HEMORRHAGIC STROKE

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Published on February 6, 2014

Author: GghNeurology

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HEMORRHAGIC STROKE : HEMORRHAGIC STROKE Dr Srikanth Vadlamudi Epidemiology: Stroke is the leading cause of adult disabilities 2nd leading cause of death worldwide 800,000 strokes per year resulting in 150,000 deaths Stroke can be divided into hemorrhagic and ischemic origins 15% hemorrhagic 85% ischemic Epidemiology CLASSIFICATION OF STROKE: CLASSIFICATION OF STROKE Adapted from Scott PA, Barsan WG. Stroke, transient ischemic attack, and other central focal conditions. In: Tintinalli J. Emergency Medicine: A Comprehensive Study Guide. 5th ed. McGraw-Hill; 2000:1430. Stroke Hemorrhagic Stroke 15-20% Ischemic Stroke 80-85% Intracerebral Hemorrhage 2/3 Subarachnoid Hemorrhage 1/3 Types Of Hematomas: Epidural hematoma: results from damaged artery  risk for bursting (e.g. meningeal artery) Commonly due to head trauma associated with skull fracture Mass effect may occur after several hours Subdural hematoma: develops from damaged veins  leakage of blood to subdural space (e.g. cortical veins bridging) Commonly due to head trauma Mass effect may occur after several days Common in elderly population Types Of Hematomas PowerPoint Presentation: Intra-axial and extra-axial Intra-axial involves intracerebral hemorrhage. Extra-axial involves epidural, subdural and subarachnoid hemorrhage. Types Of Hematomas: Types Of Hematomas http://brainandspine.titololawoffice.com/2011/09/articles/brain-injury/subdural-hematoma-and-epidural-hematoma/ PowerPoint Presentation: Berry Aneurysm http://www.strokesurvivors.ca/new/AneurysmFAQ.php MOST COMMON SITES: Basal ganglia ( Putamen ) Thalamus Cerebellum Pons MOST COMMON SITES CAUSES: Traumatic Non-traumatic Head injury Uncontrolled hypertension Anticoagulant therapy Platelet and coagulation disorders Vascular malformations Brain tumors Cerebral amyloid angiopathy Drug-induced: cocaine, amphetamines CAUSES HYPERTENSION: Main cause of ICH is hypertension. The primary role of HTN is supported by a high frequency of history of HTN, significantly higher blood pressure measurements at admission. In one study on 188 patients with primary ICH, it was determined that the cause was HTN in 72% of patients. HYPERTENSION PowerPoint Presentation: Increase in ICH incidence with advancing age, which ais also associated with an increase in the prevalence of HTN. In both hypertensive and non hypertensive patients, the circadian rhythm of ICH onset, coincides with peaks at 8 AM and 8 PM which coincides with the physiological peaks of BP. The vascular lesion produced by chronic HTN that leads to arterial rupture and ICH is probably lipohyalinosis of small intraparenchymal arteries. VASCULAR MALFORMATIONS: ICHs caused by small AVMs or cavernous angiomas are frequently located in the subcortical white matter. Has distinctive characteristics The hematoma is smaller, symptoms and signs develop more slowly, tend to occur in younger patients and have female preponderance and presence of associated subarachoid hemorrhage. These lesions are often documented by MRI, by pathological examination of specimens obtained at the time of surgical drainage or at autopsy. Cerebral angiography plays an important role in the diagnosis of these lesions. VASCULAR MALFORMATIONS INTRACRANIAL TUMORS: Accounts for less than 10% of cases. Glioblastoma multiforme , metastases from melanoma, bronchogenic ca , choriocarcinoma and renal cell ca are the tumor types that are most commonly associated with ICH. Confirmation of the diagnosis of ICH secondary to malignant brain tumor carries a dismal prognosis, with a 30 day mortality rate in the 90% range. INTRACRANIAL TUMORS CLINICAL AND IMAGING CHARACTERISTICS OF ICH ASSOCIATED WITH INTRACRANIAL TUMORS: Presence of papilledema on presentation The location of ICH in sites that are rarely affected in hypertensive ICH, such as the corpus callosum (common in malignant gliomas ) ICH in multiple sites CT scan characterized by a ring of high density hemorrhage surrounding a low density center in a noncontrast study Enhancing nodules adjacent to the hemorrhage on contrast CT or MRI A disproportionate amount of surrounding edema and mass effect associated with acute hematoma. CLINICAL AND IMAGING CHARACTERISTICS O F ICH ASSOCIATED WITH INTRACRANIAL TUMORS PowerPoint Presentation: In such circumstances, a search for a primary or metastatic brain tumor should follow and include evaluation for systemic malignancy. If there is none, cerebral angiography and eventually craniotomy for biopsy of the wall of the hematoma cavity should be considered. BLEEDING DISORDERS: Hemophilia caused by factor VIII deficiency leads to ICH in 2.5% to 6% of patients. Majority occur in young patients, generally younger than 18%. Immune mediated thrombocytopenia, especially ITP is associated with life threatening ICH in 1% of patients. Bleeding occurs when platelet count drops below 10000/ ul and hemorrhages can occur anywhere in the brain. BLEEDING DISORDERS PowerPoint Presentation: Acute leukemia, especially ALL is a common cause of ICH that favours the lobar white matter of the cerebral hemispheres. The bleeding complications of ALL are often accompanied by both thrombocytopenia and rapidly increasing numbers of abnormal circulating leukocytes of 300,000/ ul or more (blast crisis) Acute promyelocytic leukemia, a variant of AML has a particular propensity to produce ICH secondary to DIC. ANTICOAGULANTS: Account for 9-11% of cases of ICH. Rx with oral anticoagulants increases the risk of ICH by 8-11 fold compared with individuals with otherwise similar risk factors for ICH who are not receiving anticoagulants. Advanced age, htn , preceding cerebral infarcts, head trauma and prolongation of INR are the risk factors for ICH in patients on oral anticoagulants. ANTICOAGULANTS PowerPoint Presentation: Trials suggest that oral anticoagulation in patients with CVA should aim at an INR of 2-3. The presence of severe leukaraiosis on CT is an additional risk factor that independently increases the risk of ICH in patients on oral anticoagulants. DISTINCT CHARACTERISTICS OF ICH DUE TO ORAL ANTICOAGULANTS: Tend to present with a slowly progressive course, at times as long as 48-72 hours, in contrast with the usually more rapidly evloving presentation of hypertensive ICH. Volumes are on average larger than those occuring in hypertensive ICH. Signs of systemic bleeding rarely accompany ICH. Bleeding is usually from vessels different from those involved in ICH of hypertensive origin. DISTINCT CHARACTERISTICS OF ICH DUE TO ORAL ANTICOAGULANTS FIBRINOLYTICS : Complication of thrombolytic therapy may be favored by preexisting vasculopathies with bleeding potential such as CAA. Recombinant tPA for the Rx of acute ischemic stroke was complicated by ICH in 6% of cases, which is about 10 times the rate found in the placebo group. Risk factors for ICH include severe neurological deficit at presentation and documentation of hypodensity or mass effect on CT before Rx. FIBRINOLYTICS PowerPoint Presentation: Intraarterial thrombolysis with prurokinase for MCA occlusion leads to 11% of early symptomatic hemorrhages. These hemorrhages occur at the site of the preceding infarct and are generally large. Hyperglycemia at pretreatment baseline has been identified as a potential risk factor of ICH in pts treated with intraarterial prurokinase or iv tPA for acute ischemic stroke. Presence of microhemorrhages which can be easily detected by gradient ECHO MRI sequences is a risk factor for ICH after thrombolysis. CEREBRAL AMYLOID ANGIOPATHY: Characterised by selective deposition of amyloid in cerebral vessels, primarily small and medium sized arteries of the cortex and leptomeninges . Frequency increases with age. Superficial location of affected vessels in the cortex and leptomeninges is responsible for lobar location of ICH. Is associated with alzheimer’s disease, clinical and progressive dementia in 10%-30% of cases of CAA and neuritic plaques in 50% of casses . CEREBRAL AMYLOID ANGIOPATHY PowerPoint Presentation: Histological lesion in CAA is deposition of congor red positive, birefringent amyloid material in the media and adventitia of small cortical and leptomeningeal arteries. Mechanism of rupture of affected artery may be either weakening of the wall or formation of microaneurysms at sites of amyloid deposition. SYMPATHOMIMETIC AGENTS: Can cause ICH fter iv, oral or intranasal use. Hemorrhages occur within minutes to a few hours after drug use, and the majority are located in the subcortical white matter of the cerebral hemispheres. In half of reported cases, transient HTN has been documented, as well as multifocal areas of spasm and dilatation of intracranial arteries on angiography. The decongestant and apetite suppressant, phenylpropanolamine, has been associated with ICH in young patients, predominantly women usually without a history of HTN but with acute HTN on admission. SYMPATHOMIMETIC AGENTS PowerPoint Presentation: Cocaine is the most common sympathomimetic agent associated with ICH. Both ICH and subarachnoid hemorrhage can occur within short minutes of use of alkaloid form of cocaine and its precipitate form, known as crack. ICH favor subcortical white matter. Multiple simultaneous ICHs both deep and superficial, the mechanism of which is unknown. Cocaine induced vasoconstriction followed by repurfusion , heavy alcohol intake HEMORRHAGIC INFARCTION: Pathologically and pathogenically different from ICH in that It results from arterial or venous occlusion rather than from vascular rupture that causes ICH. Characteristically occurs in the setting of cerebral embolism or less frequently cerebral infarction secondary to venous occlusion, in both the bleeding reflects the mechanism of the infarct and is not due to therapeutic measures such as use of anticoagulants. HEMORRHAGIC INFARCTION GRANULOMATOUS ANGITIS OF CNS : Also called isolated angitis of the CNS. Characterized by mononuclear inflammation with giant cell formation in the media and adventitia of small and medium sized intracranial arteries and veins. GRANULOMATOUS ANGITIS OF CNS HEAD TRAUMA: ICH caused by cerebral contusion characteristically occus in the surgace of the brain because its mechanism is one of direct brain trauma against its bony covering at the time of an acceleration-deceleration head injury. Sites of predilection are basal frontal, anterior temporal and occipital areas. Frequently multiple. HEAD TRAUMA PATHOLOGY: Chronic hypertension  structural wall changes of small arteries and arterioles in the brain Fibrinoid necrosis Charcot-Bouchard aneurysms Vascular malformations Arteriovenous malformations (AVM): failure of formation of capillary beds Saccular (berry): results from developmental weakness of arteriole walls Hemorrhages can cause compression to nearby brain tissues May result in brain tissue inflammation and edema PATHOLOGY PowerPoint Presentation: Within 48 hrs macrophages begin to phagocytize the hemorrhage at its outer surface. After 1-6 months, the hemorrhage is generally resolved to a slitlike orange cavity lined with glial scar and hemosiderin laden macrophages. CLINICAL FEATURES: Has two main elements -symptoms that reflect the effects of intracranial HTN and those that are specific for the location of hematoma. Headache, vomiting and depressed level of consciousness are the general clinical manifestations of ICH. A characteristic of ICH at presentation is the frequent progression of focal neurolgical deficits over periods of hours. Reflects progressive enlargement of the hematoma. Depend on the volume and site of bleed. CLINICAL FEATURES PUTAMINAL HEMORRHAGE: Represents approximately 35% of cases. A wide spectrum of clinical severity relates to hematoma size, from minimally symptomatic cases with pure motor hemiparesis or slight hemiparesis and dysarthria to the extreme of coma with decerebrate rigidity. Ventricular extension carries an invariably poor prognosis in putaminal hemorrhage. Mortality is about 37%. PUTAMINAL HEMORRHAGE CAUDATE HEMORRHAGE: Accounts for only 5% of cases. HTN is the most common cause. Results from rupture of penetrating arteries from the anterior and middle cerebral arteries. Presentation is similar to that of subarachnoid hemorrhage. Clinical picture is dominated by signs of ICH and meningeal irritation focal neurological deficits( hemiparesis , horizontal gaze palsy and Horner’s syndrome) are minimal or absent. CAUDATE HEMORRHAGE PowerPoint Presentation: At times, the main manifestations are neuropsychological deficits including abulia , disorientation and memory disturbances occasionally accompanied by language disturbances. Ventricular extension and hydrocephalus are a regular feature of caudate ICH. Outcome is generally good and majority of pts recover without neurological sequelae . Main differential diagnosis of caudate ICH is ruptured ACA aneurysm. THALAMIC HEMORRHAGE: Represents 10-15% of ICH cases. Onset tends to be more abrupt and slow progression of deficits is less common.\ Central feature is severe multimodal sensory loss on the entire contralateral body. If large, may produce a hemiparesis by compression of adjacent internal capsule. Fluent aphasia may be present with lesions on dominant side and amorphosynthesis and contralateral neglect, with lesions on nondominant side. THALAMIC HEMORRHAGE PowerPoint Presentation: May produce a series of ocular disturbances by virtue of its extension into the subthalamus and high midbrain. Vertical and lateral gaze palsies Forced deviation of eyes downward. Inequality of pupils with absence of light reaction. Skew deviation with the eye ipsilateral to hemorrhage assuming a higher position than the contralateral eye. Ipsilateral Horner’s syndrome Absence of convergence Retraction nystagmus LOBAR HEMORRHAGE: 25% of ICH cases. Non hypertensive mechanisms like AVMs, sympathomimetic agents, and CAA are frequent causes. Lower frequency of coma due to peripheral location of these hematomas. Seizures occur in 28% of cases. Hemiparesis of UL in frontal hematomas Senorimotor deficit and hemianopia in parietal hemorrhages. Fluent aphasia with relatively preserved repetition in dominant temporal hematomas Homonymous hemianopia in occipital lobe hemorrhages. Mortality rate is lower than in those with hematomas in other locations. LOBAR HEMORRHAGE CEREBELLAR HEMORRHAGE: 5-10% of ICH cases. Characteristic clinical presentation with abrupt onset of vertigo, headache, vomiting and inability to stand and walk but absence of hemiparesis or hemiplegia . Triad of appendicular ataxia, horizontal gaze palsy and peripheral facial palsy are seen, all ipsilateral to hemorrhage. Clinical course can be difficult to predict. Tendeny for abrupt deterioration to coma and death after a period of clinical stability. Clinical evidence of compromise of brainstem function, CT features of hydrocephalus, hematomas of 3 cm or more in diameter and effacement of quadrigeminal cistern are associated with a bad prognosis. CEREBELLAR HEMORRHAGE PONTINE HEMORRHAGE: 5% of ICH cases. Classic picture of coma, quadriplegia, decerebrate posturing, horizontal ophthalmoplegia , ocular bobbing, pinpoint reactive pupils, abnormalities of respiratory rhythm and preterminal hyperthermia. Less severe forms are recognized that are compatible with survival. These are frequently located in the tegmentum , lateral to the midline and thus produce symptoms of unilateral dorsal pontine involvement( one and half syndrome, internuclear ophthalmoplegia , V and VII cranial nerve palsies) with variable degrees of long tract interuption . PONTINE HEMORRHAGE MEDULLARY HEMORRHAGE: Pure primary ICH involving the medulla alone are rare. Most cases represent medullary extension of caudal pontine hematomas. Clinical presentation reflects location of lesion on one half of the medulla, generally extending beyond the dorsolateral region both medially resulting in ipsilateral hypoglossal nerve palsy and ventrally resulting in contralateral hemiparesis . MEDULLARY HEMORRHAGE INTRAVENTRICULAR HEMORRHAGE: Rare, account for 3% of ICH. Extension into ventricles is a common feature of caudate and thalamic hemorrhages and of large putaminal and lobar hemorrhages. Causes are similar to ICH elsewhere like HTN, aneurysm, coagulation disorders, cerbral tumors, cocaine use and rare vasculopathies such as moyamoya disease. Clinical presentation is with acute onset of headache, nausea, vomiting and decreased level of consciousness with minimal or absent FND. INTRAVENTRICULAR HEMORRHAGE PowerPoint Presentation: Prognosis of IVH is strongly dependent on the severity o the initial manifestation and its mechanism. Patients who are comatose as a result of the initial hemorrhage generally succumb, especially if they have early signs of brainstem involvement. Those who remain alert or obtunded without signs of parenchymal involvement tend to recover without neurological sequelae . Pts with the idiopathic form of IVH have the best prognosis. MESENCEPHALIC HEMORRHAGE: Exceptionlly rare HTN or ruptured AVM is the cause in half of the reported cases, the others being of undetermined cause. Occasional unilateral hematomas can presen with ipsilateral III nerve palsy, cerebellar ataxia and controlateral hemiparesis . Bilateral cases have bilateral ptosis , paralysis of upward gaze and small pupils. MESENCEPHALIC HEMORRHAGE TRAUMA: Most common sites of bleed after head injury are intracerebral (especially temporal and inferior frontal lobes) and into the subarachnoid, subdural and epidural spaces. Should be considered in any patient with an unexplained acute neurologic deficit ( hemiparesis , stupor, confusion), particularly if the deficit occurred in the context of a fall. TRAUMA PowerPoint Presentation: May result from head injury, rupture of arterial aneurysm, or spread of blood from different location to subarachnoid space Most common: berry aneurysm Pts present with sudden severe headache, with or without loss of consciousness. Vomiting, photophobia, restlessness and agitation may be seen. Neck stiffness and sub hyaloid hemorrhages on fundoscopy may be seen OCULAR SIGNS FOR LOCALIZATION OF ICH: In putaminal hemorrhage, eyes are deviated to the side opposite of parlysis . In thalamic hemorrhage, downward deviation of the eyes and pupils may be unreactive In pontine hemorrhage, the eyeballs are fixed and the pupils are tiny but reactive In large cerebellar hemorrhage, the eyes may be deviated laterally to the side opposite the lesion and ocular bobbing may occur. OCULAR SIGNS FOR LOCALIZATION OF ICH DIAGNOSIS: CT scan MRI Angiography CBC Platelet count b leeding time p rothrombin /partial thromboplastin time(PT/PTT) CSF (cerebrospinal fluid) examination DIAGNOSIS DIAGNOSIS: For rapid diagnosis CT occupies the foremost position. Totally reliable in the detection of hemorrhages that are 1 cm or more in diameter. Small pontine hemorrhages may be missed because of the artifact produced by the adjacent bone. Coexisting hydrocephalus, tumor, cerebral swelling and displacement of the intracranial contents are readily appreciated. MRI is particularly useful for demonstrating brainstem hemorrhages and residual hemorrhages, which remain visible after they are no longer visible on the CT scan. DIAGNOSIS PowerPoint Presentation: Head CT http://www.uwmedicine.org/patient-care/our-services/medical-services/stroke-center/pages/articleview.aspx?subId=79 SEQUENCE OF CHANGES ON IMAGING: Fresh blood is visualised as a white mass. The mass effect and the surrounding extruded serum and edema are hypodense . After 2 to 3 weeks, density of hematoma decreases, first at the periphery and eventually becomes isodense . Aftere several weeks, it may transiently simulate a tumor or abscess. SEQUENCE OF CHANGES ON IMAGING PowerPoint Presentation: By MRI, in convention T1 or T2 weighted images, the hemorrhage is not easily visible in the 2 or 3 days after bleeding, as oxyhemoglobin is diamagnetic and only the mass effect is evident. After several days, the surrounding edema is hyperintense in T2 weighted images. The hematoma signal becomes bright on T1 weighted images and dark on T2. As the hematoma becomes subacute , the dark images gradually brighten. SPOT SIGN: The presence of small foci of contrast extravasation on CT Angiography is referred to as ‘Spot Sign’. It is predictive of hematoma enlargement. No of spot signs (3 or more), maximal diameter (5cm or more), maximal attenuation (180 Hounsfield units) are independent predictors of hematoma expansion. SPOT SIGN TREATMENT : Initial evaluation General measures for prevention of further elevation of ICP Specific treatment of increased ICP TREATMENT INITIAL EVALUATION: Should be immediately evaluated for stabilization of vital signs and airway protection. ET intubation should be done if the Glasgow Coma scale is less than 8. Best performed with the administration of short acting iv agents like thiopental and lidocaine to block the increase in ICP that result from tracheal stimulation. Followed by CT brain and relevant investigations. INITIAL EVALUATION MANAGEMENT OF COAGULATION DISORDERS: Coagulation abnormalities in pts receiving anticoagulants should be promptly treated because if it is not reversed, it can lead to progressive enlargement of hematoma. Pts with ICH in the setting of Heparin anticoagulation should receive protamine sulfate, 1mg per 100 units of heparin estimated in plasma. Those on warfarin should receive 5-25 mg of iv vit K, fresh frozen plasma or prothrombin plama concentrate. IV Factor VIIa rapidly reverses the abnormally prolonged INR in cases of warfarin related ICH.. ICH after thrombolytic therapy are best treated with 4 to 6 units of cryoprecipitate or FFP as well as single donor platelets. MANAGEMENT OF COAGULATION DISORDERS GENERAL MEASURES TO PREVENT FURTHER ELEVATION OF ICP: Control of HTN and treatment of seizures. Persistent HTN by casuing increased CPP may produce an increase in cerebral edema around the ICH, with further elevation of ICP. BP should be lowered if it is more than 180/105 mm of Hg. Goal should be maintainence of normal CPP levels of 60-70 mm of Hg, aiming at a BP of 160/90 mm of Hg. Anti hypertensive agent of choice is iv beta and alpha blocking agent, labetalol often used in combination with loop diuretics. Nicardipine can also be used as it has no cerebral vasodilatory effect. These agents have the advantage of being rapidly effective and easy to titrate. GENERAL MEASURES TO PREVENT FURTHER ELEVATION OF ICP PowerPoint Presentation: Seizures, a feature of lobar rather than deep ganglionic ICH, typically occur at onset. If the pt has no early seizures, there is negligible risk of late epilepsy. Routine use of anticonvulsants in ICH is not justified. Early tonic- clonic convulsions need immediate control because they can contribute to increased ICP. SPECIFIC Rx OF INCREASED ICP: Hyperventilation, diuretic therapy and corticosteroids are the mainstay of Rx. Hyperventilation is most effective in rapidly lowering ICP usually within minutes of achieving leels of hypocapnia in the range of 25-30 mm Hg. IV mannitol (0.25-1mg/kg) may be used. Dexamethasone reduces ICP by reducing cerebral edema.. SPECIFIC Rx OF INCREASED ICP HEMOSTATIC THERAPY: Studies show that treatment with rFVIIa , within 4 hours from symptom onset reduces hematoma growth. Phase III FAST trial compared rFVIIa in two dosages (20 and 80ug/kg) with placebo in patients with ICH treated within 4 hrs from onset. Although subjects treated with 80ug/kg had a significantly smaller increase in hematoma volume, mortality and morbidity at 90 days occurred with same frequency. HEMOSTATIC THERAPY SURGERY VS MEDICAL Rx: Considered frequently in pts with superficial lobar hematomas or cerebellar hemorrhage. Pts with deep hemorrhages(caudate, thalamic, pontine , mesencephalic and medullary) are rare surgical candidates. Putaminal hemorrhage occupies an intermediate position and is most controversial. Most pts are currently treated nonsurgically with the exception of putaminal and especially lobar hemorrhage with progressive deterioration in the level of consciousness and cerebellar hemorrhage. . SURGERY VS MEDICAL Rx PowerPoint Presentation: Presence of a lesion with potential for casuing recurrent ICH like AVM, aneurysm or cavernous angioma is another indication for surgery The best candidates for surgery are pts with lobar hemorrhages of intermediate size (hematoma volumes between 20-40 ml) located just beneath the cortical surface and pts with a declined level of consciousness and marked mass effect on CT. The other group for whom surgery is frequently considered is pts with cerebellar hemorrhage. PowerPoint Presentation: CT criteria for a early selection of candidates for surgical therapy are alrge hematomas (diameter of 3cm or more), presence of hydrocephalus and boliteration of quadrigeminal cistern In addition, early signs of pontine tegmental compression and development of obtundation and extensor plantar responses are indications for emergency surgery, because otherwise the outcome is fatal. PowerPoint Presentation: STICH trial randomized 1033 pts and found that outcome, death or disability at 6 months was virtually identical in both groups, 74% in surgical and 76% in non surgical group. Mortality at 6 months was 36% and 37% respectively. No superiority of one Rx over the other with the only exception being the hematomas located at a depth of less than 1cm from the cortical surface who fared better with surgery. PREVENTION: Reducing HTN Eliminating excessive alcohol use Discontinuing use of illicit drugs such as cocaine and amphetamines. Pts with amyloid angiopathy should avoid anti thrombotic agents. PREVENTION COURSE AND PROGNOSIS: The immediate prognosis for medium and large sized cerebral clots is grave, 30-35% die within 30 days. In these cases, the hemorrhage has extended into the intraventricular system or ICP becomes elevated to levels that preclude normal perfusion of the brain. Both the location and size predict outcome. COURSE AND PROGNOSIS PowerPoint Presentation: In pts who survive, there can be a surprising degree of restoration of function, because in contrast to infarction, the hemorrhage has to some extent pushed brain tissue aside rather than destroyed it. Function returns very slowly, because extravasated blood takes time to be removed from the tissues. ICH SCORING SYSTEM:  ICH SCORING SYSTEM

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