Cerebral edema is a pathological phenomenon of increased water in the brain, resulting in increased brain volume, and is a response of brain tissue to various pathogenic factors. It can cause intracranial hypertension and damage brain tissue, and is commonly seen in neurological diseases such as craniocerebral trauma, intracranial infections (encephalitis, meningitis, etc.), cerebrovascular diseases, intracranial occupational diseases (e.g., tumors), seizures; and systemic diseases such as toxic dysentery and severe pneumonia.
There are four categories according to the pathological pattern and pathogenesis
Vascular-derived cerebral edema: It is the most common type of cerebral edema. The experimental model is brain edema produced after brain freezing, secondary to the disruption of the blood-brain barrier, due to increased cerebrovascular permeability. The edema is characterized by (1) predominantly white matter; (2) an increase in cell volume (intracellular edema) in the gray matter, but an enlargement of the extracellular space in the white matter; (3) the most basic change in the cellular components, whether in the white matter or gray matter, is prominent in astrocytes (a kind of neuroglia, filling between capillaries and brain nerve cells), with obvious cellular drinking phenomenon; (4) the blood-brain barrier is damaged in the focal area, with increased vascular permeability The increased vascular permeability mainly occurs in the capillary endothelial cells and the tight antibody junction of endothelial cells. CT brain scan shows that this kind of cerebral edema has the following characteristics: ① the edema area has low density value; ② the edema is mainly located in the white matter; ③ there may be occupying effect and displacement of the ventricles and midline structures; ④ the edema often extends towards the normal Such edema is commonly seen in brain tumors (especially through brain metastases and malignant gliomas), brain abscesses, cerebrovascular accidents, traumatic brain injury, etc. The role of cerebral edema is greater than that of the original occupying lesion in the cultivation of brain compression symptoms.
Cytotoxic cerebral edema: It is often associated with swelling of neuronal cells, glial cells and ventricular canal cells combined with a reduction in the extracellular space. The typical experimental model is cerebral edema induced by triethyltin, amino nicotinamide, dinitrophenol and other poisoning. This type of cerebral edema is closely related to the energy metabolism of brain cells. The active Na+ migration process (Na+/K+/ATPase, sodium pump) of the cell membrane plays a decisive role in maintaining the cell volume, and the energy source of the sodium pump is adenosine triphosphate (ATP), so any factor affecting the metabolism of these high-energy phosphate compounds will lead to the failure of the sodium pump, and a large amount of Na+ stays in the cell, and a large amount of Clˉ enters the cell with Na+ enters the cell, so that the osmotic pressure of the intracellular fluid is higher than that of the extracellular fluid, and the cell relies on the inhalation of water and the excretion of K+ to bring the osmotic pressure inside and outside the cell into balance, so cell swelling occurs. Therefore, Bachelor, the impairment of the Na+ migration process of the cell membrane, the impairment of the osmotic pressure regulation mechanism and the impairment of energy metabolism are the mechanisms of cytotoxic edema, and the imbalance of Ca+ endostasis is also an important cause of cerebral edema, and in the normal state Under normal conditions, the concentration of extracellular Ca+ is 10,000 times higher than that of intracellular Ca+, and such a high concentration difference all depends on Ca pumps to maintain. When the brain is hypoxic and ischemic, Ca ions enter the cell early, activating phospholipase A, and phospholipase C, so that membrane phospholipid metabolism is impaired, and a large number of polyvalent unsaturated fatty acids, especially arachidonic acid, are released in large quantities, and the free ones form a series of bioactive substances such as leukotrienes under the action of some enzymes. These bioactive substances can have harmful effects on cell membranes and microcirculation and accelerate cell death. Polyvalent unsaturated fatty acids can also react with oxygen free radicals to produce a large amount of lipid peroxide, which aggravates the damage to membrane structure and promotes brain edema, which itself is also a substance that strongly damages the blood-brain barrier and promotes brain edema even more. CT brain scan shows: diffuse occupancy effect combined with bilateral ventricular compression and diffuse hypodense areas in both hemispheres; there is no change in the scan before and after enhancement, in general, the white matter and gray matter of the brain are involved at the same time and the ventricles become smaller, the brain sulcus and the brain pool disappear as cytotoxic cerebral edema, which is common in cerebral ischemia, cerebral hypoxia and toxic encephalopathy. It is common in cerebral ischemia, cerebral hypoxia and toxic encephalopathy. Cerebral edema
Interstitial cerebral edema: Most commonly seen in infarct hydrocephalus, because cerebrospinal fluid cannot be absorbed by researchers through normal channels, this type of edema mainly occurs in the surrounding white matter of the ventricles, also known as hydrocephalic cerebral edema, because of the enlargement of the ventricles, ventricular canal expansion, changes in the surface structure and permeability of the ventricles, part of the cerebrospinal fluid escapes from the ventricles and squeezes into the nearby white matter, so the level of intracerebrospinal fluid pressure can directly affect the degree of this type of cerebral edema. The CT brain scan shows that the ventricular canal absorbs a large amount of cerebrospinal fluid, and the white matter around the ventricles, especially around the frontal horn, shows a butterfly-shaped hypointense area.
Osmolar cerebral edema: experiments and after clinical are found to have this kind of cerebral edema and acute water intoxication, anti-diuretic hormone secretion deficiency comprehensive abdominal signs, plasma low Na + low osmolarity has a close relationship, the mechanism of occurrence is an acute drop in the osmolarity of extracellular fluid, in order to maintain the balance of osmolarity water transfer to the brain cells, close main features are: ① gray matter, white matter are edema, to white matter more obvious; ② edema fluid The main well-known aggregation in the glial cells; ③ extracellular gap does not expand, the blood-brain barrier is not destroyed; ④ edema fluid osmotic pressure is low, Na+, K+ concentration are low, K+ concentration is more obvious (cells rely on the discharge of K+ to maintain intracellular osmotic pressure), this type of edema is mainly arthritis due to the hypotonic pressure of extracellular fluid, hemodialysis-induced osmotic pressure imbalance can also lead to such brain edema.
The above types of cerebral edema rarely exist alone, most cases are mixed, such as disorders of cellular metabolism or impaired blood supply on the basis of vasogenic cerebral edema gynecology, so there is a cytotoxic cerebral edema components of the Director involved.
Pathogenesis
The basic pathogenesis of vasogenic cerebral edema is an increase in microvascular permeability. The normal blood-brain barrier allows the passage of only some small molecules of solutes, as the brain capillaries have very low permeability and the basal periphery is almost surrounded by astrocyte end-feet, which are considered as a component of the blood-brain barrier (second barrier). Therefore, the usual intertissue fluid contains almost no protein, but the edema fluid in vasogenic brain edema contains more protein indicating that microvascular permeability has increased. Experimental observation revealed an increase in the size of the drinking vesicles of capillary endothelial cells in the central area of edema; using ferritin as a tracer, the particles were found to be present in the drinking vesicles, free in the cytoplasm and basement membrane, lodged in the intercellular space, and in the edematous tissue, leading to the conclusion that the edematous fluid was leaking and expanding through the channels within and between endothelial cells. The mechanism of increased permeability is not known and may be related to the action of some chemical mediators. It has been found that 5-hydroxytryptamine is significantly increased in edematous white matter, and the introduction of the latter into the brain parenchyma via cerebrospinal fluid can lead to increased microvascular permeability; recent data suggest that free radical damage to endothelial cells is likely, and intramuscular injection of the free radical scavenger p-phenylenediamine (DPPD) can reduce experimental frostbite cerebral edema. Microvascular permeability is not increased in the development of cellular neutrophilic brain edema. This type of edema is currently considered to be swelling due to increased water uptake by brain cells.
The pathogenesis of cellular neutrophilic cerebral edema is mainly related to hyponatremic sodium pump function. The various metabolic inhibitors mentioned above and acute hypoxia may reduce ATP production, resulting in the attenuation of the sodium pump, which is dependent on ATP for energy, and the inability of Na+ to function actively outside the cell, and the entry of water into the cell to restore homeostasis, resulting in the accumulation of excess Na and water in brain cells. In acute hyponatremia, water is transferred to intracellular cells because of extracellular hypotonicity. New information shows that brain cell membranes contain more polyvalent unsaturated fatty acids, and their unsaturated double bonds are susceptible to lipid peroxidation by free radicals, thus damaging membrane structure and function. This factor may play an important role in the pathogenesis of cellular neutrophilic brain edema. Free radicals damage the mitochondrial membrane, which in turn leads to reduced ATP production due to impaired function of the latter.
Interstitial cerebral edema fluid comes from the cerebrospinal fluid, and when the pathway of cerebrospinal fluid production and return is blocked (e.g., the conduit is blocked by a tumor, or inflammatory growth), it accumulates in the ventricles, and excessive accumulation increases intraventricular pressure, resulting in increased permeability or even rupture of the ventricular canal membrane, which overflows into the nearby interstitium and causes interstitial cerebral edema in the surrounding white matter.
Treatment principles
In addition to addressing the cause, the main symptomatic treatment is to reduce swelling, reduce brain volume or surgical decompression.
Glucocorticoid therapy
High-dose glucocorticoids, especially dexamethasone, are effective in relieving vasogenic cerebral edema and have good effects on cytotoxic cerebral edema. Its effects are to inhibit inflammatory response, reduce microvascular permeability (anti-exudation), stabilize cell membranes and restore sodium pump function, improve mitochondrial function, prevent or attenuate free radical-induced lipid peroxidation, and are also effective in inflammation-induced interstitial cerebral edema.
Dehydration therapy
① Osmotherapy: The aim is to transfer water from brain tissue to blood, causing brain volume reduction and intracranial hypotension, which can be used as an emergency measure. The drugs chosen are urea, mannitol and glycerol, the first two of which are infused intravenously and the latter orally; ② diuretic therapy: the aim is to increase sodium and water excretion and reduce extracellular fluid accumulation.
Surgical decompression therapy
It is an emergency measure to relieve brain swelling and intracranial hypertension, not a routine treatment, but a better treatment for severe hematoma and abscess, etc.
Conventional treatment
Strictly control the factors that aggravate cerebral edema
(1) Limit water intake: Excessive water intake can aggravate cerebral edema, so in the first few days, the state of mild dehydration should be maintained, so that the amount of water out is slightly more than the amount of water in. In general, the amount of water intake can be calculated by adding 500ml to the previous day’s urine volume.
(2) Control blood pressure; high blood pressure will aggravate cerebral edema and low blood pressure will aggravate poor cerebral blood perfusion. Therefore, both hypertension and hypotension should be corrected.
(3) Control arterial partial pressure of oxygen above 13,3kPa (100mmHg) and partial pressure of carbon dioxide below 5,3kPa (40mmHg).
(4) The body temperature is controlled within 32-37℃. Animal experiments have shown that 40℃ for 2 hours can increase brain edema by 40% in animals with frozen cerebral edema. Therefore, the use of hibernation combination with physical cooling to control the body temperature between 32 and 37℃ is beneficial to the treatment of cerebral edema.
(5) Correct acidosis and regulate electrolyte disturbance.
Reduce intracranial pressure
(1) Mannitol; 20% mannitol 250ml, injected quietly, 20-30 minutes to finish. The hypotensive effect can be pushed for 4-6 hours, each 8 grams of mannitol can carry out 100ml of water. mannitol every 6-8/hour once.
(2) Sorbitol; use the same as mannitol.
(3) Urea: by dry will make the blood urea nitrogen rise, local irritation, so currently less common than mannitol.
(4) Glycerol: It is a cranial pressure-lowering drug that can be taken orally. 10% glycerol 1,2g per kg per day in static drip, or 50% glycerol 1,5g per kg per day in oral drip, because the half-life is only 30-40 minutes must be repeatedly taken orally or continuous static drip. It has more side effects, so it is not widely used at present.
3.Adrenocorticosteroids refer to “Ischemic cerebrovascular disease”.
4.Diuretics refer to “ischemic cerebrovascular disease”.
5.Acetazolamide can reduce intracranial pressure. Cardiac glucose or similar drugs can also reduce intracranial pressure. Acetazolamide and digoxin combined will enhance the effect of lowering intracranial pressure.
6, barbiturates have reported traumatic brain injury caused by cerebral edema, the use of thiopentone can not only reduce intracranial pressure and can improve the brain perfusion pressure, the brain damage has a protective effect. The mechanism of lowering cranial pressure: ① directly affect the cellular Na+ transport; ② inhibit the anaerobic enzyme of sugar and enhance the aerobic oxidation of sugar; ③ have antioxidant effect; ④ improve the permeability of cell membrane to ions.
7, Hyperventilation can reduce the partial pressure of carbon dioxide.
8.Etiological treatment.