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  3. Intracerebral Hemorrhage
  • Cited by 5
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    • Publisher:
      Cambridge University Press
      Publication date:
      04 May 2010
      12 November 2009
      ISBN:
      9780511691836
      9780521873314
      DOI:
      https://doi.org/10.1017/CBO9780511691836
      Dimensions:
      (246 x 189 mm)
      Weight & Pages:
      0.76kg, 276 Pages
      Dimensions:
      Weight & Pages:
      • Subjects:
      Emergency Medicine, Neurology and Clinical Neuroscience, Medicine
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    Subjects:
    Emergency Medicine, Neurology and Clinical Neuroscience, Medicine
    Information

    Book description

    Intracerebral hemorrhage is a neurovascular emergency associated with high mortality and morbidity. With in-depth reviews of the clinical and biological aspects of the condition, this text provides an up-to-date coverage of this form of stroke. The book covers epidemiology, causes, clinical presentation, management and prognosis, and describes the ongoing research advances aimed at improving our understanding of the condition. The book fills an existing gap in the medical literature. The chapters discussing the clinical aspects of intracerebral hemorrhage are aimed at the practitioner directing the care of stroke victims. Chapters exploring the biology of pathophysiological events triggered by this disease will provide readers with current data directed to facilitate experimental research in this field of cerebrovascular neurology. It will appeal to clinicians and those with a research interest in cerebrovascular diseases.

    Reviews

    'The three editors, J. Ricardo Carhuapoma, Stephan A. Mayer and Daniel F. Hanley, have clearly succeeded in compiling a standard textbook of high quality (both in writing, tables, images and pictures). It contains all recent publications in the field of spontaneous intracerebral hemorrhage … This is definitely a [highly] recommendable book - it should be on the bookshelf of any neurointensivist dealing with such patients.'

    E. Schmutzhard - Neurological Intensive Care Unit, Medical University of Innsbruck

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    Contents

    Page 1 of 2

    Contents
    • Chapter 8 - Clinical presentation of intracerebral hemorrhage
      pp 101-120
    • View abstract

      Summary

      This chapter reviews the epidemiology of non-traumatic intracerebral hemorrhage (ICH) in light of modern neuroimaging and discusses the incidence, etiology, clinical presentation, and natural history of this condition. Risk for ICH appears to be marginally greater in men than in women, driven by an excess of deep hemorrhages. Incidence rates increase dramatically among persons older than 60. Hypertension is the most important and prevalent modifiable risk factor for ICH. The clinical features used to define ICH are presentation with a gradual progression (over minutes or days) or sudden onset of focal neurological deficit, usually accompanied by signs of increased intracranial pressure such as vomiting or diminished consciousness. A variety of reports have examined clinical and radiographic factors associated with prognosis after ICH. Primary intraventricular hemorrhage (IVH) is rare among adults, comprising 2-3% of ICH admissions. Signs and symptoms of IVH frequently include headache, vomiting, and altered level of consciousness.
    • Chapter 10 - MRI of intracerebral hemorrhage
      pp 125-138
    • View abstract

      Summary

      Acute hypertensive response is the elevation of blood pressure above normal and premorbid values that initially occurs within the first 24 hours of symptom onset in patients with intracerebral hemorrhage (ICH). Hypertension is the most frequent and most important risk factor for ICH. Hypertensive patients suspected of primary intraparenchymal hematoma died and were subsequently autopsied in order to assess the alterations of extraparenchymal and intraparenchymal vascular structures. Stroke patients with a history of hypertension are at risk of critical hypoperfusion for mean arterial pressure levels usually well tolerated by normotensive individuals. Drugs recommended for use in lowering blood pressure in acute stroke include labetalol, hydralazine, nicardipine, and nitroprusside. The Antihypertensive Treatment in Acute Cerebral Hemorrhage (ATACH) trial is a prospective, open label phase I safety and tolerability study started in 2005 that plans to study 60 patients.
    • Chapter 12 - Laboratory and other ancillary testing in intracerebral hemorrhage: an algorithmic approach
      pp 149-158
    • View abstract

      Summary

      Cancer-related intracerebral bleeding is an uncommon cause of hemorrhage and represents only a fraction of all non-traumatic intracranial hemorrhages (ICHs). The mechanisms of intratumoral hemorrhage remain unclear, but include tumor necrosis, rupture of tumor blood vessels and invasion of parenchymal blood vessels by tumor. Metastatic brain tumors can cause intracerebral hemorrhage. Brain metastases from any primary tumor can cause bleeding, but the different primaries have a wide variability in their tendency to bleed. A tumor embolus may cause an aneurysm that can lead to potentially fatal intraparenchymal or subarachnoid hemorrhages. The clinical presentation of intratumoral hemorrhage is often indistinguishable from spontaneous ICH from more typical etiologies such as hypertension. Radiotherapy should be administered according to the appropriate protocol regardless of whether the tumor is associated with hemorrhage. The prognosis of a hemorrhagic neoplasm is primarily determined by the prognosis of the underlying malignancy.
    • Chapter 13 - Medical management of intracerebral hemorrhage
      pp 159-164
    • View abstract

      Summary

      Advanced cerebral amyloid angiopathy (CAA) consists of vascular deposition of amyloid and secondary breakdown of amyloid-laden vessel walls. This chapter focuses on the pathogenesis of CAA, clinical and genetic risk factors, presentations and diagnosis, and prospects for treatment. CAA-related intracerebral hemorrhage (ICH) accounts for a substantial proportion of all spontaneous ICH in the elderly. CAA-related lobar ICH presents similarly to other types of lobar ICH with acute onset of neurological symptoms and the variable presence of headache, seizures, or decreased consciousness according to hemorrhage size and location. CAA-related hemorrhages can also be small and clinically silent. CAA can also present with transient neurological symptoms, another syndrome where diagnosis during life is of particular practical importance. Future treatments for CAA are likely to focus on preventive or protective therapy aimed at decreasing the deposition or toxicity of vascular amyloid.
    • Chapter 14 - Surgical management of intracerebral hemorrhage
      pp 165-175
    • View abstract

      Summary

      This chapter focuses on the epidemiology of oral anticoagulant therapy (OAT)-associated ICH, its pathophysiology, and treatment options based on the currently available data. One of the most common indications for OAT is to prevent stroke in patients with atrial fibrillation. Intracerebral hemorrhage is the deadliest form of stroke, with a mortality rate between 30% and 55%. The incidence and dynamics of hematoma expansion in OAT-ICH remain to be established. Current data suggest that the natural course of hematoma expansion in this group of patients is more prolonged as compared to spontaneous ICH. This may provide a longer time window for treatment of OAT-ICH. However, in OAT-ICH the underlying coagulopathy prolongs the time course of bleeding or rebleeding, and repeated dosing or a higher dose might be essential. The risk of thromboembolism that is associated with current hemostatic treatment strategies which aim to normalize coagulation is unknown.
    • Chapter 15 - Future therapy in intracerebral hemorrhage and intraventricular hemorrhage: aspiration and thrombolysis
      pp 176-186
    • View abstract

      Summary

      Vascular malformations constitute an important cause of intracranial hemorrhage especially in younger patients. These malformations may arise from any segment of the different functional units of the brain vasculature, including arteries, arterioles, capillaries, venules, and veins. Among vascular malformations causing intracranial hemorrhage, brain arteriovenous malformations (AVMs) are among the most frequently encountered. Brain AVMs commonly affect distal arterial branches and in roughly half of the cases, the malformation is found in the borderzone region shared by the distal anterior, middle, and/or posterior cerebral arteries. Cerebral angiography may help to differentiate brain AVMs from other types of intracranial anomalies with arterio-venous shunting. Resection of an associated developmental venous anomaly is contraindicated as its occlusion may lead to venous stasis, brain edema, and eventual hemorrhage. A developmental venous anomaly (DVA) is found in up to 30% of cerebral cavernous malformations (CCM) patients.
    • Chapter 16 - Mathematical models of intracerebral hemorrhage and intraventricular hemorrhage outcomes prediction: their comparison, advantages, and limitations
      pp 187-192
    • View abstract

      Summary

      Cerebral venous thrombosis (CVT), a rare variety of cerebrovascular disease, is a well-established cause of intracerebral hemorrhage (ICH). Cerebral venous thrombosis in neonates is a condition that widely differs from CVT in children and adults because of the frequent association with an acute illness at time of diagnosis and the clinical presentation with seizures and lethargy. The diagnosis of CVT is based on neuroimaging but, even though some locations of hemorrhages can be suggestive of CVT, brain imaging by itself is of little positive value. Computerized tomography scan remains often the first investigation performed on an emergency basis. Antiepileptic drugs are usually prescribed only in patients who present with seizures. Patients with ICH frequently have severe headaches that may require strong analgesics such as morphine, but these usually rapidly decrease after initiation of heparin treatment. The follow-up of patients with H-CVT is similar to that of patients with non-H-CVT.

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