Craniocerebral injury principles of classification, features of the course post anoxic myoclonus

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post anoxic myoclonus


Craniocerebral injury.

Causes of TBI:

– household injury – 60%

– car accidents – 30%

– industrial, sports traumatism -10%

Clinical forms of CCT:

I.- mild: concussion of the GM, a bruise of an easy degree

– moderate severity: injury to the degree of severity, subacute and chronic compression of the GM

– severe: severe bruise, acute compression of the GM.

II. -isolated

Combined (combination of CTB with mechanical damage of other organs)

Combined (the impact of various traumatic factors – mechanical + thermal + chemical)

III.- closed

– open

– penetrating (taking into account the danger of inflammatory complications) – if the dura mater is damaged

Concussion GM (clinic): loss of consciousness from 1 to 15 minutes, headache, nausea, single vomiting, retrograde amnesia, radiography can reveal fractures of the bones of the skull.Post anoxic myoclonus the presence of a blood admixture in the LP-bruise of GM of the degree of severity and above.

GM’s bruises: this is a GM damage, has arisen. At the time of injury and accompanied by anatomic destruction of its substance with hemorrhages, ischemia, necrosis and regional edema.

Classification of GM contusions:

1) in terms of the volume of the dense part of the pathological spine, the difference is:

– shallow focal (the volume of a dense part up to 30 cubic centimeters)

-bound (the volume of the dense part is 30-50)

-distributed (the volume of the dense part is more than 50)

Separately selected:

– contusion of the cerebellum

– contusion of the brainstem

– diffuse axonal injury

Any traumatic characterization of 3 gram of symptoms:

post anoxic myoclonus

1 gr. Loss of consciousness (adults do not have TBI without losing consciousness)

2 g. General cerebral symptoms – headache, nausea, single-time vomiting-concussion, amnesia (congrade-simple, retrograde amnesia – concussion)

Concussion GM-functional damage GM neurons do not die.

When the GM is injured, an anatomical destruction of the GM substance takes place, an admixture of blood in the cerebrospinal fluid.

Clinic of a serious injury GM:

– loss of consciousness from 10 to 40 min

– retrograde amnesia up to 30 min

– severe cerebral symptoms

– mild focal symptomatology

– in 40-50% of patients with CT of GM – foci of posttraumatic hemangiopathic ischemia

– there is almost no focal symptomatology

The clinic of the GM moderate injury:

post anoxic myoclonus

– loss of consciousness from 10 minutes to 4 hours

– retrograde and anterograde amnesia

– severe cerebral symptoms

– moderate stem symptomatology

– hemorrhagic cerebrospinal fluid

– phenomena of edema of optic discs

– duration of the period of functional disorders -7-12 days

Clinic of a serious injury of GM:

– loss of consciousness from several hours to several weeks

– severe cerebral symptoms

– rough focal and meningeal symptoms

– severe stem symptomatology

– congestion of optic discs

Plan of examination with CCT:

– clinical neurologic examination

– general and biochemical analyzes of blood and urine

– blood test for alcohol and toxic profile

– X-ray of the skull and cervical spine

– ECHO – encephalography

– CT of GM

post anoxic myoclonus

– lumbar puncture (if the pink liquor is a bruise of the GM)

– EEG and AUC

– ophthalmoscopy

On MRI, you can not see fresh blood, with MRI fractures of the bones of the skull are seen very poorly, so you need to do CT.

At CT, the irradiation is small.

Fluorography 0.3 milzirta

Concussion requires anesthesia, antiemetic drugs, rest.

Pathogenesis of the injury of the GM:

– damage with CBT is divided into: primary and secondary

Factors of secondary damage: intracranial and extracranial (arterial hypotension, hypoxemia, hypercapnia, hyperthermia, hyponatremia, anemia, dvs-syndrome, hypo- and hyperglycemia).

Conditions of occurrence of WCT:

– trauma of braking – acceleration or angular rotation

– tight fit and fixation of the brainstem to the bones of the base of the skull

post anoxic myoclonus

The main symptoms of diffuse axonal lesion:

– a prolonged coma

– pronounced stem smptomatics

Principles of management of patients with bruises:

– dynamic control of neurological status

– dynamic control.

– control of intracranial hypertension

Indications for surgical treatment of brain contusions:

– presence of traumatic intracerebral hematoma, accompanying.

Mass effect

– pronounced dislocation of the brain in the presence of oppression of consciousness and gross neurologic deficit

– pronounced intracranial hypertension if it is impossible to conservatively correct (only in the presence of monitoring)

Mechanism of formation of intracranial hematomas:

– formation in the impact zone

– in the zone of a shock – basically subdural and 50% intracerebral hematomas

post anoxic myoclonus

The main clinical signs of intracranial hematomas are:

– loss of consciousness immediately after an injury

– a light period (the period when a person regains consciousness and then dies)

– repeated loss of consciousness

– bradycardia: cushing’s triad (hypertension, bradycardia, respiratory disorders)

Anisocoria

– contralateral hemiparesis (violation of movement on the opposite side)

The cerebellum is responsible for its side.

Epidural hematomas:

– more often meetings. For men

– localization in the temporal and parietal regions

– almost always localized. In the zone of bone fracture

– very rarely meetings. On the base of the skull

– have clear boundaries and less prevalence

Acute subdural hematomas – in contrast to epidural, subdural hematomas have less clear boundaries.Post anoxic myoclonus

Sources for the formation of acute subdural hematomas:

– vessels of the pia mater

– vessels of the cerebral cortex

-parasinus veins

– venous sinuses

Types of operation: open operation, application of the milling hole and drainage of the hematoma, removal through the trephination hole, fibrinolysis.

Mortality with intracranial hematomas:

– avg. Mortality – 39%

– with shkg up to 8 points -22.9%

– with shkg – 8 and less than -70% 3%

You talk and the person begins to fall asleep, gives short answers – stunning

If he does not speak, then to a pain stimulus or to open it.

If the pain stimulus is not reactive. – coma

It extends to the irritant with the hands – a moderate coma

Do not stir on any stimulus – paralytic.Midriasis

post anoxic myoclonus

Fractures of the bones of the arch and the base of the skull:

– on the mechanism of education: direct, indirect

– localization: fractures of the bones of the cranial vault, fractures of the base of the skull, fractures of bones

Battle symptom, raccoon’s eye

Anosmia and hyposmia

Liquorrhea (nasorrhea and otorrhoea) – leakage of liquor from the nose and ears

Hypacosis

Paraorbital emphysema

Complications of TBI: inflamed. And non-belligerent.

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Craniocerebral injury: principles of classification, features of the course of various forms of traumatic brain injury

• classification of craniocerebral trauma

I. Classification according to petit (1774). • commotio segrebri – concussion of the brain.Post anoxic myoclonus • sintusio segebri – brain contusion. • compression of cerebri – compression of the brain. P. Modern classification. • closed craniocerebral trauma – damage to the brain without compromising the integrity of the skin. • open craniocerebral trauma – damage to the head

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post anoxic myoclonus

• meningitis. Classification, features of the current, the principles of therapy

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• pathophysiological features that deserve attention in neurosurgical patients and patients with craniocerebral trauma

Spatial limited cranial cavity the volume of the cavity of the skull, surrounded by bones, is approximately constant.Post anoxic myoclonus increasing the volume of the contents of the cranium leads to compression of the brain and, at the same time, to relative changes in the existing ratio of the brain substance, the contents of blood vessels and cerebrospinal fluid. The consequence of the compression of the brain is drowsiness, which can

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Clinic. There are closed and open craniocerebral trauma. With a closed skull-brain injury, there is no violation of the integrity of the head cover or there are wounds of soft tissues without damage to the aponeurosis, or fracture of the bones of the cranial vault without damaging the aponeurosis and soft tissues. Damage, accompanied by wounds of the soft tissues of the head and aponeurosis, fractures of the base of the skull,

post anoxic myoclonus

• CRANIAL-BRAIN TRAUMA

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• craniocerebral injury

Craniocerebral trauma – a frequent form of pathology of the nervous system, often accompanied by pronounced changes in motor and mental functions. Craniocerebral injury is divided into closed and open. With open lesions, the integrity of the skin and skull bones is impaired.Post anoxic myoclonus the appearance of neurologic symptoms in various types of craniocerebral trauma is associated with the influence of mechanical

• craniocerebral injury

Clinical characteristics of cerebral trauma the urgency of treatment and diagnosis of craniocerebral trauma nowadays does not cause doubts: deterioration of living conditions, unemployment, growing crime, drug addiction increase criminal traumatism. Because of the increased consumption of alcohol and drugs, frequent overdoses (narcotic coma), it became more difficult to differentiate the traumatic brain injury

• complications of craniocerebral trauma

Complications of craniocerebral trauma can be early and late. Early traumatic meningitis, meningo-encephalitis, abscess, traumatic prolapse and protrusion of the brain, intra-cerebral and intracerebral hemorrhages.Post anoxic myoclonus by the late-traumatic arachnoiditis or arachnoencephalitis, parkinsonism, occlusive hydrocephalus, epilepsy, neuroses. Traumatic meningitis, mainly purulent,

• craniocerebral injury

Craniocerebral trauma can be the result of traffic accidents, falls, industrial, sports or domestic injuries (primary trauma), as well as a neurological or somatic disease (eg cardiogenic syncope or epilepsy) that causes the patient to fall (secondary trauma) . Head trauma can lead to soft tissue damage, fracture

• CRANIAL-BRAIN AND SPINAL INJURIES

L. X. Ropper (AN hopper) craniocerebral injuries are especially common in industrialized countries, with many ballroom injured in mature working age. To assess the medical and social significance of this problem, it should be pointed out that almost 10 million americans get head injuries every year and about 20% of them are so serious that they are accompanied by

post anoxic myoclonus

• craniocerebral injury

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• closed craniocerebral injury

There are three main forms of closed cranial brain damage: concussion, contusio and compression of the brain (compressio cerebri). This classification lasted more than 200 years and underwent only some unprincipled changes. Recently, in addition to the mentioned forms, the diffuse axonal lesion caused by the rotation of the head with a sharp

post anoxic myoclonus

• craniocerebral injury

TBI is a collective concept that includes damage to the skull covers (skin, aponeurosis, muscles, skeleton of the skull) and the contents of the cranium (brain membranes, brain substance, blood vessels, liquor-containing containers and liquor-conduction pathways). CCI can be closed, open non-penetrating, open penetrating, combined and combined. = closed CCT damage

• craniocerebral injury

In war zones and industrially developed countries with their extremely intensive traffic, head injuries occupy a huge share in the mortality structure of people under 45 years of age. In the clinical course of these injuries, the anatomical location of the lesion and the limited capacity for functional restoration of the brain tissue are of great importance.Post anoxic myoclonus thus, a necrosis with a volume of several cubic

• craniocerebral injury

Craniocerebral trauma is a collective concept that includes damage to the skull covers (see the standard of the wounds of the head) and the contents of the cranium – brain substances, cranial nerves, blood vessels, cerebrospinal fluid (cerebral vesicles) and liquid-conducting pathways. There are 3 types of CMT – concussion, bruise and compression of the brain. Д – ка: concussion