Brain hematoma: causes, symptoms and treatment in an article by neurosurgeon Yakovlev D.V.

Other information about different types of diseases starting with the letter “V”: Vegetative state, Ventricular, Vestibular ataxia, Vestibular neuronitis, Vibration disease, Viral meningitis, Viral encephalitis, Temporal lobe epilepsy, Intracerebral hematoma, Intracranial tumors of the cerebral hemispheres, Intracranial hypertension, Inflammatory myopathy, Inflammatory polyneuropathy, Congenital myopathy, Congenital paramyotonia, Secondary parkinsonism

Intracerebral hematoma: concept

Intracerebral hematoma is a painful condition of the body, characterized by the accumulation of blood cells in the structures of the main organ, which causes compression, displacement and various types of damage to nearby tissue. The presented disease has such symptoms as: general cerebral and focal lesions that develop from the location of the injury and its size. To obtain detailed and detailed data about the disease being described, doctors resort to the use of computer equipment, magnetic resonance imaging and angiographic examination of cerebral vessels. A small hematoma can be treated conservatively, but in other situations, when the damage becomes significantly larger in diameter, this issue can only be resolved through surgery, by removal or aspiration.

Brain hematoma - symptoms and treatment

There are two types of treatment: conservative and surgical.

Conservative treatment

Methods of conservative (medicinal) treatment normalize the vital functions of the body:

maintain blood pressure at the required level: so that the blood supply to the brain is maintained, but the volume of the hematoma does not increase;
affect the blood coagulation system;
prevent and eliminate swelling;
strengthen the vascular wall.

This is an extremely important and responsible stage of treatment. All activities are carried out by a doctor, deeply analyzing the pathogenetic processes in the human body. Many methods are based on laboratory data. Conservative therapy cannot in any way be controlled or regulated by relatives or sympathizers due to their lack of this knowledge. For example, the decrease in blood pressure during antihypertensive therapy should not be sudden. It is reduced to a level that does not coincide with the norm for a healthy person. The pressure is maintained within certain limits: it should not be too high, but also too low. This reduces the risk of continued hemorrhage and maintains adequate blood supply to the brain to protect it from secondary damage due to oxygen deprivation.

Conservative methods are used for treatment in the following cases:

hematomas are small in size and do not exert significant pressure on the brain;
hematomas do not cause displacement of brain structures, severe depression of consciousness, and are accompanied by moderate neurological disorders.

Surgery

Surgical treatment consists of mechanical removal of the hematoma. As a result, the pressure of the hematoma on the brain stops.

Several methods of surgical removal of intracerebral hematomas are used:

The puncture method is pumping out the liquid part of the hematoma (aspiration) through the hole. However, it is impossible to remove the entire hematoma in this way, since it usually consists of 80% blood clots, and the liquid component is 20% or less. The method is used only in severe cases of the disease to save lives. If the patient’s condition does not improve after surgery, then radical removal methods are used.
The open method is a traditional method of removing a hematoma by creating a hole in the bone tissue of the skull (trepanation), dissecting a section of the brain (encephalotomy) and suctioning out both liquid blood and its clots. The method allows you to completely remove the hematoma. However, it is accompanied by additional surgical trauma to the brain, which leads to an increase in edema, increased displacement and deformation of brain structures and often causes repeated hemorrhage.
The endoscopic method is a promising technology for removing intracerebral hematomas. Combines the low invasiveness of the puncture method with the possibility of complete removal of the hematoma. But the method can only be used if the environment in the operation area is transparent. For example, if there is bleeding, surgery is difficult and often impossible.
Stereotactic method is carried out using special instruments immersed in the brain through a hole with a diameter of 5–10 mm. A special feature of the method is the transfer of hematoma coordinates using computed tomography or radiography. The technology reduced the mortality rate of deep hematomas by 22% compared to conservative treatment methods. However, in 10-16% of cases, repeated hemorrhages are possible in the first few days after surgery.
Neuronavigation method - neuronavigation systems are used: OrthicaI Tracking System "Radionics Inc" Compass Cygnus PFS System, "Compass" Vectorvision BrainLAB. The method determines the location of the hematoma with high accuracy. The technology is especially effective for lesions in functionally significant areas of the brain. Its widespread use is not yet possible due to the high cost of equipment and limited surgical experience among doctors [13].

The tactics of surgical intervention, its volume, measures to eliminate compression of the brain, timing of the operation and much more depend on the specific situation. The decision is made by a neurosurgeon based on the patient’s condition, laboratory data and CT/MRI images.

Useful facts

An intracerebral bruise may have a liquid texture or consist of coagulated blood. In certain situations, in addition, detritus may be present in the bruise in much smaller quantities. The total volume of liquid can reach 100 ml. The increase in the diameter of the hematoma continues for several hours after the onset of hemorrhage, and during a failure of the coagulation function much longer. After the formation of the lesion, the process of compression of adjacent tissues begins, which subsequently leads to necrosis.

In addition, the occurrence of such a phenomenon affects the increase in the level of intracranial pressure and becomes a source of swelling. It can cause displacement of certain structures and the formation of dislocation syndrome if the bruise is large. Bleeding can lead to a reflex spasm and the onset of ischemia, first affecting the nearby cavities. Ischemia is considered an additional damaging cause, which shapes the progression of abnormal deformations far beyond the boundaries of the formation. According to average statistical information, in almost 14% of cases there is a breakthrough into the ventricles and hemorrhage.

Types of brain hematomas

Cerebral hemorrhages are usually divided into the following types:

intraparenchymal;
subarachnoid;
subdural;
epidural;
intraventricular;
intratumoral.

Intraparenchymal hematomas. They develop against the background of hemorrhagic stroke and high blood pressure syndrome. Hemorrhagic hemorrhage is caused by rupture of modified vessels during a critical increase in blood pressure. Hemorrhagic strokes account for 10-18% of all deaths. Intraparenchymal hemorrhages can affect any part of the brain, but most often the basal ganglia, thalamus, and cerebellum.

Subarachnoid hemorrhages. Formed between the arachnoid and pia mater. Most often, a hematoma occurs after injury followed by rupture of a saccular aneurysm. The patient suddenly begins to have a severe headache, develops photophobia, nausea, and vomiting. Diagnosis of hematoma on MRI shows blood clots, vasospasm, volume of spilled blood, early signs of ischemic hemorrhage.

Subdural hematomas. They become the result of venous rupture that develops after injury, treatment with anticoagulants, or decompression after bypass surgery of the ventricles of the brain. On MRI, the subdural hematoma has a crescent shape.

Epidural hemorrhages. Most often, they occur as a result of injury. A hematoma forms between the inner bone plate and the dura mater of the brain, usually over the area of the skull fracture. On MRI, the hemorrhage has a biconvex shape.

Intraventricular hematomas. They are divided into primary and secondary. Primary ones occur with tumors of intraventricular localization, aneurysms and subependymal cavernous angiomas. Secondary - after a breakthrough of blood into the ventricular cavity, with intrapanerchymal hemorrhages.

Intratumoral hematomas. They are rarely recorded, most often with pituitary apoplexy. The patient complains of headaches, vomiting, and blurred vision. The images may show hemorrhages in secondary brain metastases.

Mechanism of occurrence

The described disease can manifest itself due to the following factors:

Rupture of vascular walls due to injury (for example, head injury, concussion, etc.).
Post-traumatic diapedesis at the point of contusion.
Deformation of an aneurysm or arterial-venous malformation due to tumor formation (stroke, hypertension, atherosclerosis, etc.).
Changes in the rheological functions of blood vessels during hemophilia, leukemia, painful conditions of the liver and others.

Diagnosis of hematoma on MRI

In case of subdural hematomas on MRI images in the most acute stage (up to 12 hours), the T1-WI signal can vary from iso- to hyperintense; in acute cases (from 12 hours to 2 days) - a hypointense impulse. The T2-WI signal in the acute period is moderate hyperintense, in the acute stage it is hypointense. The FLAIR signal is expressed as hyperintensity of the signal to the cerebrospinal fluid. Signal strength may vary relative to effects at T1 and T2. The shortened T2 time is caused by intracellular methemoglobin. Acute hematomas are isointense to the cerebrospinal fluid.

The T2 GRE pulse after the acute period has a hypointense expression. DWI has a nonspecific heterogeneous response. DWI indicators exclude extracerebral empyema and differentiate hemorrhages, having a noticeable hyperintense central signal. When a contrast agent is used, the post-contrast T1-weighted signal is determined. Contrasted displaced cortical veins are identified.

MRI produces variable SDH impulses. Repeated hemorrhages may develop. The images reveal elements of acute or chronic hemorrhage. SDH may be a signal of recurrent hemorrhage. Leakage of CSF into the SDH may be a consequence of rupture of the membranes made by the pia and arachnoid membranes. There is a transformation in signal intensity due to dilution of the blood by cerebrospinal fluid.

Types of intracerebral hematoma

In modern medicine, in particular in the field of neurology, several forms of the present disease are used, which can give an idea of its different characteristics. According to location, there are the following types: central, subcortical, cortico-subcortical, and formation of damage in the cerebellum. In addition, there are such types as:

Lobar.
Medial.
Lateral.
Mixed.

With different volumes of pathology, the following differences are present:

Small bruise - the size does not exceed three centimeters.
Medium - reaches 4.5 cm.
Large - more than 4.5 cm.

The classification of such injuries due to the phenomenon can be:

Post-traumatic form.
Hypertensive.
Aneurysmal.
Tumor, etc.

What is the manifestation of an intracerebral hematoma?

Typically, the described illness occurs with fairly pronounced symptoms of a general cerebral nature. When visiting the office of a specialist in the field of neurology, patients report dizziness, painful sensations of acute heaviness in the head area, attacks of nausea and gag reflexes. Almost 50% of cases manifest with disturbances of consciousness from stupor to coma. At some points, a sharp change in mood occurs and instead of a depressed state, a person begins to experience psychomotor activity. The formation of a hematoma can occur with the presence of an erased light space. Further patient complaints are directly dependent on the size and location.

Doctors list the following symptoms as the most common problems:

Disturbances in the functioning of the speech apparatus.
Malfunctions in the operation of numeric parameters.
Asymmetry of tendon movements of both limbs.
Seizures of a convulsive and epileptic nature.
Anisocoria.
Loss of vision.
Memory disorders and behavioral problems.
Dislocation syndrome.
Displacement of brain areas.
Uncontrolled eye orbital movement activity.
Difficulty with the breathing device.
Hearing loss.
Vestibular ataxia.
Strabismus.
Increased pressure and others.

Symptoms and clinical manifestations of intracerebral hematoma and bruises

As a rule, such pathologies are manifested by clinical symptoms that are characteristic of the picture of a general brain lesion. Most patients experience nausea, dizziness, severe headache, and vomiting that does not bring relief. People with such pathologies experience confusion, even stupor or even coma. In some cases, psychomotor agitation may have occurred before the onset of such lethargy and apathy. Further clinical signs of hematoma and bruise depend on the location of the pathological focus and the degree of brain damage. Patients may experience nystagmus, swallowing and breathing disorders, hearing loss, impaired coordination of movements and fine motor skills of the hands, strabismus, elevated body temperature, slow heartbeat, drooping eyelids and elevated blood pressure.

Diagnostic options

With the help of new-fangled clinical devices, doctors have a large number of opportunities to conduct research on patients with the presenting disease. Thanks to such devices, doctors can study not only the formation itself, but also understand what causes the development. The main technology used by specialists in the capital’s medical institutions is computed tomography. Often, on the images obtained, experts see the pathology in the form of a round or oval lesion. If deviations from the norm occurred due to damage, then, as a rule, uneven boundaries are visible in photographs.

In case of diameter reduction, magnetic resonance scanning is used. In some situations, this examination may give erroneous readings, which is why doctors prefer to use two tests simultaneously. At certain points, angiographic examination or MR angiography is performed to determine vascular disorders and the formation of aneurysms.

Magnetic resonance imaging (MRI) in St. Petersburg

The skull is a combination of several thin bones. Each of them has a three-layer structure - thick outer compact bone tissue - spongy dipdoid - thin inner compact bone tissue. The dura mater is tightly adjacent to the inner bone plate. Skull fractures occur as a result of a direct blow and usually at the site of impact. The brain can be damaged during a traumatic action, not necessarily in combination with a fracture of the skull bones and not necessarily at the site of application of external force. Bone fractures as such are not life-threatening, but they are often accompanied by intracranial changes - hemorrhages, cerebral edema and damage to the brain substance. A fracture can occur in any part of the skull, but the thinnest bones, such as the squama of the parietal and temporal bones, the sphenoid sinus and the wings of the sphenoid bone, are damaged more often than others. Approximately 10% of patients with TBI require neurodiagnostics and 1% require surgical treatment. Typically, the criteria for CT or MRI are less than 13 points on the Glasgow Coma Scale, headaches and vomiting, repeated vomiting, loss of consciousness (New Orleans criteria and Canadian criteria for CT), alcohol intoxication, and childhood.

Traumatic brain injuries (TBI) are either open or closed. With open TBI, there is a violation of the integrity of the bones of the skull and meninges.

Fractures of the skull bones can be linear, diastatic (along the suture), depressed or convex. The latter occur in children when the underlying membranes and substance of the brain are involved. In severe TBI, the incidence of calvarial fractures reaches 1.5-2.7%. Severe fractures are often combined with pneumocephalus, pass through the paranasal sinuses and are combined with damage to the soft tissues of the head. Linear fractures can be visualized already on topograms, which are used to select the area of interest during CT scanning. As healing progresses, the fracture line becomes more difficult to discern. Linear fractures in children heal in less than 3-6 months, while in adults it takes 2 to 3 years.

Damage in closed TBI can be local, diffuse and secondary. Local injuries in TBI include meningeal and intracerebral hemorrhage, contusion and direct damage to the brain stem, arteries, hypothalamus and (or) cranial nerves. Diffuse axonal damage does not directly correlate with the force of external impact and appears to be associated with rotational action. With diffuse axonal damage, hemorrhages and foci of necrosis are detected in the corpus callosum, posterior parts of the pons and, sometimes, in the deep parts of the brain. Secondary post-traumatic injuries include necrosis of the medial parts (parahippocampal) of the temporal lobe, local infarction due to arterial compression, infarction of the border zones and hypoxic changes due to general hypotension, diffuse ischemic necrosis due to intracranial hypertension, secondary hemorrhages in the trunk due to increased intracranial pressure and hernia through the tentorium of the cerebellum.

CT is most informative in the diagnosis of acute hemorrhages resulting from birth and postnatal injuries. After TBI, SAH, in contrast to aneurysm ruptures, are more often local. On CT, it is possible to clearly visualize blood accumulations in the interhemispheric fissure and in the adjacent sulci, due to which an increase in the density and thickness of the posterior parts of the falx process is determined. On CT they appear as a crescent-shaped, sometimes plano-convex or irregularly shaped band of altered density. HS in the acute stage is 3-5 times less common than SAH. HS usually extends over the entire hemisphere or most of it and has a crescent shape. Certain difficulties in differentiating meningeal hematomas are caused by contusions of the cerebral hemispheres, compressed by the hematoma, and therefore a subdural hematoma can have both a concave and convex edge. The change in the shape of the SG from crescent-shaped to biconvex is also associated with its increase as a result of repeated hemorrhages. Subdural blood collections, which are thick and localized in the area of the lateral fissure, are similar to an epidural hematoma. The shape and distribution of an epidural hematoma depends on the anatomical relationship of the skull bones and the dura mater, the location of its location and the volume of blood shed. CT scan reveals a biconvex, less often plano-convex, zone of altered density adjacent to the cranial vault. HS is limited in nature and is usually localized within 1-2 lobes.

Over time, there is a gradual decrease in the density of the hematoma, starting from 3-5 days after the injury. Chronic hematomas on CT may be characterized by low or mixed density.

CT scans do not show focal or diffuse changes in concussion. Contusion lesions, depending on the severity of destructive changes, cerebral edema and the amount of blood shed, may look like this:

In the form of a zone of reduced density, as a manifestation of local cerebral edema. This type of lesion does not exclude the presence of diapedetic hemorrhages;
In the form of a zone of reduced density, including small-point increases in density, corresponding to hemorrhages;
In the form of single or multiple round or oval foci of intense homogeneous increase in density up to 60-80HU (Fig.), which corresponds to hematomas in destructive foci.

Diffuse axonal damage to the brain is characterized by small (5-9 mm) foci of increased density, localized in the semioval centers of both hemispheres, the corpus callosum, subcortical nuclei and periventricular substance of the brain.

Intracerebral hematomas on CT are revealed as cloud-like zones of homogeneous intense increase in density of various sizes, with clearly defined edges, often with perifocal edema.

A diffuse increase in brain volume due to its edema is manifested by moderate or severe compression of either the ventricular system and subarachnoid spaces, not accompanied by gross focal brain lesions.

Typically, CT is used in the first 24 hours after injury, since it is faster than MRI, more accessible, less sensitive to motion artifacts, and is good at detecting hemorrhage and bone damage. However, in the first 3 hours, CT may underestimate the severity of brain damage. MRI of TBI shows evidence of injury at a very early stage, including the hyperacute stage of hemorrhage. In addition to standard T1- and T2-WI MRI of the brain in the acute period of injury, FLAIR MRI and diffusion-weighted MRI have proven themselves well. MRI of brain contusions is applicable already on the first day, but optimally on days 2-3, when the patient’s condition is no longer so critical. After 72 hours, MRI of the brain is preferable to CT, as it is more accurate in identifying hematomas, cortical contusions, as well as minor injuries - petechial hemorrhages, axonal and neuronal damage. Edema and displacement of the midline structures can lead to vascular compression, secondary ischemia, and infarctions, which are clearly detected by MRI. Brain contusion can result from direct trauma or from progressive damage. In the acute stage, CT is more sensitive to contusions than MRI, since MRI visualizes hemorrhage worse during this period. However, as the heme molecule transforms, MRI becomes more sensitive. MRI diagnosis of cerebral hemorrhages is the most important task of neuroimaging. Subdural hematomas are observed in 10-20% of patients with TBI and are accompanied by high (50-85%) mortality. In the subacute stage, subdural hematomas are clearly identified by MRI. Subarachnoid hemorrhage (SAH) is more common in children and the elderly. They are usually adjacent to the site of contusion. Epidural hematomas are observed in 1-4% of TBI cases and usually accompany skull fractures. Intraventricular hemorrhages reach 3% and are associated with high mortality. Diffuse edema, detected on MRI of the brain, can lead to herniation. The degree of longitudinal and transverse dislocation is determined by MRI. Based on the CT and MRI performed, as well as the clinical picture, the issue of emergency surgical intervention is decided. Fractures of the bones of the base of the skull can lead to pneumocephalus, which is equally clearly visible on CT and MRI of the brain. Foreign bodies are usually identified using CT, since the capabilities of MRI are very limited here. In case of injury, vascular damage may occur. MRA and CTA can help identify ruptures, dissections, and aneurysms. In severe TBI, diffuse axonal damage may be seen on MRI. It refers to pinpoint hemorrhages and lesions directly in the white matter of the tracts. Such lesions are typical on MRI of the brain at the border of white and gray matter, the corpus callosum, and the brain stem. The clinical course of the injury in such patients is more severe and mental disorders are common as a result. weighted MRI. Lesions in the corpus callosum. The lesions may be small and difficult to see on regular MRIs of the brain.

CT native slices. Double fracture of the occipital bone, fracture of the squama of the temporal bone and the apex of the pyramid. There is moderate narrowing of the lateral ventricles and subarachnoid spaces along the convexital surface. Diffuse moderate cerebral edema.

CT.
Epidural hematoma. MRI in St. Petersburg USA

What's the forecast?

The main reasons on which further prognosis of the patient’s condition depends include:

Volume and localization.
Age range of the patient.
The presence of concomitant abnormalities (high body weight, hypertensive diseases, diabetes mellitus, etc.).
Level and extent of disturbances of consciousness.
Combination of intracerebral formations with trauma to the membranes.
Timely seeking medical help.
Adequacy and qualifications of the doctor.

The most negative prognosis can be made in the presence of a breakthrough form of the disease. The main factors of death are swelling and dislocation of the brain. According to average statistical data, more than 10% of cases end in death after recurrence of hemorrhage, and 70% of patients are diagnosed with a disabling neurological deficit.