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Consequences of traumatic brain injury ICD 10. Symptoms of closed head injury

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Closed craniocerebral injury– This is a combined injury to the skull and/or brain (BM), when there is no violation of the integrity of the scalp, or there are superficial soft tissue wounds without damage to the aponeurosis. It is possible to have fractures of the bones of the cranial vault (SC) without injuries to adjacent soft tissues and aponeurosis

ICD-10 code

S00 (superficial head injury);
S02.0 (closed fracture of the skull and facial bones);
S03 (dislocation, sprain and strain of joints and ligaments of the head);
S04 (cranial nerve injury);
S05 (injury to the eye and orbit);
S06.0 (intracranial injury without open intracranial wound);
S09 (other and unspecified head injuries)

CCI is among the TOP 10 causes of mortality and disability in the population of the entire globe under the age of 45 years.

In the world, about three thousand people for every 1 million population are hospitalized for TBI, and for every inpatient, another 4 people with TBI are diagnosed by emergency medicine doctors, hospital emergency departments and general practice, and then treated on an outpatient basis. Moreover, of all of them, about 50% are closed injuries.

The bulk of patients are patients with mild traumatic brain injury (up to 90%); moderate and severe (in a comatose state) - approximately 5% each.

Reasons

CTBI: fracture of the cranial vault. (x-ray)

In Russia, the leading cause of closed craniocerebral injury is domestic trauma received at home.

In economically developed countries, motor vehicle injuries predominate as causes.

Less common are falls from various heights - catatraumas and sports injuries.

The main risk factor that accompanies up to 70% of all victims is alcohol intoxication of varying degrees.

During injury, traumatic forces can affect bone and brain tissue, the membranes of the brain, its blood vessels and the ventricular system, causing primary damage: axonal (APM) and focal bruises and crush injuries of the brain.

Then- secondary, due to exposure to:

Intracranial factors: intracranial hypertension, cerebral edema, vasospasm, hydrocephalus, infectious disorders, seizures, cerebral blood flow disorders, neuronal metabolic disorders, transmembrane ion imbalance, neurotoxicity of excitatory amino acids and free radical cellular damage.
Systemic: hypotension - low blood pressure, hypoxia, anemia, hypercapnia, electrolyte disorders, hypoglycemia, acid-base disorders and inflammatory reactions

Leading to secondary ischemia of brain tissue and secondary damage to the brain.

Classification of closed craniocerebral injury

It is customary to distinguish three main forms of traumatic brain injury:

– occurs most often (up to 80%); accompanied by a short-term (up to several minutes) disturbance of consciousness (usually loss of consciousness); memory impairment in the form of retrograde (loss of memory for events that preceded the injury) and/or congrade (which occurred during the TBI) and/or anterograde (which occurred after the TBI) amnesia. Possible attacks of vomiting, cephalalgia (headaches), dizziness, short-term oculomotor disorders, fluctuations in blood pressure and pulse. In this type of TBI, damage to neurons, cell membranes and mitochondria can only be seen with an electron microscope and is caused by the disintegration of nervous processes between the cerebral cortex and underlying structures;
– morphologically variable (from pinpoint hemorrhages to destruction of brain tissue and edema). There are three degrees (mild, moderate and severe). Consciousness turns off for a period of time from several minutes to weeks (depending on the severity). The appearance of meningeal, stem and focal symptoms is characteristic (with moderate and severe bruises);
– occurs in almost 5% of all patients with head injury; intracranial hematomas often form, quickly compressing parts of the brain and leading to a threat to life;
– there is a prolonged loss of consciousness, paresis and impaired tone in the limbs, decerebration, changes in the functioning of the respiratory and cardiovascular systems; CT scan reveals diffuse changes indicating compression of the ventricles and subarachnoid cisterns.

First aid

First of all, you need to call an ambulance. When providing first emergency medical care to a person with a suspected closed head injury, it is necessary to lay him on his side so that vomit and blood do not enter the respiratory tract. Clean them with a cloth wrap - there should be no obstructions in the upper respiratory tract for free breathing.

If there is bleeding, it should be stopped (with a tourniquet - arterial - except for the neck area, with a pressure bandage - venous).

If there are bone fractures, immobilization with improvised or standard devices is mandatory. In parallel with this, infusion therapy is carried out, as well as therapy aimed at stabilizing the heart.

Treatment and rehabilitation

The scope of conservative treatment depends on the clinical form of traumatic brain injury and the severity of the patient’s condition.

For concussion, the use of analgesics, non-steroidal anti-inflammatory, sedative and hypnotic drugs is necessary; providing bed rest for 4-5 days.

For mild to moderate bruises, dehydration therapy with diuretics and antihistamines are additionally prescribed. If subarachnoid (subarachnoid) hemorrhage has developed, hemostatic therapy is necessary, and in the absence of signs of compression and dislocation of the brain, a diagnostic and therapeutic spinal puncture is performed.

Bed rest for mild bruises is up to a week, and for moderate bruises up to two.

In case of severe bruises (with profound impairment of consciousness) and DAP, resuscitation measures are necessary (tracheal intubation and mechanical ventilation or tracheostomy, parenteral nutrition, anticonvulsant, analgesic, infusion therapy), as well as the introduction of anti-enzyme drugs, antioxidants, vasoactive agents, broad-spectrum antibacterial drugs actions (for the purpose of preventing infectious complications - hypostatic pneumonia) and low molecular weight heparins (for the purpose of preventing vascular thrombosis).

In some cases (with extensive intracranial hematomas, depressed fractures, complications), surgical treatment is performed.

Constant and dynamic care is required to prevent the formation of trophic disorders (bedsores). Particular attention should be paid to patient care. Proper care is one of the most important factors in reducing the risk of complications associated with prolonged lying down.

To prevent the occurrence of bedsores, it is necessary to change the patient’s position in bed every 3 hours, and also use an anti-bedsore air mattress.

An important step in restoring functions is after a closed craniocerebral injury with the participation of specialists, including physiotherapy (massage, exercise therapy) and kinesiotherapy, in the presence of speech disorders, a speech therapist and aphasiologist. A frequent accompaniment of severe traumatic brain injury are mental disorders, which can lead to changes in personality and character, sometimes beyond recognition. In these conditions, the help of a psychologist, psychotherapist or psychiatrist is very popular.

Forecast for health and life

After suffering a head injury, complications may develop:

purulent meningitis (in 4%),
(if consciousness is absent for more than a day, the probability reaches 15%)
postconcussion syndrome (recurrent headaches, ringing and tinnitus, nausea, weakness, sleep changes).

In general, for concussions and bruises of mild to moderate severity, if competent medication and rehabilitation support is provided, the prognosis is favorable.

With severe injuries, mortality among inpatients reaches 30%. It should be remembered that a significant portion of the victims are drunk, which worsens their general condition and chances for a good prognosis for their health and life.

Published by author

ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. No. 170

The release of a new revision (ICD-11) is planned by WHO in 2017-2018.

With changes and additions from WHO.

Processing and translation of changes © mkb-10.com

Post-traumatic encephalopathy - what is it and how to treat it

Post-traumatic encephalopathy is the consequences of TBI, manifested in the form of changes in the functions and structure of the brain of varying severity. Mental, vestibular, mental and autonomic disorders can appear within 12 months from the moment of injury and thereby significantly limit daily life activities. In severe forms of brain damage, the patient is recognized as disabled, since his life-support functions are limited.

The disease is a complication of TBI, therefore, according to ICD-10, it is most often assigned code T90.5 - “Consequences of intracranial injury” or G93.8 - “Other specified diseases of the brain.” If post-traumatic encephalopathy is accompanied by tissue swelling and severe hydrocephalus, then it can be classified as code G91 - “Acquired hydrocephalus”.

Degrees of post-traumatic encephalopathy

According to the severity, post-traumatic encephalopathy is classified according to the following criteria:

1st degree - not recognized by visual symptoms and signs, since the nature of the damage to brain tissue is insignificant. Impairments caused by a bruise or concussion can be identified using diagnostic or laboratory tests, as well as using special tests.
2nd degree – characterized by the manifestation of neurological signs in the form of restless sleep, fatigue, emotional instability, decreased concentration and memory. Symptoms appear mildly and sporadically.
3rd degree - due to severe traumatic effects on brain tissue, the patient experiences serious disorders in the central nervous system, which can manifest themselves in the form of complications such as dementia, epileptic seizures, Parkinson's disease.

A conclusion about the severity of post-traumatic encephalopathy is made by a neurologist based on the nature of the damage to brain structures and the symptoms that appear.

Causes of the disease

Post-traumatic encephalopathy is a complication of traumatic brain injuries of the 2nd or 3rd degree, which can be obtained in the following cases:

during childbirth in infants;
accidents - car, plane crash;
a blow to the head or a heavy object falling on it;
fights, beatings received, including as a result of sports competitions;
falling, hitting your head on the ground or other hard surface.

After traumatic exposure, changes occur in brain structures that can cause the development of post-traumatic encephalopathy:

immediately after an injury, swelling forms in the brain tissue, which impedes the flow of blood through the vessels;
due to oxygen deficiency, the affected area of the brain begins to atrophy, decreasing in size;
the spaces formed as a result of drying out of the brain are filled with liquor fluid, which puts pressure on nearby tissues and irritates the nerve endings;
The pressure of the cerebrospinal fluid significantly disrupts the blood supply, as a result of which brain cells begin to split and die.

Spaces in brain structures that can also fill with fluid often occur after intracranial hematomas resulting from trauma resolve. In these same spaces, porencephalic cysts can form, which also compress the brain tissue and thereby contribute to their death.

Symptoms and signs of post-traumatic encephalopathy

The symptoms of post-traumatic encephalopathy appear and increase within 1-2 weeks, while the nature and severity of neurological disorders will depend on the size of the lesion and the area of brain damage.

The following signs indicate the development of post-traumatic encephalopathy:

Memory impairment. Short-term amnesia may be present immediately after the injury or when the victim wakes up after losing consciousness. One should be alarmed when a person begins to forget events that occurred some time after the traumatic incident.
Decreased concentration. The patient becomes distracted, inhibited, inattentive, slow, and quickly gets tired of both mental and physical work.
Violation of mental functions. A person cannot think logically and analytically; in this state, he commits rash acts and is unable to make adequate decisions in everyday life and professional activities.
Decreased coordination. It is difficult for a patient with post-traumatic encephalopathy to maintain balance and coordinate their movements. He has an unsteady gait when walking, and sometimes has difficulty getting into a doorway.
Speech disorders, manifested in the form of slow and slurred speech.
Behavior change. A person begins to exhibit behavioral qualities and character traits that were not characteristic of him previously (for example, apathy towards what is happening, outbursts of irritability and aggression).
Lack of appetite.
Insomnia.
Headaches that are difficult to relieve with painkillers.
Jumps in blood pressure, accompanied by sweating and weakness.
Nausea that comes on suddenly.
Dizziness, often appearing after physical labor.

In the delayed period, up to a year after the injury, a patient with post-traumatic encephalopathy may experience seizures of epilepsy, indicating a deeper damage to brain structures.

Diagnosis and treatment of post-traumatic encephalopathy

To diagnose post-traumatic encephalopathy, the neurologist first obtains information from the patient about the trauma he suffered, namely:

statute of limitations;
localization;
degree of severity;
manifested symptoms;
treatment method.

After this, the doctor prescribes an additional examination using instrumental methods:

MRI and CT – to identify the degree of traumatic impact and signs of brain atrophy;
electroencephalography - to study the frequency of basic rhythms and determine the degree of epileptic activity.

After the examination, the patient is prescribed medication aimed at eliminating the negative consequences of the injury and restoring brain function. Individually, the doctor selects the following groups of drugs:

diuretics – for diagnosed hydrocephalic syndrome;
analgesics – for headaches;
nootropic drugs - to restore metabolic processes between brain cells;
neuroprotectors – for the restoration and nutrition of nerve cells;
vitamins “B” - to nourish the brain and improve its activity;
anticonvulsants – for epilepsy attacks confirmed by specialists.

Auxiliary therapy plays a major role in restoring brain functions in post-traumatic encephalopathy:

physiotherapy;
therapeutic exercises;
acupuncture;
massage – classic, manual, acupressure;
help from a psychologist.

Depending on the degree of brain damage and the intensity of symptoms, the patient is prescribed treatment in courses, the time interval between which is 6 months or a year. The rest of the time, he should comply with several basic requirements:

eat right;
take daily walks - on foot and in the fresh air;
give up bad habits;
Visit a neurologist regularly to monitor your health.

Forecast and consequences

With confirmed post-traumatic encephalopathy, the patient will need long-term rehabilitation to restore impaired or lost brain functions.

Over the course of a year, a person undergoes treatment and rehabilitation courses, as well as measures for social adaptation in cases where disorders of brain activity entail limitations in personal care and discomfort in everyday life. Only after this period can the doctor make a forecast about the degree of restoration of brain function.

If, after completed rehabilitation, it is not possible to restore lost functions and ability to work, then the patient with post-traumatic encephalopathy is assigned disability. Depending on the form of the pathology, it is assigned one of the following groups:

Group II or III – with diagnosed 2nd degree of severity of the pathology, while the patient can work under the condition of light work and a shortened working day.
Group I – in case of a 3rd degree disease due to a decrease or complete lack of ability to care for oneself and the need for outside help.

Disability is not prescribed for patients with grade 1 post-traumatic encephalopathy, since exposure to symptoms characteristic of this condition does not reduce their quality of life and performance.

Choosing a doctor or clinic

©18 The information on the site is for informational purposes only and does not replace consultation with a qualified physician.

Possible consequences after traumatic brain injury and disease code according to ICD-10

1 Causes and classification of the disease

The consequences of TBI according to ICD-10 are coded T90.5. Traumatic brain injury occurs when the soft tissues of the skull and brain are damaged. Most often the cause is:

hitting the head;
road traffic accidents;
sports injuries.

All traumatic brain injuries are divided into 2 groups:

If an injury occurs and it turns out that the integrity of the soft tissues of the head is broken, then this is a group of open injuries. If the bones of the skull were damaged, but the dura mater remained intact, then the injuries are classified as non-penetrating. They are called penetrating if the bones are damaged and the hard shell is also damaged. The closed form is characterized by the fact that the soft tissues are not affected, without an aponeurosis, and the skull bones are broken.

If we take into account the pathophysiology of TBI, then there are damages:

Primary. In this case, blood vessels, skull bones, brain tissue, as well as the membrane are injured, and the cerebrospinal fluid system is also affected.
Secondary. Not directly related to brain damage. Their development occurs as a secondary ischemic change in brain tissue.

There are injuries that cause complications, the most common among them:

The degree of severity must be taken into account:

Easy. Consciousness is clear, there is no pain, there is no particular threat to health.
Average. Consciousness can be clear, but it is also possible that the person feels a little stunned. Pronounced focal signs.
Heavy. Stupor and severe stupor occur. Vital functions are disturbed, focal signs are present.
Particularly heavy. The patient falls into a coma, either short-lived or deep. Vital functions are severely impaired, as are the cardiovascular and respiratory systems. Focal symptoms are present. Consciousness is absent from a couple of hours to many days. The movements of the eyeballs are blurred, and the reaction of the pupils to bright stimuli is depressed.

2 Diagnostic methods and periods of illness

Patients with traumatic brain injuries should undergo examination. Based on determining the degree of depression of consciousness, the extent to which neurological symptoms are expressed, and whether other organs are damaged, a diagnosis is made. It is most convenient to use the Glasgow Coma Scale for these purposes. The patient's condition is checked immediately after the injury, after 12 hours and 24 hours later.

The patient is asked to make certain movements, answer questions and open and close his eyes. At the same time, they monitor the reaction to external irritating factors.

In medicine, there are several periods of the disease:

If a concussion occurs, the patient most often experiences a sharp headache. Possible loss of consciousness, vomiting, and dizziness.

The person experiences weakness and becomes lethargic. But there is no congestion in the fundus, the brain is not locally affected, the cerebrospinal fluid has the same pressure.

If a brain injury occurs, the person is haunted by a headache at the site of the impact, constant vomiting, difficulty breathing and bradycardia, pallor and fever. The examination reveals:

in the cerebrospinal fluid - the presence of blood;
in the blood - an increased number of leukocytes.

Vision and speech may be affected. At this time, it is necessary to be under the supervision of a doctor, as traumatic epilepsy may occur, accompanied by seizures. And this process often causes depression, aggressive behavior, and fatigue.

Intracranial hematomas and depressed skull fractures can cause compression of the brain. This is due to various types of hemorrhages resulting from injuries. Often, due to hemorrhage that occurred between the bones of the skull and the meninges, precisely at the point of impact, an epidural hematoma occurs. It can be determined by anisocoria with expansion. Loss of consciousness is common. This diagnosis most often requires surgical intervention.

With a subdural hematoma, severe head spasms, vomiting occur from the blow, and blood begins to collect in the subdural space. Convulsions occur. Patients cannot navigate in space, quickly get tired, but at the same time they are too excited and irritable.

To confirm the diagnosis caused by a bruise in the skull area, additional studies will be needed:

X-ray of the skull when there is a suspicion of a fracture.
EMG will help determine the extent of damage in muscle fibers and myoneural endings.
Neurosonography. With its help, intracranial hypertension and hydrocephalus are determined.
Doppler ultrasound to check whether pathology has arisen in the vessels of the brain.
Biochemical blood test.
MRI to identify lesions in the brain.
EEG to detect dysfunction of brain stem structures.

Diagnostics will help determine the consequences of a skull injury.

Consequences of head injury code according to ICD 10

1046 universities, 2204 subjects.

Closed craniocerebral injury (concussion, head contusion)

Goal of the stage: Restoring the functions of all vital systems and organs

S06.0 Concussion

S06.1 Traumatic cerebral edema

S06.2 Diffuse brain injury

S06.3 Focal brain injury

S06.4 Epidural hemorrhage

S06.5 Traumatic subdural hemorrhage

S06.6 Traumatic subarachnoid hemorrhage

S06.7 Intracranial injury with prolonged coma

S06.8 Other intracranial injuries

S06.9 Intracranial injury, unspecified

Definition: Closed traumatic brain injury (CTBI) – damage to the skull and

brain, which is not accompanied by a violation of the integrity of the soft tissues of the head and/or

aponeurotic stretching of the skull.

Open TBI includes injuries that are accompanied by a violation

integrity of the soft tissues of the head and aponeurotic helmet of the skull and/or corresponding

in the fracture zone. Penetrating injuries include a TBI that

is caused by fractures of the skull bones and damage to the dura mater of the brain with

the occurrence of cerebrospinal fluid fistulas (cerebrospinal fluid leaks).

Primary – damage is caused by direct exposure to trauma

forces on the bones of the skull, meninges and brain tissue, brain vessels and fluid

Secondary – damage is not associated with direct damage to the brain,

but are caused by the consequences of primary brain damage and develop mainly

according to the type of secondary ischemic changes in brain tissue. (intracranial and system-

1. intracranial - cerebrovascular changes, disturbances of the liquor circulation

lation, cerebral edema, changes in intracranial pressure, dislocation syndrome.

2. systemic – arterial hypotension, hypoxia, hyper- and hypocapnia, hyper- and

hyponatremia, hyperthermia, carbohydrate metabolism disorders, disseminated intravascular coagulation syndrome.

According to the severity of the condition of patients with TBI - based on an assessment of the degree of depression

the consciousness of the victim, the presence and severity of neurological symptoms,

presence or absence of damage to other organs. The greatest distribution of semi-

the Glasgow Coma Scale (proposed by G. Teasdale and B. Jennet 1974). Condition of the building

Those who gave are assessed at the first contact with the patient, after 12 and 24 hours according to three parameters:

frames: eye opening, speech response and motor reaction in response to external

fight. There is a classification of disturbances of consciousness in TBI, based on the quality

assessment of the degree of oppression of consciousness, where there are the following gradations of co-

Mild traumatic brain injury includes concussion and mild cerebral contusion

degrees. Moderate head injury – moderate brain contusion. To cha-

Yellow traumatic brain injury includes severe brain contusion and all types of head compression

2. moderate severity;

4. extremely difficult;

The criteria for a satisfactory condition are:

1. clear consciousness;

2. absence of disturbances in vital functions;

3. absence of secondary (dislocation) neurological symptoms, no

effect or mild severity of primary hemispheric and craniobasal symptoms.

There is no threat to life, the prognosis for restoration of working capacity is usually good.

The criteria for a moderately severe condition are:

1. clear consciousness or moderate stupor;

2. vital functions are not impaired (only bradycardia is possible);

3. focal symptoms – certain hemispheric and cranial symptoms may be expressed

basal symptoms. Sometimes there are single, mildly expressed stem

symptoms (spontaneous nystagmus, etc.)

To establish a condition of moderate severity, it is enough to have one of

the specified parameters. The threat to life is insignificant, the forecast for restoration of work is

abilities are often favorable.

1. change in consciousness to deep stupor or stupor;

2. disturbance of vital functions (moderate according to one or two indicators);

3. focal symptoms – trunk symptoms are moderately expressed (anisocoria, mild

decreased upward gaze, spontaneous nystagmus, contralateral pyramidal insufficiency

ity, dissociation of meningeal symptoms along the body axis, etc.); can be sharply increased

wife hemispheric and craniobasal symptoms, including epileptic seizures,

paresis and paralysis.

To establish a serious condition, it is permissible to have these disorders, although

according to one of the parameters. The threat to life is significant and largely depends on the duration

severity of a serious condition, the prognosis for restoration of working capacity is often unfavorable

1. impairment of consciousness to moderate or deep coma;

2. pronounced disturbance of vital functions in several parameters;

3. focal symptoms - stem symptoms are clearly expressed (paresis of upward gaze, pronounced

anisocoria, vertical or horizontal eye divergence, tonic spontaneous

nystagmus, weakened pupillary response to light, bilateral pathological reflexes,

decerebrate rigidity, etc.); hemispheric and craniobasal symptoms sharply

expressed (up to bilateral and multiple paresis).

When an extremely serious condition is determined, it is necessary to have pronounced abnormalities

solutions in all respects, and in one of them necessarily extreme, a threat to

maximum life. The prognosis for restoration of working capacity is often unfavorable.

The criteria for terminal condition are as follows:

1. impairment of consciousness to the level of extreme coma;

2. critical violation of vital functions;

3. focal symptoms – stem symptoms in the form of extreme bilateral mydriasis, from

absence of corneal and pupillary reactions; hemispheric and craniobasal are usually re-

covered by general cerebral and stem disorders. The prognosis for survival of a patient with unaffected

2. open: a) non-penetrating; b) penetrating;

There are different types of brain damage:

1. concussion– a condition that occurs more often due to exposure to

effects of a small traumatic force. Occurs in almost 70% of victims with TBI.

Concussion is characterized by no loss of consciousness or short-term loss of consciousness.

consciousness after injury: from 1-2 minutes. Patients complain of headaches, nausea

note, less often vomiting, dizziness, weakness, pain when moving the eyeballs.

There may be slight asymmetry of tendon reflexes. Retrograde amnesia (es-

whether it occurs) is short-lived. Anterograde amnesia does not exist. When shaken -

in the brain, these phenomena are caused by functional damage to the brain and

after 5-8 days they pass. To make a diagnosis, it is not necessary to have

all of the above symptoms. Concussion is a single form and not

divided into degrees of severity;

2. brain contusion– this is damage in the form of macrostructural destruction

brain substances, often with a hemorrhagic component that arose at the time of application

traumatic force. According to the clinical course and severity of brain damage

brain tissue bruises are divided into mild, moderate and severe bruises):

Mild brain contusion(10-15% of victims). After the injury there is a decrease in

time of consciousness from several minutes to 40 minutes. Most have retrograde amne-

zia for a period of up to 30 minutes. If anteroretrograde amnesia occurs, it is short-lived.

resident After regaining consciousness, the victim complains of a headache,

nausea, vomiting (often repeated), dizziness, loss of attention and memory. They can

nystagmus (usually horizontal), anisoreflexia, and sometimes mild hemiparesis are detected.

Sometimes pathological reflexes appear. Due to subarachnoid hemorrhage

Mild meningeal syndrome may be detected. Can observe-

brady- and tachycardia, transient increase in blood pressure mm Hg.

Art. Symptoms usually regress within 1-3 weeks after injury. Head bruise-

Mild brain damage may be accompanied by skull fractures.

Moderate brain contusion. Loss of consciousness lasts from non-

how many tens of minutes to 2-4 hours. Depression of consciousness to a level of moderate or

deep stunning can persist for several hours or days. Observation

There is a severe headache, often repeated vomiting. Horizontal nystagmus, weakened

Decreased pupillary response to light, possible convergence disorder. There is a disso-

tion of tendon reflexes, sometimes moderate hemiparesis and pathological

ski reflexes. There may be sensory disturbances and speech disorders. Menin-

geal syndrome is moderately expressed, and cerebrospinal fluid pressure is moderately increased (due to

including victims who have liquorrhea). There is tachy- or bradycardia.

Breathing disorders in the form of moderate tachypnea without rhythm disturbance and does not require apparatus

military correction. The temperature is subfebrile. On the 1st day there may be psychomotor

agitation, sometimes convulsive seizures. There is retro- and antero-retrograde amne-

Severe brain contusion. Loss of consciousness lasts from several hours to

how many days (in some patients with transition to apallic syndrome or akinetic

mutism). Depression of consciousness to the point of stupor or coma. There may be a pronounced psychomotor

arousal followed by atony. Stem symptoms are expressed - floating

movements of the eyeballs, difference of the eyeballs along the vertical axis, fixation

downward gaze, anisocoria. The reaction of the pupils to light and corneal reflexes are depressed. Glotta-

tion is broken. Sometimes hormetonia develops in response to painful stimuli or spontaneously.

Bilateral pathological foot reflexes. There are changes in muscle tone

sa, often - hemiparesis, anisoreflexia. There may be seizures. Violation

breathing - central or peripheral type (tachy- or bradypnea). Arteri-

The blood pressure is either increased or decreased (may be normal), and with atonic

Coma is unstable and requires constant medical support. Expressed me-

A special form of brain contusion includes diffuse axonal injury

brain. Its clinical signs include dysfunction of the brain stem - depression

loss of consciousness to deep coma, pronounced disturbance of vital functions, which

which require mandatory medication and hardware correction. Mortality at

diffuse axonal damage to the brain is very high and reaches 80-90%, and in high

survivors develop apallic syndrome. Diffuse axonal damage can

accompanied by the formation of intracranial hematomas.

3. Compression of the brain ( growing and non-growing) – occurs due to a decrease

filling the intracranial space with volumetric formations. It should be kept in mind

that any “non-increasing” compression during TBI can become increasing and lead to

pronounced compression and dislocation of the brain. Non-increasing compression includes

compression by fragments of the skull bones during depressed fractures, pressure on the brain of other

mi foreign bodies. In these cases, the formation itself compressing the brain does not increase

varies in volume. In the genesis of brain compression, the leading role is played by secondary intracranial

nal mechanisms. Increasing compression includes all types of intracranial hematomas

and brain contusions accompanied by mass effect.

5. multiple intrathecal hematomas;

6. subdural hydromas;

Hematomas may be: sharp(first 3 days), subacute(4 days-3 weeks) and

chronic(later 3 weeks).

The classic __________ clinical picture of intracranial hematomas includes the presence

light interval, anisocoria, hemiparesis, bradycardia, which is less common.

The classic clinical picture is typical for hematomas without concomitant brain contusion. U po-

suffered from hematomas in combination with brain contusion from the first hours

TBI has signs of primary brain damage and symptoms of compression and dislocation

cation of the brain caused by contusion of brain tissue.

1. alcohol intoxication (70%).

2. TBI as a result of an epileptic seizure.

1. road injuries;

2. domestic trauma;

3. fall and sports injury;

Pay attention to the presence of visible damage to the skin of the head.

Periorbital hematoma (“glasses symptom”, “raccoon eyes”) indicates a fracture

bottom of the anterior cranial fossa. Hematoma in the mastoid area (Batt-symptom)

la) accompanies a fracture of the pyramid of the temporal bone. Hemotympanum or drum rupture

a new membrane may correspond to a fracture of the base of the skull. Nasal or ear

liquorrhea indicates a fracture of the base of the skull and penetrating head injury. The sound of "crack"

a new pot” during percussion of the skull can occur with fractures of the bones of the cranial vault

turnip. Exophthalmos with conjunctival edema may indicate the formation of carotid

cavernous anastomosis or the resulting retrobulbar hematoma. Hematoma soft

certain tissues in the occipito-cervical region may accompany a fracture of the occipital bone

and (or) contusion of the poles and basal parts of the frontal lobes and poles of the temporal lobes.

Undoubtedly, it is mandatory to assess the level of consciousness, the presence of meningeal

symptoms, the condition of the pupils and their reaction to light, the functions of cranial nerves and motor

negative functions, neurological symptoms, increased intracranial pressure,

brain dislocation, development of acute cerebrospinal fluid occlusion.

Tactics of medical care:

The choice of treatment tactics for victims is determined by the nature of the head injury.

brain, bones of the vault and base of the skull, concomitant extracranial trauma and various

development of complications due to injury.

The main task when providing first aid to victims with TBI is not to

allow the development of arterial hypotension, hypoventilation, hypoxia, hypercapnia, so

how these complications lead to severe ischemic brain damage and accompanying

have a high mortality rate.

In this regard, in the first minutes and hours after injury, all therapeutic measures

must be subject to the ABC rule:

A (airway) – ensuring airway patency;

B (breathing) - restoration of adequate breathing: elimination of respiratory obstruction -

body tracts, drainage of the pleural cavity for pneumo-, hemothorax, mechanical ventilation (according to

C (circulation) – control over the activity of the cardiovascular system: fast

restoration of bcc (transfusion of solutions of crystalloids and colloids), in case of insufficient

accuracy of the myocardium - administration of inotropic drugs (dopamine, dobutamine) or vaso-

pressors (adrenaline, norepinephrine, mesaton). It must be remembered that without normalization

tion of circulating blood mass, the administration of vasopressors is dangerous.

Indications for tracheal intubation and mechanical ventilation are apnea and hypoapnea,

the presence of cyanosis of the skin and mucous membranes. Nasal intubation has a number of advantages:

societies, because with TBI, the likelihood of cervical spinal injury cannot be excluded (and therefore

All victims, before clarifying the nature of the injury at the prehospital stage, must

dimo fix the cervical spine by applying special cervical collars -

nicknames). To normalize the arteriovenous oxygen difference in patients with TBI

It is advisable to use oxygen-air mixtures with an oxygen content of up to

An obligatory component of the treatment of severe TBI is the elimination of hypovolatile

miia, and for this purpose, liquid is usually administered in a volume of 30-35 ml/kg per day. Exception

are patients with acute occlusive syndrome, whose rate of CSF production

directly depends on water balance, so dehydration is justified in them, allowing

to reduce ICP.

For the prevention of intracranial hypertension and its brain-damaging

consequences at the prehospital stage, glucocorticoid hormones and salure-

Glucocorticoid hormones prevent the development of intracranial hypertension

sion by stabilizing the permeability of the blood-brain barrier and reducing

transudation of fluid into brain tissue.

They help reduce perifocal edema in the area of injury.

At the prehospital stage, intravenous or intramuscular administration is advisable.

administration of prednisolone at a dose of 30 mg

However, it should be borne in mind that due to concomitant mineralocorticoid

effect, prednisolone is able to retain sodium in the body and enhance elimination

potassium, which adversely affects the general condition of patients with TBI.

Therefore, it is preferable to use dexamethasone at a dose of 4-8 mg, which

has virtually no mineralocorticoid properties.

In the absence of circulatory disorders, simultaneously with glucocorticoid

hormones for brain dehydration, it is possible to prescribe fast-acting salureti-

cove, for example, Lasix in doses (2-4 ml of 1% solution).

Ganglion-blocking drugs for high-grade intracranial hypertension

are contraindicated, since with a decrease in systemic blood pressure it can develop

There is a complete blockade of cerebral blood flow due to compression of the capillaries of the brain by edematous brain

To reduce intracranial pressure- both at the prehospital stage and in

hospital - you should not use osmotically active substances (mannitol), because

with a damaged blood-brain barrier, create a gradient of their concentration me-

I'm waiting for the brain matter and the vascular bed to fail and the condition is likely to worsen

patient due to a rapid secondary increase in intracranial pressure.

The exception is the threat of brain dislocation, accompanied by severe

breathing and circulatory disorders.

In this case, it is advisable to administer intravenously mannitol (mannitol) based on

and 0.5 g/kg body weight in the form of a 20% solution.

The sequence of emergency care measures at the prehospital stage is

No emergency care is required for a concussion.

With psychomotor agitation:

2-4 ml of 0.5% solution of seduxen (Relanium, Sibazon) intravenously;

Transportation to the hospital (to the neurological department).

For bruises and compression of the brain:

1. Provide access to the vein.

2. If a terminal condition develops, perform cardiac resuscitation.

3. In case of circulatory decompensation:

Reopoliglucin, crystalloid solutions intravenously;

If necessary, dopamine 200 mg in 400 ml of isotonic sodium solution

chloride or any other crystalloid solution intravenously at a rate that ensures

ensuring the maintenance of blood pressure at the level of mercury. Art.;

4. In an unconscious state:

Inspection and mechanical cleaning of the oral cavity;

Application of the Sellick maneuver;

Performing direct laryngoscopy;

Do not straighten the spine in the cervical region!

Stabilization of the cervical spine (light traction with hands);

Tracheal intubation (without muscle relaxants!), regardless of whether it will be

whether to use mechanical ventilation or not; muscle relaxants (succinylcholine chloride - dicilin, listenone in

dose 1-2 mg/kg; injections are carried out only by doctors of intensive care units

If spontaneous breathing is ineffective, artificial ventilation is indicated.

tion of the lungs in the mode of moderate hyperventilation (12-14 l/min for a patient with body weight

5. For psychomotor agitation, convulsions and as a premedication:

0.5-1.0 ml of 0.1% atropine solution subcutaneously;

Intravenous propofol 1-2 mg/kg, or sodium thiopental 3-5 mg/kg, or 2-4 ml 0.5%

seduxen solution, or 20% sodium hydroxybutyrate solution, or dormicum 0.1-

During transportation, control of the respiratory rhythm is necessary.

6. For intracranial hypertension syndrome:

2-4 ml of 1% solution of furosemide (Lasix) intravenously (for decompensated

blood loss due to concomitant trauma, do not administer Lasix!);

Artificial hyperventilation.

7. For pain: intramuscularly (or slowly intravenously) 30 mg-1.0

ketorolac and 2 ml of 1-2% solution of diphenhydramine and (or) 2-4 ml (mg) of 0.5% solution

Tramal or other non-narcotic analgesic in appropriate doses.

8. For head wounds and external bleeding from them:

Toilet the wound by treating the edges with an antiseptic (see Chapter 15).

9. Transportation to a hospital where there is a neurosurgical service; at cry-

in critical condition - to the intensive care unit.

List of essential medications:

1. *Dopamine 4%, 5 ml; amp

2. Dobutamine solution for infusion 5 mg/ml

4. *Prednisolone 25 mg 1 ml, amp

5. *Diazepam 10 mg/2 ml; amp

7. *Sodium oxybate 20% 5 ml, amp

8. *Magnesium sulfate 25% 5.0, amp

9. *Mannitol 15% 200 ml, fl

10. *Furosemide 1% 2.0, amp

11. Mesaton 1% - 1.0; amp

List of additional medications:

1. *Atropine sulfate 0.1% - 1.0, amp

2. *Betamethasone 1ml, amp

3. *Epinephrine 0.18% - 1 ml; amp

4. *Destran,0; fl

5. *Diphenhydramine 1% - 1.0, amp

6. * Ketorolac 30 mg - 1.0; amp

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A bruise - a focus of traumatic crushing of brain tissue - often forms in the basal parts of the frontal and anterior parts of the temporal lobes, which are in close contact with the protruding bone relief. Diffuse axonal injury is the result of rotational or linear acceleration at the time of injury. Depending on the magnitude of acceleration with diffuse axonal damage, a wide range of disorders are possible, from mild confusion and short-term loss of consciousness (with a concussion) to coma and even death. Secondary brain damage is associated with hypoxia, ischemia, intracranial hypertension, and infection.
There is an open traumatic brain injury (TBI), in which there is communication between the cranial cavity and the external environment, and a closed one.
The main clinical factors that determine the severity of the injury are: the duration of loss of consciousness and amnesia, the degree of depression of consciousness at the time of hospitalization, and the presence of brainstem neurological symptoms.
When examining a patient with a TBI, especially a severe one, you need to adhere to a specific plan.
1. First, you should pay attention to the patency of the airways, the frequency and rhythm of breathing, and the state of hemodynamics.
2. The chest and abdomen should be quickly examined to rule out hemo- or pneumothorax or abdominal bleeding.
3. Assess the state of consciousness. In case of mild TBI, it is important to assess orientation in place, time, self, attention, by asking the patient to name the months of the year in reverse order or sequentially subtracting from 40 to 3, memory, asking to remember 3 words and checking whether the patient can name them after 5 minutes.
4. Examine the head, torso, limbs, paying attention to external signs of injury (wounds, bruises, bruises, fractures).
5. It is important to identify signs of a fracture of the base of the skull: leakage of cerebrospinal fluid from the nose (unlike ordinary mucus, cerebrospinal fluid contains glucose), a symptom of glasses (delayed appearance of bilateral bruising in the periorbital area, limited to the edges of the orbit), leakage of blood and cerebrospinal fluid from the ear ( bleeding from the ear can also be associated with damage to the external auditory canal or eardrum), as well as a bruise behind the auricle in the mastoid area, appearing 24-48 hours after the injury.
6. When collecting anamnesis from the patient or those accompanying him, you should pay attention to the circumstances of the injury (trauma can provoke a stroke, epileptic seizure), the use of alcohol or medications.
7. When figuring out the duration of loss of consciousness, it is important to take into account that for an external observer, consciousness returns at the moment when the patient opens his eyes, but for the patient himself, consciousness returns at the moment when the ability to remember returns. The duration of the patient's amnesic period is one of the most reliable indicators of the severity of the injury. It is determined by asking the patient about the circumstances of the injury, preceding and subsequent events.
8. The appearance of meningeal symptoms indicates subarachnoid hemorrhage or meningitis, but neck stiffness can only be checked if cervical trauma has been ruled out.
9. All patients with TBI undergo an X-ray of the skull in two projections, which can reveal depressed fractures, linear fractures in the middle cranial fossa or at the base of the skull, fluid level in the ethmoid sinus, pneumocephalus (presence of air in the cranial cavity). In case of a linear fracture of the calvarium, attention should be paid to whether the fracture line crosses the groove in which the middle meningeal artery passes. Its damage is the most common cause of epidural hematoma.
10. Most patients (even with minimal signs of damage to the cervical spine or abrasion on the forehead) should be prescribed a radiography of the cervical spine (at least in the lateral projection, and an image of all cervical vertebrae should be obtained).
11. Displacement of the midline structures of the brain during the development of intracranial hematoma can be detected using echoencephaloscopy.
12. Lumbar puncture in the acute period usually does not provide additional useful information, but can be dangerous.
13. In the presence of confusion or depression of consciousness, focal neurological symptoms, epileptic seizure, meningeal symptoms, signs of a basal skull fracture, comminuted or depressed fracture of the calvarium, urgent consultation with a neurosurgeon is necessary. Particular vigilance regarding hematoma is necessary in the elderly, patients, alcoholics or taking anticoagulants.
Traumatic brain injury is a dynamic process that requires constant monitoring of the state of consciousness, neurological and mental status. During the first day, the neurological status, first of all, the state of consciousness should be assessed every hour, refraining, if possible, from prescribing sedatives (if the patient falls asleep, then he should be woken up periodically).
Mild TBI is characterized by a brief loss of consciousness, orientation, or other neurological functions, usually occurring immediately after injury. The Glasgow Coma Scale score during the initial examination is 13 - 15 points. After restoration of consciousness, amnesia is detected for events that immediately preceded the injury or occurred immediately after it (the total duration of the amnesic period does not exceed 1 hour), headache, autonomic disorders (blood pressure fluctuations, pulse lability, vomiting, pallor, hyperhidrosis), asymmetry of reflexes, pupillary abnormalities and other focal symptoms that usually resolve spontaneously within a few days. The criteria for mild TBI include a concussion and a mild cerebral contusion. The main feature of mild TBI is the fundamental reversibility of neurological disorders, however, the recovery process can drag on for several weeks or months, during which patients will continue to experience headache, dizziness, asthenia, memory impairment, sleep disturbance and other symptoms (post-concussion syndrome). In car accidents, mild TBI is often associated with whiplash, which occurs as a result of sudden movements of the head (most often as a result of sudden hyperextension of the head followed by rapid flexion). Whiplash injury is accompanied by a sprain of the ligaments and muscles of the neck and is manifested by pain in the cervical-occipital region and dizziness, which spontaneously disappear within a few weeks, usually leaving no consequences.
Patients with minor trauma should be hospitalized for observation for 2-3 days. The main purpose of hospitalization is not to miss a more serious injury. Subsequently, the likelihood of complications (intracranial hematoma) is significantly reduced, and the patient can be sent home provided that relatives will monitor him, and if his condition worsens, he will be quickly taken to the hospital. Particular caution should be exercised in children, in whom intracranial hematoma may develop in the absence of an initial loss of consciousness.
Moderate and severe TBI is characterized by prolonged loss of consciousness and amnesia, persistent cognitive and focal neurological disorders. In severe TBI, the likelihood of intracranial hematoma is significantly higher. Hematoma should be suspected if there is progressive depression of consciousness, the appearance of new or an increase in existing focal symptoms, or the appearance of signs of herniation. A “lucid interval” (short-term return of consciousness followed by deterioration), considered a classic sign of hematoma, is observed in only 20% of cases. The development of a long-term coma immediately after injury in the absence of an intracranial hematoma or massive contusion lesions is a sign of diffuse axonal damage. Late deterioration, in addition to intracranial hematoma, may be caused by cerebral edema, fat embolism, ischemia, or infectious complications. Fat embolism occurs several days after injury, usually in patients with fractures of long tubular bones - when fragments are displaced or attempted to reposition them; in most patients, respiratory function is impaired and small hemorrhages occur under the conjunctiva. Post-traumatic meningitis develops several days after the injury, more often in patients with open TBI, especially in the presence of a fracture of the base of the skull with the appearance of a communication (fistula) between the subarachnoid space and the paranasal sinuses or middle ear.

In Russia, the International Classification of Diseases, 10th revision (ICD-10) has been adopted as a single normative document for recording morbidity, reasons for the population's visits to medical institutions of all departments, and causes of death.

ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. No. 170

The release of a new revision (ICD-11) is planned by WHO in 2017-2018.

With changes and additions from WHO.

Processing and translation of changes © mkb-10.com

Consequences of head injury ICD 10

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