Presentation on the topic of closed craniocerebral injury. Traumatic brain injury
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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KSMU Department of General Surgery Diagnosis and tactics for acute traumatic brain injury Lecturer: MD, Professor A.S. Tutov
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The relevance of the problem of acute TBI is due to the significant frequency, difficulty of diagnosis, tactics, high mortality and poor long-term treatment results
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Classification of traumatic brain injury (III All-Union Congress of Neurosurgeons, 1982) CLOSED Concussion Brain contusion Compression of the brain due to contusion Compression of the brain without accompanying contusion Damage to the bones of the cranial vault and brain (bruise, compression) OPEN Damage to the soft tissues of the head without signs of brain damage Damage to the soft tissues of the head with impaired brain function (concussion, bruise, compression) Damage to the soft tissues of the head, bones of the cranial vault and brain (bruise, compression) - penetrating and non-penetrating Fracture of the base of the skull (bruise, compression) Gunshot wound
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SYNDROMES Hypertensive - cerebrospinal fluid pressure is increased Hypotensive - cerebrospinal fluid pressure is decreased Normotensive - cerebrospinal fluid pressure is not changed Subarachnoid hemorrhage
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The structure of some nosological forms of TBI. Compression of the brain: intracranial hematomas (epidural, subdural, intracerebral, intraventricular); bone fragments; foreign bodies; hygromas; edema and swelling of the brain. Open injuries to the skull and brain: penetrating (with damage to the dura mater); non-penetrating (without damage to the dura mater).
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Symptoms of traumatic brain injury General cerebral symptoms. Meningeal symptoms. Local symptoms. Stem symptoms.
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General cerebral symptoms Loss of consciousness (stunning, stupor, coma). Memory loss. Headache, dizziness. Nausea, vomiting, tinnitus. Instability in the Romberg pose.
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Meningeal symptoms Headache – sharp, squeezing in nature. Photophobia. Nausea and vomiting are persistent. High body temperature. Trigger pose. Stiff neck. Positive symptoms of Kernig, Brudzinsky.
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Local symptoms Paresis, paralysis. Impaired sensitivity. Loss of vision, hearing. Motor and sensory aphasia.
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Brainstem symptoms Upper brainstem (mesodiencephalic) syndrome: - consciousness: stupor, stupor; - breathing: tachypne, “orderly breathing”; - vascular activity: persistent tachycardia and hypertension (pulse up to 120 beats per minute, blood pressure up to 200/100 mm Hg); - oculomotor disorders: “floating gaze”, divergence, convergence, gaze paresis; - movement and tone: high tone, increased reflexes, pathological reflexes; - swallowing: not impaired; - thermoregulation: body temperature is high.
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Brainstem symptoms Lower brainstem (bulbar) syndrome: - consciousness: coma; - breathing: pathological forms; - vascular activity: weak pulse, tachycardia, blood pressure up to 70/40 mm Hg. Art. and below; - oculomotor disorders: pupils are wide, reaction to light is subtle; - swallowing: severely impaired; - thermoregulation: temperature is reduced or normal. Dislocation syndrome: rapid transition from upper brainstem to lower brainstem syndrome as a result of infringement of the brain stem.
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Determination of hyper- or hypotension syndrome by an indirect method (according to clinical data)
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Determination of hyper- or hypotension syndrome by direct method: Lumbar puncture with the patient lying down. Measuring the pressure of the cerebrospinal fluid with a manometer (the norm is 120-180 mm water column) or counting the drops of cerebrospinal fluid flowing from the needle (the norm is 60 drops per minute). An upward deviation (occurs in 60-70% of patients) indicates hypertension syndrome. There are: mild hypertension (pressure up to 230 mm water column), moderate (up to 280) and severe (over 280 mm water column). Reducing pressure below 100 water. Art. indicates hypotensive syndrome (occurs in 20-25% of patients). Normotensive syndrome is observed in 10-15 patients with TBI.
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If the patient has general cerebral symptoms, then one should think about either a concussion or compression of the brain by an intracranial hematoma at an early stage.
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If cerebral symptoms are combined with meningeal symptoms, then a basal skull fracture or subarachnoid hemorrhage should be suspected.
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If general cerebral symptoms are combined with meningeal + local symptoms, then brain contusion, compression of the brain by bone fragments, foreign bodies or late-stage intracranial hematoma should be excluded
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Algorithm for the differential diagnosis of TBI based on the symptom complex “general cerebral symptoms” GENERAL SYMPTOMS General cerebral only Presumptive diagnosis: Concussion. 2. Compression of the brain by intracranial hematoma at an early stage In combination with meningeal hematomas Suspicion of: Fracture of the base of the skull. 2. Subarachnoid hemorrhage. In combination with local + meningeal Presumptive diagnosis: Brain contusion. Compression of the brain by bone fragments or a foreign body. Compression of the brain by intracranial hematoma in the late stage. 1 A 1 B 1 C
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1A. Diagnosis: Concussion Confirmed by: Regression of general cerebral symptoms over time. No violations with additional research methods (according to indications). Compression of the brain by an intracranial (epi- or subdural) hematoma Confirmed by: Dynamic observation - after temporary improvement (“bright interval”), headaches intensify, nausea, vomiting, anxiety and discomfort reappear. Local and meningeal symptoms occur. Additional research methods: a) echoEG – M-echo displacement by 6-15 mm; b) carotid arteriography (CAG) – displacement of vascular structures; c) computed tomography (CG)
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1B. Diagnosis Fracture of the base of the skull Confirmed by: Bleeding and blood loss from the nose or ear. With “spectacles”, hemorrhages in the posterior wall of the pharynx or the mastoid area, appearing 12-24 hours or more after the injury. X-ray of the skull. Subarachnoid hemorrhage Confirmed: Lumbar puncture - the fluid is intensely stained with blood.
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1B. Diagnosis: Brain contusion Confirmed: Regression of cerebral and meningeal symptoms. Stability of the local system, especially in severe cases. Additional diagnostic methods: a) echoEG – displacement no more than 3-5 mm; b) CAG is not very informative; c) CG – areas of increased density. Compression of the brain by bone fragments or foreign bodies Confirmed by: Correspondence of local structures to the site of the head injury. Craniography. Inspection of the wound. Additional research methods: a) echoEG – M-echo displacement; b) CAG – displacement of vascular structures; c) CG – depressed fracture. Compression of the brain by intracranial hematoma Confirmed: “Light gap” with subsequent deterioration of the patient’s condition. Clinic for severe brain contusion. Additional diagnostic methods: a) echoEG – M-echo displacement by 6-15 mm; b) CAG – displacement of vascular structures; c) KG – change in density zone.
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Depending on the cerebrospinal fluid pressure, the following is prescribed: For hypertensive syndrome Diet No. 7. Fowler's position (raised head end. Dehydration. Diuretics. Unloading lumbar punctures. Cleansing enemas. For hypotensive syndrome Table No. 15. Trendelenburg position (lowered head end. IV administration solutions with a low concentration of salts (5% glucose, Ringer's solution, saline). Caffeine 1 ml 10% subcutaneously. Vagosimatic blockades.
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According to indications, use: Antibiotics and sulfonamide drugs. Analeptics - lobeline, cititon, cordiamine. Adrenergic agonists: adrenaline, norepinephrine, mezaton. Cardiac glycosides. Transfusion of blood and blood substitutes. Plasma replacement solutions. Analgesics (promedol, analgin).
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Indications for surgical treatment Open injuries - perform PSO of the wound. Compression of the brain - osteoplastic or resection trepanation of the skull is performed, the causes of compression of the brain are eliminated, a final stop of bleeding is performed, wound care is performed, and tissue is sutured layer-by-layer.
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Presentation on the topic: Damage to the skull and brain
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Open injuries With an open craniocerebral injury, the skin, aponeurosis and the bottom of the wound are bone or deeper tissue. A penetrating injury is one in which the dura mater is damaged. A special case of penetrating trauma is otoliquorrhea resulting from a fracture of the bones of the base of the skull.
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Closed injuries With a closed craniocerebral injury, the aponeurosis is not damaged, although the skin may be damaged. All craniocerebral 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. The main criteria for the severity of a concussion are the duration (from several seconds to hours) and the subsequent depth of loss of consciousness and the state of amnesia. Non-specific symptoms - nausea, vomiting, pale skin, cardiac dysfunction. Compression of the brain (hematoma, foreign body, air, contusion). Brain contusion: mild, moderate and severe. Diffuse axonal damage. Subarachnoid hemorrhage. 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.
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Classification of traumatic brain injuries (TBI). The following main clinical forms of traumatic brain injury are distinguished: concussion, mild, moderate and severe brain contusion, compression of the brain. The causes of traumatic brain injury can be: 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, 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 its fractures.
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Brain contusion due to TBI A brain contusion is a violation of the integrity of the brain matter in a limited area. It usually occurs at the point of application of the traumatic force, but can also be observed on the side opposite to the injury (contusion from a counter-impact). In this case, destruction of part of the brain tissue, blood vessels, and histological cell connections occurs, with the subsequent development of traumatic edema. The area of such violations is different and is determined by the severity of the injury. Brain contusions are distinguished between mild, moderate and severe.
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Mild degree of brain contusion A mild degree of brain contusion is characterized by a loss of consciousness after an injury lasting from several to tens of minutes. After restoration of consciousness, complaints of headache, dizziness, nausea, etc. are typical. As a rule, retro-, con-, and anterograde amnesia is noted. Amnesia (Greek: amnesia forgetfulness, memory loss) is a memory impairment in the form of loss of the ability to retain and reproduce previously acquired knowledge. Vomiting, sometimes repeated. Moderate bradycardia may be observed. Bradycardia is a decrease in heart rate to 60 or less per minute in an adult. tachycardia - an increase in heart rate over 90 beats per minute for adults. sometimes - systemic arterial hypertension; hypertension - increased hydrostatic pressure in blood vessels, hollow organs or body cavities. Breathing and body temperature without significant deviations. Neurological symptoms are usually mild (clonic nystagmus - involuntary rhythmic biphasic movements of the eyeballs, drowsiness, weakness), slight anisocoria, signs of pyramidal insufficiency, meningeal symptoms, etc., often regressing within 2-3 weeks. after injury.
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Moderate degree of brain contusion Moderate degree of brain contusion is characterized by loss of consciousness after an injury lasting from several tens of minutes to several hours. Amnesia is pronounced (retro-, con-, anterograde). The headache is often severe. Repeated vomiting may occur. Mental disorders are sometimes observed. Transient disorders of vital functions are possible: bradycardia or tachycardia, increased blood pressure, tachypnea - rapid shallow (not deep) breathing without disturbing the rhythm of breathing and airway patency, low-grade fever - increased body temperature within 37-37.9 ° C.
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Severe degree of brain contusion Severe brain contusion, intracerebral hematomas (limited accumulation of blood in closed and open injuries to organs and tissues with rupture (injury) of blood vessels; a cavity is formed containing liquid or coagulated blood) of both frontal lobes.
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Severe brain contusion Severe brain contusion is characterized by loss of consciousness after injury lasting from several hours to several weeks. Motor agitation is often pronounced. Severe disturbances in vital functions are observed: arterial hypertension (sometimes hypotension), bradycardia or tachycardia, disorders of the frequency and rhythm of breathing, which may be accompanied by disturbances in the patency of the upper respiratory tract. Hyperthermia is pronounced. Primary brainstem neurological symptoms often dominate (floating movements of the eyeballs, gaze paresis, tonic nystagmus, swallowing disorders, bilateral mydriasis or ptosis - drooping of the upper eyelid, divergence of the eyes along the vertical or horizontal axis, changing muscle tone, decerebrate rigidity, depression or increased tendon reflexes, reflexes from the mucous membranes and skin, bilateral pathological foot signs, etc.), which in the first hours and days after injury obscures focal hemispheric symptoms. Paresis of the limbs (up to paralysis), subcortical disorders of muscle tone, reflexes of oral automatism, etc. can be detected. Generalized or focal epileptic seizures are sometimes observed.
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Compression of the brain Compression of the brain is a progressive pathological process in the cranial cavity that occurs as a result of trauma and causes dislocation and infringement of the trunk with the development of a life-threatening condition. With TBI, compression of the brain occurs in 3-5% of cases, both with and without UGM. Among the causes of compression, intracranial hematomas come first - epidural, subdural, intracerebral and intraventricular; This is followed by depressed fractures of the skull bones, areas of brain crushing, subdural hygromas, and pneumocephalus. .Compression of the brain. The main cause of brain compression during traumatic brain injury is the accumulation of blood in a closed intracranial space. Depending on the relationship to the membranes and the substance of the brain, epidural (located above the dura mater), subdural (between the dura mater and the arachnoid mater), intracerebral (in the white matter of the brain and intraventricular (in the cavity of the ventricles of the brain) hematomas are distinguished. The cause of compression of the brain can be There may also be depressed fractures of the bones of the cranial vault, especially penetration of bone fragments to a depth of more than 1 cm.
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Literature Clinical guide to traumatic brain injury, volume 3, Konovalov A.N. 2002 Potapov A.A., Likhterman L.B., Kravchuk A.D. Chronic subdural hematomas. M.: Antidor, 1997. Potapov A.A., Okhlopkov V.A., Likhterman L.B., Kravchuk A.D. Post-traumatic basal liquorrhea. M.: Antidor, 1997. Neurotraumatology. Directory. Under. ed. acad. RAMS A.N. Konovalova, prof. L.B. Likhterman, prof. A.A.Potapova. Rostov-on-Don: Phoenix, 1999. Clinical guidelines for traumatic brain injury. Ed. acad. RAMS Konovalov A.N., Potapov A.A., Likhterman L.B. and others. Surgery of the consequences of traumatic brain injury. M., 2006.
Description of the presentation TRAUMATIC BRAIN INJURY TBI - by slides
TBI is a type of head injury in which, along with damage to the brain, the skull and soft tissues of the head are injured.
41 238. 8 27. 2 injuries as a result of road accidents criminal injuries domestic injuries other injuries CAUSES of TBI
CRANIO-BRAIN INJURIES ARE DIFFERENTIATED: TBI By degree of severity: mild, moderate, severe By clinical form: concussion, bruise, compression, diffuse local damage. By the nature of the injury: open, closed By the outcome of the injury: good recovery, moderate disability, severe disability, death
MODERN CLASSIFICATION OF TRANO BRAIN INJURY closed open. Types of TBI Cerebral pressure Cerebral contusion Diffuse -LOCAL DAMAGE CONCUSSION OF THE BRAIN INJURY expectations, in which there are soft tissue wounds of the head, includin g apo neurosis Fracture of the base of the skull, accompanied by The current rate of wear and tear, evidence tone and tightness of the skull box
The mildest and most common type of closed traumatic brain injury, which is characterized by only minor changes in cell membranes and intercellular contacts of nerve cells; a concussion is not divided into degrees and is a functional, reversible damage to the nervous system; Patients with concussion account for 75-80% of all hospitalized patients. BRAIN CONCUSSION
CLINIC OF BRAIN CONCUSSION The leading ones are three syndromes: general cerebral autonomic neurotic. Manifested by impaired consciousness (stunning or short-term loss for a few seconds), headaches, dizziness, vomiting. It manifests itself as general weakness, apathy, drowsiness, sleep disturbance, loss of appetite, irritability, sometimes euphoria, and decreased criticism of one’s condition. It manifests itself as hyperhidrosis of the palms, pallor or hyperemia of the skin, instability of blood pressure, changes in pulse, attacks of chills, fever.
They are distinguished by the predominance of irreversible morphological changes in the area of contusion lesions; Subarachnoid hemorrhage always accompanies a brain contusion, since inevitable damage to the vessels of the pia mater at the site of contusion leads to blood entering the cerebrospinal fluid. BRAIN CONUSIONS
Brain contusions Mild contusions Moderate contusions Severe contusions Focal symptoms are caused by damage to the cortical parts of one hemisphere of the brain. Due to subarachnoid hemorrhage, cerebral, autonomic and neurotic disorders are more pronounced than with a concussion. They are characterized by the appearance of foci of damage to the basal parts of the cerebral hemispheres and the convexital surface of the brain. This type of brain injury is diagnosed in 100% of patients with basal skull fractures. Characterized by the appearance of foci of contusion not only in the cortex and basal parts of the brain, but to a greater extent by damage to the stem parts of the brain and the diencephalic region.
CLINIC OF BRAIN CONUSIONS Mild brain contusions Moderate brain contusions Severe brain contusions loss of consciousness for several minutes or hours; mild focal symptoms (weakness in the limbs; nystagmus (pendulum-like eye movements, “eyes darting” from side to side); mild motor disturbances in the form of asymmetry of reflexes, pathological foot signs on one side; meningeal syndrome: stiffness of the neck muscles, Kernig’s, Brudzinski’s symptoms , photophobia, pain when moving the eyeballs; duration of clinical manifestations is usually 2-3 weeks. prolonged loss of consciousness (from a few seconds to 1-2 hours); psychomotor agitation, euphoria, mental disorders may occur; with damage to the central gyri - motor and sensory disorders; the duration of clinical manifestations is 3-6 weeks; persistent focal symptoms of damage to the nervous system may remain, which leads to disability of patients. from the moment of severe injury, the victims are in a coma. The duration of loss of consciousness can be from several days to several weeks, months; characterized by a violation of muscle tone (a sharp increase in the extensor muscles of the arms and legs); strabismus; prolonged increase in body temperature; floating eye movements; convulsive seizures (contractions of the muscles of the arms and legs, sometimes with tongue biting);
The consequence of severe brain damage is more common in children and adolescents. Pathomorphological changes - tension and rupture of axons in the white matter of the hemispheres and the brain stem. clinic The person is in a coma (there is no reaction to a call or pain stimulation); there are breathing disorders (irregular breathing rhythm, respiratory arrest); a sharp decrease in arterial (blood) pressure; characteristic posture (a sharp increase in tone in the extensor muscles of the arms and legs); strabismus; prolonged increase in body temperature; floating eye movements; compression of the brain - characterized by the so-called “lucid interval” after injury. Diffuse axonal brain injury
May be caused by: 1. Intracranial hematoma (epidural, subdural, intracerebral, intraventricular). 2. Depressed fracture of the bones of the calvarium. 3. Contusion lesion, causing swelling and displacement of the brain. 4. Subdural hydroma. BRAIN COMPRESSION
An epidural hematoma is a localized collection of blood between the outer surface of the dura mater and the bones of the skull. The source of an epidural hematoma is a damaged branch of the meningeal arteries. Most often, the middle meningeal artery ruptures. A subdural hematoma is a collection of blood under the dura mater. It occurs, most often, when the veins running from the surface of the brain to the venous sinuses are damaged. An intracerebral hematoma is formed when blood vessels are damaged in areas of contusion and crushing of the brain. Clinic: First, compensation for compression of the brain occurs due to the displacement of cerebrospinal fluid from the ventricles and subarachnoid fissures of the brain. This is manifested by an asymptomatic period after the injury - the so-called “lucid interval”. Brain dislocation is manifested by: paresis of the limbs (mono- or hemiparesis) on the side opposite to the hematoma; dilation of the pupil on the side of the hematoma; bradycardia; epileptic seizures. If the victim has a combination of any three of the listed signs (for example, “light gap”, bradycardia, focal epileptic seizure), the probability of diagnosing an intracranial hematoma reaches 90%. INTRACRANIAL HEMATOMA
Brain contusions in 20–35% of cases are accompanied by fractures of the bones of the vault and base of the skull. Fractures of the bones of the skull vault are open (the soft tissue in the area of the bone fracture is damaged); closed (soft tissues are not damaged); penetrating (with damage to the dura mater); non-penetrating (dura mater remains intact). Fractures of the skull bones
Clinical manifestations of fractures of the base of the skull Fracture of the anterior cranial fossa Fracture of the middle cranial fossa Fracture of the posterior cranial fossa Symptom of “glasses” - hemorrhage into the paraorbital tissue, which appears several hours or days after the injury Nasal liquorrhea - leakage of cerebrospinal fluid from the nose. To detect the presence of cerebrospinal fluid in bloody fluid, the symptom of a “blurring spot” on a gauze napkin is used; bleeding and cerebrospinal fluid leakage from the ear; on the side of the fracture, the functions of the vestibulocochlear and facial nerves are lost (deafness, paresis of facial muscles); hemorrhage under the temporalis muscle. Hematoma under the aponeurosis behind the mastoid process.
METHODS OF DIAGNOSIS OF TBI Clinical examination Neurological examination Analysis of complaints and medical history: nature of head injury, duration of loss of consciousness, damage to soft tissues of the head, skull bones, etc. Level of consciousness - assessment of the patient’s response to a call, painful stimuli; Assessment of pupil size and symmetry; Presence of symptoms of meningeal irritation, Presence of neurological focal symptoms, CP, Echoencephaloscopy. A consultation with a neurosurgeon is possible.
Quantitative assessment of disturbances of consciousness (Glasgow Coma Scale) Eye opening Scores Speech Points Movements on command 6 Spontaneous speech 5 Localization of painful stimuli 5 Spontaneous opening of eyes 4 Individual phrases 4 Withdrawal of a limb in response to pain 4 Opening to sound 3 Individual words 3 Pathological flexion movements 3 Opening for pain 2 Indistinct muttering 2 Pathological extension movements 2 Lack of reaction 1 Lack of speech 1 Lack of motor reactions
3 -7 points - severe traumatic brain injury. 8 -12 points – moderate traumatic brain injury. 13 -15 points - mild traumatic brain injury. Assessment of brain injury severity using the Glasgow Coma Scale
All patients with traumatic brain injury are subject to hospitalization in medical institutions. Patients with concussion and brain contusions of all degrees are treated conservatively. Cases of brain compression require emergency surgery. TREATMENT OF TRANO BRAIN INJURY
Conservative therapy Mild traumatic brain injury Bed rest Taking medications aimed at eliminating cerebral, focal and autonomic disorders, normalizing sleep (analgesics, antihistamines, sleeping pills). Moderate traumatic brain injury Therapeutic agents are added: Neurovegetative blockade with lytic mixtures (droperidol, aminazine, diphenhydramine). Restoring cerebral microcirculation (Cavinton, aminophylline). At the prehospital stage, first of all, it is necessary to restore the patency of the upper respiratory tract: clear the oral cavity, nasopharynx of mucus, saliva, vomit, using a mouth dilator, tongue depressor. In cases of severe respiratory disorders, it is necessary to provide ventilation of the lungs in any way (mouth-to-mouth breathing mouth", "mouth to nose"). Patients are indicated for urgent tracheal intubation, and if it is impossible, a tracheostomy is performed.
Artificial ventilation. Medicinal agents are added: Barbiturates and sodium hydroxybutyrate are used as antihypoxants. Constant neurovegetative blockade with lytic mixtures. Regular sanitation of the tracheo-bronchial tree Parenteral, and after 5-8 days - enteral nutrition of patients through a tube. IN THE HOSPITAL
TBI IN CHILDREN Traumatic brain injury in children is one of the important problems of pediatric neurology and ranks first among injuries requiring hospitalization. Causes of trauma to the skull and brain: in infancy - a fall from a small height (from a bed, sofa, table, from a stroller, etc.), often a child falling from the hands of adults. children of middle and high school age - falls from a height (3rd -5th floor), injuries received during outdoor games, as well as in road accidents, predominate. The severity of the child’s general condition and the clinical course of MT in children depends on: 1 the mechanism and the force of influence. 2 localization and nature of damage. Differences in the clinical course of TBI in children are due to the anatomical and physiological characteristics of childhood: incompleteness of the process of ossification of the skull, immaturity of brain tissue, lability of the vascular system
Already a few hours after a mild brain injury, it is not uncommon for there to be no significant neurological symptoms at the time of examination. very rare loss of consciousness at the time of injury in young children, and in older children it occurs in 57% of cases, vagueness and therefore subjectivity in the interpretation of the neurological picture, transience of neurological symptoms, predominance of cerebral symptoms over focal ones, absence of meningeal symptoms in young children with subarachnoid hemorrhages, the relative rarity of intracranial hematomas, cerebral edema more often than in adults, good regression of neurological symptoms. Features of the clinical course of brain injury in childhood
Headaches Increased fatigue, decreased performance, impaired concentration Disturbances in the psycho-emotional sphere (psycho-emotional instability, sleep disturbance, fear, hyperdynamic syndrome) In severe cases, the development of post-traumatic epilepsy and paralytic syndromes is possible. Typically, such consequences are associated with severe traumatic brain injury, but they can also occur after a seemingly mild injury. . In the long-term post-traumatic period, children retain and sometimes increase vegetative lability, memory decreases, academic performance deteriorates, and behavior is disrupted. An important condition for preventing serious complications and ensuring the fastest possible recovery is the correct management of the acute post-traumatic period. Consequences of TBI in children
Provide rest, lay the child down, apply a cold vessel to the site of the bruise; call a doctor or “emergency”; carefully monitor the child; even if the child is in good condition, do not refuse the doctor’s offers to examine him or hospitalize him, at least for a while, in order to clarify the degree of brain damage - concussion, compression or bruise. The basic rule for treating children with brain injury is strict bed rest. For mild brain injury, bed rest lasts up to 10-14 days. Compliance with restrictions on physical activity prevents the development of long-term consequences of traumatic brain injury. For a month after a mild brain injury, the child should not attend a nursery, kindergarten, or school. After a concussion, schoolchildren are exempted from physical education for 1-2 months. The question of its volume and necessary medications is decided by the attending physician. Parents should be aware that after suffering a traumatic brain injury of any severity, long-term consequences may occur. So, after six months to a year, and sometimes later, headaches, sleep disturbances, memory loss, and epileptic seizures may appear. Any deviations from the normal state of the child in the coming years after the injury require consultation with a neurologist and a thorough examination. Typically, after a traumatic brain injury, the doctor actively monitors the child. So, after suffering a concussion, a child should visit a neurologist several times during the year; in case of a brain contusion, such observation lasts two years. If the consequences of injury are identified, patients are observed and treated for many years. Actions of parents in case of head injuries in children.
Traumatic brain injury is a complex of contact injuries (soft tissues of the face and head, skull bones and facial skeleton) and intracranial injuries (damage to the substance of the brain and its membranes), having a single mechanism and age of formation.
Classification Based on the severity of the injury, a distinction is made between mild, moderate and severe TBI. The Glasgow Coma Scale is used to determine severity. In this case, the patient receives from 3 to 15 points depending on the level of impairment of consciousness, which is assessed by eye opening, speech and motor reactions to stimuli.
Glasgow Coma Scale Eye opening Voluntary 4 points – As a reaction to a verbal stimulus 3 points – As a reaction to painful stimulation 2 points – Absent 1 point Speech reaction – The patient is oriented, quick and correct answer to the question asked 5 points – The patient is disoriented, confused speech 4 points – Verbal hash, the answer in meaning does not correspond to the question 3 points – Inarticulate sounds in response to the question asked 2 points – Lack of speech 1 point Motor reaction – Performing movements on command 6 points – Purposeful movement in response to painful stimulation (repulsion) 5 points – Withdrawal of a limb in response to painful stimulation 4 points – Pathological flexion in response to painful stimulation 3 points – Pathological extension in response to painful stimulation 2 points – Lack of movement 1 point
Interpretation of results – 15 points clear consciousness. – points moderate stun. – 1211 points deep stun. – 108 points sopor. – 7-6 points moderate coma. – 5-4 points deep coma. – 3 points extreme coma, brain death.
Clinical forms of TBI Concussion Brain contusion Diffuse axonal damage. Compression of the brain Intracranial hemorrhage (hemorrhage in the cranial cavity: Subarachnoid hemorrhage, Subdural hematoma, Epidural hematoma)
Concussion Concussion is a mild form of traumatic brain injury with short-term loss of consciousness (acute short-term impairment of brain function). Pathomorphological changes can be detected only at the cellular and subcellular levels. Clinic: possible loss of consciousness lasting up to 5 minutes. After regaining consciousness, patients may complain of headache, dizziness, nausea, often vomiting, tinnitus, sweating, and sleep disturbances. Vital functions without significant deviations. In the neurological status, transient microsymptoms can be noted (Babinski reflex, nystagmus, transient anisoreflexia). The general situation usually improves during the first, or less often the second, days after the injury.
Brain contusion Brain contusion (lat. contusio cerebri) is a traumatic brain injury in which the brain tissue is directly damaged, always accompanied by the presence of a focus of necrosis of the nervous tissue. Most often, lesions are located in the frontal, temporal and occipital lobes. Damage caused by trauma can be either unilateral or bilateral. Brain contusions are classified into mild, moderate and severe severity depending on the depth and duration of loss of consciousness.
A mild brain contusion is characterized by a short loss of consciousness after the injury (from several to tens of minutes). After a bruise, patients complain of headache, dizziness, nausea, and vomiting. Sometimes moderate bradycardia or tachycardia occurs, and arterial hypertension occurs. Body temperature is normal. Fractures of the calvarial bones and subarachnoid hemorrhage are possible. Moderate brain contusion is characterized by a longer loss of consciousness after injury (from several tens of minutes to several hours). After a bruise, patients complain of a severe headache and repeated vomiting. Mental disorders may occur. Bradycardia or tachycardia, increased blood pressure, and tachypnea occur. Meningeal symptoms are often prominent. Fractures of the calvarial bones and subarachnoid hemorrhage are possible. Cerebrospinal fluid with a pronounced admixture of blood. Severe brain contusion is characterized by prolonged loss of consciousness after injury (from several hours to several weeks). Motor excitement is usually pronounced. There is a dominance of stem neurological symptoms (multiple nystagmus, swallowing disorders, bilateral mydriasis or miosis). Paresis of the limbs may be detected. Meningeal symptoms are often prominent. Fractures of the calvarial bones and massive subarachnoid hemorrhage are possible. Severe brain contusions are often fatal.
Diffuse axonal brain injury Diffuse axonal brain injury (DAB) is a common type of traumatic brain injury in which sudden acceleration or deceleration of the head, for example, at the time of an accident, leads to tension and rupture of axons. Other, less common causes of DAP include falls, blows during a fight or beating, and in young children, axonal damage is noted in “shaking syndrome.” With diffuse axonal damage to the brain, microscopic small focal hemorrhages are detected in the corpus callosum, centrum semiovale, and upper parts of the brain stem. Clinically, it manifests itself as a prolonged coma, which in most cases turns into a vegetative state. The latter is characterized by the absence of cortical activity and lasts for months and years.
Brain compression Brain compression (CBC) is a progressive pathological process in the cranial cavity that occurs as a result of trauma (intracranial hematomas, subdural hygromas, areas of contusion or crushing, depressed fractures, pneumocephalus) leading to filling the capacity of the reserve spaces of the skull and depletion of compensatory mechanisms, to dislocation and/or infringement of the brain stem with the development of a life-threatening condition. Compression of the brain is observed in 35% of victims with traumatic brain injury. In recent years, compression of the brain has been positioned as a clinical form of traumatic brain injury.
Clinical picture Depending on the severity of the injury and other factors that led to compression of the brain, the increase in symptoms can be rapid (immediately after the injury) or delayed in time. Symptoms consist of: general cerebral (various types of disturbances of consciousness, headache, repeated vomiting, psychomotor agitation); focal (appearance/deepening of hemiparesis, unilateral mydriasis, partial epileptic seizures); stem symptoms (appearance/deepening of bradycardia, increased blood pressure, limitation of upward gaze, tonic spontaneous nystagmus, bilateral pathological signs);
Intracranial hemorrhage Intracranial hemorrhage is hemorrhage in the cranial cavity. It is a serious pathology that requires emergency medical care, since blood spilling into the cranial cavity causes an increase in intracranial pressure, which can lead to damage to nervous tissue, disruption of its blood supply and dislocation of brain structures (with the risk of wedging into the foramen magnum). Intracranial hemorrhages are conventionally divided into intra-axial and extra-axial. Hemorrhage refers to local brain injury (that is, damage to the brain that is not diffuse). Based on size, hematomas are classified into small (up to 50 ml), medium volume (ml) and large (more than 100 ml).
Intra-axial hemorrhage Intra-axial hemorrhage is hemorrhage within the brain. This category includes intraparenchymal hemorrhage (bleeding into brain tissue) and intraventricular hemorrhage (bleeding into the ventricular system). Intra-axial hemorrhages are more dangerous and less treatable than extra-axial hemorrhages.
Epidural hematoma Epidural hematoma is a traumatic hematoma between the dura mater (the most superficial) and the skull. May be caused by rupture of an artery, usually the middle meningeal artery. This type of hemorrhage is extremely dangerous due to the flow of blood from the arterial system under high pressure, which causes a rapid (within minutes, hours) increase in intracranial pressure. However, this type of hemorrhage is the least common and occurs in 1% to 3% of traumatic brain injury cases. During epidural hematomas, there is a period of loss of consciousness, which is replaced by a “light interval”, after which a sharp deterioration of the condition occurs (vomiting, anxiety, impaired consciousness). – CT scan of the brain demonstrates a superficial biconcave hematoma.
Subdural hematoma A subdural hematoma develops when the bridging veins rupture in the subdural space between the dura mater and the arachnoid mater; its volume increases over several hours. – A CT scan of the brain reveals a superficial hematoma of a concave (crescent) shape. – If there is significant compression of the brain, a craniotomy with removal of the hematoma is indicated. Compression of the brain is accompanied by dislocation and secondary ischemia, focal (corresponding to localization) and general cerebral symptoms.
Subarachnoid hemorrhage Subarachnoid hemorrhage develops between the arachnoid and pia mater in the subarachnoid space. Like intracerebral hemorrhage, it can be caused by both trauma and damage to a vessel (in the area of an aneurysm or arteriovenous malformation). – Classic symptoms of subarachnoid hemorrhage are acute headache (resembling a “blow to the head”), nausea, repeated vomiting, and loss of consciousness often occurs. This type of hemorrhage requires immediate consultation with a neurosurgeon, sometimes with emergency surgery.
Treatment of TBI If there is an episode with loss of consciousness, the patient, regardless of his current condition, needs to be transported to a hospital. If possible, collect anamnesis and clarify the nature of the injury from the victim or those accompanying them. The method of choice for this type of injury is computed tomography. The main goal of treatment is to prevent damage to brain tissue, and as a result maintain normal intracranial pressure and protect the cerebral cortex from hypoxia. In some cases, trepanations are performed for this purpose to drain intracranial hematomas. In the absence of bleeding into the cranial cavity, patients are usually treated with conservative therapy.
