MRI can detect underlying causes of secondary hemorrhages, such as vascular malformations, including cavernomas, tumors, and cerebral vein thrombosis.Įxtravasation of contrast in CT angiogram (CTA) indicates ongoing bleeding associated with fatality. MRI can distinguish between the hemorrhagic transformation of infarct and primary hemorrhage. Gradient echo (GRE) imaging is as good as CT in detecting acute bleed. The paramagnetic properties of deoxyhemoglobin allow early detection of hemorrhage in MRI. The other poor prognostic factors are hematoma expansion, intraventricular hemorrhage, infra-tentorial location, and contrast extravasation on CT scan (spot sign). Intracerebral hemorrhage with a volume of more than 60 ml is associated with high mortality. C is the vertical height of the hematoma. The volume of the hematoma can be measured by the formula AxBxC/2, where A and B are the largest diameter and the diameter perpendicular to that. In the subacute phase, the hematoma may be isodense to brain tissue, and magnetic resonance imaging (MRI) may be necessary. These sequences are more sensitive than CT for identification of prior hemorrhage. However, gradient echo and T2* susceptibility-weighted magnetic resonance imaging (MRI) has the same sensitivity as CT to detect acute hemorrhage. Vasogenic edema around the hematoma may increase for up to 2 weeks. CT is considered the “gold standard” in detecting acute hemorrhage due to its sensitivity. The attenuation may be decreased in anemia and coagulopathy. The hemorrhage increases in attenuation from 30-60 Hounsfield units (HU) in the hyperacute phase to 80 to 100 HU over hours. Ĭomputerized tomography (CT) is usually the initial investigation. There is diffuse blood distribution in non-perimesencephalic SAH (NPM-SAH). Physical exertion, such as the Valsalva maneuver producing increased intrathoracic pressure, and elevated intracranial venous pressure, is a predisposing factor for perimesencephalic nonaneurysmal SAH (PM-SAH). In perimesencephalic SAH, bleeding is mainly in the interpeduncular cistern. Non-aneurysmal spontaneous subarachnoid hemorrhage may be either perimesencephalic or non-perimesencephalic SAH. Cerebellar hematoma produces hydrocephalus by compression of the fourth ventricle in the early stage. The factors causing deterioration in ICH are an expansion of hematoma, intraventricular hemorrhage, perihematomal edema, and inflammation. There is an area of hypoperfusion around the hematoma. The perihematomal edema increases within 24 hours, peaks around 5 to 6 days, and lasts up to 14 days. The enlargement of hematoma occurs in 3 hours in one-third of cases. Usually, the hematoma enlarges in 3 hours to 12 hours. Secondary injury is contributed to by inflammation, disruption of the blood-brain barrier (BBB), edema, overproduction of free radicals such as reactive oxygen species (ROS), glutamate-induced excitotoxicity, and release of hemoglobin and iron from the clot. The primary injury is due to the compression of brain tissue by the hematoma and an increase in the intracranial pressure(ICP). Thrombin activates microglia and causes inflammation and edema. This results in oligaemia, neuro-transmitter release, mitochondrial dysfunction, and cellular swelling. The hematoma disrupts the neurons and glia. The common sites of the bleed are the basal ganglia (50%), cerebral lobes (10% to 20%), the thalamus (15%), pons and the brain stem (10% to 20%), and the cerebellum(10%)(fig.1,2,3).
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