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Figure 34-20 An unenhanced CT scan showing the typical picture of a massive primary (hypertensive) hemorrhage in the basal ganglia The third ventricle and ipsilateral lateral ventricle are compressed and displaced by the expanding mass (12 h after onset of stroke)

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tions In the rst hours and days following the hemorrhage, a limited amount of edema accumulates around the clot and adds to the mass effect Hydrocephalus may occur as a result of bleeding into the ventricular system or from compression of the third ventricle Extravasated blood undergoes a predictable series of changes At rst uid, it clots within hours Before the clot forms, red cells may settle in the dependent part of the hematoma and form a meniscus with the plasma above; this is particularly prone to occur in cases of anticoagulant-induced hemorrhage A uid- uid level is then observed on scans ( hematocrit effect ) Only masses of red blood cells (RBCs) and proteins are found within the hematoma; rarely one sees a few remnants of destroyed brain tissue The hematoma is surrounded by petechial hemorrhages from torn arterioles and venules Within a few days, hemoglobin products, mainly hemosiderin and hematoidin, begin to appear The hemosiderin forms within histiocytes that have phagocytized RBCs and takes the form of ferritin granules, which stain positively for iron As oxyhemoglobin is liberated from the RBCs and becomes deoxygenated, methemoglobin is formed This begins within a few days and imparts a brownish hue to the periphery of the clot Phagocytosis of RBCs begins within 24 h, and hemosiderin is rst observed around the margins of the clot in 5 to 6 days The clot changes color gradually, over a few weeks, from dark red to pale red, and the border of golden-brown hemosiderin widens The edema disappears over many days or weeks In 2 to 3 months, larger clots are lled with a chrome-colored mush, which is slowly absorbed, leaving a smooth-walled cavity (slit hemorrhage) or a yellow-brown scar The iron pigment (hematin) becomes dispersed and studs adjacent astrocytes and neurons It may persist well beyond the border of the hemorrhage for years In CT scans, fresh blood is visualized as a white mass as soon as it is shed The mass effect and the surrounding extruded serum and edema are hypodense After 2 to 3 weeks, the surrounding edema begins to recede and the density of the hematoma decreases, rst at the periphery Gradually the clot becomes isodense with brain There may be a ring of enhancement from the hemosiderin lled macrophages and the reacting cells forming the capsule of the hemorrhage By MRI, either in conventional T1- or T2weighted images, the hemorrhage is not easily visible in the 2 or 3 days after bleeding, since oxyhemoglobin is diamagnetic or, at most, is slightly hypointense, so that only the mass effect is evident After several days the surrounding edema is hyperintense in T2weighted images As deoxyhemoglobin and methemoglobin form, the hematoma signal becomes bright on T1-weighted images and dark on T2 As the hematoma becomes subacute, the dark images gradually brighten When methemoglobin disappears and only hemosiderin remains, the entire remaining mass is hypodense on T2weighted images, as are the surrounding deposits of iron MR images that display areas of magnetic susceptibility will show hemorrhages earlier and detect remnants of deposited hemosiderin even years afterwards Hemorrhages may be described as massive, moderate, small, slit, and petechial Massive refers to hemorrhages several centimeters in diameter; small applies to those 1 to 2 cm in diameter and less than 20 mL in volume; a moderate-sized hemorrhage, of course, falls between these two, both in diameter and in volume Slit refers to an old collapsed hypertensive or traumatic hemorrhage that lies just beneath the cortex Pathogenesis The hypertensive vascular lesion that leads to arterial rupture in some cases appears to arise from an arterial wall.

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