Subdural hematoma

Subdural hematoma is a volumetric accumulation of blood, located between the solid and arachnoid medullary membranes and causing compression of the brain.

Isolated subdural hematomas account for approximately 2/5 of the total number of intracranial hemorrhages and occupy the first place among various species of hematomas. Among the victims with craniocerebral trauma, an acute subdural hematoma is 1-5%, reaching 9-22% with severe craniocerebral trauma. Subdural hematomas predominate in men compared with women (3: 1), they are met in all age categories, but more often in individuals over 40 years old.

[1], [2], [3], [4], [5],

Epidemiology

The vast majority of subdural hematomas are formed as a result of craniocerebral trauma. Much less often they arise in the vascular pathology of the brain (for example, hypertension, arterial aneurysms, arterio-venous malformations, etc.), and in some cases are the result of taking anticoagulants. Isolated subdural hematomas account for approximately 2/5 of the total number of intracranial hemorrhages and occupy the first place among various species of hematomas. Among the victims with craniocerebral trauma, an acute subdural hematoma is 1-5%, reaching 9-22% with severe craniocerebral trauma. Subdural hematomas predominate in men compared with women (3: 1), they are met in all age categories, but more often in individuals over 40 years old.

[6], [7], [8], [9], [10], [11], [12]

Causes of the subdural hematoma

The vast majority of subdural hematomas are formed as a result of craniocerebral trauma. Much less often they arise in the vascular pathology of the brain (for example, hypertension, arterial aneurysms, arterio-venous malformations, etc.), and in some cases are the result of taking anticoagulants.

[13], [14], [15]

Pathogenesis

Subdural hematomas develop with a head injury of varying severity. For acute subdural hematomas, a severe craniocerebral injury is more common, and for subacute and (especially) chronic hematomas - a relatively minor trauma. In contrast to epidural subdural hematomas occur not only on the side of the application of the traumatic agent, but also on the opposite side (approximately at the same frequency).

The mechanisms of subdural hematoma formation are different. In homolateral lesions, it is to a certain extent similar to the formation of epidural hematomas, that is, a traumatic agent with a small application area affects the motionless or inactive head, causing a local brain injury and rupture of the pial or cortical vessels in the area of trauma.

The formation of subdural hematomas, the contralateral site of application of the traumatic agent, is usually caused by a displacement of the brain that occurs when the head is in a relatively fast motion, a massive motionless or inactive object (falling from a relatively high altitude, from moving vehicles to pavement, collision of motor vehicles, motorcycles, falling backwards, etc.). This breaks the so-called bridge veins that flow into the upper sagittal sinus.

The development of subdural hematomas is also possible in the absence of a direct application of a traumatic agent to the head. A sudden change in the speed or direction of movement (when a sudden stop of a fast moving vehicle, falling from height to toe, buttocks, etc.) can also cause a shift in the brain hemispheres and breaks in the corresponding veins.

In addition, subdural hematomas on the opposite side can occur when a traumatic agent with a wide application area is exposed to a fixed head, when there is not so much a local deformation of the skull as a displacement of the brain, often with a rupture of veins flowing into the sagittal sinus (impact by a log falling an object, a snow block, a side of a motor vehicle, etc.). Often different mechanisms participate in the formation of subdural hematomas, which explains the significant frequency of their bilateral arrangement.

In some cases, subdural hematomas are formed due to direct injury of the venous sinuses, in violation of the integrity of the dura mater with the rupture of its vessels, as well as with damage to the cortical arteries.

In the development of subacute and (especially) chronic subdural hematomas, secondary hemorrhages, which occur as a result of vascular dysfunction under the influence of dystrophic, angioedema and angioedrotic factors, also play an important role.

[16], [17], [18]

Symptoms of the subdural hematoma

Symptoms of subdural hematomas are extremely variable. Along with their volume, the source of bleeding, the rate of formation, localization, distribution, and other factors, this is due to heavy concomitant brain damage more frequent than with epidural hematomas; Often (in connection with the mechanism of a counter-attack) they are two-sided.

The clinical picture consists of cerebral, local and secondary stem symptoms, which is caused by compression and dislocation of the brain with the development of intracranial hypertension. Typically, there is a so-called "light" interval - time after injury, when clinical manifestations of subdural hematoma are absent. The duration of the "light" gap (unfolded or erased) with subdural hematomas varies very widely - from several minutes and hours (with acute development) to several days (with subacute development). In chronic course this interval can reach several weeks, months and even years. In such cases, the clinical manifestations of the hematoma can be triggered by a variety of factors: additional trauma, fluctuations in blood pressure, etc. With accompanying brain contusions, a "light" gap is often absent. With subdural hematomas brighter than with epidural, there is a waveform and a gradual change in the state of consciousness. However, sometimes the patients suddenly fall into a coma, as with epidural hematomas.

Thus, the three-phase nature of the disorders of consciousness (primary loss of consciousness after trauma, its restoration for a certain period and subsequent re-shutdown), which is often described when characterizing the clinical course of subdural hematoma, may be absent.

In contrast to epidural hematomas, in which disorders of consciousness proceed mainly through the stem type, subdural hematomas, especially in subacute and chronic hematomas, are often noted for the disintegration of consciousness by the cortical type with the development of aminic, onyroid, deliriform-like conditions, memory disorders with features of the Korsakov syndrome, as well as "frontal psyche" with a decrease in criticism to his condition, aspontaneity, euphoria, ridiculous behavior, violation of control over the functions of pelvic organs.

In the clinical picture of subdural hematomas, psychomotor agitation is often noted. With subdural hematomas, epileptic seizures occur somewhat more often than with epidural. Most generalized convulsive paroxysms predominate.

Headache in patients with contact with subdural hematoma is almost a constant symptom. Along with cephalalgia, which has a shelling shade (irradiation of pain in the eyeballs, occiput, soreness in eye movements, photophobia, etc.), and objectified local soreness with percussion of the skull with subdural hematomas, and diffuse hypertensive headaches, accompanied by a feeling of "bursting" of the head. The period of headache intensification with subdural hematoma is often accompanied by vomiting.

Approximately half of the observations with subdural hematomas register a bradycardia. With subdural hematomas, in contrast to epidural, congestive phenomena on the fundus are a more frequent component of the compression syndrome. In patients with chronic hematomas, it is possible to identify stagnant discs with reduced visual acuity and elements of optic disc atrophy. It should be noted that in connection with severe concomitant brain contusions, subdural hematomas, especially acute ones, are often accompanied by stem disorders in the form of respiratory disorders, arterial hypertension or hypotension, early hyperthermia, diffuse changes in muscle tone and reflex sphere.

For subdural hematomas, in contrast to epidural, the predominance of general cerebral symptoms over a relatively common focal is more characteristic. However, concomitant bruises, as well as dislocation phenomena, sometimes cause the presence in the clinical picture of the disease of complex relationships of different groups of symptoms.

Among focal features with subdural hematomas, the most important role is played by unilateral mydriasis with a decrease or loss of the pupil's response to light. Mydrias homolateral to subdural hematoma is observed in half of the observations (and in acute subdural hematomas - in 2/3 of cases), which significantly exceeds the number of similar findings with epidural hematomas. The dilatation of the pupil on the side opposite to the hematoma is noted much less often, it is due to a bruise of the opposite hemisphere or infringement of the opposite hematoma of the brain stem in the aperture of the cerebellum whine. With acute subdural hematoma, the limiting dilatation of the homolateral pupil predominates, with the loss of its reaction to light. With subacute and chronic subdural hematomas, mydriasis is more often mild and dynamic, without photoreaction. Often the change in the diameter of the pupil is accompanied by the ptosis of the upper eyelid on the same side, as well as the limitation of the mobility of the eyeball, which may indicate the craniobasal root genesis of the oculomotor pathology.

Pyramidal hemisindrom in acute subdural hematoma, in contrast to epidural, is inferior to mydriasis for diagnostic significance. With subacute and chronic subdural hematoma, the lateral role of pyramidal symptomatology increases. If pyramidal hemisindrom reaches the degree of deep paresis or paralysis, it is more often due to concomitant brain contusion. When subdural hematomas appear in a "pure form", the pyramidal hemisindrom is usually characterized by anisoreflexia, a slight increase in tone and a moderate decrease in force in the contralateral hematoma s extremities. The deficiency of the VII cranial nerve with subdural hematomas usually has a facial shade.

With subdural hematomas, the pyramidal hemisindrom is more often than epidural, homolateral or bilateral due to concomitant bruising or dislocation of the brain. The differentiation of the cause is facilitated by a rapid significant decrease in dislocation hemiparesis during the refraction of the trunk infringement and the comparative stability of the hemisyndrome due to brain contusion. It should also be remembered that the bilaterality of pyramidal and other focal symptoms may be due to the bilateral location of subdural hematomas.

With subdural hematomas, irritation symptoms in the form of focal seizures, as a rule, appear on the opposite side of the body.

When localizing the subdural hematoma over the dominant hemisphere, verbal disturbances, often sensory ones, are often detected.

Sensitivity disorders in frequency are much inferior to pyramidal symptoms, but still with subdural hematomas they occur more often than with epidural, characterized not only by hypalgesia, but also by disorders of epicritic sensitivities. The specific gravity of extrapyramidal symptoms in subdural hematomas, especially chronic ones, is comparatively large. Discover plastic changes in muscle tone, general stiffness and slowness of movements, reflexes of oral automatism and a grasping reflex.

Forms

The opinion of the relatively slow development of subdural hematomas, compared with epidural, for a long time prevailed in the literature. At present, it has been established that acute subdural hematomas are often not inferior to epidural by their rapid development rate. Subdural hematomas downstream divide into acute, subacute and chronic. To acute carry hematomas, in which compression of the brain is clinically manifested in 1-e-3 days after traumatic brain injury, to subacute - on the 4-10th day, and to chronic subdural hematomas - manifesting in 2 weeks or more after injury. Non-invasive imaging methods have shown that these terms are very conventional, nevertheless the division into acute, subacute and chronic subdural hematomas retains its clinical significance.

[19], [20]

Acute subdural hematoma

An acute subdural hematoma in approximately half of the observations is manifested by a pattern of compression of the brain in the first 12 hours after trauma. It is necessary to distinguish 3 basic variants of development of a clinical picture of acute subdural hematomas.

[21], [22], [23], [24], [25]

Classic Edition

The classical variant is rarely met. It is characterized by a three-phase change in the state of consciousness (primary loss at the time of injury, unfolded "light" gap and secondary shutdown of consciousness).

At the time of craniocerebral trauma, which is relatively mild (brain contusion of mild or moderate degree), they note a brief loss of consciousness, during the recovery of which only mild stunning or its elements are observed.

During the light period, lasting from 10-20 minutes to several hours, occasionally 1-2 days, patients complain of a headache, nausea, dizziness, amnesia appears. With the adequacy of behavior and orientation in the surrounding environment, rapid exhaustion and slowing of intellectual-mnestic processes are revealed. Focal neurological symptoms in the period of light interval, if present, it is usually soft and diffuse.

In the future there is a deepening of stunning with the appearance of increased drowsiness or psychomotor agitation. The patients become inadequate, the headache sharply increases, there is a repeated vomiting. More clearly manifested focal symptomatology in the form of homolateral mydriasis, contralateral pyramidal insufficiency and sensitivity disorders, as well as other disorders of the relatively large cortical zone. Along with the deenergization of consciousness, a secondary stem syndrome with bradycardia, an increase in blood pressure, a change in the rhythm of breathing, bilateral vestibuloglazodvigatelnymi and pyramidal disorders, tonic convulsions develops.

[26], [27]

Option with an erased "light" gap

This option is often met. Subdural hematoma is usually combined with severe bruises of the brain. Primary loss of consciousness often reaches a degree of coma. Focal and stem symptomatology caused by primary damage to brain substance is expressed. In the future, a partial restoration of consciousness is noted until deafening, usually deep. During this period, the disorders of vital functions are somewhat reduced. The victim, who emerges from a coma, is sometimes noted psychomotor agitation, the search for an antialgic position. Often it is possible to identify a headache, expressed meningeal symptoms. After this or that period (from several minutes to 1-2 days), the erased "light" interval is replaced by a repeated switch-off of consciousness to soporus or coma with deepening of disturbances of vital functions, development of vestibular-oculomotor disorders and decerebral rigidity. As the onset of coma, the focal symptomatology determined by the action of the hematoma is aggravated, in particular, the unilateral mydriasis appears or becomes extreme, hemiparesis increases, epileptic seizures can sometimes develop.

Option without a "light" gap

The variant without a "light" gap is often met, usually with multiple severe brain injuries. Sopor (and often coma) from the moment of injury to surgery or the death of the patient does not undergo any significant positive dynamics.

Subacute subdural hematoma

Subacute subdural hematoma in contrast to acute hematoma is characterized by a relatively slow development of the compression syndrome and a significantly longer duration of the "light" gap. In this regard, it is often regarded as a concussion or bruise of the brain, and sometimes as a nontraumatic disease (influenza, meningitis, spontaneous subarachnoid disease, alcohol intoxication, etc.). Despite the often early formation of subacute subdural hematomas, their threatening clinical manifestation usually occurs 3 days after the trauma. The severity of the injury with it is often inferior to that of acute infection. In most cases, they occur with relatively light head injuries.

Three-phase in the change of consciousness is much more characteristic for subacute subdural hematoma, than for acute. The duration of primary loss of consciousness in the majority of victims ranges from a few minutes to an hour. The subsequent "light" gap can last up to 2 weeks, manifesting in a more typically developed version.

During the "light" gap, the victims are in clear consciousness or there are only elements of stunning. Vital functions do not suffer, and if they mark increase of arterial pressure and a bradycardia, then very insignificant. Neurological symptoms are often minimal, sometimes it is manifested by any one symptom.

The dynamics of secondary deenergia in the affected is variable.

At times, there are wavy oscillations of consciousness within the limits of stunning of various degrees, and sometimes also of a sopor. In other cases, secondary deenergizing of consciousness develops progressively: more often - gradually over hours and days, less often - with a stormy entrance to a coma. At the same time, among the victims with subdural hematomas, there are those who, with the growth of other symptoms of brain compression, persistently have a disturbance of consciousness within moderate stunning.

With subacute subdural hematomas, changes in the psyche are possible in the form of reducing criticism to one's condition, disorientation in place and time, euphoria, inadequacy of behavior, and apatiko-abulic phenomena.

Subacute subdural hematoma is often manifested by psychomotor agitation, provoked by headaches. In connection with the accessibility of patients, contact is more pronounced than with acute hematomas, an increasing headache appears, playing the role of the main symptom. Along with vomiting, bradycardia, hypertension, stagnant phenomena on the fundus are an important component of the diagnosis of compression syndrome. They tend to initially develop on the side of the location of the hematoma.

Stem symptoms with subordinal subdural hematoma are much less common than in acute, and almost always they are secondary in origin - compression. Among the lateral features, homolateral mydriasis and contralateral pyramidal insufficiency are most significant, they appear or grow during the course of observation. It should be borne in mind that in the phase of gross clinical decompensation, the pupil expansion may appear on the opposite hematoma side. Pyramidal hemisindrom in subacute subdural hematomas is usually expressed moderately and much less frequently than with acute hematomas, it is bilateral. Due to the patient's access to contact, it is almost always possible to detect focal hemispheric symptoms, even if it is mild or selectively represented by sensitivity disorders, visual fields, and disorders of higher cortical functions. When localized with hematomas over the dominant hemisphere, aphasic disturbances occur in half of the cases. Part of the patients develop focal cramps on the opposite side of the body.

Chronic subdural hematomas

To chronic carry subdural hematomas, if they are detected or removed after 14 days or more after a traumatic brain injury. However, their main distinguishing feature is not the period of verification in itself, but the formation of a capsule that gives a certain autonomy in coexistence with the brain and determines all subsequent clinical and pathophysiological dynamics.

[28], [29], [30], [31], [32], [33], [34], [35]

Diagnostics of the subdural hematoma

When subdural hematoma is recognized, one often has to overcome the difficulties caused by the variety of forms of clinical manifestation and course. In cases where subdural hematoma is not accompanied by severe concomitant brain damage, its diagnosis is based on a three-phase change in consciousness: a primary loss at the time of injury, a "light" gap, a repeated de-activation of consciousness due to compression of the brain.

If, with a relatively slow development of cerebral compression in the clinical picture, along with other symptoms, diffuse, bursting headaches, changes in the "frontal" type of mind and psychomotor agitation are revealed, there are grounds to assume the development of a subdural hematoma. The mechanism of damage may be inclined to this conclusion: a blow to the head with a blunt object (more often in the occipital, frontal or sagittal area), a blow to the head about a massive object or a sudden change in the speed of movement, resulting not so much in local impression as in displacement of the brain in the cranial cavity with the possibility of rupture of the bridge veins and the formation of subdural hematoma on the side opposite the place of application of the traumatic agent.

When recognizing subdural hematomas, one should take into account the frequent predominance of cerebral symptoms over focal, although these relationships are variable. The nature of focal symptoms with isolated subdural hematoma (their comparative softness, prevalence, and often bilaterality) can contribute to diagnosis. The assumption of subdural hematoma may be indirectly supported by the characteristics of hemispheric symptoms. Detection of sensitivity disorders is more typical for subdural hematomas. Craniobasal symptoms (and among them, primarily, homolateral mydriasis) are more often expressed than in epidural hematomas.

Diagnosis of subdural hematomas is especially difficult in victims with severe concomitant brain damage, when the "light" gap is absent or is erased. In patients who are in a sore or coma, a bradycardia, an increase in blood pressure, epileptic seizures are alarming regarding the possibility of compression of the brain. The emergence or tendency to deepen the respiratory distress, hyperthermia, reflex vision upward, decerebral rigidity, bilateral pathological signs and other stem pathology reinforce the assumption of compression of the brain with hematoma.

Detection of traces of trauma in the occipital, frontal or sagittal region (especially if the mechanism of damage is known), clinical (bleeding, liquorrhea from the nose, ears) and radiographic signs of fracture of the base of the skull allow tentatively to bend to the diagnosis of subdural hematoma. For its lateralization, the side of mydriasis should first of all be taken into account.

With subdural hematoma, in contrast to epidural, craniographic findings are not so characteristic and important for local diagnosis. In acute subdural hematoma, fractures of the base of the skull are often detected, usually extending to the middle and posterior, and less often to the anterior cranial fossa. There are combinations of damage to the bones of the base and the cranial vault. Isolated fractures of individual bones of the cranial vault are less common. If a severe subdural hematoma reveals damage to the bones of the arch. Then usually they are extensive. It should be borne in mind that, unlike epidural, with subdural hematomas, bone injuries are often found on the side opposite to the hematoma. In general, bone injuries are absent in a third of the victims with acute subdural hematomas and in 2/3 - with subacute hematomas.

Linear Echo can promote recognition of subdural hematoma, revealing lateralization of a traumatic substrate that compresses the brain.

At a cerebral angiography for subdural hematomas on direct pictures the symptom of "border" - sickle-shaped avascular zone in the form of a strip of various width is typical. "Kayma" more or less evenly displaces the vascular pattern of the squeezed hemisphere from the cranial vault from the sagittal suture to the base of the skull, which can be seen in the photographs in the frontal plane. It should be borne in mind that the "border" symptom is often more clearly expressed in the capillary or venous phase. The displacement of the anterior cerebral artery is also characteristic. Lateral angiograms with convectional subdural hematomas are less demonstrative. However, with subdural hematomas located in the interhemispheric fissure, lateral shots are also convincing: they detect pitting down the pericalliform artery.

A decisive role in the recognition of subdural hematoma and in the refinement of its localization, size, influence on the brain is played by CT and MRI.

Acute subdural hematoma on a computer tomogram is usually characterized by a sickle-like zone of homogeneous increase in density.

In most cases, subdural hematoma extends to the entire hemisphere or most of it. Often subdural hematomas can be bilateral, and also spread to the interhemispheric fissure and to the nasal mucosa. The absorption coefficients of acute epidural hematoma are higher than the density of subdural hematoma due to mixing of the latter with liquor and / or detritus. For this reason, the inner edge of the acute and subacute subdural hematoma. Repeating the relief of the surface of the subject brain, can have a fuzzy outline. Atypical localization of subdural hematomas - in the interhemispheric fissure, above or below the mound, on the basis of the middle cranial fossa - is a much more rare finding than the convectional fossa.

Over time, as a result of liquefaction of the contents of the hematoma, the decomposition of blood pigments, a gradual decrease in its density occurs, making it difficult to diagnose, especially when the absorption coefficients of the altered blood and the surrounding cerebral matter become the same. Subdural hematomas become identifiable within 1-6 weeks. The diagnosis is then based on secondary symptoms, such as compression or medial displacement of convective subarachnoid fissures, narrowing of the homolateral lateral ventricle and dislocation of the median structures. After the isodensic phase, a phase of reduced density follows, in which the absorption coefficient of the outflowing blood approaches the density of the liquor. With subdural hematoma, the phenomenon of sedimentation is encountered: the lower part of the hematoma as a result of the deposition of high-density blood elements is hyperdense, and the upper part is iso- or hypodensitive.

With subdural hematomas, the signs of a decrease in intracranial reserve spaces predominate on the tomogram: narrowing of the ventricular system, compression of the convectional subarachnoid cracks, moderate or severe deformation of the basal cisterns. A significant displacement of the median structures is accompanied by the development of dislocation hydrocephalus, which is combined with the compression of subarachnoid spaces. When localized hematoma in the posterior cranial fossa develops acute occlusive hydrocephalus.

After removal of the subdural hematoma, the position and size of the ventricular system, the brain base cisterns and subarachnoid cracks are normalized.

On MRI images with acute subdural hematomas, low contrast of the image is possible due to the absence of methemoglobin. In 30% of cases, chronic subdural hematomas look hypo- or isodensic on tomograms in T1 mode, but almost all of them are characterized by increased signal intensity in T2 mode. In cases of repeated hemorrhages in subacute or chronic subdural hematomas, heterogeneity of their structure is noted. Capsule of chronic hematomas, as a rule, intensively accumulates a contrast substance, which allows them to differentiate from gigrom and arachnoid cysts. MRI provides an opportunity to successfully detect subdural hematomas that are isodensial with CT. MRI also has advantages with planar subdural hematomas, especially if they enter the interhemispheric cleft or spread basally.

[36], [37]

Treatment of the subdural hematoma

Treatment of subdural hematomas can be conservative and surgical. The choice of tactics depends on the volume of the hematoma, the phase of its development and the condition of the patient.

Surgical treatment of subdural hematomas

Absolute indications for surgical treatment are as follows.

• Acute subdural hematoma, which causes compression and displacement of the brain. The operation should be carried out as soon as possible after the injury. The earlier the subdural hematoma was removed, the better the outcome.
• Subacute subdural hematoma with increased focal symptomatology and / or signs of intracranial hypertension.

In other cases, the decision on surgery is made on the basis of a set of clinical and radiological data.

Procedure for acute subdural hematoma

A complete craniotomy is usually indicated for the complete removal of acute subdural hematoma and reliable hemostasis. The size and location of osteoplastic trepanation depends on the extent of subdural hematoma and the localization of concomitant parenchymal lesions. When a subdural hematoma is combined with contusions of the pole-basal parts of the frontal and temporal lobes, the lower boundary of the trepanation window should reach the base of the skull, and the other boundaries correspond to the dimensions and localization of the subdural hematoma. Removing the hematoma can stop bleeding if it continues from the brain clefts. With a rapidly increasing dislocation of the brain, craniotomy should begin with the application of a milling hole through which a part of the subdural hematoma can be quickly aspirated and thereby reduce the degree of compression of the brain. Then the remaining stages of craniotomy should be performed quickly. However, there was no significant difference in the comparison of mortality in the groups of patients where the "quick" removal of subdural hematoma through the trephination hole was originally used, and in the group of patients where bone-plastic trepanation was performed immediately.

With subdural hematoma, a tense, cyanotic, non-pulsating or weakly pulsing hard dura mater is thrust into the trepanation window.

In the presence of concomitant pole-basal bruises of the frontal and temporal lobes on the side of the subdural hematoma, it is preferable to open the dura mater in an arch-shaped base to the baseline, since in these cases, the source of bleeding is most often the cortical vessels in the area of the contusion foci. With convectional-parasagittal localization of subdural hematoma, dissection of the dura mater can be made by the base to the superior sagittal sinus.

In the presence of intracranial hematomas and foci of crushing, the swabs of blood and cerebral detritus are removed by irrigation and gentle aspiration. Hemostasis is performed by bipolar coagulation, haemostatic sponge or fibrin-thrombin adhesive compositions. After suturing the dura mater or her plasty, the bone flap can be laid in place and sealed. If the brain material prolapses into a trephination defect, the bone flap is removed and preserved, that is, the operation is completed by decompressive trepanation of the skull.

To errors of surgical tactics is the removal of subdural hematoma through a small resection window without the closure of the dura mater. This really allows you to quickly remove the main part of subdural hematoma, but it is fraught with prolapse of the brain substance in the bone window with compression of convective veins, violation of venous outflow and increased edema of the brain. In addition, in conditions of cerebral edema after removal of subdural hematoma through a small trepanation window, it is not possible to audit the source of bleeding and perform reliable hemostasis.

Drug treatment of subdural hematomas

Victims with subdural hematoma in clear consciousness with a thickness of the hematoma of less than 10 mm, displacement of the median structures not more than 3 mm, without compression of basal cisterns usually do not need surgical intervention.

In patients who are in a sore or coma, with stable neurological status, absence of signs of compression of the brainstem, intracranial pressure not exceeding 25 mm Hg, and the volume of subdural hematoma of not more than 40 ml, conservative therapy with dynamic clinical CT and MRI monitoring.

Resorption of the plane subdural hematoma usually occurs within a month. In some cases, a capsule forms around the hematoma and the hematoma is transformed into a chronic one. If, during dynamic observation, the gradual transformation of subdural hematoma into a chronic one is accompanied by deterioration of the patient's condition or an increase in headaches, the appearance of stagnation on the fundus, there is a need for surgical intervention by closed external drainage.

[38], [39], [40], [41], [42]

Forecast

An acute subdural hematoma is often less favorable in prognosis than an acute epidural hematoma. This is due to the fact that subdural hematomas usually occur with primarily severe brain damage, and are also accompanied by a rapid rate of brain displacement and infringement of stem structures. Therefore, despite the introduction of modern diagnostic methods, acute subdural hematomas register a relatively high lethality, and among the survivors of the disease, profound disability is significant.

The rapid detection and removal of subdural hematoma is also important for the prognosis. The outcomes of surgical treatment are much better for the victims, operated in the first 4-6 hours after the trauma, in comparison with the group of patients operated at a later date. The volume of subdural hematoma, as well as the age of the affected, increases with an increasing negative role in outcomes.

Unfavorable results with subdural hematoma are caused, in addition, by the development of intracranial hypertension and cerebral ischemia. Recent studies have shown that with the rapid elimination of cerebral compression, these ischemic disorders can be reversible. Important prognostic factors include brain edema, which often progresses after the removal of acute subdural hematoma.

[43], [44], [45], [46], [47], [48], [49]