In approximate order of frequency, the most common sites of a cerebral hemorrhage are (1) the putamen and adjacent internal capsule (50 percent); (2) the central white matter of the temporal, parietal, or frontal lobes (lobar hemorrhages, not strictly associated with hypertension); (3) the thalamus; (4) one or the other cerebellar hemisphere; and (5) the pons. The vessel that ruptures, giving rise to the hemorrhage, is usually a small penetrating artery that originates from a larger trunk. Approximately 2 percent of primary hemorrhages are multiple. Multiple, nearly simultaneous intracerebral hemorrhages raise the possibility of amyloid angiopathy or a bleeding diathesis (see further on) but may occur when one conventional hypertensive intracerebral hemorrhage causes hypertension, which in turn leads to one or more additional hemorrhages.
The extravasation of blood into the substance of the brain forms a roughly circular or oval mass that disrupts the tissue and can grow in volume if the bleeding continues. Adjacent brain tissue is distorted and compressed. If the hemorrhage is large, midline structures are displaced to the opposite side of the cranium and the reticular activating and respiratory centers are compromised, leading to coma and death in the manner described in Chap. 16. It has been long known that both the size and the location of the clot determine the degree of secondary brainstem compression and this was confirmed by Andrew and associates. Rupture or seepage of blood into the ventricular system or rarely to the surface subarachnoid space may occur, and the CSF becomes bloody in these cases. In the first hours and days following the hemorrhage, varying degrees of edema evolve around the clot and add to the mass effect. Hydrocephalus may occur as a result of bleeding into the ventricular system or from compression of the third ventricle.
The extravasated blood undergoes a predictable series of changes. At first fluid, the collection becomes a clot within hours. Before the clot forms, red cells 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. The resultant fluid–fluid level can be observed on CT and MRI (“hematocrit effect”). Hematomas, when examined in autopsy material, contain only masses of red blood cells and proteins; rarely one sees a few remnants of destroyed brain tissue. The hematoma is often 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 red blood cells (RBCs) and takes the form of ferritin granules that stain positively for iron. As oxyhemoglobin is liberated from the RBCs and becomes deoxygenated, methemoglobin appears. This begins within a few days and imparts a brownish hue to the periphery of the clot. Phagocytosis of red cells begins within 24 h, and hemosiderin is first 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 filled with a chrome-colored thick fluid, which is slowly absorbed, leaving a smooth-walled cavity or a yellow-brown scar. The iron pigment (hematin) becomes dispersed and studs adjacent astrocytes and neurons and may persist well beyond the border of the hemorrhage for years.