Intracranial hemorrhage is a form of stroke (see Chap. 426). Compared to ischemic stroke, patients with intracranial hemorrhage are more likely to present with headache; however, brain imaging is required to distinguish these entities. CT imaging of the head is highly sensitive and specific for intracranial hemorrhage and determines the location(s) of bleeding. Hemorrhages are classified by their location and the underlying vascular pathology. Hemorrhage directly into the brain parenchyma, also known as intracerebral hemorrhage (ICH), and arteriovenous malformations (AVMs) of the brain will be considered here. Other categories of hemorrhage include bleeding into subdural and epidural spaces, usually caused by trauma (Chap 443), and subarachnoid hemorrhage due to trauma or the rupture of an intracranial aneurysm (Chap. 429).
Intracranial hemorrhage is often identified on noncontrast CT imaging of the brain during the acute evaluation of stroke. Because CT is more widely available and may be logistically easier to perform than MRI, CT imaging is generally the preferred method for acute stroke evaluation (Fig. 428-1). The location of the hemorrhage narrows the differential diagnosis to a few entities. Table 428-1 lists the causes and anatomic spaces involved in hemorrhages.
Hypertensive hemorrhage. Transaxial noncontrast computed tomography scan through the region of the basal ganglia reveals a hematoma involving the left putamen in a patient with rapidly progressive onset of right hemiparesis.
++ Table Graphic Jump Location TABLE 428-1Causes of Intracranial Hemorrhage ||Download (.pdf) TABLE 428-1 Causes of Intracranial Hemorrhage
|CAUSE ||LOCATION ||COMMENTS |
|Head trauma ||Intraparenchymal: frontal lobes, anterior temporal lobes; subarachnoid; extra-axial (subdural, epidural) ||Coup and contrecoup injury during brain deceleration |
|Hypertensive hemorrhage ||Putamen, globus pallidus, thalamus, cerebellar hemisphere, pons ||Chronic hypertension produces hemorrhage from small (~30–100 μm) vessels in these regions |
|Transformation of prior ischemic infarction ||Basal ganglion, subcortical regions, lobar ||Occurs in 1–6% of ischemic strokes with predilection for large hemispheric infarctions |
|Metastatic brain tumor ||Lobar ||Lung, choriocarcinoma, melanoma, renal cell carcinoma, thyroid, atrial myxoma |
|Coagulopathy ||Any ||Risk for ongoing hematoma expansion |
|Drug ||Any, lobar, subarachnoid ||Cocaine, amphetamine |
|Arteriovenous malformation ||Lobar, intraventricular, subarachnoid ||Risk is ~2–3% per year for bleeding if previously unruptured |
|Aneurysm ||Subarachnoid, intraparenchymal, rarely subdural ||Mycotic and nonmycotic forms of aneurysms |
|Amyloid angiopathy ||Lobar ||Degenerative disease of intracranial vessels; associated with dementia, rare in patients <60 years |
|Cavernous angioma ||Intraparenchymal ||Multiple cavernous angiomas linked to mutations in KRIT1, CCM2, and PDCD10 genes |
|Dural arteriovenous fistula ||Lobar, subarachnoid ||Produces bleeding by venous hypertension |
|Dural sinus thrombosis ||Along sagittal sinus, posterior temporal/inferior parietal ||Sagittal sinus thrombosis can cause hemispheric parasagittal hemorrhage with edema; vein of Labbé occlusion from transverse sinus occlusion produces posterior temporal/inferior parietal hemorrhage |
|Capillary telangiectasias ||Usually brainstem ||Rare cause of hemorrhage |
Close attention should be paid to airway management ...