Hemorrhage

10.1055/b-0034-102658

Hemorrhage

Parenchymal Hemorrhage

Hemorrhage has a specific but varied appearance on MR, dependent on time frame ( Fig. 1.40 ). The appearance is much more straightforward on CT. In normotensive young adults, vascular malformations are the most common cause of spontaneous hemorrhage. In adults, parenchymal hemorrhage is commonly due to hypertension ( Fig. 1.41 ), whereas subarachnoid hemorrhage is commonly due to rupture of an intracranial aneurysm. Typical locations for hypertensive hemorrhage include, in order of decreasing frequency, the basal ganglia (in particular the putamen), thalamus, pons ( Fig. 1.42 ), and cerebellar hemisphere. The descriptions of the appearance of hemorrhage in the literature are predominantly for parenchymal bleeds. To some extent, the appearance of subarachnoid hemorrhage is similar.

**Fig. 1.41** Hypertensive hemorrhage. A large acute parenchymal hematoma is seen on the initial CT in this patient (left upper image), with its epicenter in the right putamen. There has also been extravasation of blood into the ventricular system, with hemorrhage seen in the frontal horns, third ventricle, and atria of the lateral ventricles. On the follow-up CT 3 weeks later, the hematoma is smaller and is in transition from hyperdense to isodense to brain. On the MR obtained after an additional 3 weeks, the hematoma is high signal intensity on both T2- and T1-weighted scans (consistent with methemoglobin), with a hemosiderin rim seen on the T2-weighted scan and a thin peripheral rim of enhancement (*black arrow*) post-contrast. Both are characteristic features on MR in a subacute hematoma, with the enhancement blending into the margin of the high signal intensity hemorrhage.

**Fig. 1.42** Acute pontine hemorrhage. A large acute hemorrhage is seen centrally in the pons on axial unenhanced and sagittal enhanced CT. A small amount of hemorrhage is also seen in the fourth ventricle posteriorly, which is compressed due to mass effect. The pons and cerebellum, considered together, are the third most common site for hypertensive hemorrhage, after the putamen/external capsule (first) and the thalamus (second). This known hypertensive patient presented in hypertensive crisis.

Hyperacute hemorrhage on CT is of moderate density, rapidly increasing further in density (attenuation) over the first few hours due to clot formation and retraction. After a few days, in the subacute time frame, a progressive loss in attenuation begins. By 1 to 4 weeks, a hematoma will be isodense to brain, and in the chronic phase may appear hypodense.

The subsequent description of hemorrhage on MR is for field strengths of 1.5T and above, covering the vast majority of clinical systems today. Magnetic susceptibility effects, which cause decreased signal intensity depending on the time frame of the hemorrhage, are much less evident at lower field strengths. On MR, hemorrhage follows a regular well-defined temporal progression of changes in signal intensity ( Fig. 1.43 ).

**Fig. 1.43** Parenchymal hemorrhage on MR, the spectrum of signal intensity appearance. Initially, but for a very short time, a parenchymal hemorrhage contains oxygenated hemoglobin and is seen as a fluid collection, with slight hyperintensity on a T2-weighted scan. A large, basal ganglia, hyperacute hemorrhage (*black asterisk*) illustrates this appearance. There is a small amount of associated vasogenic edema and marked mass effect upon the right lateral ventricle. In the next patient, FLAIR scans are shown both on presentation and long term follow-up. This large, acute, left external capsule hematoma evolves from a fluid collection containing deoxyhemoglobin (*white asterisk*, with low signal intensity on T2-weighted scans), to a hemosiderin lined cleft (also low signal intensity). Note the associated vasogenic edema and mass effect in the acute stage. The third patient illustrates a subacute, extracellular methemoglobin hematoma, with high signal intensity on both T2- and T1-weighted scans, in the left parietal region. Note the peripheral hemosiderin rim, with low signal intensity, already present on the T2-weighted scan. The fourth patient illustrates on an unenhanced T1-weighted scan a methemoglobin hematoma in the right occipital lobe. This case emphasizes the importance of looking for the cause of a hemorrhage, as the post-contrast scan reveals the associated enhancing metastasis (*black arrows*).

Oxyhemoglobin (hyperacute) progresses to deoxyhemoglobin (acute), to intracellular methemoglobin (early subacute), then extracellular methemoglobin (late subacute), and eventually to hemosiderin (chronic). Oxyhemoglobin (hyperacute hemorrhage) has the signal intensity of fluid, high on T2- and low on T1-weighted scans. This imaging appearance is relatively nonspecific. Within hours, however, deoxyhemoglobin (acute hemorrhage) is evident with distinctive low signal intensity on T2-weighted scans. Deoxyhemoglobin does not have a unique appearance on T1-weighted scans, on which it appears isointense to mildly hypointense. Methemoglobin (subacute hemorrhage) has distinctive high signal intensity on T1-weighted scans, and bleeds can be further subdivided temporally into intracellular and extracellular methemoglobin. Initially, in the intracellular phase, blood will be high signal intensity on a T1-weighted scan and low signal intensity on a T2-weighted scan (the latter due to a susceptibility effect). With red blood cell lysis, methemoglobin becomes extra-cellular in location, with distinctive high signal intensity on both T1- and T2-weighted scans ( Fig. 1.44 ).

**Fig. 1.44** Parenchymal hemorrhage, involving the globus pallidus and putamen (the lentiform nucleus). High signal intensity on both T1- and T2-weighted scans is consistent with extracellular methemoglobin, in this late subacute hypertensive hemorrhage. An additional characteristic finding is the faint hemosiderin rim, with low signal intensity on the T2-weighted scan.

With time, methemoglobin is converted into hemosiderin (and to a lesser degree ferritin), with chronic hemorrhage thus exhibiting pronounced low signal intensity on T2-weighted scans again due to susceptibility effects. The appearance of a chronic parenchymal hemorrhage on MR also depends on whether the central fluid collection is resorbed or not. If resorbed, a hemosiderin cleft will be left. If not resorbed, there will be a central fluid collection with high signal intensity on both T1- and T2-weighted scans, surrounded by a hemosiderin rim. With the passage of years, the fluid collection may change in appearance on T1-weighted scans from high to low signal intensity. It is important to note that the evolution of parenchymal hemorrhage on MR does not always follow the characteristic pattern described. Additional factors can be very important, including dilution, clotting, and hematocrit. One key to the recognition of parenchymal hemorrhage, not discussed in detail, is the presence of edema surrounding the hematoma, which is seen in the hyperacute, acute, and early subacute stages.

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