What causes brain swelling. Cerebral edema - emergency measures and proper treatment. Consequences of edema in infants

Cerebral edema (CED) is a nonspecific reaction to the effects of various damaging factors (trauma, hypoxia, intoxication, etc.), expressed in excessive accumulation of fluid in the brain tissue and increased intracranial pressure. Being essentially a defensive reaction, AGM, if diagnosed and treated untimely, can become the main reason determining the severity of the patient’s condition and even death.

Etiology.

Brain edema occurs with traumatic brain injury (TBI), intracranial hemorrhage, embolism cerebral vessels, brain tumors. In addition, various diseases and pathological conditions leading to cerebral hypoxia, acidosis, disturbances of cerebral blood flow and liquor dynamics, changes in colloid-osmotic and hydrostatic pressure and acid-base status can also lead to the development of AMS.

Pathogenesis.

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

1) Cytotoxic. It is a consequence of the effects of toxins on brain cells, resulting in a disorder of cellular metabolism and disruption of ion transport through cell membranes. The process is expressed in the cell losing mainly potassium and replacing it with sodium from the extracellular space. Under hypoxic conditions, pyruvic acid is reduced to lactic acid, which causes disruption 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. A lactate content above 6-8 mmol/l in the blood flowing from the brain indicates brain edema. The cytotoxic form of edema is always generalized, spreading to all parts, including the stem, so signs of herniation may develop quite quickly (within several hours). Occurs in cases of poisoning, intoxication, ischemia.

2) Vasogenic. It develops as a result of damage to brain tissue with disruption of the blood-brain barrier (BBB). This mechanism for the development of cerebral edema is based on the following pathophysiological mechanisms: increased capillary permeability; increase in hydrostatic pressure in capillaries; accumulation of fluid in the interstitial space. Changes in the permeability of brain capillaries occur as a result of damage to endothelial cell membranes. 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, blood plasma, along with the electrolytes and proteins it contains, moves from the vascular bed to the perivascular areas of the brain. Plasmorrhagia, increasing oncotic pressure outside the vessel, helps to increase the hydrophilicity of the brain. Most often observed with head injury, intracranial hemorrhage, etc.

3) Hydrostatic. It manifests itself when the volume of brain tissue changes and the ratio of blood inflow and outflow is disturbed. Due to the difficulty 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 when there is a disruption of the normally existing small osmotic gradient between the osmolarity of the brain tissue (it is higher) and the osmolarity of the blood. Develops as a result of water intoxication of the central nervous system due to hyperosmolarity of brain tissue. Occurs in metabolic encephalopathies (renal and liver failure, hyperglycemia, etc.).

Clinic.

Several groups of children with a high degree of risk of developing AMS can be identified. 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 common in children with an allergic predisposition.

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

All symptoms of AMS 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 caused by increased 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 convulsions appear. Typically, first-time seizures are clonic or tonic-clonic in nature; They are characterized by comparative short duration and a completely favorable outcome. With a prolonged course of convulsions or their frequent repetition, the tonic component increases and the unconsciousness worsens. An early objective symptom of increased ICP is congestion of the veins and swelling of the optic discs. At the same time or somewhat later, radiological signs of intracranial hypertension appear: increased pattern of digital impressions, thinning of the bones of the vault.

With a rapid increase in ICP, the headache is bursting in nature, and 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 when palpating the skull due to 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 in the pathological process of first the cortical, then subcortical and ultimately brain stem structures. When the cerebral hemispheres swell, consciousness is impaired and generalized, clonic convulsions appear. 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.

Dislocation of brain structures is accompanied by the development of signs of herniation: the upper - midbrain into the notch of the cerebellar tentorium and the lower - with pinching in the foramen magnum ( bulbar syndrome). The main symptoms of damage to the midbrain: loss of consciousness, unilateral changes in the pupil, mydriasis, strabismus, spastic hemiparesis, often unilateral convulsions of the extensor muscles. Acute bulbar syndrome indicates a preterminal increase in intracranial pressure, accompanied by a drop in blood pressure, a decrease heart rate and a decrease in body temperature, muscle hypotonia, 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 AMS 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 of age.

The most important diagnostic method is CT, which, in addition to identifying intracranial hematomas and areas of contusion, allows one to visualize the localization, extent and severity of cerebral edema, its dislocation, as well as evaluate the effect of treatment measures during repeated studies. NMR imaging complements CT, in particular in visualizing small structural changes in diffuse damage. NMR imaging also makes it possible to differentiate different types of cerebral edema, and, therefore, to correctly build treatment tactics.

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

A patient with suspected AGM should undergo a neurological examination based on the assessment of behavioral reactions, verbal-acoustic, pain and some other specific responses, including ocular and pupillary reflexes. Additionally, more subtle tests, for example, vestibular tests, can be carried out.

An ophthalmological examination reveals swelling of the conjunctiva, increased intraocular pressure, and swelling of the optic nerve head. An ultrasound scan of the skull is performed x-rays in two projections; topical diagnostics for suspected massive 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 AMG 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 of the most complete and rapid restoration of basic 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 that aggravate primary brain damage.

General principles intensive care patients with AGM:

1. mechanical ventilation. It is considered advisable to maintain PaO 2 at a level of 100-120 mm Hg. with moderate hypocapnia (PaCO 2 - 25-30 mm Hg), i.e. perform mechanical ventilation in the mode of moderate hyperventilation. Hyperventilation prevents the development of acidosis, reduces ICP and helps reduce intracranial blood volume. If necessary, small doses of muscle relaxants are used that do not cause complete relaxation in order to be able to notice the restoration of consciousness, the appearance 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, and practically do not penetrate the BBB and other cell membranes. Contraindications to the administration of mannitol are acute tubular necrosis, BCC deficiency, and severe cardiac decompensation. Mannitol is highly effective for short-term reduction of ICP. With excessive administration, recurrent cerebral edema, disturbance of water-electrolyte balance and the development of a hyperosmolar state may be observed, therefore constant monitoring of osmotic parameters of blood plasma is required. The use of mannitol requires simultaneous monitoring and replenishment of blood volume to the level of normovolemia. When treating with mannitol, you must adhere to the following recommendations: a) use the smallest effective doses; b) administer the drug no more often than every 6-8 hours; c) maintain serum osmolarity below 320 mOsm/L.

Daily dose of mannitol for children infancy- 5-15 g, younger age- 15-30 g, older age - 30-75 g. The diuretic effect is very well expressed, but depends on the rate of infusion, so the calculated dose of the drug should be administered within 10-20 minutes. Daily dose(0.5-1.5 g dry matter/kg) should be divided into 2-3 administrations.

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

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

After stopping the administration of osmodiuretics, a “recoil” phenomenon 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 cerebrospinal fluid 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 kidney tubules. Their advantage lies in the rapid onset of action, and side effects are hemoconcentration, hypokalemia and hyponatremia. Furosemide is used in doses of 1-3 (in severe cases up to 10) mg/kg several times a day to complement the effect of mannitol. Currently, there is convincing evidence in favor of the pronounced synergism of furosemide and mannitol.

4. Corticosteroids. The mechanism of action is not fully understood; perhaps 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, increased cerebral vascular permeability is normalized.

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

5. Barbiturates reduce the severity of cerebral edema, suppress convulsive activity and thereby increase the chances of survival. They should not be used in cases of arterial hypotension and unreplenished blood volume. Side effects include hypothermia and arterial hypotension due to a decrease in total peripheral vascular resistance, which can be prevented by the administration of dopamine. The decrease in ICP as a result of a slowdown in 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. Recommended initial doses are 20-30 mg/kg; maintenance therapy - 5-10 mg/kg/day. During intravenous administration of large doses of barbiturates, patients should be under constant and careful monitoring. 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. Small doses can be prescribed to reduce these symptoms. sedatives(diazepam - 0.2 mg/kg, phenobarbital - 10 mg/kg).

6. Hypothermia reduces the rate of metabolic processes in brain tissue, has a protective effect during 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 increases susceptibility to bacterial infection.

To safely use hypothermia, it is necessary to block the body's protective reactions to cooling. Therefore, cooling must be carried out in conditions of complete relaxation with the use of medications that prevent the appearance of tremors, the development of hypermetabolism, vasoconstriction and heart rhythm disturbances. This can be achieved by slow intravenous administration of antipsychotics, for example aminazine 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 and wrapped in damp sheets. Cooling with fans or using special devices is even more effective.

In addition to the above specific therapy, measures should be taken aimed at maintaining adequate cerebral perfusion, systemic hemodynamics, CBS and water-electrolyte balance. It is advisable to maintain pH at 7.3-7.6 and RaO 2 at 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 (Kontrikal, Gordox), drugs that stabilize cell membranes and angioprotectors (Dicinone, Troxevasin, Ascorutin).

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

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

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

Cerebral edema is a serious pathology that inevitably leads to death if left untreated. The disease is especially dangerous for children because it has hidden symptoms and causes a number of violations. In adults, it is easier, but it cannot be cured on your own. What kind of disease is this and what factors provoke it?

Cerebral edema is a reactive process that occurs when there is an excessive concentration of fluid in the brain cavities and tissues. This serious illness is accompanied by an increase in intracranial pressure and damage to blood vessels, as a result of which nerve cells die.

Pathology develops with hypoxia, accompanied by an increase in carbon dioxide levels in the body.

Cerebral edema is provoked by the following factors:

Damage to the skull. Sometimes the brain is injured by fragments of cranial bones. All this causes severe swelling, preventing the outflow of fluid.
Brain contusion.
Ischemic stroke, disrupting cerebral circulation due to blockage by a blood clot. It prevents cells from receiving normal amounts of oxygen, after which they die, causing swelling.
Hemorrhagic stroke, which develops with damage and aneurysm of blood vessels and provokes an increase in intracranial pressure.
Meningitis- inflammation of the meninges.
Intracranial hematomas.
Metastasis of tumors in brain tissue.
Toxoplasmosis– a disease caused by the protozoan Toxoplasma. It is especially dangerous for the fetus developing in the mother's womb.
Purulent infection, which, when rapidly flowing, becomes a source of swelling, preventing the outflow of fluid.
Tumors, disrupting blood circulation when certain areas of the brain are compressed.
Encephalitis– inflammation of the brain viral nature carried by insects.
Height changes. Above 1.5 km above sea level, due to lack of oxygen, cerebral edema begins. This is one of the symptoms of altitude sickness.
Intoxication neuroparalytic poisons, alcohol, chemicals.
Damage to the liver and bile ducts.
Operations on brain tissue.
Anaphylactic reactions.
Anasarca– edema accompanied by heart failure.

Cerebral edema is dangerous because this organ is limited by the size of the skull and is not able to increase its volume without consequences for the entire body. Compression of the skull, combined with a drop in oxygen levels, leads to a complete cessation of blood supply to neurons, increasing swelling.

What contributes to the disease

The following factors contribute to the occurrence of the disease:

Promotion blood pressure due to its increase in capillaries. This is due to the dilation of the cerebral arteries. In fact, water accumulates in the intercellular space.
Violation of vascular permeability. As a result, the pressure in the intercellular space rises, which causes damage to cell membranes.

In an adult, intracranial pressure in the supine position ranges from 3-15 mm Hg. Art. In some situations (when coughing, sneezing, increased intra-abdominal pressure), the indicator reaches 50–60 mmHg. Art., but this does not cause disturbances in the human nervous system, since it quickly passes due to the internal mechanisms of cerebral protection.

At-risk groups

The following are more susceptible to cerebral edema:

People, having problems with the cardiovascular system. These include transferred ischemic disease, hypertension, atherosclerosis.
Sick, whose professions involve the risk of injury, falling from a height.
Adults, alcoholics. At excessive consumption alcoholic drinks, under the influence of ethanol, nerve cells die, and fluid accumulates in their place.
Newborns passing through the birth canal.

Symptoms

Having appeared locally, the pathology quickly covers the entire organ. In some cases, the disease develops gradually, therefore, by detecting the first signs of edema, the patient’s life can be saved.

Symptoms depend on the origin of the formation and the severity of the disease. The most common signs are:

nausea and vomiting;
headache, manifested in acute brain diseases;
memory disorders;
forgetfulness;
blurred vision;
decreased blood pressure, unstable pulse;
pain in the neck;
uneven breathing;
speech problems;
frequent dizziness;
lack of coordination;
paralysis of limbs;
cramps turning into muscle atony (inability to contract);
hallucinations;
with alcoholic edema, swelling of the face is observed with the formation of many hematomas;
loss of consciousness, which, as the situation worsens, turns into a coma.

Brain edema occurs:

local affecting a specific area of the brain;
diffuse, covering the brain stem and hemispheres.

In this case, diffuse edema has more pronounced symptoms.

But they also highlight the following types edema:

Cytotoxic swelling occurs due to hypoxia, intoxication and ischemia. Pathologically increases the number gray matter.
Vasogenic edema forms when the blood-brain barrier is broken. It occurs in the presence of a tumor, abscess, ischemia, and also after surgical intervention. This pathology manifests itself in an increase in the amount of white matter and is perifocal, which leads to compression of the brain.
Osmotic edema develops with an increase in blood glucose and sodium. It leads to brain dehydration, and then to complete dehydration of the body.
Interstitial edema is formed due to the penetration of water into the brain tissue.

What does pathology lead to?

Edema is often fatal, causing irreversible damage to brain tissue. Modern medicine cannot guarantee the patient's recovery even with proper therapy.

Cerebral edema threatens the following conditions:

Progression of edema causing death of the patient. These consequences are typical for most victims. A person is in a stable condition if there is free space in the cranial cavity. When it becomes completely filled with fluid, constriction of the brain occurs. At the same time, dense brain structures turn into soft ones. Thus, the cerebellar tonsils become wedged into the trunk, resulting in the cessation of a person’s breathing and heartbeat.
Elimination of edema without consequences for the brain. This outcome is rare and is possible for young people if the swelling is caused by intoxication.
Getting rid of edema, while the patient becomes disabled. This is how the swelling that occurs due to infectious diseases, minor injuries and hematomas ends. In this case, the disability may not be visually manifested.

After such a pathology in adults the following are observed:

frequent headaches;
absent-mindedness;
convulsions;
problems with coordination;
poor sleep;
physical development defects;
communication skills disorder;
breathing problems;
depression;
epilepsy;
paralysis;
coma;
a vegetative state, when the patient is not aware of and does not respond to the environment because the function of the cerebral cortex is lost.

Brain edema in children

The skull of newborns has its own characteristics. The skull bones are connected by cartilage as the baby's brain continues to grow.

Reasons for appearance

The accumulation of fluid in the brain in children is provoked by:

intrauterine fetal hypoxia;
congenital pathologies of the nervous system;
birth injury;
accumulation of pus in the brain;
previous infections in utero;
meningitis and encephalitis;
increased amount of sodium in the blood (observed in premature babies);
congenital tumors in the head.

Symptoms of swelling

The following signs indicate cerebral edema in an infant:

drowsiness;
anxiety;
breast refusal;
tachycardia;
strong cry;
dilated pupils;
lethargy;
temperature increase;
tension or swelling of the fontanel;
vomit;
increase in head size;
convulsions.

If timely assistance is not provided, the child’s condition worsens, the disease develops quickly and ends in death.

If a child is prone to edema, he should be observed by a neurologist to exclude intracranial pathology, which will increase the chances of survival. The most dangerous period for a baby is the month after birth.

Possible complications

The consequences of the disease in children are:

decrease in intellectual skills;
impaired functioning of the body (lack of reflexes, inability to hold up the head);
insufficient development of communication abilities;
epilepsy;
death.

Diagnostic features

If swelling of the brain is suspected, the patient is prescribed:

examination by a neurologist and ophthalmologist;
blood analysis;
examination of the cervical spine;
MRI and CT of the brain;
neurosonography for children under one year old.

On early stages diseases, when the symptoms are not clearly expressed, an examination of the fundus will be required. Edema will be indicated by congestion of the optic discs, the reaction of the pupils, and characteristic movements of the eyeballs.

Treatment of swelling

The therapeutic course consists of a set of procedures aimed at:

fight against progression swelling of the brain;
eliminating the cause swelling;
treatment of symptoms causing complications and aggravating the patient’s well-being.

The causes of cerebral edema are eliminated:

treatment with antibiotics: cefepime, cefuroxime;
prescribing blockers calcium channels: phendiline, verapamil, nimodipine;
removal of toxins;
normalization of vascular tone;
elimination of the tumor if the patient’s condition is stable;
improving blood circulation;
drainage of cerebrospinal fluid.

When treating this pathology, it is necessary to control the cardiovascular system and body temperature, since its increase exacerbates swelling.

When cerebral edema is diagnosed, the patient must be hospitalized. He is placed in the intensive care unit, and the patient’s vital functions are supported artificially.

Only swelling that is small or caused by mountain sickness can go away on its own.

Main treatment methods:

medicinal;
oxygen therapy;
with the help of surgery.

Drug treatment

A complex of medications is prescribed for treatment:

Diuretics to remove excess fluid from tissues: lasix, sorbitol, furosemide, mannitol. They have a diuretic effect and are used in combination with glucose and magnesium sulfate to enhance the effect.
Decongestant drug L-lysine escinate.
Installations to increase oxygen saturation of tissues, and, if necessary, artificial ventilation.
Mexidol, contexten, actovegin, ceraxon improve metabolism.
Muscle relaxants to relieve cramps.
Glucocorticoid hormones: prednisolone, dexamethasone, cortisone, hydrocortisone. They stabilize the membrane of affected cells, strengthening the vascular walls.

Oxygen therapy

This method involves introducing oxygen directly into the blood artificially. This manipulation provides nutrition to the brain, helping to eliminate swelling.

Surgical intervention

With the help of surgery, the cause that caused the swelling of the brain tissue is removed. This is the only way to get rid of dangerous disease, if it was provoked by a neoplasm, a violation of the integrity of blood vessels, or traumatic injuries to the skull.

The fluid accumulated in the head is drained with a catheter, which reduces intracranial pressure.

Surgeries performed on the brain are among the most complex.

Forecast

The prognosis of the disease is influenced by the timeliness of treatment. When swelling occurs on the brain, it appears strong pressure, which can damage vital nerve centers. As a result of the death of neurons, paralysis or coma occurs.

The degree of development of the disease plays a huge role.

Perifocal edema is easier to cure, but not all of the patient’s lost functions can be restored.

Prevention

Illness can be avoided if you follow safety rules. These include:

fastening seat belts;
wearing a helmet when riding a bicycle, rollerblading, or working on a construction site;
undergoing acclimatization during mountaineering;
to give up smoking;
constant monitoring of blood pressure.

Conclusion

Brain edema – dangerous condition, most often resulting from skull trauma or infection. When the first signs of the disease appear, you should consult a doctor, who, after a series of procedures, will prescribe a course of treatment. If the disease is detected in the early stages, it can be treated with medications. In this case, prolonged pathology can only be treated surgically and will leave complications varying degrees heaviness for life.

Cerebral edema is considered one of the most dangerous conditions, life-threatening person. If this pathology is present, it is important to immediately identify the provoking factor and begin treatment immediately. Delaying time can contribute to severe damage to the central nervous system.

What is cerebral edema

Cerebral edema is an accumulation of fluid in the cerebral tissues, which develops rapidly and creates pressure on the membranes of the organ. This pathology is not an independent disease, but occurs under the influence of a number of provoking factors. As a result of the accumulation of fluid in the intercellular space, the brain increases in size.

Normally, a small amount of fluid (CSF) should circulate in the brain

Since the bones of the skull are hard and unable to expand, a life-threatening condition occurs caused by significant compression of the organ tissue. If the pathological process is not detected in time, more and more fluid accumulates. In this case, the brain is in a cramped position, in which important centers, including those regulating breathing, suffer.

When cerebral edema occurs, tissue swelling occurs

Interesting fact: cerebral edema was first described by the famous doctor and scientist Nikolai Ivanovich Pirogov in 1865. His contribution to this pathology allowed for timely recognition of a dangerous condition and immediate initiation of treatment.

Causes and provoking factors

The pathogenesis is based on microcirculatory disorders, which initially have a focal nature. If left untreated, the pathological process covers all brain tissue. In the latter case, a life-threatening condition develops. The most common cause of swelling of brain tissue is injury to the organ. Factors provoking this pathological condition:

strong head impacts;
skull fracture;
various types of hematomas (blood clots formed as a result of traumatic injury);
diffuse ruptures of the nerve endings of the brain;
surgery in the brain area;
brain tumors, including malignant and benign;
purulent processes;
encephalitis.

Tissue swelling can occur as a result of an acute allergic reaction to any component, as well as poisoning with toxic substances. The development of pathology is possible with alcoholism, which is associated with thinning and increased permeability of blood vessels.

Inflammation of the meninges during meningitis provokes the accumulation of fluid in the tissues

The disease often manifests itself in newborns whose mothers suffered from severe toxicosis during pregnancy. In infants, edema forms as a result of injury during childbirth and when the umbilical cord is entangled.

A slight accumulation of fluid in the brain tissue is possible during a sharp climb up the mountain. This often happens to unprepared people. Symptoms quickly disappear when descending from altitude.

Causes of cerebral edema: closed craniocerebral injury - video

Classification

There are several forms of pathology, the main of which are focal and generalized. The first is characterized by a limited area of tissue swelling and often occurs in the initial stages. The generalized form is a consequence of lack of treatment. In this case, all tissues of the left or right hemisphere swell. Swelling occurs under the influence of three factors:

tissue - fluid accumulates in the intercellular space when microcirculation is disrupted;
circulatory - vasodilation occurs, in which the pressure on the tissue increases;
vascular - the walls of blood vessels become permeable and some of the blood sweats through them.

80% of the brain is cerebral tissue, 15% is occupied by circulating fluid (CSF) and 5% is blood. When edema occurs, intracranial pressure increases. The pathological process develops due to an increase in the volume of cerebral tissue. In this case, the vessels are compressed, hypoxia occurs, as a result of which neurons die.

Increased intracranial pressure and edema occur when there is a violation of the circulation of fluid (CSF) in the brain

The following types of pathology are distinguished:

vasogenic, characterized by pathological permeability of the blood-brain barrier (can be provoked by tumors and diseases of the vascular system);
perifocal, which is swelling that occurs in the area of ischemia, abscess, tumor or in the area of surgical intervention;
cytotoxic, which occurs when the functions of glial cells and the regulation of neurons are disrupted (often provoked viral diseases, exposure to toxic substances, etc.);
diffuse - edema occurs evenly and covers all brain tissues;
traumatic - is a consequence of a bruise, blow, car accident, etc., first affects a certain limited area of the brain, subsequently covering nearby tissues;
osmotic, which appears as a result of an increase in osmolarity of cerebral tissues (there is more fluid than there should be). May occur due to unsuccessful hemodialysis or drowning);
interstitial (paraventricular), which occurs when the pressure inside the ventricles increases, at which the surrounding brain tissues become saturated with fluid.

A brain tumor is often the cause of perifocal edema

The blood-brain barrier (BBB) is a kind of physiological boundary between the central nervous system and the circulatory system. This is necessary to prevent toxins and certain types of substances from reaching the neurons. Such a barrier performs protective functions. If the permeability of the BBB increases under the influence of pathological factors, then cerebral edema may occur.

Clinical picture

The main symptom characterizing the presence of cerebral edema is impaired consciousness. In the initial stages it is mild, but in advanced cases a person can fall into a coma. Additional signs of pathology:

convulsions;
epileptic seizures;
prolonged headache;
nausea and vomiting;
hallucinations;
visual impairment;
increased blood pressure;
impaired coordination of movements;
increased body temperature;
breathing and heartbeat disorders;
lack of pupillary response;
photophobia.

Intense headache that does not go away after taking medications may indicate cerebral edema

A characteristic symptom The pathological process is fainting, which differs in its duration.

How to give first aid

With cerebral edema, every hour counts, so you shouldn’t tempt fate, but even with a slight suspicion of pathology, you need to call an ambulance. It is recommended to put the victim to bed before medical workers arrive. If the person is conscious, then you can give him any diuretic medicine that is in the medicine cabinet, for example: Furosemide, Lasix, etc. Such drugs remove excess fluid from the body, which will reduce the intensity of tissue swelling.

Furosemide is a loop diuretic that has a diuretic effect.

It is also advisable to open a window or vent, thereby ensuring a flow of fresh air into the room. If there is a severe headache, then you can use any analgesic. If your blood pressure has risen, you need to take antihypertensive drug, for example: Enalapril, Adelfan, etc.

Enalapril lowers blood pressure

These methods do not replace visiting a doctor. Even if the condition has returned to normal, it is necessary to call an ambulance, since in the initial stages of cerebral edema, the symptoms are slightly dulled when taking analgesics and diuretics.

Take diuretics in large quantities. 1 tablet is enough.
Drink plenty of fluids.
Trying to get rid of pathology using traditional methods.
Refuse hospitalization.

A patient with cerebral edema must be taken to the intensive care unit of the neurosurgical department. The more time has passed since the first symptoms appeared, the higher the likelihood of death.

What conditions require an urgent call to the ambulance?

If the patient’s condition is satisfactory, then you can take him to the neurosurgical department yourself by car. Ambulance You should call immediately if you have the following symptoms:

fainting;
intense headache;
uncontrollable vomiting;
seizures;
blurred vision;
intermittent breathing.

If the patient has lost consciousness, then first of all you need to look at his pupils, opening his eyelids slightly. If the gaze is scattered and the eyes look in different directions, then this is a symptom of cerebral edema.

Diagnostic methods

CT scan of the brain. Computed tomography is performed using x-rays, which are used in minimal quantities. In this case, the doctor determines the characteristic cerebral edema using a series of images, which he receives from different projections. The method helps to identify provoking factors: tumors, abscesses, etc.
MRI. Magnetic resonance imaging is considered a more reliable research method than CT. In addition, the specialist obtains images using nuclear magnetic resonance. This method is safe and reliable. On a computer monitor you can get a 3D image of the organ being examined. With cerebral edema, swollen tissues and compressed centers are visible.
General blood analysis. Used as an auxiliary method to determine the condition of the body as a whole. At the same time, deviations from the norm of leukocytes, erythrocyte sedimentation rate, and platelet count are assessed. However, in the initial stages of cerebral edema, general indicators may remain unchanged.
Encephalography. Used as an auxiliary method to identify the degree of neurological disorders. In this case, a special device with lots of wiring. The electrodes transmit impulses from the brain, which are recorded on a special diagram, with the help of which the doctor can detect the presence of disturbances in the functioning of the organ.

MRI of the brain is the most reliable method definition of cerebral edema

Additionally, in rare cases, lumbar puncture may be used, in which spinal cord A small amount of fluid is withdrawn for examination. The procedure is carried out using a thin and long needle, which is placed between the 3rd and 4th or 4th and 5th vertebrae. The puncture is performed only in extreme cases, as it has a number of contraindications and side effects.

Diagnosis criteria

Cerebral edema is confirmed if there is:

characteristic neurological symptoms;
high rate of increase in intracranial pressure;
papilledema;
increased tendon reflexes;
decreased reaction of the pupils to a light stimulus;
divergence of eyeballs;
pronounced swelling of the conjunctiva.

The diagnosis is confirmed only through a brain scan using computed tomography or magnetic resonance imaging.

Treatment tactics

In the presence of this pathology, treatment is aimed at gradually removing excess fluid from the brain, as well as restoring cerebral metabolism. It is important to determine the root cause of edema and eliminate it. In this case they use different ways treatment. For edema that is not caused by tumors and hematomas, you can do without drug therapy. In addition, they often resort to drainage of the cranium to reduce intracranial pressure. Treatment of cerebral edema is always complex.

Traditional methods of therapy in the presence of this pathology will not only not bring results, but can also provoke life-threatening consequences.

Surgical intervention

If the pathology is caused by trauma, as a result of which a hematoma is formed, then surgical intervention is indicated. This approach is also used in the presence of brain tumors of benign and malignant origin.

Brain hematoma is a common cause of edema

In this case, the pathological area is most often removed using a special neuroendoscope. First, the doctor creates access to the organ by making a small hole in the skull. Then, using an endoscope, he reaches the pathological focus and carefully excises it. However, this method is not always possible, because some tumors are located near vital centers, accidental injury to which can cause death or paralysis.

Brain surgery is monitored using images on a computer monitor

For cerebral edema caused by bruises, infectious diseases and stroke, craniotomy is used. This type of surgery can reduce intracranial pressure. This reduces the risk of compression of important brain centers. The operation consists of draining the skull. A small hole is created, which is covered by the temporalis muscle. This measure is necessary when severe swelling, which can be fatal. Once the cause is eliminated, the hole is closed with a skull bone or an implant.

Craniotomy is an operation to reduce intracranial pressure

Surgery on the brain is always associated with risks, since this organ regulates all processes in the body. A correctly performed operation promises a favorable prognosis, but the slightest mistake can cost a person his life.

Conservative methods of therapy

To remove excess fluid, intravenous infusion is used. loop diuretics, such as Torasemide, Furosemide and others. The effect of these drugs is enhanced by injection of 40% glucose solution and 25% magnesium sulfate. This combination of drugs helps not only reduce intracranial pressure, but also nourish cerebral neurons.

Magnesium sulfate in combination with glucose is administered intravenously for cerebral edema

Additionally used for treatment:

Metabolites: Mexidol, Citicoline, etc. Improve blood circulation in the brain, relieve hypoxia and have an antioxidant effect. It is used both for intravenous infusion and prescribed for oral administration. The course is individual in each case.
Glucocorticoids: Prednisolone, Hydrocortisone, etc. Prescribed to eliminate the symptoms of edema, as well as to stabilize cell membranes. These medications are used for a short course. It is also used either for intravenous administration or prescribed for oral administration.
Painkillers: Analgin, Tempalgin, etc. Used to eliminate intense symptoms that are accompanied by headache.
Antibiotics: Amoxicillin, Flemoxin, etc. This group of medications is used for treatment if the cause is an infectious disease or its complications, such as an abscess.

If the cause of edema is meningitis, then antiviral or antibacterial drugs are prescribed. Treatment tactics depend on the etiology of the disease. Additionally, diuretic medications are used.

Medicines used for treatment - photo gallery

Amoxicillin destroys pathogenic microflora Prednisolone is a systemic glucocorticoid Mexidol is a complex action drug Analgin eliminates pain symptoms

Rehabilitation period

Rehabilitation after cerebral edema often takes at least 3 months. In this case, the patient must remain in bed for 4–8 weeks. During the period of recovery of the body, it is necessary to eat properly, the diet should include more vegetable fiber, cereals, freshly squeezed juices and fish. The menu should also include lean first courses, nuts and dried fruits. The drinking regime is determined by the doctor depending on the cause of the edema. Often, the amount of liquid you drink per day should not exceed 1–1.5 liters.

Vegetables and fruits are recommended to be consumed during the period of recovery of the body

Recovery period may include light gymnastics, short walks on fresh air, as well as taking medications that improve blood circulation in the brain. Rehabilitation excludes mental and physical activity. It is also forbidden to be nervous and stay in one position for a long time.

Rehabilitation after cerebral edema takes different times for each patient, as it depends on the provoking factor that caused the pathology.

Prognosis and complications

If you managed to get rid of cerebral edema in the initial stages, then the prognosis is favorable. In advanced cases, irreversible processes and death of neurons occur with the further appearance of pathologies. To prevent complications, you need to follow all the doctor’s recommendations during the rehabilitation period: eat right, take medications and get plenty of rest.

Frequent dizziness may occur after cerebral edema

Long-term consequences that may occur 6–12 months after rehabilitation:

epileptic seizures;
decreased visual acuity;
mental disorders;
feeling of spasms in the head;
convulsions.

To eliminate the consequences, medications are prescribed that improve brain function and the conduction of nerve impulses, as well as antioxidant drugs.

Features of pathology in children and pregnant women

Pathology in newborns is often associated with hydrocephalus, a disease in which cerebral fluid accumulates in the area of the ventricles of the brain. This illness accompanies many congenital diseases and manifests itself as an enlargement of the skull (due to the fact that bone infants are susceptible to sprains), headaches, nausea, and frequent regurgitation. Treatment consists of taking diuretics, as well as eliminating the cause of hydrocephalus - hematoma, brain development abnormalities, etc.

Hydrocephalus causes an increase in the size of the skull

In pregnant women, pathology can occur for the same reasons as in all other people. The disease can be caused by tumors, injuries and infectious diseases. Treatment during pregnancy is conservative. In this case, diuretics and intravenous infusions of magnesium sulfate and glucose are prescribed. If there is a risk to the woman’s life, then surgical intervention is performed and the pregnancy is terminated.

What is cerebral edema and how to eliminate it - video

In many cases, cerebral edema requires urgent surgical intervention. If you ignore your doctor’s recommendations, you may encounter a number of dangerous consequences which often lead to disability. At the first signs of increasing cerebral edema, you should call a doctor.

EDEMA AND Swelling of the brain- a reactive process characterized by disruption of water-salt and other types of metabolism in the brain, as well as disorders of cerebral circulation and expressed in both intra- and interstructural hyperhydration, which usually leads to an increase in the volume of the contents of the skull and an increase in intracranial pressure. Edema and swelling are also possible in the spinal cord; they obey basically the same laws as in the brain, but this process in the spinal cord has not been sufficiently studied.

Many researchers equate the concepts of “edema” and “swelling” of the brain, giving preference to the first term; others believe that swelling represents more high degree edema, in particular intracellular; Most research schools clearly distinguish between edema and swelling of the brain, understanding edema as an increase in the content of free fluid (with a relative decrease in dry matter), and swelling as an increase in bound fluid. In practice, the accumulation of fluid in the intercellular space is regarded as edema (see), and its accumulation inside the cells is considered swelling (see).

The most consistent with reality is the idea that edema and swelling of the brain are, in principle, independent, but closely related and always combined processes, usually poorly differentiated by the time of occurrence; the primacy of a particular process varies depending on the characteristics of each individual case. The development of the doctrine of edema and swelling of the brain is associated with the works of N.I. Pirogov, M. Reichardt, N.N. Burdenko, A. I. Arutyunova, L. I. Smirnov, V. K. Beletsky, G. I. Mchedlishvili, K. Zulch and others.

Classification

The most recognized classifications of cerebral edema and swelling are based on etiological and pathogenetic principles. According to etiol, the signs are tumor, traumatic, postoperative, toxic (intoxication), inflammatory, ischemic, osmotic, hydrostatic edema and swelling of the brain. However, this division is very relative; combination possible various forms. By pathogenetic principle a distinction is made between vasogenic and cytotoxic edema and swelling of the brain, although the vasogenic form, as a rule, also includes a cytotoxic component, which is manifested by a certain “readiness” of the brain parenchyma for the development of this process in it.

Etiology

Pathogenesis

Pathophysiol, the mechanisms of development of edema and swelling of the brain are similar to the mechanisms of edema in other organs, however, the brain is characterized by more rapid swelling of cellular elements. Among these mechanisms, an important role belongs to circulatory factors, tissue changes, as well as increased permeability of vascular walls (see Blood-brain barrier).

A circulatory factor, which directly affects the filtration of water from blood vessels into brain tissue, is intravascular pressure. Its level in the vessels of the brain is determined both by the general pressure in the arteries and veins of the body, and by the resistance to blood flow in the arterial system of the brain. The rate of development of edema and swelling of the brain after injuries, ischemia, etc. increases significantly with a significant increase in total blood pressure. A sharp increase in it, causing a breakdown in autoregulation, can itself cause edema and swelling of the brain without additional influences. In hypertensive crises, edema and swelling of the brain can result from the use of vasodilators in doses that increase cerebral blood flow. An increase in total venous pressure significantly increases the pressure inside the vessels of the brain and is more conducive to the occurrence of edema and swelling than an increase in total blood pressure, since the resistance in the venous system is small and there are no autoregulation mechanisms that limit this effect.

Decreasing blood osmolarity changes its osmotic pressure, increasing the filtration of water into brain tissue, which can also cause edema and swelling of the brain. In experiments, this is observed when animals are injected with distilled water into a vein or abdominal cavity. Under natural conditions, the main role in the development of edema is played by a decrease in the concentration in the blood of macromolecular particles that determine colloid-osmotic pressure, but not ions such as Na +, Cl -, etc., the concentration of which is in the blood plasma and interstitial fluid brain is approximately the same.

Tissue changes in the brain play a particularly important role in the development of its edema and swelling. In this case, the main importance is to reduce the hydrostatic pressure of the interstitial fluid and increase its osmolarity. Hydrostatic pressure is determined both by the mechanical properties of the structural elements surrounding the tissue spaces and by the amount of fluid in them. Of no small importance in reducing hydrostatic pressure is the size of these spaces, which, during swelling, stretch the more easily, the larger their diameter. Already in the pre-edema state, brain tissue becomes more extensible and plastic, which contributes to the retention of water in its interstitial spaces.

An increase in the osmolarity of the interstitial fluid of the brain can occur with increased catabolism in brain tissue observed after injury, during cerebral ischemia and other damaging influences. In these cases, as well as when blood plasma directly enters the brain tissue as a result of hemorrhage or exudation, the concentration of macromolecular compounds in the interstitial fluid increases, i.e. its osmolarity increases, and consequently, the flow of water into the brain from the blood increases. It is possible that the concentration of macromolecular compounds in the interstitial fluid of the brain also increases the movement of water into the cellular elements during swelling of the gray matter of the brain.

An increase in the permeability of the vascular walls of the brain is detected simultaneously with the development of edema and swelling after injury as one of the components of brain damage. However, the role of this factor in the transition of water from blood to tissue is apparently small, since there is no barrier to water in the vascular walls and is normal. But this role increases significantly with such a violation of the blood-brain barrier, in which it becomes possible for blood proteins to enter the interstitial fluid of the brain, causing an increase in its osmolarity.

Edematous fluid accumulates in the brain tissue unevenly: in the white matter it is located mainly in the interstitial spaces, in the gray matter it is intracellular, and the heads swell. arr. glial elements, and neurons are often even wrinkled. The movement of excess amounts of water from outside to intracellular spaces is caused by a violation of the active transport of ions through plasma membranes (see Biological membranes).

TO compensatory mechanisms, which can act during edema and swelling of the brain and delay or stop the development of this process, include: a decrease in intracapillary pressure in the brain as a result of a drop in general arterial and venous pressure and narrowing of the main arteries and arteries of the soft shell of the brain; normalization of the mechanical properties of brain tissue (reducing flabbiness and pliability of its structures), as a result of which the pressure of the interstitial fluid increases and the resorption of water into the bloodstream increases; strengthening the active transport of ions and colloidal particles through the membranes of cellular elements, as well as the vascular wall from the brain tissue into the blood, as a result of which the osmolarity of the interstitial fluid of the brain decreases and the transition of water into the blood increases blood vessels, and possibly into the cerebrospinal fluid.

Biochem, changes during edema and swelling of the brain are expressed in an increase in the water content in the brain tissue: in the white matter it can be St. 80% At the same time, Na+ and Cl- ions are retained, the content of various nitrogenous fractions, nucleic acids, phosphoproteins increases, and the ratio of albumin to globulins increases. Changes in the enzymatic systems of the brain are observed, associated with a disorder of cell energy metabolism and transport in plasma membranes, acidic products and osmotically active substances accumulate. Tissue acidosis contributes to changes in the intra- and extracellular concentration gradient (see Gradient), and this leads to fluid redistribution. With edema and swelling in the brain tissue, disturbances of anaerobic glycolysis, quantitative and qualitative changes in the activity of mitochondrial and Na+-K+-dependent ATPases, a decrease in the content of creatine sulfate and ATP with an increase in the content of ADP, AMP, inorganic phosphorus, as well as disorders of lipid metabolism ( reduction in lecithin content, etc.).

In the rare independent (or predominant over edema) form of swelling, the brain substance is even in a state of water deficiency (the dry residue increases); it shows significant changes in the metabolism of proteins and lipids, in particular, polymerization (formation of high-molecular hydrophilic polymers) and increased binding of water by sphingomyelin occur.

Pathological anatomy

Macroscopically, edema and swelling of the brain are characterized by a number of signs: moisture and turbidity of the surface, an increase in volume, increased flabbiness (water content) of the brain matter, which has a yellowish-pink color, and unclear boundaries between the gray and white matter (Fig.). Due to the general increase in the volume of the brain, deep depressions are found in the area of the cerebellar hemispheres and protrusion of its tonsils, which is a morphological sign of strangulation of the stem sections in the foramen of the tentorium of the cerebellum. However, differences in the signs of edema and swelling are also noted. With predominant edema, there is plethora and swelling of the soft membrane of the brain, and a clear liquid drains from the surface along with blood. There is an increased amount of cerebrospinal fluid in the ventricles of the brain. On sections, the brain substance appears to be excessively moist, it can be easily cut with a knife, and clear liquid flows from the cut surface. With predominant swelling of the structural elements of the brain, the soft meninges, on the contrary, are dry, the brain substance is dense, the knife sticks to the cut surface. In the ventricles of the brain, cerebrospinal fluid is absent or contained in small quantities; the ventricles are slit-like.

Features of the microscopic picture are determined by the presence in the medulla of interstructural spaces filled with interstitial fluid, which occupy up to 10-15% of the organ’s volume. Electron microscopic data on the gapless fit of the structural elements of brain tissue and the predominantly intraglial nature of cerebral edema require correction. The possibility of rupture of astrocytic processes overloaded with fluid is also recognized by some supporters of the intrastructural theory of edema. Increased hydration of brain tissue under light microscopy is manifested by its loosening, more or less widespread dystrophic changes in neurons of the cortex and subcortical centers, as well as the walls of intracerebral vessels, swelling of the myelin sheaths of nerve fibers with the formation of balloon-shaped swellings, dystrophic and proliferative changes in astrocytic neuroglia with decay phenomena processes (clasmatodendrosis), hydropic transformation of hyperplastic oligodendroglia (especially along the brain capillaries), sometimes activation of microglia.

In pathomorphology, diagnosis, it is necessary to take into account the complex of macro- and microscopic signs, as well as their relationship with each other. Availability individual signs, for example, expansion of the perivascular spaces, does not yet indicate edema and swelling of the brain, since it may be a consequence of the redistribution of tissue fluid without increasing its quantity. Therefore, the common term “perivascular cerebral edema” is relative. One of the reliable indicators of edema and swelling is a violation of the specific density of brain tissue. Edema and swelling of the brain can be predominantly local (perifocal) or diffuse. The process usually involves both gray and white matter, but according to some researchers, it predominates in white matter. It is not possible to clearly identify areas of brain tissue that are particularly susceptible (or resistant) to edema and swelling.

Clinical picture

The clinical picture of edema and swelling of the brain is characterized by general cerebral and focal symptoms. General cerebral phenomena are determined by an increase in intracranial pressure (see Hypertensive syndrome), when the process affects large parts of the brain or becomes generalized. In this case, characteristic attacks of exacerbation of headaches are observed, at a height of which vomiting may occur; sometimes a disturbance of consciousness such as stunning; change in activity of cardio-vascular system(pulse rate, blood pressure, etc.), respiration; congestive papillae of the optic nerves are determined.

Focal brain lesions develop due to its displacement during edema and swelling and herniation of the basal-medial parts temporal lobe or superomedial parts of the cerebellar hemisphere into the tentorial foramen with compression of the midbrain and cerebellar tonsils in the foramen magnum, as well as compression of the lower parts of the medulla oblongata and upper sections spinal cord (see Brain dislocation). When the midbrain is compressed, signs of damage are observed oculomotor nerve(dilation of the pupil and disappearance of the pupillary reaction, upward gaze paralysis, etc.), with compression of the posterior cerebral artery - temporary visual impairment or homonymous hemianopsia. Decerebrate rigidity, hemiparesis, vestibular disorders, etc. may also develop.

Herniation of the cerebellum into the foramen magnum is accompanied by symptoms of dysfunction of the cranial nerves (bradycardia, dysphagia, sudden vomiting); Rigidity of the neck and paresthesia in the arms may develop. In advanced stages it is possible sudden stop breathing.

Whether local edema and swelling of the brain cause focal symptoms has not been established, since in practice their influence cannot be separated from the influence of the cause that caused them. These symptoms are also caused by tumors, abscesses, traumatic lesions, and cerebral infarction.

Diagnosis

Diagnosis general edema and swelling of the brain is based on taking into account clinical data and the results of additional research methods. The cardinal symptom of this process, increased intracranial pressure, is diagnosed by measuring the pressure of the cerebrospinal fluid using tensiometric sensors, as well as on the basis radiological signs hypertensive changes in the bones of the skull, EEG data(appearance of slow waves), slowdown of the general cerebral circulation; reduction in the volume of the brain ventricles and subarachnoid spaces, detected by encephalo- or ventriculography (see Encephalography).

Local edema and swelling of the brain are diagnosed using echoencephalography (see), when the cut is determined by the displacement of the affected area of the brain; pneumoencephalo- or ventriculography, in which a displacement of the ventricular system in the opposite direction and possible deformations of the ventricle in the focal area are detected; angiography, in which a slowdown in local blood flow, displacement of the vessels of the affected area, and the appearance of a seemingly avascular area are observed in the cut; radioisotope scanning (see), based on the fact that certain isotopes (labeled albumin, 32 P, etc.) accumulate in increased quantities in the area of edema and swelling of the brain. A particularly highly informative and largely differentiated understanding of edema and swelling of the brain, their relationship and dynamics of development is provided by the determination of the electrical impedance of brain tissue (see Impedance), carried out using deep electrodes and currents of a certain frequency.

Treatment

Treatment of edema and swelling of the brain requires an in-depth analysis of each individual case. Treatment measures are always aimed, on the one hand, at eliminating the cause that gave rise to the development of edema and swelling of the brain, and on the other, at normalizing cerebral circulation, removing excess fluid from the brain (see Dehydration therapy), normalizing the permeability of the blood-brain barrier, correcting metabolic disorders. For this purpose they are used intravenously hypertensive solutions(glucose, sodium chloride, magnesium sulfate, urea, mannitol, glycerin, isosorbitol), diuretics, vitamins, analgesics, corticosteroids (dexamethasone, etc.), ganglion blockers, antihypoxants. Moderate hypothermia is sometimes used.

Forecast

By its nature, edema and swelling of the brain is a reversible process; the prognosis for it largely depends on the severity of the disease that caused it. With progressive development, edema and swelling of the brain can result in death from entrapment of the brain stem in the foramen of the cerebellar tentorium or from dislocation of the hemispheres with an uneven increase in their volume.

Bibliography: Avtsyn A. P. and Shakhlamov V. A. Ultrastructural foundations of cell pathology, M., 1979; Arkhangelsky V.V. Pathological anatomy traumatic brain injury, Disorders of water metabolism and cerebrospinal fluid formation, Guide to neurotraumatology, ed. A. I. Arutyunova, part 1, p. 19, M., 1978; B a k iL.iLiD. Cerebral edema, trans. from English, M., 1969, bibliogr.; Zhab o-tinsky Yu. M. Normal and pathological morphology of a neuron, JI., 1965; K in and t n and c to and y-R y about in Yu. N. Edema and swelling of the brain, Kyiv, 1978, bibliogr.; To about l t about in e r A. N. et al. Pathological anatomy of cerebral circulation disorders, M., 1975; Multi-volume guide to surgery, ed. B.V. Petrovsky, vol. 3, part 1, p. 137, M., 1968; Mchedlishvili G.I. On the pathogenesis of post-ischemic cerebral edema, Anest. and resuscitation, No. 2, p. 47, 1980; M h e d l and sh v i l and G. I., H and k o-laishvili JI. S. and I t kis M. JI. Transcapillary filtration of water with increased intravascular pressure as a factor in the development of cerebral edema, Vopr, neurosurgeon, “Nb 4, p. 15, 1978; Peters A., Paley S. and Webster G. Ultrastructure of the nervous system, trans. from English, M., 1972; Tuma

new V.P. and MalamudM. D. Changes in the central nervous system during thermal, radiation and combined trauma, Chisinau, 1977; Brain edema, ed. by I. Klatzo a. F. Seitelberger, Wien-N.Y., 1967; Dynamics of brain edema, ed. by H. M. Pappius a. W. Feindel, V. a. o., 1976; R e u 1 e n H. J. Vasogenic brain oedema, Brit. J. Anaesth., v. 48, p. 741, 1976; Steroids and brain, ed. by H. J. Reulen a. K. Schiirmann, V. a. o., 1972.

A. P. Romodanov, Yu. N. Kvitnitsky-Ryzhov; G. I. Mchedlishvili (pathogenesis).

Cerebral edema is the result of interconnected physical and biochemical processes occurring in the body due to diseases or pathological conditions.

This complication, depending on its severity, can go almost unnoticed, for example, with a mild concussion. But most often the consequences of cerebral edema are severe complications:

changes in mental and mental activity;

motor dysfunction;

auditory;

visual;

coordination functions, which leads to disability of the patient;

Quite often, cerebral edema causes death.

What is cerebral edema?

The essence of the definition this state consists in a nonspecific response of the whole organism to the influence of severe damaging factors. The latter may be the reason:

changes in plasma protein (oncotic) and electrolyte (osmotic) pressure;

violations of the acid-base state (pH) of the blood;

disruption of energy, protein and water-electrolyte metabolism and accumulation of lactic acid in nerve fibers;

oxygen starvation of brain tissue, especially if it is combined with excessive accumulation of carbon dioxide in the blood;

disturbance of blood microcirculation in brain tissue.

All these reasons provoke the development of swelling and edema of the brain. Edema provokes a violation of the permeability of the capillary walls and the release of the liquid part of the blood into the surrounding tissues. When swelling occurs due to the difference in oncotic pressure, water molecules begin to flow directly into the nerve cells through the membrane. Here they interact with intracellular proteins, as a result, the cells increase in volume.

However, most authors scientific research swelling is considered as one of the stages of edema, which leads to an increase in brain volume. This situation provokes its displacement around its axis in a confined space, which is limited by the bones of the skull.

The spread of cerebral edema causes compression of the medulla oblongata and other underlying structures in the foramen magnum. This zone contains vital regulatory centers that control thermoregulation, cardiovascular activity, and respiration.

Signs of cerebral edema are manifested by impaired functioning of brain centers and nerve cells even before the onset of complete damage to the structures of the latter, which is determined only with the help of modern methods diagnostics

Types and causes of cerebral edema

There are 2 types of cerebral edema:

regional or local edema - limited to a certain area that surrounds the pathological formation in the brain tissue; cyst, hematoma, tumor, abscess;

widespread or generalized – covers the entire brain. Develops as a result of the loss of a large volume of protein in the urine during poisoning and various diseases, intoxication, drowning, suffocation, traumatic brain injury, and hypertensive encephalopathy, which occurs against the background severe forms increased blood pressure and other disorders.

In many cases, excluding asphyxia and traumatic brain injury, identifying cerebral edema is a difficult task against the background of clinical manifestations of other pathological conditions and diseases. The onset of the development of edema can be suspected when, against the background of a lack of progress or a decrease in the symptoms of the underlying disease, neurological symptoms begin to increase and progress.

The main reasons for the development of cerebral edema:

traumatic brain injury, laryngeal stenosis if the child has an acute respiratory infection, asphyxia with vomit after an alcoholic coma, brain contusion;

subarachnoid hemorrhage, which occurs due to a stroke in the presence of high blood pressure;

brain tumors;

subdural hematoma, which forms under the dura mater as a result of exposure to mechanical factors without compromising the integrity of the bones of the skull;

cerebral edema in newborns due to birth trauma to the child’s brain, severe gestosis in the mother, prolonged labor, umbilical cord entanglement;

poisoning with medications, gases, chemical poisons;

severe allergic reactions, anaphylactic shock;

severe course diabetes mellitus, especially if it occurs with episodes of hypoglycemic state, hepatorenal or liver failure chronic or acute form;

diseases that are accompanied by convulsive syndrome - epilepsy, heat stroke, hyperthermia in children with infectious diseases;

gestosis in the second half of pregnancy - eclampsia, preeclampsia, severe nephropathy;

acute infectious diseases – encephalitis, meningitis, influenza, including severe childhood infections – chicken pox, scarlet fever, measles, mumps.

In addition, cerebral edema is almost always observed after cranial surgery. In some cases - after operations that are performed under epidural or spinal anesthesia or are accompanied by significant blood loss due to a prolonged and pronounced decrease in blood pressure, with intravenous administration excessive amounts of hypotonic or saline solutions during surgery, as a result of difficulties in tracheal intubation to ensure artificial ventilation lungs or inadequate anesthesia, ventilation.

Symptoms of cerebral edema

Depending on the duration of the disease, the location of the lesion, the rate of increase and the extent of the process, the clinical manifestations of cerebral edema may differ. Limited (local) edema is manifested by general cerebral symptoms, much less often these are signs that are characteristic of a specific part of the brain. With the increase or presence of initially generalized edema, but slowly increasing, there is a gradual increase in the number of symptoms, which mean damage to several parts of the brain at once. All symptoms can be divided into groups.

Signs of increased intracranial pressure:

headache;

lethargy and drowsiness;

gradual increase in depression of consciousness with the appearance of nausea and vomiting;

dangerous convulsions - clonic (short-term, sweeping contractions of the muscles of the face and limbs), tonic (prolonged muscle contractions, as a result of which certain parts of the body acquire an unusual position for themselves), clonic-tonic, provoking an increase in cerebral edema;

a rapid increase in intracranial pressure provokes the development of bursting headaches, disturbance of eyeball movement, and repeated vomiting;

cerebral edema in infants (children under 1 year of age) provokes an increase in head circumference; after the fontanelles close, their opening develops due to displacement of the bones.

The appearance of scattered (diffuse) neurological symptoms

The phenomenon is reflected by the increase in the pathological process, which carries the risk of developing coma in the presence of cerebral edema. This is provoked by the involvement of the cerebral cortex in the initial process, after which subcortical structures are also involved. In addition to impaired consciousness and the patient’s transition into a coma, the following develop:

pathological grasping and defensive reflexes;

psychomotor agitation in the intervals between attacks of convulsions, the latter are of the epileptic type and occur with a predominance of muscle hypertonicity;

widespread (generalized) repeated seizures.

Group of the most dangerous symptoms

They are associated with the continued increase in cerebral edema and dislocation of its structures, followed by herniation or pinching in the area of the foramen magnum. Signs include:

Coma (various degrees).

Hyperthermia (above 40 degrees), it cannot be controlled with antipyretics and vasodilators. In some cases, a slight decrease in temperature can be achieved only by applying cold to areas of large vessels or by performing general hypotremia.

There are different pupil sizes and lack of reaction to light, floating eyeballs, strabismus, unilateral convulsive contraction of the extensor muscles and unilateral paresis, absence of tendon and pain reflexes, heart rhythm disturbances, and a tendency to reduce the number of heart beats.

If the patient is not subjected to artificial ventilation, the depth of breathing and frequency first increase, then the breathing rhythm is disrupted, and as a result, respiratory and cardiac activity stops.

Diagnostics

IN outpatient setting diagnosing cerebral edema is quite difficult, since the phenomenon has no special neurological symptoms. In the early stages, the complication may be asymptomatic or minimally symptomatic. The diagnosis is made based on the symptoms of the underlying disease or injury that caused the swelling; an examination of the fundus is also informative.

If cerebral edema is suspected, the patient should be kept in the neurosurgery or intensive care unit. In a hospital setting, a decision is made regarding the need to perform lumbar puncture, angiography. In the diagnostic process, CT and MRI are also informative, which help diagnose edema and determine the degree of its prevalence and severity.

Consequences of cerebral edema in children and adults

The earlier this pathological condition is diagnosed and intensive medical care is provided, the higher the chances of a full recovery. In the intensive care unit, restoration of blood supply to the brain, dehydration therapy, and restoration of liquor dynamics are carried out; the prognosis depends on the severity of the pathology.

In the presence of small perifocal edema, it is possible full recovery, whereas with the development of cystic-atrophic processes in the brain tissue, only partial restoration of functionality can be achieved. When treating only the underlying pathology, which is accompanied by cerebral edema, recovery is not always possible, but the high risk fatal outcome.

The success of therapy and the consequences for the patient depend on the severity of the pathology that provoked the development of such serious condition and the degree of edema itself, which in some cases ends in complete recovery. In severe cases, the following are observed:

When the swelling is localized in medulla oblongata, the location of the main life support centers, the consequences of cerebral edema can be impaired blood supply, epilepsy, convulsions, and breathing problems.

Even after appropriate treatment, the patient may experience increased intracranial pressure, which greatly worsens the patient’s quality of life, as it is accompanied by headache, drowsiness, lethargy, decreased social communication skills, loss of patient orientation in time, and disturbance of consciousness.

Infringement of the brain stem is especially dangerous; its displacement is also dangerous, which threatens the development of paralysis and respiratory arrest.

After therapy and rehabilitation, many patients have residual adhesions between meninges, in the liquor spaces or in the ventricles of the brain. This also provokes the development of headaches, depressive states, disorders of neuropsychic activity.

With prolonged cerebral edema without appropriate therapy, brain function disorders may subsequently occur, which are manifested by a decrease in a person’s mental abilities.

Children may also experience complete recovery or:

mental retardation and neuropsychic instability;

impaired motor coordination and speech;

dysfunction of internal organs and epilepsy;

development of hydrocephalus and cerebral palsy.

Cerebral edema is a serious, in most cases extremely severe, pathology that requires immediate diagnosis, adequate treatment and observation in adults by a psychoneurologist and neurologist, and in children by a neurologist and pediatrician. The duration of observation and therapy after suffering from cerebral edema depends on the severity of residual pathology.