Laboratory Studies
See the list below:
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Complete blood count (CBC) with platelets: Monitor for infection and assess hematocrit and platelet count to identify hemorrhagic risk and complications.
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Prothrombin time (PT)/activated partial thromboplastin time (aPTT): Identify a coagulopathy.
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Serum chemistries including electrolytes and osmolarity: Assess for metabolic derangements, such as hyponatremia, and monitor osmolarity for guidance of osmotic diuresis.
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Toxicology screen and serum alcohol level if illicit drug use or excessive alcohol intake is suspected: Identify exogenous toxins that can cause intracerebral hemorrhage.
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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 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:
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Lumbar puncture in the setting of IVH may reveal xanthochromia and a biochemical profile similar to that observed in subarachnoid hemorrhage.
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Ventriculostomy allows for external ventricular drainage in patients with intraventricular extension of blood products. Intraventricular administration of thrombolytics may assist clot removal.
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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:
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Gross examination reveals focal accumulation of blood with adjacent destruction of parenchyma.
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Microscopically, bleeding sites appear as round collections of platelets surrounded by fibrin.
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Charcot-Bouchard microaneurysms may be seen at bifurcations of distal lateral lenticulostriate vessels in hypertensive intracerebral hemorrhage.
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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 |
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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.
Tables
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 |
