ICb code closed craniocerebral injury. Closed craniocerebral injury (concussion, brain contusion, intracranial hematomas, etc.). S08 Traumatic amputation of part of head

• eyes
• face (any part)
• gums
• jaws
• oral cavity
• periocular area
• scalp
• language

Ceeh uhtaPa: Restoration of the functions of all vital systems and organs

Toone (toaboutds) Pabout MToB- 10 - 10:

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

ODAfoodleneithere: Zakrstand ICheReMonabout- brainGnewtRavma(ZTCHMT) - 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.

To abouttkrstoh HMT include injuries that are accompanied by a violation of the integrity of the soft tissues of the head and the aponeurotic helmet of the skull and / or

correspond to the fracture zone. Penetrating injuries include such TBI,

which is accompanied by fractures of the skull bones and damage to the dura mater

membranes of the brain with the occurrence of cerebrospinal fluid fistulas (liquorrhea).

TolassandfikaqiI:

According to the pathophysiology of TBI:

- PeRinandhns- damage caused by direct impact

traumatic forces on the skull bones, meninges and brain tissue, brain vessels and the cerebrospinal fluid system.

- ATtaboutrihns- damage is not associated with direct brain damage, but is due to the consequences of primary brain damage and develops mainly along

type of secondary ischemic changes in brain tissue. (intracranial and systemic).

1. innattriCheReMons- cerebrovascular changes, liquor circulation disorders,

cerebral edema, changes in intracranial pressure, dislocation syndrome.

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

hyponatremia, hyperthermia, impaired carbohydrate metabolism, DIC.

By tIandeWithtand WithaboutWithtoyaneitherI bolbns With HMT – based on an assessment of the degree of oppression

consciousness of the victim, the presence and severity of neurological symptoms, the presence or absence of damage to other organs. The Glasgow coma scale (proposed by G. Teasdale and B. Jennet 1974) has received the greatest distribution. The condition of the victims is assessed at the first contact with the patient, after 12 and 24 hours according to three parameters: eye opening, speech response and motor response in response to external stimulation. There is a classification of disorders of consciousness in TBI, based on a qualitative assessment of the degree of depression of consciousness, where there are the following gradations of the state of consciousness:

Moderate stun;

Deep stun;

Sopor;

deep coma;

Outrageous coma;
Mild PTBI includes concussion and mild contusion of the brain. CTBI of moderate severity - brain contusion of moderate severity. Severe CBI includes severe brain contusion and all types of cerebral compression.

ATsdelaYut 5 gradaqith WithaboutWithtoyaneitherI bolbns With HMT:

1. oudaboutownoinorithoseflaxaboute;

2. WithRunitsneth chaandeuti;

3. chaandelaboute;

4. toparadisene chaandelaboute;

5. thoserminaflaxaboute;

Toriteriyami atdovletinaboutritelbnaboutGabout WithaboutWithtoyanandI isYutXia:

1. I'm withnoh Withabouthnanande;

2. abouttsustinienaratshenuy inandtaehnsXfatntotions;

3. abouttsustinie intorichoh(dandWithlabouttoazionnoh) neinrolaboutGandheutoohWithimptohmtandtoand abouttsustinie andlandneRehtoand IyouRaandennaboutWithbe PeRinandchnyx bylatsharnsx and toranand aboutbahaflaxWithimptomoin. AtGrohadlI andandhnand abouttsustinyet, aboutGnoz inaboutsstanaboutowenand I tRoudaboutWithonWithaboutbnaboutWithti obychabout Xoroshuy.

Toriteriyami WithaboutWithtaboutIneitherI WithRunitsneth tIandeutand isYutXia:

1. clear consciousness or moderate stupor;

1-3 weeks after injury. Brain contusion of mild severity may be accompanied by fractures of the bones of the skull.

4. Atshandb GtinnaboutGabout brainGa WithRunitsneth WithtePenand tIandeWithtand. Loss of consciousness lasts from several tens of minutes to 2-4 hours. Depression of consciousness to the level of moderate or

deep stunning can persist for several hours or days.

There is severe headache, often repeated vomiting. Horizontal

nystagmus, weakening of the reaction of pupils to light, a violation of convergence is possible. There is dissociation of tendon reflexes, sometimes moderate hemiparesis and pathological reflexes. There may be sensory disturbances, speech disorders. The meningeal syndrome is moderately expressed, and the CSF pressure is moderately increased (with the exception of victims who have liquorrhea).

Atshandb brainGa tIandeloy WithtePeneither. Loss of consciousness lasts from several hours to

several days (in some patients with the transition to apallic syndrome or akinetic mutism). Oppression of consciousness to stupor or coma. There may be pronounced psychomotor agitation, followed by atony. Stem symptoms are pronounced - floating movements of the eyeballs, eyeball separation along the vertical axis, gaze fixation down, anisocoria. Pupillary reaction to light and corneal reflexes are depressed. Swallowing is impaired. Sometimes hormetonia develops to painful stimuli or spontaneously. Bilateral pathological foot reflexes. There are changes in muscle tone, often - hemiparesis, anisoreflexia. There may be seizures. Respiratory failure - according to the central or peripheral type (tachy- or bradypnea). Blood pressure is either increased or decreased (may be normal), and in atonic coma it is unstable and requires constant medical support. Pronounced meningeal syndrome.

A special form of brain contusion is dandffbondsnoh atoWithaboutnalbnoh PovReanddeniebrainGa. Its clinical signs include dysfunction of the brain stem - depression of consciousness to a deep coma, a pronounced violation of vital functions, which require mandatory medical and hardware correction. Mortality in diffuse axonal brain damage is very high and reaches 80-90%, and apallic syndrome develops in survivors. Diffuse axonal damage may be accompanied by the formation of intracranial hematomas.

5. FROM d a in l e neither e m about h G a ( growing and non-growing ) – happens due to

reduction of intracranial space by volumetric formations. It should be borne in mind that any "non-increasing" compression in TBI can become progressive and lead to severe compression and dislocation of the brain. Non-increasing compressions include compression by fragments of the skull bones with depressed fractures, pressure on the brain by other foreign bodies. In these cases, the formation itself squeezing the brain does not increase in volume. Secondary intracranial mechanisms play a leading role in the genesis of brain compression. Increasing compressions include all types of intracranial hematomas and brain contusions, accompanied by a mass effect.

AT n at t R and Che R e stumps e G eat a t about m s :

1. epidural;

2. subdural;

3. intracerebral;

4. intraventricular;

5. multiple intrathecal hematomas;

6. subdural hydromas;

Hematomas can be: acute (first 3 days), subacute (4 days-3 weeks) and

chronic (after 3 weeks).

The classic clinical picture of intracranial hematomas includes the presence of

light gap, anisocoria, hemiparesis, bradycardia, which is less common. The classic clinic is characterized by hematomas without concomitant brain injury. In victims with hematomas combined with brain contusion, already from the first hours of TBI, there are signs of primary brain damage and symptoms of compression and dislocation of the brain due to brain tissue contusion.

F a to t about R s R and With to a P R and World Cup T :

1. alcohol intoxication (70%).

2. TBI as a result of an epileptic seizure.
ATunitsatschandeathins HMT:

1. road traffic injuries;

2. domestic injury;

3. falls and sports injury;

DandaMraboutWithtandcheskie Creeteriand: Look out for visible damage.

skin of the head. Periorbital hematoma ("symptom of glasses", "raccoon eyes") indicates a fracture of the floor of the anterior cranial fossa. Hematoma in the area of ​​the mastoid process (Battle's symptom) accompanies a fracture of the pyramid of the temporal bone. A hemotympanum or ruptured tympanic membrane may correspond to a skull base fracture. Nasal or ear liquorrhea indicates a fracture of the base of the skull and penetrating TBI. The sound of a "cracked pot" on percussion of the skull can occur with fractures of the bones of the cranial vault. Exophthalmos with conjunctival edema may indicate the formation of a carotid-cavernous fistula or a retrobulbar hematoma. Soft tissue hematoma in the occipito-cervical region may be accompanied by 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 state of the pupils and their reaction to light, the functions of cranial nerves and motor functions, neurological symptoms, increased intracranial pressure, dislocation of the brain, the development of acute cerebrospinal fluid occlusion.

Tatotika abouttoazaneitherI munitsicinWithtoaboutth Pomoschand:

The choice of tactics for treating victims is determined by the nature of damage to the brain, bones of the vault and base of the skull, concomitant extracranial trauma and

the development of complications due to trauma.

OWithnovnand I perdaha etcand abouttoazaneitherand PeRhowl Pohmaboutschand PaboutWithtRadainshandm with TBI - prevent

the development of arterial hypotension, hypoventilation, hypoxia, hypercapnia, since these complications lead to severe ischemic brain damage and are accompanied by high mortality.

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

0.5-1.0 ml of a 0.1% solution of atropine subcutaneously;

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

seduxen solution, or 15-20 ml of 20% sodium oxybutyrate solution, or dormicum 0.1-

During transportation, control of the respiratory rhythm is necessary.

6. With intracranial hypertension syndrome:

2-4 ml of a 1% solution of furosemide (lasix) intravenously (with decompensated

blood loss due to concomitant trauma manholeikWithne introdandtb! );

Artificial hyperventilation of the lungs.

7. In pain syndrome: intramuscularly (or intravenously slowly) 30 mg-1.0 ketorolac and 2 ml of 1-2% solution of diphenhydramine and (or) 2-4 ml (200-400 mg) of 0.5% solution of tramal or other non-narcotic analgesic in appropriate doses.

Opieats ne introdandtb!

8. For head wounds and external bleeding from them:

Wound toilet with antiseptic treatment of the edges (see Ch. 15).

9. Transportation to a hospital where there is a neurosurgical service; in critical condition - to the intensive care unit.

PeReven morenb aboutWithnovns munitsikamentov:

1. *Dopamine 4%, 5 ml; amp

2. Dobutamine solution for infusions 5 mg/ml

4. *Prednisolone 25mg 1ml, 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. Mezaton 1% - 1.0; amp

PeReven morenb daboutPolnandtelbns munitsikamentov:

1. * Atropine sulfate 0.1% - 1.0, amp

2. *Betamethasone 1ml, amp

3. * Epinephrine 0.18% - 1 ml; amp

4. *Destran 70400.0; fl

5. * Diphenhydramine 1% - 1.0, amp

6. * Ketorolac 30mg - 1.0; amp

FROMpiWithOK andWithPaboutlbcallnnoh landteRatatRs:

1. "Diseases of the nervous system" / Guide for doctors / Edited by N.N. Yakhno,

D.R. Shtulman - 3rd edition, 2003

2. V.A. Mikhailovich, A.G. Miroshnichenko. A guide for emergency physicians. 2001

4. Birtanov E.A., Novikov S.V., Akshalova D.Z. Development of clinical guidelines and protocols for diagnosis and treatment, taking into account modern requirements. methodical

No. 883 “On Approval of the List of Basic (Vital) medicines».

"On approval of the Instructions for the formation of the List of the main (vital)

medicines".

FROMpiWithOK RazRababoutthikov:

Head of the Department of Emergency and Urgent Care, Internal Medicine No. 2 of the Kazakh National medical university them. S.D.

Asfendiyarova - Doctor of Medical Sciences, Professor Turlanov K.M. Employees of the Department of Emergency and Urgent Care, Internal Medicine No. 2 of the Kazakh National

Medical University. S.D. Asfendiyarova: Candidate of Medical Sciences, Associate Professor Vodnev V.P.; PhD,

associate professor Dyusembaev B.K.; Candidate of Medical Sciences, Associate Professor Akhmetova G.D.; Candidate of Medical Sciences, Associate Professor Bedelbayeva G.G.;

Almukhambetov M.K.; Lozhkin A.A.; Madenov N.N.

Head of the Department of Emergency Medicine, Almaty State

Institute for Advanced Training of Doctors - Candidate of Medical Sciences, Associate Professor Rakhimbaev R.S. Employees of the Department of Emergency Medicine of the Almaty State Institute for the Improvement of Doctors: Candidate of Medical Sciences, Associate Professor Silachev Yu.Ya.; Volkova N.V.; Khairulin R.Z.; Sedenko V.A.

* - drugs included in the list of essential (vital) drugs

In Russia, the International Classification of Diseases of the 10th revision (ICD-10) is adopted as a single regulatory document for accounting for morbidity, reasons for the population to contact 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. №170

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

With amendments and additions by WHO.

Processing and translation of changes © mkb-10.com

Consequences of chmt mcb 10

1047 universities, 2204 subjects.

Closed craniocerebral injury (concussion, head contusion)

The purpose of the stage: Restoration of the functions of all vital systems and organs

S06.1 Traumatic cerebral edema

S06.2 Diffuse brain injury

S06.3 Focal brain injury

S06.4 Epidural hemorrhage

Definition: Closed craniocerebral injury (CTBI) is an injury 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

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

vuyut fracture zone. Penetrating injuries include such a TBI, which is accompanied by

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

the occurrence of liquor fistulas (liquorrhea).

Primary - damage is caused by the direct impact of trauma-

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

Secondary - damage not associated with direct brain damage,

but are due to the consequences of primary brain damage and develop mainly

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

1. intracranial - cerebrovascular changes, disorders of the cerebrospinal fluid

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

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

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

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

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

chila Glasgow coma scale (proposed by G. Teasdale and B. Jennet 1974). The state of the building

those who gave are evaluated at the first contact with the patient, after 12 and 24 hours according to three parameters

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

irritation. There is a classification of impaired consciousness in TBI, based on the quality

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

Light traumatic brain injury includes concussion and mild cerebral contusion.

degree. CTBI of moderate severity - brain contusion of moderate severity. To cha-

zhelee CTBI include severe brain contusion and all types of head compression

2. moderate;

4. extremely heavy;

The criteria for a satisfactory condition are:

1. clear consciousness;

2. absence of violations of 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 recovery is usually good.

The criteria for a state of moderate severity are:

3. focal symptoms - certain hemispheric and cranio-

basic symptoms. Sometimes there are single, mildly pronounced stem

symptoms (spontaneous nystagmus, etc.)

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

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

abilities are often favorable.

3. focal symptoms - stem symptoms are moderately pronounced (anisocoria, mild

downward gaze, spontaneous nystagmus, contralateral pyramidal

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

wife hemispheric and craniobasal symptoms, including epileptic seizures,

paresis and paralysis.

by one of the parameters. The threat to life is significant, largely depends on the duration

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

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

anisocoria, vertical or horizontal eye divergence, tonic spontaneous

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

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

expressed (up to bilateral and multiple paresis).

When ascertaining an extremely serious condition, it is necessary to have pronounced disorders

decisions on all parameters, and one of them is necessarily limiting, a threat to

life is maximum. The prognosis for recovery is often unfavorable.

The criteria for the terminal state are as follows:

3. focal symptoms - stem in the form of limiting bilateral mydriasis,

absence of corneal and pupillary reactions; hemispheric and craniobasal usually change

covered with cerebral and stem disorders. The prognosis for the survival of the patient is unfavorable

The types of brain damage are:

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

effects of a small traumatic force. It occurs in almost 70% of patients with TBI.

A concussion is characterized by the absence of loss of consciousness or a short-term loss of consciousness.

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

note, rarely vomiting, dizziness, weakness, pain when moving the eyeballs.

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

whether it occurs) is short-lived. There is no anteroretrograde amnesia. When shaken-

in the brain, these phenomena are caused by a functional lesion of the brain and

pass after 5-8 days. It is not necessary to have a diagnosis to establish a diagnosis.

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

subdivided into degrees of severity;

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

brain matter, often with a hemorrhagic component that occurred 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 injury(10-15% affected). After the injury, ut-

Rata of consciousness from several minutes to 40 minutes. Most have retrograde amnesia

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

lively. After regaining consciousness, the victim complains of headache,

nausea, vomiting (often repeated), dizziness, weakening of attention, memory. Can

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

Sometimes there are pathological reflexes. Due to subarachnoid hemorrhage

the influence can be detected easily expressed meningeal syndrome. Can watch-

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

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

mild brain injury may be accompanied by skull fractures.

Moderate brain injury. Loss of consciousness lasts from

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

deep stunning can persist for several hours or days. Observing-

severe headache, often repeated vomiting. Horizontal nystagmus, weakened

decrease in pupillary response to light, a violation of convergence is possible. Disso-

cation of tendon reflexes, sometimes moderately pronounced hemiparesis and pathological

sky reflexes. There may be sensory disturbances, speech disorders. menin-

heal syndrome is moderately pronounced, and CSF pressure is moderately increased (due to

including victims who have liquorrhea). There is tachycardia or bradycardia.

Respiratory disorders in the form of moderate tachypnea without rhythm disturbance and does not require application

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

agitation, sometimes convulsive seizures. There is retro- and anteroretrograde amnesia

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

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

mutism). Oppression of consciousness to stupor or coma. There may be a pronounced psychomotor-

noe excitation, followed by atony. Pronounced stem symptoms - floating

eyeball movements, eyeball distance along the vertical axis, fixation

downward gaze, anisocoria. Pupillary reaction to light and corneal reflexes are depressed. Swallow-

is violated. Sometimes hormetonia develops to painful stimuli or spontaneously.

Bilateral pathological foot reflexes. There are changes in muscle tone

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

respiration - according to the central or peripheral type (tachy- or bradypnea). Arteri-

nal 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 is diffuse axonal injury

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

shading of consciousness to a deep coma, a pronounced violation of vital functions, which

which require mandatory medical and hardware correction. Lethality at

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

living develops apallic syndrome. Diffuse axonal injury

accompanied by the formation of intracranial hematomas.

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

sheniya intracranial space space-occupying formations. It should be borne in mind

that any “non-building” compression in TBI can become progressive and lead to

severe compression and dislocation of the brain. Non-increasing pressures include

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

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

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

nye mechanisms. Increasing pressures include all types of intracranial hematomas

and brain contusions, accompanied by a mass effect.

6. subdural hydromas;

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

chronic(after 3 weeks).

The classic __________ clinical picture of intracranial hematomas includes the presence of

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

The classic clinic is characterized by hematomas without concomitant brain injury. At the

suffering from hematomas combined with brain contusion from the very first hours

TBI, there are signs of primary brain damage and symptoms of compression and dislo-

cations of the brain caused by contusion of the brain tissue.

1. road traffic injuries;

2. domestic injury;

3. fall and sports injury;

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

Periorbital hematoma ("spectacle symptom", "raccoon eye") indicates a fracture

floor of the anterior cranial fossa. Hematoma in the area of ​​the mastoid process (symptom Butt-

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

noah 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 TBI. The sound of "trem-

broken pot" with percussion of the skull can occur with fractures of the bones of the arch of the skull

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

cavernous anastomosis or on the formed retrobulbar hematoma. Hematoma soft-

some tissues in the occipito-cervical region may be accompanied by a fracture of the occipital bone

and (or) contusion of the poles and basal regions 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 state of the pupils and their reaction to light, the functions of the cranial nerves and movement

negative functions, neurological symptoms, increased intracranial pressure,

dislocation of the brain, the development of acute cerebrospinal fluid occlusion.

Medical care tactics:

The choice of tactics for the treatment of 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 trauma.

The main task in providing first aid to victims of TBI is not to

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

how these complications lead to severe ischemic brain damage and accompanying

are associated with high mortality.

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

must be subject to the ABC rule:

A (airway) - ensuring the patency of the respiratory tract;

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

tracts, drainage of the pleural cavity with 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), with insufficient

myocardial accuracy - the introduction of inotropic drugs (dopamine, dobutamine) or vaso-

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

tion of the mass of circulating blood, the introduction 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.

creatures, because with TBI, the probability of a cervicospinal injury is not excluded (and therefore

all victims before clarifying the nature of the injury at the prehospital stage

dimo to fix the cervical spine, imposing a special cervical gate-

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 hypovola-

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

are patients with acute occlusive syndrome, in which the rate of CSF production

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

reducing ICP.

For the prevention of intracranial hypertension and her brain-damaging

consequences at the prehospital stage, glucocorticoid hormones and salure-

Glucocorticoid hormones prevent the development of intracranial hypertension

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

extravasation of fluid into the brain tissue.

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

nie prednisolone at a dose of 30 mg

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

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

salureti-

kov, for example, lasix in dozemg (2-4 ml of a 1% solution).

Ganglion blocking drugs for high degree of intracranial hypertension

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

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

To reduce intracranial pressure both at the prehospital stage and in

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

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

waiting for the substance of the brain and the vascular bed is not possible and deterioration is likely

patient due to a rapid secondary increase in intracranial pressure.

In this case, it is advisable to intravenously administer mannitol (mannitol) from the calculation

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

The sequence of measures to provide emergency care at the prehospital stage

With a concussion, emergency care is not required.

In case of bruising and compression of the brain:

1. Provide access to the vein.

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

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

baking maintenance of blood pressure at the level of RT. Art.;

Application of the Sellick maneuver;

Do not bend the spine in the cervical region!

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

to be driven by a ventilator or not; muscle relaxants (succinylcholine chloride - dicilin, listenone in

dose of 1-2 mg/kg; injections are carried out only by doctors of resuscitation and surgical brigades

If spontaneous breathing is ineffective, artificial ventilation is indicated.

lung circulation in the mode of moderate hyperventilation (12-14 l/min for a patient weighing

blood loss due to a combined injury, do not administer Lasix!);

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

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

tramala or other non-narcotic analgesic in appropriate doses.

Wound toilet with antiseptic treatment of the edges (see Ch. 15).

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

in a mental state - to the intensive care unit.

List of essential medicines:

1. *Dopamine 4%, 5 ml; amp

4. *Prednisolone 25mg 1ml, amp

5. * Diazepam 10 mg/2 ml; amp

9. *Mannitol 15% 200 ml, fl

10. * Furosemide 1% 2.0, amp

11. Mezaton 1% - 1.0; amp

List of additional medicines:

2. *Betamethasone 1ml, amp

4. *Destran,0; fl

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Traumatic brain injury concussion

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

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

correspond to the fracture zone. Penetrating injuries include such TBI,

which is accompanied by fractures of the skull bones and damage to the dura mater

membranes of the brain with the occurrence of cerebrospinal fluid fistulas (liquorrhea).

According to the pathophysiology of TBI:

traumatic forces on the skull bones, meninges and brain tissue, brain vessels and the cerebrospinal fluid system.

type of secondary ischemic changes in brain tissue. (intracranial and systemic).

cerebral edema, changes in intracranial pressure, dislocation syndrome.

hyponatremia, hyperthermia, impaired carbohydrate metabolism, DIC.

consciousness of the victim, the presence and severity of neurological symptoms, the presence or absence of damage to other organs. The Glasgow coma scale (proposed by G. Teasdale and B. Jennet 1974) has received the greatest distribution. The condition of the victims is assessed at the first contact with the patient, after 12 and 24 hours according to three parameters: eye opening, speech response and motor response in response to external stimulation. There is a classification of disorders of consciousness in TBI, based on a qualitative assessment of the degree of depression of consciousness, where there are the following gradations of the state of consciousness:

Mild PTBI includes concussion and mild contusion of the brain. CTBI of moderate severity - brain contusion of moderate severity. Severe CBI includes severe brain contusion and all types of cerebral compression.

1. clear consciousness or moderate stupor;

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

3. focal symptoms - certain hemispheric and

craniobasal symptoms. Sometimes there are single, mild stem symptoms (spontaneous nystagmus, etc.)

To state a state of moderate severity, it is sufficient to have one of the indicated parameters. The threat to life is insignificant, the forecast of recovery

working capacity is more often favorable.

1. change in consciousness to a deep stupor or stupor;

2. violation of vital functions (moderate in one or two indicators);

3. focal symptoms - stem symptoms are moderately pronounced (anisocoria, slight upward gaze restriction, spontaneous nystagmus, contralateral pyramidal insufficiency, dissociation of meningeal symptoms along the body axis, etc.); hemispheric and craniobasal symptoms, including epileptic seizures, paresis and paralysis, may be pronounced.

To state a serious condition, it is permissible to have these violations, although

by one of the parameters. The threat to life is significant, largely depends on the duration of the serious condition, the prognosis for recovery is often unfavorable.

1. impaired consciousness to moderate or deep coma;

2. a pronounced violation of vital functions in several ways;

3. focal symptoms - stem symptoms are clearly expressed (paresis of upward gaze, severe anisocoria, divergence of the eyes vertically or horizontally, tonic spontaneous nystagmus, weakening of the pupil's reaction to light, bilateral pathological reflexes, decerebrate rigidity, etc.); hemispheric and craniobasal symptoms are pronounced (up to bilateral and multiple paresis).

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

violations in all respects, and in one of them necessarily the limit, the threat to life is maximum. The prognosis for recovery is often unfavorable.

1. violation of consciousness to the level of transcendental coma;

2. critical violation of vital functions;

3. focal symptoms - stem in the form of limiting bilateral mydriasis, the absence of corneal and pupillary reactions; hemispheric and craniobasal are usually blocked by cerebral and stem disorders. The patient's survival prognosis is unfavorable.

By types distinguish:

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

1. concussion – a condition that occurs more often as a result of exposure to a small traumatic force. Occurs in almost 70% of patients with

TBI. A concussion is characterized by the absence of loss of consciousness or a short-term loss of consciousness after an injury: from 1-2 minutes. Patients complain of headaches

pain, nausea, rarely vomiting, dizziness, weakness, pain when moving the eyeballs.

There may be slight asymmetry of the tendon reflexes. retrograde amnesia

(if it occurs) is short-lived. There is no anteroretrograde amnesia. At

concussion, these phenomena are caused by a functional lesion of the brain and disappear after 5-8 days. It is not necessary to have all of these symptoms to make a diagnosis. A concussion is a single form and is not divided into degrees of severity;

1-3 weeks after injury. Brain contusion of mild severity may be accompanied by fractures of the bones of the skull.

deep stunning can persist for several hours or days.

There is severe headache, often repeated vomiting. Horizontal

nystagmus, weakening of the reaction of pupils to light, a violation of convergence is possible. There is dissociation of tendon reflexes, sometimes moderate hemiparesis and pathological reflexes. There may be sensory disturbances, speech disorders. The meningeal syndrome is moderately expressed, and the CSF pressure is moderately increased (with the exception of victims who have liquorrhea).

There is tachycardia or bradycardia. Respiratory disorders in the form of moderate tachypnea without rhythm disturbance and does not require hardware correction. The temperature is subfebrile. On the 1st day there may be psychomotor agitation, sometimes convulsive seizures. There is retro- and anteroretrograde amnesia.

several days (in some patients with the transition to apallic syndrome or akinetic mutism). Oppression of consciousness to stupor or coma. There may be pronounced psychomotor agitation, followed by atony. Stem symptoms are pronounced - floating movements of the eyeballs, eyeball separation along the vertical axis, gaze fixation down, anisocoria. Pupillary reaction to light and corneal reflexes are depressed. Swallowing is impaired. Sometimes hormetonia develops to painful stimuli or spontaneously. Bilateral pathological foot reflexes. There are changes in muscle tone, often - hemiparesis, anisoreflexia. There may be seizures. Respiratory failure - according to the central or peripheral type (tachy- or bradypnea). Blood pressure is either increased or decreased (may be normal), and in atonic coma it is unstable and requires constant medical support. Pronounced meningeal syndrome.

Diffuse axonal damage to the brain is a special form of brain contusion. . Its clinical signs include dysfunction of the brain stem - depression of consciousness to a deep coma, a pronounced violation of vital functions, which require mandatory medical and hardware correction. Mortality in diffuse axonal brain damage is very high and reaches 80-90%, and apallic syndrome develops in survivors. Diffuse axonal damage may be accompanied by the formation of intracranial hematomas.

reduction of intracranial space by volumetric formations. It should be borne in mind that any "non-increasing" compression in TBI can become progressive and lead to severe compression and dislocation of the brain. Non-increasing compressions include compression by fragments of the skull bones with depressed fractures, pressure on the brain by other foreign bodies. In these cases, the formation itself squeezing the brain does not increase in volume. Secondary intracranial mechanisms play a leading role in the genesis of brain compression. Increasing compressions include all types of intracranial hematomas and brain contusions, accompanied by a mass effect.

5. multiple intrathecal hematomas;

6. subdural hydromas;

Hematomas can be: acute (first 3 days), subacute (4 days-3 weeks) and

chronic (after 3 weeks).

The classic clinical picture of intracranial hematomas includes the presence of

light gap, anisocoria, hemiparesis, bradycardia, which is less common. The classic clinic is characterized by hematomas without concomitant brain injury. In victims with hematomas combined with brain contusion, already from the first hours of TBI, there are signs of primary brain damage and symptoms of compression and dislocation of the brain due to brain tissue contusion.

1. alcohol intoxication (70%).

2. TBI as a result of an epileptic seizure.

1. road traffic injuries;

2. domestic injury;

skin of the head. Periorbital hematoma ("symptom of glasses", "raccoon eyes") indicates a fracture of the bottom of the anterior cranial fossa. Hematoma in the area of ​​the mastoid process (Battle's symptom) accompanies a fracture of the pyramid of the temporal bone. A hemotympanum or ruptured tympanic membrane may correspond to a skull base fracture. Nasal or ear liquorrhea indicates a fracture of the base of the skull and penetrating TBI. The sound of a "cracked pot" on percussion of the skull can occur with fractures of the bones of the cranial vault. Exophthalmos with conjunctival edema may indicate the formation of a carotid-cavernous fistula or a retrobulbar hematoma. Soft tissue hematoma in the occipito-cervical region may be accompanied by 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 state of the pupils and their reaction to light, the functions of cranial nerves and motor functions, neurological symptoms, increased intracranial pressure, dislocation of the brain, the development of acute cerebrospinal fluid occlusion.

The choice of tactics for treating victims is determined by the nature of damage to the brain, bones of the vault and base of the skull, concomitant extracranial trauma and

the development of complications due to trauma.

the development of arterial hypotension, hypoventilation, hypoxia, hypercapnia, since these complications lead to severe ischemic brain damage and are accompanied by high mortality.

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

be subject to the ABC rule:

restoration of BCC (transfusion of solutions of crystalloids and colloids), with myocardial insufficiency - the introduction of inotropic drugs (dopamine, dobutamine) or vasopressors (adrenaline, norepinephrine, mezaton). It must be remembered that without the normalization of the mass of circulating blood, the introduction of vasopressors is dangerous.

An obligatory component of the treatment of severe TBI is the elimination of hypovolemia, and for this purpose, liquid is usually administered in a volume of 30-35 ml / kg per day. An exception are patients with acute occlusive syndrome, in whom the rate of CSF production directly depends on the water balance, so dehydration is justified in them, which allows them to reduce ICP.

They contribute to the subsidence of perifocal edema in the area of ​​injury.

At the prehospital stage, intravenous or intramuscular injection prednisolone at a dose of 30 mg

However, it should be borne in mind that, due to the concomitant mineralocorticoid effect, prednisolone is able to retain sodium in the body and increase the 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

practically does not have mineralocorticoid properties.

In the absence of circulatory disorders simultaneously with glucocorticoid

hormones for dehydration of the brain, it is possible to prescribe high-speed

Ganglion blocking drugs with a high degree of intracranial hypertension are contraindicated, since with a decrease in systemic blood pressure, a complete blockade of cerebral blood flow may develop due to compression of the brain capillaries by edematous brain tissue.

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

respiratory and circulatory disorders.

In this case, intravenous administration of mannitol (mannitol) from

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

With psychomotor agitation:

2-4 ml of 0.5% solution of seduxen (relanium, sibazon) intravenously;

Transportation to the hospital (to the neurological department).

1. Provide access to the vein.

2. With the development of a terminal state, perform cardiac resuscitation.

3. In case of circulatory decompensation:

Reopoliglyukin, crystalloid solutions intravenously;

If necessary, dopamine 200 mg in 400 ml of isotonic sodium chloride solution or any other crystalloid solution intravenously at a rate that maintains blood pressure at the level of RT. Art.;

4. When unconscious:

Inspection and mechanical cleaning of the oral cavity;

Application of the Sellick maneuver;

Performing direct laryngoscopy;

Stabilization of the cervical spine (slight stretching by hands);

IVL is carried out or not; muscle relaxants (succinylcholine chloride - dicilin, listenone

at a dose of 1-2 mg/kg; injections are carried out only by doctors of resuscitation and surgical teams).

If spontaneous breathing is ineffective, artificial

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

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

0.5-1.0 ml of a 0.1% solution of atropine subcutaneously;

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

seduxen solution, or ml of 20% sodium oxybutyrate solution, or dormicum 0.1-

During transportation, control of the respiratory rhythm is necessary.

6. With intracranial hypertension syndrome:

2-4 ml of a 1% solution of furosemide (lasix) intravenously (with decompensated

Artificial hyperventilation of the lungs.

7. In pain syndrome: intramuscularly (or intravenously slowly) 30 mg-1.0 ketorolac and 2 ml of 1-2% solution of diphenhydramine and (or) 2-4 ml (mg) of 0.5% solution of tramal or other non-narcotic analgesic in the appropriate doses.

8. For head wounds and external bleeding from them:

9. Transportation to a hospital where there is a neurosurgical service; in critical condition - to the intensive care unit.

1. *Dopamine 4%, 5 ml; amp

2. Dobutamine solution for infusions 5 mg/ml

4. *Prednisolone 25mg 1ml, 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. Mezaton 1% - 1.0; amp

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 30mg - 1.0; amp

1. "Diseases of the nervous system" / Guide for doctors / Edited by N.N. Yakhno,

D.R. Shtulman - 3rd edition, 2003

2. V.A. Mikhailovich, A.G. Miroshnichenko. A guide for emergency physicians. 2001

4. Birtanov E.A., Novikov S.V., Akshalova D.Z. Development of clinical guidelines and protocols for diagnosis and treatment, taking into account modern requirements. methodical

No. 883 "On Approval of the List of Essential (Essential) Medicines".

"On approval of the Instructions for the formation of the List of the main (vital)

Head of the Department of Emergency and Urgent Care, Internal Medicine No. 2 of the Kazakh National Medical University. S.D.

Asfendiyarova - Doctor of Medical Sciences, Professor Turlanov K.M. Employees of the Department of Emergency and Urgent Care, Internal Medicine No. 2 of the Kazakh National

Medical University. S.D. Asfendiyarova: Candidate of Medical Sciences, Associate Professor Vodnev V.P.; PhD,

associate professor Dyusembaev B.K.; Candidate of Medical Sciences, Associate Professor Akhmetova G.D.; Candidate of Medical Sciences, Associate Professor Bedelbayeva G.G.;

Almukhambetov M.K.; Lozhkin A.A.; Madenov N.N.

Head of the Department of Emergency Medicine, Almaty State

Institute for Advanced Training of Doctors - Candidate of Medical Sciences, Associate Professor Rakhimbaev R.S. Employees of the Department of Emergency Medicine of the Almaty State Institute for the Improvement of Doctors: Candidate of Medical Sciences, Associate Professor Silachev Yu.Ya.; Volkova N.V.; Khairulin R.Z.; Sedenko V.A.

Closed cranium- brain injury(brain concussion, head injury-

leg brain, intracranial hematomas, etc.. d.)

Protocol code: SP-008

Purpose of the stage: Restoration of the functions of all vital systems and organs

ICD codes-10:

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 cranium- brain injury(ZTCHMT) - 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.

To open TBI includes injuries that are accompanied by a violation

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

vuyut fracture zone. Penetrating injuries include such a TBI, which is accompanied by

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

the occurrence of liquor fistulas (liquorrhea).

Classification:

According to the pathophysiology of TBI:

- Primary- damage is caused by the direct impact of trauma -

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

thief system.

- Secondary- damage not associated with direct brain damage,

but are due to the consequences of primary brain damage and develop mainly

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

1. intracranial- cerebrovascular changes, disorders of liquor circulation;

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

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

hyponatremia, hyperthermia, impaired carbohydrate metabolism, DIC.

According to the severity of the condition of patients with TBI– is based on an assessment of the degree of oppression

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

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

chila Glasgow coma scale (proposed by G. Teasdale and B. Jennet 1974). The state of the building

those who gave are evaluated at the first contact with the patient, after 12 and 24 hours according to three parameters

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

irritation. There is a classification of impaired consciousness in TBI, based on the quality

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

standing of consciousness:

Moderate stun;

Deep stun;

moderate coma;

deep coma;

Outrageous coma;

Light traumatic brain injury includes concussion and mild cerebral contusion.

degree. CTBI of moderate severity - brain contusion of moderate severity. To cha-

zhelee CTBI include severe brain contusion and all types of head compression

leg brain.

Allocate 5 gradations of the state of patients with TBI :

1. satisfactory;

2. moderate;

3. heavy;

4. extremely heavy;

5. terminal;

The criteria for a satisfactory condition are :

1. clear consciousness;

2. absence of violations of 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 recovery is usually good.

The criteria for a state of moderate severity are :

1. clear consciousness or moderate stupor;

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

3. focal symptoms - certain hemispheric and cranio-

basic symptoms. Sometimes there are single, mildly pronounced stem

symptoms (spontaneous nystagmus, etc.)

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

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

abilities are often favorable.

Severe Condition Criteria (15-60 min .):

1. change in consciousness to a deep stupor or stupor;

2. violation of vital functions (moderate in one or two indicators);

3. focal symptoms - stem symptoms are moderately pronounced (anisocoria, mild

downward gaze, spontaneous nystagmus, contralateral pyramidal

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

wife hemispheric and craniobasal symptoms, including epileptic seizures,

paresis and paralysis.

To state a serious condition, it is permissible to have these violations, although

by one of the parameters. The threat to life is significant, largely depends on the duration

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

pleasant.

The criteria for an extremely serious condition are (6-12 hours):

1. impaired consciousness to moderate or deep coma;

2. a pronounced violation of vital functions in several ways;

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

anisocoria, vertical or horizontal eye divergence, tonic spontaneous

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

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

expressed (up to bilateral and multiple paresis).

When ascertaining an extremely serious condition, it is necessary to have pronounced disorders

decisions on all parameters, and one of them is necessarily limiting, a threat to

life is maximum. The prognosis for recovery is often unfavorable.

The criteria for the terminal state are as follows :

1. violation of consciousness to the level of transcendental coma;

2. critical violation of vital functions;

3. focal symptoms - stem in the form of limiting bilateral mydriasis,

absence of corneal and pupillary reactions; hemispheric and craniobasal usually change

covered with cerebral and stem disorders. The prognosis for the survival of the patient is unfavorable

pleasant.

Clinical forms of TBI.

Distinguish by type:

1. insulated;

2. combined;

3. combined;

4. repeated;

Cranial- brain injury is divided into:

1. closed;

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

There are different types of brain damage:

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

effects of a small traumatic force. It occurs in almost 70% of patients with TBI.

A concussion is characterized by the absence of loss of consciousness or a short-term loss of consciousness.

consciousness after injury: from 1-2 to 10-15 minutes. Patients complain of headaches, nausea

note, rarely vomiting, dizziness, weakness, pain when moving the eyeballs.

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

whether it occurs) is short-lived. There is no anteroretrograde amnesia. When shaken-

in the brain, these phenomena are caused by a functional lesion of the brain and

pass after 5-8 days. It is not necessary to have a diagnosis to establish a diagnosis.

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

subdivided into degrees of severity;

2. Brain contusion is damage in the form of macrostructural destruction

brain matter, often with a hemorrhagic component that occurred 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 injury (10-15% affected). After the injury, ut-

Rata of consciousness from several minutes to 40 minutes. Most have retrograde amnesia

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

lively. After regaining consciousness, the victim complains of headache,

nausea, vomiting (often repeated), dizziness, weakening of attention, memory. Can

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

Sometimes there are pathological reflexes. Due to subarachnoid hemorrhage

the influence can be detected easily expressed meningeal syndrome. Can watch-

brady- and tachycardia, a transient increase in blood pressure by 10-15 mm Hg.

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

mild brain injury may be accompanied by skull fractures.

Moderate brain injury . Loss of consciousness lasts from

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

deep stunning can persist for several hours or days. Observing-

severe headache, often repeated vomiting. Horizontal nystagmus, weakened

decrease in pupillary response to light, a violation of convergence is possible. Disso-

cation of tendon reflexes, sometimes moderately pronounced hemiparesis and pathological

sky reflexes. There may be sensory disturbances, speech disorders. menin-

heal syndrome is moderately pronounced, and CSF pressure is moderately increased (due to

including victims who have liquorrhea). There is tachycardia or bradycardia.

Respiratory disorders in the form of moderate tachypnea without rhythm disturbance and does not require application

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

agitation, sometimes convulsive seizures. There is retro- and anteroretrograde amnesia

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

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

mutism). Oppression of consciousness to stupor or coma. There may be a pronounced psychomotor-

noe excitation, followed by atony. Pronounced stem symptoms - floating

eyeball movements, eyeball distance along the vertical axis, fixation

downward gaze, anisocoria. Pupillary reaction to light and corneal reflexes are depressed. Swallow-

is violated. Sometimes hormetonia develops to painful stimuli or spontaneously.

Bilateral pathological foot reflexes. There are changes in muscle tone

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

respiration - according to the central or peripheral type (tachy- or bradypnea). Arteri-

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

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

ningeal syndrome.

A special form of brain contusion is diffuse axonal injury

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

shading of consciousness to a deep coma, a pronounced violation of vital functions, which

which require mandatory medical and hardware correction. Lethality at

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

living develops apallic syndrome. Diffuse axonal injury

accompanied by the formation of intracranial hematomas.

A contusion - a focus of traumatic crushing of the brain tissue - is often formed in the basal sections of the frontal and anterior sections 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 in diffuse axonal damage, it is possible wide range disorders from mild confusion and short-term loss of consciousness (with concussion) to coma and even death. Secondary brain damage is associated with hypoxia, ischemia, intracranial hypertension, infection.
Allocate open craniocerebral injury (TBI), in which there is communication between the cranial cavity and the external environment, and closed.
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, the presence of stem neurological symptoms.
When examining a patient with TBI, especially severe, you need to follow a certain plan.
1. First, you should pay attention to the patency of the airways, the frequency and rhythm of breathing, the state of hemodynamics.
2. You should quickly examine the chest and abdomen to exclude hemo- or pneumothorax, abdominal bleeding.
3. Assess the state of consciousness. With 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 take away from 40 to 3 memory, asking to remember 3 words and checking if the patient can name them after 5 minutes.
4. Examine the head, torso, limbs, paying attention to external signs injuries (wounds, bruises, bruises, fractures).
5. It is important to identify signs of a fracture of the base of the skull: the outflow of cerebrospinal fluid from the nose (unlike ordinary mucus, the cerebrospinal fluid contains glucose), the symptom of glasses (delayed appearance of bilateral bruising in the periorbital region, limited by the edges of the orbit), the outflow 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 bruising behind auricle in the area of ​​the mastoid process, appearing 24-48 hours after the injury.
6. When collecting an anamnesis from the patient or those accompanying him, you should pay attention to the circumstances of the injury (the injury can provoke a stroke, an epileptic seizure), the use of alcohol or drugs.
7. When determining the duration of the 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, for the patient himself, consciousness returns at the moment when the ability to remember returns. The duration of the amnestic period for patients 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, previous and subsequent events.
8. The appearance of meningeal symptoms indicates a subarachnoid hemorrhage or meningitis, but neck stiffness can only be checked if cervical trauma is excluded.
9. All patients with TBI undergo x-ray of the skull in two projections, which can reveal depressed fractures, linear fractures in the region of the middle cranial fossa or at the base of the skull, the level of fluid in the ethmoid sinus, pneumocephalus (presence of air in the cranial cavity). With a linear fracture of the cranial vault, attention should be paid to whether the fracture line crosses the groove in which the middle meningeal artery passes. Her injury is the most common cause epidural hematoma.
10. Most patients (even with minimal signs of damage to the cervical spine or abrasions on the forehead) should be assigned a cervical x-ray (at least in the lateral projection, while all the cervical vertebrae should be imaged).
11. Displacement of the median structures of the brain during the development of intracranial hematoma can be detected using echoencephaloscopy.
12. Lumbar puncture in 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 fracture of the base of the skull, comminuted or depressed fracture of the cranial vault, urgent consultation neurosurgeon. Particular vigilance for hematoma is necessary in the elderly, patients suffering from alcoholism or taking anticoagulants.
Traumatic brain injury is a dynamic process requiring constant control behind 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 from prescribing sedatives if possible (if the patient falls asleep, you should periodically wake him up).
Mild TBI is characterized by a brief loss of consciousness, orientation, or other neurological function, usually occurring immediately after injury. The score on the Glasgow Coma Scale at the initial examination is 13-15 points. After the restoration of consciousness, amnesia is detected for events that immediately preceded the injury or occurred immediately after it (the total duration of the amnesiac period does not exceed 1 hour), headache, autonomic disorders (fluctuations in blood pressure, 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 correspond to concussion and mild brain contusion. main feature mild TBI - the fundamental reversibility of neurological disorders, however, the recovery process may take several weeks or months, during which patients will continue to have headache, dizziness, asthenia, impaired memory, sleep and other symptoms (post-commotion syndrome). In car accidents, mild head injury is often combined with whiplash injury of the neck resulting from sudden head movements (most often as a result of sudden overextension 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 mild 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 allowed to go home, provided that relatives follow him, and if his condition worsens, he will be quickly taken to the hospital. Particular care should be taken in children who may develop intracranial hematoma in the absence of initial loss of consciousness.
Moderate and severe TBI are 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 with progressive depression of consciousness, the appearance of a new or an increase in already existing focal symptoms, the appearance of signs of wedging. The "light interval" (a short-term return of consciousness with subsequent deterioration), which is considered a classic sign of a hematoma, is observed in only 20% of cases. The development of a prolonged coma immediately after injury in the absence of intracranial hematoma or massive contusion foci is a sign of diffuse axonal damage. Delayed deterioration, in addition to intracranial hematoma, may be due to cerebral edema, fat embolism, ischemia, or infectious complications. Fat embolism occurs several days after injury, usually in patients with fractures of the long tubular bones- when the fragments are displaced or attempted to be repositioned, in most patients, the respiratory function is disturbed and small hemorrhages occur under the conjunctiva. Post-traumatic meningitis develops a few days after injury, more often in patients with open TBI, especially in the presence of a skull base fracture with a message (fistula) between the subarachnoid space and the paranasal sinuses or middle ear.