AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
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• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
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INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
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• Medication
• Follow-up
• Miscellaneous
• Multimedia
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Background

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. ICH accounts for 8-13% of all strokes and results from a wide spectrum of disorders. ICH is more likely to result in death or major disability than ischemic stroke or subarachnoid hemorrhage. ICH 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 ICH 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 ICH.

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 ICH 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%).

IVH occurs in one third of ICH cases from extension of thalamic ganglionic bleeding into the ventricular space. Isolated IVH frequently arise from subependymal structures including the germinal matrix, AVMs, and cavernous angiomas.

Frequency

United States

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

International

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

Mortality/Morbidity

• Annually, more than 20,000 individuals in the United States die of ICH.
• ICH has a 30-day mortality rate of 44%.
• Pontine or other brainstem ICH has a mortality rate of 75% at 24 hours.

Race

ICH has a higher incidence among populations with a higher frequency of hypertension, including African Americans. A higher incidence of ICH 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

ICH 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 ICH in young women.

Age

Incidence of ICH increases in individuals older than 55 years and doubles with each decade until age 80 years.

• The relative risk of ICH 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.

CLINICAL

Section 3 of 11  

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• Follow-up
• Miscellaneous
• Multimedia
• References

History

• Onset of symptoms of ICH 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 (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 ICH 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
• • 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
  • Brain stem - Quadriparesis, facial weakness, decreased level of consciousness, gaze paresis, ocular bobbing, miosis, or autonomic instability
  • Cerebellum - Ataxia, usually beginning in the trunk, ipsilateral facial weakness, ipsilateral sensory loss, gaze paresis, skew deviation, miosis, or decreased level of consciousness

Causes

• Hypertension
• 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 IVH
• Trauma

DIFFERENTIALS

Section 4 of 11  

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• Differentials
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• Follow-up
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Other Problems to be Considered

Vasculitis

WORKUP

Section 5 of 11  

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• Medication
• Follow-up
• Miscellaneous
• Multimedia
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Lab Studies

• 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 ICH
• Screening for hematologic, infectious, and vasculitic etiologies in select patients - Selective testing for more uncommon causes of ICH

Imaging Studies

• Parenchymal imaging
• • CT scan
  • • CT scan readily demonstrates acute hemorrhage as hyperdense signal intensity (see Image 1). Multifocal hemorrhages at the frontal, temporal, or occipital poles suggest a traumatic etiology.
    • 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.
  • 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 ICH reliably within the first 1-2 hours of onset (see Images 2-3).
    • 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.

    Table 1. MRI Appearance of ICH

    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 (intracellular)	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 ICH 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

• 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

• 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 ICH.
• 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

TREATMENT

Section 6 of 11  

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Medical Care

Medical therapy of ICH is principally focused on adjunctive measures to minimize injury and to stabilize individuals in the perioperative phase. Promising clinical trial data suggest 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. This intervention, however, may result in a small increase in the frequency of thromboembolic adverse events.

• 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.
• Rapidly stabilize vital signs, and simultaneously acquire emergent CT scan.
• Intubate and hyperventilate if ICP 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.
• Facilitate transfer to the operating room or ICU.

Surgical Care

• Consider nonsurgical management for patients with minimal neurological deficits or with ICH volumes less than 10 cc.
• Consider surgery for patients with cerebellar hemorrhage greater than 3 cm, for patients with ICH 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:
• • Clinical course and timing
  • Patient's age and comorbid conditions
  • Etiology
  • Location of the hematoma
  • Mass effect and drainage patterns
• Surgical approaches include the following:
• • Craniotomy and clot evacuation under direct visual guidance
  • Stereotactic aspiration with thrombolytic agents
  • Endoscopic evacuation

Consultations

• Neurosurgeon
• Neurologist
• Interventional neuroradiologist
• Rehabilitation specialist

Diet

• 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

• Maintain bedrest during the first 24 hours.
• Follow with progressive increase in activity.
• Avoid strenuous exertion.

MEDICATION

Section 7 of 11  

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Antihypertensive agents reduce blood pressure to prevent exacerbation of ICH. Osmotic diuretics, such as mannitol, may be used to decrease ICP. 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. Vitamin K and protamine may be used to restore normal coagulation parameters. Antacids are used to prevent gastric ulcers associated with ICH.

Drug Category: Antihypertensive agents

These agents reduce blood pressure to prevent exacerbation of ICH.

Drug Category: Osmotic diuretics

Osmotic diuretics reverse pressure gradient across the blood-brain barrier, reducing ICP.

Drug Category: Antipyretics, analgesics

These agents reduce fever and relieve pain.

Drug Category: Anticonvulsants

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

Drug Category: Antidotes

This agent reverses some coagulopathies or bleeding diatheses.

Drug Category: Antacids

These agents provide prophylaxis of gastric ulcers.

FOLLOW-UP

Section 8 of 11  

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• Follow-up
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Further Inpatient Care

• Initial management of ICH generally is conducted in the ICU. Subsequent care generally includes the following:
• • Serial neurologic examinations
  • Treatment of elevated ICP
  • 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

Further Outpatient Care

• 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.

In/Out Patient Meds

• Antihypertensives for modification of blood pressure
• Mannitol or other osmotic diuretics for elevated ICP
• 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 ICH should be transferred to a medical facility with neurosurgical expertise.

Deterrence/Prevention

• 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 ICH
• 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 IVH due to germinal matrix hemorrhage

Complications

• Neurological deficits or death
• Seizures
• Hydrocephalus
• Spasticity
• Urinary complications
• Aspiration pneumonia
• Neuropathic pain
• Deep venous thrombosis
• Pulmonary emboli
• Cerebral herniation

Prognosis

• Early reduction in the level of consciousness carries an ominous prognosis.
• The size and location of ICH provide useful prognostic information.
• • Larger hematomas have a worse outcome.
  • Lobar hemorrhage has a better outcome than deep hemorrhage.
  • 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 ICH can be predicted on admission by neurologic severity, ICH location, and fibrinogen levels.

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

MISCELLANEOUS

Section 9 of 11  

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• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• Delayed transfer and triage
• Failure to consider clinical diagnosis of ICH
• Failure to obtain emergent CT scan
• Failure to perform serial neurologic assessments and detect delayed deterioration

Special Concerns

• Consider the relative risks and benefits of anticoagulation for individuals with ICH at high risk of embolic phenomena, such as mechanical cardiac valves. Anticoagulation usually may be restarted within 2-3 weeks after ICH.
• Diagnosis and management of pregnant women with ICH require careful selection of neuroradiologic studies and medications, with due consideration of teratogenic effects.

MULTIMEDIA

Section 10 of 11  

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• Multimedia
• References

Media file 1:  Intracranial hemorrhage. CT scan of right frontal intracerebral hemorrhage complicating thrombolysis of an ischemic stroke.
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Media file 2:  Intracranial hemorrhage. Fluid-attenuated inversion-recovery, T2-weighted, and gradient echo MRI illustration of intracerebral hemorrhage associated with a right frontal arteriovenous malformation.
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Media file 3:  Intracranial hemorrhage. Fluid-attenuated inversion-recovery, T2-weighted, and gradient echo MRI depiction of left temporal intracranial hemorrhage due to sickle cell disease.
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Media type:  MRI

Media file 4:  This MRI reveals petechial intracerebral hemorrhage (ICH) due to cerebral venous thrombosis.
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Media type:  MRI

Media file 5:  This CT scan and MRI revealed midbrain intracerebral hemorrhage (ICH) and intraventricular hemorrhage (IVH) associated with a cavernous angioma.
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Media file 6:  This MRI reveals hemorrhagic transformation of an ischemic infarct.
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Media type:  MRI

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Media file 8:
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Media file 9:
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Media type:  MRI

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
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• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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Article Last Updated: Aug 7, 2006