Dr. Hashemi MD Hemorrhagic stroke Intracerebral Hemorrhage (ICH)

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Text of Dr. Hashemi MD Hemorrhagic stroke Intracerebral Hemorrhage (ICH)

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  • Dr. Hashemi MD
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  • Hemorrhagic stroke
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  • Intracerebral Hemorrhage (ICH)
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  • What Is ICH? A hemorrhagic stroke is bleeding (hemorrhage) that suddenly interferes with the brain's function. This bleeding can occur either within the brain or between the brain and the skull.
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  • ICH background 10-18% of strokes. Mortality rate : 25% and 60%. Mortality is strongly dependent on hematoma size and, to a lesser extent, location. The main cause of ICH is hypertension~ 60-70% In both hypertensive and nonhypertensive patients, the circadian rhythm of ICH onset, with peaks at 8 AM and 8 PM, coincides with the physiological daily peaks of blood pressure, pointing to the importance of blood pressure rises in the pathogenesis of ICH.
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  • Subarachnoid hemorrhage Bleeding from a damaged blood vessel causes blood to accumulate at the surface of the brain. As blood flows into the cerebral spinal fluid, it increases pressure on the brain, which causes an immediate headache. In the days immediately following the bleeding, chemical irritation from clotted blood can cause brain arteries near to the clot to go into spasm. Artery spasm can damage brain tissue. Most often, a subarachnoid hemorrhage happens because of a saccular aneurysm, but it also can occur because of leakage from an AVM.
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  • Ischemic versus hemorrhagic stroke
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  • VASCULAR ANATOMY
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  • anatomy Knowledge of cerebrovascular arterial anatomy and the brain regions supplied by the arteries is useful in determining which vessels are involved in acute stroke. Atypical patterns that do not conform to a vascular distribution may indicate another diagnosis, such as venous infarction. The cerebral hemispheres are supplied by 3 paired major arteries: the anterior, middle, and posterior cerebral arteries. The anterior and middle cerebral arteries are responsible for the anterior circulation and arise from the supraclinoid internal carotid arteries. The posterior cerebral arteries arise from the basilar artery and form the posterior circulation, which also supplies the thalami, brainstem, and cerebellum. The angiograms in the images below demonstrate some portions of the circulation involved in hemorrhagic strokes.
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  • Anterior circulation
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  • Posterior circulation
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  • Territories of the principle cerebral arteries ArteryTerritory Anterior circulation Internal carotid Anterior choroidalHippocampus, globus pallidus, lower internal capsule Anterior cerebral Medial frontal and parietal cortex and subjacent white matter, anterior corpus callosum Middle cerebralLateral frontal, parietal, occipital, and temporal cortex and subjacent white matter Lenticulostri ate branchesCaudate nucleus, putamen, upper internal capsule Posterior circulation Vertebral PICA Medulla, lower cerebellum Basilar AICALower and midpons, mid cerebellum SCAUpper pons, lower midbrain, upper cerebellum Posterior cerebral Medial occipital and temporal cortex and subjacent white matter, posterior corpus callosum, upper midbrain Thalamoperforat e branchesThalamus Thalamogenicul ate branchesThalamus
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  • Distribution of major supratentorial arterial territories
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  • Frontal view of a cerebral angiogram with selective injection of the left internal carotid artery illustrates the anterior circulation. The anterior cerebral artery consists of the A1 segment proximal to the anterior communicating artery with the A2 segment distal to it. The middle cerebral artery can be divided into 4 segments: the M1 (horizontal segment) extends to the limen insulae and gives off lateral lenticulostriate branches, the M2 (insular segment), M3 (opercular branches), and M4 (distal cortical branches on the lateral hemispheric convexities)
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  • Lateral view of a cerebral angiogram illustrates the branches of the anterior cerebral artery (ACA) and sylvian triangle. The pericallosal artery has been described as arising distal to the anterior communicating artery or distal to the origin of the callosomarginal branch of the ACA. The segmental anatomy of the ACA has been described as follows: (1) the A1 segment extends from the internal carotid artery (ICA) bifurcation to the anterior communicating artery, (2) A2 extends to the junction of the rostrum and genu of the corpus callosum, (3) A3 extends into the bend of the genu of the corpus callosum, and (4) A4 and A5 extend posteriorly above the callosal body and superior portion of the splenium. The sylvian triangle overlies the opercular branches of the middle cerebral artery, with the apex representing the sylvian point.
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  • Frontal projection from a right vertebral artery angiogram illustrates the posterior circulation. The vertebral arteries join to form the basilar artery. The posterior inferior cerebellar arteries (PICA) arise from the distal vertebral arteries. The anterior inferior cerebellar arteries (AICA) arise from the proximal basilar artery. The superior cerebellar arteries (SCA) arise distally from the basilar artery before its bifurcation into the posterior cerebral arteries.
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  • Diagnosis Brain imaging is a crucial step in the evaluation of suspected hemorrhagic stroke and must be obtained on an emergent basis. Brain imaging aids in excluding ischemic stroke, and it may identify complications of hemorrhagic stroke such as intraventricular hemorrhage, brain edema, and hydrocephalus. Either noncontrast computed tomography (NCCT) scanning or magnetic resonance imaging (MRI) is the modality of choice.
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  • Risk factors The risk of hemorrhagic stroke is increased with the following factors: Advanced age Hypertension (up to 60% of cases) Previous history of stroke Alcohol abuse Use of illicit drugs (cocaine, other sympathomimetic drugs)
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  • Hypertension Hypertensive small-vessel disease results from tiny lipohyalinotic aneurysms that subsequently rupture and result in intraparenchymal hemorrhage. Typical locations include the basal ganglia, thalami, cerebellum, and pons.
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  • Nonhypertensive Causes of Intracerebral Hemorrhage Vascular malformations (saccular or mycotic aneurysms, arteriovenous malformations, cavernous angiomas) Intracranial tumors Bleeding disorders, anticoagulant and fibrinolytic treatment Cerebral amyloid angiopathy Granulomatous angiitis of the central nervous system and other vasculitides, such as polyarteritis nodosa Sympathomimetic agents (including amphetamine and cocaine) Hemorrhagic infarction Trauma
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  • Arteriovenous malformations Numerous genetic causes may predispose to AVMs in the brain, although AVMs are generally sporadic. Hereditary hemorrhagic telangiectasia (HHT), previously known as Osler-Weber-Rendu syndrome, is an autosomal dominant disorder that causes dysplasia of the vasculature. HHT is most frequently diagnosed when patients present with telangiectasias on the skin and mucosa or with chronic epistaxis from AVMs in the nasal mucosa. Additionally, HHT can result in AVMs in any organ system or vascular bed.
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  • Arteriovenous malformations
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  • Intracranial tumors
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  • Noncontrast CTscan of acute left putaminal intracerebral hemorrhage (CT done 3 hours after symptom onset) with a large amount of surrounding hypodensity edema and mass effect. Biopsy of tissue adjacent to the hemorrhage at the time of surgical drainage revealed typical features of gliobastoma multiform.
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  • Amyloidosis Cerebral amyloidosis affects people who are elderly and may cause up to 10% of intracerebral hemorrhages. Rarely, cerebral amyloid angiopathy can be caused by mutations in the amyloid precursor protein and is inherited in an autosomal dominant fashion. 80-year-old woman with numerous punctate foci of hypointensity (black dots) on MRI gradient-echo (GRE) sequence (left), suggesting multiple lobar microbleeds caused by cerebral amyloid angiopathy.
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  • Coagulopathies Coagulopathies may be acquired or inherited. Liver disease can result in a bleeding diathesis. Inherited disorders of coagulation such as factor VII, VIII, IX, X, and XIII deficiency can predispose to excessive bleeding, and intracranial hemorrhage has been seen in all of these disorders.
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  • Hemorrhagic transformation of ischemic stroke Hemorrhagic transformation represents the conversion of a bland infarction into an area of hemorrhage (20-40% of patients with ischemic infarction). Mechanisms: Reperfusion of ischemically injured tissue, either from recanalization of an occluded vessel or from collateral blood supply to the ischemic territory Disruption of the blood-brain barrier
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  • Hemorrhagic transformation of ischemic stroke Hemorrhagic transformation of an ischemic infarct occurs within 2-14 days postictus, usually within the first week. It is more commonly seen following cardioembolic strokes and is more likely with larger infarct size. Hemorrhagic transformation is also more likely following administration of tissue plasminogen activator (tPA) in patients