The Changing Magnetic Resonance Imaging Appearance Of Haemorrhage - Essay Example

MRES7013
a. Characteristics of blood
They do it by membrane proteins called hemoglobin, which binds or releases oxygen, depending on the concentration of the gas in the tissue. Thus, it is oxygenated in the lungs, and de-oxygenated once it passes through tissues (Guyton and Hall, 2006 p. 78).

b. Causes and effects of brain hemorrhage
Because of its liquid nature, it is able to seep through spaces once a vascular injury occurs. We usually see it as bruising of the skin, when trauma causes breakage in the thin-walled capillaries in the dermis. The bruising then recede with time, and the skin goes back to its previous appearance as if nothing happened. The same may not be applicable to other organs, more notably the brain. Although there is no obvious bruising similar to that seen on the skin, brain hemorrhages present with more serious signs of paralysis or changes in the sensorium, as caused by the ischemia and neuronal death of the area in the brain that should have been perfused by the injured vessel. Soon, ischemia of some brain tissue results in irreversible neurologic dysfunction. Prompt management is thus needed before neurologic defects become permanent (Kumar et al., 2010, p. 41).

c. Different stages of a hematoma
The age of hemorrhage is important because it determines the management of intracranial hemorrhage, as will be discussed later. The stages of hematoma are based on the form of hemoglobin in RBCs. Initially, during the hyper-acute phase or hours after the development of the lesion, the hematoma is made up of a liquid suspension of intact RBCs containing oxy- or deoxyhemoglobin. If the blood came from an arterial source, which is the case in most non-traumatic etiologies such as aneurysms, approximately 95% of hemoglobin molecules are oxygenated. Later, water is resorbed by the brain tissue, resulting in a solidified aggregation of RBCs. As the blood ages further, the hemoglobin denatures from oxy- or deoxy- to met-hemoglobin. This transformation is dependent on the oxidation of ferrous (Fe+2) heme iron contained by oxy- and deoxyhemoglobin to ferric (Fe+3) state, turning the protein into methemoglobin. After which, met-hemoglobin becomes she microsomes. When RBCs are lysed, Hemi chromes are broken down into heme iron and globins. Phagocytosis of these organic molecules by macrophages and glial cells results in protein-bound ferritin or water-insoluble hemosiderin(Nitz, et al., 2010, p. 75).

The necrosis of intracranial hematoma thus may thus result in cavitation.
Still, it should be noted that hemorrhages cause heterogeneous signal intensity. Thus, in determining the age of hematoma, it is beneficial to get both T1- and T2-weighted images. Based on Table 1, hemorrhages that are hypo-dense in T2-weighted MRI can be old hemorrhage, containing ferritin and/or hemosiderin, sub-acute hemorrhage, with predominantly intracellular methemoglobin, or acute hemorrhage, containing oxy- and deoxy-hemoglobin. However, sub-acute hemorrhage can also produce a hyper-intense lesion in T2-weighted MRI. Thus, to confirm the true age of the hemorrhage, we can obtain a T1-weighted MRI. Although the information about the hemorrhage obtained from this sequence is relatively limited, since the hematoma is usually hypo- or iso-dense, sub-acute hemorrhages are distinctly hyper-dense. Thus, a finding of hyper-dense hematoma in T1-weighted MRI is definitive for sub-acute hemorrhage. Aside from sub-acute hemorrhage, hyper-acute and chronic hematomas also have distinct MRI imaging. The hours-old hemorrhages are hyper-dense in TW-weighted imaging, while they are hypo-dense in T1-weighted imaging, because of the longer T1 times of water. Since MRI imaging is highly dependent on water in the early stages of hemorrhage, it is more advantageous to use Computer Tomography. On the other hand, chronic hematomas in T2-weighted imaging, as seen in Figure 1, have a characteristic hypo-dense ring surrounding the lesion. This is the hemosiderin membrane, which is prone to susceptibility effects of MRI (Nitz, et al., 2010, p. 94).

The evaluation, as well as the appearance of hemorrhage on MRI, mainly relies on the imaging parameters or sequence and the hematoma age.