The chronic phase of a hematoma is arbitrarily defined to begin at about 2 months after the initial hemorrhage. By this time the original blood-containing cavity has largely collapsed, surrounding reactive edema has disappeared, RBCs have completely lysed, hemoglobin species have undergone degradation, and heme iron has been released and deposited in the surrounding tissues. The center and periphery of chronic hematomas have different pathological and imaging characteristics and must therefore be considered separately.
Chronic Hematoma Center
Diffusion characteristics also reflect high free water content, with only minimally restricted diffusion noted that depends on the protein content of the fluid. Thus the center of old hematomas will be dark on DWI/Trace images and bright on ADC maps.
Ferritin and hemosiderin are superparamagnetic, with creating large microscopic susceptibility gradients in the areas where they accumulate. As water molecules diffuse through these gradients their resonance frequencies change with resultant T2/T2* dephasing.
The iron centers of ferritin and hemosiderin are sequestered and do not allow close approach of water for inner sphere relaxation. Hence only a minimal amount of T1 shortening occurs.
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The peripheral microstructure of chronic hematomas depends on their anatomic location and thus may vary across the body. For example, chronic subdural hematomas develop an organized fibrovascular neomembrane attaching to the inner surface of the dura and surrounding the clot. Multiple membranes may develop formed by proliferating fibroblasts and thin-walled capillaries at risk for rebleeding. The walls of chronic subdural hematomas may thus have a thick, lamellated appearance.
Allkemper T, Tombach B, Schwindt W, et al. Acute and subacute intracerebral hemorrhages: comparison of MR imaging at 1.5 and 3.0 T–initial experience. Radiology 2004; 232:874–81.
Bradley WG Jr. MR appearance of hemorrhage in the brain. Radiology 1993; 189:15-26.
Gomori JM, Grossman RI. Mechanisms responsible for the MR appearance and evolution of intracranial hemorrhage. Radiographics 1988; 8:427-440.
Wagner KR, Sharp FR, Ardizzone TD, et al. Heme and iron metabolism: role in cerebral hemorrhage. J Cerebral Blood Flow Metabolism 2003; 23:629-652.
What is ferritin? How is it different from hemosiderin?
What happens after the met-Hb stage and how do these later degradation products affect the MR signal?