Practice Essentials

In hemorrhagic stroke, bleeding occurs directly into the brain parenchyma. The usual mechanism is thought to be leakage from small intracerebral arteries damaged by chronic hypertension. The terms intracerebral hemorrhage and hemorrhagic stroke are used interchangeably in this article and are regarded as separate entities from hemorrhagic transformation of ischemic stroke. See the image below.

Axial noncontrast computed tomography scan of the brain of a 60-year-old man with a history of acute onset of left-sided weakness. Two areas of intracerebral hemorrhage are seen in the right lentiform nucleus, with surrounding edema and effacement of the adjacent cortical sulci and right sylvian fissure. Mass effect is present upon the frontal horn of the right lateral ventricle, with intraventricular extension of the hemorrhage.See Acute Stroke, a Critical Images slideshow, for more information on incidence, presentation, intervention, and additional resources.

Also, see the Vertigo: 5 Case-Based Diagnostic Puzzles slideshow to help recognize diagnostic clues in vertigo cases.

Essential update: Inpatient statin use and maintenance may improve outcomes post intracerebral hemorrhage

In a retrospective multicenter cohort study of 3481 patients with intracerebral hemorrhage over a 10-year period, Flint et al found that inpatients who received a

statin (lovastatin, simvastatin, atorvastatin, pravastatin sodium) had better 30-day survival rates following the bleeding event and were more likely to be discharged home or to a rehabilitation center than those who didn’t receive a statin while hospitalized—despite the fact that the statin users had significantly more severe illness and more comorbidities than non statin users.[1, 2] Moreover, those whose statins were discontinued during their hospitalization had worse outcomes than those who remained on statins.

Inpatients treated with a statin had an 18.4% unadjusted 30-day mortality rate compared to 38.7% for those not treated with a statin during their admission.[1, 2] After adjustment for various factors (age, sex, race/ethnicity, comorbidities, number of intracerebral hemorrhage cases by hospital, dysphagia), statin users were also more likely to be alive at 30 days (odds ratio [OR], 4.25; 95% confidence interval [CI], 3.46-5.23; P < .001). Inpatients treated with statins had a 51.1% rate of discharge to home or to a rehabilitation facility compared to 35.0% for patients not treated with statins while hospitalized. Furthermore, patients who discontinued statin therapy after hospital admission had an unadjusted mortality rate of 57.8% compared to 18.9% for patients using a statin before and during hospitalization; they were also significantly less likely to be alive at 30 days (OR, 0.16; 95% CI, 0.12-0.21; P < .001).[1, 2]

Signs and symptoms

Patients with intracerebral bleeds are more likely than those with ischemic stroke to have headache, altered mental status, seizures, nausea and vomiting, and/or marked hypertension. Even so, none of these findings reliably distinguishes between hemorrhagic and ischemic stroke.

Focal neurologic deficits

The type of deficit depends on the area of brain involved. If the dominant (usually the left) hemisphere is involved, a syndrome consisting of the following may result:

• Right hemiparesis • Right hemisensory loss • Left gaze preference • Right visual field cut • Aphasia • Neglect (atypical) If the nondominant (usually the right) hemisphere is involved, a syndrome consisting of the following may result:

• Left hemiparesis • Left hemisensory loss • Right gaze preference • Left visual field cut See Clinical Presentation for more detail.

Diagnosis

Laboratory tests should include a complete blood count (CBC), a metabolic panel, and—particularly in patients taking anticoagulants—coagulation studies (ie, prothrombin time or international normalized ratio [INR] and an activated partial thromboplastin

time).[3]

Brain imaging is a crucial step in the evaluation of suspected hemorrhagic stroke and must be obtained on an emergent basis. Brain imaging aids diagnosing hemorrhage, and it may identify complications such as intraventricular hemorrhage, brain edema, or hydrocephalus. Either noncontrast computed tomography (NCCT) scanning or magnetic resonance imaging (MRI) is the modality of choice.

See Workup for more detail.

Management

The treatment and management of patients with acute intracerebral hemorrhage depends on the cause and severity of the bleeding. Basic life support, as well as control of bleeding, seizures, blood pressure (BP), and intracranial pressure, are critical. Medications used in the treatment of acute stroke include the following:

• Anticonvulsants - To prevent seizure recurrence • Antihypertensive agents - To reduce BP and other risk factors of heart disease • Osmotic diuretics - To decrease intracranial pressure in the subarachnoid space A potential treatment for hemorrhagic stroke is surgical evacuation of the hematoma. However, the role of surgical treatment for supratentorial intracranial hemorrhage remains controversial. Outcomes in published studies are conflicting.

Endovascular therapy using coil embolization, as an alternative to surgical clipping, has been increasingly employed with great success, although controversy still exists over which treatment is ultimately superior.

See Treatment and Medication for more detail.

Background

The terms intracerebral hemorrhage and hemorrhagic stroke are used interchangeably in this article and are regarded as separate entities from hemorrhagic transformation of ischemic stroke. Hemorrhagic stroke is less common than ischemic stroke (ie, stroke caused by thrombosis or embolism); epidemiologic studies indicate that only 8-18% of strokes are hemorrhagic.[4] However, hemorrhagic stroke is associated with higher mortality rates than is ischemic stroke. (See Epidemiology.)[5]

Patients with hemorrhagic stroke present with focal neurologic deficits similar to those of ischemic stroke but tend to be more ill than are patients with ischemic stroke. However, though patients with intracerebral bleeds are more likely to have headache, altered mental status, seizures, nausea and vomiting, and/or marked hypertension, none of these findings reliably distinguishes between hemorrhagic and ischemic stroke. (See Presentation.)[6]

Brain imaging is a crucial step in the evaluation of suspected hemorrhagic stroke and must be obtained on an emergent basis (see the image below). 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. For more information, see Ischemic Stroke in Emergency Medicine. (See Workup.)

Axial noncontrast computed tomography scan of the brain of a 60-year-old man with a history of acute onset of left-sided weakness. Two areas of intracerebral hemorrhage are seen in the right lentiform nucleus, with surrounding edema and effacement of the adjacent cortical sulci and right sylvian fissure. Mass effect is present upon the frontal horn of the right lateral ventricle, with intraventricular extension of the hemorrhage.The treatment of patients with acute stroke depends on the cause and severity of the bleeding. Basic life support, as well as control of bleeding, seizures, blood pressure (BP), and intracranial pressure, are critical. Surgical evacuation of the hematoma is a potential therapeutic option, but it remains controversial. (See Treatment.)

For patient education information, see the Stroke Health Center, as well as Stroke.

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.

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).

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.

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.

Pathophysiology

In intracerebral hemorrhage, bleeding occurs directly into the brain parenchyma. The usual mechanism is thought to be leakage from small intracerebral arteries damaged by chronic hypertension. Other mechanisms include bleeding diatheses, iatrogenic anticoagulation, cerebral amyloidosis, and cocaine abuse.

Intracerebral hemorrhage has a predilection for certain sites in the brain, including the thalamus, putamen, cerebellum, and brainstem. In addition to the area of the brain injured by the hemorrhage, the surrounding brain can be damaged by pressure produced by the mass effect of the hematoma. A general increase in intracranial pressure may occur.

Subarachnoid hemorrhage

The pathologic effects of subarachnoid hemorrhage (SAH) on the brain are multifocal. SAH results in elevated intracranial pressure and impairs cerebral autoregulation. These effects can occur in combination with acute vasoconstriction,

microvascular platelet aggregation, and loss of microvascular perfusion, resulting in profound reduction in blood flow and cerebral ischemia.[7] See the images below.

Noncontrast computed tomography (CT) scanning was performed emergently in a 71-year-old man who presented with acute onset of severe headache and underwent rapid neurologic deterioration requiring intubation. The noncontrast CT scan (left image) demonstrates diffuse, high-density subarachnoid hemorrhage in the basilar cisterns and both Sylvian fissures. There is diffuse loss of gray-white differentiation. The fluid-attenuated inversion-recovery (FLAIR) image (right) demonstrates high signal throughout the cortical sulci and in the basilar cisterns, as well as in the dependent portions of the ventricles. FLAIR is highly sensitive to acute subarachnoid hemorrhage; the suppression of high cerebrospinal fluid signal aids in making subarachnoid hemorrhage more conspicuous than do conventional magnetic resonance imaging sequences.

Computed tomographic angiography examination and subsequent cerebral angiography were performed in 71-year-old man who presented with acute onset of severe headache and underwent rapid neurologic deterioration. Multiple aneurysms were identified, including a 9-mm aneurysm at the junction of the anterior cerebral and posterior communicating arteries seen on this lateral view of an internal carotid artery injection. Balloon-assisted coil embolization was performed.

Lateral view of a selective injection of the left internal carotid artery demonstrates a microcatheter passing distal to the aneurysm neck. This lateral view from an angiogram performed during balloon-assisted coil embolization demonstrates significantly diminished filling of the aneurysm.

Etiology

The etiologies of stroke are varied, but they can be broadly categorized into ischemic or hemorrhagic. Approximately 80-87% of strokes are from ischemic infarction caused by thrombotic or embolic cerebrovascular occlusion. Intracerebral hemorrhages account for most of the remainder of strokes, with a smaller number resulting from aneurysmal subarachnoid hemorrhage.[8, 9, 10, 11]

In 20-40% of patients with ischemic infarction, hemorrhagic transformation may occur within 1 week after ictus.[12, 13]

Differentiating between the different types of stroke is an essential part of the initial workup of patients with stroke, as the subsequent management of each disorder will be vastly different.

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 (eg, cocaine, other sympathomimetic drugs) Causes of hemorrhagic stroke include the following[11, 12, 14, 15, 16] :

• Hypertension • Cerebral amyloidosis • Coagulopathies • Anticoagulant therapy • Thrombolytic therapy for acute myocardial infarction (MI) or acute ischemic stroke

(can cause iatrogenic hemorrhagic transformation) • Arteriovenous malformation (AVM), aneurysms, and other vascular malformations

(venous and cavernous angiomas) • Vasculitis • Intracranial neoplasm 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.

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.

Anticoagulant therapy

Anticoagulant therapy is especially likely to increase hemorrhage risk in patients who metabolize warfarin inefficiently. Warfarin metabolism is influenced by polymorphism in the CYP2C9 genes. Three known variants have been described. CYP2C9*1 is the normal variant and is associated with typical response to dosage of warfarin. Variations *2 and *3 are relatively common polymorphisms that reduce the efficiency of warfarin metabolism.[17]

Arteriovenous malformations

Numerous genetic causes may predispose to AVMs in the brain, although AVMs are generally sporadic. Polymorphisms in the IL6 gene increase susceptibility to a number of disorders, including AVM. Hereditary hemorrhagic telangiectasia (HHT), previously known as Osler-Weber-Rendu syndrome, is an autosomal dominant disorder that causes dysplasia of the vasculature. HHT is caused by mutations in ENG, ACVRL1, or SMAD4 genes. Mutations in SMAD4 are also associated with juvenile polyposis, so this must be considered when obtaining the patient’s history.

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. AVM in the gastrointestinal tract, lungs, and brain are the most worrisome, and their detection is the mainstay of surveillance for this disease.

Hypertension

The most common etiology of primary hemorrhagic stroke (intracerebral hemorrhage) is hypertension. At least two thirds of patients with primary intraparenchymal hemorrhage are reported to have preexisting or newly diagnosed 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.

Aneurysms and subarachnoid hemorrhage

The most common cause of atraumatic hemorrhage into the subarachnoid space is rupture of an intracranial aneurysm. Aneurysms are focal dilatations of arteries, with the most frequently encountered intracranial type being the berry (saccular) aneurysm. Aneurysms may less commonly be related to altered hemodynamics associated with AVMs, collagen vascular disease, polycystic kidney disease, septic emboli, and neoplasms.

Nonaneurysmal perimesencephalic subarachnoid hemorrhage may also be seen. This phenomenon is thought to arise from capillary or venous rupture. It has a less severe clinical course and, in general, a better prognosis.

Berry aneurysms are most often isolated lesions whose formation results from a combination of hemodynamic stresses and acquired or congenital weakness in the

vessel wall. Saccular aneurysms typically occur at vascular bifurcations, with more than 90% occurring in the anterior circulation. Common sites include the following:

• The junction of the anterior communicating arteries and anterior cerebral arteries—most commonly, the middle cerebral artery (MCA) bifurcation

• The supraclinoid internal carotid artery at the origin of the posterior communicating artery

• The bifurcation of the internal carotid artery (ICA) Genetic causes of aneurysms

Intracranial aneurysms may result from genetic disorders. Although rare, several families have been described that have a predisposition—inherited in an autosomal dominant fashion—to intracranial berry aneurysms. A number of genes, all categorized as ANIB genes, are associated with this predisposition. Presently, ANIB1 through ANIB11 are known.

Autosomal dominant polycystic kidney disease (ADPKD) is another cause of intracranial aneurysm. Families with ADPKD tend to show phenotypic similarity with regard to intracranial hemorrhage or asymptomatic berry aneurysms.[18]

Loeys-Dietz syndrome (LDS) consists of craniofacial abnormalities, craniosynostosis, marked arterial tortuosity, and aneurysms and is inherited in an autosomal dominant manner. Although intracranial aneurysms occur in LDS of all types, saccular intracranial aneurysms are a prominent feature of LDS type IC, which is caused by mutations in the SMAD3 gene.[19]

Ehlers-Danlos syndrome is a group of inherited disorders of the connective tissue that feature hyperextensibility of the joints and changes to the skin, including poor wound healing, fragility, and hyperextensibility. However, Ehlers-Danlos vascular type (type IV) also is known to cause spontaneous rupture of hollow viscera and large arteries, including arteries in the intracranial circulation.

Patients with Ehlers-Danlos syndrome may also have mild facial findings, including lobeless ears, a thin upper lip, and a thin, sharp nose. The distal fingers may appear prematurely aged (acrogeria). In the absence of a suggestive family history, it is difficult to separate Ehlers-Danlos vascular type from other forms of Ehlers-Danlos. Ehlers-Danlos vascular type is caused by mutations in the COL3A1 gene; it is inherited in an autosomal dominant manner.

See Genetic and Inflammatory Mechanisms in Stroke, as well as Blood Dyscrasias and Stroke. Information on metabolic diseases and stroke can be found in the following articles:

• Methylmalonic Acidemia • Homocystinuria/Homocysteinemia • Fabry Disease • MELAS – Mitochondrial Encephalomyopathy, Lactic Acidosis, Strokelike

Episodes • Hyperglycemia/Hypoglycemia Hemorrhagic transformation of ischemic stroke

Hemorrhagic transformation represents the conversion of a bland infarction into an

area of hemorrhage. Proposed mechanisms for hemorrhagic transformation include reperfusion of ischemically injured tissue, either from recanalization of an occluded vessel or from collateral blood supply to the ischemic territory or disruption of the blood-brain barrier. With disruption of the blood-brain barrier, red blood cells extravasate from the weakened capillary bed, producing petechial hemorrhage or frank intraparenchymal hematoma.[11, 12, 20] (For more information, see Reperfusion Injury in 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.[11, 13, 21] Hemorrhagic transformation is also more likely following administration of tissue plasminogen activator (tPA) in patients whose noncontrast computed tomography (CT) scans demonstrate areas of hypodensity.[20, 22, 23] See the image below.

Noncontrast computed tomography scan (left) obtained in a 75-year-old man who was admitted for stroke demonstrates a large right middle cerebral artery distribution infarction with linear areas of developing hemorrhage. These become more confluent on day 2 of hospitalization (middle image), with increased mass effect and midline shift. There is massive hemorrhagic transformation by day 6 (right), with increased leftward midline shift and subfalcine herniation. Obstructive hydrocephalus is also noted, with dilatation of the lateral ventricles, likely due to compression of the foramen of Monroe. Intraventricular hemorrhage is also noted layering in the left occipital horn. Larger infarctions are more likely to undergo hemorrhagic transformation and are one contraindication to thrombolytic therapy.

Epidemiology

Occurrence in the United States

Each year in the United States, approximately 795,000 people experience new or recurrent stroke. Of these, approximately 610,000 represent initial attacks, and 185,000 represent recurrent strokes. Epidemiologic studies indicate that approximately 87% of strokes in the United States are ischemic, 10% are secondary to intracerebral hemorrhage, and another 3% may be secondary to subarachnoid hemorrhage.[8, 24]

A 2010 retrospective review from a stroke center found that 40.9% of the 757 patients in the study had suffered hemorrhagic strokes.[25] The researchers speculate that improved availability and implementation of computed tomography (CT) scanning

may have unmasked a previous underestimation of the actual percentage of hemorrhagic strokes, or increased use of antiplatelet agents and warfarin may have led to a higher incidence of hemorrhage. Alternatively, this higher rate may represent referral bias of patients with intracerebral hemorrhages to medical centers with neurosurgical capabilities.

The incidence of stroke varies with age, sex, ethnicity, and socioeconomic status. For example, American Heart Association (AHA) researchers found that rates of intracerebral hemorrhage are higher in Mexican Americans, Latin Americans, blacks, Native Americans, Japanese people, and Chinese people than they are in whites.[8]

Flaherty et al found that excess risk of intracranial hemorrhage in African Americans is largely attributable to higher hemorrhage rates in young and middle-aged persons, particularly for deep cerebral and brainstem locations. Hypertension is the predominant risk factor.[26]

International occurrence

According to the World Health Organization (WHO), 15 million people suffer stroke worldwide each year. Of these, 5 million die and another 5 million are left permanently disabled.[27]

The global incidence of stroke has at least a modest variation from nation to nation, suggesting the importance of genetics and environmental factors, such as disparities in access to health care in developing countries. The age-adjusted incidence of total strokes per 1000 person-years for people 55 years or older has been reported in the range of 4.2 to 6.5. The highest incidences have been reported in Russia, Ukraine, and Japan.

In a prospective, population-based registry study from Italy, the crude annual incidence rate of intracerebral hemorrhage was 36.9 per 100,000 population. When standardized to the 2006 European population, the rate was 32.9 per 100,000 population; standardized to the world population, the rate was 15.9 per 100,000 population.[28]

Overall, the incidence of acute stroke has demonstrated a constant decline over the past several decades, most notably during the 1970s-1990s, although in recent years the rate trend has begun to plateau. However, the increased survival among stroke victims will place an increased demand on health-care systems globally.[11, 29]

Stroke subtypes also vary greatly in different parts of the world and between different races. For example, the proportion of hemorrhagic strokes may be higher in certain populations, such as the Chinese population, in which it has been reported to be up to 39.4%, and the Japanese, in which it is reportedly up to 38.7%.[4, 29]

Prognosis

The prognosis in patients with hemorrhagic stroke varies depending on the severity of stroke and the location and the size of the hemorrhage. Lower Glasgow Coma Scale (GCS) scores are associated with poorer prognosis and higher mortality rates. A larger volume of blood at presentation is also associated with a poorer prognosis. Growth of

the hematoma volume is associated with a poorer functional outcome and increased mortality rate.

The intracerebral hemorrhage score is the most commonly used instrument for predicting outcome in hemorrhagic stroke. The score is calculated as follows:

• GCS score 3-4: 2 points • GCS score 5-12: 1 point • GCS score 13-15: 0 points • Age ≥80 years: Yes, 1 point; no, 0 points • Infratentorial origin: Yes, 1 point; no, 0 points • Intracerebral hemorrhage volume ≥30 cm 3: 1 point • Intracerebral hemorrhage volume < 30 cm 3: 0 points • Intraventricular hemorrhage: Yes, 1 point; no, 0 points In a study by Hemphill et al, all patients with an Intracerebral Hemorrhage Score of 0 survived, and all of those with a score of 5 died; 30-day mortality increased steadily with the Score.[30]

Other prognostic factors include the following:

• Nonaneurysmal perimesencephalic stroke has a less severe clinical course and, in general, a better prognosis

• The presence of blood in the ventricles is associated with a higher mortality rate; in one study, the presence of intraventricular blood at presentation was associated with a mortality increase of more than 2-fold

• Patients with oral anticoagulation-associated intracerebral hemorrhage have higher mortality rates and poorer functional outcomes

In studies, withdrawal of medical support or issuance of Do Not Resuscitate (DNR) orders within the first day of hospitalization predict poor outcome independent of clinical factors. Because limiting care may adversely impact outcome, American Heart Association/American Stroke Association (AHA/ASA) guidelines suggest that new DNR orders should probably be postponed until at least the second full day of hospitalization. Patients with DNRs should be given all other medical and surgical treatment, unless the DNR explicitly says otherwise.[3]

History

Obtaining an adequate history includes determining the onset and progression of symptoms, as well as assessing for risk factors and possible causative events. Such risk factors include the following:

• Previous transient ischemic attack (TIA) and stroke • Hypertension • Diabetes • Smoking • Arrhythmia and valvular disease • Illicit drug use • Use of anticoagulants • Risk factors for thrombosis A history of trauma, even if minor, may be important, as extracranial arterial dissections can result in ischemic stroke.

Hemorrhagic versus ischemic stroke

Symptoms alone are not specific enough to distinguish ischemic from hemorrhagic stroke. However, generalized symptoms, including nausea, vomiting, and headache, as well as an altered level of consciousness, may indicate increased intracranial pressure and are more common with hemorrhagic strokes and large ischemic strokes.

Seizures are more common in hemorrhagic stroke than in the ischemic kind. Seizures occur in up to 28% of hemorrhagic strokes, generally at the onset of the intracerebral hemorrhage or within the first 24 hours.

Focal neurologic deficits

The neurologic deficits reflect the area of the brain typically involved, and stroke syndromes for specific vascular lesions have been described. Focal symptoms of stroke include the following:

• Weakness or paresis that may affect a single extremity, one half of the body, or all 4 extremities

• Facial droop • Monocular or binocular blindness • Blurred vision or visual field deficits • Dysarthria and trouble understanding speech • Vertigo or ataxia • Aphasia Subarachnoid hemorrhage

Symptoms of subarachnoid hemorrhage may include the following:

• Sudden onset of severe headache • Signs of meningismus with nuchal rigidity • Photophobia and pain with eye movements • Nausea and vomiting • Syncope - Prolonged or atypical The most common clinical scoring systems for grading aneurysmal subarachnoid hemorrhage are the Hunt and Hess grading scheme and the World Federation of Neurosurgeons (WFNS) grading scheme, which incorporates the Glasgow Coma Scale. The Fisher Scale incorporates findings from noncontrast computed tomography (NCCT) scans.

Physical Examination

The assessment in patients with possible hemorrhagic stroke includes vital signs; a general physical examination that focuses on the head, heart, lungs, abdomen, and extremities; and a thorough but expeditious neurologic examination.[3] However, intracerebral hemorrhage may be clinically indistinguishable from ischemic stroke. (Though stroke is less common in children, the clinical presentation is similar.)

Hypertension (particularly systolic blood pressure [BP] greater than 220 mm Hg) is commonly a prominent finding in hemorrhagic stroke. Higher initial BP is associated with early neurologic deterioration, as is fever.[3]

An acute onset of neurologic deficit, altered level of consciousness/mental status, or

coma is more common with hemorrhagic stroke than with ischemic stroke. Often, this is caused by increased intracranial pressure. Meningismus may result from blood in the subarachnoid space.

Examination results can be quantified using various scoring systems. These include the Glasgow Coma Scale (GCS), the Intracerebral Hemorrhage Score (which incorporates the GCS; see Prognosis), and the National Institutes of Health Stroke Scale.

Focal neurologic deficits

The type of deficit depends upon the area of brain involved. If the dominant hemisphere (usually the left) is involved, a syndrome consisting of the following may result:

• Right hemiparesis • Right hemisensory loss • Left gaze preference • Right visual field cut • Aphasia • Neglect (atypical) If the nondominant (usually the right) hemisphere is involved, a syndrome consisting of the following may result:

• Left hemiparesis • Left hemisensory loss • Right gaze preference • Left visual field cut Nondominant hemisphere syndrome may also result in neglect when the patient has left-sided hemi-inattention and ignores the left side.

If the cerebellum is involved, the patient is at high risk for herniation and brainstem compression. Herniation may cause a rapid decrease in the level of consciousness and may result in apnea or death.

Specific brain sites and associated deficits involved in hemorrhagic stroke include the following:

• Putamen - Contralateral hemiparesis, contralateral sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, aphasia, neglect, or apraxia

• Thalamus - Contralateral sensory loss, contralateral hemiparesis, gaze paresis, homonymous hemianopia, miosis, aphasia, or confusion

• Lobar - Contralateral hemiparesis or sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, abulia, aphasia, neglect, or apraxia

• Caudate nucleus - Contralateral hemiparesis, contralateral conjugate gaze paresis, or confusion

• Brainstem - Quadriparesis, facial weakness, decreased level of consciousness, gaze paresis, ocular bobbing, miosis, or autonomic instability

• Cerebellum – Ipsilateral ataxia, facial weakness, sensory loss; gaze paresis, skew deviation, miosis, or decreased level of consciousness

Other signs of cerebellar or brainstem involvement include the following:

• Gait or limb ataxia • Vertigo or tinnitus • Nausea and vomiting • Hemiparesis or quadriparesis • Hemisensory loss or sensory loss of all 4 limbs • Eye movement abnormalities resulting in diplopia or nystagmus • Oropharyngeal weakness or dysphagia • Crossed signs (ipsilateral face and contralateral body) Many other stroke syndromes are associated with intracerebral hemorrhage, ranging from mild headache to neurologic devastation. At times, a cerebral hemorrhage may present as a new-onset seizure

iagnostic Considerations

Intracerebral hemorrhage may be clinically indistinguishable from ischemic stroke, and a thorough history and physical examination are important. An acute onset of neurologic deficit, altered level of consciousness/mental status, or coma is more common with hemorrhagic stroke than with ischemic stroke. A history of trauma, even if minor, may be important, as extracranial arterial dissections can result in ischemic stroke.

Seizures are more common in hemorrhagic stroke than in ischemic stroke and occur in up to 28% of hemorrhagic strokes, generally at the onset of the intracerebral hemorrhage or within the first 24 hours. Postictal (Todd) paralysis and hyperosmolality should also be considered.

Other problems to consider are as follows:

• Hyponatremia or hypernatremia• Migraine headache• Hyperosmolar hyperglycemic nonketotic comaDifferential Diagnoses

• Acute Hypoglycemia

• Brain Neoplasms

• Encephalitis

• Headache, Migraine

• Hypernatremia in Emergency Medicine

• Hyperosmolar Hyperglycemic Nonketotic Coma

• Hypertensive Emergencies

• Hyponatremia

• Labyrinthitis Ossificans

• Meningitis

• Stroke, Ischemic

• Subarachnoid Hemorrhage

• Subdural Hematoma

Transient Ischemic Attack

Approach Considerations

Laboratory tests should include a complete blood count, a metabolic panel, and—particularly in patients taking anticoagulants—coagulation studies (ie, prothrombin time or international normalized ratio [INR] and an activated partial thromboplastin time).[3]

Brain imaging is a crucial step in the evaluation of suspected hemorrhagic stroke and must be obtained on an emergent basis. Brain imaging aids diagnosing hemorrhage, and it may identify complications such as intraventricular hemorrhage, brain edema, or hydrocephalus. Either noncontrast computed tomography (NCCT) scanning or magnetic resonance imaging (MRI) is the modality of choice.

Computed tomography (CT)-scan studies can also be performed in patients who are unable to tolerate a magnetic resonance examination or who have contraindications to MRI, including pacemakers, aneurysm clips, or other ferromagnetic materials in their bodies. Additionally, CT-scan examination is more easily accessible for patients who require special equipment for life support. See the image below.

Noncontrast computed tomography scan of the brain (left) demonstrates an acute hemorrhage in the left gangliocapsular region, with surrounding white matter hypodensity consistent with vasogenic edema. T2-weighted axial magnetic resonance imaging scan (middle image) again demonstrates the hemorrhage, with surrounding high-signal edema. The coronal gradient-echo image (right) demonstrates susceptibility related to the hematoma, with markedly low signal adjacent the left caudate head. Gradient-echo images are highly sensitive for blood products.CT angiography and contrast-enhanced CT scanning may be considered for helping identify patients at risk for hematoma expansion. Extravasation of contrast within the hematoma indicates high risk.

When clinical or radiologic findings suggest an underlying structural lesion, useful techniques include CT angiography, CT venography, contrast-enhanced CT scanning, contrast-enhanced MRI, magnetic resonance angiography (MRA), or magnetic resonance venography.[3]

Conventional angiography is the gold standard in evaluating for cerebrovascular disease and for providing less-invasive endovascular interventions. This modality can be performed to clarify equivocal findings or to confirm and treat disease seen on MRA, CTA, transcranial Doppler, or neck ultrasonograms. However, Zhu et al found that in patients with spontaneous intracranial hemorrhage, angiographic yield was significantly lower in patients older than 45 years and those who had preexisting hypertension.[31]

Although the traditional approach to excluding underlying vascular abnormalities in patients with spontaneous intracerebral hemorrhage is to use digital subtraction angiography (DSA) in the acute and subacute phases, Wong et al found that MRA was able to detect most structural vascular abnormalities in the subacute phase in most patients. Consequently, they recommend MRA as the screening test.

Treatment & Management

Blood Pressure Control

No controlled studies have defined optimum BP levels for patients with acute hemorrhagic stroke, but greatly elevated BP is thought to lead to rebleeding and hematoma expansion. Stroke may result in loss of cerebral autoregulation of cerebral perfusion pressure.

Intensive BP reduction (target BP < 140 mm Hg systolic) early in the treatment of patients with intracerebral hemorrhage appears to lessen the absolute growth of hematomas, particularly in patients who have received previous antithrombotic therapy, according to a combined analysis of the Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trials 1 and 2 (INTERACT).[32]

Suggested agents for use in the acute setting are beta blockers (eg, labetalol) and angiotensin-converting enzyme inhibitors (ACEIs) (eg, enalapril). For more refractory hypertension, agents such as nicardipine and hydralazine are used. Avoid nitroprusside because it may raise intracranial pressure.

The 2010 AHA/ASA guidelines acknowledge that evidence for the efficacy of managing BP in hemorrhagic stroke is currently incomplete. With that caveat, the AHA/ASA recommendations for treating elevated BP are as follows[3] :

• If systolic BP is over 200 mm Hg or mean arterial pressure (MAP) is over 150 mm Hg, then consider aggressive reduction of BP with continuous IV infusion; check BP every 5 minutes

• If systolic BP is over 180 mm Hg or MAP is over 130 mm Hg and intracranial pressure may be elevated, then consider monitoring intracranial pressure and reducing BP using intermittent or continuous intravenous medications, while maintaining a cerebral perfusion pressure of 60 mm Hg or higher

• If systolic BP is over 180 or MAP is over 130 mm Hg and there is no evidence of elevated intracranial pressure, then consider modest reduction of BP (target MAP of 110 mm Hg or target BP of 160/90 mm Hg) using intermittent or continuous intravenous medications to control it, and perform clinical reexamination of the patient every 15 minutes

• In patients presenting with a systolic BP of 150 to 220 mm Hg, acute lowering of systolic BP to 140 mm Hg is probably safe

For patients with aneurysmal subarachnoid hemorrhage, the 2012 AHA/ASA guidelines recommend lowering BP below 160 mmHg acutely to reduce rebleeding.[35]

The ongoing Antihypertensive Treatment in Acute Cerebral Hemorrhage-II (ATACH-II) phase 3 randomized clinical trial is designed to determine whether the likelihood of death or disability at 3 months after spontaneous supratentorial intracerebral hemorrhage is lower when systolic BP has been reduced to 180 mm Hg or below or to 140 mm Hg or below. In ATACH-II, intravenous nicardipine is started within 3 hours of stroke onset and continued for the next 24 hours. 

Intracranial Pressure Control

Elevated intracranial pressure may result from the hematoma itself, from surrounding edema, or from both. The frequency of increased intracranial pressure in patients with intracerebral hemorrhage is not known.

Elevate the head of the bed to 30°. This improves jugular venous outflow and lowers intracranial pressure. The head should be midline and not turned to the side. Provide analgesia and sedation as needed. Antacids are used to prevent gastric ulcers associated with intracerebral hemorrhage.

More aggressive therapies, such as osmotic therapy (ie, mannitol, hypertonic saline), barbiturate anesthesia, and neuromuscular blockage, generally require concomitant monitoring of intracranial pressure and BP with an intracranial pressure monitor to maintain adequate cerebral perfusion pressure of greater than 70 mm Hg. A randomized, controlled study of mannitol in intracerebral hemorrhage failed to demonstrate any difference in disability or death at 3 months.[36]

Hyperventilation (partial pressure of carbon dioxide [PaCO2] of 25 to 30-35 mm Hg) is not recommended, because its effect is transient, it decreases cerebral blood flow, and it may result in rebound elevated intracranial pressure.[5] Glucocorticoids are not effective and result in higher rates of complications with poorer outcomes.

Treatment of Anticoagulation-associated Intracranial Hemorrhage

Patients on warfarin have an increased incidence of hemorrhagic stroke. Morbidity and mortality for warfarin-associated bleeding is high, with over one half of patients dying within 30 days. Most episodes occur with a therapeutic international normalized ratio (INR), but overanticoagulation is associated with an even greater risk of bleeding.

The need to reverse warfarin anticoagulation is a true medical emergency, and reversal must be accomplished as quickly as possible to prevent further hematoma expansion. Options for reversal therapy include the following:

• Intravenous vitamin K • Fresh frozen plasma (FFP) • Prothrombin complex concentrates (PCC)

• rFVIIa FFP versus PCC

Because vitamin K requires more than 6 hours to normalize the INR, it should be administered with either FFP or PCC. FFP is the standard of care in the United States[42] ; however, FFP needs to be given in a dose of 15-20 mL/kg and therefore requires a large-volume infusion. PCC contains high levels of vitamin K-dependent cofactors and thus involves a smaller-volume infusion than FFP and more rapid administration.[43, 44] However, PCC is associated with high rates of thrombotic complications.

No randomized, controlled trial has studied the safety and efficacy of FFP versus PCC for reversing the effects of warfarin in patients with intracranial hemorrhage. The International Normalised ratio normalisation in patients with Coumarin-related intracranial Haemorrhages (INCH) trial, a prospective, randomized, controlled, multicenter trial comparing the 2 agents, began recruiting subjects in 2009.[45]

FVIIa

Based upon the available medical evidence, the use of FVIIa is currently not recommended over other agents. The PCC available in the United States contains only low levels of FVII, however, and Sarode et al have described successful, rapid reversal of vitamin K antagonist–related coagulopathy using a combination of low-dose FVIIa with PCC, although they note the need for caution in patients at high risk for thrombosis.[42]

Patients on heparin (either unfractionated or low molecular weight heparin [LMWH]) who develop a hemorrhagic stroke should immediately have anticoagulation reversed with protamine.[5] The dose of protamine is dependent upon the dose of heparin that was given and the time elapsed since that dose.

Patients with severe deficiency of a specific coagulation factor who develop spontaneous intracerebral hemorrhage should receive factor replacement therapy.[3]

Reversal of antiplatelet therapy and platelet dysfunction

There is controversy about whether patients on antiplatelet medications (eg, aspirin, aspirin/dipyridamole [Aggrenox], clopidogrel) should be given desmopressin (DDAVP) and/or platelet transfusions. Patients with renal failure and platelet dysfunction may also benefit from the administration of desmopressin (DDAVP). The 2010 AHA/ASA guideline for management of spontaneous intracerebral hemorrhage recommends platelet transfusions only when such hemorrhaging complicates severe thrombocytopenia.[3]

SAHPractice Essentials

The term subarachnoid hemorrhage (SAH) refers to extravasation of blood into the subarachnoid space between the pial and arachnoid membranes (see the image below). It occurs in various clinical contexts, the most common being head trauma. However, the familiar use of the term SAH refers to nontraumatic (or spontaneous) hemorrhage, which usually occurs in the setting of a ruptured cerebral aneurysm or arteriovenous malformation (AVM).

A 47-year-old woman presented with headache and vomiting; her CT scan in the emergency department revealed subarachnoid hemorrhage.Signs and symptoms

Signs and symptoms of SAH range from subtle prodromal events to the classic presentation. The most common premonitory symptoms are as follows:

• Headache (48%) • Dizziness (10%) • Orbital pain (7%) • Diplopia (4%) • Visual loss (4%) Signs present before SAH include the following:

• Sensory or motor disturbance (6%) • Seizures (4%) • Ptosis (3%) • Bruits (3%) • Dysphasia (2%) Prodromal signs and symptoms usually are the result of sentinel leaks, mass effect of aneurysm expansion, emboli, or some combination thereof.

The classic presentation can include the following:

• Sudden onset of severe headache (the classic feature) • Accompanying nausea or vomiting • Symptoms of meningeal irritation • Photophobia and visual changes • Focal neurologic deficits • Sudden loss of consciousness at the ictus • Seizures during the acute phase Physical examination findings may be normal or may include the following:

• Mild to moderate BP elevation • Temperature elevation • Tachycardia • Papilledema • Retinal hemorrhage • Global or focal neurologic abnormalities Complications of SAH include the following:

• Hydrocephalus • Rebleeding • Vasospasm • Seizures • Cardiac dysfunction See Clinical Presentation for more detail.

Diagnosis

Diagnosis of SAH usually depends on a high index of clinical suspicion combined with radiologic confirmation via urgent noncontrast CT, followed by lumbar puncture or CT angiography of the brain. After the diagnosis is established, further imaging should be performed to characterize the source of the hemorrhage.

Laboratory studies should include the following:

• Serum chemistry panel • Complete blood count • Prothrombin time (PT)/activated partial thromboplastin time (aPTT) • Blood typing/screening • Cardiac enzymes • Arterial blood gas (ABG) determination Imaging studies that may be helpful include the following:

• CT (noncontrast, contrast, or infusion) • Digital subtraction cerebral angiography • Multidetector CT angiography • MRI (if no lesion is found on angiography) • Magnetic resonance angiography (MRA; investigational for SAH) Other diagnostic studies that may be warranted are as follows:

• Baseline chest radiograph • ECG on admission • Lumbar puncture and CSF analysis See Workup for more detail.

Management

Current treatment recommendations include the following:

• Antihypertensive agents (eg, IV beta blockers) when mean arterial pressure exceeds 130 mm Hg

• Avoidance of nitrates (which elevate ICP) when feasible • Hydralazine and calcium channel blockers • Angiotensin-converting enzyme (ACE) inhibitors (not first-line agents in acute

SAH) • In patients with signs of increased ICP or herniation, intubation and

hyperventilation Other interventions for increased ICP are as follows:

• Osmotic agents (eg, mannitol) • Loop diuretics (eg, furosemide) • IV steroids (controversial but recommended by some) Additional medical management is directed toward the following common complications:

• Rebleeding • Vasospasm • Hydrocephalus • Hyponatremia • Seizures • Pulmonary complications • Cardiac complications Surgical treatment to prevent rebleeding includes the following options:

• Clipping the ruptured aneurysm • Endovascular treatment [1] (ie, coiling) The choice between coiling and clipping usually depends on the location of the lesion, the neck of the aneurysm, and the availability and experience of hospital staff.

Screening is not recommended in the general population. However, it can lower cost and improve quality of life in patients at relatively high risk for aneurysm formation and rupture.

See Treatment and Medication for more detail.

Background

The term subarachnoid hemorrhage (SAH) refers to extravasation of blood into the subarachnoid space between the pial and arachnoid membranes. SAH constitutes half of all spontaneous atraumatic intracranial hemorrhages; the other half consists of bleeding that occurs within the brain parenchyma.

Subarachnoid hemorrhage (see the image below) occurs in various clinical contexts, the most common being head trauma. However, the familiar use of the term SAH refers to nontraumatic (or spontaneous) hemorrhage, which usually occurs in the setting of a ruptured cerebral aneurysm or arteriovenous malformation (AVM).

CT scan reveals subarachnoid hemorrhage in the right sylvian fissure; no evidence of hydrocephalus is apparent.Intracranial saccular aneurysms (“berry aneurysms”) represent the most common etiology of nontraumatic SAH; about 80% of cases of SAH result from ruptured aneurysms. SAH is responsible for the death and/or disability of 18,000 persons each year in North America alone. In the United States, it is associated with an annual cost of $1.75 billion. Unfortunately, the difficulties in detecting unruptured aneurysms in asymptomatic patients practically preclude the possibility of preventing most instances of SAH.

About 6-8% of all strokes are caused by SAH from ruptured berry aneurysms. Over the past several decades, the incidence of other types of strokes has decreased; however, the incidence of SAH has not decreased.

The history and physical examination, especially the neurologic examination, are essential components in the diagnosis and clinical staging of SAH (see Presentation). The diagnosis is confirmed radiologically via urgent computed tomography (CT) scan without contrast. Traditionally, a negative CT scan is followed with lumbar puncture. However, noncontrast CT followed by CT angiography (CTA) of the brain can rule out SAH with greater than 99% sensitivity.[2] (See Workup.)

Current treatment recommendations involve management in an intensive care unit setting. The blood pressure is maintained with consideration of the patient’s

neurologic status, and additional medical management is directed toward the prevention and treatment of complications. Surgical treatment to prevent rebleeding consists of clipping the ruptured berry aneurysm. Endovascular treatment[1] (ie, coiling) is an increasingly practiced alternative to surgical clipping (see Treatment).

Pathophysiology

Aneurysms are acquired lesions related to hemodynamic stress on the arterial walls at bifurcation points and bends. Saccular or berry aneurysms are specific to the intracranial arteries because their walls lack an external elastic lamina and contain a very thin adventitia—factors that may predispose to the formation of aneurysms. An additional feature is that they lie unsupported in the subarachnoid space.

Aneurysms usually occur in the terminal portion of the internal carotid artery and the branching sites on the large cerebral arteries in the anterior portion of the circle of Willis. The early precursors of aneurysms are small outpouchings through defects in the media of the arteries.

These defects are thought to expand as a result of hydrostatic pressure from pulsatile blood flow and blood turbulence, which is greatest at the arterial bifurcations. A mature aneurysm has a paucity of media, replaced by connective tissue, and has diminished or absent elastic lamina.

The probability of rupture is related to the tension on the aneurysm wall. The law of La Place states that tension is determined by the radius of the aneurysm and the pressure gradient across the wall of the aneurysm. Thus, the rate of rupture is directly related to the size of the aneurysm. Aneurysms with a diameter of 5 mm or less have a 2% risk of rupture, whereas 40% of those with a diameter of 6-10 mm have already ruptured upon diagnosis.

Although hypertension has been identified as a risk factor for aneurysm formation, the data with respect to rupture are conflicting. However, certain hypertensive states, such as those induced by use of cocaine and other stimulants, clearly promote aneurysm growth and rupture earlier than would be predicted by the available data.

Brain injury from cerebral aneurysm formation can occur in the absence of rupture. Compressive forces can cause injury to local tissues and/or compromise of distal blood supply (mass effect).

When an aneurysm ruptures, blood extravasates under arterial pressure into the subarachnoid space and quickly spreads through the cerebrospinal fluid around the brain and spinal cord. Blood released under high pressure may directly cause damage to local tissues. Blood extravasation causes a global increase in intracranial pressure (ICP). Meningeal irritation occurs.

Rupture of AVMs can result in both intracerebral hemorrhage and SAH. Currently, no explanation can be provided for the observation that small AVMs (< 2.5 cm) rupture more frequently than large AVMs (>5 cm).

In a 25-year autopsy study of 125 patients with ruptured or unruptured aneurysms conducted at Johns Hopkins, the following conditions correlated positively with the

formation of saccular aneurysms:

• Hypertension • Cerebral atherosclerosis • Vascular asymmetry in the circle of Willis • Persistent headache • Pregnancy-induced hypertension • Long-term analgesic use • Family history of stroke The occurrence of aneurysms in children indicates the role of intrinsic vascular factors. A number of disease states resulting in weakness of the arterial wall are associated with an increased incidence of berry aneurysms.

Mechanisms and disease states associated with higher incidence of berry aneurysms include the following:

• Increased blood pressure: Fibromuscular dysplasia, polycystic kidney disease, aortic coarctation

• Increased blood flow: Cerebral arteriovenous malformation (AVM); persistent carotid-basilar anastomosis; ligated, aplastic, or hypoplastic contralateral vessel

• Blood vessel disorders: Systemic lupus erythematosus (SLE), Moyamoya disease, [3] granulomatous angiitis

• Genetic disorders: Marfan syndrome, Ehlers-Danlos syndrome, Osler-Weber-Rendu syndrome, pseudoxanthoma elasticum, Klippel-Trenaunay-Weber syndrome

• Congenital conditions: Persistent fetal circulation, hypoplastic/absent arterial circulation

• Metastatic tumors to cerebral arteries: Atrial myxoma, choriocarcinoma, undifferentiated carcinoma

• Infections: Bacterial, fungal Complications

Complications of SAH include the following:

• Hydrocephalus • Rebleeding • Delayed cerebral ischemia from vasospasm • Intracerebral hemorrhage • Intraventricular hemorrhage • Left ventricular systolic dysfunction • Subdural hematoma • Seizures • Increased intracranial pressure • Myocardial infarction [4] Hydrocephalus

SAH can cause hydrocephalus by 2 mechanisms: obstruction of CSF pathways (ie, acute, obstructive, noncommunicating type) and blockage of arachnoid granulations by scarring (ie, delayed, nonobstructive, communicating type). Acute hydrocephalus is caused by compromise of CSF circulation pathways by interfering with CSF

outflow through the sylvian aqueduct, fourth ventricular outlet, basal cisterns, and subarachnoid space. CSF production and absorption rates are unaltered.

Intraventricular blood is the strongest determinant for the development of acute hydrocephalus. Other risk factors include the following:

• Bilateral ambient cisternal blood • Increased age • Vasospasm • Use of antifibrinolytic drugs • Intraventricular hemorrhage • Left ventricular systolic dysfunction • Subdural hematoma • Seizures Rebleeding

Rebleeding of SAH occurs in 20% of patients in the first 2 weeks. The rebleeds in the first days ("blow out" hemorrhages) are thought to be related to the unstable nature of the aneurysmal thrombus, as opposed to lysis of the clot sitting over the rupture site. Clinical factors that increase the likelihood of rebleeding include hypertension, anxiety,[5] agitation, and seizures.

Cerebral ischemia

Delayed cerebral ischemia from arterial smooth muscle contraction is the most common cause of death and disability following aneurysmal SAH. Vasospasm can lead to impaired cerebral autoregulation and may progress to cerebral ischemia and infarction.[6] Most often, the terminal internal carotid artery or the proximal portions of the anterior and middle cerebral arteries are involved. The arterial territory involved is not related to the location of the ruptured aneurysm.

Vasospasm is believed to be induced in areas of thick subarachnoid clot. The putative agent responsible for vasospasm is oxyhemoglobin, but its true etiology and pathogenesis remain to be elucidated.

Intracerebral hemorrhage

The mechanism of intracerebal hemorrhage (ICH) is direct rupture of aneurysm into the brain. ICH commonly results from internal cerebral artery (ICA), pericallosal, and anterior cerebral artery (ACA) aneurysms. Secondary rupture of a subarachnoid hematoma into the brain parenchyma most commonly arises from middle cerebral artery aneurysms.

Intraventricular hemorrhage

Found in 13-28% of clinical cases of ruptured aneurysms and in 37-54% of autopsy cases, intraventricular hemorrhage (IVH) is a significant predictor of poor neurologic grade and outcome. Sources of IVH include the following:

• Anterior cerebral artery (40%) • Internal cerebral artery (25%) • Middle cerebral artery (21%)

• Vertebrobasilar artery (14%) Left ventricular systolic dysfunction

LV systolic dysfunction in humans with SAH is associated with normal myocardial perfusion and abnormal sympathetic innervation. These findings may be explained by excessive release of norepinephrine from myocardial sympathetic nerves, which could damage both myocytes and nerve terminals.[7]

Subdural hematoma

Subdural hematoma (SDH) is rare following aneurysmal SAH, with reported incidence of 1.3-2.8% in clinical series and as high as 20% in autopsy series. The mechanisms of SDH involve tearing of arachnoid adherent to the dome of the aneurysm at the time of rupture, direct tearing of arachnoid by a jet of blood, and disruption of arachnoid by ICH, with secondary decompression of ICH into the subdural space.

Increased intracranial pressure

Elevations in ICP are due to mass effect of blood (subarachnoid, intracranial, intraventricular, or subdural hemorrhage) or acute hydrocephalus. Once ICP reaches mean arterial pressure (MAP), cerebral perfusion pressure becomes zero and cerebral blood flow stops, resulting in loss of consciousness and death.

Etiology

Of nontraumatic subarachnoid hemorrhages, approximately 80% are due to a ruptured berry aneurysm. Rupture of arteriovenous malformations (AVMs) is the second most identifiable cause of SAH, accounting for 10% of cases of SAH. Most of the remaining cases result from rupture of the following types of pathologic entities:

• Mycotic aneurysm • Angioma • Neoplasm • Cortical thrombosis SAH may reflect a secondary dissection of blood from an intraparenchymal hematoma (eg, bleeding from hypertension or neoplasm).

Both congenital and acquired factors are thought to play a role in SAH. Evidence supporting the role of congenital causes in aneurysm formation includes the following:

• Clusters of familial occurrence, such as in Finland, where the incidence of familial cerebral aneurysm is 10%

• Significant incidence of multiple aneurysms in patients with SAH (15%) • The association of aneurysms with specific congenital diseases (eg, coarctation of

the aorta, Marfan syndrome, Ehlers-Danlos syndrome, fibromuscular dysplasia, polycystic kidney disease)

Familial cases of AVM are rare, and the problem may result from sporadic abnormalities in embryologic development. AVMs are thought to occur in approximately 4-5% of the general population, of which 10-15% are symptomatic.

Congenital defects in the muscle and elastic tissue of the arterial media in the vessels of the circle of Willis are found in approximately 80% of normal vessels at autopsy. These defects lead to microaneurysmal dilation (< 2 mm) in 20% of the population and larger dilation (>5 mm) and aneurysms in 5% of the population.

Acquired factors thought to be associated with aneurysmal formation include the following:

• Atherosclerosis • Hypertension • Advancing age • Smoking • Hemodynamic stress Less common causes of SAH include the following:

• Fusiform and mycotic aneurysms • Fibromuscular dysplasia • Blood dyscrasias • Moyamoya disease • Infection • Neoplasm • Trauma (fracture at the base of the skull leading to internal carotid aneurysm) • Amyloid angiopathy (especially in elderly people) • Vasculitis Reversible cerebral vasoconstriction syndrome (RCVS) is characterized by recurrent thunderclap headaches and reversible segmental multifocal cerebral artery narrowing, and it results in SAH in more than 30% of cases. Muehlschlegel and colleagues found that clinical and imaging findings can differentiate RCVS with SAH from other causes of SAH.[8, 9]

After analyzing clinical and imaging features of 38 patients with RCVS-SAH, 515 patients with aneurysmal SAH, and 93 patients with cryptogenic (angiogram negative) SAH, Muehlschlegel et al identified clinical characteristics and radiological findings that can differentiate RCVS-SAH from aneurysmal SAH or cryptogenic SAH. These researchers concluded that these differences may be useful for improving diagnostic accuracy, clinical management, and resource utilization.[8, 9]

Risk factors

Although risk factors for SAH have been evaluated extensively, little conclusive evidence has been derived. Smoking appears to be a significant risk factor, as does heavy alcohol consumption. The risk of AVM rupture is greater during pregnancy. Data regarding the relationship between hypertension and SAH are conflicting. Previously documented acute severe hypertension with diastolic pressure over 110 mm Hg has been linked to SAH.

The following do not appear to be significant risk factors for SAH:

• Use of oral contraceptives • Hormone replacement therapy • Hypercholesterolemia • Vigorous physical activity

Epidemiology

United States statistics

The frequency of ruptured and unruptured aneurysms has been estimated at 1-9% in different autopsy series, with a prevalence of unruptured aneurysms of 0.3-5%. Retrospective arteriographic studies show a prevalence of less than 1% with the limitation that some cases did not receive adequate evaluation and thus some aneurysms may have been missed. Annual incidence increases with age and probably is underestimated because death is attributed to other reasons that are not confirmed by autopsies.

The annual incidence of aneurysmal SAH in the United States is 6-16 cases per 100,000 population, with approximately 30,000 episodes occurring each year. Unlike other subcategories of stroke, the incidence of SAH has not decreased over time. However, since 1970, population-based survival rates have improved.

International statistics

The reported incidence of subarachnoid hemorrhage is high in the United States, Finland, and Japan, while it is low in New Zealand and the Middle East. In Finland, the estimated incidence based on different studies is 14.4-19.6 cases per 100,000 population, although numbers as high as 29.7 have been reported.

In Japan, the reported rates vary between 11 and 18.3 cases per 100,000 population, with one study showing an incidence of 96.1 cases per 100,000 population (this study included only patients aged 40 and older in the data collection, and results were not adjusted for sex and age to the same reference population). In New Zealand, age-adjusted incidence was reported as 14.3 cases per 100,000 population.

An Australian study reported an incidence of 26.4 cases per 100,000 population but only for patients older than 35 years, as age was not adjusted in the reference population. In the Netherlands, the age-specific incidence was reported as 7.8 cases per 100,000 population (this is believed to be an underestimate).

Iceland reported 8 cases per 100,000 population, but a significant portion of the affected rural population was believed to be missed. Greenland Eskimos had 9.3 cases per 100,000 population; ethnic Danes there had an incidence of 3.1 cases per 100,000 population. This latter figure is consistent with the figures in Denmark—marked differences are postulated to be related to genetic factors. On the Faeroe Islands (part of Denmark with an isolated population of the same genetic ancestry), the reported incidence is 7.4 cases per 100,000 population.

In China, the reported incidence is low, but no good studies have been published to support this statement. The incidence among Indians and Rhodesian Africans is significantly lower than in those from European nations; this can be explained partly by the low incidence of atherosclerosis in these populations. In the Middle East, the numbers are very low as well; the best available estimate is 5.1 cases per 100,000 population in Qatar.

Race-, sex-, and age-related demographics

The risk is higher in blacks than in whites; however, people of all ethnic groups

develop intracranial aneurysms. The disparity in frequency of rupture has been attributed to population variance with respect to prevalence of risk factors and age distribution.

The incidence of SAH in women is higher than in men (ratio of 3 to 2). The risk of SAH is significantly higher in the third trimester of pregnancy, and SAH from aneurysmal rupture is a leading cause of maternal mortality, accounting for 6-25% of maternal deaths during pregnancy. A higher incidence of AVM rupture also has been reported during pregnancy.

Incidence increases with age and peaks at age 50 years. Approximately 80% of cases of SAH occur in people aged 40-65 years, with 15% occurring in people aged 20-40 years. Only 5% of cases of SAH occur in people younger than 20 years. SAH is rare in children younger than 10 years, accounting for only 0.5% of all cases.

Prognosis

Although mortality rates of SAH have decreased in the past 3 decades, it remains a devastating neurologic problem. An estimated 10-15% of patients die before reaching the hospital. Approximately 25% of patients die within 24 hours, with or without medical attention. Hospitalized patients have an average mortality rate of 40% in the first month. About half of affected individuals die in the first 6 months. Rebleeding, a major complication, carries a mortality rate of 51-80%.

Age-adjusted mortality rates are 62% greater in females than in males and 57% greater in blacks than in whites. Morbidity and mortality increase with age and are related to the overall health status of the patient.

More than one third of survivors have major neurologic deficits. Cognitive deficits are present even in many patients considered to have a good outcome.

Al-Khindi et al found that survivors of aneurysmal SAH commonly experience deficits in memory, executive function, and language that affect their day-to-day functioning, including activities of daily living, instrumental activities of daily living, return to work, and quality of life. Deficits in cognition and day-to-day functioning are further compounded by depression, anxiety, fatigue, and sleep disturbances.[10]

Factors that affect morbidity and mortality rates are as follows:

• Severity of hemorrhage • Degree of cerebral vasospasm • Occurrence of rebleeding • Presence of comorbid conditions and the hospital course (eg, infections, myocardial

infarction) Other factors that affect the prognosis of patients who have suffered an SAH include age, Hunt and Hess grade (see below), smoking history, and location of the aneurysm. Younger patients do better. Patients with a history of cigarette smoking have a poorer prognosis. Anterior circulation aneurysms carry a more favorable prognosis.

Acute cocaine use was associated with higher rates of in-hospital death and a significantly increased risk for aneurysm rerepture in a retrospective study of 1134

patients with aneurysmal SAH. Compared with patients who had not used cocaine in the 72 hours preceding their event, those who had used cocaine had a nearly 3-fold increased risk for in-hospital mortality. Mortality remained higher among cocaine users after patients with rerupture were excluded from the analysis, suggesting that rerupture was not entirely responsible for the higher mortality rate in these patients.[11]

Clinical grading scales

Clinical assessment of SAH severity commonly utilizes grading scales. The 2 clinical scales most often employed are the Hunt and Hess and the World Federation of Neurological Surgeons (WFNS) grading systems. A third, the Fisher scale, classifies SAH based on CT scan appearance and quantification of subarachnoid blood.

The WFNS scale is as follows:

• Grade 1 - Glasgow Coma Score (GCS) of 15, motor deficit absent • Grade 2 - GCS of 13-14, motor deficit absent • Grade 3 - GCS of 13-14, motor deficit present • Grade 4 - GCS of 7-12, motor deficit absent or present • Grade 5 - GCS of 3-6, motor deficit absent or present The Fisher scale (CT scan appearance) is as follows:

• Group 1 - No blood detected • Group 2 - Diffuse deposition of subarachnoid blood, no clots, and no layers of

blood greater than 1 mm • Group 3 - Localized clots and/or vertical layers of blood 1 mm or greater in

thickness • Group 4 - Diffuse or no subarachnoid blood, but intracerebral or intraventricular

clots are present The Hunt and Hess grading system is as follows:

• Grade 0 - Unruptured aneurysm • Grade I - Asymptomatic or mild headache and slight nuchal rigidity • Grade Ia - Fixed neurologic deficit without acute meningeal/brain reaction • Grade II - Cranial nerve palsy, moderate to severe headache, nuchal rigidity • Grade III - Mild focal deficit, lethargy, or confusion • Grade IV - Stupor, moderate to severe hemiparesis, early decerebrate rigidity • Grade V - Deep coma, decerebrate rigidity, moribund appearance In the Hunt and Hess system, the lower the grade, the better the prognosis. Grades I-III generally are associated with favorable outcome; these patients are candidates for early surgery. Grades IV and V carry a poor prognosis; these patients need stabilization and improvement to grade III before surgery is undertaken. Some recommend more aggressive management for patients with poor clinical grade.

Survival correlates with the grade of subarachnoid hemorrhage upon presentation. Reported figures include a 70% survival rate for Hunt and Hess grade I, 60% for grade II, 50% for grade III, 40% for grade IV, and 10% for grade V.

The Hunt and Hess and the WFNS grading systems have been shown to correlate well with patient outcome. The Fisher classification has been used successfully to predict the likelihood of symptomatic cerebral vasospasm, one of the most feared

complications of SAH. All 3 grading systems are useful in determining the indications for and timing of surgical management. For an accurate assessment of SAH severity, these grading systems must be used in concert with the patient's overall general medical condition and the location and size of the ruptured aneurysm.

Complications

Complications of SAH include the following:

• Hydrocephalus • Rebleeding • Delayed ischemia • Intracerebral hemorrhage • Intraventricular hemorrhage (IVH) • Left ventricular systolic dysfunction • Subdural hematoma • Seizures • Increased intracranial pressure • Myocardial infarction [4] The incidence of rebleeding complication is greatest in the first 2 weeks. The peak is within 24-48 hours following initial SAH (approximately 6%), with a rate of 1.5% per day for the next 12-13 days. The cumulative 2-week incidence is 20-30% in unoperated patients. After the first 30 days, rebleed rate decreases to 1.5% per year for the first 10 years. In another study, rebleeding was reported at a rate of 3% per year after 6 months, with a 67% mortality rate at 20 years.

Delayed ischemia

Delayed ischemia from cerebral vasospasm is currently the most common cause of death and disability following aneurysmal SAH. It has to some degree cancelled out the improvement in morbidity and mortality from the lower rebleed rate related to early surgical clipping.

An estimated 10-20% of patients with aneurysmal SAH suffer delayed cerebral ischemia, resulting in permanent disability or death. This complication alone accounts for 14-32% of deaths and permanent disability in large studies, while the direct effect of aneurysm rupture accounts for 25% and rebleeding for 17.6%. Approximately 15-20% of patients with symptomatic vasospasm will have a poor outcome despite maximal medical therapy, including mortality in 7-10% of patients and severe morbidity in 7-10% of patients.

Intraventricular hemorrhage

Found in 13-28% of clinical cases of ruptured aneurysms and in 37-54% of autopsy cases, intraventricular hemorrhage (IVH) is a significant predictor of poor neurologic grade and outcome. Patients with IVH are at higher risk of developing hydrocephalus. In one study of 91 patients, IVH was associated with an overall mortality rate of 64%. The key prognostic indicator is the degree of ventricular dilatation.

ICHntracerebral hemorrhage (ICH)

A+ | Reset | A-OverviewIntracerebral hemorrhage (ICH) is a type of stroke caused by bleeding within the brain tissue itself – a very life-threatening situation. A stroke occurs when the brain is deprived of oxygen due to an interruption of its blood supply. ICH is most commonly caused by hypertension, arteriovenous malformations, or head trauma. Treatment focuses on stopping the bleeding, removing the blood clot (hematoma), and relieving the pressure on the brain.What is an intracerebral hemorrhage (ICH)?Tiny arteries bring blood to areas deep inside the brain (see Anatomy of the Brain). High blood pressure (hypertension) can cause these thin-walled arteries to rupture, releasing blood into the brain tissue. The blood collects and forms a clot, called a hematoma, which grows and causes pressure on surrounding brain tissue (Fig. 1). Increased intracranial pressure (ICP) makes a person confused and lethargic. As blood spills into the brain, the area that artery supplied is now deprived of oxygen-rich blood – called a released that further damage brain cells in the area surrounding the hematoma.

Figure 1. An intracerebral hemorrhage (ICH) is usually caused by rupture of tiny arteries within the brain tissue (left). As blood collects, a hematoma or blood clot forms causing increased pressure on the brain. Arteriovenous malformations (AVMs) and tumors can also cause bleeding into brain tissue (right).An ICH can occur close to the surface or in deep areas of the brain. Sometimes deep hemorrhages can expand into the ventricles – the fluid filled spaces in the center of the brain.What are the symptoms?If you experience the symptoms of an ICH, call 911 immediately! Symptoms usually come on suddenly and can vary depending on the location of the bleed. Common symptoms include:

• headache, nausea, and vomiting• lethargy or confusion• sudden weakness or numbness of the face, arm or leg, usually on one side• loss of consciousness• temporary loss of vision• seizures

What are the causes?• Hypertension: an elevation of blood pressure that may cause tiny arteries to burst inside the brain.• Blood thinner therapy: drugs such as coumadin, heparin, and warfarin used to treat heart and stroke conditions.• AVM : a tangle of abnormal arteries and veins with no capillaries in between.• Aneurysm : a bulge or weakening of an arterial wall.• Head trauma: fractures to the skull and penetrating wounds (gunshot) can damage an artery and cause bleeding.• Bleeding disorders: hemophilia, sickle cell anemia, DIC, thrombocytopenia.• Tumors: highly vascular tumors such as angiomas and metastatic tumors can bleed into the brain tissue.• Amyloid angiopathy: a degenerative disease of the arteries.• Drug usage: cocaine and other illicit drugs can cause ICH.• Spontaneous: ICH by unknown causes.

Who is affected?Ten percent of strokes are caused by ICH (approximately 70,000 new cases each year). ICH is twice as common as subarachnoid hemorrhage (SAH) and has a 40% risk of death. ICH occurs slightly more frequently among men than women and is more common among young and middle-aged African Americans and Japanese. Advancing age and hypertension are the most important risk factors for ICH. Approximately 70% of patients experience long-term deficits after an ICH.How is a diagnosis made?When you or a loved one is brought to the emergency room with an ICH, the doctor will learn as much about your symptoms, current and previous medical problems, current medications, family history, and perform a physical exam. Diagnostic tests help doctors determine the source and location of the bleeding.Computed Tomography Angiography (CTA) scan is a noninvasive X-ray to review the anatomical structures within the brain to see if there is any blood in the brain (Fig. 2). A newer technology called CT angiography involves the injection of contrast into the blood stream to view arteries of the brain.

Figure 2. CT scan showing a large ICH.Angiogram is an invasive procedure, where a catheter is inserted into an artery and passed through the blood vessels to the brain. Once the catheter is in place, a contrast dye is injected into the bloodstream and X-ray images are taken.Magnetic resonance imaging (MRI) scan is a noninvasive test, which uses a magnetic field and radio-frequency waves to give a detailed view of the soft tissues of your brain. An MRA (Magnetic Resonance Angiogram) is the same non-invasive study, except it is also an angiogram, which means it examines the blood vessels as well as the structures of the brain.What treatments are available?Once the cause and location of the bleeding is identified, medical or surgical treatment is performed to stop the bleeding, remove the clot, and relieve the pressure on the brain. If left alone the brain will eventually absorb the clot within a couple of weeks – however the damage to the brain

caused by ICP and blood toxins may be irreversible.Generally, patients with small hemorrhages (<10 cm3) and minimal deficits are treated medically. Patients with cerebellar hemorrhages (>3 cm3) who are deteriorating or who have brainstem compression and hydrocephalus are treated surgically to remove the hematoma as soon as possible. Patients with large lobar hemorrhages (50 cm3) who are deteriorating usually undergo surgical removal of the hematoma.Medical treatmentBlood pressure is managed to decrease the risk of more bleeding yet provide enough blood flow (perfusion) to the brain.Controlling intracranial pressure is the biggest factor in the outcome of ICH. A device called an ICP monitor is placed directly into the ventricles or within the brain to measure pressure. Normal ICP is 20mm HG.Removing cerebrospinal fluid (CSF) from the ventricles is a common method to control ICP. A ventricular catheter (VP shunt) may be placed in the ventricles to drain CSF fluid to allow room for the hematoma to expand without damaging the brain. Hyperventilation also helps control ICP. In some cases, coma may be induced with drugs to bring down ICP.Surgical treatment The goal of surgery is to remove as much of the blood clot as possible and stop the source of bleeding if it is from an identifiable cause such as an AVM or tumor. Depending on the location of the clot either a craniotomy or a stereotactic aspiration may be performed.

• Craniotomy involves cutting a hole in the skull with a drill to expose the brain and remove the clot. Because of the increased risk to the brain, this technique is usually used only when the hematoma is close to the surface of the brain or if it is associated with an AVM or tumor that must also be removed.

• Stereotactic aspiration is a less invasive technique preferred for large hematomas located deep inside the brain. The procedure requires attaching a stereotactic frame to your head with four pins (screws). The pin site areas are injected with local anesthesia to minimize discomfort. A metal cage, which looks like a birdcage, is placed on the frame. Next, you undergo a CT scan to help the surgeon pinpoint the exact coordinates of the hematoma. In the OR, the surgeon drills a small hole about the size of quarter in the skull. With the aid of the stereotactic frame, a hollow needle is passed through the hole, through the brain tissue, directly into the clot. The hollow needle is attached to a large syringe, which the surgeon uses to suction out the contents of the blood clot.

Recovery & preventionImmediately after an ICH, the patient will stay in the intensive care unit (ICU) for several weeks where doctors and nurses watch them closely for signs of rebleeding, hydrocephalus, and other complications. Once their condition is stable, the patient is transferred to a regular room.ICH patients may suffer short-term and/or long-term deficits as a result of the bleed or the treatment. Some of these deficits may disappear over time with healing and therapy. The recovery process may take weeks, months, or years to understand the level of deficits incurred and regain function.Clinical trialsClinical trials are research studies in which new treatments—drugs, diagnostics, procedures, and other therapies—are tested in people to see if they are safe and effective. Research is always being conducted to improve the standard of medical care. Information about current clinical trials, including eligibility, protocol, and locations, are found on the Web. Studies can be sponsored by the National Institutes of Health (see clinicaltrials.gov) as well as private industry and pharmaceutical companies (see

Lobar Intracerebral Hemorrhage

An intracerebral hemorrhage (ICH) occurs when blood suddenly bursts into brain tissue, causing damage to the brain, which may present symptoms similar to that of a stroke. Lobar intracerebral hemorrhages occur in the cerebral lobes outside of the basal ganglia. The basal ganglia are a structure located in the cerebrum (the largest part of the brain) that aids in motor control, procedural learning, eye movement, and cognitive function.

Stroke-like symptoms usually appear suddenly during ICH, causing symptoms that include headache, weakness, confusion, and paralysis, particularly on one side of the body. The buildup of blood puts pressure on the brain and interferes with its oxygen supply. This can quickly cause brain and nerve damage.

This is a medical emergency requiring immediate treatment. ICH is not as common as ischemic stroke (when a blood vessel is blocked by a clot), but is more serious.

Treatment generally involves surgery to repair damaged blood vessels. Depending on the location of the hemorrhage and the amount of damage, long-term treatment may include physical, speech, and occupational therapy. Most people have some level of permanent disability.

Part 2 of 8: SymptomsSymptoms of Intracerebral Hemorrhage

Symptoms of ICH include:

• sudden weakness, tingling, or paralysis in the face, arm, or leg, especially if it occurs on only one side of the body

• sudden onset of severe headache• trouble swallowing• trouble with vision in one or both eyes• loss of balance and coordination, dizziness• trouble with language skills (reading, writing, speaking, understanding)• nausea, vomiting• apathy, sleepiness, lethargy, loss of consciousness• confusion, deliriumThis is a serious medical condition. If you or someone near you is having symptoms of stroke, call 911 immediately.

Part 3 of 8: CausesCauses of Intracerebral Hemorrhage

High blood pressure is the most common cause of intracerebral hemorrhage. In younger people, another common cause is abnormally formed blood vessels in the brain. Other causes include:

• head injury or trauma• blood clot that blocks an artery in the brain• ruptured cerebral aneurysm (weak spot in a blood vessel that bursts)• arteriovenous malformation (a grouping of malformed blood vessels in the

brain that disrupts normal blood flow)• use of blood thinners• bleeding tumors• cocaine use, which can cause severe hypertension and lead to hemorrhage• bleeding disorders such as hemophilia and sickle cell anemiaAnyone can have an intracerebral hemorrhage, but your risk increases with age. According to the Mayfield Clinic, men are at higher risk than women, as are middle-aged people of Japanese or African-American descent (Mayfield Clinic, 2009).

Part 4 of 8: DiagnosisDiagnosing Intracerebral Hemorrhage

If you have some symptoms of ICH, a neurological exam will be performed. Imaging tests are used to determine if you are having an ischemic stroke (blockage) or a hemorrhagic (bleeding) stroke. Diagnostic testing for ICH may

include:

Computed tomography (CT scan): This type of test creates images of the brain, which can detect skull fractures or confirm bleeding.

Magnetic resonance imaging (MRI): This type of imaging test may help your doctor see the brain more clearly to better identify the cause of the bleeding.

Angiogram: This test uses X-ray technology to take pictures of blood flow within an artery.

Blood tests may also be used to identify immune system disorders, inflammation, and blood clotting problems that can cause bleeding in the brain.

Part 5 of 8: TreatmentTreatment for Intracerebral Hemorrhage

Treatment within the first three hours of the onset of symptoms generally results in a better outcome.

Surgery can relieve pressure on the brain and repair torn arteries. In addition, certain medications may be prescribed to manage symptoms, such as painkillers to ease severe headaches. Antianxiety drugs may be necessary to control blood pressure. If your doctor determines that you are at risk for seizures, antiepileptic drugs may be prescribed.

Long-term treatment will be needed to overcome symptoms caused by damage to the brain. Depending on your symptoms, treatment may include physical and speech therapy to help restore muscle function or improve communication. Occupational therapy may help a person regain certain skills and independence by practicing and modifying everyday activities.

Part 6 of 8: ComplicationsComplications from Intracerebral Hemorrhage

Depending on the location of the hemorrhage and how long your brain was deprived of oxygen, complications may include:

• impaired language skills• fatigue• problems with swallowing• vision loss• difficulty with sensations or movements on one side of the body• pneumonia• cognitive dysfunction (memory loss, difficulty reasoning), confusion• swelling on the brain• seizures• depression, emotional problemsPart 7 of 8: OutlookLong-Term Outlook for Intracerebral Hemorrhage

Recovery following ICH differs greatly from person to person, and will depend on a variety of factors, including your age and overall health, the location of the hemorrhage, and the extent of the damage.

Some people may take months or years to recover. Most ICH patients have some long-term disability. In some cases, around-the-clock or nursing home care may be needed. According to The University of Washington Medical Center (UWM), about 40 percent of ICH patients die within the first month (UWM).

Stroke support groups can help people and families cope with long-term care. Your doctor or hospital can provide information about support groups that meet in your area.

Part 8 of 8: PreventionPreventing Intracerebral Hemorrhage

You can decrease your chances of ICH by:

• not smoking• treating heart disease• treating high blood pressure• keeping diabetes under controlmaintaining a healthy lifestyle