Closed craniocerebral injury. Diagnosis of a lower limb fracture

Diagnostic tactics. Anamnesis.. In the anamnesis, not only current complaints are important, but also those that have already disappeared.. All previous diseases should be identified, including operations, injuries and mental disorders.. Details such as family history may also be significant anamnesis, vaccination and medication data, professional anamnesis, clarification of the travel route, information about the sexual partner, the presence of animals in the environment. Physical examination...

Anamnesis. Burdened family anamnesis regarding anemia, any manifestations of liver and biliary tract diseases. Contact with patients with infectious hepatitis, stay in hepatitis-endemic regions during the last 2 months, parenteral interventions, drug administration, casual sexual intercourse during the last 6 months. Working with hepatotoxic substances. Alcohol abuse. Treatment with hepatotoxic drugs. Biliary colic...

Pathomorphology. The spleen is enlarged and full of blood. The vessels of the portal system and spleen are enlarged, tortuous, they may contain aneurysms, hemorrhages, and parietal thrombi. Changes in the liver depend on the cause of PG. Varicose veins of the esophagus, stomach, rectum. Anamnesis. Presence of cirrhosis or chronic hepatitis. Indication of a history of gastrointestinal bleeding. Indications of alcohol abuse, blood transfusions, viral hepatitis B, C...

The true conjugate is less than 6.5 cm. Vaginal delivery is impossible even with the use of fetal destruction surgery. Diagnostics. Anamnesis: infantilism, past illnesses and injuries, obstetric anamnesis. Objective examination: general examination, height 150 cm and below, assessment of the Michaelis rhombus, spinal curvature, joint mobility; a saggy belly in multiparous women and a pointed belly in primiparous women.

Huntington's chorea (choric dementia) is a hereditary disease. Choreic hyperkinesis appears at the age of 30-40 years, and later progressive dementia occurs, reaching the complete collapse of the personality. When differentiating from senile chorea, family history is of decisive importance. anamnesis; at the onset of the disease, diagnosis is facilitated by the administration of L-DOPA, which leads to a sharp increase in hyperkinesis.

Etiology. The vast majority of cases (more than 95%) are of rheumatic etiology. Overt rheumatic anamnesis can be collected from 50-60% of patients. Almost always debuting before the age of 20 years, after 10-30 years the defect becomes clinically pronounced. Non-rheumatic cases of the defect include severe calcification of the cusps and annulus of the mitral valve, congenital anomalies (for example, Lutembasche syndrome - 0.4% of all congenital heart diseases), neoplasms and blood clots in the mitral valve area and...

Risk factors. Gluten enteropathy. Family anamnesis dermatitis herpetiformis. Oncological diseases. Insolation. Clinical picture. Skin changes.. True polymorphic rashes: urticarial, erythematous elements, tense blisters on an edematous erythematous background (can also occur on unaltered skin) with a pronounced tendency to group and herpetiform arrangement.. The cover of the blisters is dense, the contents are first serous, then becomes cloudy...

Anamnesis. Contact with a patient with SI (hospital patients or care staff with inflammatory changes on the skin, mucous membranes or other organs, definitely or presumably of staphylococcal etiology) 1-10 days before the present illness. Consumption of food products infected with staphylococcus. The development of a purulent-inflammatory disease in a hospital setting, most often after 3 days from the moment of hospitalization. Surgical intervention With...

Clinical picture. Anamnesis. Chronic diseases of the stomach, duodenum, liver, blood. Complaints of weakness, dizziness, drowsiness, fainting, thirst, vomiting of fresh blood or coffee grounds, tarry stools. Objective data. Pale skin and visible mucous membranes, dry tongue, rapid and soft pulse, blood pressure with minor blood loss is initially elevated, then normal.

to subepicardial, which can lead to the development of secondary MI. The mechanism of rupture of the heart wall during blunt trauma is a sharp increase in pressure in the chambers of the heart during its anterior-posterior compression or a sharp influx of blood from the inferior vena cava during a seat belt injury. Clinical picture and diagnosis. . Complaints and anamnesis.. The main complaints in case of heart contusion are chest pain, shortness of breath and interruptions in the functioning of the heart.. Often numerous complaints...

Anamnesis. Indication of the consumption of thermally unprocessed products, home-canned products and those preserved under anaerobic conditions, mainly vegetables and mushrooms, as well as sausage, ham, smoked and salted fish, contaminated with bacteria. With wound botulism - lacerated or crushed wounds with significant tissue necrosis. Periods of illness. Incubation, lasting from 2 hours to 7 days (rarely up to 14 days).

. The acute form of Hirschsprung's disease manifests itself in newborns in the form of low congenital intestinal obstruction. Anamnesis. Hirschsprung's disease, unlike other forms of megacolon (tumor, megacolon against the background of atonic constipation in the elderly, toxic megacolon with ulcerative colitis), is characterized by the appearance of constipation from birth or early childhood. Parents often note the presence of endocrine, mental and neurological abnormalities.

HSV-1 infection in people over 4 years of age in the population is more than 80% (European countries and the USA). Anamnesis. Indication of contact with a patient with a clinically manifest form of herpes infection during the last 2 weeks. If perinatal infection is suspected, information about the presence of herpetic infection in the pregnant woman in various clinical forms (including latent). Classification. Localized form. Disseminated form. Latent form. Clinical picture.

Clinical picture. Anamnesis. Contact with a patient with chickenpox or herpes zoster 11-21 days before illness; Direct contact is not required. . Periods of the disease.. Duration of the incubation period - 11-21 days.. Prodromal period (optional) - up to 1 day.. Period of rashes (main clinical manifestations) - 4-7 days.. Convalescence period - 1-2 weeks. . Clinical symptoms.. Intoxication syndrome: usually 3-5 days of fever with...

Diagnostics. Anamnesis. Visual field examination. Visual acuity study. Ophthalmoscopy. Treatment is etiotropic. Course and prognosis. With a stagnant disc, normal visual functions are maintained for a long time, even with severe swelling. Subsequently, the field of view narrows.

Classification. Latent (subclinical) form. Congenital form.. Acute form.. Chronic form. Acquired form. Anamnesis. Indication of possible infection (fact of maternal infection according to laboratory data, miscarriage, stillbirth, blood transfusions and parenteral interventions in the past, sexual and/or close household contact with an infected or sick person, organ and tissue transplantation). Presence of possible primary manifestations...

Differential diagnosis. Great importance has a carefully assembled anamnesis, establishing the possibility of professional or household intoxication, taking into account the epidemiological situation in identifying the nature and cause of the disease. In unclear cases, the first consideration should be viral hepatitis. The detection of the so-called Australian antigen is characteristic of serum hepatitis B (it is also detected in virus carriers, rarely in other diseases).

Diagnostics. Anamnesis life (obstetric and postnatal) - the course of pregnancy, toxicosis, maternal diseases; course of labor, duration of the anhydrous interval, use of obstetric aids; monthly weight gain of the child, previous diseases in the early neonatal period. Social anamnesis(housing and living conditions, socio-economic condition of the family). Hereditary anamnesis- metabolic, endocrine diseases, enzymopathies in family members...

The clinical picture of the primary septic or primary pulmonary form is not fundamentally different from the secondary forms, but the primary forms often have a shorter incubation period - up to several hours. Diagnosis. The most important role in diagnosis in modern conditions plays epidemiological anamnesis. Arrival from zones endemic for plague (Vietnam, Burma, Bolivia, Ecuador, Turkmenistan, Karakalpak Autonomous Soviet Socialist Republic, etc.), or from anti-plague stations of a patient with the above...

Anamnesis: contact with a patient with polio 3 weeks before the onset of the first symptoms of the disease, stay in a region unfavorable for the incidence of polio. The fact of vaccination with live polio vaccine one month before the onset of the first symptoms of the disease or contact with a vaccinated person within the last two months (situations associated with a vaccine-associated form of the disease).

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Traumatic brain injury

Traumatic brain injury - damage to the bones of the skull and/or soft tissues (meninges, brain tissue, nerves, blood vessels). Based on the nature of the injury, a distinction is made between closed and open, penetrating and non-penetrating TBI, as well as concussion or contusion of the brain. The clinical picture of traumatic brain injury depends on its nature and severity. The main symptoms are headache, dizziness, nausea and vomiting, loss of consciousness, memory impairment. Brain contusion and intracerebral hematoma are accompanied by focal symptoms. Diagnosis of traumatic brain injury includes medical history, neurological examination, skull x-ray, CT or MRI of the brain.

Traumatic brain injury

Traumatic brain injury - damage to the bones of the skull and/or soft tissues (meninges, brain tissue, nerves, blood vessels). The classification of TBI is based on its biomechanics, type, type, nature, shape, severity of injury, clinical phase, treatment period, and outcome of the injury.

Based on biomechanics, the following types of TBI are distinguished:

• shock-anti-shock (the shock wave propagates from the site of the received blow and passes through the brain to the opposite side with rapid pressure changes);
• acceleration-deceleration (movement and rotation of the cerebral hemispheres in relation to a more fixed brain stem);
• combined (simultaneous impact of both mechanisms).

By type of damage:

• focal (characterized by local macrostructural damage to the brain matter, with the exception of areas of destruction, small and large focal hemorrhages in the area of ​​impact, counter-impact and shock wave);
• diffuse (tension and spread of primary and secondary axonal ruptures in the centrum semiovale, corpus callosum, subcortical formations, brain stem);
• combined (a combination of focal and diffuse brain damage).

According to the genesis of the lesion:

• primary lesions: focal contusions and crushes of the brain, diffuse axonal damage, primary intracranial hematomas, brainstem ruptures, multiple intracerebral hemorrhages;
• secondary lesions:

1. due to secondary intracranial factors (delayed hematomas, disturbances in cerebrospinal fluid and hemocirculation due to intraventricular or subarachnoid hemorrhage, cerebral edema, hyperemia, etc.);
2. due to secondary extracranial factors (arterial hypertension, hypercapnia, hypoxemia, anemia, etc.)

According to their type, TBIs are classified into: closed - injuries that do not violate the integrity of the skin of the head; fractures of the bones of the calvarium without damage to the adjacent soft tissues or a fracture of the base of the skull with developed liquorrhea and bleeding (from the ear or nose); open non-penetrating TBI - without damage to the dura mater and open penetrating TBI - with damage to the dura mater. In addition, isolated (absence of any extracranial damage), combined (extracranial damage as a result of mechanical energy) and combined (simultaneous exposure to various energies: mechanical and thermal/radiation/chemical) traumatic brain injury are distinguished.

Based on severity, TBI is divided into 3 degrees: mild, moderate and severe. When correlating this rubric with the Glasgow Coma Scale, mild traumatic brain injury is assessed at 13-15, moderate at 9-12, severe at 8 points or less. A mild traumatic brain injury corresponds to a mild concussion and contusion, a moderate one corresponds to a moderate brain contusion, a severe one corresponds to a severe brain contusion, diffuse axonal damage and acute compression of the brain.

According to the mechanism of occurrence of TBI, there are primary (the impact of traumatic mechanical energy on the brain is not preceded by any cerebral or extracerebral catastrophe) and secondary (the impact of traumatic mechanical energy on the brain is preceded by a cerebral or extracerebral catastrophe). TBI in the same patient can occur for the first time or repeatedly (twice, three times).

The following clinical forms of TBI are distinguished: concussion, mild brain contusion, moderate brain contusion, severe brain contusion, diffuse axonal damage, brain compression. The course of each of them is divided into 3 basic periods: acute, intermediate and long-term. The time duration of the periods of traumatic brain injury varies depending on the clinical form of TBI: acute - 2-10 weeks, intermediate - 2-6 months, long-term with clinical recovery - up to 2 years.

Brain concussion

The most common injury among possible traumatic brain injuries (up to 80% of all TBIs).

Clinical picture

Depression of consciousness (to the level of stupor) during a concussion can last from several seconds to several minutes, but may be absent altogether. Retrograde, congrade and antegrade amnesia develops for a short period of time. Immediately after a traumatic brain injury, a single vomiting occurs, breathing becomes more frequent, but soon returns to normal. Blood pressure also returns to normal, except in cases where the medical history is aggravated by hypertension. Body temperature during a concussion remains normal. When the victim regains consciousness, there are complaints of dizziness, headache, general weakness, cold sweat, flushing of the face, and tinnitus. The neurological status at this stage is characterized by mild asymmetry of skin and tendon reflexes, small horizontal nystagmus in the extreme abductions of the eyes, and mild meningeal symptoms that disappear during the first week. With a concussion as a result of a traumatic brain injury, after 1.5 - 2 weeks, an improvement in the patient’s general condition is noted. It is possible that some asthenic phenomena may persist.

Diagnosis

Recognizing a concussion is not an easy task for a neurologist or traumatologist, since the main criteria for diagnosing it are the components of subjective symptoms in the absence of any objective data. It is necessary to familiarize yourself with the circumstances of the injury, using the information available to witnesses to the incident. Of great importance is an examination by an otoneurologist, with the help of which the presence of symptoms of irritation of the vestibular analyzer in the absence of signs of prolapse is determined. Due to the mild semiotics of a concussion and the possibility of a similar picture arising as a result of one of many pre-traumatic pathologies, special importance in diagnosis is given to the dynamics of clinical symptoms. The justification for the diagnosis of “concussion” is the disappearance of such symptoms 3-6 days after receiving a traumatic brain injury. With a concussion, there are no fractures of the skull bones. The composition of the cerebrospinal fluid and its pressure remain normal. CT scan of the brain does not detect intracranial spaces.

Treatment

If a victim with a traumatic brain injury has come to his senses, first of all he needs to be given a comfortable horizontal position, his head should be slightly raised. A victim with a traumatic brain injury who is in an unconscious state must be given the so-called. “saving” position - lay him on his right side, his face should be turned to the ground, his left arm and leg should be bent at a right angle at the elbow and knee joints(if fractures of the spine and limbs are excluded). This position promotes the free passage of air into the lungs, preventing the tongue from retracting and vomit, saliva and blood from entering the respiratory tract. Apply an aseptic bandage to bleeding wounds on the head, if any.

All victims with traumatic brain injury are necessarily transported to a hospital, where, after confirmation of the diagnosis, they are placed on bed rest for a period that depends on the clinical characteristics of the course of the disease. The absence of signs of focal brain lesions on CT and MRI of the brain, as well as the patient’s condition, which allows one to refrain from active drug treatment, allows us to resolve the issue in favor of discharging the patient for outpatient treatment.

For a concussion, overactive drug treatment is not used. Its main goals are to normalize the functional state of the brain, relieve headaches, and normalize sleep. For this purpose, analgesics and sedatives (usually in tablet forms) are used.

Brain contusion

Mild brain contusion is detected in 10-15% of victims with traumatic brain injury. A bruise of moderate severity is diagnosed in 8-10% of victims, a severe bruise - in 5-7% of victims.

Clinical picture

A mild brain contusion is characterized by loss of consciousness after injury of up to several tens of minutes. After regaining consciousness, complaints of headache, dizziness, and nausea appear. Retrograde, congrade, and anterograde amnesia are noted. Vomiting is possible, sometimes with repetitions. Vital functions are usually preserved. Moderate tachycardia or bradycardia and sometimes increased blood pressure are observed. Body temperature and respiration without significant deviations. Mild neurological symptoms regress after 2-3 weeks.

Loss of consciousness with a moderate brain contusion can last from minutes to 5-7 hours. Retrograde, congrade and anterograde amnesia are strongly expressed. Repeated vomiting and severe headache are possible. Some vital functions are impaired. Bradycardia or tachycardia, increased blood pressure, tachypnea without respiratory distress, and increased body temperature to subfebrile are detected. The manifestation of meningeal signs, as well as stem symptoms, is possible: bilateral pyramidal signs, nystagmus, dissociation of meningeal symptoms along the body axis. Pronounced focal signs: oculomotor and pupillary disorders, paresis of the limbs, speech and sensitivity disorders. They regress after 4-5 weeks.

Severe brain contusion is accompanied by loss of consciousness from several hours to 1-2 weeks. It is often combined with fractures of the bones of the base and vault of the skull, and profuse subarachnoid hemorrhage. Disorders of vital functions are noted: respiratory rhythm disturbances, sharply increased (sometimes decreased) blood pressure, tachy- or bradyarrhythmia. Possible blockage of the airways, intense hyperthermia. Focal symptoms of hemispheric damage are often masked behind stem symptoms that come to the fore (nystagmus, gaze paresis, dysphagia, ptosis, mydriasis, decerebrate rigidity, changes in tendon reflexes, the appearance of pathological foot reflexes). Symptoms of oral automatism, paresis, focal or generalized seizures can be detected. Restoring lost functions is difficult. In most cases, gross residual motor and mental disorders remain.

Diagnosis

The method of choice for diagnosing a brain contusion is a CT scan of the brain. A CT scan reveals a limited area of ​​low density, possible fractures of the calvarial bones and subarachnoid hemorrhage. With a brain contusion of moderate severity, CT or spiral CT in most cases reveals focal changes (non-compactly located areas of low density with small areas of increased density).

In case of severe contusion, CT scan reveals areas of heterogeneous increase in density (alternating areas of increased and decreased density). Perifocal cerebral edema is severe. A hypodense track is formed in the area of ​​the nearest section of the lateral ventricle. Through it, fluid with breakdown products of blood and brain tissue is discharged.

Diffuse axonal brain injury

Diffuse axonal brain damage is typically long-term coma after traumatic brain injury, as well as pronounced brain stem symptoms. Coma is accompanied by symmetrical or asymmetrical decerebration or decortication, both spontaneous and easily provoked by irritations (for example, painful ones). Changes in muscle tone are very variable (hormetonia or diffuse hypotension). A typical manifestation is pyramidal-extrapyramidal paresis of the limbs, including asymmetric tetraparesis. In addition to gross disturbances in the rhythm and frequency of breathing, autonomic disorders also appear: increased body temperature and blood pressure, hyperhidrosis, etc. Characteristic feature The clinical course of diffuse axonal brain damage is the transformation of the patient’s condition from a prolonged coma to a transient vegetative state. The onset of this state is indicated by spontaneous opening of the eyes (with no signs of tracking or fixation of gaze).

Diagnosis

The CT picture of diffuse axonal brain damage is characterized by an increase in brain volume, as a result of which the lateral and third ventricles, subarachnoid convexital spaces, and also the cisterns of the base of the brain are under compression. The presence of small focal hemorrhages in the white matter of the cerebral hemispheres, corpus callosum, subcortical and brain stem structures is often detected.

Brain compression

Brain compression develops in more than 55% of cases of traumatic brain injury. The most common cause of brain compression is an intracranial hematoma (intracerebral, epi- or subdural). Rapidly increasing focal, brainstem and cerebral symptoms pose a danger to the life of the victim. Availability and duration of the so-called the “light gap” - expanded or erased - depends on the severity of the victim’s condition.

Diagnosis

A CT scan reveals a biconvex, less often a flat-convex, limited zone of increased density, which is adjacent to the cranial vault and is localized within one or two lobes. However, if there are several sources of bleeding, the area of ​​​​increased density can be significant in size and have a crescent shape.

Treatment of traumatic brain injury

When a patient with a traumatic brain injury is admitted to the intensive care unit, the following measures must be taken:

• Examination of the victim’s body, during which abrasions, bruises, joint deformities, changes in the shape of the abdomen and chest, bleeding and/or liquor leakage from the ears and nose, bleeding from the rectum and/or urethra, and a specific odor from the mouth are detected or excluded.
• Comprehensive x-ray examination: skull in 2 projections, cervical, thoracic and lumbar spine, chest, pelvic bones, upper and lower extremities.
• Ultrasound of the chest, ultrasound of the abdominal cavity and retroperitoneal space.
• Laboratory tests: general clinical analysis of blood and urine, biochemical blood test (creatinine, urea, bilirubin, etc.), blood sugar, electrolytes. These laboratory tests must be carried out in the future, daily.
• ECG (three standard and six chest leads).
• Testing urine and blood for alcohol content. If necessary, consult a toxicologist.
• Consultations with a neurosurgeon, surgeon, traumatologist.

A mandatory method of examining victims with traumatic brain injury is computed tomography. Relative contraindications to its implementation may include hemorrhagic or traumatic shock, as well as unstable hemodynamics. Using CT, the pathological focus and its location, the number and volume of hyper- and hypodense zones, the position and degree of displacement of the midline structures of the brain, the condition and degree of damage to the brain and skull are determined. If meningitis is suspected, a lumbar puncture and dynamic examination of the cerebrospinal fluid are indicated, which allows monitoring changes in the inflammatory nature of its composition.

A neurological examination of a patient with a traumatic brain injury should be performed every 4 hours. To determine the degree of consciousness impairment, the Glasgow Coma Scale is used (state of speech, response to pain and ability to open/close eyes). In addition, the level of focal, oculomotor, pupillary and bulbar disorders is determined.

For a victim with impaired consciousness of 8 points or less on the Glasgow scale, tracheal intubation is indicated, due to which normal oxygenation is maintained. Depression of consciousness to the level of stupor or coma is an indication for auxiliary or controlled mechanical ventilation (at least 50% oxygen). With its help, optimal cerebral oxygenation is maintained. Patients with severe traumatic brain injury (hematomas, cerebral edema, etc. detected on CT) require monitoring of intracranial pressure, which must be maintained below 20 mmHg. For this purpose, mannitol, hyperventilation, and sometimes barbiturates are prescribed. To prevent septic complications, escalation or de-escalation antibacterial therapy is used. For the treatment of post-traumatic meningitis, modern antimicrobial drugs approved for endolumbar administration (vancomycin) are used.

Patients begin feeding no later than 3 days after TBI. Its volume is increased gradually and at the end of the first week following the date of the traumatic brain injury, it should provide 100% of the patient’s caloric needs. The route of nutrition can be enteral or parenteral. To relieve epileptic seizures, anticonvulsants are prescribed with minimal dose titration (levetiracetam, valproate).

The indication for surgery is an epidural hematoma with a volume of over 30 cm³. It has been proven that the method that provides the most complete evacuation of the hematoma is transcranial removal. Acute subdural hematoma with a thickness of more than 10 mm is also subject to surgical treatment. In comatose patients, acute subdural hematoma is removed by craniotomy, retaining or removing a bone flap. An epidural hematoma with a volume of more than 25 cm³ is also subject to mandatory surgical treatment.

Prognosis for traumatic brain injury

Concussion is a predominantly reversible clinical form of traumatic brain injury. Therefore, in more than 90% of cases of concussion, the outcome of the disease is the recovery of the victim with full restoration of ability to work. Some patients, after the acute period of concussion, experience certain manifestations of post-concussion syndrome: disturbances in cognitive functions, mood, physical well-being and behavior. 5-12 months after a traumatic brain injury, these symptoms disappear or are significantly smoothed out.

Prognostic assessment in severe traumatic brain injury is carried out using the Glasgow Outcome Scale. A decrease in the total number of points on the Glasgow scale increases the likelihood of an unfavorable outcome of the disease. Analyzing the prognostic significance of the age factor, we can conclude that it has a significant impact on both disability and mortality. The combination of hypoxia and arterial hypertension is an unfavorable prognosis factor.

Traumatic brain injury - treatment in Moscow

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Traumatic brain injury

Compiled by: Candidate of Medical Sciences, Associate Professor Melnikov V.L., Art. teacher Matrosov M.G.

Traumatic brain injury is one of the most common injuries and accounts for >40% of the total number; the mortality rate for severe injuries of the skull and brain reaches 70-80%. The mechanism of traumatic brain injury can be direct or indirect. An example of an indirect mechanism would be traumatic brain injury resulting from a fall from a height onto the legs or pelvis. When landing and stopping the movement of the skeleton, the skull, due to inertia, seems to be pushed onto the spine and a fracture of the base of the skull can occur. If this does not happen, the skull stops, and the brain, continuing to move, hits its base and standing bones.

Classification of traumatic brain injury Tab.1.

1. Concussion

I. Damage to the soft tissues of the head without signs of brain injury

2. Brain contusion (1st, 2nd, 3rd degree)

2. Damage to the soft tissues of the head with impaired brain function (concussion, bruise, compression).

3. Compression of the brain due to its contusion.

3. Damage to the soft tissues of the head, bones of the cranial vault and brain (bruise, compression) - penetrating and non-penetrating.

4. Compression of the brain without accompanying contusion.

4.Fracture of the base of the skull (bruise and compression).

5. Damage to the bones of the cranial vault and brain (bruise, compression).

Syndromes: Hypertensive - cerebrospinal fluid pressure is increased. Hypotensive - cerebrospinal fluid pressure is reduced. Normotensive - cerebrospinal fluid pressure is not changed.

Diagnosis of traumatic brain injury: There are four main groups of clinical symptoms: general cerebral, local, meningeal and brainstem.

General cerebral symptoms. Their formation is based on functional (reversible) changes in the substance of the brain. Appearing after injury, these signs gradually regress and, ultimately, disappear without a trace. These include:

1. Loss of consciousness. It proceeds according to the stem type and is characterized by three forms of manifestation: a) stunning - expressed by a short-term disturbance of orientation followed by mild drowsiness. Particular attention should be paid to this form of disorder of consciousness, since victims remain on their feet and do not regard the state of stupor as a loss of consciousness; b) stupor - a more severe degree of impairment of consciousness, in which the reaction to gross stimuli (pain, loud cry) in the form of coordinated defensive movements, opening of the eyes is still preserved; c) coma - prostration with a complete loss of perception of the surrounding world, deepening, characterized by adynamia, atony, areflexia, depression of vital functions.

2. Memory loss (amnesia). It may be: retrograde, when patients do not remember the events immediately preceding the injury; anterograde - loss of memory for events that occurred after the injury; anterograde - a combined form of memory loss for events before and after injury.

Headache. There can be both diffuse and local pain, bursting or squeezing the head.

Dizziness. Instability in the Romberg pose.

Nausea, vomiting. Depending on the type and nature of the injury, nausea can be short-term with one or two vomiting and long-term with frequently repeated vomiting, even indomitable.

Positive Mann-Gurevich sign. The doctor asks the patient to follow with his eyes, without turning his head, any object in his hand, and makes several (3-5) oscillatory movements of the object in the frontal plane. If the patient’s well-being has worsened, cerebral and autonomic manifestations have intensified, and tachycardia has appeared, then the symptom is considered positive.

7. Autonomic symptoms. Weakness, noise or ringing in the ears, pallor or hyperemia of the skin, their high humidity or dryness, pulse lability and other vegetative manifestations.

Local (aka focal) symptoms. The reason for their appearance is organic damage to some part of the brain and loss of function in the zone of its innervation. Clinically defined local signs are nothing more than paresis, paralysis, sensitivity disorders and dysfunction of the sensory organs. For example: motor or sensory aphasia, anisokaria, smoothness of the nasolabial fold, deviation of the tongue, monoparesis of the limbs, hemiparesis, etc.

Meningeal (meningeal) symptoms. They are the result of irritation of the meninges directly by trauma (bruises, ruptures), pressure from bone fragments, foreign bodies, hematomas (the dura mater has baroreceptors), blood, infection and other ingredients. Typical severe meningeal symptoms can be identified during an external examination of the patient. He takes a forced position, lying on his side with his head thrown back and his legs bent at the knees and hip joints (the “trigger” pose). Other characteristic symptoms are photophobia. The victim tries to turn away from the light source or covers his face with a blanket. There is increased excitability, and an extreme reaction to harsh stimuli can be a convulsive seizure.

Patients complain of intense headaches that get worse when moving their heads. Localization of pain is the frontal and occipital areas with irradiation to the neck or eyeballs. Often there is pain in the eyeballs. When the meninges are irritated, nausea and vomiting are observed, the latter being repeated and debilitating.

Pathognomonic meningeal signs are nuchal rigidity and positive Kernig and Brudzinski signs. An increase in body temperature to 39-40°C is typical, especially if an infection occurs.

Stem symptoms. In their genesis they are no different from local ones, but the damage affects only the brain stem and its structures that regulate vital functions. Injury to the brain stem can be primary, or arise as a result of brain dislocation and pinching of the brain stem into the foramen of the cerebellar tentorium or in the occipito-cervical dural infundibulum.

Stem symptoms are divided into non-upper-trunk, lower-trunk and dislocation.

Upper stem(mesodiencephalic syndrome) is characterized by a disorder of consciousness in the form of stupor or stupor. Mild breathing disorders - tachypnea and “orderly breathing”, when the duration of inhalation and exhalation becomes the same. Cardiovascular disorders consist of increased heart rate up to 120 per minute. and an increase in blood pressure to 200/100 mm Hg.

Upper brainstem symptoms include a large number of oculomotor disorders. This is a symptom of “floating gaze”, divergence in the vertical and horizontal planes, convergence, gaze paresis, etc.

Muscle tone is high, reflexes are animated or increased, bilateral pathological reflexes from the feet appear (Babinsky, Gordon, Oppenheim). Swallowing is not impaired. Body temperature is high.

Nizhnestvolova(bulbar) syndrome is characterized by a more severe condition. There is no consciousness - coma. Respiratory disorder reaches an extreme degree, pathological forms of breathing occur. The pulse is weak and frequent. Blood pressure drops to 70/40 mm Hg. and below. The pupils are wide, the reaction to light is subtle. Swallowing is severely impaired. Thermoregulation is reduced.

Dislocation syndrome- this is a rapid transition from the upper brainstem to the lower brainstem syndrome as a result of brain infringement.

Traumatic brain injury can occur with increased, normal or decreased cerebrospinal fluid pressure, depending on which hyper-, normo- and hypotensive syndromes are distinguished. Diagnosis of the syndrome can be carried out on the basis of clinical manifestations and using auxiliary methods.

Hypertension syndrome occurs in 65% of victims with traumatic brain injury. It occurs more often in older people. It occurs with a bursting headache, high blood pressure, and bradycardia. A positive symptom of “raised head” (pillow) is noted - patients take a forced position with the head end raised, since an elevated position reduces headaches.

Traumatic brain injury with hypotension syndrome occurs in 25% of victims. A decrease in cerebrospinal fluid pressure is more often observed in young people, occurring with a compressive headache, with normal or low blood pressure, and tachycardia. Vegetative signs are pronounced, most often manifested by pallor and sweating. Increased fatigue, lethargy, and mental exhaustion are noted. A positive symptom of “lowered head” is that giving the patient a Trandelenburg position reduces headaches.

During a lumbar puncture with the patient in a supine position, cerebrospinal fluid flows out in drops at a rate of 60 per minute, and the pressure measured by a pressure gauge is mm of water. These numbers are considered the norm. An increase in the frequency of drops and cerebrospinal fluid pressure is regarded as hypertension, and a decrease is considered as hypotension.

Lumbar puncture should be performed in all patients with concussion and more severe TBI.

Additional research methods

Craniography is the most common method. When examining patients with traumatic brain injury, two panoramic craniograms are required: straight and lateral. .

Schemes of craniograms in overview projections with explanations are presented in Fig. 1.

Rice. 1. Scheme of craniograms in direct (A) and lateral (B) projections:

(A) 1. Pyramid. 2. Lesser wing of the main bone. 3. Mastoid process. 4. Atlantooccipital

joint. 5. Atlantoaxial joint. 6. Frontal sinus. 7. Sagittal suture. 8. Lambdoid suture. 9. Coronal suture. 10. Maxillary sinus.

(B) 1. Pyramid. 2. Main bone. 3. Turkish saddle. 4. The anterior part of the large wings of the main bone. 5. Frontal sinus. 6. Coronal suture. 7. Lambdoid suture. 8, 9. Anterior and posterior branches of the meningeal artery, 10. Internal and external auditory canals. 11. Shadow of the cartilage of the auricle. 12. Nasal bones. 13. Cheekbones. 14. Maxillary sinus

Echoencephalography is the registration of the position of the midline structures of the brain (epiphysis, third ventricle, interhemispheric fissure, etc.) by receiving a reflected ultrasound signal from them (M-echo). The method is based on the ability of ultrasound to propagate in various media and give reflection at the border of structural formations with inhomogeneous acoustic resistance. The ultrasonic wave reflected from the object is recorded on the screen of the echoencephalograph in the form of a peak located along midline. During volumetric processes in the cranial cavity (hematomas, hygromas, traumatic cysts, abscesses, tumors), the midline structures of the brain shift towards the healthy hemisphere. This is revealed on the echoencephalogram in the form of a displacement of the M-echo from the midline by 3 mm or more. With pronounced volumetric processes, for example, with epi- and subdural hematomas, the displacement of the M-echo can reach 8-15 mm (Fig. 2).

Normal echogram (A). Displacement of midline structures and M-echo with intracranial hematoma (B)

Carotid angiography. This research method is based on the introduction into the carotid artery of substances that have the property of absorbing X-rays, which ensures the visibility of blood vessels on an X-ray at different phases of cerebral circulation. By changes in the filling and location of the vessels, the degree of circulatory disturbance in the brain and its causes are judged.

Computed tomography is an X-ray research method using a computer, which allows one to obtain images of the structures of the brain and bones of the skull both in whole form and in sections with a thickness of 3 to 13 mm. The method allows you to see changes and damage to the bones of the skull, structures of the brain, identify intracerebral and intracranial hemorrhages and much more.

Patients with traumatic brain injury should undergo ophthalmological and otorhineurological examination.

A lumbar puncture is done to clarify the pressure of the cerebrospinal fluid, determine its composition and the patency of the cerebrospinal fluid pathways.

The manipulation is performed with the patient lying on his side, on a hard table with his legs bent towards the stomach. The back is bent as much as possible. The place for puncture is the space between the III and IV lumbar vertebrae. Treat the skin with iodine tincture, then with alcohol until traces of iodine disappear, the entry of which into the lumbar canal is extremely undesirable. The puncture site is anesthetized with a 1% solution of novocaine in an amount of 5-10 ml. The puncture is performed with a special needle with a mandrel, directing its course strictly sagittally and at an angle to the frontal plane. The angle corresponds to the inclination of the spinous processes. The sensation of needle failure usually corresponds to the needle being in the subarachnoid space. When removed from the mandrin needle, cerebrospinal fluid begins to flow out. The pressure is measured with a manometer, and then 2 ml of cerebrospinal fluid is taken for examination. In case of high blood pressure, the cerebrospinal fluid should be slowly released by drip until the cerebrospinal fluid pressure normalizes.

Normally, cerebrospinal fluid is clear. In an adult, the subarachnoid space and ventricles contain ml of cerebrospinal fluid, which is completely renewed up to 6 times a day. It is absorbed and in return produced mainly by the choroid plexuses of the ventricles.

Laboratory examination: colorless transparent liquid, cytosis in 1 μl - 2-3; pH - 7.35-7.80; protein - 0.15-0.33 g/l; glucose - 0.5-0.8 g/l.

CLINICAL AND DIAGNOSTICS OF INDIVIDUAL

NOSOLOGICAL FORMS OF TRANAIOUS BRAIN INJURY

Brain concussion

The cause of a concussion is a mechanical injury of direct or indirect impact, followed by the development of general cerebral symptoms. The nature of the headaches and the position in bed depend on the cerebrospinal fluid pressure, and the severity of clinical manifestations depends on the severity of the injury.

Nystagmus, slight asymmetry of the face may appear due to the smoothness of the nasolabial fold and drooping of the corner of the mouth, deviation of the tongue. These and other local “microsymptoms” usually occur within 1-2 days. Longer persistence of these signs indicates the presence of a brain contusion.

Additional research methods practically do not provide information that reliably confirms the diagnosis. An exception is lumbar puncture, which can be used to determine changes in cerebrospinal fluid pressure.

At proper treatment the patient's condition improves by the end of the first week, and complete regression of clinical signs occurs after 2-4 weeks. The most stable are headache and the Mann-Gurevich symptom, the test of which should be used to determine the timing of bed rest. Once it disappears (becomes negative), patients are allowed to sit up in bed and then get up and walk.

Brain contusion

Brain contusion occurs due to direct and indirect mechanisms of impact. An example of an indirect mechanism of injury is a counter-impact, when a wave of “perturbed” brain matter, consisting of 80% water, reaches the opposite wall of the skull and hits its superior parts or is destroyed by tightly stretched areas of the dura mater.

A brain contusion is an organic lesion. As a result of the injury, areas of crushing and necrosis of brain tissue, severe vascular disorders with phenomena of hemorrhagic softening occur. Around the area of ​​brain contusion there is a zone of severe molecular concussion. Subsequent pathomorphological changes are expressed in encephalomalacia and lysis of a portion of the medulla, its resorption. If an infection occurs during this period, a brain abscess is formed. In an aseptic course, the brain tissue defect is replaced by a scar of neuroglia or brain cysts are formed.

The clinical picture of brain contusion is that immediately after the injury, victims experience general and local symptoms, and in severe forms, meningeal and brainstem symptoms are added.

There are three degrees of brain contusions.

/ degree (mild bruise). Loss of consciousness from several minutes to 1 hour. Upon restoration of consciousness, pronounced general cerebral symptoms and local, predominantly microfocal signs are determined. The last ones are saved for days. Violations of vital functions are not determined.

Grade I brain contusion may be accompanied by moderate subarachnoid hemorrhage and fractures of the bones of the vault and base of the skull, which are detected on craniograms.

// degree (moderate). Switching off consciousness after injury reaches 4-6 hours. During the period of coma, and sometimes in the first days of recovery of consciousness, moderately severe disorders of vital functions (upper brainstem signs) are detected in the form of bradycardia, tachypnea, increased blood pressure, nystagmus, etc. As a rule, these phenomena are transient.

Upon return of consciousness, amnesia, intense headache, and repeated vomiting are noted. In the early post-comatose period, mental disorders may be observed.

When examining the patient, distinct local symptoms are found that last from 3-5 weeks to 6 months.

In addition to the listed signs, with a second degree brain contusion, pronounced meningeal symptoms are always detected, fractures of the vault and base of the skull can be found, and in all cases significant subarachnoid hemorrhage.

Additional research methods: with lumbar puncture, increased cerebrospinal fluid pressure and a significant admixture of blood in it are determined. Craniograms show fractures of the skull bones. Echoencephalography gives a displacement of the M-echo of no more than 3-5 mm.

Ill degree. Loss of consciousness after injury is prolonged - from several hours to several weeks. The condition is extremely serious. Severe disturbances of vital functions come to the fore: changes in heart rate (bradycardia or tachycardia), arterial hypertension, disturbances in the frequency and rhythm of breathing, hyperthermia. Primary brainstem symptoms are clearly expressed: floating movements of the eyeballs, gaze paresis, tonic nystagmus, bilateral mydriasis or miosis, impaired swallowing. If the patient is in stupor or in a state of moderate coma, it is possible to identify local symptoms in the form of paresis or paralysis with impaired muscle tone and reflexes. Meningeal symptoms include stiff neck, positive Kernig and Brudzinski signs.

Grade III brain contusion is usually accompanied by fractures of the vault and base of the skull and massive subarachnoid hemorrhage.

Electroencephalography - with a brain contusion and crushing, high-amplitude delta waves appear in the destruction zone. With extensive convexital lesions, zones of electrical silence are found corresponding to the most severely affected area.

BRAIN COMPRESSION

The causes of compression of the brain can be: intracranial hematomas, bone fragments, foreign bodies, hygromas, pneumocephalus, hydrocephalus, subarachnoid hemorrhage, edema and swelling of the brain. The first four of these causes cause local compression of the brain and are the true root causes of intracranial catastrophes with a fairly typical course and frequent tragic outcome. The remaining nosological forms arise as a consequence of the listed or other severe injuries of the skull and brain, or as a natural subsequent stage of local compression of the brain. They lead to a total increase in brain volume and, as the pathology progresses, can cause dislocation and pinching of the brain in the foramen magnum.

Compression of the brain by bone fragments and foreign bodies

Compression of the brain by bone fragments occurs during fractures of the skull vault with prolapse of fragments deeper than the internal bone plate. Depressed fractures of the calvarium are mainly of two types. The first is when, as a result of mechanical action, the fragments are displaced at an angle, the apex of which “looks” into the cranial cavity, and the peripheral ends of the fragments retain connection with the mother bone. Such fractures are called impression fractures. The second type of fracture (depression) occurs when the injury is inflicted with great force, and the damaging agent has a small contact area. For example, a blow with a hammer, brass knuckles or a similar object. As a result of the injury, a fenestrated fracture occurs, the size and shape of the wounding object. The bone plate that covered the resulting “window” falls into the cranial cavity and leads to compression of the brain (Fig. 3).

Foreign bodies enter the cranial cavity mainly as a result of gunshot (bullet, shrapnel) wounds. However, penetrating injuries to the skull are also possible with cold steel or household objects, parts of which, breaking off, remain in the cranial cavity.

Rice. 3. Depressed fractures of the calvarium: A - impression; B - depressed.

Preliminary data allow us to make a diagnosis of brain contusion (of varying severity), which in fact accompanies depressed fractures and foreign bodies of the skull with compression of the brain. The final diagnosis is made after craniography, computed tomography, echoencephalography, with the help of which depressed skull fractures or foreign bodies in it are identified, and clinical data and the results of additional research methods on the topography of the location of the ingredient causing pressure on the brain tissue must match.

Compression of the brain by intracranial hematomas

Intracranial hematomas occur in 2-9% of the total number of traumatic brain injuries. There are epidural, subdural, subarachnoid, intracerebral, intraventricular hematomas (Fig. 4).

Fig4. Intracranial hematomas: 1 - epidural; 2 - subdural; 3 - intracerebral; 4 - intraventricular

The clinical manifestations of various hematomas are not the same, but in their course a number of patterns can be traced that allow intracranial hematomas to be considered in one group. Schematically, it looks like this: a history of head trauma with loss of consciousness (often for a short period). Upon return of consciousness, general cerebral symptoms are identified, on the basis of which a diagnosis of “concussion” can be made. Optimally, the patient is hospitalized and appropriate treatment is prescribed: rest, sedatives, etc. In some cases, victims may not seek help, since short bed rest, as a rule, relieves general cerebral symptoms. Moderate headaches and amnesia persist. The patient's condition improves significantly. Thus, rupture of an intracranial vessel at the time of injury due to the lack of clinical evidence of brain compression remains unnoticed. As compression increases, meningeal and then local symptoms appear (anisokaria, mono- or hemiparesis, etc.). A disorder of consciousness of the cortical type occurs. Psychomotor and speech agitation occurs, which subsequently turns into depressed consciousness (stupor), often with convulsive seizures and subsequent cerebral coma. The outcome of brain compression if left untreated is usually death. Thus, intracranial hematoma is characterized by a three-phase course: injury with loss of consciousness - improvement of the condition (“bright interval”) - deterioration of the condition with a tragic outcome.

Light interval refers to the time from the return of consciousness after the initial injury to the appearance of signs of brain compression. The duration of the light interval can be from several hours to several days, weeks and even months. Depending on this, hematomas are divided into acute (light period up to 3 days), subacute (from 4 to 21 days) and chronic (more than three weeks).

What determines the duration of the light interval?

It has now been proven that hematomas are mainly formed during the first three hours, and their volume, significantly exceeding ml, does not always interrupt the light interval. The reason is that the brain is not “squeezed” into the skull, but has certain spaces between it and the membranes with a certain intracranial pressure. A formed hematoma at an early stage does not cause pronounced compression of the brain, since it, like any living organ, sacrifices its volume to a certain extent, compensating for its functional state. Gradual vascular disorders, hypoxia, increasing edema, and then swelling of the brain lead to an increase in its volume and a sharp increase in pressure along the area of ​​contact between the hematoma and the brain. A breakdown of the compensatory capabilities of the central nervous system occurs, which is expressed in the end of the light interval. A further increase in brain volume leads to displacement of the midline structures, and then dislocation of the brain stem into the foramen of the cerebellar tentorium and the occipito-cervical dural infundibulum.

An increase in the duration of the clear interval in the acute stage may be due to the absorption of the liquid part of the blood from the hematoma and a decrease in its volume. The duration of imaginary well-being is also facilitated by dehydration carried out in a hospital for patients diagnosed with a concussion or bruise of the brain, which does not allow the development of pronounced swelling of the brain tissue.

With subacute and chronic hematomas, it is possible to increase their volume (naden) due to the influx of fluid. The decomposition of spilled blood and the increase in the content of high molecular weight proteins increase the oncotic pressure in the hematoma. This causes diffusion of the cerebrospinal fluid until an osmotic equilibrium is created between the liquid contents of the hematoma and the cerebrospinal fluid.

It is possible that the lucid interval may be interrupted by repeated hemorrhages into the epi- or subdural space when a blood clot breaks off from a damaged vessel. This can occur with a sudden sharp change in arterial and intracranial pressure - when sneezing, coughing, straining, etc.

Thus, the duration of the clear interval depends on many factors, and not just on the time and intensity of bleeding.

Epidural hematoma - This is a limited accumulation of blood between the bones of the skull and the dura mater of the brain. Suprathecal hemorrhages occur as a result of a direct mechanism of injury when exposed to a traumatic agent with a small area of ​​application of force of varying intensity and account for 0.6-5% of all traumatic brain injuries.

The source of epidural hematoma formation most often is damage to the branches of the middle meningeal artery, the vein of the same name, or the spongy substance of a broken bone. This explains the fact that epidural hematomas in 73-75% of cases are located in the temporal region. The dura mater is tightly adjacent to the bones of the skull and is fused with them along the suture lines, therefore the area of ​​epidural hematomas is limited and most often is 6-8 cm in diameter.

Suprathecal hematomas usually have a semi- spherical shape with a height in the central part of up to 4 cm. The amount of blood poured into the epidural space is often within ml, although local accumulation of blood in the volume leads to compression of the brain.

The clinical picture of acute epidural hematoma is characterized by a predominantly classical course.

The history reveals the presence of a head injury, accompanied by loss of consciousness. Upon return of consciousness, only general cerebral symptoms are found in the patient.

In the further clinical course of epidural hematoma, 4 stages can be distinguished: a light interval, a stage of excitation, inhibition and cerebral coma.

The light period is short, from several hours to 1.5-2 days, in most cases it does not exceed 24 hours. This stage begins with the return of consciousness and is characterized by the presence of the already described cerebral symptoms. During the first hours after injury, the severity of cerebral symptoms fades. At rest, dizziness and vomiting disappear, nausea and headache decrease. The victim is adequate, oriented in time and space, critically assesses his condition.

In the next stage, the patient develops unconscious anxiety. He is overly active, strives to change the position of his limbs, sit down, stand up, and leave the room. The face is hyperemic, there is aloofness or fear in the eyes. Patients cannot stand bright light or noise. This excitement is caused by increased headaches, which are painful and bursting in nature. The victim covers his head with his hands, takes a forced position, begs or demands immediate help, agrees and insists on surgical treatment.

Persistent nausea, repeated vomiting, terrifying dizziness appear - everything floats before your eyes. The pulse rate slows down, moderate bradycardia occurs (51-59 beats/min), blood pressure increases (from 140/80 to 180/100 mm Hg). Breathing increases moderately (21-30 breaths per minute). At this stage, focal microsymptoms may appear: mild anisokaria - slight dilation of the pupil on the side of the hematoma, smoothness of the nasolabial fold, moderate deviation of the tongue. Percussion of the skull can reveal areas of increased pain (usually above the hematoma), to which the patient reacts with a pained grimace.

During the inhibition stage, the patient's behavior changes radically. He no longer rages or asks for anything. A secondary disorder of consciousness occurs, beginning with stupor and progressing to stupor. The victim is indifferent to his surroundings, his gaze is pointlessly directed into the distance. Bradycardia (41-50 beats/min.) and tachypnea (31-40 breaths per minute) increase. Asymmetry in blood pressure appears. On the arm opposite the lesion, the blood pressure will be nmm Hg. higher than on the arm on the side of the hematoma. Focal symptoms increase. Among them, the main diagnostic role is played by: dilation of the pupil on the side of the hematoma, smoothness of the nasolabial fold, abnormal grins, deviation of the tongue, spastic hemiparesis with a predominant lesion of the arm on the opposite half of the body. Meningeal signs are identified in the form of stiff neck and positive Kernig and Brudzinski signs.

The final stage of untreated epidural hematoma is the stage of cerebral coma. It is caused by displacement and compression of the brain. It is characterized by dislocation signs: the transition of bradycardia to tachycardia (120 beats/min. and above), tachypnea to pathological types of breathing, blood pressure begins to steadily decrease, reaching critical numbers (below 60 mm Hg), swallowing disorders, a symptom of floating gaze, gross anisocaria and dissociation of meningeal symptoms, muscle tone and reflexes along the body axis. In the final phase, bilateral mydriasis with lack of pupillary response to light, areflexia, muscle atony, and death occurs.

A favorable outcome for epidural hematoma is possible if early diagnosis and timely adequate treatment. In addition to clinical signs, craniography, computed tomography, echoencephalography and carotid angiography are of diagnostic value, with the help of which they can identify fractures of the cranial vault, most often the scales of the temporal bone, an area of ​​​​increased density of a plano-convex or biconvex shape adjacent to the skull, displacement of the median M-echo by 6-15 mm and displacement of intracerebral vascular structures.

An ophthalmological examination reveals congestion in the fundus.

Subdural hematomas

A subdural hematoma is a limited accumulation of blood between the dura and arachnoid membranes of the brain. The incidence of these hemorrhages ranges from 1 to 13% of all traumatic brain injuries. Subdural hematomas most often occur with an indirect mechanism of injury, such as a counter-strike on the side opposite to the application of force. The area of ​​contact with the traumatic agent is large, so significant destruction occurs in this place: skull fractures, brain contusions, subarachnoid hemorrhages.

The source of the formation of subdural hematomas is most often damage to the transitional veins in the area between the surface of the brain and the sagittal sinuses as a result of displacement of the brain or bone fragments. Another reason is the rupture of the delicate pial vessels during sharp rotation of the head and displacement of the hemispheres around the vertical or horizontal axes. These same vessels are damaged during brain contusions.

Subdural hematomas can reach ml, but more often their volume is ml. In 60% of cases, hematomas form over the convex surface of the brain in the form of a cloak 1-1.5 cm thick, covering 1-2 lobes over an area of ​​4x6 to 13x15 cm.

Clinical manifestations of subdural hematomas in classic version are close to the course of epidural hemorrhages, but at the same time have a large number distinctive features and signs that allow differential diagnosis of these nosological forms of injury in the acute period. (Table 2).

Thus, there are quite a few signs that make it possible to distinguish the clinical picture of an epidural from a subdural hematoma.

Subdural hygroma - It is a localized collection of cerebrospinal fluid in the space beneath the dura mater resulting from trauma.

Subdural hygromas are much less common than hematomas in a similar situation. The issue of pathogenesis of hygroma has not been completely resolved. The reasons for the limited accumulation of cerebrospinal fluid under the dura mater are considered to be damage to the arachnoid membrane, like a valve that allows the cerebrospinal fluid to move in only one direction - from the subarachnoid to the subdural space. Hygromas can also occur due to changes in the vessels of the dura mater, creating conditions for blood plasma to leak into the subdural space, or as a result of severe brain damage when communications arise between the intrathecal spaces and lateral ventricles.

The clinical manifestations of subdural hygromas are heterogeneous, since they can occur both in isolation and in combination with many nosological forms of traumatic brain injury, most often accompanying severe brain contusion.

If the hygroma occurs in isolation, then its clinical picture is very similar to that of a subdural hematoma, especially in its three-phase course. As a rule, after an injury with a short-term loss of consciousness, a clear interval occurs, usually lasting 1-3 days and with typical cerebral symptoms. Then the headache intensifies, stupor appears and increases, meningeal and local symptoms appear in the form of facial nerve paresis, mono- or hemiparesis, and sensory disturbances.

However, in the classic clinic of intracranial hematoma, one can notice some features typical of subdural hygroma, or signs that are most often found with it. This is a long clear period (1-10 days) - hygromas often have a subacute course. Headaches are paroxysmal, radiating to the eyeballs and cervical-occipital region. Photophobia and local pain upon percussion of the skull are characteristic. The general condition of the patients deteriorates slowly, as do the signs of brain compression, which increase relatively more gently and gradually. Mental disorders such as frontal syndrome are often observed (decreased criticism of one’s condition, euphoria, disorientation, apathetic-abulic symptoms), proboscis and grasping reflexes appear. Psychomotor agitation often develops.

Paresis of the limbs of a spastic type with hypertonicity and revitalization of reflexes. Quite often, patients with hygromas have convulsive seizures starting from the muscles of the face or on the contralateral side. Subdural hygromas are characterized by a gradual, wave-like deepening of secondary disturbances of consciousness. So, in the early stages, after a convulsive seizure, consciousness is restored and contact can be made with the patient.

Acute hygromas are characterized by the absence of anisocaria, and if it is present, then, unlike hematomas, the reaction of the pupil to light is preserved.

Intracerebral hematoma - This is a post-traumatic hemorrhage into the substance of the brain with the formation of a cavity filled with blood. The incidence of intracerebral hemorrhages is approximately 5-7% of all intracranial hematomas. The favorite localization is the frontotemporal lobe. The size of intracerebral hematomas is relatively small and is 1-3 cm in diameter, but can reach 7-8 cm. The volume of spilled blood is most often within ml, sometimes more massive hematomas are found.

The source of cerebral hemorrhages is damaged vessels of the brain substance due to its contusion or other types of traumatic brain injury

The clinical picture of isolated intracerebral hemorrhages tends to be three-phase and have acute, subacute and chronic stages of the course. The latter depend on the volume of the hematoma and the brain’s response to injury, expressed by edema and swelling.

In the acute course of a hematoma, a clear gap is observed in half of the patients, in the rest it is absent or in an erased form. After the initial loss of consciousness, which can last from several minutes to several days, a period of imaginary well-being begins, which differs from meningeal hematomas in its short duration (no more than 6 hours), the presence, in addition to general cerebral, meningeal and gross focal symptoms in the form of hemiparesis and plegia. It should be emphasized that paresis and paralysis in patients with intracerebral hematomas always develop contralaterally, while pupil dilation in 50% of victims occurs on the side of the hematoma, in the rest - on the opposite side. The light interval, as a rule, ends with a sudden entry into a coma. Vegetative-stem symptoms appear early in the form of respiratory failure, cardiovascular

activities. Hormetonia syndrome often develops, characterized by strong tonic tension in the muscles of the limbs and trunk with a predominance of extensors. Sometimes there are epileptic seizures. All symptoms tend to increase.

Computed tomography, echoEG, angiography and pneumoencephalography can facilitate diagnosis, with the help of which it is possible to respectively identify an area of ​​altered density in the brain substance, a displacement of the M-echo, a displacement of the vascular and median structures of the brain.

Intraventricular hematomas - These are post-traumatic hemorrhages in the cavities of the lateral, III and IV ventricles of the brain. This type of hemorrhage occurs only against the background of a severe brain contusion and practically never occurs in isolation.

Intraventricular hematomas account for 1.5 to 4% of all intracerebral hemorrhages. They are caused by rupture of the choroid plexuses of the ventricles as a result of hydrodynamic shock at the time of injury. Most often, one of the lateral ventricles is affected. Even 100 ml of blood can flow into it.

The clinical picture of intraventricular hematoma depends on the rate of bleeding into the ventricle and the severity of the concomitant brain contusion. Blood pressure on the walls of the ventricle and irritation of the reflexogenic zones embedded in them not only aggravate the severity of the injury, but also gives the clinical picture some originality. There is a disorder of consciousness in the form of stupor or coma. Literally after the injury, vegetative-stem disorders appear and quickly increase. Against the background of progressive intracranial hypertension, combined with arterial hypertension, hyperthermia occurs, reaching 38-41°C. The victim's face and neck are hyperemic with symptoms of hyperhidrosis.

Severe motor agitation with the presence of hormetonia is considered characteristic of intraventricular hematomas. Extensor spasms can be provoked by external stimuli, even by neurological examination techniques. Sometimes they are combined with epileptic seizures.

Neurological symptoms with intraventricular hematomas are usually bilateral.

Dysregulation of breathing appears quite early in the form of tachypnea (30-70 breaths per minute), which persistently progress, reaching pathological forms (Cheyne-Stokes, Biota). Subsequently, signs of brain dislocation appear (transition of bradycardia to tachycardia, reaching 160 or more beats per minute with bilateral mydriasis, the appearance of pathological reflexes from the feet.

In patients with intraventricular hematomas, motor-tonic phenomena are often detected in the form of automated gestures, stereotypical hand movements (“scratching”, “stroking”, “pulling the blanket”), as well as oral and manual hyperkinesis of the subcortical type (sucking and smacking movements of the lips, tremor limbs), which manifest from the initial period and can persist until the agonal state.

Lumbar puncture reveals copious amounts of blood in the cerebrospinal fluid.

Subarachnoid hemorrhage - This is a post-traumatic accumulation of blood in the subarachnoid space, which does not cause local compression of the brain. This intracranial hemorrhage does not occur in isolation, but is a companion to traumatic brain injuries, mainly brain contusion. Subarachnoid hemorrhages occur in 15-42% of all traumatic brain injuries, and in severe forms they reach 79%. Even higher figures are given by forensic doctors, who observed subarachnoid hemorrhages in 84-92% of cases, and some in 100% of all traumatic brain injuries.

The source of subarachnoid hemorrhages is ruptured vessels of the membranes that limit the subarachnoid space, or increased vascular permeability as a result of injury. The spilled blood spreads over large areas (from 50 to 300 cm 2 or more), taking on a lamellar character. Subsequently, most of the blood is absorbed into the subdural space and further into the blood vessels of the dura mater, the remaining red blood cells undergo decay. It has been established that blood and its toxic breakdown products (bilirubin, serotonin) irritate the meninges and cause disturbances in cerebral circulation, liquor dynamics, and sharp fluctuations in intracranial pressure with a disorder of brain functions.

What is pathognomic for subarachnoid hemorrhages is that loss of consciousness after the initial injury is replaced by a state of stupor, disorientation, and often psychomotor agitation. The restoration of consciousness is accompanied by retro- and anterograde amnesia, memory impairment of the asthenic type and Korsakoff traumatic amnestic syndrome.

In victims with subarachnoid hemorrhage, by the end of the first day, meningeal syndrome develops as a response to irritation of the membranes with blood. It is characterized by intense headache in the occipital and frontal regions, pain in the eyeballs and neck, photophobia, nausea and repeated vomiting, stiff neck and positive Kernig syndrome. The syndrome increases, reaching a peak on days 7-8, and then declines and disappears by the day.

As a result of irritation by blood of the recurrent branch trigeminal nerve(1st branch) cerebellar tentorium syndrome occurs, manifested by photophobia, injection of conjunctival vessels, lacrimation, and rapid blinking. As the flow of fresh blood into the cerebrospinal fluid decreases, the syndrome fades and completely disappears by 6-7 days.

The breakdown products of blood and brain detritus inhibit the cortical section of the motor analyzer. Because of this, from 2-3 days there is a weakening of the tendon and periosteal reflexes (especially the knee), which disappear completely by 5-6 days. By 8-9, sometimes on days and even more late dates reflexes are restored and return to normal.

For 7-14 days after the injury, an increase in body temperature remains 1.5-2 degrees above normal.

A reliable sign of subarachnoid hemorrhage is the presence of blood in the cerebrospinal fluid.

SKULL FRACTURES

Fractures of the skull bones account for up to 10% of fractures of all skeletal bones and are classified as severe injuries, because they are unthinkable without damage to the underlying structures - the membranes and substance of the brain. 18-20% of all severe traumatic brain injuries are accompanied by skull fractures. There are fractures of the facial and cerebral skull, and fractures of the vault and base are distinguished among injuries of the cerebral skull.

Fractures of the base of the skull

Fractures of the base of the skull arise predominantly from an indirect mechanism of injury when falling from a height onto the head, pelvis, lower limbs due to impact through the spine, and also as a continuation of fractures of the vault. If the fracture is single, then the fracture line can pass through one of the cranial fossae of the base: the anterior, middle or posterior, which will subsequently determine the clinical picture of the injury. The latter has characteristic manifestations also because a fracture of the base of the skull is accompanied by a rupture of the dura mater, which is intimately fused to it and often forms a connection between the cranial cavity and the external environment. Thus, the picture of a fracture of the base of the skull consists of clinical manifestations of concomitant brain injury (contusion of varying severity) and symptoms that are pathognomonic for a violation of the integrity of the anterior, middle or posterior cranial fossa.

In the first case, hemorrhages occur in the paraorbital tissue (symptom of “glasses”) and leakage of cerebrospinal fluid mixed with blood from the nasal passages. It should be noted that with traumatic brain injuries, multiple bruises of the soft tissues of the head are possible with the formation of a large number of different sizes and localizations of bruises and bleeding from the nose, ear canals, etc. It is necessary to be able to differentiate bruises and bleeding as a result of the direct mechanism of injury from the symptom of “glasses” and liquorrhea.

Traumatic “spectacles” appear an hour or more after the injury, often symmetrical. The color of the bruise is homogeneous and does not extend beyond the orbit. Palpation is painless. There are no signs of mechanical impact - wounds, abrasions, eye injuries. A fracture of the base of the skull may be accompanied by exophthalmos (hemorrhage into the retrobulbar tissue) and subcutaneous emphysema when the air cavities are damaged.

With direct trauma, bruising appears immediately after the blow. They are not symmetrical and often extend beyond the orbit and are painful on palpation. There are signs of direct mechanical impact: skin abrasions, wounds, hemorrhages in the sclera, bruises of uneven color, etc.

Blood mixed with cerebrospinal fluid on white cotton fabric produces a stain in the form of two rings of different colors. In the center, the color is more intense due to the formed elements of blood, but at the periphery it has a sterile color, formed by an excess of the liquid part.

In case of a fracture of the middle cranial fossa, characteristic signs should be considered a bruise in the back wall pharynx and liquorrhea from the ear canals.

A fracture of the posterior cranial fossa is accompanied by severe bulbar disorders (damage to the brain stem) and bruising into the subcutaneous tissue of the mastoid region. It should be noted that all bruises from a fracture of the base of the skull appear, as well as the symptom of “glasses,” no earlier than hours from the moment of injury. The clinic is the leader in diagnosing fractures of the base of the skull, since primary radiographs in standard settings can detect bone damage in only 8-9% of victims. This is due to the complexity of the anatomical structure of the bones that form the bottom of the skull, and the no less complex course of the fracture line, which selects holes in the weakest places of the base of the skull. For reliable diagnosis, special techniques are required, which cannot always be used due to the severity of the patient’s condition.

Cranial vault fractures

Cranial vault fractures result from a direct mechanism of injury, where the point of application of force and the site of injury coincide. An indirect mechanism is also possible when the skull, which has a spherical shape, is compressed; a fracture occurs at the intersection point power lines with an extreme load, and not in a pressure zone.

Fractures of the calvarium are divided into linear (cracks), depressed (impression and depression) and comminuted.

Clinical diagnosis of closed calvarial fractures, which account for about 2/3 of all fractures, is extremely difficult. Subperiosteal and subgaleal hematomas and severe pain complicate palpation, which should already be extremely gentle to avoid

displacement of the comminuted fracture and injury to the underlying formations. Anamnesis information about the severity may suggest a possible fracture. mechanical injury and a symptom of axial load - compression of the head in the sagittal and frontal planes. In this case, the pain radiates to the fracture site. To clarify the diagnosis, it is necessary to perform craniography in standard settings, but even then, according to forensic autopsies, about 20% of fractures remain unrecognized.

The greatest difficulty in diagnosis is presented by linear fractures, which are often mistaken for a vascular pattern. The latter differs from a linear fracture in that it has a tree-like shape with a wider base and a thin apex. In addition, twisted branches extend from the trunk, which in turn have the same branches, but thinner.

Rice. 5. X-ray signs of a calvarial fracture:

A - normal vascular pattern; B - symptom of enlightenment and zigzag;

B - symptom of line doubling (symptom of “ice flake”)

Linear fractures have a number of distinctive features:

1. Symptom of transparency (linear clearing) - is associated with a break in the bone and is often distinct, but sometimes it may be due to the vascular pattern or the contour of the cranial sutures.

Symptom of bifurcation - Along the course of the cracks, in some areas the line bifurcates, and then again goes single. Bifurcation occurs with through cracks, when a beam coming at an angle to the fracture line can separately reflect the edges of the outer and inner vault plates. An illusion is created that islands of bone are gouged out along the fracture line, which is why this sign is called the “ice flake” symptom. The symptom of bifurcation absolutely confirms the diagnosis of a fracture.

Zigzag symptom(lightning) - expressed by a zigzag line of enlightenment. Refers to reliable signs of a fracture that have absolute diagnostic value (Fig. 5).

Sometimes, along with cracks, seams come apart.

Treatment of patients with traumatic brain injury

Treatment of patients with traumatic brain injury is a complex and extensive range of medical measures, the choice of which in each specific case depends on the type, severity and progression of the injury, the stage at which therapy was started, age, concomitant diseases and much more.

Assistance to victims with traumatic brain injury can be divided into three periods: assistance for prehospital stage, treatment in a hospital (hospital stage) and “follow-up treatment” in a polyclinic setting (outpatient stage) or under the supervision of a family doctor.

Providing assistance at the prehospital stage is as follows:

Place the patient in a horizontal position. Create peace of mind with the means at hand: pillow, bolsters, clothes.

Check and, if necessary, clear the airways from vomit, tongue retraction, etc.

Stop external bleeding by pressing the edges of the wound with your fingers or a pressure bandage.

Give oxygen inhalation.

According to indications, the following are used: analeptics (cordiamin, cititon, lobeline), cardiac glycosides (strophanthin K, korglykon).

Transport the patient urgently (necessarily in a supine position) to a medical facility.

All patients with traumatic brain injury must be hospitalized! Treatment in a hospital can be conservative or surgical. Bloodless treatment methods are used much more often, while surgical interventions are performed according to strict indications.

Patients with concussion, brain contusion, closed calvarial fractures, fractures of the base of the skull, and subarachnoid hemorrhages are treated conservatively.

All patients, regardless of the type of injury, are prescribed:

Strict bed rest. Its duration depends on the severity of the injury. So, with a 1st degree concussion, strict bed rest lasts 5-7 days, 2nd degree - days. For a cerebral contusion of the first degree, days, second degree, a week and third degree - at least 3-4 weeks. To determine the termination of strict bed rest, in addition to the specified periods, the Mann-Gurevich symptom is used. If it is negative, the patient can sit up in bed, and after adaptation, stand up and walk under the supervision of staff.

Cold to the head. Use ice packs wrapped in a towel to prevent frostbite. To cool the head, helmets of various designs were offered (with a system of constantly circulating cold water, with a system of thermoelements, etc.). Unfortunately, our industry does not produce these necessary devices for treating patients. Exposure to head hypothermia depends on the severity of the injury. For mild injuries (concussion and cerebral contusion of the first degree), its exposure is limited to 2-3 hours, and for severe injuries, exposure lasts 7-8 hours or more, up to 1-2 days. But it should be remembered that when using cold for a long time, take a break for 1 hour every 2-3 hours.

The purpose of using cold is to normalize vascular disorders, reduce the production of cerebrospinal fluid, prevent cerebral edema, reduce the need for oxygen in brain tissue, and reduce headaches.

3. Sedatives(sodium bromide, bromocamphor, corvalol), etc. tranquilizers(Elenium, Seduxen, Tazepam).

4. Sleeping pills(phenobarbital, barbamyl, etaminal sodium). Strict bed rest, the prescription of tranquilizers, sedatives and hypnotics are a set of measures aimed at creating rest for the damaged organ, i.e. brain. Medicines weaken external stimuli, prolong physiological sleep, which has a beneficial effect on the functions of the central nervous system.

5. Antihistamines(diphenhydramine, fenkarol, diazolin).

As a result of vascular disorders and hypoxia of the brain, destruction and resorption of intracranial hemorrhages, and disintegration of the destroyed brain matter, a mass of histamine-like substances (serotonin, etc.) is formed, therefore the prescription of antihistamines is mandatory.

The further choice of treatment prescriptions depends on the height of the patient’s cerebrospinal fluid pressure. With increased cerebrospinal fluid pressure (hypertension syndrome), treatment should be as follows: position in bed according to Fowler - with the head end elevated, diet No. 7 with limited salt and liquid.

To reduce cerebral edema, dehydration is used. Concentrated hypertonic solutions are administered intravenously to increase the osmotic pressure in the vascular bed and cause the outflow of fluid from the interstitial spaces of the brain. For osmotherapy, use 40% glucose solution, 40% sodium chloride solution, 25% magnesium sulfate solution, 15% mannitol solution at the rate of -1-1.5 per 1 kg of body weight. The last two drugs have pronounced diuretic properties. Of the diuretics, furosemide (Lasix) is most often used for tissue dehydration. Cleansing enemas help remove fluid from the body.

Unloading lumbar punctures directly reduce cerebrospinal fluid pressure, when, following a lumbar puncture, 8-12 ml of cerebrospinal fluid are slowly released.

For hypotensive syndrome, the following is prescribed: diet No. 15, position in bed according to Trandelenburg - with the leg end raised. Solutions with low salt concentrations (isotonic Ringer-Locke, 5% glucose solution) are administered intravenously. Subcutaneous injections of caffeine-sodium benzonate 1 ml of 10% solution and vagosympathetic novocaine blockades have a good therapeutic effect.

In some cases, it becomes necessary to prescribe certain groups of drugs and medicines. So, for open injuries, when there is a threat of developing infectious complications, antiseptics, antibiotics and sulfonamides are used.

In case of violation of vital functions, analeptic drugs are administered that stimulate the respiratory center and vascular tone (cordiamin, lobeline hydrochloride, cititon); to normalize blood pressure in the entire vascular bed, adrenomimetic substances are used (adrenaline hydrochloride, norepinephrine hydrotartrate, mesatone). Weakness of the heart muscle is treated with cardiac glycosides (strophanthin K, corglycon).

Traumatic brain injury is often part of a polytrauma accompanied by shock and blood loss. In the complex of anti-shock therapy, blood and plasma-substituting solutions (reopolyglucin, gelatinol, Acesol) are transfused, analgesics (morphine hydrochloride, promedol, analgin), hormones (hydrocortisone) and other drugs are administered.

Surgical treatment of patients with acute traumatic brain injury is inevitable in case of open injuries and in the presence of signs of brain compression. For open injuries, primary surgical treatment is performed. The wound is closed with sterile material. The hair around it is shaved off. The skin is washed with soapy water, wiped with napkins and treated twice with a solution of 5% iodine tincture. Local infiltration anesthesia is performed with a 0.25% solution of novocaine with the addition of antibiotics. After anesthesia, the wound is thoroughly washed with an antiseptic solution (furacilin, hydrogen peroxide, rivanol) and examined. If only soft tissue is damaged, nonviable tissue is excised. For compressed wounds with crushed edges, it is better to excise them to a width of 0.3-0.5 cm to the bone. The bleeding is stopped and the wound is sutured.

If a fracture is detected during inspection of the wound, then it is necessary to carefully remove all small loose fragments with tweezers and examine the dura mater. If there is no damage, normal color, or preserved pulsation, the shell is not opened. The edges of the bone wound are resected with pliers to a width of 0.5 cm. Hemostasis is performed and sutures are placed on the wound.

If the dura mater is damaged, i.e. If there is a penetrating wound to the skull, then primary surgical treatment is performed as described above, but with economical excision of the edges of the shell. For better inspection of the subdural space, the wound of the dura mater is expanded. Loose bone fragments, brain detritus, and blood are washed out with hydrogen peroxide and warm isotonic sodium chloride solution. After stopping the bleeding, the dura mater is sutured, if possible, and layer-by-layer sutures are applied to the soft tissues of the skull.

Compression of the brain, regardless of the reasons that caused it, must be eliminated immediately after diagnosis.

For depressed closed fractures of the calvarium, an incision is made into the soft tissue down to the bone with the expectation of exposing the fracture site. A milling hole is placed next to it, through which they try to lift the depressed fragment using a levator. If the fragments were able to be lifted, which happens very rarely, and they do not move, then the operation can be completed, having first made sure that there are no indications for extended surgery. If the fragments cannot be lifted, then the depressed portion of the bone is resected from the side of the burr hole. The further course of the intervention is the same as during primary surgical treatment, but without excision in the dura mater.

If the brain is compressed by hematomas or hygroma, resection or osteoplastic surgery can be performed. The first option of the operation is that a search burr hole is placed in the projection of the suspected hematoma. If a hematoma is detected, the hole is widened by gradual resection of the bone until required sizes(6x6, 7x7 cm). Through the created window, intervention is performed on the brain and membranes. The operation is completed by suturing the soft tissue, leaving a large defect in the skull bones. This operation creates good decompression of the brain, especially when compression of the brain is combined with severe contusion. But resection trepanation also has negative sides. After this, another intervention is necessary to close the skull defect with synthetic material (steractyl) or autologous bone taken from the rib. If this is not done, post-trepanation syndrome will develop. Changes in intracranial pressure caused by physical stress (straining, coughing, sneezing, etc.) lead to frequent movements of the brain matter into the “window” of the skull defect. Trauma to the brain from the edges of the burr hole causes the development of a fibrotic process in this area. Adhesions are formed between the brain and the membranes, bones and integument of the skull, which cause local pain and headaches, and subsequently epileptic seizures. Osteoplastic trepanation does not leave skull defects requiring subsequent plastic surgery. A semi-oval incision is made from the base downwards in the soft tissue down to the bone. Along the incision line, without separating the soft tissue flap, five milling holes are drilled - two at the base of the flap and three along the arc. Using a guide, a Gigli saw is passed through two milling holes and the bone bridge is sawed through. All holes are gradually connected into a single one, and the bone-soft tissue flap on the feeding pedicle is turned downwards. The further course of the operation depends on the type of injury. After completing the intervention in the cranial cavity, the bone flap is placed in place and the soft tissue is sutured layer by layer.

Test task for self-study on the topic “Craniobrain injury”

Mechanisms of traumatic brain injury.

Classification of traumatic brain injury.

Name the general cerebral symptoms.

Name local symptoms.

Name meningeal symptoms.

Name the stem symptoms.

What is hyper-, hypo- and normotensive syndrome and how to define it?

How is a concussion diagnosed?

On what basis is the diagnosis of “brain contusion” made?

Gradation of injury severity, clinical differences in degrees of severity.

Causes of compression of the brain.

Clinic of compression of the brain by bone fragments and foreign bodies, as distinguished from brain contusion.

Clinic of brain compression by intracerebral and intraventricular hematomas.

Clinic of brain compression by epi- and subdural hematomas, as distinguished from brain contusion.

What is a subdural hygroma?

Difference between the clinic of concussion, bruise and compression by epi- and subdural hematomas.

Clinic of subarachnoid hemorrhage.

Fracture of the base of the skull, diagnosis.

Traumatic glasses and liquorrhea, their diagnosis. Signs of damage to the anterior, middle and posterior cranial fossae.

Fractures of the cranial vault, diagnosis, tactics.

First aid for traumatic brain injuries.

Conservative treatment of acute traumatic brain injury, give a pathogenetic rationale.

Conservative treatment of brain damage during the recovery period.

Surgical treatment of traumatic brain injury (TBI): puncture, trephination, trepanation.

Techniques of various types of trepanations, necessary instruments.

What is post-trepanation syndrome, its treatment.

Outcomes and long-term consequences of TBI.

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Historically, the treatment of injuries was of primary importance in the development of surgery. And to this day, damage (trauma) is one of the largest and most diverse sections of surgery.

THE CONCEPT OF TRAUMA, TRAUMATISM, HISTORY OF TRAUMATOLOGY

Basic concepts Definitions

Injury(Greek trauma- damage) - simultaneous exposure to an external factor that causes local anatomical and functional disorders in tissues, accompanied by general reactions of the body.

Traumatology- the science of trauma.

Injuries- a set of injuries in a certain territory (in a country, city, etc.) or among a certain group of people (in agriculture, in production, in sports, etc.).

Injuries are divided into industrial and non-industrial. This division has important social and legal aspects. If non-production injuries are to some extent a problem, the misfortune of the victim, then in the case of an industrial injury, a certain share of the blame is borne by the enterprise or organization where it occurred. Occupational injuries are usually the result of non-compliance with safety regulations at the enterprise. Therefore, production management may receive serious administrative and financial penalties. In particular, by a court decision, an enterprise may be closed altogether, and in case of gross violations of safety regulations, its owners may also bear criminal liability. In addition, the company in most cases fully pays the costs of treatment of the victim, pays a special pension and compensation.

In Russia, an industrial injury is considered to be an injury received at the workplace while performing official duties, as well as while traveling to and from work. Moreover, if an injury occurs at a state-owned enterprise, from the first day the victim is issued a certificate of incapacity for work with 100% payment (unlike a non-working, domestic injury, when a certificate of incapacity for work is issued from the 6th day and is paid in accordance with the rules accepted in the industry: length of service, position, etc.).

Depending on the type of activity, place and circumstances in which the injury was sustained, domestic, transport, industrial (agricultural, military, etc.), and sports types of injuries are distinguished. Separately, combat injuries received by military personnel and civilians during wars and military conflicts should be highlighted.

Statistics

The importance of treating patients with various injuries is evidenced by the following facts. In terms of mortality, traumatism usually ranked 2-3rd after mortality from diseases of the cardiovascular system, along with cancer. In recent years, the mortality rate from injuries has come in second place.

Injuries rank third among all causes of disability. In men, injuries occur twice as often as in women, and in young people under 40 years of age they take first place in the structure of overall morbidity.

Up to 8-10% of trauma patients require hospitalization.

The mortality rate from various injuries per 100,000 population in Russia is about 230 people, in the USA - about 80, in European countries - 40-50.

In Russia, approximately half of all cases are domestic injuries, transport - about 40%, industrial - 5-6%.

The incidence of injury is significantly higher in individuals with alcoholism.

History of traumatology

The first information about methods of treating fractures and their results was obtained through archaeological excavations. Thus, when analyzing 36 Neanderthal skeletons with consequences of fractures (more than 10,000 BC), only 11 showed unsatisfactory treatment results. In Egypt, during the excavations of the pyramids (2500 BC) there were

mummies were found with traces of fused fractures of the limb bones, enclosed in a case made of palm leaves. Works devoted to issues of traumatology - “On fractures”, “On joints”, “On levers” - back in the 4th century BC. left for us by the great scientist Hippocrates. Drawings of his apparatus for comparing bone fragments have also been preserved, and the method of managing shoulder dislocation according to the Hippocratic method is still widely used in practice.

In ancient Rome (1st-2nd centuries AD), Cornelius Celsus described the technique of operations on bones and proposed special instruments for this, and Claudius Galen, studying the issues of damage and deformation of the skeleton, introduced terms such as “lordosis”, “ kyphosis" and "scoliosis".

Ambroise Pare (1510-1590) made a great contribution to the development of traumatology and orthopedics. He introduced special devices for immobilization and for the first time paid attention to the issues of correction of deformities (corset, special shoes) and prosthetics, thereby laying the foundations of orthopedics.

A significant accumulation of descriptive information about various injuries and deformations of the skeleton was prepared by the appearance in 1741 of a two-volume work by the dean of the medical faculty of the University of Paris Andry, which became the first manual on orthopedics, and the drawing he provided depicting a method for straightening a curved young tree by fixing it to a straight pole (Fig. . 11-1) has since become the emblem of orthopedics.

Rice. 11-1. The straightening tree is the emblem of orthopedics (drawing from Andri’s book)

The first chiropractic school in Rus' was founded in 1654 in Moscow under the Ankor order. In 1767, Peter I established the Medical-Surgical School in Moscow, in which much attention was paid to chiropractic sciences.

The further development of traumatology in Russia was associated with the Moscow and St. Petersburg schools. The Moscow one was headed by the dean of the medical faculty of the university E.O. Mukhin, who developed many methods of conservative and surgical treatment of injuries. He wrote the first textbook on traumatology in Russian (1806).

In St. Petersburg, at the Medical-Surgical Academy, the school of traumatologists was headed by adjunct Kh.Kh. Solomon, who paid more attention to the development of orthopedics.

N.I. made a significant contribution to the development of traumatology. Pirogov (1810-1881). He developed the first osteoplastic amputation and proposed a “stick-on alabaster bandage” for the treatment of fractures and transportation of the wounded, which in many ways was the prototype of the modern plaster cast.

The discovery in 1895 was of great importance for traumatology and orthopedics. x-rays which made it possible to radically improve the diagnosis of skeletal injuries and deformities.

At the beginning of the twentieth century, two fundamental schools of traumatology were formed in Russia, headed by G.I. Turner and R.R. Harmful.

G.I. Turner in 1900 created the first department of orthopedics, achieved the construction of an orthopedic clinic at the Medical-Surgical Academy in St. Petersburg, which was opened in 1913. He also headed a shelter for poor and crippled children, which in 1931 became the “Institute of Restoration working ability of physically handicapped children named after. G.I. Turner."

R.R.

Vreden entered the world of orthopedics as a pioneer of surgical orthopedics. They offered more than 20 types of new surgical interventions on bones and joints for a wide variety of pathologies. R.R. Vreden created an orthopedic hospital in St. Petersburg, which later became the Institute of Traumatology and Orthopedics (currently the Russian Research Institute of Traumatology and Orthopedics named after R.R. Vreden).

Technological progress led to a qualitative change in traumatology and orthopedics in the twentieth century. The range of surgical interventions has expanded significantly. Methods of skeletal traction, compression-distraction osteosynthesis, bone plastic surgery, and surgical treatment of injuries and diseases of the spine have been developed and are successfully used. An achievement in recent decades has been joint replacement. Significant advances have been made in limb prosthetics. At the same time, it should be noted the priority role in the main achievements of world traumatology and orthopedics of domestic scientists (G.A. Ilizarov, O.N. Gudushauri, K.M. Sivash, Ya.L. Tsivyan, G.S. Yumashev, etc.).

Modern traumatology

The initial cause of changes occurring in the body during injury is the impact of some external factor. The nature of this factor can be different: mechanical force, high or low temperature (thermal factor), electric current, radioactive radiation, chemicals.

Thus, exposure to thermal factors, electric current, as well as radiation and chemicals lead to burns (frostbite). The changes that occur in the victim’s body turn out to be so unique that their treatment requires special training of both medical personnel and hospitals where they provide care to this group of patients. In this regard, the treatment of burns and frostbite became a separate discipline from traumatology - combustiology.

Thus, the subject of modern traumatology is the changes in the body that occur when exposed to external factors mechanical in nature. However, there are also a number of peculiarities.

1. Injuries to internal organs are usually considered in matters of private surgery, since the methods of their diagnosis and treatment are quite specific and, above all, are determined by the characteristics of the location, structure and functions of the damaged organs. Moreover, patients with injuries to internal organs are usually treated in the appropriate specialized departments. Thus, victims with injuries to the brain and spinal cord are treated in the neurosurgery department, with abdominal injuries - in the emergency or abdominal surgery department, with chest injuries - in the emergency or thoracic surgery department, with injuries to the urinary and reproductive systems - in the urology department, etc. . Recently, due to the increase in the number of severe stab and gunshot wounds in major cities Specialized departments for thoracoabdominal trauma are being created, significantly different from departments with a purely traumatological profile. Taking into account the increasing frequency of combined injuries,

significantly different from isolated injuries of individual anatomical areas not only in severity, but also in approaches to organizing treatment, special departments with this direction are also created in large hospitals.

2. All injuries, depending on the presence of damage to the integumentary tissues, are divided into open and closed. At the same time, the treatment of open injuries, or wounds, is, first of all, a general surgical problem. The study of wounds is the basis of the work of any surgeon, as it covers the problems of diagnosis and treatment not only of accidental mechanical damage, but also of surgical wounds, purulent wounds, etc. (see chapter 4).

Taking into account the listed features of modern injuries and providing assistance to victims, the subject of traumatology at present is essentially the diagnosis and treatment of mechanical damage to soft tissues and bones, that is, the musculoskeletal system. In this regard, orthopedics is very close to traumatology.

Orthopedics(Greek orthos- straight, pedie- child) - the science of recognizing and treating developmental disorders, injuries and diseases of the musculoskeletal system and their consequences.

Treatment methods in traumatology and orthopedics are very close, if not identical. That is why the specialty “traumatology and orthopedics” is currently designated, patients with traumatology and orthopedic profiles are treated in the same hospitals (or institutes), students in the fifth year of a medical university also study the discipline “traumatology and orthopedics”.

This chapter deals exclusively with issues of damage to the musculoskeletal system. The problems of diagnosis and treatment of injuries to internal organs are practically not covered, since they are discussed in detail in textbooks on private surgery, military field surgery and are studied by students in senior years.

Organization of trauma care

Organizing the provision of care to trauma victims is of great importance for achieving a positive outcome. It is important to note the need for early assistance to the victim at the scene of the incident, ensuring continuity of treatment measures at subsequent stages and high quality specialized care.

The provision of trauma care consists of the following components: first aid, evacuation to a medical facility, outpatient and inpatient treatment, as well as rehabilitation.

First aid

First aid can be provided either by a doctor or paramedical personnel (a doctor or paramedic at an ambulance or a first aid station at an enterprise), or by other people in the form of self- and mutual assistance. In this regard, the role of sanitary educational work and improving the general culture of the population turns out to be very important. In addition to medical workers, representatives of the police, fire service, employees of the Ministry of Emergency Situations, military personnel, vehicle drivers, etc. must have first aid skills.

In Western countries there is a special system of paramedical services, the main task of which is to provide first aid medical care at the scene of the incident. Representatives of this service, the so-called “paramedics,” are not professional medical workers, but they all undergo about 200 hours of medical training under a special program. Firefighters, police officers, and volunteers who want to acquire first aid skills are trained under the same program.

When providing assistance at the scene of an incident, it is always advisable to perform pain relief, carry out transport immobilization, apply a bandage, etc. The role of first aid is especially indispensable when it is necessary to stop external bleeding and perform basic cardiopulmonary resuscitation, since the time factor here is of paramount importance for saving the victim's life.

Evacuation to a medical facility

In some cases, especially with minor injuries, providing first aid to the victim is sufficient. But much more often, patients need qualified medical care, for which they should be taken to the appropriate medical facility. Usually, the ambulance service handles the evacuation of victims; less often, they can be transported by police representatives or private individuals (in case of road accidents, etc.).

When evacuating a victim in serious condition, it is important to deliver him to the hospital as quickly as possible, but we must not forget about the parallel administration of infusion therapy, anesthesia, and transport immobilization, if there are appropriate indications for their implementation.

Ambulatory treatment

Not all victims need to be hospitalized: in 90% of cases, patients suffering from injuries can be provided with care on an outpatient basis.

Outpatient treatment of trauma patients is carried out in specialized trauma centers. They are equipped with everything necessary to perform an X-ray examination, primary surgical treatment of a wound, application of regular and plaster bandages, etc.

At the trauma center, victims receive comprehensive treatment until they are discharged to work. Patients are also treated here after their discharge from trauma hospitals.

Primary outpatient care can be provided in the emergency room of a trauma hospital if, after examining the patient, no indications for hospitalization have been identified.

Hospital treatment

Inpatient treatment of traumatological patients is carried out in specialized departments of hospitals, clinics at the departments of traumatology and orthopedics of medical universities, research institutes of traumatology and orthopedics, the largest of which are the Russian Institute of Traumatology and Orthopedics named after. R.R.

Vreden in St. Petersburg and the Central Institute of Traumatology and Orthopedics (CITO) in Moscow. These centers also conduct scientific and methodological work, training and specialization of orthopedic traumatologists. Currently in Russia there are 80,000 trauma beds, which is 30% of all surgical beds, there are twelve research institutes of traumatology and orthopedics, as well as 73 departments of this profile at medical universities.

Rehabilitation

The peculiarity of diseases and injuries of the musculoskeletal system is the duration of treatment and restoration of lost

functions.

In this regard, the role of rehabilitation is increasing. Rehabilitation is carried out in trauma hospitals, trauma centers and clinics at the patients’ place of residence. In addition, there are many special rehabilitation centers and specialized sanatoriums, where it is possible to carry out a complex of rehabilitation measures (massage, special exercise equipment, physical therapy [physical therapy], physiotherapy, mud therapy, etc.). Features of examination and treatment of trauma patients When examining trauma victims, it is necessary to follow all the rules for examining surgical patients, adhering to the general outline of the medical history (see Chapter 10). The diagnosis is also based on the collection of complaints and anamnesis, an objective examination with a detailed study

status localis

and the use of special diagnostic methods. Moreover, it is necessary to maintain careful medical records, since many domestic and work-related injuries subsequently become the subject of litigation. But at the same time, the examination of trauma patients has its own distinctive features, which is associated with the following features:

Victims are usually examined in the acute period, immediately after injury against the background of pain and a stressful situation;

Complaints

When collecting complaints and anamnesis, the doctor may encounter objective difficulties associated with the characteristics of the general condition of the victim.

These difficulties are usually due to the following reasons:

The severity of the patient's condition does not allow collecting complaints and anamnesis to the extent necessary for making a diagnosis;

The state of stress, mental affect, and alcohol intoxication is often accompanied by an inadequate assessment by the patient of his feelings.

Among the complaints in trauma patients, complaints of pain and impaired motor or support function of the damaged limb segment deserve special attention.

The pain immediately after an injury is usually intense and quite clearly localized. An important point is to clarify the connection between pain syndrome and active and passive movements in the area of ​​injury and load.

Functional dysfunction is usually expressed in limited movement, which can be caused by both anatomical damage and pain.

You should pay attention to the ability to move independently and rely on the injured limb, which can immediately indicate the severity of the injuries received.

We must not forget that damage can lead to disruption of innervation and blood supply. Therefore, it is necessary to find out whether the victim has sensory disturbances, paresthesia, convulsions, coldness of the extremities, etc.

Features of anamnesis collection

There are some specific features of collecting anamnesis of the disease and life history of victims. When collected anamnesis morbi

Two concepts are of great importance: the mechanism of injury and the circumstances of injury.

Mechanism of injury

A feature of collecting anamnesis in trauma patients is that the time and cause of the development of the pathological condition, as a rule, are precisely known. Moreover, due to the fundamentally identical structure of the musculoskeletal system, the nature of the disorders that occur in the body is largely typical and is determined by the magnitude, point of application and direction of action of the external force. These factors combine into the concept of mechanism of injury, which thus includes:

The magnitude of the external force;

Application point;

Direction of action;

The nature of the changes that occurred.

The same mechanism of injury leads to the development of typical injuries. Example 1. When hit by a car bumper in the area of ​​the victim’s shin,: a large external force (a moving car with a large mass) acts on the tibial diaphysis (point of application) in a direction perpendicular to the axis of the bone. Typically, this results in a transverse fracture of the tibia with displacement at an angle and the formation of a triangular fragment. This kind of damage is called a “bumper fracture.”

Example 2. A fall from a great height onto straight lower limbs (external force = mg 2, point of application - feet, direction - axis of the body) often leads to a compression fracture of the lumbar spine, fracture of the calcaneus, and central dislocation of the hip.

Example 3. When you fall, for example, by slipping on the street in winter, on an outstretched and outstretched upper limb, a fracture of the radius occurs in a “typical place.”

There are many similar examples. In some cases, victims may feel and hear the crunch of breaking bones, especially when twisting or sharply straightening a limb, etc.

Rice. 11-2.The mechanism of injury in a fracture of the radius in a typical location: a - Collis type fracture; b - Smith type fracture

Circumstances of injury

Determining the circumstances of the injury, in contrast to its mechanism, contributes to a lesser extent to determining the type of injury, but it establishes important associated details at the time of its occurrence. It matters whether the injury occurred at work or at home, on the street or at home; whether it is associated with violent actions, whether it is associated with a suicide attempt, what state the victim was in when receiving the injury (mental affect, alcohol intoxication, cold), the degree of contamination of the wound, etc. matters. It is imperative to find out what happened to the victim after impact of force (whether he lost consciousness, could get up, walk), whether first aid was provided and in what form.

Underestimation of the circumstances of the injury can lead to diagnostic errors. So, if after a fall from a height the victim could walk or run, he is unlikely to have serious bone damage (fractures, dislocations). But if this happened in a state of severe alcoholic intoxication or mental agitation, serious damage is very likely.

Life history features

Collecting anamnesis vitae, In addition to general provisions, it is necessary to find out whether the victim has often had traumatic injuries in the past. The presence of frequent fractures, for example, if a person is not an athlete, indicates fragility of the bones, which may be due to certain metabolic disorders (hyperparathyroidism), long-term hormonal therapy, etc. In addition, you should always remember the possibility of a so-called pathological fracture, which occurred as a result of an underlying disease with damage to bone tissue. Therefore, you should make sure that the patient has no history of cancer, osteomyelitis, tuberculosis, or syphilis.

Of certain prognostic significance is how fractures healed and wounds healed in the past, and whether there are any aggravating processes for the healing process. additional factors(diabetes mellitus, immunodeficiency, anemia, circulatory failure, etc.).

Features of an objective examination of the patient

An objective examination of the victim has its own characteristics due to the fact that it is carried out in the acute period, when the pain syndrome is especially pronounced, and there may also be life-threatening consequences of the injury itself.

Assessing the severity of the condition

Assessing the patient's general condition is of great importance. In case of severe mechanical damage, one should always expect the occurrence of life-threatening conditions that require emergency assistance as early as possible:

Asphyxia;

Continued external or internal bleeding;

Traumatic shock;

Damage to internal organs.

Identification of a threat to the patient’s life entails urgent actions both at the scene of the incident and en route and after delivery of the victim to the hospital: elimination of asphyxia, stopping external bleeding, elimination of tension (valvular) and open pneumothorax, infusion therapy, transport immobilization and other emergency measures - up to the provision of cardiopulmonary resuscitation in case of cardiac arrest.

When assessing the severity of the condition, they are based on clinical signs (state of consciousness, adequacy of breathing, hemodynamic parameters, etc.).

Features of the local survey

During a local examination, it is necessary to carefully identify all existing clinical symptoms, allowing the diagnosis to be made as accurately as possible, but this should not cause unnecessary pain to the patient, much less aggravate existing damage.

Inspection

During examination, in order to more clearly identify deformation or swelling, it is necessary to compare the damaged limb with the uninjured one. The forced position of the limb and its shortening can be of great importance for making a correct diagnosis, for which special measurements are sometimes used. Should

pay attention to the presence of hematomas, existing violation of the integrity of the skin.

Palpation

Palpation must be done very carefully. When determining pain, one should find out not only its local prevalence, but also its appearance during axial loading. Thus, the load on the spinal axis is in some cases determined in a horizontal position of the patient by lightly tapping the feet. More intense impacts in the damaged area can lead to displacement of bone fragments, increased pain and possible additional damage to large vessels, nerve trunks and soft tissues.

During a local study, a number of specific symptoms(crepitus of bone fragments, pathological mobility in the damaged segment, subcutaneous emphysema, etc.).

Determination of range of motion

Determining the volume of active and passive movements is very important to identify the full extent of the damage.

Active movements are movements that the victim performs independently. Their disruption may be associated not only with anatomical changes in bones and joints, but also with damage to nerves or tendons, as well as severe pain.

Passive movements are movements that occur passively under the influence of the examiner’s hands. A decrease in the range of passive movements is associated with pain caused by direct damage to bones and joints.

Comparing the volume of active and passive movements greatly facilitates making an accurate diagnosis. Thus, if the motor nerve is damaged, active movements may be absent, but passive movements will be preserved in full. If there is an intra-articular fracture, both active and passive movements will be impossible due to severe pain in the joint.

When determining the range of motion, it is necessary to evaluate not only flexion and extension, but also rotation (supination and pronation), adduction and abduction. In this case, the results can be assessed both by eye and with the help of special protractors and rulers, which is especially important in orthopedic patients.

Study of peripheral circulation and innervation

When examining a victim with a limb injury, one should not forget about possible damage to the great vessels and nerves. In all cases, the state of blood circulation (color, temperature of the skin, the nature of the pulsation of the main arteries, the severity of the venous pattern, the presence of edema) and the safety of the innervation (impaired sensitivity and motor activity) of the injured limb should be assessed.

Additional methods of examining a trauma patient

Among additional objective methods, the main place is occupied by x-ray diagnostics, while we must not forget about other special techniques.

X-ray examination

The results of X-ray examination are critical for accurate diagnosis and localization of bone and joint damage. However, it should be remembered that a preliminary diagnosis can and should be made on the basis of clinical symptoms, and an x-ray examination can only confirm or refute it. Moreover, in doubtful cases, for example, with rib fractures, clinical symptoms are of decisive importance.

When performing an X-ray examination, the following rules must be observed.

1. The damaged area must be in the center of the radiograph, otherwise