What can be swelling of the brain

Cerebral edema (OGM) is a pathologicala disorder characterized by excessive accumulation of fluid in the intercellular brain space or inside cells, which leads to an increase in brain size and is clinically manifested by the syndrome of intracranial hypertension. With edema of the brain, accumulation of non-extracellular fluid rather than water is observed more often, and water inside cells, primarily glial ones. Therefore, this deviation is often referred to as swelling of the brain.

Quite often, the initial development of edemaoccurs in limited areas of the brain, and eventually spreads to more extensive areas. It arises as a nonspecific protective reaction to the effects of any damaging factors (hypoxia, trauma, intoxication), most often associated with pathologies characterized by impairment of the nervous system. In the absence of timely treatment, OCM can cause serious violations and even death. Edema of the brain is a secondary symptomatic manifestation. There are generalized and local (perifocal, local) forms of lesions.

The development of cerebral edema can beprovoked by a craniocerebral trauma, embolism of cerebral vessels, intracranial hemorrhage, brain tumors. The cause of OCM development can also be pathologies leading to acidosis, cerebral hypoxia, disorders of liquorodynamics and cerebral blood flow, changes in hydrostatic and colloid osmotic pressure and acid-base state.

Depending on the characteristics of pathophysiological mechanisms, five types of OCM are distinguished.

The most common is the vasogenictype, the development of which occurs when the work of the blood-brain barrier is violated, which entails an increase in the hydration of glia. As the most common reasons for the development of this form of abnormality can be noted metabolic disturbances of transport systems of the endothelium, hypercapnia, hyperthermia, arterial hypertension, neovascularization of the tumor bed.

When the channels of the outflow of liquor overlaphydrocephalic form of OGM. The main causes can be noted hemorrhages in the ventricular system of the brain, inflammatory processes, significant intracranial processes that promote brain deformation.

The osmotic form of OGM develops as a result ofdisorders of osmotic gradients of intravascular and intracellular sectors in the absence of damage to the blood-brain barrier. The main causes of this form of deviation are: the load inside the veins with hypo-osmolar solutions, hyperproduction of vasopressin, polydipsia, hypervolemia, inadequate hemodialysis.

Ischemic or reperfusion edema of the headthe brain is characterized by the accumulation of intracellular fluid as a result of the blockade of Na + K + - pump, hypoergosis and transmineralization. As the main causes of development, we can note hypoxia of various origins, hyperammonemia, postischemic reperfusion, hypoglycemia. The cytotoxic form of OGM develops as a result of blockade of the mitochondrial respiratory chain. The main causes are viral infections, poisoning with cyanides, carbon monoxide, the products of decomposition of hemoglobin. Most often, several types of brain edema are combined. For example, as a result of a traumatic brain injury, the vasogenic form of edema first develops, to which cytotoxic and ischemic is subsequently attached. By itself, cerebral edema is a secondary symptom of the underlying disease.

With edema of the brain can be identifiedthe following mechanisms for the development of its violations. Gradually there is an increase in brain volumes, which is limited by the size of the intracranial space. In this case, there are phenomena of mass effect. As a result, secondary damage develops in the form of compression of the brain. There is an increase in intracranial pressure, a decrease in cerebral perfusion pressure (normal difference between ICP and mean systolic blood pressure is 75-80 mmHg). As a result, cerebral ischemia develops, that is, cerebral circulation is impaired. Metabolism of brain tissue changes to an anaerobic type.

It is known that in the process of origin and developmentedema of the brain a certain role is played by vascular, circulatory and tissue factors. The circulatory factor consists of two links. As a result of the expansion of the cerebral arteries and the increase in arterial pressure, there is an increase in the pressure in the capillaries, from which the filtration of water into the intercellular space begins, resulting in damage to the tissue elements. The second link is due to the lack of blood supply to the brain, which entails damage to the tissue elements and the appearance of a propensity to accumulate water in them. Vascular factor is represented by a violation of the permeability of blood vessels, which causes individual components of blood plasma and protein to penetrate the space of the brain tissue. This leads to an increase in osmolarity of the intercellular fluid and damage to cell membranes. In turn, damage to the cytoplasm of neurons and cell membranes belongs to the tissue factor of the pathogenesis of OGM.

Depending on the degree of prevalence of cerebral edema, there is a shared hemispheric, trifocal, local, and diffuse form.

Cerebral edema is not characterizedby any specific clinical manifestations, which differ significantly from the symptoms of the underlying disease. In most cases, with the development of cerebral edema as a result of the brain injury, the involvement of the brain stem into the pathological process is observed. Progressive edema of the brain stem, in the first place, is characterized by an increase in the diencephalic syndrome, which manifests itself in the form of developing hyperthermia, changes in the respiratory rhythm according to the diencephalic type, increased respiration, increased blood pressure, and a pulse rate of 120-150 beats per minute. In some cases, a Weiss-Edelman symptom (the appearance of Babinski's symptom during extension of the knee joint) is observed.

Cerebral edema is characterized, in the first placeturn, cerebral syndrome, which develops as a result of increased intracranial pressure. The patient has a bursting paroxysmal headache, against which vomiting and various changes in the performance of the cardiovascular system may appear. There is a disturbance of consciousness, psychomotor agitation with the subsequent progression of the symptomatology. Stagnant nipples of the optic nerves often arise. With OCM, a common symptom of a remitting-progredient character is usually observed.

You can also highlight the syndrome rostrokaudalnogodiffuse growth of neurological symptoms, the clinical manifestations of which depend on the degree of involvement of various brain structures in the pathological process.

In addition, with OCM there is a syndromedislocation of individual brain structures. Due to the development of edema and dislocation, there are corresponding focal symptoms. As the basic it is possible to allocate the stem symptoms accompanied by defeat of oculomotor nerves. The compression of the posterior cerebral artery can be accompanied by homonymous hemianopsia. The pronounced dislocation of the brain is accompanied by bradycardia, decerebral rigidity, dysphagia, and so on. There may be sudden vomiting, stiff neck, sometimes stopping breathing.

Diagnostic procedures for suspected edemathe brain is usually determined by clinical manifestations. It should be borne in mind that the initial stages of development of OCM can be asymptomatic. At this stage, the examination of the fundus, in which stagnation of the optic discs is observed, can reveal the deviation. Neurological manifestations of brain edema are primarily characterized by a violation of consciousness in the form of stunning, delirium, sopor or coma. With the progression of the edema, impaired consciousness also increases. To determine the extent of this violation, the Glasgow coma scale is often used. In addition, it is important to study the movement of eyeballs and oculovestibular reactions, reactivity and pupil type, the nature of breathing, motor reactions of skeletal muscles. Of great importance are the results of nuclear magnetic resonance imaging, which allows to identify foci of hyperhydration of the brain substance, change in the size of basal subarachnoidal cisterns and ventricles. Also as diagnostic techniques can be noted computer / magnetic resonance imaging and neurosonography (assigned to children up to one year). Additional information can be obtained during electroencephalography, echoencephalography, pneumo-encephalography, brain scanning with the help of radioactive isotopes, cerebral angiography. Conducting differential diagnosis is necessary with pathologies accompanied by coma and convulsive syndrome (eg, thromboembolism of cerebral vessels, traumatic brain damage, epileptic status, infection, metabolic disorders).

When treating cerebral edema is importanttimely and accurate diagnosis and determination of the causes of deviation. As the main goals of intensive care, it is possible to note the elimination of the underlying disease that caused the cerebral edema; treatment of disorders of vital functions (cardiovascular system and respiration); decreased intracranial pressure; pathogenetic treatment, whose goal is to normalize perfusion pressure, eliminate brain hypoxia and stabilize water-electrolyte metabolism; symptomatic therapy aimed at eliminating symptomatic manifestations (hyperthermia, convulsive syndrome). Also, antibiotics are prescribed for preventive purposes, somatic disorders are corrected, adequate parenteral nutrition is prescribed.

All treatment procedures can be divided intogeneral and specific. General measures include correction of metabolic processes, respiratory disorders and other homeostatic systems, normalization of peripheral and systemic hemodynamics. As specific measures, we can note correction of local disorders of hemo- and lymphodynamics, normalization of permeability of the vascular wall, therapy with diuretics. For cessation of edematous processes and their regression, corticosteroids and barbiturates are used. In some cases, surgical intervention can be administered, implying formulation CSF drainage when occlusive hydrocephalus, removal intracranial volume in abscess, contusions, hematoma.

The prognosis for edema of the brain is largely determinedadequacy of infusion therapy. A pathology of this type is dangerous for the patient's life, since it can lead to death, which most often occurs as a result of compression of vital stem cells (in children under two years old it does not occur). One of the options for developing OCM is posthypoxic encephalopathy with a decerebral or decortication syndrome. An important threat is the development of specific infectious complications in the form of encephalitis, meningitis and meningo-encephalitis.