NeuroradiologyHaematoma
collection of blood within body tissues or cavities. In this volume of the encyclopaedia the term is used to include intracranial blood collections.
A haematoma is the inevitable consequence of the rupture of a blood vessel, either artery, vein or capillary. The immediate consequence of the rupture is a haemorrhage, that is, a dynamic event characterized by the outflowing of blood from the vessel. The collection of blood outside the vessel forms the haematoma and haemodynamically this is a static event. If the haemorrhage occurs within a fluid, such as CSF, the blood cannot collect and remains dispersed; for this reason the term used to describe the situation is subarachnoid haemorrhage. The two terms then, haemorrhage and haematoma, should not be used as synonyms.
Intracranial haematomas can be classified according to location, age and aetiology. The location of a haematoma may be, from peripheral to central: epidural, subdural, intracerebral or intraventricular (see haematoma epidural, haematoma subdural, intraventricular haemorrhage). Despite what has been said above, a subarachnoid haematoma is possible if, during subarachnoid haemorrhage, blood pools and collects within a cistern; for this reason "sylvian haematomas" are a possibility.
Further subdivisions relate to cerebral lobes or parts (frontal, parietal haematoma etc.; pontine, cerebellar, cortical, subcortical, deep, basal ganglia, thalamic haematoma etc.). The most common, classical intracerebral haematoma results from rupture of the peripheral lenticulostriate arteries in the region of the external capsule. The haemorrhage strips the soft tissue under the cortex and may rupture into the lateral ventricle (see intraventricular haemorrhage). The typical clinical picture is of a sudden fulminating headache, hemiplegia and impairment of consciousness deepening into coma.
Blood within the brain tissue may be the result of infarction (haemorrhagic infarction) (Fig.1); in this case, however, the blood usually oozes outside the ischaemic vessel walls and is not a homogeneous blood collection as in haematomas. An infarction becomes haemorrhagic after an interval that may be a few hours or several days, and sometimes following revascularization of the infarcted area, when an embolus migrates or dissolves from a main arterial trunk.
With regard to age, the criteria are relatively arbitrary and take into account both clinical and imaging factors. From a clinical point of view an epidural or subdural haematoma is acute within the first 1 to 24 hours; an intracerebral haematoma is considered acute within the first few days. Subacute haematomas are usually between a week and a fortnight old; after this time they are considered to be chronic. With regard to imaging, the density or signal characteristics of the haematoma examined with CT or MR respectively vary with the age of the haematoma.
As for aetiology, apart from trauma (see traumatic intracranial haemorrhage), the main causes of intracranial haemorrhage and haematoma are: hypertension, aneurysm rupture, arteriovenous malformation rupture, infarction cerebral, coagulopathies and blood dyscrasias, amyloid angiopathy, drug abuse. Less common causes are venous infarction, fungal or bacterial vasculitis with pseudoaneurysm formation (see mycotic aneurysm in bacterial endocarditis), encephalitis and tumours. tumours.
The clinical presentation of a haematoma varies according to size, location and aetiology. In general the presentation is acute and is that of a stroke.
Imaging
On CT the imaging characteristics of the haematoma in different phases are not determined mainly by iron, as originally thought, but by the globin component of haemoglobin and its high proton density.The typical hyperdense appearance of the fresh clot in the acute phase is due to the fact that the haematocrit of the acute clot is around 90% and that globin is then its main component. If blood accumulates very rapidly semiliquid clots may result in the initial phase and hence hypodense areas within the hyperdensity of the haematoma will be observed.
Coagulation and haematological disorders may lead to unusual appearances of the acute haematoma due to abnormal clotting: isodense haematomas will be observed with a low haematocrit fluid–fluid levels within a clot in the case of coagulopathies.The attenuation of haematomas decreases with time, from the periphery to the centre. Around the second week the haematoma becomes isodense and then rapidly hypodense, as it becomes chronic. Contrast enhancement may be seen at the periphery of the clot due to blood–brain barrier disruption.
While an acute haematoma may produce a space-occupying effect owing to its size, and subsequent peripheral oedema, chronic haematoma is usually a smaller posthaemorrhagic porencephalic cavity, possibly associated with atrophic dilatation of the adjacent ventricle or subarachnoid space. A haematoma is definitely stable around 3 to 6 months. Some small posthaemorrhagic cavities, particularly in the basal ganglia, may be indistinguishable at CT, but not at MR, from small postischaemic lesions.
MR imaging
The MR appearance of a haematoma at different stages is less straightforward and varies according to physical parameters of the machine and the sequences employed and to the intrinsic composition of the haematoma itself, mainly concerning oxidation states of haemoglobin and macroscopic structure of the clot (protein concentration, clot hydration, red blood cell morphology). The most important factor that determines the signal intensity of blood is related to the magnetic properties of iron in the various haemorrhage breakdown products (Fig.2).
In the hyperacute phase oxyhaemoglobin is still present within the red cells and being diamagnetic does not affect the MR signal; for the first few hours the clot is isointense on T1-weighted and hyperintense on T2-weighted images due to the water content of the clot. Desaturation from oxyhaemoglobin to deoxyhaemoglobin produces a progressive T2 shortening, particularly when deoxyhaemoglobin becomes entirely extracellular within the first few days. In the early phases, intracellular deoxyhaemoglobin does not influence T1 significantly. In subacute phases, after 35 days methaemoglobin develops and persists for months. The haematoma will then become progressively hyperintense on both T1- and T2-weighted images.
In the chronic phases residual haemosiderin will be responsible for low signal intensity at the rim of the porencephalic cavity which will display a CSF-like signal.
GS