Key Words
Brain, Parenchymal, Hemorrhage, Hematoma
Introduction
Magnetic resonance imaging (MRI) can differentiate between acute, subacute, and chronic hemorrhage because of its sensitivity and specificity to hemoglobin degradation products. Therefore the imaging interpreter is, with proper knowledge, able to estimate the age of a brain parenchymal hematoma. The blood products in a hematoma evolve through a predictable variation in hemoglobin oxygenation states and hemoglobin byproducts. This predictable pattern of hematoma evolution over time leads to a specific pattern of changing signal intensities on conventional MRI.
There are limitations to the accuracy of hematoma age interpretation. Several direct and indirect factors, including the operating field strength of the magnet, the mode of image acquisition, and a wide range of biologic factors particular to the patient, may affect the imaging evolution of a parenchymal hematoma. Despite substantial variability, it is generally accepted that five stages of parenchymal hemorrhage can be distinguished by MRI. A basic understanding of the biochemical evolution of brain parenchymal hemorrhage and magnetic properties that affect MRI signal are essential for interpretation.
Temporal Evolution: Overview
A well-described pathophysiologic process of evolution and resorption for parenchymal hemorrhage involves five distinct phases ( Fig. 1.1 ).
With this knowledge, the imaging interpreter can often identify the relative age of a brain parenchymal hematoma based on the T1 and T2 characteristics of the collection. However, it is important to realize that hematoma evolution is a fluid process (without static or punctuated steps). Therefore, stages of hemorrhage commonly coexist within the same hematoma because hemoglobin degradation proceeds at variable rates in the center versus the periphery of a single hematoma cavity. By convention, the most mature form of hemoglobin present defines the stage of hematoma evolution ( Fig. 1.2 ).
Temporal Evolution: in Greater Depth
Extravascular blood in a hemorrhagic collection remains as oxyhemoglobin for 2 to 3 hours. The immediate activation of the clotting cascade begins the process of clot formation. Deoxyhemoglobin begins to form at the periphery of the hematoma. Eventually, the failure of metabolic pathways preventing oxidation of heme iron results in conversion of hemoglobin to methemoglobin.
In the hyperacute stage, parenchymal hemorrhage is a liquid almost completely composed of intracellular oxygenated hemoglobin. Over the course of a few hours, a heterogeneous blood clot forms within the hematoma cavity, composed of red blood cells, platelets, and serum. In the acute phase, intracellular hemoglobin becomes deoxygenated. Vasogenic edema develops in the surrounding brain parenchyma. In the early subacute phase, deoxyhemoglobin is gradually converted to intracellular methemoglobin. Then, in the late subacute phase, lysis of red blood cells leads to the release of methemoglobin into the extracellular space. During this time, the surrounding vasogenic edema slowly begins to decrease and the clot slowly retracts. In the chronic stage, macrophages and glial cells phagocytose the hematoma, leading to intracellular ferritin and hemosiderin. Eventually, the hematoma resolves and leaves a posthemorrhagic cavity with hemosiderin-stained walls.
It is critical to realize that Fig. 1.1 represents a simplified version of events designed to aid in memory. As noted previously, hematoma evolution is a fluid process (without static or punctuated steps). Stages of hemorrhage commonly coexist within the same hematoma because hemoglobin degradation proceeds at variable rates in the center versus the periphery of a single hematoma cavity ( Figs. 1.3 and 1.4 ).
