TBI: pathogenesis, clinical picture, diagnosis, IT. Traumatic brain injury Presentation on the topic closed traumatic brain injury

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Definition: Traumatic brain injury (TBI) - combined damage by mechanical energy to the skull and intracranial contents (brain, membranes, blood vessels, cranial nerves)

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Relevance of the topic 50% of all injuries 50% combined with injuries to other organs Mortality up to 10%, postoperative mortality - 30% Severe forms of TBI > 40% of cases, mortality - 70% High disability Mainly those of working age suffer

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Mechanical factors Vascular factors Hypoxemia Hypotension Hyperthermia Hyper- and hypoglycemia Hyper- and hypocapnia Intracranial hypertension

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Pathophysiology of TBI: primary and secondary damage The formation of a zone of irreversible primary damage under the influence of primary factors does not depend on the treatment measures taken. The goal of intensive therapy is to eliminate secondary damaging factors and areas of secondary structural and functional changes. The time factor is important!

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Classification of TBI (A.N. Konovalov 1998) Type of damage focal, diffuse, combined Pathogenesis primary lesion, secondary lesion Type of TBI isolated, combined, combined Nature of TBI closed, open penetrating, open non-penetrating Severity of TBI mild, moderate, severe Clinical forms concussion, brain contusion without compression, brain contusion with compression, diffuse axonal damage, head compression Clinical phases compensation, subcompensation, moderate decompensation, severe decompensation Periods of TBI acute, intermediate, residual, period of persistent residual effects Consequences of TBI autonomic cerebral dysfunction , cerebroorganic syndromes Outcome of TBI good recovery, moderate, severe disability, vegetative state, death

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Characteristics of closed and open traumatic brain injury Closed TBI: injuries in which there is no violation of the integrity of the scalp or there are soft tissue wounds without damage to the aponeurosis; fractures of the bones of the cranial vault, not accompanied by injury to the adjacent soft tissues and aponeurosis Open TBI: injuries in which there are wounds to the soft tissues of the head with damage to the aponeurosis; fracture of the base of the skull with damage to the brain, accompanied by bleeding or liquorrhea (from the ear, nose). There is a risk of infection of the intracranial contents.

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Clinical forms of TBI - Concussion - Diffuse axonal brain injury - Head compression - Brain compression - intracranial hematoma - depressed fracture - other causes Focal brain contusion - mild - moderate - severe

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Concussion Blackout of consciousness for up to 15 minutes Retro-, anterograde amnesia Nausea, vomiting, headache, dizziness Autonomic dysfunction: feeling of heat, tinnitus, sweating, blood pressure fluctuations, tachybradycardia, flushing Sleep disturbance Improvement within 7-10 days Labile anisoreflexia Small-scale nystagmus Mild meningeal symptoms that disappear within 3-7 days No damage to the skull bones CSF is normal Differential diagnosis: from a brain contusion (longer loss of consciousness, the presence of focal neurological symptoms)

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Mild brain contusion Loss of consciousness 15 min - 1 hour Headache, nausea, vomiting, dizziness Retrograde amnesia Vital functions without pronounced changes Regression of symptoms on days 14 - 18 Clonic nystagmus Mild anisocoria Pyramidal insufficiency Meningeal symptoms Possible calvarial fractures and subarachnoid hemorrhage

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Moderate brain contusion Loss of consciousness from 1 to 6 hours Expressed retro-, con-, anterograde amnesia Severe headache, repeated vomiting Transient vital disorders: bradycardia, tachycardia Increased blood pressure Tachypnea without disturbance of the respiratory rhythm Changes in the sleep-wake cycle Low-grade fever Symptoms regress to for 21-35 days or more Brainstem symptoms: nystagmus, dissociation of muscle tone and tendon reflexes Bilateral pathological signs Subarachnoid hemorrhage Otorrhea, nazorrhea Distinct focal symptoms - pupillary and oculomotor disorders, paresis, hyperesthesia, aphasia

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Severe brain contusion Loss of consciousness from several days/weeks to several months Psychomotor agitation is often observed Severe vital disturbances Tachypnea Hyperthermia Symptoms regress slowly 2-4-6 months / ??? Brainstem signs: floating eyeballs, gaze paresis, tonic nystagmus Bilateral mydriasis or miosis Swallowing disorders Variable tone, decerebrotic rigidity or ↓ tendon reflexes Oral automatism reflexes Convulsive seizures Fractures of the base of the skull Threatening hyperthermia Otorrhea, nazarea

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Compression of the brain (hematoma) Presence of a “light” gap Mydriasis on the side of the hematoma (40-60%) Bradycardia General cerebral symptoms Focal symptoms (hemiparesis, anisocoria) Convulsive syndrome Stem symptoms Asymptomatic course (light gap) Increased ICP (worsening headache, vomiting, stun or excitement) Initial symptoms of dislocation and compression of the upper parts of the trunk. Symptoms of dislocation and compression of the midbrain are expressed - deep coma with gross disturbances of muscle tone, respiratory disorders, bradycardia, arterial hypertension, pupillary and oculomotor disorders

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Changes in pupils with temporotentorial herniation on the right 1 – NORMAL 2,3, 4 – ANISOCORIA 5 – MYDRIASIS (bilateral damage to the oculomotor nerve, pupils do not react to light)

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Diffuse axonal damage Prolonged coma Hyperthermia Hyperhidrosis Hypersalivation Respiratory disturbance Symmetric or asymmetrical decerebration or decortication Changes in muscle tone - from diffuse muscle hypotonia to hormotonia Transition from coma to a persistent vegetative state Paresis of upward gaze Decreased or absent corneal reflexes Depression or loss of the oculocephalic reflex Men inhalation syndrome Stiffness Mental disorders Increased ICP Facial synkenesis - chewing, smacking, yawning and swallowing automatisms Tetrasyndromes of a pyramidal-extrapyramidal nature

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Diffuse axonal damage to the DAP occurs as a result of tension in the nerve tracts during acceleration-deceleration and rotation of brain structures. DAP is a very severe brain injury because it involves the brain pathways.

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Compression of the head deformation of the head damage and swelling of the soft coverings of the head, skull and brain depressed fractures subsequently - extensive tissue necrosis intoxication possible infection respiratory failure repeated vomiting psycho-emotional stress Amnesia dyspeptic phenomena general weakness general cerebral phenomena visual, oculomotor disturbances due to swelling of the periorbital tissue phenomenon “pseudoparesis” of the facial nerve due to asymmetrical swelling of the face pseudomeningism

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Severity of TBI 1. Mild TBI Concussion Mild brain contusion 2. Moderate TBI Moderate brain contusion 3. Severe TBI Severe brain contusion Brain compression Diffuse axonal brain injury Head compression

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Glasgow scale 2 Incoherent sounds 1 No response 3 Unintelligible speech 4 Disoriented 5 Oriented Speech response... 1 No movement 2 Extension (decerebration) 3 Flexion (decortication) 4 Protective flexion 5 Localizes a painful stimulus 6 At the request of Movement... 1 Does not open 2 To a painful stimulus 3 Upon request 4 Spontaneously Opens eyes... Point Indicator

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Study of the reflex-motor sphere Convulsive seizures do not have a topical diagnostic value, but indicate the preservation of the motor pathways from the cortex to the muscle. Pathological postures: Decortication - the focus of damage localized above the midbrain Decerebrate - damage to the upper part of the brain stem and is prognostically unfavorable

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The patient's reaction to pain A - differentiated reaction B - undifferentiated reaction C - flexion postnotonic reaction (decortication pose) D - extensor posturetonic reaction (decerebrate pose) E - twitching of the arms and legs (hormetonic convulsions)

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Pathological postures (postural reactions) Decortication lesion above the midbrain Decerebrate damage to the upper part of the brain stem

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TBI severity rating Mild - 13-15 points on the Glasgow scale Moderate - 9-12 points on the Glasgow scale Severe - 3-11 points on the Glasgow scale

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Severe TBI - mechanical damage to the skull and (or) intracranial formations, accompanied by a decrease in the level of consciousness below 9 points on the Glasgow Coma Scale - severe brain contusions, diffuse axonal damage and compression of the brain.

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Diagnostic principles Assessment of vital functions Assessment of TBI severity Exclusion of combined injuries Exclusion of spinal injury

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1. Clinical diagnosis and observation Clinical observation is the main type of monitoring. Periodic assessment of the severity of the condition (once every 4-6 hours or more often) in the first 3 days, and then once every 6-24 hours (under deep sedation) using the Glasgow coma scale and Ramsay. Assessment should be carried out during the provision of care before administration sedatives. It is important to examine the entire body of a naked patient. Pay special attention to: bad breath, abrasions, bruises, joint deformities, changes in the shape of the chest and abdomen, leakage of blood and cerebrospinal fluid from the ears and nose, bleeding from the urethra and rectum.

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Clinical examination: Neurological status using the Glasgow Coma Scale. Somatic status – blood pressure, heart rate, respiratory rate, control of airway patency, gas exchange disorders (pulse oximetry). 3. Combined and combined nature of the injury (damage to other segments, smell of alcohol). 4. Degree of shock (shock is not typical for isolated TBI!). A decrease in blood pressure is most often observed with massive external bleeding or combined head injury. 5. Simultaneously with clarifying the degree of depression of consciousness, the open nature of TBI (cerebrospinal fluid rhinorrhea, the presence of head wounds), focal symptoms (anisocoria, paresis, convulsions), and signs of hypertensive-dislocation syndrome should be assessed. 6. Signs of impaired external respiration are retraction of the lower jaw and tongue, lack of sufficient excursion of the chest, the presence of blood, foreign bodies and gastric contents in the oropharynx, auscultatory signs of hypoventilation, cyanosis, decreased saturation

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Clinical examination: 7. Depression of consciousness< 9 баллов по ШКГ, анизокория, артериальная гипертензия с брадикардией свидетельствуют о тяжелом и крайне тяжелом состоянии пострадавшего. Тяжелой ЧМТ соответствует угнетение сознания: 9-10 баллов по ШКГ - сопор (резкая заторможенность пострадавшего, приоткрывание глаз, выполнение простых команд), менее 8 баллов – кома («неразбудимость», отсутствие осознанного поведения и целенаправленности реакций). 3-5 баллов по ШКГ в 70% случаев свидетельствует о неблагоприятном прогнозе. Диагностика менее тяжелого повреждения не отменяет необходимости экстренного обследования!

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Additionally, you should pay attention to pupillary reactions, namely: significant asymmetry of 1 mm or more, fixed pupil - lack of reaction (more than 1 mm) to bright light (flashlight, laryngoscope), orbital damage, duration (minutes) of the following events: unilateral or bilateral dilation of the pupil, one- or two-sided fixation of the pupil, fixation and dilation of the pupil (pupils).

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2. Diagnostic measures and laboratory tests Computed tomography of the brain is mandatory Main tasks: Timely diagnosis of intracranial volumes (hematomas, foci of contusions, etc.). Non-invasive diagnosis of ICH. Diagnosis of brain dislocation. Relative contraindications for emergency research: unstable hemodynamics: SBP below 90 mm. rt. Art., the need for constant infusion of vasopressors; unresolved hemorrhagic or traumatic shock No positive dynamics after 12-24 hours - CT scan of the brain again. If new neurological symptoms increase and appear, urgently. In case of craniofacial damage and suspected liquorrhea, a CT scan of the head in a frontal projection is necessary.

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2. Diagnostic measures and laboratory tests 2. X-ray examination of the skull in two projections, cervical, thoracic and lumbar spine, chest, pelvic bones, bones of the upper and lower extremities according to indications, an early diagnostic procedure to exclude combined TBI and protect the patient from iatrogenic injuries during transportation and manipulation 3. Other diagnostic methods a. Ultrasound of the abdominal cavity, retroperitoneum, heart b. Laparoscopy (laparocentesis).

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2. Diagnostic measures and laboratory tests 4. Laboratory diagnostics Particular attention to the level of glucose, sodium, plasma osmolarity, total protein and albumin, state of hemostasis (APTT, PTI, ICT). Blood and urine tests for alcohol content are mandatory. If necessary, examine the contents in biological environments other toxic substances (barbiturates, phenothiazines, benzodiazepines, barbiturates, phenothiazines, benzodiazepines, higher alcohols and opiates).

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4. Neuromonitoring Neuromonitoring provides adequate therapy for severe TBI (1 level of evidence) Invasive: Installation of an ICP sensor using standard methods: parenchymal, epidural, ventricular, Pressure manometry in the ventricular drainage or during lumbar (cisternal) puncture (low pressure manometer MND-01 - Triton Electronics) Non-invasive Clinical signs: - Fundus of the eye - Signs of increasing dislocation of stem structures - Increasing depression of the level of consciousness Neurophysiological - Transcranial Dopplerography (TCDG) using a special technique gives a semi-quantitative assessment of ICP in dynamics - EEG in monitoring mode: differential diagnosis of the level of consciousness and diagnosis of convulsive patterns brain activity

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Principles of treatment Prevention and treatment of secondary cerebral ischemic attacks - providing the affected brain with oxygen-rich blood Oxygenation Maintaining the necessary hemodynamic parameters Prevention and treatment of ICH Prevention and treatment of GSO

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The goal of IT TBI is to maintain a correspondence between the delivery and consumption of O2 and nutrients consumption delivery To achieve balance, 2 strategies are possible: increase delivery (perfusion, oxygenation, changes in cerebral vascular tone, improving blood fluidity) reduce the need (hypothermia, barbiturates, propofol, sevoflurane.. .)

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Intensive care of ICH I Monroe-Kelly concept. II Concept of primary and secondary brain damage. III Rosner concept: cascade of vasodilation - vasoconstriction

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I Monroe-Kelly concept Intracranial volumes are contained in an incompressible, completely isolated bone formation. Inside the cranial cavity, pressure is distributed evenly. The sum of intracranial volumes is constant. An increase in the volume of one of the components is equalized by a decrease in the volume of other components. Violation of this balance leads to an increase in ICP.

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II Concept of primary and secondary brain damage in TBI 1. Primary damage (at the site of injury and at the time of injury) 2. Secondary damage (delayed)

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III Cascade of vasodilation (Rosner) CPP Vasodilation Cerebral blood filling (CBV) ICP cerebral ischemia Arterial hypotension Blood loss Hypovolemia Vasodilators The bottom line is this: regardless of the reasons leading to a decrease in CPP, this ultimately leads to vasodilation of cerebral vessels - to an increase in blood filling of the brain brain—an increase in ICP, which contributes to a further decrease in CPP. The pathological circle closes and the cascade can be started again and again, leading to cerebral ischemia.

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III Cascade of vasoconstriction (Rosner) CPP Vasoconstriction Cerebral blood filling (CBV) ICP Arterial hypertension Infusion therapy Hypervolemia Vasopressors The task of the intensivist: to stop this cascade by increasing CPP - to start the vasoconstriction cascade, which will reduce the blood filling of the brain and ICP

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ICH therapy Goal of therapy: reduction of ICH, prevention of autonomic dysautonomia (hyperthermia, cerebrocardial, cerebrorespiratory syndromes, hypercatabolism-hypermetabolism), optimization of central hemodynamics Carried out against the background of continuous ICP monitoring The duration of the entire protocol from the beginning to the decision on decompressive craniotomy does not exceed 6 hours NB! act from simple to complex clearly justify each step of increasing IT aggressiveness

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ICP protocol External ventricular drainage Sedation Analgesia Myoplegia Osmotic diuretics Hyperventilation Barbitus coma Decompression Protocol goal: ICP ≤ 20 mm Hg Today, two protocols are generally accepted: these are the ICP and CPP protocols. The ICP protocol, as the earliest, dates back to the 70s and has been used since the introduction of invasive ICP monitoring into practice. This protocol aims to reduce ICP below 20 mm Hg. The multi-stage structure of therapy implies a step-by-step escalation of therapy. However, as aggressiveness increases, the risk of side complications increases, and therefore 2 levels of therapy are distinguished.

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ICP CPP Target: ICP< 20 мм рт ст АД – норма Адреномиметики только для стабилизации гемодинамики Нормоволемия Гипервентиляция Цель: ЦПД >70 mm Hg blood pressure - above normal Adrenergic agonists - active to increase CPP Hypervolemia Refusal of hyperventilation Another, more well-known, CPP protocol. This protocol requires maintaining a CPP above 70 mmHg. The fundamental difference between the CPP protocol: artificial arterial hypertension and refusal of hyperventilation. In this protocol, the IT element is replaced at the 2nd level of therapy: it is quite effective, but potentially dangerous for the development of cerebral ischemia, replaced by a CPP element aimed at preventing this ischemia.

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Reasons for the development of ICH in TBI: Cerebral edema Hyperemia Additional intracranial volume Hydrocephalus Hypoventilation Arterial hypertension Impaired venous outflow Epileptic seizure

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Diagnosis of ICH Assessment of neurological status. CT scan. ICP monitoring. ICP sensor for parenchymal or subdural installation. ICP sensor for ventricular placement with drain option

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ICH clinically 1. Hypertension 2. Bradycardia Cushing's triad 3. Dyspnea. The complete Cushing's triad occurs in only 33% of patients with ICH.

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CT signs of ICH Absence of subarachnoid fissures. Smoothness of furrows and convolutions. Displacement of midline structures

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Indications for ICP monitoring 1. Comatose state (GCS< 8) и наличие: А. Изменений на КТ Наличие очаговых изменений высокой или низкой плотности (контузии, гематомы). Наличие компрессии базальных цистерн. Отек. В. N на КТ, но 2 и >risk factors Age > 40 years Systolic blood pressure< 90 мм рт. ст. Декортикация или децеребрация (одно- или двухсторонняя) 2. Сочетанная травма с нарушением уровня сознания. 3. Состояние после удаления внутричерепных объемов(гематом, контузий, вдавленных переломов).

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Relative contraindications for implantation of an ICP sensor: Conscious patients. Disorders of the coagulation system. Indications for stopping ICP monitoring 48-72 hours after ICP normalization N.B: development of delayed ICH!

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ICH therapy stage I Infusion therapy Infusion of 500 ml of 0.9% NaCl solution (with stable blood pressure at a rate of no more than 1 ml/min). For blood pressure less than 120 mmHg - up to 1000 ml bolus + 500 ml colloidal drug. If there is no effect within 10 minutes, inotropic support with dopamine (400 mg per 400 ml), drip under blood pressure control. Hypoosmolar solutions (5% glucose solution) are contraindicated. It is possible to use synthetic plasma substitutes. When the condition stabilizes, the infusion rate should be moderate.

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ICH therapy Stage I Infusion therapy A symptomatic increase in blood pressure to 200 mm Hg is unacceptable. for a normotensive person. When blood pressure exceeds the established limit, it is more physiological to deepen sedation and analgesia through drugs that reduce ICP (for example, benzodiazepines, barbiturates). Hypotension is an independent factor of central nervous system damage. It is recommended not to delay the use of vasopressors. The desired blood pressure level is 25-30% higher than normal for the corresponding age category. The volume of infusion therapy on the first day should not be less than 30 ml/kg/day

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ICH therapy stage II CSF drainage When using ventriculostomy to monitor ICP, it is advisable to evacuate the CSF to an ICP level of 15-20 mm Hg (if it exceeds 30 mm Hg). If normalization of ICP in this way is ineffective, as well as negative neurological symptoms, a repeat CT examination is indicated to exclude “surgical” causes of ICH syndrome, as well as to clarify the indications for decompressive craniotomy (retrepanation, removal of a bone flap).

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ICH therapy Stage II Liqueur drainage If consciousness is depressed, do not carry out. With CT control, the individual drainage option (external, internal) is specified. Ventriculostomy is the most indicated method of ICP control (measurement and therapy). In some cases, the use of this method is technically impossible due to displacement or compression of the ventricular system of the brain. In such cases, the decision to use other methods of ICP control should be made on the basis of monitoring this indicator by other methods (parenchymal, subdural, etc. sensors). Assessment of the ICP level based on pressure in the final tank, CT, and TCD is very conditional. Regardless of the method of assessment, ICP should be compared with the neurological and clinical status of the victim.

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ICH therapy stage III Dehydration Dehydration does not imply hypovolemia (mild hypervolemia is preferable) Stop if osmolarity >320 mmol/l or blood pressure.

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ICH therapy stage III Mannitol with an osmolarity of 310 mOsmol/l Hyperglycemia Obesity 3 degrees General dehydration Decompensated heart failure Complications Increased hematocrit with dehydration ARF Acidosis Hypokalemia Recoil phenomenon (if the BBB is damaged) To prevent complications Use the rectal route Control of hematocrit Administration of potassium-containing solutions Dehydration

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ICH therapy Stage III Dehydration Hypertonic solution (3rd level) 3%-20% (7.5%) 100 ml IV 5 times a day Maintains euvolemic hyperosmolar status of the brain Reduces dislocation in case of injury and in postoperative patients Evenly dehydrates both hemispheres of the brain Modulates inflammatory response to brain injury

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ICH therapy stage III Dehydration Furosemide (3rd level) 10-20 mg IV every 6 hours with osmolarity >320 mmol/l and hypernatremia >150 mmol/l synergism with mannitol, slows down the production of cerebrospinal fluid

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ICH therapy Stage III Hyperventilation During the transportation stage. Shown when obvious signs dislocation: -pathological reaction to pain -increasing mydriasis -progressive depression of consciousness If cerebrospinal fluid drainage, osmotherapy are ineffective, but pCO2 is not lower than 32 mm Hg. Art. (TCDG is desirable for the prevention of ischemia)

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ICH therapy stage III Hyperventilation can be used in patients whose condition worsens secondary to increased intracranial pressure, including patients with dislocation syndrome (level 4). Excessive vasoconstriction can lead to ischemia in areas with impaired MB autoregulation unless O2 extraction increases compensatoryly. Negative effects of HPV: Reduced threshold of convulsive activity Increased oxygen affinity for hemoglobin Impaired autoregulation of MB Paradoxical increase in ICP When CO2 decreases to 30 mm Hg, ICP decreases by 25-30% after 30 seconds with a maximum at 8-10 minutes. The effect lasts up to an hour. The transition to normocapnia should be slow (average 4-6 hours) to avoid rebound effects.

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ICH therapy Stage III Hypothermia 35-36.0C Complications: Decreased CO Arrhythmia Thrombocytopenia

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ICH therapy Stage III Inotropic support If infusion therapy is insufficiently effective to achieve adequate CPP (>70 mm Hg), sympathomimetics (dopamine, adrenaline, norepinephrine, mesatone). All sympathomimetics can induce polyuria. The rate of diuresis can increase 2-5 times and reach 200-400 ml/h, which requires a corresponding increase in the rate of infusion therapy. Indications: as for hyperventilation

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ICH therapy Stage III Inotropic support Arterial hypertension is a compensatory reaction in response to compression of the brain and ICH. A decrease in media blood pressure with an increase in ICP leads to a decrease in CPP. The desired level of CPP is at least 70 mmHg, which determines the desired level of media blood pressure. - not less than 100 mm Hg, and blood pressure syst. - at least 140-150 mm Hg. The use of sympathomimetics to maintain arterial hypertension helps maintain CPP and prevents the progression of ICH. The advisability of increasing blood pressure is questionable with the combined nature of the damage and signs of ongoing internal bleeding.

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ICH therapy stage IV The decision on “therapy of despair” (“barbituric coma” and moderate hypothermia) is made by a council consisting of: a neurologist, a resuscitator, a neurophysiologist ESTS1, a neurosurgeon after assessing the neurological status without sedation based on the recognition of the patient’s non-transportability. Use only for absolute indications, ICH syndrome uncontrolled by other means, absence of surgical problems, consolidated consent of all doctors involved in the treatment of this victim. EEG monitoring and invasive blood pressure measurement are desirable.

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ICH therapy stage IV Barbitus coma 1. Introductory dose of thiopental – 3-5 mg/kg IV over 10 minutes 2. Infusion 5 mg/kg/hour over 24 hours 3. Dose titration according to clinical effect or EEG control (“EEG”) -silence") 4. After 24 hours - cumulation - dose reduction to 2.5 mg/kg/hour 5. After 48 hours - stop infusion 6. If pathological muscle phenomena resume - propofol situationally 5-10 mg/kg/min 7 Assessing the neurological status 24 hours after stopping the infusion (preferably monitoring plasma concentrations) To prevent the cardiotoxic effect of barbiturates, it is recommended to administer small doses of colloids in combination with dopamine (2-4 mcg/kg/min). You should not stop administering the drug for the purpose of stage-by-stage assessment of the neurological status until the ICH syndrome is completely relieved.

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ICH therapy Stage V Neurosurgical treatment Absolute therapy of despair. Resection of 4-5 cm of the temporal lobe of the dominant and 6-7 cm of the non-dominant hemisphere. The rationale for performing decompression surgery is the possibility of expanding the space for edematous tissue, which leads to ↓ ICP, MV, preventing compression of collateral vessels.

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Stages of care for TBI Pre-hospital stage Hospital stage Emergency measures Urgent measures Delayed measures

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Prehospital stage Diagnostics Assessment of the degree of depression of consciousness using the Glasgow Coma Scale Diagnosis of respiratory and hemodynamic disorders Diagnosis of combined injuries Diagnosis of spinal injury

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Prosthetics of the respiratory tract Tracheal intubation in case of breathing disorders, massive aspiration, depression of consciousness to coma Pre-hospital stage In case of technical difficulties, a double tube of the Easy-Tube type laryngeal mask In case of asphyxia and impossibility of intubation - conicotomy

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Fixation of the spine Indications for rigid fixation of the cervical spine Automobile injury Fall from a height Drowning Prehospital stage

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Oxygenation Prehospital stage of mechanical ventilation Breathing disorders Coma Assistive regimen Normoventilation Increased oxygenation FiO2=0.5-1.0 Sedatives Diazepam Midazolam Droperidol

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CRANIO BRAIN INJURY -

mechanical damage to the skull and intracranial formations - the brain, blood vessels, cranial nerves, meninges. The main causes are road traffic accidents, falls, industrial, sports and household injuries.

Traumatic brain injury (TBI) in children, due to its unusually high prevalence (50% of all cases of traumatic injuries in childhood) is an important medical and social problem and ranks first among injuries requiring hospitalization. Even a mild TBI received in childhood leaves an imprint on the entire subsequent period of the child’s life.

CLASSIFICATION OF TRANO BRAIN INJURY

(Research Institute of Neurosurgery named after N. N. Burdenko of the Russian Academy of Sciences)

I. Characteristics of closed and open traumatic brain injury.

1.1 Closed TBI:

▪ there are no violations of the integrity of the bones and soft tissues of the head;

▪ fractures of the bones of the cranial vault, not accompanied by injury to adjacent soft tissues and aponeurosis;

▪ there are soft tissue wounds without damage to the internal aponeurosis, bone structures are not damaged.

1.2 Open TBI:

▪ injuries in which there are wounds of the soft tissues of the head with damage to the internal aponeurosis;

▪ a fracture of the base of the skull with damage to the brain, the fracture line passes through the pyramid of the temporal bone or through the sinuses, accompanied by bleeding or liquorrhea (from the ear, nose).

All open TBIs with integrity of the dura mater are considered

non-penetrating, with its violation

integrity - penetrating.

II. Clinical forms

2.1. Concussion (only with traumatic brain injury).

2.2. Mild brain contusion.

2.3. Moderate brain contusion.

2.4. Severe brain contusion.

2.5. Compression of the brain (intracranial hematomas, combined or subdural hygromas, compression by bone fragments, pneumocephalus, swelling)

swelling of the brain) - there is compression with a brain contusion and compression without a brain contusion.

2.6.

2.7. Compression of the head.

III. Severity

3.1. Mild TBI:

▪ Brain concussion.

▪ Mild brain contusion

3.2. Moderate TBI:

▪ Moderate brain contusion.

3.3. Severe TBI:

▪ Severe brain contusion.

▪ Compression of the brain.

▪ Diffuse axonal brain damage.

▪ Compression of the head.

IV. Periods of TBI

4.1. Acute period:

- with a concussion - 1-2 weeks;

- with a slight injury - 2-3 weeks;

- with a moderate injury - 4-5 weeks;

- in case of severe brain contusion - 6-8 weeks;

- with diffuse axonal damage – 8-10 weeks;

For compression – 3-8 weeks.

4.2. Interim period(early recovery period)

- for mild TBI – up to 2 months;

- for moderate TBI – 4 months;

- for severe TBI – up to 6 months.

4.3. Remote period(late recovery period)

- with clinical recovery – up to 2 years;

With a progressive course of TBI, it is not limited.

Complications of TBI are pathological processes attached to the injury (usually purulent-inflammatory), which are not necessary for damage to the brain and its integument, but arise when exposed to various additional exo- and endogenous factors.

The consequences of TBI are an evolutionarily predetermined and genetically fixed set of processes in response to damage to the brain and its integument or persistent violations of the anatomical integrity of the brain, its membranes and skull bones, resulting from acute TBI, persisting in the intermediate and long-term period and requiring treatment and rehabilitation .

Clinical picture of the acute period of concussion:

▪ absence of loss of consciousness or short-term loss of consciousness (from several seconds to 1 minute);

▪ anterograde (loss of memory for the trauma and events that followed it) or retrograde (for the events preceding the trauma) amnesia;

▪ absence of meningeal and focal neurological symptoms;

▪ general cerebral symptoms (nausea, vomiting, dizziness, headache),

▪ asthenia (general weakness, lethargy, drowsiness, insomnia, irritability, loss of appetite);

▪ Autonomic disorders were always present (pallor of the face, marbling of the skin, excessive sweating, tachycardia, arterial hypotension).

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The presentation on the topic “Medical care for traumatic brain injuries” can be downloaded absolutely free on our website. Subject of the project: life safety. Colorful slides and illustrations will help you engage your classmates or audience. To view the content, use the player, or if you want to download the report, click on the corresponding text under the player. The presentation contains 15 slide(s).

Presentation slides

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First aid for traumatic brain injuries and spinal injuries

Completed by: life safety teacher Savustyanenko Viktor Nikolaevich G. Novocherkassk MBOUSOSH No. 6

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CRANIOUS BRAIN INJURY Causes What is happening? How to recognize? What to do? Diagnosis Treatment Procedure for providing first aid to a victim of an accident Procedure for providing first aid medical care to the victim

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CRANIOUS BRAIN TRAUMA

Treatment of victims with open and closed injuries to the skull and brain has much in common, since they almost always involve a concussion or bruise of the brain, which requires protective therapy, rest, the use of sedatives, and careful monitoring of patients, starting from the advanced stages of evacuation. First aid consists primarily of preventing blood, cerebrospinal fluid or vomit from entering the respiratory tract, for which the wounded person or his head is turned to the side. An aseptic bandage is applied to the wound. At the stage of first medical aid, if necessary, the bandage is corrected and an antibiotic, tetanus toxoid, is administered intramuscularly.

Slide 4

Concussion, traumatic brain injury

It would seem that there is little threat to our brain, because it is protected like no other organ. It is washed by a special liquid, which not only provides the brain extra food, but also serves as a kind of shock absorber. The brain is covered by several membranes. After all, it is securely “hidden” in the skull. However, head injuries very often result in serious brain problems for a person. All traumatic brain injuries are divided into open and closed. Open injuries are those that damage the soft tissues of the head (skin, subcutaneous tissue, fascia) and the bones of the skull. Closed injuries are somewhat less dangerous, but still unpleasant. They, in turn, are divided into concussion, contusion and compression. Among all brain injuries, concussion ranks first in frequency. Moreover, according to the observations of traumatologists, it occurs more often in women. Although, perhaps they simply seek professional help more often than men.

Slide 5

A concussion can occur as a result of blows, bruises and sudden movements: acceleration or deceleration, such as a fall. The causes of concussions are usually road traffic accidents, domestic accidents, sports accidents, and work injuries, as well as injuries received as a result of street fights.

Slide 6

What's happening?

What exactly happens to our brain as a result of a concussion is still difficult for doctors to answer unambiguously. After all, if you examine the injured brain using computed tomography, then practically no organic disorders will be detected. Most likely, as a result of a concussion, certain problems arise with the functioning of nerve cells in the brain. At the same time, their nutrition may deteriorate, a slight displacement of the layers of brain tissue may appear, and the connection between some brain centers may be disrupted. A severe concussion can rupture blood vessels and seriously injure certain areas of the brain. The main danger with traumatic brain injuries is intracranial bleeding, since leaked blood can compress and permeate brain structures, disrupting their function and viability. In addition, injury can lead to another serious complication - cerebral edema. Particularly severe are brain injuries complicated by shock and injuries affecting the brain stem, where breathing and blood pressure are regulated.

Slide 7

How to recognize?

After an injury, a person often loses consciousness. This can last from a few seconds to several minutes. The time spent in this state may be one indicator of the severity of the concussion. The extreme degree of loss of consciousness is coma. When a concussion occurs, a person often does not understand where he is, what happened, and has difficulty recognizing the people around him. One more important sign, by which one can judge the severity of brain damage, is memory loss: whether a person remembers the moment of injury, and if not, then how much of the time before the injury has disappeared from his memory. The greater the memory loss, the more serious the injury. When the victim comes to, he may feel sick and vomit. He often turns pale, feels dizzy and has a headache, there is noise in his ears, it is difficult for him to focus his eyes, his breathing becomes rapid, and his pulse jumps. In the first hours after a concussion, the victim’s pupils are dilated or constricted - a traumatic brain injury of any severity leads to disruption of the nerve pathways responsible for the functioning of the eyes. Surely in the movies you have seen more than once how, when examining an unconscious person, a doctor directs a flashlight beam into the victim’s eyes. This is done to determine the reaction of the pupils. With a mild concussion, the pupils react to light, but sluggishly, and with a severe concussion, there is no reaction at all. In this case, the dilation of only one of the pupils and the lack of reaction in the second is a formidable symptom and may indicate severe damage to one of the hemispheres of the brain.

Slide 8

What to do?

If you suspect a concussion, you must provide first aid to the victim. First, you need to provide the person with complete peace, put him on the bed in a quiet, darkened room. It is better to raise your head slightly. It is very useful to apply cold compresses to the head. Drinking a lot if you have a concussion is not recommended. If the victim is thirsty, make him sweet tea. Alcohol is strictly contraindicated for him! And, of course, be sure to call a doctor, since it is possible that the brain damage is more severe than it seems at first glance. If the patient is in shock, carefully monitor his breathing and blood pressure before the ambulance arrives. In emergency cases, begin artificial respiration and chest compressions.

Slide 9

If you have a concussion, you should consult a traumatologist. He will examine and interview the patient, check reflexes, prescribe an X-ray of the skull, and if more complex brain damage is suspected, refer him for a consultation with a neurologist. There, the patient will undergo a full-scale examination: electroencephalography (EEG), echoencephalography, computed tomography or magnetic resonance imaging of the brain, Dopplerography of cerebral vessels, and spinal puncture. An MRI of the spine may be needed to rule out spinal problems.

Slide 10

Patients with a concussion should remain in bed for at least several days. However, you cannot read, listen to loud music or watch TV. It is necessary to follow all the doctor’s instructions and carefully take the medications prescribed by him. In case of a concussion, the general condition of the victims usually normalizes during the first, less often, the second week after the injury. It must be remembered that a person who has suffered even a mild concussion may develop post-traumatic neurosis or other more serious complications, such as epilepsy. Therefore, some time after recovery, you should definitely visit a neurologist and undergo electroencephalography. Treatment for more serious traumatic brain injuries depends on their severity. In some complicated cases, the help of neurosurgeons may be required.

Slide 11

Procedure for providing first aid to a victim of an accident

In most cases, road traffic accidents occur far from medical facilities and you have to wait a long time for an ambulance. It is this circumstance, as well as the fact that drivers can be useful to victims before others, that obliges them to be able to provide first aid, that is, carry out the simplest emergency measures to save the lives of victims. Drivers of cars and others Vehicle, both those involved and not involved in the traffic accident, but who are nearby, are obliged to immediately stop and provide assistance to those in need. Failure to provide assistance to a person in a life-threatening condition is punishable by law. The sequence of actions when providing assistance to victims should be as follows.

Slide 12

Procedure for providing first aid to the victim

1. Organizing an ambulance call. 2. Extracting victims from a broken car. Traffic accidents on the roads are often accompanied by complex fractures, traumatic brain injuries, and spinal injuries. The victim may have several injuries at once. Therefore, you should take it out of the car very carefully. You cannot pull or bend his torso, arms or legs, or pull them out by force. We must first try to eliminate everything that holds the victim back. If a person has lost consciousness and is in an unnatural position, two or three people need to carry him out of the car, trying not to change this position. WITH special attention If you suspect a spinal fracture, you should treat victims and not move them unless absolutely necessary, as this can cause paralysis. Such a person must be placed on his back or stomach in such a way that the injury site is not infringed. 3. Providing first aid. When removed from the car, you need to loosen your tie, unfasten your collar and belt so that breathing does not become difficult. For fractures and dislocations of the limbs, it is necessary in all cases to apply splints, and in their absence, fix them with improvised objects (boards, sticks); If the victim experiences bleeding, measures should be taken to temporarily stop it. First aid should be provided quickly and not cause unnecessary pain to the victim. 4. Transportation of victims to a medical facility. When everything possible to save the victims at the scene has been done, but an ambulance cannot be called or it is clear that it will arrive late, care must be taken to transport the victims to the nearest medical facility. You must act with the same caution and attention as when removing them from an emergency vehicle.

Slide 13

When it becomes necessary to lift the victim, you should use the following methods: kneel on the side of the victim, place your hands under the shoulder blade, head, neck and lift him; kneel at the head of the victim, place your hands under the shoulders and lift him up. Under no circumstances is a victim allowed to move independently if the lower extremities, skull, or thoracic or abdominal organs are damaged. If it is necessary to transfer the victim on a stretcher, he is placed carefully, without shaking and in a position comfortable for him. The stretcher is placed next to the victim on the side of the injury. Two people stand next to the patient on one knee, one of them puts his hands under the head, neck and back, the other - under the sacrum and legs. A third person moves a stretcher under the victim. You need to lift the stretcher carefully and at the same time, be sure to walk in step, in short steps, slightly bending your knees. The person walking in front is obliged to warn the person behind about all obstacles on the road. When climbing uphill, the victim is carried head first, when descending from the mountain - feet first, with the exception of cases of damage to the lower extremities. You should always try to keep the victim horizontal. Transportation, depending on the nature of the damage, is carried out according to following rules: for fractures of the skull bones, injuries to the head and brain, for fractures of the spine and pelvic bones, the victim is transported only in a horizontal position; for fractures of the ribs and collarbones, transportation in a sitting position is most painless, but when the victim cannot sit, transportation is carried out on a stretcher, giving him a semi-sitting position; for chest injuries, the victim is placed on the wounded side or on the back in a semi-sitting position; when the neck is wounded from the front, the victim is given a semi-sitting position with the head tilted to the chest in the direction of the wound; in case of abdominal wounds and internal bleeding, the victim is placed on his back, a pillow or other object replacing it is placed under the knees and sacrum; in case of fainting, the victim is placed so that his head is lower than his legs.

Slide 14

It is necessary to provide for all the features of the upcoming transportation: its distance and quality of the road, frost and bad weather, the nature of the injuries received, the condition of the victim; take care that it does not deteriorate as a result of transportation. In all cases, take measures to prevent and combat traumatic shock. If there is a large hospital or clinic relatively nearby, it is better to take the victim directly there, bypassing even the nearest medical center. If to large medical institution far away, the wounded person must be taken to the nearest medical facility. Upon arrival, do not take it out of the car, but ask medical workers approach the victim, examine him and resolve the issue further actions The wounded must never be left unaided or sent without an attendant who may be required to provide the necessary assistance along the way. In addition, through his behavior and conversations, he must strengthen the victim’s confidence in the successful outcome of the incident.

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Slide captions:

Damage to the bones of the skull and brain

Anatomy

Skull (brain) Paired parietal and temporal Unpaired frontal, sphenoid, ethmoid and occipital

Meninges of the brain Dura mater Arachnoid mater Pia mater

Head injury (traumatic brain injury, TBI) Traumatic brain injury is damage to the bones of the skull or soft tissues, such as brain tissue, blood vessels, nerves, and meninges. There are two groups of traumatic brain injuries - open and closed

Open injuries In open traumatic brain injury, the skin and aponeurosis are damaged. The bottom of the wound is bone or deeper tissue. When the dura mater is damaged, the injury is considered penetrating.

Closed injuries In a closed head injury, the aponeurosis is not damaged, although the skin may be damaged. All traumatic brain injuries are divided into: Concussion - an injury in which there are no permanent disturbances in the functioning of the brain. All symptoms that occur after a concussion usually disappear over time (within a few days). Persistent symptoms are a sign of more serious brain damage.

Closed injuries Compression of the brain (hematoma, foreign body, air, contusion). Brain contusion: mild, moderate and severe. Diffuse axonal damage. Subarachnoid hemorrhage.

Closed injuries At the same time, various combinations of types of traumatic brain injury can be observed: bruise and compression by a hematoma, bruise and subarachnoid hemorrhage, diffuse axonal damage and bruise, brain contusion with compression by a hematoma and subarachnoid hemorrhage.

Causes of traumatic brain injury: skull fracture with tissue displacement and rupture of the protective membranes around the spinal cord and brain; bruises and ruptures of brain tissue due to concussions and blows in a confined space inside the hard skull; bleeding from damaged vessels into the brain or into the space around it (including bleeding due to a ruptured aneurysm). Brain damage can also occur due to: direct injury to the brain by objects penetrating the cranial cavity (for example, bone fragments, bullets); increased pressure inside the skull as a result of cerebral edema; a bacterial or viral infection that penetrates the skull in the area of its fractures.

Concussion Acute traumatic brain injury due to exposure to mechanical force, as a result of which extreme inhibition develops in the central nervous system Changes in brain tissue are functional (reversible) in nature

Concussion Clinical picture Loss of consciousness from a few seconds to 1-2 hours Retrograde amnesia (the patient does not remember the moment of injury and the immediate events before the injury) Vomiting General cerebral symptoms: weakness, fatigue, headache, irritability, pallor or hyperemia of the skin, pupillary reaction decreased to light, nystagmus

Brain contusion due to TBI Brain contusion is an injury in which brain tissue or its membranes are destroyed. It usually occurs at the point of application of a traumatic force, but can also be observed on the side opposite to the injury (contusion from a counter-impact) Brain contusions are distinguished between mild , moderate and severe

Brain contusions (mechanism of occurrence)

Mild brain contusion

Moderate brain contusion

Severe brain contusion

Clinical picture of a brain contusion Loss of consciousness from several hours to several days Retrograde amnesia (loss of memory about events preceding the onset of the disease) Repeated vomiting Severe cerebral symptoms Focal symptoms: paralysis, paresis, speech impairment, swallowing, uneven pupil size, convulsive seizures, nystagmus , i.e. loss of brain function depending on the area of damage

Wounds of the soft tissues of the head Feature – significant bleeding When the aponeurosis is dissected, the wound gapes Contused wounds can be accompanied by detachment of soft tissues and contamination When hair gets into the moving mechanisms, scalped wounds of the head occur

Emergency care Stop the bleeding using any temporary method Place the patient in bed and calm down Treat the skin around the wound with an antiseptic solution Apply an aseptic bandage Apply cold to the injury site If possible, numb the pain Transport to a health care facility

Compression of the brain The main reason is the accumulation of blood in a closed intracranial space with the formation of an intracranial hematoma. To compress the substance of the brain, an accumulation of 50 ml of blood is sufficient

Causes of brain compression Based on the rate of development, they are distinguished: acute intracranial hematomas, which appear in the first 3 days after the injury, subacute - in the first 2 weeks after the injury and chronic - after 2 weeks after the injury. Hematomas: intracranial - epidural and subdural; intracerebral; intraventricular; Depressed fractures of the skull bones; Foci of brain crush, subdural hygromas, pneumocephalus.

Compression of the brain CT scan of the brain. Acute subdural hematoma in the right fronto-parietal-temporal region with brain dislocation and compression.

Epidural hematoma

Acute Subdural Hematoma

Chronic subdural hematoma

Subdural hematoma

Intracerebral hematoma

Compression of the brain Clinical picture Loss of consciousness at the time of injury The lucid interval is the period between the restoration of consciousness and the development of clinical signs of compression of the brain After the formation of a hematoma (several hours or days after the injury), consciousness is lost again Focal symptoms Cheyne-Stokes respiration

Emergency care Place on a stretcher in a half-turned position on your back with immobilization of the head Anesthetize If there is a wound, use an aseptic bandage Cold to the head Hospitalization in the neurosurgery department Monitoring of general condition, blood pressure, respiratory rate, pulse Assistance with vomiting, prevention of tongue retraction and aspiration Administration of medications as prescribed doctor

Treatment Creation of absolute rest, bed rest for 2-4 weeks Local application of cold Prevention and treatment of cerebral edema - dehydration therapy (glucose 20-40%, sodium chloride 10%) Analgesics, hypnotics, sedatives (not earlier than 2-3 days after injury - so as not to miss the symptoms of compression of the brain. If there is a sharp increase in ICP - lumbar puncture. If a hematoma has formed - craniotomy, removal of the hematoma, stopping the bleeding.

Fractures of the skull bones By location 1. Fractures of the bones of the cranial vault 2. Fractures of the base of the skull 3. Fractures of the bones of the facial skeleton By type of fracture 1. Linear 2. Depressed 3. Comminuted

Fractures of the bones of the cranial vault Clinical picture: Local hematoma without clear boundaries. Loss of consciousness after some time due to trauma. With an increasing subdural hematoma, there is a clear interval (period between the restoration of consciousness and the development of clinical signs of brain compression). Focal symptoms in comminuted fractures with brain compression, brain contusions, subdural hematomas: paralysis, paresis, speech impairment.

Fractures of the bones of the vault and base of the skull

Fractures of the bones of the base of the skull Clinical picture Severe condition Consciousness lost General cerebral symptoms Hyperthermia, tachycardia Decreased tendon reflexes and muscle strength Deep inhibition is replaced by excitation Bleeding and liquorrhea from the nose, nasopharynx, ears “Symptom of glasses” In case of a fracture of the frontal bone - subcutaneous emphysema

Clinical signs of a skull base fracture

First aid Apply a bandage to the wound (cap, bridle, Hippocratic cap, bandages on the eyes, cross-shaped on the back of the head) Transport on a stretcher in a half-turned position on the back with immobilization of the head (the head is placed on a cotton-gauze roll made in the shape of a bagel) to the neurosurgical hospital department Monitoring general condition, pulse, blood pressure, respiratory rate Assistance with vomiting In case of bleeding and cerebrospinal fluid from the nose and ear canals, loose tamponade of the nose and ear with an antiseptic solution is indicated

Treatment B surgical department PSO of wounds is performed under local anesthesia or anesthesia. For depressed fractures - craniotomy. For perforated fractures - the edges of the bone wound are bitten off, removing sharp protrusions. Wounds are sutured tightly. Patients with fractures of the base of the skull are treated conservatively. The nasal or ear cavities are tamponed with dry or moistened gauze in an antiseptic solution, not rinse - possible infection of the meninges. Feeding through a tube.

Craniotomy

A set of tools for craniotomy 1. Tools of a general set 2. A rotator with a set of cutters - for making a hole on the bones 3. Gigli wire saw 4. Luer, Dahlgren bone cutters - for biting off an inert fragment 5. Chisel, osteom: straight, grooved; bone hammer - for separating bone chips 6. Raspators: Farabefa (straight, curved) - for separating from bone 7. Spatulas: brain spatula - for protecting the brain

Bandage "Cap" Applied to wounds of the scalp

Cross-shaped bandage Apply when wounding the neck, larynx or back of the head

Bandage “Frenulum” Applied for extensive wounds of the head and face

Sling bandage. Place on the nose, forehead and chin on the nose on the forehead on the chin

Thank you for your attention.

It might be useful to read:

TBI: pathogenesis, clinical picture, diagnosis, IT. Traumatic brain injury Presentation on the topic closed traumatic brain injury

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