Научная статья на тему 'Clinical course of traumatic intracranial hematomas'

Clinical course of traumatic intracranial hematomas Текст научной статьи по специальности «Клиническая медицина»

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TRAUMATIC BRAIN INJURY / HEMATOMA / TREATMENT

Аннотация научной статьи по клинической медицине, автор научной работы — Hazratkulov Rustam Bafoevich

Studied the features of clinical course of 64 patients with traumatic intracranial hematoma in acute period. Were chosen 2 ways of clinical passing decompensate and sub compensated. Decompensate way of clinical passing marked at 71.0% of victims, when at the first hours after injury had been developed heavy, very heavy, and at one third of sick’s terminal state, depression of consciousness level 8 and less marks by Glasgow Coma Scale, (GCS), prevails rude dislocation syndrome. Subcompensated variant develops at 29.1%, state might be as satisfacted, as heavy with depression of consciousness level from 9 to 15 marks by GCS, during expressed cerebral and dislocation symptom otology, focal hemispheric neurological symptoms at half of patients.

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Текст научной работы на тему «Clinical course of traumatic intracranial hematomas»

Hazratkulov Rustam Bafoevich, Republican Scientific Practical Medical Center of Neurosurgery, Uzbekistan E-mail: arslanovazera@gmail.com

CLINICAL COURSE OF TRAUMATIC INTRACRANIAL HEMATOMAS

Abstract: Studied the features of clinical course of 64 patients with traumatic intracranial hematoma in acute period. Were chosen 2 ways of clinical passing - decompensate and sub compensated. Decompensate way of clinical passing marked at 71.0% of victims, when at the first hours after injury had been developed heavy, very heavy, and at one third of sick's terminal state, depression of consciousness level 8 and less marks by Glasgow Coma Scale, (GCS), prevails rude dislocation syndrome. Subcompensated variant develops at 29.1%, state might be as satisfacted, as heavy with depression of consciousness level from 9 to 15 marks by GCS, during expressed cerebral and dislocation symptom otology, focal hemispheric neurological symptoms at half of patients.

Keywords: traumatic brain injury, hematoma, treatment.

Trauma in the past and now days remains one of the ter of Neurosurgery. They were examined and treated.

main causes of mortality. It is the second leading cause of death after cardiovascular and oncology diseases. Epidemiological data shows that among different types of injuries craniocerebral trauma is one of the main causes of mortality and morbidity and significantly influence on decrease of population labor activity in the industrial countries [1, 2, 4, 9].

The incidence of craniocerebral trauma is 36-40% of all trauma cases [7, 8]. The majority ofvictims are people of working age. Among the causes of disability, the leading place is occupied by a severe craniocerebral injury (SCCT). It leads to irreversible health disorders in 2530% ofthe cases, and the lethality at it is - 68-70% [3, 11].

Serious craniocerebral trauma include now brain damage, which causes a violation of the patient's consciousness level in 3-8 points on the Glasgow coma scale (GCS), when assessing it not less than 6 hours after the injury, in conditions of correction of arterial hypotension, hypoxia and the absence of any intoxication and hypothermia [6, 10].

One type of T SCCT is traumatic intracranial hematomas of large volume. They range from 2% to 16.6% of the total CCT [5, 12].

The purpose of the study: to investigate the clinical course in patients with traumatic intracranial hematomas.

Materials and methods. 64 patients were hospitalized in the Republican Scientific Practical Medical Cen-

Among them men - 55 (85.9%), women - 9 (14.1%). All patients recieved urgent care. The majority of patients 48 (75.0%) were delivered in severe or extremely serious condition (the level of oppression on the Glasgow coma scale was 8 or less, 45 (70.3%), acute subdural hematomas. epidural hematomas were 14 (21.9%), and in 7.8% (5 patients) episubdural hematomas were detected.

All patients underwent a comprehensive examination: general and neurologic examination, craniography, ECHO-ES, CT or MRI of the brain. Consciousness was evaluated on the Glasgow coma scale: clear (GCS15 points), moderate stunning (13-14 points), deep stunning (11-12 points), sopor (9-10 points), moderate coma (7-8 points), deep coma (4-6 points), terminal coma (3 points). The task of CT and MRI was to determine the localization, type and volume of hematomas, the volume of foci of brain contusions and all foci of pathological density (hemoangiopathic posttraumatic ischemia, perifocal edema around the hematoma, limited and widespread foci of brain contusion, hygroma).

In patients, the volume of hematomas was 100-160 cm3 (average volume -130 cm3). In 75% of the affected patients, the volume of acute subdural hematoma is up to 150 cm3 (the average volume is 130 cm3). The volume of acute epidural hematoma in patients varied from 100 to 250 cm3 (the average size of the acute epidural hematoma was 120 cm3). The volume of episubdural hematoma

Section 5. Medicine

with an average value of130 cm3 did not exceed 180 cm3. In 4 (0,6%) patients bilateral hematomas were detected, their volume in the total exceeded 100 cm3.

Results and its discussion. Neurological symptoms were divided into cerebral, focal hemispheric and stem. Contraindication to the intervention was only an extremely serious condition of the patient, which required resuscitation (unstable hemodynamics, blood pressure below 80 mmHg). After stabilization of the condition, such patients were also operated. During the traumatic intracranial hematomas surgery, decompressive or osteoplastic craniotomy was performed.

The clinical picture with traumatic intracranial hematomas (TIH) of large volume already in the first hours significantly differed from the classical one. The so-called "light gap" in high-volume TIH was observed rarely in 7 (10,9%) patients. The majority of patients 48 (75,0%) who arrived from the scene were taken in a serious and extremely serious condition, in a coma. Three (0,5%) patients were affected in terminal condition (GCS - 3 points), 4 (0,6%) patients were delivered in extremely serious condition - 4 points according to GCS. Only in 2 (0,3%) patients with high-volume TIH, the level of consciousness during admission was determined by 15 points.

Of the 45 patients with acute subdural hematomas, 25 (39,0%) reported with an inhibition of consciousness of 8 or fewer points in the GCS, with epidural hematomas in 7 (50,0%), and of 5 patients with episubdural hematomas, there were 3 (60,0%)). Severe condition and expressed disorders of consciousness, observed in most cases in patients with high-volume TIH, were characteristic features in the clinical picture. Since most patients came in a coma, to identify verbal disorders, sensitive disorders were often not possible. Of all the victims with traumatic intracranial hematomas of large volume, hemispheric focal neurological symptoms were detected in 19 (29,7%). In the remaining patients, against the background of oppression of consciousness to the coma, clinical signs of dislocation took place. The more severe the condition of the victims, the less frequent and difficult it was to identify focal symptoms. Out of 48 patients admitted with depression of consciousness of 3-8 points, focal symptomatology was detected in 20 (21,7%), out of 13 patients admitted in the state of 9-11 points, local neurologic symptoms were noted in 5 (35,7%). Local neurologic symptoms were more common in acute epi-

dural hematomas 47,6% and less often with acute subdural hematomas - 24,2%. Less detectable focal symptomatology in patients with acute subdural hematomas is most likely due to the severity of their condition. As it was already shown, in the patients with acute subdural hematomas the condition was more severe. The absence of focal neurological symptoms is also attributed to the distinctive features of the clinical picture of traumatic intracranial hematomas of large volume. Lethality in the absence or presence in the clinical picture of traumatic intracranial hematomas of a large volume of local neurologic symptoms was 71,9%, respectively.

Symptoms ofbrain stem lesions in these patients testified to the induction of the brain in the stage of gross decompensation. Depending on the severity of the patients' condition, the clinical signs of brainstem lesions were manifested by a combination of symptoms, the most frequent of which were eyeballs (83%) mydriasis on the side of the hematoma (80%), bilateral pathological step reflexes (64%). Bilateral mydriasis was noted in 62% of patients admitted in terminal and extremely serious condition. Mortality among patients with a decompensated variant of the clinical course was 71.9% (46 patients out of 64 died).

Subcompensated variant of the clinical course. With this variant of the clinical course, the patients' condition was assessed as satisfactory (2 patients), moderate (5 patients) and severe (12 patients). The level of oppression of consciousness in these observables was estimated from 9 to 15 points according to the GCS. Even with oppression of consciousness to the level of sopor, respiratory disturbances and hemodynamics requiring urgent instrumental correction in patients of this variant of the clinical course of traumatic intracranial hematomas, we did not note. Just like in patients with a decompensated variant of the clinical course, the frequency of detectable hemispheric neurological symptoms depended on the patient's level of consciousness. Focal neurological symptoms were detected in 33% of the patients who received 9-12 GCS depression, and in 62% ofpatients with a consciousness level of 13-15. Local signs ofbrain damage (verbal disorders, flattening of the nasolabial fold, deviation of the tongue, hemiparesis or hemiplegia) necessarily accompanied by certain stem symptoms in the form of anisocoria, a decrease in pupillary response to light, diverging strabismus, unstable bilateral patho-

logical reflexes, bradycardia. In 38.3% of patients with HF in the clinical picture prevalent cerebral symptoms (headache, nausea, vomiting), accompanied by moderately expressed stem symptoms (anisocoria, bradycardia, unstable bilateral pathological stop reflexes).

Thus, as in the case of a decompensated variant, the dislocation syndrome prevailed in patients with a subcompensated variant of a large volume of TIH in a clinical picture, and focal neurological symptoms were manifested only in half of the observations. Mortality with a subcompensated option was 33.3%.

Increased mortality among patients with a lack of local neurological symptoms compared with patients who had local neurological symptoms was also associated with a rapidly developing dislocation syndrome and impaired vital brain stem function. The clinical picture of the expressed dislocation syndrome was determined by the damage to the brain stem sections, which often had an irreversible character.

Conclusion. Two variants of the clinical course of acute traumatic intracranial hematomas of large volume are distinguished: decompensated and subcompensated. The decompensated variant of the clinical course was noted in 71.0% of the victims, during which, in the first hours after the trauma, a severe, extremely severe, and in a third of patients the terminal state, the level of oppression of consciousness corresponds to 8 or less points in the GCS, a rough dislocation syndrome predominates hemispheric symptoms. The lethality with this variant reaches 71.9%.

A subcompensated variant of the clinical course develops in 29.1% of the patients - the condition can be either satisfactory or severe with depression of consciousness from 15 to 9 points according to the GCS; on the background of severe cerebral and dislocation symptoms focal hemispheric neurologic symptoms were noted in half of the patients. Mortality with a subcompensated version of the clinical course is 33.3%

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