TBI: pathogenesis, clinical picture, diagnostics, IT. Traumatic brain injury Presentation on the topic of 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 of other organs Mortality up to 10%, postoperative mortality - 30% Severe forms of TBI\u003e 40% of cases, mortality - 70% High disability Mainly working age suffers
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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 therapeutic measures taken. The goal of intensive care is to eliminate secondary damaging factors and areas of secondary structural and functional changes. The time factor is important!
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TBI classification (A.N. Konovalov 1998) Type of injury focal, diffuse, combined Pathogenesis primary lesion, secondary lesion Type of TBI isolated, combined, combined Type of TBI closed, open penetrating, open non-penetrating The severity of TBI mild, moderate, severe Clinical forms concussion, cerebral contusion without compression, cerebral 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 vegetative cerebral dysfunction , cerebroorganic syndromes TBI outcome good recovery, moderate, severe disability, vegetative state, death
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Characteristics of closed and open craniocerebral trauma Closed craniocerebral trauma: injuries in which there is no violation of the integrity of the integument of the head 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 of the soft tissues of the head with damage to the aponeurosis; fracture of the base of the skull with damage to the GM, accompanied by bleeding or liquorrhea (from the ear, nose). There is a risk of infection of intracranial contents.
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Clinical forms of TBI - Concussion - Diffuse axonal brain injury - Compression of the head - Compression of the brain - intracranial hematoma - depressed fracture - other causes Focal brain contusion - mild - moderate - severe
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Concussion Switching off consciousness up to 15 min Retro, anterograde amnesia Nausea, vomiting, headache, dizziness Autonomic dysfunction: feeling of heat, tinnitus, sweating, fluctuations in blood pressure, tachybradycardia, flushing of the face Sleep disturbance Improvement of the state during 7-10 days Labile anisoreflexia Small-sweeping nystagmus Mild shell symptoms that disappear in 3-7 days Absence of damage to the bones of the skull CSF is normal Differential diagnosis: from brain contusion (more prolonged 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 Symptom regression on days 14-18 Clonic nystagmus Mild anisocoria Pyramidal insufficiency Meningeal symptoms Possible fractures of the cranial vault and subarachnoid
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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 disturbing the rhythm of breathing Changes in the sleep-wake cycle Subfebrile regress Symptoms for 21-35 days or more Stem symptoms: nystagmus, dissociation of muscle tone and tendon reflexes Bilateral pathological signs Subarachnoid hemorrhage Otorrhea, nasorrhea Clear focal symptoms - pupillary and oculomotor disorders, paresis, hyperesthesia, aphasia
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Severe brain injury 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 / ??? Stem signs: floating eyeballs, gaze paresis, tonic nystagmus Bilateral mydriasis or miosis Swallowing disorders Variable tone, decerebrotation rigidity or ↓ tendon reflexes Oral automatism reflexes Convulsive seizures Skull base fractures Threatening hyperthermia Otorrhea, nasarrhea
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Compression of the brain (hematoma) The 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 (aggravated, headache, vomiting stunning or agitation) Initial symptoms of dislocation and compression of the upper sections of the trunk Symptoms of dislocation and infringement of the midbrain are expressed - a deep coma with gross violations of muscle tone, respiratory disorders, bradycardia, arterial hypertension, pupillary and oculomotor disorders
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Change of pupils with temporo-tentorial wedging on the right 1 - NORM 2,3, 4 - ANISOCORIA 5 - MIDRIASIS (bilateral lesion of the oculomotor nerve, pupils do not react to light)
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Diffuse axonal damage Prolonged coma Hyperthermia Hyperhidrosis Hypersalivation Respiratory failure Symmetric or asymmetric decerebration or decortication Changes in muscle tone - from diffuse muscular hypotonia to hormoneotony Transition from coma to persistent vegetative state Paresis of gaze upward reduction or protrusion of reflexes Mental disorders Increased ICP Facial synkenesia - chewing, smacking, yawning and swallowing automatisms Tetrasyndromes of a pyramidal-extrapyramidal nature
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Diffuse axonal damage to 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 pathways in the brain.
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Head compression head deformity damage and edema of the soft integument of the head, skull and brain depressed fractures in the future - extensive tissue necrosis intoxication possible infection respiratory failure repeated vomiting psychoemotional tension Amnesia dyspeptic symptoms general weakness general cerebral phenomena visual, oculomotor disorders due to edema of paraorrha "Pseudoparesis" of the facial nerve due to asymmetric facial edema pseudomeningism
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Severity of TBI 1. Mild TBI Concussion of the brain Mild brain injury 2. Moderate TBI Brain injury of moderate degree 3. Severe TBI Brain injury of severe degree Brain compression Diffuse axonal brain injury Head compression
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Glasgow Scale 2 Disjointed sounds 1 No response 3 Indistinct speech 4 Disoriented 5 Oriented Speech response ... 1 No movement 2 Extension (decerebration) 3 Flexion (decortication) 4 Protective flexion 5 Localizes pain stimulus 6 At the request of Movement ... 1 Does not open 2 To pain stimulus 3 At the request 4 Spontaneously Opens eyes ... Score Indicator
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Examination of the reflex-motor sphere. Convulsive seizures have no topical-diagnostic value, but indicate the preservation of the motor pathways from the cortex to the muscle. Pathological postures: Decortication - a lesion localized above the midbrain Decerebration - damage to the upper brain stem and prognostically unfavorable
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The patient's reaction to pain A - differentiated reaction B - undifferentiated reaction C - flexion posnotonic reaction (decortication posture) D - extensor poznotonic reaction (decerebration posture) E - twitching of the arms and legs (hormonal convulsions)
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Pathological postures (poznotonic reactions) Decortication focus above the midbrain Decerebral damage to the upper part of the brain stem
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Assessment of TBI severity Easy - 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 associated injuries Exclusion of spinal trauma
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1. Clinical diagnostics and observation Clinical observation is the main type of monitoring. Periodic assessment of the severity of the condition (1 time in 4-6 hours or more) in the first 3 days, and then 1 time in 6-24 hours (under conditions of deep sedation) on the Glasgow coma and Ramsay scale. Assessment should be carried out during the provision of care before administration sedatives. Examination of the entire body of a naked patient is important.Pay special attention to: bad breath, abrasions, bruises, deformities of the joints, changes in the shape of the chest and abdomen, the presence of bleeding 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, the 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 concomitant TBI. 5. Along with the specification of the degree of depression of consciousness, the open nature of TBI (liquorrhea, presence of head wounds), focal symptoms (anisocoria, paresis, convulsions), 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 chest excursion, 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, attention should be paid to pupillary reactions, namely: significant asymmetry of 1 mm or more, fixed pupil - no reaction (more than 1 mm) to bright light (flashlight, laryngoscope) orbital damage, duration (minutes) of the following events: one- or two-sided pupil dilation, one - or bilateral fixation of the pupil, fixation and dilation of the pupil (pupils).
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2. Diagnostic measures and laboratory investigations Computed tomography of GM - mandatory. Main tasks: Timely diagnosis of intracranial volumes (hematomas, contusion foci, etc.). Non-invasive diagnostics of ICH. Brain dislocation diagnostics. Relative contraindications for urgent research: unstable hemodynamics: SBP below 90 mm. rt. Art., the need for constant infusion of vasopressors; intact hemorrhagic or traumatic shock No positive dynamics in 12-24 hours - CT scan again. With an increase and the appearance of new neurological symptoms - urgently. In case of craniofacial injury and suspicion of liquorrhea, a CT scan of the head in frontal projection is necessary.
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2. Diagnostic measures and laboratory studies 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 that allows to exclude combined TBI and protect the patient from iatrogenic injuries during transportation and handling 3. Other diagnostic methods a. Ultrasound of OBP, retroperitoneal space, 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, osmolarity of plasma, total protein and albumin, the state of hemostasis (APTT, PTI, VSC) It is obligatory to perform blood and urine tests for alcohol content. If necessary, investigate the content of other toxic substances in biological media (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: Installing the ICP sensor according to the standard technique: parenchymal, epidural, ventricular, Ventricular pressure manometry or with lumbar (cisternal) pressure - T-01 Electronics) Non-invasive Clinical signs: - The fundus of the eye - Signs of increasing dislocation of the stem structures - Increasing suppression of the level of consciousness Neurophysiological - Transcranial Doppler ultrasonography (TCD) using a special technique gives a semi-quantitative assessment of ICP in dynamics - EEG in monitoring mode: differential diagnosis of pathological levels of consciousness and vascular disease 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 consistency between delivery and consumption of O2 and nutrient intake. Delivery. To achieve balance, 2 strategies are possible: to increase delivery (perfusion, oxygenation, changes in cerebral vascular tone, improve blood flow); reduce the need (hypothermia, barbiturates, propofol, sevoflurane ... .)
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Intensive ICH therapy I Monroe-Kelly concept. II Concept of primary and secondary brain damage. III Rosner's concept: the cascade of vasodilation - vasoconstriction
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I Monroe-Kelly concept The intracranial volumes are enclosed in an incompressible, completely isolated bone formation. The pressure is evenly distributed inside the cranial cavity. The sum of intracranial volumes is constant. The increase in the volume of one of the components is balanced by the decrease in the volume of the other components. Violation of this balance leads to an increase in ICP.
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II Concept of primary and secondary brain injury in TBI 1. Primary injury (at the site of injury and at the time of injury) 2. Secondary injury (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, an increase in cerebral blood flow - - brain - an increase in ICP, which contributes to a further decrease in CPP. The pathological circle is closed and the cascade can start 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 intensiveist: to stop this cascade by increasing the CPP - to start the vasoconstriction cascade, which will decrease the cerebral blood supply and ICP
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ICH therapy Purpose of therapy: reduction of ICH, prevention of autonomic dysautonomy (hyperthermia, cerebrocardiac, cerebro-respiratory syndromes, hypercatabolism-hypermetabolism), optimization of central hemodynamics Conducted against the background of continuous monitoring of ICP The duration of the entire protocol from the beginning to the decision on decompressive craniotomy does not exceed 6 hours! act from simple to complex to clearly justify each step of increasing IT aggressiveness
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ICP protocol External ventricular drainage Sedation Anesthesia Myoplegia Osmotic diuretics Hyperventilation Barbituric coma Decompression Protocol goal: ICP ≤ 20 mm HgThere are two generally accepted protocols today: the ICP and CPP protocol. 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 lower ICP below 20 mm Hg. A multi-stage therapy structure implies a gradual escalation of therapy. However, as aggressiveness increases, the risk of side complications increases, and therefore there are 2 levels of therapy.
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ICP CPP Purpose: ICP< 20 мм рт ст АД – норма Адреномиметики только для стабилизации гемодинамики Нормоволемия Гипервентиляция Цель: ЦПД > 70 mm Hg BP - above normal Adrenomimetics - active to increase CPP Hypervolemia Refusal of hyperventilation Another, better known, CPP protocol. The implementation of this protocol implies maintaining the CPP above 70 mm Hg. The fundamental difference between the CPP protocol: artificial arterial hypertension and refusal of hyperventilation.In this protocol, the replacement of the IT element occurs at the 2nd level of therapy: this way, the rather effective, but potentially dangerous for the development of cerebral ischemia, is replaced by the 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 Violation of 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 transducer for ventricular placement with drainage capability
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ICH clinically 1. Hypertension 2. Bradycardia Cushing's triad 3. Dyspnea. The complete Cushing 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\u003e 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 ICP transducer implantation. Patients are awake. Disorders from the coagulation system. Indications for discontinuing ICP monitoring 48-72 hours after ICP normalization N.B: development of delayed ICP!
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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). With blood pressure less than 120 mm Hg - up to 1000 ml of a jet + 500 ml of a colloidal preparation. In the absence of effect within 10 minutes - inotropic support with dopamine (400 mg per 400 ml), drip under the control of blood pressure. Hypoosmolar solutions (5% glucose solution) are contraindicated. It is possible to use synthetic plasma substitutes. When the condition is stabilized, the rate of infusion should be moderate.
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ICH therapy stage I Infusion therapy Symptomatic increase in blood pressure up to 200 mm Hg is unacceptable. for normotonic. When the blood pressure exceeds the established limit, it is more physiological to deepen sedation and analgesia due to drugs that reduce ICP (for example, benzodiazepines, barbiturates). Hypotension is an independent factor in damage to the central nervous system. It is recommended not to postpone the use of vasopressors. The desired blood pressure level is 25-30% higher than the 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 for monitoring ICP, it is advisable to evacuate CSF to an ICP level of 15-20 mm Hg (if 30 mm Hg is exceeded). If ICP normalization is ineffective in this way, as well as negative neurological symptoms, a repeated CT scan is indicated to exclude "surgical" causes of ICH syndrome, as well as to clarify the indication for decompressive craniotomy (retrapanation, removal of a bone flap).
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ICH therapy Stage II CSF drainage Do not carry out in case of depression of consciousness During CT control, an individual variant of drainage (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, and other sensors). Estimation of the ICP level according to the pressure in the terminal cistern, CT, TKDG is very conditional. Regardless of the method for assessing ICP, it 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 preferred) Stop if osmolarity\u003e 320 mmol / L or BPav.
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ICH therapy stage III Mannitol with osmolarity 310 mOsm / L Hyperglycemia Grade 3 obesity General dehydration Decompensated heart failure Complications Increased hematocrit with dehydration ARF Acidosis Hypokalemia Recoil phenomenon (in case of BBB damage) To prevent complications Use the rectal pathway Control of hematocorrhagic route
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ICH therapy stage III Dehydration Hypertonic solution (level 3) 3% -20% (7.5%) 100 ml IV 5 times a day Maintains euvolemic hyperosmolar status of the brain Reduces dislocation in trauma and in postoperative patients Uniformly dehydrates both hemispheres of the brain Modulates inflammatory response to brain injury
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ICH therapy stage III Dehydration Furosemide (level 3) 10-20 mg IV every 6 hours with osmolarity\u003e 320 mmol / L and hypernatremia\u003e 150 mmol / L synergism with mannitol, slows down the production of cerebrospinal fluid
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ICG therapy Stage III Hyperventilation During transportation. It is shown with obvious signs of dislocation: - pathological reaction to pain - growing mydriasis - progressive depression of consciousness; with ineffective liquor drainage, osmotherapy, but pCO2 is not lower than 32 mm Hg. Art. (in this case, TCD is desirable for the prevention of ischemia)
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ICH therapy stage III Hyperventilation can be used in patients whose condition worsens for the second time against the background of increased intracranial pressure, including patients with dislocation syndrome (level 4). Excessive vasoconstriction can lead to ischemia in areas with impaired MV autoregulation, if O2 extraction does not increase compensatory. The negative effects of HPV: Decrease in the threshold of seizure activity Increase in oxygen affinity for hemoglobin Violation of MV autoregulation Paradoxical increase in ICP With a decrease in CO2 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 (4-6 hours on average) to avoid the rebound effect.
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ICH therapy stage III Hypothermia 35-36.0 C Complications: Decreased CO Arrhythmia Thrombocytopenia
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ICH therapy stage III Inotropic support In case of insufficient efficiency of infusion therapy to achieve adequate CPP (\u003e 70 mm Hg), sympathomimetics (dopamine, adrenaline, norepinephrine, mezaton). 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. Indication: 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 blood pressure of the media with an increase in ICP leads to a decrease in CPP. The desired level of CPP is at least 70 mm Hg, which determines the desired level of blood pressure of the media. - not less than 100 mm Hg, and blood pressure of the system. - not less than 140-150 mm Hg. The use of sympathomimetics to maintain arterial hypertension contributes to the maintenance of CPP and prevents the progression of ICH. The feasibility 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 “despair therapy” (“barbituric coma” and moderate hypothermia) is made by a council consisting of: a neurologist, resuscitator, neurophysiologist ESTS1, a neurosurgeon after assessing the neurological status outside sedation on the basis of recognition of the patient's non-transportability. Application only for absolute indications, ICH syndrome, uncontrolled by other means, absence of surgical problems, consolidated consent of all doctors involved in the treatment of the victim. EEG monitoring and invasive blood pressure measurement are desirable.
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ICG therapy Stage IV Barbituric 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 by 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 Evaluation of neurological status 24 hours after stopping the infusion (preferably control of plasma concentration) To prevent the cardiotoxic effect of barbiturates, it is recommended to administer small doses of colloids in combination with dopamine (2-4 μg / kg / min). You should not stop the administration of the drug for the purpose of a staged assessment of the neurological status until the moment of complete relief of the ICH syndrome.
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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 Prehospital stage Hospital stage Emergency measures Urgent measures Delayed measures
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Prehospital stage Diagnostics Assessment of the degree of depression of consciousness according to the Glasgow Coma Scale Diagnostics of respiratory and hemodynamic disorders Diagnosis of associated injuries Diagnosis of spinal trauma
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Prosthetics of the respiratory tract Intubation of the trachea in case of breathing disorders massive aspiration depression of consciousness to coma Prehospital stage In case of technical difficulties double tube of the Easy-Tube type laryngeal mask In case of asphyxiation and impossibility of intubation - conicotomy
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Spinal fixation Indications for rigid fixation of the cervical spine Autoinjury Fall from a height Drowning Prehospital stage
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Oxygenation Pre-hospital mechanical ventilation Respiratory disorders Coma Auxiliary mode Normoventilation Increased oxygenation FiO2 \u003d 0.5-1.0 Sedatives Diazepam Midazolam Droperidol
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CRANIAL TRAUMA -
mechanical damage to the skull and intracranial formations - the brain, blood vessels, cranial nerves, meninges. The main reasons are traffic accidents, falls, industrial, sports and domestic 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 a child's life.
CLASSIFICATION OF Craniocerebral 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 the adjacent soft tissues and aponeurosis;
▪ there are soft tissue wounds without damage to the internal aponeurosis, bone structures are not damaged.
1.2 Open head injury:
▪ injuries in which there are wounds of the soft tissues of the head with damage to the internal aponeurosis;
▪ fracture of the skull base 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 the integrity of the dura mater are considered
non-penetrating, in violation of its
integrity - penetrating.
II. Clinical forms
2.1. Concussion (only for CCI).
2.2. Mild brain contusion.
2.3. Brain contusion of moderate degree.
2.4. Severe contusion of the brain.
2.5. Compression of the brain (intracranial hematomas, combined or subdural hygromas, compression by bone fragments, pneumocephalus, edema
swelling of the brain) - there is compression with a bruised brain and compression without bruising the brain.
2.6.
2.7. Compression of the head.
III. Severity
3.1. Mild TBI:
▪ Brain concussion.
▪ Mild brain contusion
3.2. Moderate TBI:
▪ Medium 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 bruise -2-3 weeks;
- with moderate injury -4-5 weeks;
- with severe brain injury -6-8 weeks;
- with diffuse axonal damage -8-10 weeks;
With compression - 3-8 weeks.
4.2. Interim period(early recovery period)
- with mild TBI - up to 2 months;
- with moderate TBI - 4 months;
- with 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 (more often purulent-inflammatory) that have joined the trauma, not necessary for damage to the brain and its integuments, but arising under the influence of 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 integuments or persistent violations of the anatomical integrity of the brain, its membranes and bones of the skull, resulting from acute TBI, persisting in the intermediate and long-term period and requiring treatment and rehabilitation. ...
The clinical picture of the acute period of concussion of the brain:
▪ 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 past events) or retrograde (for the events preceding the trauma) amnesia;
▪ absence of meningeal and focal neurological symptoms;
▪ cerebral symptoms (nausea, vomiting, dizziness, headache),
▪ asthenia (general weakness, lethargy, drowsiness, insomnia, irritability, decreased appetite);
▪ vegetative 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 in traumatic brain injury" can be downloaded absolutely free of charge on our website. Project subject: OBZH. 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 craniocerebral and spinal injuries
Completed by: teacher of health and safety Savustyanenko Viktor Nikolaevich G. Novocherkassk MBUSOSH №6
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CRANIAL - BRAIN TRAUMA Causes What is happening? How to recognize? What to do? Diagnosis Treatment Procedure for providing first aid to the victim of an accident Procedure for providing first aid to the victim
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CRANIAL - BRAIN TRAUMA
Treatment of victims with open and closed injuries to the skull and brain has much in common, since they almost always have a concussion or contusion 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 is primarily to prevent blood, cerebrospinal fluid or vomit from entering the respiratory tract, for which the wounded or his head is turned on the side. An aseptic bandage is applied to the wound. At the stage of first aid, if necessary, the bandage is corrected and an antibiotic, tetanus toxoid is injected intramuscularly.
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Concussion, traumatic brain injury
It would seem that our brain is in little threat, because it is protected like no other organ. It is washed by a special fluid, which not only provides the brain with additional nutrition, but also serves as a kind of shock absorber. The brain is covered with several membranes. After all, it is safely "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. Concussion ranks first among all brain injuries. Moreover, according to the observation of traumatologists, it is more common in women. Although, perhaps, they simply seek professional help more often than men.
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Concussion can occur as a result of impacts, bruises, and sudden movements such as acceleration or deceleration, such as falling. Concussions are commonly caused by road traffic accidents, domestic, sports and work injuries, and injuries from street fights.
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What's happening?
What exactly happens as a result of a concussion to our brain, doctors still find it difficult to answer unequivocally. After all, if you examine the injured brain using computed tomography, then practically no organic disorders can be detected. Most likely, as a result of a concussion, certain problems arise with the functioning of the nerve cells of the brain. In this case, their nutrition may deteriorate, there may be a slight displacement of the layers of brain tissue and the connection between some brain centers may go wrong. A severe concussion can rupture blood vessels and severely injure certain parts of the brain. The main danger in traumatic brain injuries is intracranial bleeding, since the leaked blood is capable of squeezing and saturating the brain structures, disrupting their work and vitality. In addition, trauma can lead to another formidable complication - brain edema. Brain injuries complicated by shock and those affecting the brainstem, where breathing and blood pressure are regulated, are especially severe.
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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 condition can be one indicator of the severity of the concussion. The extreme degree of loss of consciousness is a coma. With a concussion, a person often does not understand where he is, what happened, and hardly recognizes the people around him. Another important sign by which one can judge the severity of brain damage is memory loss: does a person remember the moment of injury, and if not, how much time before the injury fell out of his memory. The larger the memory lapse, the more serious the injury. When the victim regains consciousness, he may vomit and vomit. Often he turns pale, his head is spinning and hurts, his ears are noisy, it is difficult for him to focus his gaze, his breathing becomes rapid, and his pulse jumps. In the first hours after a concussion, the victim's pupils are dilated or narrowed - 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 a person who is unconscious, the doctor directs the 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. At the same time, the expansion 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 cerebral hemispheres.
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What to do?
If a concussion is suspected, first aid should be given 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 slightly raise the head. It is very helpful to apply cold compresses to the head. Drinking a lot for 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, as it is possible that the brain damage is more severe than meets the eye. If the patient is in shock, carefully monitor his breathing and pressure before the ambulance arrives. In an emergency, start with artificial respiration and chest compressions.
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With a concussion, you need to see a trauma doctor. He will examine and interview the patient, check reflexes, prescribe an X-ray of the skull and, if a more complex brain damage is suspected, will refer you to a neurologist for consultation. There the patient will have a full-scale examination: electroencephalography (EEG), echoencephalography, computed or magnetic resonance imaging of the brain, Doppler ultrasonography of the cerebral vessels, spinal puncture. Magnetic resonance imaging of the spine may be needed to rule out spinal problems.
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Patients with concussion should stay in bed for at least several days. In this case, you cannot read, listen to loud music and watch TV. It is necessary to follow all the instructions of the doctor, carefully take the medications prescribed by him. With a concussion, the general condition of the victims usually returns to normal 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, for example, epilepsy. Therefore, after some time after recovery, you should definitely visit a neurologist and undergo an electroencephalography. Treatment for more serious head injuries depends on the severity of the injury. In some complicated cases, the help of neurosurgeons may be required.
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The procedure for providing first aid to the victim of an accident
In most cases, road accidents occur far from medical facilities and an ambulance has to wait a long time. It is this circumstance, as well as the fact that drivers can be useful to victims earlier than others, obliges them to be able to provide first aid, that is, to carry out the simplest urgent measures to save the lives of victims. Drivers of cars and other vehicles, both involved and not involved in a traffic accident, but who are nearby, must 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.
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Procedure for providing first aid to the victim
1. Organization of an ambulance call. 2. Removing the injured from the wrecked car. Road traffic accidents are often accompanied by complex fractures, craniocerebral trauma, and spinal injuries. The victim may have several injuries at once. Therefore, take it out of the car very carefully. You cannot jerk and bend his torso, arms or legs, pull them out by force. We must first try to eliminate everything that holds the victim. If a person has lost consciousness and is in an unnatural position, two or three people need to take him out of the car, trying not to change this position. Particular attention should be paid to the victims if a spinal fracture is suspected, not to move them unless absolutely necessary, because this can cause paralysis. Such a person should be placed on his back or stomach in such a way that the site of injury is not impaired. 3. Providing first aid. When you are removed from the car, you need to loosen the tie, unfasten the collar, belt so that breathing is not difficult. In case of 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 has bleeding, measures should be taken to temporarily stop it. First aid should be done quickly and not cause unnecessary pain to the victim. 4. Transportation of victims to a medical institution. When everything possible has been done to save the victims at the scene of the incident, and it is impossible to call an ambulance or it is clear that it will arrive late, you need to take care of the delivery of the victims to the nearest medical institution. It is necessary to proceed with the same care and attention as when removing them from an emergency vehicle.
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When it becomes necessary to raise the victim, you should use the following methods: kneel on the side of the victim, bring your hands under the shoulder blade, head, neck and lift him; kneel at the head of the victim, bring your hands under your shoulders and raise him. Under no circumstances is independent movement of the victim allowed in case of damage to the lower extremities, skull, chest and abdominal organs. If it is necessary to transfer the victim on a stretcher, he is laid down carefully, without concussion and in a position comfortable for him. The stretcher is placed next to the victim from the side of the injury. Two people stand next to the patient on one knee, one of them brings his hands under the head, neck and back, the other - under the sacrum and shins. The third person moves a stretcher under the victim. You need to lift the stretcher carefully and at the same time, be sure to keep pace, in short steps, slightly bending your knees. The one in front is obliged to warn the rear one about all obstacles on the road. When climbing a mountain, the victim is carried head first, when descending a mountain - feet first, except in cases of damage to the lower limbs. You should always try to keep the victim horizontal. Transportation, depending on the nature of the damage, is carried out according to the following rules: in case of fractures of the bones of the skull, injuries of the head and brain, in case of fractures of the spine and pelvic bones, the victim is transported only in a horizontal position; in case of fractures of ribs, collarbones, transportation is most painless in a sitting position, but when the victim cannot sit, transportation is carried out on a stretcher with a half-sitting position; in case of chest injuries, the victim is placed on the wounded side or back in a semi-sitting position; when the neck is injured in front, the victim is given a half-sitting position with the head tilted to the chest towards the wound; with injuries to the abdomen and with internal bleeding, the victim is placed on his back, a pillow or other item 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.
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All the features of the forthcoming transportation should be foreseen: 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 a large hospital or clinic is located relatively nearby, it is better to deliver the victim directly there, bypassing even the nearest first-aid post. If it is far from a large medical institution, the wounded must be taken to the nearest medical institution. On arrival, do not take him out of the car, but ask the medical staff to approach the victim to examine him and decide on further actions. Never leave the injured without help and send them without an accompanying person who may be required to provide the necessary assistance on the way. In addition, by his behavior, conversations, he must strengthen in the victim confidence in the successful outcome of what happened.
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Slide captions:
Damage to the bones of the skull and brain
Anatomy
Skull (brain) Paired parietal and temporal Unpaired frontal, wedge-shaped, ethmoid and occipital
Meninges of the brain Dura mater Arachnoid Soft membrane
Head trauma (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, meninges. There are two groups of traumatic brain injuries - open and closed
Open injuries With an open traumatic brain injury, the skin and aponeurosis are damaged. The bottom of the wound is bone or deeper tissues. In case of damage to the dura mater, the injury is considered to be penetrating.
Closed injuries In a closed traumatic brain injury, the aponeurosis is intact, although the skin may be damaged. All traumatic brain injuries are divided into: Concussion is an injury in which there are no persistent disorders in the brain. All symptoms following a concussion usually resolve over time (within a few days). Persistent persistence of symptoms is a sign of more serious brain damage.
Closed injuries Compression of the brain (hematoma, foreign body, air, bruised focus). Brain contusion: mild, moderate and severe. Diffuse axonal injury. Subarachnoid hemorrhage.
Closed injuries At the same time, various combinations of types of traumatic brain injury can be observed: contusion and compression by hematoma, contusion and subarachnoid hemorrhage, diffuse axonal damage and contusion, contusion of the brain with compression by hematoma and subarachnoid hemorrhage.
The causes of traumatic brain injury: a fracture of the skull with displacement of tissues and rupture of the protective membranes around the spinal cord and brain; contusion and tears of brain tissue during concussion and impacts in a confined space inside a hard skull; bleeding from damaged vessels into the brain or into the space around it (including bleeding due to rupture of an aneurysm). Brain damage can also occur as a result of: direct injury to the brain by objects penetrating into the cranial cavity (for example, bone fragments, a bullet); increased pressure inside the skull as a result of cerebral edema; a bacterial or viral infection that penetrates the skull in the area of \u200b\u200bits fractures.
Concussion Acute traumatic brain injury due to mechanical force, as a result of which transcendental inhibition develops in the central nervous system Changes in brain tissues are functional (reversible)
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 nearest events before the injury) Vomiting Cerebral symptoms: weakness, weakness, headache, irritability, pallor or hyperemia of the skin, reaction of the pupils reduced to light, nystagmus
Brain contusion in TBI Brain contusion is an injury in which the tissues of the brain or its membranes are destroyed.It usually occurs at the point of application of the traumatic force, but it can also be observed on the side opposite to the injury (contusion from the shock). There are lung contusions , moderate and severe
Brain contusions (mechanism of occurrence)
Mild brain contusion
Moderate cerebral contusion
Severe contusion of the brain
The clinical picture of brain contusion Loss of consciousness from several hours to several days Retrograde amnesia (loss of memory of 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 in accordance with the site of damage
Wounds of the soft tissues of the head Feature - significant bleeding When dissecting the aponeurosis - the wound gapes Bruised wounds can be accompanied by detachment of soft tissues and pollution When hair gets into the moving mechanisms, scalped wounds of the head appear
Emergency care Stop bleeding by any means of temporary stopping Place the patient down, calm down Treat the skin around the wound with an antiseptic solution Apply an aseptic bandage Cold to the injury site If possible, anesthetize Transportation to the healthcare 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.An accumulation of 50 ml of blood is sufficient to compress the substance of the brain
Causes of cerebral compression The rate of development is distinguished: acute intracranial hematomas, which appear in the first 3 days from the moment of injury, subacute - in the first 2 weeks after injury, and chronic - after 2 weeks after injury. Hematomas: intracranial - epidural and subdural; intracerebral; intraventricular; Depressed fractures of the skull bones; Foci of crushing of the brain, subdupal hygromas, pneumocephalus.
Compression of the brain CT of the brain. Acute subdural hematoma in the right fronto-parietal-temporal region with dislocation of the brain and its compression.
Epidural hematoma
Epidural hematoma
Acute Subdural Hematoma
Chronic subdural hematoma
Subdural hematoma
Intracerebral hematoma
Intracerebral hematoma
Compression of the brain Clinical picture Loss of consciousness at the moment of trauma Light interval - the period between the restoration of consciousness and the development of the clinic of compression of the brain After the formation of a hematoma (a few hours or days after the injury), consciousness is again lost Focal symptoms Cheyne-Stokes breathing
Emergency care Lay on a stretcher in the supine position, half-turned with the head immobilization Anesthetize If there is a wound, aseptic dressing Cold to the head Hospitalization in the neurosurgery department Control of the general condition, blood pressure, respiratory rate, pulse Help 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 GM With a sharp increase in ICP - lumbar puncture With a hematoma formed - craniotomy, removal of the hematoma, stopping bleeding
Fractures of the bones of the skull P about localization 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 P about the type of fracture 1. Linear 2. Impressed 3. Comminuted
Fractures of the bones of the cranial vault Clinical picture: Locally hematoma without clear boundaries. Loss of consciousness after a while, the field of trauma. With an increasing subdural hematoma, there is a light interval (the period of m / y recovery of consciousness and the development of a clinic for brain compression) Focal symptoms in comminuted fractures with brain compression, in 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 is lost General cerebral symptoms Hyperthermia, tachycardia Decreased tendon reflexes and muscle strength Deep inhibition is replaced by excitement Bleeding and liquorrhea from the nose, nasopharynx, ears "Symptom of glasses" With a fracture of the frontal bone -
Clinical signs of fracture of the bones of the base of the skull
First aid Apply a bandage to the wound (cap, bridle, Hippocratic cap, blindfolds, cruciform on the back of the head) Transportation on a stretcher in the supine position half-turned with head immobilization (the head is placed on a cotton-gauze roller made in the form of a donut) in neurosurgical Department of the hospital Control of the general condition, pulse, blood pressure, respiratory rate Help with vomiting With bleeding and cerebrospinal fluid from the nose and ear canals, loose tamponade of the nose and ear with an antiseptic solution is shown
Treatment In the surgical department, under local anesthesia or anesthesia, PCO of wounds is performed; 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 Cavities of the nose or ear are tamponed with dry or moistened solution with gauze, do not rinse - infection of the meninges is possible.
Craniotomy
Set of instruments for craniotomy 1. Tools of the general set 2. Brace with a set of cutters - for making a hole on the bone 3. Wire saw Jigli 4. Bone nippers Luer, Dahlgren - for biting off an oblique fragment 5. Chisel, osteome: straight, grooved; bone hammer - for separating bone chips 6. Raspators: Farabefa (straight, curved) - for separating from the bone 7. Spatula: cerebral spatula - to protect the brain
Bandage "Cap" Applied to the wounds of the scalp
A cruciform bandage Apply when the neck, larynx or occiput is injured
Bandage "Bridle" Applied in case of extensive wounds of the head, in the face
Sling-like bandage. Apply to nose, forehead and chin to nose to forehead to chin
Thanks for your attention.
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