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.
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.
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.
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.
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
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 readily demonstrates acute hemorrhage as hyperdense signal intensity (see image below). Multifocal hemorrhages at the frontal, temporal, or occipital poles suggest a traumatic etiology.
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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).
View Image
Intracranial hemorrhage. Fluid-attenuated inversion-recovery, T2-weighted, and gradient echo MRI illustration of intracerebral hemorrhage associated w....
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Intracranial hemorrhage. Fluid-attenuated inversion-recovery, T2-weighted, and gradient echo MRI depiction of left temporal intracranial hemorrhage du....
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]
View Image
This MRI reveals petechial intracerebral hemorrhage (ICH) due to cerebral venous thrombosis.
View Image
This MRI reveals hemorrhagic transformation of an ischemic infarct.
View Image
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
View Table
See Table
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.
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]
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 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]
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:
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
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.
Clinical Context:
Calcium channel blocker. Potent rapid onset of action, ease of titration, and lack of toxic metabolites. Effective but limited reported experience in hypertensive encephalopathy.
Clinical Context:
Reduces cerebral edema with help of osmotic forces and decreases blood viscosity, resulting in reflex vasoconstriction and lowering of intracranial pressure.
Clinical Context:
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.
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
Following prehospital and emergent stabilization, patients with intracerebral hemorrhage should be transferred to a medical facility with neurosurgical expertise.
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
Early reduction in the level of consciousness carries an ominous prognosis.
The size and location of intracerebral hemorrhage 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 intracerebral hemorrhage can be predicted on admission by neurologic severity, intracerebral hemorrhage location, and fibrinogen levels.[19]
What is intracranial hemorrhage (ICH)?What is the pathophysiology of intracranial hemorrhage (ICH)?What is the role of chronic hypertension in the pathogenesis of intracranial hemorrhage (ICH)?What is the frequency of intracranial hemorrhage (ICH) in different sites of the brain?What is the role of intraventricular hemorrhage in the pathogenesis of intracranial hemorrhage (ICH)?What is the incidence of intracranial hemorrhage (ICH) in the US?What is the global incidence of intracranial hemorrhage (ICH)?What is the mortality rate for intracranial hemorrhage (ICH)?What are the racial predilections for intracranial hemorrhage (ICH)?How does the incidence of intracranial hemorrhage (ICH) vary by sex?How does the incidence of intracranial hemorrhage (ICH) vary by age?What is the progression of symptoms in intracranial hemorrhage (ICH)?What are the signs and symptoms of intracranial hemorrhage (ICH)?What are possible causes of intracranial hemorrhage (ICH)?What are the differential diagnoses for Intracranial Hemorrhage?What is the role of lab studies in the evaluation of intracranial hemorrhage (ICH)?What is the role of CT angiography in the evaluation of intracranial hemorrhage (ICH)?How is intracranial hemorrhage (ICH) characterized on a CT scan?When is CT scanning indicated in the evaluation of intracranial hemorrhage (ICH)?How is hematoma volume determined in the evaluation of intracranial hemorrhage (ICH)?Which CT findings suggest intracranial hemorrhage (ICH)?What is the role of iodinated contrast in the evaluation of intracranial hemorrhage (ICH)?What is the role of MRI in the diagnosis of intracranial hemorrhage (ICH)?Which MRI findings are associated with intracranial hemorrhage (ICH)?What is the role of paramagnetic contrast MRI in the diagnosis of intracranial hemorrhage (ICH)?What is the role of gradient echo in the diagnosis of intracranial hemorrhage (ICH)?When are permeability techniques used in the diagnosis of intracranial hemorrhage (ICH)?What is the indication for CT angiography in the evaluation of intracranial hemorrhage (ICH)?What is the indication for MRI angiography in the evaluation of intracranial hemorrhage (ICH)?What is the role of conventional catheter angiography in the evaluation of intracranial hemorrhage (ICH)?When is conventional catheter angiography indicated in the evaluation of intracranial hemorrhage (ICH)?Which factors affect the timing of angiography in the evaluation of intracranial hemorrhage (ICH) depend on?What is the role of ECG in the diagnosis of intracranial hemorrhage (ICH)?Which diagnostic procedures may be performed in the evaluation of suspected intracranial hemorrhage (ICH)?Which histologic findings are characteristic of intracranial hemorrhage (ICH)?What are the grades of intracranial hemorrhage (ICH)?What is the focus of medical therapy for intracranial hemorrhage (ICH)?What is the initial treatment of intracranial hemorrhage (ICH)?What are the surgical options for the treatment of intracranial hemorrhage (ICH)?Which specialists should be consulted in the management of intracranial hemorrhage (ICH)?What are the nutritional interventions for intracranial hemorrhage (ICH)?What activity modifications are needed during treatment of intracranial hemorrhage (ICH)?What is the role of antihypertensive agents in the treatment of intracranial hemorrhage (ICH)?What is the role of acetaminophen in the treatment of intracranial hemorrhage (ICH)?What is the role of anticonvulsants in the treatment of intracranial hemorrhage (ICH)?What is the role of statins in the treatment of intracranial hemorrhage (ICH)?Which medications in the drug class Antacids are used in the treatment of Intracranial Hemorrhage?Which medications in the drug class Antidotes are used in the treatment of Intracranial Hemorrhage?Which medications in the drug class Anticonvulsants are used in the treatment of Intracranial Hemorrhage?Which medications in the drug class Antipyretics, analgesics are used in the treatment of Intracranial Hemorrhage?Which medications in the drug class Osmotic diuretics are used in the treatment of Intracranial Hemorrhage?Which medications in the drug class Antihypertensive agents are used in the treatment of Intracranial Hemorrhage?What long-term care is needed following treatment of intracranial hemorrhage (ICH)?What is included in the ICU care of intracranial hemorrhage (ICH)?Which medications are used for the treatment of intracranial hemorrhage (ICH)?When is patient transfer indicated in cases of intracranial hemorrhage (ICH)?How is intracranial hemorrhage (ICH) prevented?What are the possible complications of intracranial hemorrhage (ICH)?What is the prognosis of intracranial hemorrhage (ICH)?What information about intracranial hemorrhage (ICH) should patients receive?
David S Liebeskind, MD, FAAN, FAHA, FANA, Professor of Neurology and Director, Neurovascular Imaging Research Core, Director, Vascular Neurology Residency Program, Department of Neurology, University of California, Los Angeles, David Geffen School of Medicine; Director, UCLA Outpatient Stroke and Neurovascular Programs; Director, UCLA Cerebral Blood Flow Laboratory; Associate Neurology Director, UCLA Stroke Center
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Howard S Kirshner, MD, Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center
Disclosure: Nothing to disclose.
Chief Editor
Helmi L Lutsep, MD, Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, OHSU Stroke Center
Disclosure: Medscape Neurology Editorial Advisory Board for: Stroke Adjudication Committee, CREST2; Physician Advisory Board for Coherex Medical; National Leader and Steering Committee Clinical Trial, Bristol Myers Squibb; Consultant, Abbott Vascular, Inc. .
Additional Contributors
Jeffrey L Saver, MD, FAHA, FAAN, Professor of Neurology, Director, UCLA Stroke Center, University of California, Los Angeles, David Geffen School of Medicine
Disclosure: Received the university of california regents receive funds for consulting services on clinical trial design provided to covidien, stryker, and lundbeck. from University of California for consulting.
Intracranial hemorrhage. CT scan of right frontal intracerebral hemorrhage complicating thrombolysis of an ischemic stroke.
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.
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.
Intracranial hemorrhage. CT scan of right frontal intracerebral hemorrhage complicating thrombolysis of an ischemic stroke.
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.
This MRI reveals petechial intracerebral hemorrhage (ICH) due to cerebral venous thrombosis.
This CT scan and MRI revealed midbrain intracerebral hemorrhage (ICH) and intraventricular hemorrhage (IVH) associated with a cavernous angioma.
This MRI reveals hemorrhagic transformation of an ischemic infarct.
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
Grade
Hemorrhage Location
I
Subependymal hemorrhage
II
Intraventricular hemorrhage without ventriculomegaly
III
Intraventricular hemorrhage with ventriculomegaly
IV
Intraventricular hemorrhage with parenchymal hemorrhage