The traumatic brain injury (TBI) is a physical damage to brain tissue that limits brain function temporarily or permanently. The diagnosis is clinically suspected and confirmed by imaging methods, mainly computed tomography (CT). The first treatment consists of a reliable airway and maintenance of breathing, oxygenation and blood pressure. Surgery is often required in patients with more severe injuries to place monitors, monitor the evaluation of intracranial pressure and control. These devices decompress z. As when the intracranial pressure is increased or remove intracranial hematomas. In the first days after the injury, it is important to ensure the maintenance of adequate cerebral blood flow and oxygen supply and preventing complications of an altered sensorium. Then, many patients require rehabilitation.

In the United States, as in much of the world, TBI is a common cause of death and disability. Among the causes of traffic accidents include (z. B. motorcycle accidents, collisions with pedestrians), falls (v. A. In old people and children), assaults and sports injuries. (Exact .: epidemiological data on frequency, severity and type of TBI in Germany there is not, however, n. D. Red. Estimates of 200-300 patients with SHT all severities per 100,000 inhabitants and year out.) (Sport-related concussion)

The traumatic brain injury (TBI) is a physical damage to brain tissue that limits brain function temporarily or permanently. The diagnosis is clinically suspected and confirmed by imaging methods, mainly computed tomography (CT). The first treatment consists of a reliable airway and maintenance of breathing, oxygenation and blood pressure. Surgery is often required in patients with more severe injuries to place monitors, monitor the evaluation of intracranial pressure and control. These devices decompress z. As when the intracranial pressure is increased or remove intracranial hematomas. In the first days after the injury, it is important to ensure the maintenance of adequate cerebral blood flow and oxygen supply and preventing complications of an altered sensorium. Then, many patients require rehabilitation. In the United States, as in much of the world, TBI is a common cause of death and disability. Among the causes of traffic accidents include (z. B. motorcycle accidents, collisions with pedestrians), falls (v. A. In old people and children), assaults and sports injuries. (Sport-related concussion) (. N. D Red .: Precise epidemiological data on frequency, severity and type of TBI in Germany, it does not exist. It is estimated 200-300 patients with SHT all severities per 100,000 inhabitants and year.) Pathology structural changes which are caused by head injury, may be greater or microscopically small, depending on the particular circumstances of the accident and the forces involved. Patients with less severe injuries may have no serious structural damage. Severity and impact of the clinical manifestations are highly variable. The injuries are usually divided “open” and “closed”. Open injuries penetrate the scalp and the skull (and usually also the meninges and the underlying brain tissue). Typically, they are formed by balls or sharp objects, but also a skull with overlying laceration due to severe blunt force is referred to as an open head injury. To closed injury occurs when hitting head is struck by an object or shaken violently, so that the brain is greatly accelerated and decelerated. The frontal and temporal lobe are particularly sensitive. As a result, the tissue at the site of action of force (coupling), on the opposite side (Contrecoup) or be damaged diffuse. Axons and / or vessels can be sheared or tear. Impaired blood vessels are leaky, which, intracerebral or subarachnoid hemorrhage and epidural or subdural hematoma resulting in effusions (see Table: Common types of craniocerebral trauma). Common types of craniocerebral trauma disorder Clinical Findings Diagnosis Acute subdural hematoma Typically acute neurological dysfunction, either focally, nonfokal or both for small hematoma, is a normal function possible CT: hyperdensity in subdural space, classic crescent Important: the degree of midline shift basilar skull fracture leakage of cerebrospinal fluid from the nose or ear blood behind the eardrum (Hämotympanum) or in the outer ear behind the ear ecchymosis (So-called Battle sign) or around the eye (raccoon eyes) CT: Generally visible brain contusion Stark varying degrees of neurological dysfunction or normal function CT: hyperdensity caused (by punctate hemorrhages of various sizes concussion Temporary changes in mental status such. As loss of consciousness or memory) via <6 h persistently If due to clinical criteria. CT: Rarely abnormal Chronic subdural hematoma worsened headache, drowsiness, confusion, sometimes with focal deficits or seizures CT: h Hypodensity in the subdural space (isodense anomaly during the subacute transition from hyperattenuating to hypodense) Diffuser Axonschaden loss of consciousness about> 6, but without focal deficits or motor gestures his If on the basis of clinical criteria. CT: Can initially be normal or small Hyperdensitäten (micro-bleeding) in the corpus callosum, semiovale Centrum, in the basal ganglia or brainstem show MRI: Often abnormal epidural headache, altered consciousness ipsilateral within hours, sometimes with a lucid interval herniation typically causes contralateral hemiparesis and pupil dilation CT: hyperdensity in the epidural space, classic lentikularförmig and located above the middle meningeal artery (temporal fossa) due to a temporary bone fracture subarachnoid hemorrhage Typically normal function Occasionally, acute neurological dysfunction CT: hyperdensity in the subarachnoid space on the surface of the brain, often sketched furrows concussion A concussion (sports-related concussion) is (as a temporary and reversible post-traumatic loss of consciousness for. B. consciousness or amnesia) defined, the seconds to minutes, and – by establishing arbitrary – lasts <6 hours. Gross structural brain lesions and severe neurological residues are not part of the concussion, although a temporary disability due to symptoms such as nausea, headache, dizziness, Gedächtnisstörungenund difficulties (postkommotionelles syndrome) can occur to concentrate, the auflöst.Hirnkontusionen after a few weeks, the brain contusion ( brain contusion) can arise and lead depending on the extent and the location of the contusion to a variety of impairments of the cerebral functions in open (and penetrating) or closed injury. Larger bruises cause cerebral edema and increased intracranial pressure (ICP). Bruises can relax in the hours and days after the initial injury and enlarge a neurological deterioration verursachen.Diffuser Axonschaden A diffuse Axonschaden arises as a result of rotating Dezelerationstraumas and consists in a generalized, extended disruption of axons and myelin sheaths. In some cases, a minor head injury can be the cause. Gross structural lesions are not typical of a diffuse Axonschaden, but often can be found in the CT (and the histopathological examination) small petechial hemorrhages in the white matter. The diffuse Axonschaden is sometimes clinically defined as loss of consciousness over 6 hours in the absence of specific focal lesion. The resulting from the breach edema often increases the intracranial pressure (ICP), which in various ways manifests (traumatic brain injury: pathophysiology). Typically, the diffuse Axonschaden is also the Shaken Baby Syndrome zugrunde.Hämatome hematoma (accumulation of blood in the brain or around the brain) may occur and go back to an epidural, subdural, or intracerebral hemorrhage in open or closed injury. Subarachnoid hemorrhage (SAH bleeding inside the Subarachnoidalraum- subarachnoid hemorrhage (SAH)) are common in traumatic brain injuries, although its appearance on CT is usually different from the aneurysmal SAH one. Subdural hematomas are accumulations of blood between the dura mater and the pia mater. Acute subdural hematoma caused by injury of cortical vein or veins avulsions from bridging between the cortex and the dural sinuses. They often occur in the context of head injuries from falls and car accidents. A compression of the brain by the hematoma and swelling of the brain due to edema or hyperemia (increased blood flow due to swollen blood vessels) can increase the ICP. If both occur these processes, the mortality and morbidity can be high. After a trauma, a chronic subdural hematoma can occur with a gradually over weeks developing symptoms. These hematomas encountered more frequently in alcoholics and elderly patients (particularly with concomitant use of anticoagulant drugs or those with brain atrophy). Elderly patients may regard as relatively trivial or even forget the head injury. Edema and increased ICP here are rare in contrast to acute subdural hematoma. Epiduralhämatome are accumulation of blood between the skull and the dura mater, which are less common than the subdural hematoma. Large or fast-spreading Epiduralhämoatome are usually triggered by an arterial bleeding, which typically results from a violation of the middle meningeal artery temporal at fracture of the Os. Without treatment, the condition of patients can deteriorate rapidly with arterial epidural hematoma and death. Small venous Epiduralhämatome are rarely fatal. Intracerebral hematomas are accumulations of blood in the brain itself. In the traumatic constellation they arise from a confluence of effusions. The exact point at which one or more bruising to a hematoma, is not well defined. Subsequently, an increase in ICP, a Hirnstammeinklemmung and a brain stem failure can adjust, especially in lesions in the temporal lobe or Kleinhirn.Schädelfrakturen By definition, one of the most penetrating injuries, the fracture. Closed injuries can also cause a skull fracture. A distinction between linear skull fracture, skull fracture and skull comminuted fracture. The presence of a fracture suggests that in case of injury was a strong force in the game. Although most patients with simple linear fractures without neurological impairment do not have a high risk of brain damage, have patients with fractures with neurologic influence an increased risk of intracranial hematomas. Fractures that pose special risks, including depressed fractures: These fractures often occur to crack the dura and / or brain damage. Fractures in which the temporal bone, the area of ??the middle meningeal artery crosses: these fractures the emergence of a Epiduralhämatoms is a risk. Fractures that run through one of the dural Hauptsinusse: These fractures significant bleeding with a venous or epi subdural hematoma can be triggered. Injured venous sinuses can cause thrombosis and stroke later. Fractures that affect the carotid canal: These fractures can lead to carotid dissection. Fractures of the occipital bone and skull base: These bones are thick and strong, so to speak fractures in these areas for a very severe trauma and a significant risk of brain injury. Skull base fractures that affect the petrous temporal, often also destroy the inner ear structures, thereby possibly also the Nn. facial and vestibulocochlear. Fractures in children: The meninges can become trapped in a linear skull fracture and to form a leptomeningeal cyst with an expanding fracture, a so-called "growing skull fracture," lead. The pathophysiology of brain function can immediately by a direct injury (z. B. accident, injury section) of the brain tissue to be affected. More damage is possible a short time later by the triggered by the initial injury events. A traumatic brain injury of any kind can lead to cerebral edema and decreased blood flow in the brain. The cranial cavity is fixed in size (defined by the skull bone) and filled with the incompressible cerebrospinal fluid and brain tissue. Thus, a swelling can expand by edema or intracranial hematoma nowhere and increases the ICP. The cerebral blood flow depends on the cerebral perfusion pressure (CPP), which represents the difference between the mean arterial pressure (MAP) and the mean ICP. Thus, when the ICP increases (or decreases MAD), the CPP increases. When the CPP drops below 50 mmHg, the brain can be ischemic. Ischemia and edema can cause various secondary damaging mechanisms such. As the release of excitatory neurotransmitters, intracellular calcium, free radicals and cytokines, leading to further cell damage, further edema and further increases in ICP. And systemic complications of trauma (eg. As hypotension, hypoxia) may contribute to cerebral ischemia and are referred to as "Sekundärinsulte". An excessive ICP causes global cerebral dysfunction. If an excessive ICP is left untreated, it can suppress the brain tissue through the tentorial or through the foramen magnum and a Hirnstammeinklemmung cause (entrapment of brain tissue.), Whereby the morbidity and mortality increased. To complete brain ischemia with rapid brain death occurs when the ICP has the same value as the MAD and the CPP goes to zero. A lack of cerebral blood flow is an objective evidence to determine brain death (brain death). Hyperemia and increased blood flow in the brain can result from shaking injuries in adolescents or children. The Second-impact syndrome is a rare and much-discussed disease, which is defined by a suddenly increased ICP and sometimes death. It is caused by a traumatic injury that lasts before the recovery from the previous minor head injury has occurred. This is attributed to a loss of autoregulation of cerebral blood flow, which leads to a vascular congestion, increased ICP and a herniation. Symptoms and complaints Initially, most patients lose a moderate or severe TBI awareness (usually for seconds or minutes), while it sometimes occurs in patients with minor injuries only to confusion or amnesia (amnesia is usually retrograde and leads to memory loss a period of seconds to a few hours before the injury). Small children are perhaps only slightly irritable. Some patients suffer seizures, often within the first hour or the first day. After these initial symptoms, patients can awake and be fully conscious, or consciousness and function are disrupted to varying degrees between slight confusion and stupor or coma. However, the duration of unconsciousness and the severity of Eingetrübtheit not correlate roughly with the severity of the injury, in a specific way. The Glaskow Coma Scale (GCS -see Table: Glasgow Coma Scale *) is a fast and reproducible tool in the early diagnosis, with the severity of TBI can be estimated. It is based on eye opening, verbal response and the best motor response. Lowest total value of 3 indicates a potentially fatal injury, especially in light Rigid both pupils and lack okulovestibularem reflex. Higher input values ??argue for greater recreational opportunities. By convention, the seriousness of head injuries is defined initially by the GCS: 14 or 15: light SHT 9-13 mittelgradiges SHT 3-8: severe TBI Clinical computer: Glasgow coma scale Glasgow Coma Scale * Evaluated region reaction points eye opening Spontaneous opening 4 Capable of verbal articulation 3 opening in response to pain caused to the limbs or chest legs 2 None 1 Verbal Oriented 5 Lost, but able to respond to questions 4 Inappropriate e answers to questions; not understanding words 3 Incomprehensible speech 2 No 1 motor obey commands 6 Responds to pain with purposeful movement 5 moves to of the pain back 4 Responds to pain with abnormal flexion (Dekortikationshaltung) 3 Responds to pain with abnormal (rigid) Extension (Dezerebrationsstarre) 2 None 1 * Combined values ??<8 are considered coma normally. Adapted from Teasdale G, Jennett B: Assessment of coma and impaired consciousness. A practical scale. Lancet 2: 81-84; 1974 predictions about the severity of a TBI and a forecast may be specified in the light of CT results and other factors. Some patients with an initially moderate TBI and some with an initial mild TBI still deteriorate. In infants and young children to apply the modified Glasgow Coma Scale for Children (see table: Modified Glasgow Coma Scale for infants and children). Since hypoxia and hypotension may reduce the GCS, the GCS-values ??determined according to the cardiopulmonary resuscitation the extent of brain damage more accurate than the values ??before resuscitation. Likewise Sedidativa and Paralytika can reduce the GCS values ??and should not be given before full neurological examination. Tips and risks delaying the use of sedatives and paralytic drugs by the end of the complete neurological examination, if possible. Modified Glasgow Coma Scale for infants and children Evaluated area Infants Children Value * eye opening open spontaneously, open spontaneously 4 opening in response to verbal stimuli open in response to verbal stimuli 3 Open only in response to pain No response Open only in response to pain 2 None 1 Verbal response reaction cooing and babbling Clear, logical 5 overwrought shouting Confused 4 Cries in response to pain episode right words moans 3 in response to pain unintelligible words or sounds nonspecific 2 No response No response 1 Motorized reaction † moves spontaneously and specifically obey commands 6 Takes place on contact back Isolated painful stimulus 5 rotates in response to pain away rotates in response to pain was gone 4 Responds to pain with Dekortikationshaltung (abnormal flexion) Responds to pain with Dekortikationshaltung (abnormal flexion) 3 Responds to pain with Dezerebrationsstarre (abnormal extension ) Reacts (on pain with Dezerebrationsstarre abnormal Extension) 2 No response No response 1 * A value ? 12 indicates a severe head injury. A value <8 indicates the need for intubation and mechanical ventilation. A value ? 6 refers to the need for a Überachung intracranial pressure. † If the patient is intubated, unconscious or too young to speak, provides the motor response the most important part of this evaluation. This area should be carefully checked. Adapted from Davis RJ, et al: Head and spinal cord injury. In: Textbook of Pediatric Intensive Care, ed. v. MC Rogers. Baltimore, Williams & Wilkins, 1987; James H, N Anas, Perkin RM: Brain Insults in Infants and Children. New York, Grune & Stratton, 1985; and Morray JP et al: Coma Scale for use in brain-injured children. Critical Care Medicine 12: 1018, 1984. Symptoms of certain types of TBI symptoms of different types of TBI may overlap considerably. Epiduralhämatome develop usually within minutes to several hours after the injury (the period without symptoms is the so-called lucid interval) and consist of increasing headache, reduced-consciousness and focal neurological deficits (z. B. hemiparesis). A pupil dilation with lack of reactivity to light usually indicates a herniation. Some patients lose consciousness and then have a vorübergehnde lucid phase gefolt by an increasing neurological deterioration. Most patients with subdural hematomas have an immediate loss of consciousness. Intracerebral hematoma and subdural hematomas can cause focal neurological deficits such as hemiparesis, progressive loss of consciousness, or both. A progressive loss of consciousness may be caused by anything that increases the ICP such. B. hematoma, edema, hyperemia. Increased ICP sometimes causes vomiting, but vomiting is nonspecific. A clearly increased ICP manifests itself as a rule in a combination of hypertension (usually with an increased pulse pressure), bradycardia and respiratory depression (Cushing's triad); breathing is usually slow and irregular. A severe diffuse brain injury or a greatly increased ICP can lead to Dekortikations- or Dezerebrationshaltung, both are considered unfavorable prognostic sign. Entrapment in tentorial notch (entrapment of brain tissue.) Can lead to coma, one or both wide and fixed pupil, hemiplegia (usually contralateral the light-rigid pupil) and lead to the so-called Cushing's triad. A base of the skull fracture may lead to leakage of cerebrospinal fluid from the nose (Rhinorhoe) or from the ear (otorrhea). Furthermore, the blood can accumulate behind the eardrum (Hämotympanum) or in the external auditory meatus when the tympanic membrane has ruptured. can bruising behind the ear (Battle's sign) or around the eyes (raccoon eyes or hematoma) can occur. The loss of smell and hearing occurs usually immediately, although these losses are sometimes not noticed until the patient regains consciousness. The facial nerve may be affected immediately or with a delay. Other skull fractures are sometimes, especially with injuries to the skull rind, as impression or Stufendeformität palpable. Allerdings kann auch eine Blutansammlung unter der Galea aponeurotica eine Stufendeformität vortäuschen. Chronische Subduralhämatome können sich mit zunehmenden tägliche Kopfschmerzen, fluktuierende Benommenheit oder Verwirrtheit manifestieren (die wie eine beginnende Demenz aussehen kann) sowie über eine leichte bis mäßige Hemiparese oder andere fokale neurologische Defizite.Langfristige Symptome Die Amnesie kann fortdauern, sowohl als retrograde als auch als anterograde Amnesie (d.h. für Ereignisse, die auf die Verletzung folgen). Das postkommotionelle Syndrom, das sich an eine mittelschwere bis schwere Gehirnerschütterung anschließen kann, umfasst Kopfschmerzen, Schwindel, Müdigkeit, Konzentrationsstörung, variable Amnesie, Depression, Apathie und Ängstlichkeit. Oft sind Geruchsinn (und somit auch der Geschmacksinn), manchmal das Hören und selten das Sehen verändert oder ausgefallen. Die Beschwerden klingen gewöhnlich spontan nach Wochen bis Monaten ab. Nach einem schweren, mittelgradigen und sogar leichten SHT können kognitive und neuropsychologische Defizite persistieren, besonders wenn eine erhebliche strukturelle Schädigung vorlag. Häufige Probleme sind dabei Amnesie, Verhaltensänderungen (z. B. Agitiertheit, Impulsivität, Enthemmung, Motivationsverlust), emotionale Labilität, Schlafstörungen und vermindertes intellektuelles Vermögen. Bei einigen Patienten kommt es zu spät

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