How does cerebral edema occur? Edema of the brain. The development of cerebral edema: what are the symptoms and how is it treated

Cerebral edema (CSE) is a non-specific reaction to the impact of various damaging factors (trauma, hypoxia, intoxication, etc.), which is expressed in excessive accumulation of fluid in the brain tissues and increased intracranial pressure. Being essentially a protective reaction, HMO, with untimely diagnosis and treatment, can become the main cause that determines the severity of the patient's condition and even death.

Etiology.

Cerebral edema occurs with traumatic brain injury (TBI), intracranial hemorrhage, cerebral embolism, brain tumors. In addition, various diseases and pathological conditions leading to cerebral hypoxia, acidosis, disorders of cerebral blood flow and liquorodynamics, changes in colloid osmotic and hydrostatic pressure and acid-base state can also lead to the development of BT.

Pathogenesis.

In the pathogenesis of cerebral edema, 4 main mechanisms are distinguished:

1) Cytotoxic. It is a consequence of the effects of toxins on brain cells, resulting in a breakdown of cellular metabolism and a violation of the transport of ions through cell membranes. The process is expressed in the loss of mainly potassium by the cell, and its replacement with sodium from the extracellular space. Under hypoxic conditions, pyruvic acid is reduced to lactic acid, which causes a violation of the enzyme systems responsible for removing sodium from the cell - a blockade of sodium pumps develops. A brain cell containing an increased amount of sodium begins to intensively accumulate water. The content of lactate above 6-8 mmol / l in the blood flowing from the brain indicates its edema. The cytotoxic form of edema is always generalized, spreads to all departments, including the stem ones, so signs of herniation may develop quite quickly (within a few hours). Occurs with poisoning, intoxication, ischemia.

2) Vasogenic. It develops as a result of damage to brain tissue with a violation of the blood-brain (BBB) ​​barrier. The following pathophysiological mechanisms underlie this mechanism for the development of cerebral edema: increased capillary permeability; increase in hydrostatic pressure in capillaries; accumulation of fluid in the interstitial space. The change in the permeability of the capillaries of the brain occurs as a result of damage to the cell membranes of the endothelium. Violation of the integrity of the endothelium is primary, due to direct injury, or secondary, due to the action of biologically active substances, such as bradykinin, histamine, arachidonic acid derivatives, hydroxyl radicals containing free oxygen. When the vessel wall is damaged, the blood plasma, together with the electrolytes and proteins contained in it, passes from the vascular bed to the perivascular zones of the brain. Plasmorrhagia, by increasing the oncotic pressure outside the vessel, increases the hydrophilicity of the brain. Most often observed with head injury, intracranial hemorrhage, etc.

3) Hydrostatic. It manifests itself with a change in the volume of brain tissue and a violation of the ratio of blood inflow and outflow. Due to obstruction of venous outflow, hydrostatic pressure increases at the level of the venous knee of the vascular system. In most cases, the cause is compression of large venous trunks by a developing tumor.

4) Osmotic. It is formed in violation of the normal small osmotic gradient between the osmolarity of the brain tissue (it is higher) and the osmolarity of the blood. It develops as a result of water intoxication of the central nervous system due to hyperosmolarity of the brain tissue. Occurs in metabolic encephalopathies (renal and liver failure, hyperglycemia, etc.).

Clinic.

There are several groups of children with a high risk of developing BT. These are, first of all, young children from 6 months to 2 years, especially with neurological pathology. Ecephalitic reactions and cerebral edema are also more often observed in children with an allergic predisposition.

In most cases, it is extremely difficult to differentiate the clinical signs of cerebral edema and the symptoms of the underlying pathological process. Beginning cerebral edema can be assumed if there is confidence that the primary focus is not progressing, and the patient develops and increases negative neurological symptoms (appearance of convulsive status and, against this background, depression of consciousness up to coma).

All symptoms of OGM can be divided into 3 groups:

symptoms characteristic of increased intracranial pressure (ICP);

diffuse increase in neurological symptoms;

dislocation of brain structures.

The clinical picture, due to an increase in ICP, has various manifestations depending on the rate of increase. An increase in ICP is usually accompanied by the following symptoms: headache, nausea and/or vomiting, drowsiness, and later seizures appear. Usually, convulsions that first appear are clonic or tonic-clonic in nature; they are characterized by comparative short duration and quite favorable outcome. With a long course of convulsions or their frequent repetition, the tonic component increases and the unconscious state worsens. An early objective symptom of an increase in ICP is plethora of veins and swelling of the optic discs. Simultaneously or somewhat later, radiological signs of intracranial hypertension appear: increased pattern of finger impressions, thinning of the bones of the arch.

With a rapid increase in ICP, the headache is bursting in nature, vomiting does not bring relief. Meningeal symptoms appear, tendon reflexes increase, oculomotor disorders occur, an increase in head circumference (up to the second year of life), bone mobility during palpation of the skull due to the divergence of its sutures, in infants - the opening of a previously closed large fontanel, convulsions.

The syndrome of diffuse increase in neurological symptoms reflects the gradual involvement of the cortical, then subcortical, and ultimately brain stem structures in the pathological process. With swelling of the cerebral hemispheres, consciousness is disturbed, and generalized, clonic convulsions appear. The involvement of subcortical and deep structures is accompanied by psychomotor agitation, hyperkinesis, the appearance of grasping and protective reflexes, and an increase in the tonic phase of epileptic paroxysms.

The dislocation of the brain structures is accompanied by the development of signs of wedging: the upper - the middle brain into the notch of the cerebellar tenon and the lower - with infringement in the foramen magnum (bulbar syndrome). The main symptoms of damage to the midbrain: loss of consciousness, unilateral pupil change, mydriasis, strabismus, spastic hemiparesis, often unilateral extensor muscle spasms. Acute bulbar syndrome indicates a preterminal increase in intracranial pressure, accompanied by a drop in blood pressure, a decrease in heart rate and a decrease in body temperature, muscle hypotension, areflexia, bilateral dilation of the pupils without reaction to light, intermittent bubbling breathing and then its complete stop.

Diagnostics.

According to the degree of accuracy, methods for diagnosing BT can be divided into reliable and auxiliary. Reliable methods include: computed tomography (CT), nuclear magnetic resonance (NMR) tomography and neurosonography in newborns and children under 1 year old.

The most important diagnostic method is CT, which, in addition to detecting intracranial hematomas and foci of contusions, allows visualizing the localization, extent and severity of cerebral edema, its dislocation, and also assessing the effect of therapeutic measures during repeated studies. NMR imaging complements CT, particularly in visualizing small structural changes in diffuse lesions. NMR tomography also makes it possible to differentiate various types of cerebral edema, and, consequently, to correctly build treatment tactics.

Ancillary methods include: electroencephalography (EEG), echoencephalography (Echo-EG), neuroophthalmoscopy, cerebral angiography, brain scan using radioactive isotopes, pneumoencephalography and X-ray examination.

A patient with suspected BT should undergo a neurological examination based on an assessment of behavioral reactions, verbal-acoustic, pain and some other specific responses, including eye and pupillary reflexes. Additionally, more subtle tests, such as vestibular ones, can be performed.

An ophthalmological examination reveals conjunctival edema, increased intraocular pressure, and papilledema. An ultrasound of the skull is performed, x-rays in two projections; topical diagnostics in case of suspected volumetric intracranial process, EEG and computed tomography of the head. EEG is useful in detecting seizures in patients with cerebral edema, in whom seizure activity manifests itself at a subclinical level or is suppressed by the action of muscle relaxants.

Differential diagnosis of BT is carried out with pathological conditions accompanied by convulsive syndrome and coma. These include: traumatic brain injury, cerebral thromboembolism, metabolic disorders, infection, and status epilepticus.

Treatment.

Therapeutic measures upon admission of the victim to the hospital consist in the most complete and rapid restoration of the main vital functions. This is, first of all, the normalization of blood pressure (BP) and circulating blood volume (CBV), indicators of external respiration and gas exchange, since arterial hypotension, hypoxia, hypercapnia are secondary damaging factors aggravating primary brain damage.

General principles of intensive care for patients with BT:

1. IVL. It is considered appropriate to maintain PaO 2 at the level of 100-120 mm Hg. with moderate hypocapnia (PaCO 2 - 25-30 mm Hg), i.e. carry out IVL in the mode of moderate hyperventilation. Hyperventilation prevents the development of acidosis, reduces ICP and contributes to a decrease in intracranial blood volume. If necessary, small doses of muscle relaxants that do not cause complete relaxation are used in order to be able to notice the restoration of consciousness, the onset of seizures, or focal neurological symptoms.

2. Osmodiuretics are used to stimulate diuresis by increasing plasma osmolarity, as a result of which fluid from the intracellular and interstitial space passes into the vascular bed. For this purpose, mannitol, sorbitol and glycerol are used. Currently, mannitol is one of the most effective and common drugs in the treatment of cerebral edema. Mannitol solutions (10, 15 and 20%) have a pronounced diuretic effect, are non-toxic, do not enter into metabolic processes, practically do not penetrate through the BBB and other cell membranes. Contraindications to the appointment of mannitol are acute tubular necrosis, BCC deficiency, severe cardiac decompensation. Mannitol is highly effective for short-term reduction of ICP. With excessive administration, recurrent cerebral edema, a violation of the water and electrolyte balance and the development of a hyperosmolar state can be observed, therefore, constant monitoring of the osmotic parameters of the blood plasma is required. The use of mannitol requires simultaneous control and replenishment of BCC to the level of normovolemia. When treating with mannitol, it is necessary to adhere to the following recommendations: a) use the smallest effective doses; b) administer the drug no more than every 6-8 hours; c) maintain serum osmolarity below 320 mOsm/l.

The daily dose of mannitol for infants is 5-15 g, for younger children 15-30 g, for older children 30-75 g. The diuretic effect is very good, but depends on the infusion rate, so the estimated dose of the drug should be administered 10 -20 minutes. The daily dose (0.5-1.5 g dry matter/kg) should be divided into 2-3 injections.

Sorbitol (40% solution) has a relatively short duration of action, the diuretic effect is not as pronounced as that of mannitol. Unlike mannitol, sorbitol is metabolized in the body with energy production equivalent to glucose. Doses are the same as for mannitol.

Glycerol, a trihydric alcohol, increases plasma osmolarity and thus provides a dehydrating effect. Glycerol is non-toxic, does not penetrate the BBB and therefore does not cause a recoil phenomenon. Intravenous administration of 10% glycerol in isotonic sodium chloride solution or oral (in the absence of pathology of the gastrointestinal tract) is used. Initial dose 0.25 g/kg; other recommendations are the same as for mannitol.

After the cessation of the administration of osmodiuretics, the phenomenon of "recoil" is often observed (due to the ability of osmodiuretics to penetrate into the intercellular space of the brain and attract water) with an increase in CSF pressure above the initial level. To a certain extent, the development of this complication can be prevented by infusion of albumin (10-20%) at a dose of 5-10 ml/kg/day.

3. Saluretics have a dehydrating effect by inhibiting the reabsorption of sodium and chlorine in the tubules of the kidneys. Their advantage lies in the rapid onset of action, and side effects are hemoconcentration, hypokalemia and hyponatremia. Use furosemide at doses of 1-3 (in severe cases up to 10) mg/kg several times a day to supplement the effect of mannitol. Currently, there is convincing evidence in favor of a pronounced synergy between furosemide and mannitol.

4. Corticosteroids. The mechanism of action is not fully understood, it is possible that the development of edema is inhibited due to the membrane-stabilizing effect, as well as the restoration of regional blood flow in the area of ​​edema. Treatment should begin as early as possible and continue for at least a week. Under the influence of corticosteroids, the increased permeability of cerebral vessels is normalized.

Dexamethasone is prescribed according to the following scheme: the initial dose is 2 mg/kg, after 2 hours -1 mg/kg, then every 6 hours during the day - 2 mg/kg; then 1 mg/kg/day for a week. It is most effective in vasogenic cerebral edema and ineffective in cytotoxic.

5. Barbiturates reduce the severity of cerebral edema, suppress convulsive activity and thereby increase the chances of survival. You can not use them for arterial hypotension and not replenished BCC. Side effects are hypothermia and arterial hypotension due to a decrease in total peripheral vascular resistance, which can be prevented by the administration of dopamine. Reducing ICP as a result of slowing down the rate of metabolic processes in the brain is directly dependent on the dose of the drug. A progressive decrease in metabolism is reflected in the EGG in the form of a decrease in the amplitude and frequency of biopotentials. Thus, the selection of the dose of barbiturates is facilitated under conditions of constant EEG monitoring. The recommended initial doses - 20-30 mg/kg; maintenance therapy - 5-10 mg / kg / day. During the intravenous administration of large doses of barbiturates, patients should be under constant and careful supervision. In the future, the child may experience symptoms of drug dependence ("withdrawal" syndrome), expressed by overexcitation and hallucinations. They usually last no more than 2-3 days. To reduce these symptoms, small doses of sedatives (diazepam - 0.2 mg / kg, phenobarbital - 10 mg / kg) can be prescribed.

6. Hypothermia reduces the rate of metabolic processes in the brain tissue, has a protective effect in cerebral ischemia and a stabilizing effect on enzyme systems and membranes. Hypothermia does not improve blood flow and may even reduce it by increasing blood viscosity. In addition, it contributes to increased susceptibility to bacterial infection.

For the safe use of hypothermia, it is necessary to block the body's defense responses to cooling. Therefore, cooling must be carried out in conditions of complete relaxation with the use of medications that prevent the appearance of trembling, the development of hypermetabolism, vasoconstriction and heart rhythm disturbance. This can be achieved by slow intravenous administration of antipsychotics, such as chlorpromazine at a dose of 0.5-1.0 mg/kg.

To create hypothermia, the head (craniocerebral) or body (general hypothermia) is covered with ice packs, wrapped in wet sheets. Cooling with fans or with the help of special devices is even more efficient.

In addition to the above specific therapy, measures should be taken to maintain adequate brain perfusion, systemic hemodynamics, CBS, and fluid and electrolyte balance. It is desirable to maintain pH at the level of 7.3-7.6, and PaO 2 at the level of 100-120 mm Hg.

In some cases, complex therapy uses drugs that normalize vascular tone and improve the rheological properties of blood (cavinton, trental), inhibitors of proteolytic enzymes (kontrykal, gordox), drugs that stabilize cell membranes and angioprotectors (dicynone, troxevasin, ascorutin).

In order to normalize metabolic processes in brain neurons, nootropics are used - nootropil, piracetam, aminalon, cerebrolysin, pantogam.

Course and outcome largely depends on the adequacy of the ongoing infusion therapy. The development of cerebral edema is always dangerous for the life of the patient. Swelling or compression of the vital centers of the trunk is the most common cause of death. Compression of the brainstem is more common in children older than 2 years, tk. at an earlier age, there are conditions for natural decompression due to an increase in the capacity of the subarachnoid space, compliance of sutures and fontanelles. One of the possible outcomes of edema is the development of posthypoxic encephalopathy with decortication or decerebration syndrome. An unfavorable prognosis includes the disappearance of spontaneous activity on the EEG. In the clinic - tonic convulsions of the type of decerebrate rigidity, a reflex of oral automatism with an expansion of the reflexogenic zone, the appearance of reflexes of newborns that have faded with age.

A great threat is posed by specific infectious complications - meningitis, encephalitis, meningo-encephalitis, which greatly aggravate the prognosis.

Cerebral edema is an excessive accumulation of fluid in its tissues, accompanied by an increase in intracranial pressure, and is the body's response to any irritation (presence of infection, intoxication as a result of poisoning, head trauma). Usually, this reaction develops rapidly, and if the necessary medical care is not provided to the patient in time, it leads to death. An increase in intracranial pressure leads, in turn, to impaired blood circulation in the brain and the death of its cells.

There can be several reasons for the occurrence of cerebral edema. Among them: a skull injury, an infectious disease, diseases associated with disruption of the brain, a brain tumor, intracranial hemorrhage. When receiving a traumatic brain injury, mechanical damage to the brain occurs, sometimes it is complicated by the ingress of fragments of the cranial bone into the brain.

The resulting swelling prevents the normal outflow of fluid from the brain tissue. A similar phenomenon can occur as a result of a fall from a great height, an accident, a strong blow to the head. Directly to the development of cerebral edema is ischemic - a violation of blood circulation in the brain as a result of blockage of the vessel by a thrombus. With a stroke, the brain cells do not receive the required amount of oxygen, which leads to their starvation and gradual death, as a result of which edema develops.

Many infectious diseases cause cerebral edema. The most common of them are:

• Encephalitis is a viral disease associated with an inflammatory process localized in the brain. Most often, various insects become carriers of encephalitis.
• - inflammation of the lining of the brain as a result of a viral infection or uncontrolled intake of medications.
• Subdural empyema is a purulent complication of brain infection.
• Toxoplasmosis is an infection caused by the presence in the human body of the simplest microorganism - toxoplasma.

The presence of a tumor in the brain is often accompanied by its edema. Growing rapidly, tumor cells put pressure on healthy brain cells, thereby causing it to swell. In newborns, cerebral edema is most often caused by trauma received at birth. Predisposing factors in this case are the diseases suffered by the mother during pregnancy. Climbers often have the so-called mountain cerebral edema, which occurs when climbing to a height of more than one and a half thousand meters above sea level. This phenomenon is associated with a sharp drop in altitude.

Symptoms of cerebral edema

The occurrence of cerebral edema can be suspected not by several main symptoms:

• Strong ;
• Dizziness accompanied by nausea and vomiting;
• Partial visual impairment;
• Loss of orientation in space;
• Uneven breathing;
• Difficulty in speech and falling into a stupor;
• Memory losses;
• short-term convulsions;
• Fainting.

If these symptoms appear, you should immediately seek medical help. Diagnosis of cerebral edema is based on the results of computed tomography and magnetic resonance imaging of the brain. The cause of the development of edema can be established by a blood test.

Treatment of cerebral edema and its consequences

Cerebral edema resulting from a small concussion usually resolves on its own and does not require treatment. In all other cases, in the presence of pronounced symptoms of brain damage, qualified treatment is required, which is aimed primarily at supplying the brain with a sufficient amount of oxygen. It involves the intravenous infusion of drugs to the patient that help reduce intracranial pressure and eliminate the infection (if it was the infection that caused the development of edema). The choice of drugs depends on the cause of the edema and the severity of its main symptoms.

If necessary, for example, in case of a traumatic brain injury as a result of an accident, the method of oxygen therapy is used, which involves the artificial introduction of oxygen into the body of the victim. The blood saturated with oxygen nourishes the damaged brain and contributes to the speedy removal of its edema.

In especially severe cases of edema, surgical methods of treatment are used. With excessive accumulation of fluid in the ventricles of the brain, it is removed using a special catheter. This procedure helps to eliminate fluid and reduce intracranial pressure.

Brain surgeries are among the most difficult, but in some cases they are the only way to save the patient's life. So, surgical intervention is necessary in the presence of a tumor, the entry of the skull bone into the brain, and the restoration of a damaged blood vessel. The outcome of such an operation always depends on the level of professionalism of the surgeon.

The consequences of cerebral edema can be varied. First of all, you should pay attention to the consequences of those diseases that lead to it. A stroke is accompanied by the death of brain tissue that cannot be restored even after treatment. The consequence of a stroke and increased intracranial pressure may be partial or complete paralysis of the body and, accordingly, disability. Removing a brain tumor is only the first step in cancer treatment. Therefore, the outcome of the disease depends on its further therapy.

For most patients, cerebral edema does not go away without a trace. Each of them in the future will have to face such unpleasant consequences as frequent headaches, insomnia, impaired ability to communicate with other people, depression, absent-mindedness and forgetfulness. With a slight swelling of the brain, for example, with a concussion as a result of a small accident, the consequences are usually minimal and disappear with time.

Cerebral edema can have various consequences. In rare cases, a complete cure occurs. But in the majority, various kinds of pathologies are observed.

Cerebral edema, like its other pathologies, can have very deplorable consequences. After all, this organ of the human body is responsible for all vital functions without exception. Therefore, the result can be disturbances in the work of various body systems.

What influences the consequences

Regardless of the cause and mechanism of edema, its clinical consequences are almost the same: increased intracranial pressure, impaired cellular nutrition and gas exchange.

As a result, massive cell death begins, which endangers not only the functioning of the body, but also the life of the patient.

The consequences of cerebral edema can be varied. They are affected by:

• the degree and localization of brain tissue damage, which depends on the cause of the pathology;
• timeliness of medical care.

Naturally, the greater the degree of damage, the more serious the consequences will be. The effectiveness of medical care is reduced by the fact that edema develops in most cases not immediately, but after a few days. The transience of this brain disorder is characteristic of a few precedents, for example, for skull fractures.

As a rule, the effects of edema are superimposed on the results of the impact of the cause that caused it - various disorders of the central nervous system under the influence of hemorrhages, strokes, intoxications and other processes.

Possible Scenarios

Doctors believe that cerebral edema (swelling) is a reversible phenomenon. If you remove the causes of its occurrence, regression is possible. But if the effect on the brain cells took place for a long time, then the destructive stage begins. As you know, nerve cells are not restored, and if they are restored, then very slowly. The death of part of the nerve fibers entails irreversible processes.

There are three options for the development of the consequences of cerebral edema:

1. Complete cure of the patient without further pathologies. Unfortunately, this option is the exception rather than the rule. It is typical for healthy people with a small brain injury, for example, with intoxication, a slight concussion;
2. The appearance of pathologies that entail the disability of the victim even after the elimination of edema. It usually manifests itself with lesions of moderate severity. This includes timely treated infectious diseases, small hematomas;
3. The growth of edema, leading to the death of the patient. Sadly, this is how most cases end.

The fact is that until a critical amount of fluid accumulates in the cranium, a brain tumor may not manifest itself in any way. When the space in which the swollen cells can be placed ends, the dislocation of the nervous tissue occurs. When crushing the centers responsible for vital functions, death may occur due to respiratory arrest or heart failure.

Consequences of cerebral edema

Consider some specific pathologies that develop as a result of cerebral edema. Their development depends on the degree of damage. The lighter ones are characteristic of focal edema, capturing small areas of the brain. With generalized edema affecting one or both hemispheres, the consequences are severe, irreversible.

Paresis and paralysis

Slight swelling can provoke the occurrence of paresis - an incomplete loss of muscle movement. With an unfavorable prognosis, paralysis can develop - a complete violation of motor function. If one hemisphere is affected, then this pathology is noted on the side opposite to it. That is, with swelling of the right hemisphere, the left limbs suffer and vice versa. The process can also be observed when the edema is eliminated. Then apply symptomatic treatment aimed at restoring motor functions.

Loss of speech (aphasia)

May be partial or complete. It develops with a local lesion of the cerebral cortex in the left hemisphere (if we are talking about right-handers). Depending on the degree of development of the pathology, various violations of the speech function are possible: a person does not speak; does not perceive speech or individual words.

Coma

One of the most severe consequences of disruption of the central nervous system. The highest stage of slowing down her work. The patient has a lack of consciousness and reactions to stimuli, extinction of reflexes, general disorganization of vital functions. The main reason is the disorder of cellular nutrition and gas exchange, which leads to a breakdown in the basic function of the nervous tissue. Nerve cells cannot fully generate, conduct and perceive nerve impulses.

The longer the coma lasts, the greater the danger to the life of the patient. Although there are cases when people came out of a long-term coma. But such cases are not so common. Basically, coma develops into brain death, leading to death. Even if a person comes out of a coma, one cannot be completely sure that all functions will be fully restored.

Other violations

A patient who has undergone cerebral edema needs to be prepared for the fact that headaches, sleep dysfunction, impaired orientation in space and motor functions, depression, sometimes attacks of aggressiveness and other mental disorders can become his constant companions. The consequences of cerebral edema in newborns has its own characteristics.

There are symptomatic treatments for most of the consequences of cerebral edema. But the best, as with other ailments, is still prevention and timely seeking medical help.

Edema and swelling of the brain come from excessive accumulation of fluid in tissue cells and intercellular space. The scientific world has not come to a final conclusion in which cases and whether it is generally correct to call this condition - cerebral edema or swelling.

The role of the brain as a leading link in the management of the functions of the whole organism is difficult to overestimate. Any violations in his work turn into undesirable consequences. Therefore, it is so important to know the signs of brain disorders and what they come from.

The saturation of the material with specific medical terminology does not make the topic more understandable, but only frightens with the unknown. Given that this material is not intended to improve the skills of specialists, we will adhere to the rule of maximum accessibility of the presentation.

What is cerebral edema? This is either an increase in the entire volume of brain tissue, or hypertrophy of one of its sections. The causes of cerebral edema can be different, but without timely treatment, they always threaten with serious consequences, even death.

Symptoms of the disease

It is almost impossible to distinguish signs of cerebral edema from diseases that occur with similar symptoms and do not pose a great danger. Only a comprehensive examination using special equipment can give an affirmative or negative answer.

A trip to the clinic cannot be postponed for a long time if a person has been experiencing a combination of unpleasant sensations for some time:

• severe pain spreading to the entire head area;
• loss of appetite;
• nausea, turning into vomiting;
• inhibited perception of the phenomena of the surrounding reality;
• constant desire to sleep;
• restless sleep that does not bring rest;
• pain associated with the movement of the eyeballs.

The list of signs can be continued, but for the patient's personal conclusions, they will no longer be important. Firstly, with these symptoms, a state occurs in which a person can no longer adequately perceive what is happening. Secondly, convulsions, loss of consciousness, coma mean that the time has come that no longer tolerates delay. Calling an ambulance will be the only right decision.

Prior to the arrival of the medical team, you should:

• put the patient to bed, after taking off his clothes;
• open windows, thereby ensuring a sufficient flow of oxygen;
• in case of vomiting, turn the head to a position that avoids the ingress of vomit into the respiratory system;
• in case of convulsions, hold the head and limbs of the patient to avoid accidental injury.

Further resuscitation can only be performed by specialists.

Risk group

Cerebral edema is not an independent disease. Causes of edema: current and past illnesses, surgical interventions, injuries, intoxication of the body, tumor formations, infection. Some of them are worth talking about in more detail.

1. People suffering from impaired functions of the cardiovascular system: hypertension, coronary heart disease, vascular atherosclerosis should closely monitor the manifestations of symptoms of cerebral edema.
2. Any, more or less serious head injury (fall from a height, blows), as a rule, causes a concussion. Edema is the result of a concussion. These are usually easily reversible. Treatment is limited to bed rest, general tonic and diuretics.
3. Regrettably, the most common cause of cerebral edema, with views of a disappointing prognosis, in adults is alcohol intoxication.

The consequences of cerebral edema depend on the location of the affected area, along with the progression of the provoking disease.

Possible Complications

The results of untimely started treatment, as well as the uncontrolled development of the underlying disease, can be severe disorders of the whole organism, and sometimes the death of the patient.

But even when the treatment is started on time and carried out quite successfully, it is possible to consolidate residual fatal consequences that fall under the signs of cerebral edema:

• persistent headaches;
• lethargy of consciousness;
• partial memory loss;
• inappropriate behaviour.

The rehabilitation period can take a very long time, but a return to normal is more than likely. Brain cells still recover, only much more slowly than it happens in the tissues of other organs.

In older people, complications are exacerbated by an age-related decrease in immunity, together with acquired diseases of the heart and blood vessels. Increased permeability of the vascular walls rarely eliminates the manifestations of puffiness once and for all. What is the danger of edema for the older age category? What consequences does it cause?

1. Acute strokes leading to partial and complete paralysis.
2. Destruction of the structure of the cerebral cortex, which leads the patient to a state of dementia.
3. Significant deterioration (up to complete loss) of hearing and vision.
4. Violation of the functions of the respiratory and digestive organs.

The mortality rate among the elderly is much higher than among young people and the middle age category of citizens.

But still, the degree of danger of possible consequences largely depends on the type and intensity of cerebral edema.

Mechanisms of the pathogenesis of the disease

External signs of cerebral edema are manifested by similar symptoms, regardless of the provoking causes. The initial phase of the disease is expressed by the following factors:

• accumulation of fluid in the cells of the brain tissue and extracellular space;
• increase in brain volume;
• an increase in intracranial pressure.

In order to understand how to treat cerebral edema, the doctor needs to clearly identify the cause that initiates the pathology. The classification of the disease adopted as a basis reads four types:

1. Hydrostatic. It develops due to the predominance of the volume of blood entering the brain tissue over its outflow. Most often it is caused by compression of large veins by tumor formations.
2. Osmotic. The reason is a violation of the balanced electrochemical activity of brain tissues and blood substances.
3. Vasogenic. An increase in the permeability of brain capillaries leads to the release of blood plasma from the vascular bed and an increase in the volume of fluid in the intercellular space and in the space surrounding the bloodstream.
4. Cytotoxic. The impact of toxins on brain cells disrupts the process of cellular metabolism, which is marked by the replacement of cellular potassium with sodium. The latter exhibits the effect of a sponge, strongly drawing in and holding water. Intoxication affects the blood vessels of the brain, destroys the protective barrier, and this increases the penetrating and destructive ability of neurotoxins.

Cerebral edema in alcoholism is one of the complications that occurs due to external intoxication of the body. And since voluntary alcohol poisoning is practiced everywhere and with enthusiasm, it is impossible not to consider this point in a special order.

The destructive effect of alcohol on the brain

The serpent curled up into a ring and swallowing its tail symbolizes Infinity in Eastern teachings. The green serpent, by analogy, symbolizes the vicious circle of alcoholism. Only this circle is predictably finite.

The impact of alcohol on the body is determined not only by the one-time amount of alcohol consumed, the age and gender of the recipient, but also by its hereditary predisposition and even race. But in any case, alcohol dependence occurs according to the general scheme.

After taking a certain dose of alcohol, a state of euphoria sets in, followed by hangover symptoms, which can be removed with a new dose. Sitting on this "carousel" becomes addicted to alcohol. Alcohol becomes both the cause of the disease and the cure for it. A drinking person does not notice (or can no longer notice) the changes that occur in his body. He ceases to adequately assess his physical and moral condition. First of all, because alcohol destroys the main organ that induces evaluation criteria.

Alcohol destroys the nerve connections between brain cells, leaving them face to face with the enemy. Alcohol dramatically and significantly lowers blood sugar levels. Lack of glucose causes cells to starve. Brain dystrophy develops, manifested by a decrease in communication and reflex functions. The offensive is carried out slowly, but inevitably and mercilessly.

Post-mortem studies of the brains of alcoholics have shown brain atrophy, especially in the frontal lobes. It would seem that there is no connection between reduction and swelling. This is another insidious property of alcohol-containing liquids, the systematic use of which violates all the functional foundations of brain tissues. Taking a critical dose against the background of general dehydration of the body blocks the removal of fluid from the cells. The defensive reaction turns suicidal. Cerebral edema in alcoholism is the finish line, beyond which only coma and death. This should sound like a warning to all drinkers.

Treatment of the disease

Cerebral edema, regardless of the cause, requires urgent medical attention. What is dangerous edema?

1. General and focal structural changes:

• deformation of departments;
• displacement of the skull in the occipital region and compression of the cerebellum;
• compression of the brainstem.

2. Partial or complete damage to the cerebral cortex.

3. Many capillary ruptures with extensive hemorrhage.

The first and main task of physicians is to relieve cerebral edema, thereby preventing damage to its main and stem parts. This will be enough to buy time and start intensive care.

In critical cases, treatment can begin with the necessary surgical intervention:

• removal of part of the bone plate of the skull;
• installation of catheters for pumping fluid.

Intravenous infusions help restore blood circulation.

It is very important to establish what caused the functional impairment. The medical approach provides for a fundamental difference in the treatment of edema caused by a tumor and, for example, alcohol intoxication.

Medicine has a large arsenal of tools for obtaining the most accurate diagnosis. Along with the measures taken to relieve cerebral edema, therapeutic measures are taken to eliminate the cause itself. In each individual case, drug treatment has a narrow focus, taking into account the degree of development of the disease provoking edema and the general condition of the patient.

If you or your loved ones show signs of such a serious illness as cerebral edema, you should immediately consult a doctor. Alarming factors may be recent infectious diseases, head trauma, epilepsy, alcoholism.

The passage of computed tomography and x-rays of the skull, at best, will dispel your fears, and at worst, help to cure brain dysfunction without negative consequences.

In no case should you self-medicate or be limited to traditional medicine. The disease tends to progress rapidly and cause irreparable damage to the brain.

After inpatient treatment and elimination of the main symptoms, one should strictly adhere to the doctor's recommendations and continue treatment at home. Patients with alcoholism are recommended to undergo a rehabilitation course in special institutions. Repeated alcoholic cerebral edema, as a rule, ends in death or disability.

People who have had the disease should give up all bad habits and lead a healthy lifestyle. Physical exercise in the fresh air, with increasing load, will save brain cells from oxygen starvation and will help restore the walls of blood vessels.

The basis of preventive measures to prevent swelling of brain cells is the normal functioning of the hematopoietic and cardiovascular systems.

The processes of cerebral edema (CSE) are one of the most pressing problems of modern medicine. They accompany various neurosurgical, neurological and somatic pathologies. The causes of cerebral edema are multifactorial in nature.

What it is

Cerebral edema (ICD-10 code G 93.6) is a universal non-specific response of the body to the action of pathogenic factors. It is a companion of critical conditions, in some cases leads to death. The term "edema" is interpreted as an excessive accumulation of fluid in the brain tissue. This process is characterized by a violation of water-salt metabolism, circulatory disorders in the structures of the brain. It entails an increase in the volume of the contents of the skull and an increase in (ICP).

The space of the cranium consists of the parenchyma of the brain, cerebrospinal fluid and blood in the vessels. If one of the components increases in volume, the others decrease. With cerebral edema, the amount of cerebrospinal fluid is reduced, blood vessels are compressed. Inside the skull, a reserve may be maintained for changing spatial relationships. In this case, ICP does not go beyond the norm. An increase in the size of the brain, the displacement of cerebrospinal fluid and blood increases the likelihood of raising pressure. This leads to compression of thin-walled veins and a decrease in venous blood in the brain.

The depletion of the described compensatory mechanisms leads to the onset of subcompensation with a noticeable increase in intracranial pressure and occlusion of the CSF pathways. In the phase of decompensation, a slight change in the volume of the brain provokes a pronounced increase in pressure. These processes lead to the cessation of CSF absorption, compression of arterial vessels and the development of cerebral ischemia due to oxygen starvation.

An increase in brain volume due to edema may be accompanied by neuronal damage. The degree of their damage and reversibility is proportional to the decrease in cerebral circulation. Up to a certain point, focal neurological deficit is reversible. With a decrease in blood flow to 11 ml per 100 g/min, the death of nerve cells occurs in about 8 minutes.

The rate of development of edema after ischemia increases with a significant increase in blood pressure. Its sharp rise itself can provoke HMO without additional interactions.

In children

The predisposition to edematous syndrome and its severity is determined by the peculiarities of blood flow in the affected area and the absorbency of the tissue. The structure and specificity of its functioning predisposes to the frequent development of cerebral edema.

Newborn

Mechanical forces affect the fetal head during childbirth. The rise and fall of intracranial pressure alternates with contractions and attempts of the woman in labor. Usually, such a head massage does not lead to significant pathological manifestations. But the rate of increase, the force of pressure, the frequency of oscillations varies over a wide range. A strong impact can be an irritant, leading to a violation of the water balance. In newborns, this is expressed by cerebral edema. It leads to hernial herniation of the brain in the natural openings of the skull.

The level of damage to the fetal head during labor varies. A minor injury can cause cerebral edema, a severe one can cause trauma and damage to the dura mater.

Time passes from the moment of exposure to the traumatic force to the development of edema and herniation. Childbirth with a dead fetus occurs if it has been in the birth canal all this period. If the injuries were received at birth, then time passes before the appearance of dangerous phenomena, and the child is born with signs of a live birth. Medical care for a relatively minor injury can prevent death.

In older children

There are several groups of children with a high risk of developing pathology. First of all, this applies to young children up to 2 years old, especially with neurological diseases. BT is more often diagnosed in children with a tendency to allergies.

The development of edema is always unsafe for life. Of particular danger is the compression of the brain stem. Affecting its important centers ends in death. This process is observed in children older than 2 years. At an earlier age, due to the plasticity of the sutures and fontanelles of the skull, an increase in the capacity of the subarachnoid space, there are conditions for natural decompression. With an increase in ICP and an increase in edema up to the 2nd year of life, the head circumference increases, the sutures of the skull diverge, and a large fontanel opens in infants. This is clearly shown in the figure below.

In adults

In adults, the brain and tissues that surround it occupy a certain fixed volume, which is limited by the bones of the skull. When analyzing the processes observed in the brain during trauma or stroke, the similarity of the factors that potentiate damage to the brain tissue is manifested. One of them is the development of edema.

After a stroke

Regardless of the mechanism of stroke development, the patient develops swelling of the brain tissue due to excessive accumulation of fluid in it. In patients with hemorrhagic stroke, complex pathophysiological processes are diagnosed, including the development of edema, microcirculation disorders, and ischemic changes.

At first, after an intracranial hemorrhage, a clot is formed, which is compacted due to the release of plasma to the periphery to the substance of the brain.

At the end of the 1st day after the stroke, perifocal vasogenic edema develops. It reaches its peak at 2-5 days. The larger the size of the vascular injury, the more pronounced the edema. The degree of BT determines the severity of the course of acute circulatory disorders. Severe edema sharply aggravates the stroke clinic. Cortical compression ischemia occurs, which can cause brain death.

Traumatic brain injury and edema

Due to injury, oxygen consumption decreases. Metabolic processes are disturbed due to which the brain receives less energy. A shift in his work leads to edema. In turn, this impedes blood circulation. One of the vicious circles of severe brain damage is formed. Hypoxia occurs in the area of ​​reduced blood flow. As a result, there is a violation of the function of the brain, which is especially sensitive to oxygen starvation.

Symptoms

The resulting pathological symptoms are due to a violation of the functions of all brain structures. The destructive process can lead to focal neurological symptoms. There are 3 clinical syndromes most characteristic of BT:

Thus, OGM does not have etiological specifics. The clinic is determined by the localization and severity of the process.

Causes

Edema syndrome is a reactive condition that develops secondarily, as a reaction to any brain damage. The reason is an increase in the permeability of the physiological barrier between the circulatory system and the central nervous system. The blood-brain barrier protects nerve tissue from toxic substances, immune system factors that circulate in the blood and regard brain tissue as foreign. Its damage leads to disruption of mediator metabolism, blockade of signal transmission between nerve cells.

Causes of swelling:

infectious diseases (bacterial meningitis, encephalitis, meningoencephalitis);

severe traumatic brain injury of varying severity;

oncological diseases of the central nervous system;

acute violation of cerebral circulation;

surgical interventions;

acute toxic poisoning.

Edema significantly aggravates the course of a particular pathological process. It leads to the development of ischemic and hypoxic disorders, necrosis of cellular structures. The most dangerous consequence of edema is the development of a dislocation syndrome with wedging of brain structures into the foramen magnum or under the meninges. As a result, the cerebellum, parietal and frontal lobes are infringed. Long-term effects may be cognitive impairment and persistent neurological symptoms.

Treatment

Treatment is determined by the characteristics of the pathological process. Depends on the origin and clinical signs of edema. It is an obligatory component of resuscitation measures carried out by a resuscitator in the intensive care unit.

Edema with signs of dislocation primarily requires early artificial ventilation of the lungs with an oxygen-air mixture. First line events:

normalization of venous outflow from the cranial cavity (achieved by the position of the patient with the head end raised by 30°);

oxygenation;

maintenance of normal CO2 content in the blood;

body temperature control;

sedation (immersion of the patient in a relaxed state) and analgesia.

If the above measures are ineffective, hyperventilation is indicated for 20-30 minutes. Persistent high intracranial pressure is an indication for the administration of hyperosmolar solutions. In the absence of positive dynamics, they proceed to the stage of the second line, which includes barbituric coma, therapeutic hypothermia up to 32-34°C, craniotomy in neurosurgical patients.

Surgery often saves lives. The need for this appears with intracranial hemorrhages of traumatic and non-traumatic origin, occlusive hydrocephalus, neoplasms. Surgical tactics include removal of a hematoma, abscess, setting up CSF drainage.

Consequences

By its nature, edema - the process is reversible. The forecast essentially depends on many factors. Not the last role is given to the age of the patient. In children under 1 year of age with non-united bones of the skull, dislocation is usually not diagnosed. In older people, BT often progresses, aggravated by the development of dislocation.

The course of the pathological process is aggravated by the presence of factors that increase the oxygen starvation of the brain. These include pneumonia, anemia, arterial hypotension.

Cause of death

A feature of OGM is the likelihood of developing fatal infringements: lower and upper. Inferior infringement occurs due to wedging of the medulla oblongata and cerebellar tonsils into the foramen magnum. Significant compression of the medulla oblongata, the development of hypoxia leads to disruption of the respiratory center. Breathing stops and death occurs.

Fatal edema develops quickly, within a few hours and increases over 1-2 days. May be the direct cause of death when severe. Many unclear cases of rapidly occurring death are explained by the occurrence of edematous syndrome.