Intracranial hemorrhage (ie, the pathological accumulation of blood within the cranial vault)

may occur within brain parenchyma or the surrounding meningeal spaces. Hemorrhage
within the meninges or the associated potential spaces, including epidural hematoma,
subdural hematoma, and subarachnoid hemorrhage, is covered in detail in other articles.
Intracerebral hemorrhage (ICH) and extension of parenchymal bleeding into the ventricles
(ie, intraventricular hemorrhage [IVH]) are detailed here.

Intracerebral hemorrhage accounts for 8-13% of all strokes and results from a wide spectrum
of disorders. Intracerebral hemorrhage is more likely to result in death or major disability
than ischemic stroke or subarachnoid hemorrhage. Intracerebral hemorrhage and
accompanying edema may disrupt or compress adjacent brain tissue, leading to neurological
dysfunction. Substantial displacement of brain parenchyma may cause elevation of
intracranial pressure (ICP) and potentially fatal herniation syndromes.

Pathophysiology
Nontraumatic intracerebral hemorrhage most commonly results from hypertensive damage to
blood vessel walls (eg, hypertension, eclampsia, drug abuse), but it also may be due to
autoregulatory dysfunction with excessive cerebral blood flow (eg, reperfusion injury,
hemorrhagic transformation, cold exposure), rupture of an aneurysm or arteriovenous
malformation (AVM), arteriopathy (eg, cerebral amyloid angiopathy, moyamoya), altered
hemostasis (eg, thrombolysis, anticoagulation, bleeding diathesis), hemorrhagic necrosis (eg,
tumor, infection), or venous outflow obstruction (eg, cerebral venous thrombosis).

Nonpenetrating and penetrating cranial trauma are also common causes of intracerebral
hemorrhage.Patients who experience blunt head trauma and subsequently receive warfarin or
clopidogrel are considered at increased risk for traumatic intracranial hemorrhage. According
to one study, patients receiving clopidogrel have a significantly higher prevalence of
immediate traumatic intracranial hemorrhage compared with patients receiving warfarin.
Delayed traumatic intracranial hemorrhage is rare and occurred only in patients receiving
warfarin.[1]

Chronic hypertension produces a small vessel vasculopathy characterized by lipohyalinosis,

fibrinoid necrosis, and development of Charcot-Bouchard aneurysms, affecting penetrating
arteries throughout the brain including lenticulostriates, thalamoperforators, paramedian
branches of the basilar artery, superior cerebellar arteries, and anterior inferior cerebellar
arteries.

Predilection sites for intracerebral hemorrhage include the basal ganglia (40-50%), lobar
regions (20-50%), thalamus (10-15%), pons (5-12%), cerebellum (5-10%), and other
brainstem sites (1-5%).

Intraventricular hemorrhage occurs in one third of intracerebral hemorrhage cases from

extension of thalamic ganglionic bleeding into the ventricular space. Isolated intraventricular
hemorrhage frequently arise from subependymal structures including the germinal matrix,
AVMs, and cavernous angiomas.

Epidemiology
Frequency

United States

Each year, intracerebral hemorrhage affects approximately 12-15 per 100,000 individuals,
including 350 hypertensive hemorrhages per 100,000 elderly individuals. The overall
incidence of intracerebral hemorrhage has declined since the 1950s.

International

Asian countries have a higher incidence of intracerebral hemorrhage than other regions of the
world.

Mortality/Morbidity

Annually, more than 20,000 individuals in the United States die of intracerebral hemorrhage.
Intracerebral hemorrhage has a 30-day mortality rate of 44%. Pontine or other brainstem
intracerebral hemorrhage has a mortality rate of 75% at 24 hours. Hallevi et al reviewed the
charts and CT scans of patients with intraventricular hemorrhage (IVH) to determine if the
extension of the hemorrhage could be measured. Clinical outcome was determined by the
modified Rankin Scale (mRS). IVH was also classified with an IVH score. The IVH score
allowed rapid estimate of IVH volume by the practitioner and increased predictability for
outcome.[2]

Race

Intracerebral hemorrhage has a higher incidence among populations with a higher frequency
of hypertension, including African Americans. A higher incidence of intracerebral
hemorrhage has been noted in Chinese, Japanese, and other Asian populations, possibly due
to environmental factors (eg, a diet rich in fish oils) and/or genetic factors.

Sex

Intracerebral hemorrhage has a slight male predominance, though study results have been
conflicting.

Cerebral amyloid angiopathy may be more common among women.

Phenylpropanolamine use has been associated with intracerebral hemorrhage in young

women.[3]

Age

Incidence of intracerebral hemorrhage increases in individuals older than 55 years and

doubles with each decade until age 80 years. The relative risk of intracerebral hemorrhage is
greater than 7 in individuals older than 70 years.

In individuals younger than 45 years, lobar hemorrhage is the most common site of and
frequently is associated with AVMs.
Subependymal hemorrhage or germinal matrix hemorrhage is primarily seen in premature
infants.

History
Onset of symptoms of intracerebral hemorrhage is usually during daytime activity, with
progressive (ie, minutes to hours) development of the following:

 Alteration in level of consciousness (approximately 50%)

 Nausea and vomiting (approximately 40-50%)
 Headache (approximately 40%)
 Seizures[4] (approximately 6-7%)
 Focal neurological deficits

Lobar hemorrhage due to cerebral amyloid angiopathy may be preceded by prodromal

symptoms of focal numbness, tingling, or weakness.

A history of hypertension, trauma, illicit drug abuse, or a bleeding diathesis may be elicited.

Physical
Clinical manifestations of intracerebral hemorrhage are determined by the size and location
of hemorrhage, but may include the following:

 Hypertension, fever, or cardiac arrhythmias

 Nuchal rigidity
 Subhyaloid retinal hemorrhages
 Altered level of consciousness
 Anisocoria
 Focal neurological deficits
o Putamen - Contralateral hemiparesis, contralateral sensory loss, contralateral
conjugate gaze paresis, homonymous hemianopia, aphasia, neglect, or apraxia
o Thalamus - Contralateral sensory loss, contralateral hemiparesis, gaze paresis,
homonymous hemianopia, miosis, aphasia, or confusion
o Lobar - Contralateral hemiparesis or sensory loss, contralateral conjugate gaze
paresis, homonymous hemianopia, abulia, aphasia, neglect, or apraxia
o Caudate nucleus - Contralateral hemiparesis, contralateral conjugate gaze
paresis, or confusion
o Brain stem - Quadriparesis, facial weakness, decreased level of consciousness,
gaze paresis, ocular bobbing, miosis, or autonomic instability
o Cerebellum - Ataxia, usually beginning in the trunk, ipsilateral facial
weakness, ipsilateral sensory loss, gaze paresis, skew deviation, miosis, or
decreased level of consciousness

Causes
Possible causes are as follows:
  Hypertension[5]
 Arteriovenous malformation
 Aneurysmal rupture
 Cerebral amyloid angiopathy
 Intracranial neoplasm
 Coagulopathy
 Hemorrhagic transformation of an ischemic infarct
 Cerebral venous thrombosis
 Sympathomimetic drug abuse
 Moyamoya
 Sickle cell disease
 Eclampsia or postpartum vasculopathy
 Infection
 Vasculitis
 Neonatal intraventricular hemorrhage
 Trauma

Differential Diagnoses
 Acute Management of Stroke
 Acute Subdural Hematoma
 Anisocoria
 Blood Dyscrasias and Stroke
 Cardioembolic Stroke
 Cerebellar Hemorrhage
 Cerebral Amyloid Angiopathy
 Cerebral Aneurysms
 Cerebral Venous Thrombosis
 Dissection Syndromes
 Emergent Management of Subarachnoid Hemorrhage
 Epidural Hematoma in Emergency Medicine
 Head Injury
 Herpes Simplex Encephalitis
 Hydrocephalus
 Lumbar Puncture (CSF Examination)
 Magnetic Resonance Imaging in Acute Stroke
 Moyamoya Disease
 Neonatal Injuries in Child Abuse
 Neurologic Effects of Cocaine
 Neurological Sequelae of Infectious Endocarditis
 Pediatric Status Epilepticus
 Posttraumatic Epilepsy
 Reperfusion Injury in Stroke
 Secondary CNS Melanomas
 Stroke Anticoagulation and Prophylaxis
 Subdural Empyema
 Thrombolytic Therapy in Stroke
 Vascular Surgery for Arteriovenous Malformations
 Vein of Galen Malformation
Laboratory Studies
See the list below:

 Complete blood count (CBC) with platelets: Monitor for infection and assess
hematocrit and platelet count to identify hemorrhagic risk and complications.
 Prothrombin time (PT)/activated partial thromboplastin time (aPTT): Identify a
coagulopathy.
 Serum chemistries including electrolytes and osmolarity: Assess for metabolic
derangements, such as hyponatremia, and monitor osmolarity for guidance of osmotic
diuresis.
 Toxicology screen and serum alcohol level if illicit drug use or excessive alcohol
intake is suspected: Identify exogenous toxins that can cause intracerebral
hemorrhage.
 Screening for hematologic, infectious, and vasculitic etiologies in select patients:
Selective testing for more uncommon causes of intracerebral hemorrhage.

Imaging Studies
CT scan

CT scan readily demonstrates acute hemorrhage as hyperdense signal intensity (see image
below). Multifocal hemorrhages at the frontal, temporal, or occipital poles suggest a
traumatic etiology.

Intracranial hemorrhage. CT scan of

right frontal intracerebral hemorrhage complicating thrombolysis of an ischemic stroke.
Patients with mild blunt head trauma and preinjury anticoagulant or antiplatelet use are at
increased risk of intracranial hemorrhage and should undergo urgent and liberal CT
scanning.[6]

Hematoma volume in cubic centimeters can be approximated by a modified ellipsoid

equation: (A x B x C)/2, where A, B, and C represent the longest linear dimensions in
centimeters of the hematoma in each orthogonal plane.

Perihematomal edema and displacement of tissue with herniation also can be appreciated.

Iodinated contrast may be injected to increase screening yield for underlying tumor or
vascular malformation.

CT angiography "spot sign" may be used to predict growth of intracerebral hematomas.[7]

MRI

The MRI appearance of hemorrhage on conventional T1 and T2 sequences evolves over time
because of chemical and physical changes within and around the hematoma (see Table 1
below).

Conventional T1 and T2 sequences are not highly sensitive to hemorrhage in the first few
hours, but newer gradient refocused echo sequences appear to be able to detect intracerebral
hemorrhage reliably within the first 1-2 hours of onset (see following images).

Intracranial hemorrhage. Fluid-

attenuated inversion-recovery, T2-weighted, and gradient echo MRI illustration of
intracerebral hemorrhage associated with a right frontal arteriovenous malformation.

Intracranial hemorrhage. Fluid-

attenuated inversion-recovery, T2-weighted, and gradient echo MRI depiction of left
temporal intracranial hemorrhage due to sickle cell disease.

AVMs and cavernous angiomas may be identified by the presence of multiple flow voids
adjacent to the hematoma.
Paramagnetic contrast may be injected to increase screening yield for underlying tumor or
vascular malformation.

Gradient echo sequences may reveal multiple foci of hypointensity attributable to

hemosiderin deposition from prior silent cerebral microbleeds. A multilobar distribution of
hypointense foci on gradient echo imaging may provide supportive evidence of cerebral
amyloid angiopathy, while multiple deep foci may suggest an underlying hypertensive
arteriopathy.

MRI studies incorporating gradient echo or susceptibility-weighted sequences may be used as

the sole imaging modality for patients with acute stroke, readily identifying intracranial
hemorrhage.

Permeability techniques, including use of source perfusion imaging data, may be used to
detect blood-brain derangements that precede hemorrhagic transformation after
thrombolysis.[8]

This MRI reveals petechial

intracerebral hemorrhage (ICH) due to cerebral venous thrombosis.

This MRI reveals hemorrhagic

transformation of an ischemic infarct.
 This CT scan and MRI revealed
midbrain intracerebral hemorrhage (ICH) and intraventricular hemorrhage (IVH) associated
with a cavernous angioma.

Table 1. MRI Appearance of Intracerebral Hemorrhage (Open Table in a new window)

Phase Time Hemoglobin T1 T2

Hyperacute < 24 hours Oxyhemoglobin (intracellular) Iso or hypo Hyper
Acute 1-3 days Deoxyhemoglobin (intracellular) Iso or hypo Hypo
Early subacute >3 days Methemoglobin Hyper Hypo
Late subacute >7 days Methemoglobin (extracellular) Hyper Hyper
Chronic >14 days Hemosiderin (extracellular) Iso or hypo Hypo

Vessel imaging

CT angiography permits screening of large and medium-sized vessels for AVMs, vasculitis,
and other arteriopathies.

MR angiography permits screening of large and medium-sized vessels for AVMs, vasculitis,
and other arteriopathies.

Conventional catheter angiography definitively assesses large, medium-sized, and sizable

small vessels for AVMs, vasculitis, and other arteriopathies.

Consider catheter angiography for young patients, patients with lobar hemorrhage, patients
without a history of hypertension, and patients without a clear cause of hemorrhage who are
surgical candidates. Angiography may be deferred for older patients with suspected
hypertensive intracerebral hemorrhage and patients who do not have any structural
abnormalities on CT scan or MRI.

Timing of angiography depends on clinical status and neurosurgical considerations.

Other Tests
ECG frequently identifies cerebrum-induced dysrhythmia or cardiac injury.
Procedures
See the list below:

 Lumbar puncture in the setting of IVH may reveal xanthochromia and a biochemical
profile similar to that observed in subarachnoid hemorrhage.
 Ventriculostomy allows for external ventricular drainage in patients with
intraventricular extension of blood products. Intraventricular administration of
thrombolytics may assist clot removal.
 Endoscopic hematoma evacuation may be a promising ultra-early stage treatment for
intracerebral hemorrhage that improves long-term prognosis. [9]

Histologic Findings
See the list below:

 Gross examination reveals focal accumulation of blood with adjacent destruction of

parenchyma.
 Microscopically, bleeding sites appear as round collections of platelets surrounded by
fibrin.
 Charcot-Bouchard microaneurysms may be seen at bifurcations of distal lateral
lenticulostriate vessels in hypertensive intracerebral hemorrhage.
 Lobar hemorrhages of cerebral amyloid angiopathy may reveal pathological
deposition of beta-amyloid protein within the media of small cortical and meningeal
vessels.

Staging
Table 2. Grading of Subependymal Hemorrhage (Open Table in a new window)

Grade Hemorrhage Location

I Subependymal hemorrhage
II Intraventricular hemorrhage without ventriculomegaly
III Intraventricular hemorrhage with ventriculomegaly
IV Intraventricular hemorrhage with parenchymal hemorrhage

Medical Care
Medical therapy of intracranial hemorrhage is principally focused on adjunctive measures to
minimize injury and to stabilize individuals in the perioperative phase. Recent clinical trial
data suggests that treatment with recombinant factor VIIa (rFVIIa) within 4 hours after the
onset of intracerebral hemorrhage limits the growth of the hematoma, reduces mortality, and
improves functional outcomes at 90 days.[10] However, further study of this medication in a
broader cohort did not result in improved clinical outcomes. This intervention may also result
in a small increase in the frequency of thromboembolic adverse events. The early use of
rFVIIa in patients with head injury without systemic coagulopathy may reduce the occurrence
of enlargement of contusions, the requirement of further operation, and adverse outcome.[11]
  Perform endotracheal intubation for patients with decreased level of consciousness
and poor airway protection.
 Cautiously lower blood pressure to a mean arterial pressure (MAP) less than 130 mm
Hg, but avoid excessive hypotension. Early treatment in patients presenting with
spontaneous intracerebral hemorrhage is important as it may decrease hematoma
enlargement and lead to better neurologic outcome.[12]
 Rapidly stabilize vital signs, and simultaneously acquire emergent CT scan.
 Intubate and hyperventilate if intracranial pressure is increased; initiate administration
of mannitol for further control.
 Maintain euvolemia, using normotonic rather than hypotonic fluids, to maintain brain
perfusion without exacerbating brain edema.
 Avoid hyperthermia.
 Correct any identifiable coagulopathy with fresh frozen plasma, vitamin K,
protamine, or platelet transfusions.
 Initiate fosphenytoin or other anticonvulsant definitely for seizure activity or lobar
hemorrhage, and optionally in other patients.Levetiracetam has shown efficacy in
children for prophylaxis of early posthemorrhagic seizures.[13] Additional data suggest
that levetiracetam is more effective than phenytoin for seizure prophylaxis without
suppression of cognitive abilities in patients with ICH.[14]
 Facilitate transfer to the operating room or ICU.
 While reducing SBP with intravenous nicardipine hydrochloride does not
significantly reduce hematoma expansion in patients with ICH, the Antihypertensive
Treatment of Acute Cerebral Hemorrhage study supports further studies to evaluate
the efficacy of aggressive pharmacologic SBP reduction.[15]

Surgical Care
See the list below:

 Consider nonsurgical management for patients with minimal neurological deficits or

with intracerebral hemorrhage volumes less than 10 mL.
 Consider surgery for patients with cerebellar hemorrhage greater than 3 cm, for
patients with intracerebral hemorrhage associated with a structural vascular lesion,
and for young patients with lobar hemorrhage. The common hypertensive
hemorrhages in the basal ganglia have not been shown clearly to benefit from surgery,
although case series with favorable outcomes after stereotactic needle evacuation or
endoscopic drainage have been reported. In the past, standard craniotomy with
evacuation of the hematoma did not appear to improve outcomes.
 Other surgical considerations include the following:
o Clinical course and timing
o Patient's age and comorbid conditions
o Etiology
o Location of the hematoma
o Mass effect and drainage patterns
 Surgical approaches include the following:
o Craniotomy and clot evacuation under direct visual guidance
o Stereotactic aspiration with thrombolytic agents
o Endoscopic evacuation
Consultations
See the list below:

 Neurosurgeon
 Neurologist
 Interventional neuroradiologist
 Rehabilitation specialist

Diet
See the list below:

 Employ aspiration precautions and obtain evaluation of patient's swallowing.

 Initiate enteral feedings as soon as possible. The patient may require placement of a
nasogastric tube or percutaneous device.

Activity
See the list below:

 Maintain bedrest during the first 24 hours.

 Follow with progressive increase in activity.
 Avoid strenuous exertion.
 Medication Summary
 Antihypertensive agents reduce blood pressure to prevent exacerbation of
intracerebral hemorrhage. Osmotic diuretics, such as mannitol, may be used to
decrease intracranial pressure.
 As hyperthermia may exacerbate neurological injury, acetaminophen may be given to
reduce fever and to relieve headache.
 Anticonvulsants are used routinely to avoid seizures that may be induced by cortical
damage. Levetiracetam has shown efficacy in children for prophylaxis of early
posthemorrhagic seizures.[13] Additional data suggest that levetiracetam is more
effective than phenytoin for seizure prophylaxis without suppression of cognitive
abilities in patients with ICH.[14] Vitamin K and protamine may be used to restore
normal coagulation parameters. Antacids are used to prevent gastric ulcers associated
with intracerebral hemorrhage.
 Accumulating data suggest that statins have neuroprotective effects; however, their
association with intracerebral hemorrhage outcome has been inconsistent.[16]
Antecedent use of statins prior to intracerebral hemorrhage is associated with
favorable outcome and reduced mortality after intracerebral hemorrhage. This
phenomenon appears to be a class effect of statins.
 Antihypertensive agents
 Class Summary
 These agents reduce blood pressure to prevent exacerbation of intracerebral
hemorrhage.
 View full drug information
 Labetalol (Normodyne, Trandate)

 Antagonizes adrenergic receptors, thereby reducing blood pressure.
 View full drug information
 Nicardipine (Cardene, Cardene SR)

 Calcium channel blocker. Potent rapid onset of action, ease of titration, and lack of
toxic metabolites. Effective but limited reported experience in hypertensive
encephalopathy.
 Osmotic diuretics
 Class Summary
 Osmotic diuretics reverse pressure gradient across the blood-brain barrier, reducing
intracranial pressure.
 View full drug information
 Mannitol (Osmitrol, Resectisol)

 Reduces cerebral edema with help of osmotic forces and decreases blood viscosity,
resulting in reflex vasoconstriction and lowering of intracranial pressure.
 Antipyretics, analgesics
 Class Summary
 These agents reduce fever and relieve pain.
 View full drug information
 Acetaminophen (Tylenol, Feverall, Aspirin Free Anacin)

 Reduces fever, maintains normothermia, and reduces headache.
 Anticonvulsants
 Class Summary
 These agents reduce the frequency of seizures and provide seizure prophylaxis.
 View full drug information
 Fosphenytoin (Cerebyx)

 Diphosphate ester salt of phenytoin that acts as water-soluble prodrug of phenytoin.
Following administration, plasma esterases convert fosphenytoin to phosphate,
formaldehyde, and phenytoin. Phenytoin in turn stabilizes neuronal membranes and
decreases seizure activity.
 To avoid need to perform molecular weight-based adjustments when converting
between fosphenytoin and phenytoin sodium doses, express dose as phenytoin sodium
equivalents (PE). Although can be administered IV and IM, IV route is route of
choice and should be used in emergency situations.
 Concomitant administration of IV benzodiazepine usually necessary to control status
epilepticus. Full antiepileptic effect of phenytoin, whether given as fosphenytoin or
parenteral phenytoin, not immediate.
 Antidotes
 Class Summary
 This agent reverses some coagulopathies or bleeding diatheses.
 View full drug information
 Phytonadione; vitamin K (Konakion, Mephyton, AquaMEPHYTON)
 
 Promotes hepatic synthesis of clotting factors that inhibit warfarin effects.
 View full drug information
 Protamine

 Forms a salt with heparin and neutralizes its effects.
 Antacids
 Class Summary
 These agents provide prophylaxis of gastric ulcers.
 View full drug information
 Famotidine (Pepcid)

 Minimizes development of gastric ulcers.
 Competitively inhibits histamine at H2 receptor of gastric parietal cells, resulting in
reduced gastric acid secretion, gastric volume, and hydrogen concentration.

Further Outpatient Care

See the list below:

 After hospital discharge, continued physical, occupational, and speech therapy may be
required.
 Administer medications to control hypertension and to prevent complications such as
seizures, urinary tract infections, or venous thromboses.

Further Inpatient Care

Initial management of intracerebral hemorrhage generally is conducted in the ICU.
Subsequent care generally includes the following:

 Serial neurologic examinations

 Treatment of elevated intracranial pressure
 Placement of ventricular catheter should hydrocephalus develop
 Avoidance of hypotension or hypertension (MAP = 70-130 mm Hg)
 Use of isotonic solutions, such as normal saline, to minimize cerebral edema
 Treatment with 3 X isotonic saline should hyponatremia due to cerebral salt wasting
occur
 Avoidance of hyperthermia
 Treatment or prophylaxis of seizures
 Treatment of urinary tract infections
 Prevention of venous thrombosis with intermittent compression stockings plus or
minus low-dose subcutaneous unfractionated or low molecular weight heparin
 Prophylaxis for gastric ulcers
 Physical, occupational, and speech therapy
 Psychological support with cautious use of sedatives, if necessary
 Repeat CT scan in case of clinical deterioration

Inpatient & Outpatient Medications

See the list below:

 Antihypertensives for modification of blood pressure

 Mannitol or other osmotic diuretics for elevated intracranial pressure
 Acetaminophen for fever and headache relief
 Fosphenytoin or other anticonvulsants for posttraumatic seizures
 Famotidine or other antacids for gastric ulcer prophylaxis
 Anticholinergics for bladder complications
 Baclofen, diazepam, or tizanidine for spasticity
 Amitriptyline, carbamazepine, or gabapentin for neuropathic pain

Transfer
Following prehospital and emergent stabilization, patients with intracerebral hemorrhage
should be transferred to a medical facility with neurosurgical expertise.

Deterrence/Prevention
See the list below:

 Early detection and aggressive treatment of hypertension

 Cautious management of anticoagulation and other antithrombotic medications
 Careful selection of subjects suitable for thrombolysis
 Consideration of cerebral amyloid angiopathy as a significant risk factor for
intracerebral hemorrhage[17, 18]
 Public education campaigns emphasizing the dangers of heavy alcohol intake and
sympathomimetic use
 Public education regarding traumatic brain injury, including appropriate use of safety
equipment, precautions, and measures that may reduce the incidence of head injury
 Prevention and management of preterm labor that may reduce intraventricular
hemorrhage due to germinal matrix hemorrhage

Complications
See the list below:

 Neurological deficits or death

 Seizures
 Hydrocephalus
 Spasticity
 Urinary complications
 Aspiration pneumonia
 Neuropathic pain
 Deep venous thrombosis
 Pulmonary emboli
 Cerebral herniation

Prognosis
See the list below:

 Early reduction in the level of consciousness carries an ominous prognosis.

 The size and location of intracerebral hemorrhage provide useful prognostic
information.
o Larger hematomas have a worse outcome.
o Lobar hemorrhage has a better outcome than deep hemorrhage.
o Significant volume of intraventricular blood is a poor prognostic indicator.
 The presence of hydrocephalus is associated with a poor outcome.
 Good outcome in medium to large intracerebral hemorrhage can be predicted on
admission by neurologic severity, intracerebral hemorrhage location, and fibrinogen
levels.[19]

Patient Education
Educate patients regarding the following:

 Treatment of hypertension
 Warning signs and symptoms of stroke as well as preventive measures
 Traumatic brain injury
 Adverse effects of alcohol and sympathomimetic substances