Cerebral edema

Cerebral edema (oedema cerebri) is a pathological process characterized by the accumulation of water in the brain, an increase in its mass and volume. Water can accumulate both in the intercellular spaces and inside the cells. Often, cerebral edema is at first limited, and later spreads to more and more extensive areas of the brain. Edema usually leads to increased intracranial pressure.

The pathophysiological factor contributing to the development of brain edema is hypoxia. It entails a peculiar cascade of pathophysiological phenomena: an increase in the partial pressure of carbon dioxide in the blood (PaCO 2 ) => tissue acidosis => incipient edema of the brain tissue => slowing of arterial blood flow => disruption of liquor circulation => difficulty of venous outflow from the cranial cavity => growth the severity of brain edema, wherein, as a rule, there is disruption of the blood brain barrier function, changes in membrane potential of cells of the brain, impaired transport of ions across cell membranes, their pas accumulation and excess fluid in the extracellular and intracellular spaces.

Previously, intracellular accumulation of water was recognized as swelling, edema was considered only an increase in the amount of water in the intercellular spaces. However, these processes usually take place in parallel and their differentiation is therefore not justified.

Therefore, all the processes of accumulation of water in the brain began to be called his edema, although some authors prefer to speak about edema-swelling.


Cerebral edema always leads to an increase in its volume and mass and, consequently, to an increase in intracranial pressure. Not only the prevalence of edema, but also its localization is significant. The edema of the mediobasal divisions of the temporal lobe, which often leads to the penetration of its tissue into the cutout of the cerebellum (in the tentorial opening), has increased danger for the patient,

cerebellar edema , early causing blockade of the cerebrospinal fluid and the development of occlusive hydrocephalus, as well as swelling of the brain stem.

Various causes of cerebral edema are possible: brain injury, impaired cerebral circulation, in particular hypertensive crisis, acute hypertensive encephalopathy, hemorrhagic stroke, heart attacks, as well as brain tumors, encephalitis or meningoencephalitis, hypoxic or toxic (endogenous or exogenous), exogenous or exogenous), hypoxic or toxic (endogenous or exogenous); brain irradiation, status epileptic.

In the pathogenesis of cerebral edema, vascular (vasogenic), tissue (interstitial) factors, cytotoxic (dysmetabolic) and osmotic processes may be predominant. They differ from each other by the features of the biochemical and pathophysiological mechanisms of development and distribution of edematous fluid in the brain tissue.

The predominance of manifestations of a particular form of brain edema depends on many circumstances, in particular on the nature of the pathological process that caused it and the age of the patient.

The basis of vasogenic edema is a significant increase in pressure in the capillaries of the brain, the expansion of interendothelial slits in them, this increases the perfusion pressure in the vessels of the brain tissue, increases the permeability of the blood-brain barrier , the output of colloidal plasma components in the extracellular fluid, which contributes to enhanced filtration in the intercellular spaces of the brain water that accumulates in a significant amount in white matter.

Vasogenic edema develops in acute disorders of cerebral circulation, encephalitis, an immature glial tumor.

Interstitial cerebral edema is also a form of intercellular edema, caused primarily by a violation of the liquor circulation, especially pronounced in occlusive hydrocephalus.

The fluid penetrates the layer of ependymal cells (ependymocytes) lining the brain ventricles into the paraventricular structures of the white matter of the brain.

Cytotoxic (dismetabolic) edema of the brain is caused by exogenous and endogenous factors damaging the brain and disruption of metabolic processes in it, manifested in impaired function of energy-dependent membrane sodium-potassium ion pumps and depolarization of cell membranes, which occurs with a decrease in cerebral blood flow.

Membrane depolarization leads to electrolyte imbalance, an increase in osmotic pressure in the cellular elements of brain tissue and the accumulation of fluid in them.

Osmotic edema develops as a result of pathological changes in the osmotic gradient between blood plasma and fluid in the intercellular spaces of the brain tissue, especially pronounced in acute brain damage in children, and also develops in overly accelerated hemodialysis in patients with uremia in the presence of acute or chronic renal failure and manifestation – It is found in both white and gray matter of the brain.

In the experiments on monkeys demonstrated that the osmotic swelling in the brain is changed number of enzymes such as lactate dehydrogenase, creatine phosphokinase, increase the amount of lactic acid.

The prevalence distinguish local, trifocal, lobar hemispheric and diffuse cerebral edema. The clinical picture arising from cerebral edema is caused by dysfunction of the edema of the brain tissue, disorder of microcirculation, metabolic processes and the resulting increase in the volume of brain tissue, which can be accompanied by displacement and sometimes penetration of certain brain structures, and blood flow disorders in the brain and liquorodynamics.

In severe cerebral edema, usually a combination of all the manifestations characteristic of the options noted occurs. In the edematous tissue, a decrease in the arteriovenous difference in oxygen is pronounced, the oxygen consumption of cellular structures decreases, and the accumulation of metabolic products increases.

For the clinical picture of marked cerebral edema, cerebral symptoms (decreased mental activity, congestion, diffuse headache) are characteristic, which can be combined with the appearance or increase of focal neurological symptoms, the severity of which increases dramatically in cases of displacement and penetration of edematous brain structures.

On MRI, the edematous tissue of the brain is characterized by a lower density. According to the results of repeated MRI studies, it is possible to monitor changes in the volume of brain tissue and the edema zone detected in it, the accompanying deformations of brain structures and changes in the shape and size of the ventricles of the brain and thus control the dynamics of the swelling. Based on MRI studies, it has been established that when edema spreads to the deep structures of the brain, the clearance vector of the edematous fluid is directed towards the nearest wall of the ventricular system of the brain. This is evidenced by the occasional detection of a hypo-intensive path from the zone of perifocal edema to the adjacent sections of the ventricular system.

In a macroscopic examination of the edema brain, attention is drawn to the increase in its volume and humidity, on the cut – the vagueness of the boundaries between the gray and white matter. Histological examination reveals the expansion of the intercellular and perivascular cracks, changes in the capillary endothelium, an increase in the volume of neurons and especially of glial cells (astrocytes and oligodendrocytes), thickening of the nerve fibers, and disruption of the myelin sheath.


If signs of brain edema appear, it is necessary to identify its cause, which can be achieved by clarifying the clinical diagnosis. It is desirable, of course, that the cause of cerebral edema be eliminated, which can sometimes be achieved by conducting appropriate etiological and pathogenetic conservative treatment, for example, in hypertensive crisis, contusion of the brain, encephalitis, or surgery: removal of hematoma, abscess, tumor, and trauma – bone fragments, foreign bodies, occipital or epidural hematomas.

In all cases of cerebral edema, accompanied by intracranial hypertension, drug therapy is shown, aimed at dehydration of brain tissue. Osmotic diuretics, saluretics and corticosteroids are used for this purpose. The pathogenetic features, the pace of development of the brain edema, and the degree of its manifestation, which are different in each specific case, do not allow one to recommend rigid standard regimens for the use of drugs exerting an anti-edema effect.

The indications for osmotic diuretics are signs of marked cerebral edema, an acute or progressive increase in

shenie intracranial pressure, accompanied by rising cerebral and focal neurological symptoms, the displacement of brain structures, risk of herniation of brain tissue, as well as preparation for emergency neurosurgery.

From osmotic diuretics used frequently mannitol (15% solution intravenously for 10-20 min at the rate of 0, 5, 1.5 g / kg of patient weight, repeating the administration of the drug at the same dose every 6 hours) or glycerol (0 , 5-1.0 g / kg by mouth, can be mixed with syrup, if necessary, through a nasogastric tube).

In the process of treatment, the osmolarity of the blood should be maintained at a level not higher than 300-310 mosm / l. The effect of mannitol is manifested after 10-20 minutes and lasts 4-6 hours. Mannitol or the combined drug Reogluman containing it is administered (intravenously, first 5-10 drops, and then 30 drops in 1 minute); It is recommended to take a break after 2-3 minutes and, in the absence of side effects, continue the introduction of the drug at a rate of up to 40 drops / min, while 200-400 ml are injected.

These drugs give a pronounced dehydrating effect, reduce the aggregation of blood corpuscles, reduce blood viscosity and contribute to the restoration of blood flow in the capillaries, increase tissue oxygenation. The daily dose of mannitol should not exceed 140-180 g p .

It should be borne in mind manifest with the introduction of mannitol and other osmotic diuretics unwanted side effects:

  • due to an increase in the introduction of osmotic diuretics, the volume of blood circulating in the vessels, an increase in heart failure and pulmonary edema are possible;
  • dehydration due to diuresis stimulation, accompanied by manifestations of hypokalemia;
  • at the end of the effect of mannitol in the event of damage to the BBB, a recoil effect may manifest itself — a further increase in cerebral edema due to the return of water from the blood plasma to the tissue.

In addition, osmotic diuretics provide dehydration and a decrease in the total volume of brain tissue, affecting mainly the unaffected brain structures. This makes it advisable to use it primarily with obvious signs of brain compression.

Indicators of blood osmolality above 300 mOsm / l and diuresis exceeding 4-6 liters per day ki, to be regarded as DOS o- Bani for limiting further application of osmotic diuretics.

The effectiveness of glycerol is lower than mannitol: it begins to act 12 hours after ingestion, but practically does not cause a recoil phenomenon. The effectiveness of glycerol is observed only in patients with mild cerebral edema, mainly in ischemic stroke.

For the purpose of dehydration with cerebral edema, saluretics from the group of loop diuretics are also used, more often – furosemide (lasix), usually 20–40 mg intramuscularly or intravenously up to 3 times a day, sometimes it is advisable to combine them with osmotic diuretics. ace after administration of mannitol).

Furosemide begins to act after 35-105 minutes, the duration of action is 30 minutes-2.5 hours. Indications for the appointment of loop diuretics:

1) The desirability of amplification effect caused Osmotic diuretic;

2) Equalization of water balance in case of pronounced accumulation of fluid in the body;

3) Dehydration with mild swelling of the brain.

Loop diuretics, like osmotic ones, also have a greater effect on the intact parts of the brain, so their prophylactic use in acute neurological diseases can be useless or even harmful, as it causes an electrolyte imbalance (decrease in potassium in the blood).

Corticosteroids reduce the permeability of the blood-brain barrier, contribute to the normalization of membrane permeability and microcirculation, block the synthesis of prostaglandins and other substances that contribute to the formation of edema in inflammatory, particularly infectious, processes, as well as in brain tumors.

Where indicated, the use of corticosteroids is usually administered dexamethasone in a dose of 12-16 mg; in severe cases 24-48 mg per day.

Its initial dose (1/4 daily) is administered intravenously, drip. Re-drug is administered intravenously or intramuscularly every 6 hours of aces .

In very severe cases, up to 60-100 mg of dexamethasone is administered per day with a gradual decrease in the dose of the drug.

In appointing prednisone, it should be borne in mind that its action is more short-term than dexamethasone; the calculation of the required doses of prednisolone should be made on the basis that its therapeutic activity in comparison with dexamethasone is 7 times less. Contraindications to the appointment of corticosteroids can be a pronounced increase in blood pressure.

When high doses of corticosteroids shown early administration of antacids (Almagelum 2 teaspoons 4 times a day or magnesium oxide in the powder tablespoon 4 times a day, etc.) For 15-30 minutes before meals u naturally or before administration nutrient mixture through c trawling probe.

The use of antacids is aimed at preventing gastric bleeding and the development of Mendelssohn’s syndrome (abscess pneumonia due to aspiration of gastric juice if its pH is <2).

With prolonged use of corticosteroids, a number of side effects and complications are possible: delayed wound healing, provocation of exacerbation of existing infectious foci, depression and psychosis, peptic ulcers, subcapsular cataracts, osteoporosis, signs of Cushing’s syndrome.

The frequency of side effects depends on the nature of the drug, its dose, duration of treatment; in general, it is quite large and appears in about 50% of cases with corticosteroid treatment. The indications for the use of corticosteroids for purulent meningitis are severely limited. They should be used only for severe cerebral edema, usually as an adjunct to intravenous administration of mannitol.

The anti-edema effect of corticosteroids usually appears after 12 hours of aces . Corticosteroids are especially effective in vasogenic edema caused by a brain tumor, their effectiveness in traumatic brain injury, especially in adults, in brain hemorrhage, as well as in cytotoxic edema associated with hypoxia and ischemia of the brain is controversial.

The treatment with corticosteroids requires regular monitoring of glucose and electrolytes in the blood for the timely diagnosis of occasionally arising hyperglycemia and hypernatremia.

Patients with cerebral edema, along with dehydration, need to monitor the level of ventilation of the lungs and the state of central hemodynamics, as well as taking measures to normalize microcirculation and general cerebral blood flow.

In case of cerebral edema, patients may need non-specific treatment aimed at normalizing respiration (restoration of airway patency, ensuring sufficient oxygenation, prevention and timely treatment of pulmonary complications), cardiac activity, arterial pressure.

To facilitate the venous outflow from the cranial cavity, it is necessary to raise the head end of the blood and set it at an angle of 15-30 . Necessary to control the state of the water-electrolyte balance, CBS and their correction, it is desirable to limit the amount of fluid injected to 1 -2 5 liters per day.

If possible, avoid using vasodilators.

Conducting dehydration, it is necessary to stop excessive hypertension at the same time, to take appropriate measures in case of hyperthermia, psychomotor agitation, epileptic seizures. According to the testimony used antihypoxants, metabolically active agents, in particular nootropics, vitamin complexes.



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