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

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

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.

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.

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).

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.

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.

Medical Care

Medical therapy of intracranial hemorrhage is principally focused on adjunctive measures to

minimize injury and to stabilize individuals in the perioperative phase. Clinical trial data had
suggested that treatment with recombinant factor VIIa (rFVIIa) within 4 hours after the onset
of intracerebral hemorrhage limited the growth of the hematoma, reduced mortality, and
improved 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.

Labetalol (Normodyne, Trandate)

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Antagonizes adrenergic receptors, thereby reducing blood pressure.

Nicardipine (Cardene, Cardene SR)

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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.

Mannitol (Osmitrol, Resectisol)

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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.

Acetaminophen (Tylenol, Feverall, Aspirin Free Anacin)

 • View full drug information

Reduces fever, maintains normothermia, and reduces headache.

Anticonvulsants

Class Summary

These agents reduce the frequency of seizures and provide seizure prophylaxis.

Fosphenytoin (Cerebyx)

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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.

Phytonadione; vitamin K (Konakion, Mephyton, AquaMEPHYTON)

• View full drug information

Promotes hepatic synthesis of clotting factors that inhibit warfarin effects.

Protamine

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Forms a salt with heparin and neutralizes its effects.

Antacids

Class Summary

These agents provide prophylaxis of gastric ulcers.

Famotidine (Pepcid)

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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

rimary ICH type n (%) M:F ratio Mean age (years) 30-day mortality (%)
Lobar 154 (36.4) 1.1 66.7 29 (18.8)
Nonlobar 269 (63.6) 1.3 65.3 87 (32.3)
•
52 (12.3) 1.2 68.7 14 (26.9)
Cerebellar
•
73 (17.3) 1.1 67.0 21 (28.8)
Thalamic
•
121 (28.6) 1.5 65.1 43 (35.5)
Putamenal/caudate
• 21 (5.0) 2.0 52.5 8 (38.1)
 rimary ICH type n (%) M:F ratio Mean age (years) 30-day mortality (%)

Brainstem
•
2 (0.5) 1 (50.0)
Unspecified
Total 423 1.2 65.9 116 (27.4)