke
- cerebral amyloid angiopathy
- autosomal dominant mutations in the COL4A1 gene
- hereditary haemorrhagic telangiectasia
- autosomal dominant mutations in the KRIT1 gene
- autosomal dominant mutations in the CCM2 gene
- autosomal dominant mutations in the PDCD10 gene
- illicit sympathomimetic drugs
- vascular malformations
- non-steroidal anti-inflammatories (NSAIDs)
- diabetes mellitus
- heavy alcohol abuse
- sympathomimetic medications
- cerebral vasculitis
- Moyamoya disease
Clinical Associate of Neurology
Medical Director, Neuroscience ICU
Director, Neurocritical Care Education
Co-Director, Stroke Center
University of Chicago
FDG declares that he has no competing interests.
Neurocritical Care Fellow
Department of Neurology
University of Chicago
RCM declares that she has no competing interests.
Dr Fernando Goldenberg and Dr Raisa Martinez would like to gratefully acknowledge Dr Alejandro Hornik, Dr Eric E. Smith, and Dr T. Dion Fung, the previous contributors to this monograph. EES is an author of a number of references cited in this monograph. AH and TDF declare that they have no competing interests.
Lecturer in Neurology
Beth Israel Deaconess Medical Center
Division of Cerebrovascular/Stroke
LRC declares that he has no competing interests.
Centre Hospitalier Universitaire Vaudois (CHUV)
JM declares that he has no competing interests.
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