Cerebral edema of the brain

Craniocerebral trauma can cause structural disturbances of various types. Structural changes can be macro- or microscopic, depending on the mechanism of injury and the strength of the effect.

A patient with a less severe traumatic brain injurycan not have large structural damage. Symptoms of craniocerebral injury vary widely in severity and consequences. Damage is usually divided into open and closed.

To open craniocerebral injuries includedamage that penetrates through the scalp and the skull (and usually the dura mater and brain tissue). Open lesions are observed in gunshot wounds or injuries inflicted by sharp objects, but fractures of the skull with the wound of the tissues covering it as a result of the force exposure by a heavy blunt object are also considered to be open.

Closed craniocerebral trauma usuallyarise when the head strikes against an object or with a sudden shaking, which leads to an instant acceleration and slowing down of the brain's movement in the cranial cavity. Acceleration and deceleration can damage the brain tissue at the site of a direct impact or in the opposite zone (shock), and diffusely. Frontal and temporal lobes suffer most often. Possible tears or detachments of nerve fibers, blood vessels, or both. Damaged vessels become excessively permeable, which leads to the formation of zones of injury, intracerebral or subarachnoid hemorrhages. as well as hematomas (epidural and subdural).

Concussion is defined as posttraumatica temporary and reversible change in the level of consciousness (for example, loss of consciousness or memory), lasting from a few seconds and minutes to a conditionally determined period of 6 hours in the absence of focal neurological symptoms. Traumatic edema often increases intracranial pressure (ICP), which leads to a variety of clinical manifestations. The WCT usually underlies the so-called baby shaking syndrome.

Contusion (concussion) of the brain is possible both with open(including penetrating), and with closed damages. A pathological condition can disrupt a wide range of brain functions, depending on the size and location of the focus. Large bruises can cause extensive brain swelling and a sharp increase in intraocular pressure.

Hematomas (blood clots in the brain substance oraround it) are possible both with penetrating and with closed damages; they can be epidural, subdural and intracerebral. Subarachnoid hemorrhage (SAH) is characteristic of craniocerebral trauma.

Subdural hematoma is the accumulation of blood betweensolid brains and arachnoid shells. Acute subdural hematomas are often caused by the destruction of the veins of the brain or its cortex, or by the rupture of communicative veins between the cortex and the sinuses of the dura mater, most often occurring after falls and auto accident. As a result of compression of brain tissue with hematoma, edema development may occur with an increase in intra-arterial pressure, the manifestations of which are different. Mortality and complications after hematomas are significant.

Symptoms of chronic subdural hematoma mayappear gradually, within a few weeks after the injury. Often occur in the elderly (especially those who take antithrombocytic drugs and anticoagulants), who may find the head injury insignificant and even forget about what happened. Unlike acute subdural hematomas, edema and increased intracranial pressure for chronic hematomas are not characteristic.

Epidural hematomas (blood accumulation betweenbones of the skull and dura mater) are less common subdural. Epidural hematoma is usually caused by arterial bleeding, classically due to the rupture of the middle meningeal artery in fractures of the temporal bone. Without emergency intervention, the condition of a patient with a large or arterial epidural hematoma can quickly deteriorate and he may die. Small, venous epidural hematomas are rare, mortality is not high.

Intracerebral hematomas (accumulation of blood in thebrain tissue) are often a consequence of the progression of the injury, so clinically the boundary between the bruise and intracranial hematoma is not clearly defined. Subsequently, increased intraocular pressure, herniation, functional failure of the brain stem, especially with hematomas in the temporal lobes or in the cerebellum.

Penetrating damage, by definition,are accompanied by fractures. However, with closed craniocerebral trauma, fractures of the skull bones are possible, which are divided into linear, dented and comminuted. Although severe and even fatal craniocerebral injury is possible without fractures, their presence indicates a significant impact force. Fractures in patients with diffuse traumatic brain injury indicate a high risk of intracranial lesions. Fractures with a local craniocerebral trauma (for example, a small object hit), in contrast, do not necessarily indicate a high risk of intracranial lesions. A simple linear fracture is also usually not associated with a high risk unless accompanied by neurologic symptoms or if it does not occur in the infant.

With depressed fractures, the risk of rupture of the dura mater and / or brain tissue is greatest.

If a fracture of the temporal bone crosses the zonepassage of the middle meningeal artery, it is very likely the development of epidural hematoma. Fractures passing through any of the large sinuses of the dura mater can cause massive bleeding and the formation of a venous epidural or subdural hematoma. Fractures passing through the carotid can lead to rupture of the carotid artery.

The bones of the occiput and the base of the skull are very thick andstrong, and their fractures indicate a high-intensity external impact. Fractures of the base of the skull passing through the stony part of the temporal bone, often damage the structure of the external and internal ear, can disrupt the function of the facial, pre-door, cochlear and pre-nerve nerves.

In children, it is possible to infringe the meninges in a linear fracture of the skull with the subsequent development of leptomeningeal cysts and an increase in the primary fracture (a "growing" fracture).

With a direct injury (for example, stroke, injury), the function of the brain can be disturbed immediately. Soon after the initial injury, a cascade of processes may begin, leading to further damage.

Any craniocerebral injury can cause swellingdamaged tissue. The volume of the skull is fixed by its bones and is almost entirely occupied by incompressible cerebrospinal fluid (CSF) and a slightly compressible tissue of the brain; in connection with this, any increase in volume due to edema, bleeding or bruising does not have a free space for this and inevitably leads to an increase in intra-arterial pressure. The cerebral blood flow is proportional to the level of cerebral perfusion pressure (MTD), which is the difference between mean arterial pressure (SBP) and mean intraocular pressure. Thus, as the intracranial pressure increases (or the SBP decreases), the MTD decreases and when it falls below 50 mm Hg. begins ischemia of the brain. This mechanism can lead to ischemia at the local level, when pressure as a result of local edema or hematomas worsen cerebral blood flow in the area of ​​injury. Ischemia and edema can provoke the release of stimulating neurotransmitters and free radicals, which further aggravate edema and increase internal blood pressure. Systemic complications of trauma (eg, arterial hypotension, hypoxia) can also contribute to the formation of cerebral ischemia, which is often called a secondary cerebral stroke.

Excessive internal pressure in the beginningleads to a global impairment of brain function. If the intraocervical pressure does not decrease, it can lead to the destruction of brain tissue in the large occipital foramen and under the cerebellar nest with the formation of cerebral hernias, which significantly increases the risk of complications and death. In addition, if the intra-arterial pressure is compared with SBP, the MTD becomes zero, which leads to complete cerebral ischemia, which quickly leads to brain death. The absence of cerebral blood flow can be used as one of the criteria for brain death.