Brain edema

Introduction Cerebral edema refers to the pathological phenomenon in which the water in the brain increases and the volume of the brain increases, which is the response of brain tissue to various pathogenic factors. Can cause intracranial hypertension, damage brain tissue, clinically common in nervous system diseases, such as craniocerebral trauma, intracranial infection (encephalitis, meningitis, etc.), cerebrovascular disease, intracranial space-occupying diseases (such as tumors), Seizures and systemic diseases such as toxic dysentery, severe pneumonia. Cerebral edema mainly shows signs of intracranial hypertension. The most effective means of diagnosis are CT scan and magnetic resonance examination.

Cause

1, craniocerebral injury: all kinds of craniocerebral injury, directly or indirectly caused by brain contusion and laceration can cause cerebral edema, and intracranial hematoma, so that local brain tissue pressure can also cause brain edema. Skull sag fracture, compression on the brain tissue, or fracture of the fracture piece directly into the brain tissue, cerebral edema in the affected area, blast shock wave impact on the chest, or the chest directly directly squeezed, making the superior vena cava pressure sharp Elevated, the pressure spreads to the brain and impacts the brain tissue, causing extensive diffuse punctiform hemorrhage of the capillaries in the brain tissue, increased capillary permeability, often diffuse brain edema, diffuse axonal damage of the brain, can continue Severe diffuse brain edema.

2, intracranial space-occupying lesions: tumors surrounding the brain tissue pressure or obstruction of cerebral venous return, increased venous pressure, intracranial congestion, cerebrospinal fluid circulation machine absorption disorders, and tumor biotoxic effects, so that the brain tissue around the tumor Affected, the blood-brain barrier is damaged or destroyed, and the permeability of the blood vessel wall is increased, resulting in localized cerebral edema. Brain edema associated with primary malignant tumors of the brain is particularly pronounced. Brain metastases such as lung cancer and choriocarcinoma, whether single or multiple, have severe cerebral edema around the lesion.

3, intracranial inflammation: encephalitis, meningitis, ventriculitis, brain abscess and sepsis caused by intracranial diffuse inflammation, often secondary to varying degrees of cerebral edema, which is related to the toxicity and pathogenesis of pathogenic microorganisms.

4, cerebrovascular disease: internal carotid artery or cerebral artery thrombosis or embolism, brain fat embolism, the arterial blood flow is reduced or interrupted, so that the arterial blood supply area has acute cerebral insufficiency and cerebral infarction, while secondary limitations or extensive Sexual cerebral edema, cerebral aneurysm or arteriovenous malformation rupture, subarachnoid hemorrhage, intraventricular hemorrhage and cerebral vasospasm, secondary to cerebral edema.

5, cerebral hypoxia: epileptic state, chest trauma, dyspnea or asphyxia caused by different causes, cardiac arrest, prolonged hypotension, shock, high altitude hypoxia, carbon monoxide poisoning and other pulmonary encephalopathy, the brain In hypoxia, accompanied by cerebral edema.

6, exogenous or endogenous poisoning: lead poisoning or other causes of systemic poisoning, often complicated by diffuse brain edema.

7, brain metabolism disorders: a variety of causes, systemic or localized brain metabolism disorders, causing brain edema.

8, the brain's radioactive damage: including electromagnetic damage such as microwave, infrared, X-ray, gamma ray, beta ray, fast neutron and so on.

an examination

Related inspection

Intracranial pressure monitoring EEG examination Brain CT examination Brain MRI examination Brain nerve examination

1. History: Pay attention to whether there is a large amount of drinking water or excessive water input after burns, whether there is brain trauma, history of poisoning, whether there is severe shock, inhalation injury or other serious or long-term hypoxia or acidosis and alkalosis Wait.

2. Clinical manifestations: increased intracranial pressure and cerebral palsy, respiratory, mental changes and mental symptoms. Children can have high fever and convulsions.

3. Check: whether there is a change in pupil and optic nerve head edema, with or without conjunctival edema or increased intraocular pressure, in the baby with or without a full stomach, increased tension.

4. Test: Pay attention to the presence or absence of hyponatremia, low blood chlorine, plasma protein, acidosis and other poisoning.

5. Lumbar puncture can cause sacral stenosis and infection (especially through burn wounds), generally not suitable.

Differential diagnosis

Differential diagnosis

Angiogenic cerebral edema: is the most common brain edema. The experimental model is brain edema produced after brain freezing, secondary to the destruction of the blood-brain barrier, due to increased cerebral vascular permeability. Its characteristics are:

1 edema is mainly white matter;

2 in the gray matter is the increase in cell volume (intracellular edema), but in the white matter is the expansion of the extracellular space;

Cytotoxic cerebral edema: often associated with swelling of nerve cells, glial cells and ependymal cells with decreased extracellular space. A typical experimental model is brain edema induced by triethyltin-aminonicotinamide-dinitrophenol poisoning. Such cerebral edema is closely related to the energy metabolism of brain cells. The Na+ active migration process of cell membrane (Na+/K+/ATPase, sodium pump) plays a decisive role in maintaining cell capacity. The energy of sodium pump is adenosine triphosphate (ATP). Therefore, any factors affecting the metabolism of these high-energy phosphate compounds will lead to the failure of the sodium pump. Na+ stays in the cells in a large amount, and a large amount of Cl enters the cells with Na+, so that the osmotic pressure of the intracellular fluid is higher than that of the extracellular fluid, and the cells are inhaled. Moisture and excretion of K+ to balance the osmotic pressure inside and outside the cell, so that cell swelling occurs. Therefore, the barrier of Na+ migration process, the disorder of osmotic pressure regulation mechanism and energy metabolism disorder are the mechanisms of cytotoxic edema, and the imbalance of Ca+ homeostasis is also An important cause of cerebral edema, under normal conditions, the extracellular Ca+ concentration is higher than 10,000 times in the cell. Such a high concentration difference depends on the Ca pump to maintain During cerebral hypoxia-ischemia, Ca ions enter the cells early, activate phospholipase A and phospholipase C, and cause membrane phospholipid metabolism disorder. A large number of polyunsaturated fatty acids, especially established, are a large release of arachidonic acid, free in some Under the action of enzymes, a series of biologically active substances such as leukotrienes are formed. These biologically active substances can have harmful effects on cell membranes and microcirculation, accelerate cell death, and multivalent unsaturated fatty acids can also react with oxygen radicals to produce a large amount of Oxidized lipids, increase membrane structure damage, promote brain edema, itself is also a strong destruction of blood-brain barrier substances, but also promote brain edema, this type of brain edema has the following characteristics:

1 no vascular injury, the blood-brain barrier is relatively intact;

2 edema in the cell, the extracellular space does not expand;

3 edema fluid does not contain protein, has the characteristics of plasma ultrafiltrate, CT brain scan shows: diffuse mass effect combined with bilateral ventricular pressure and diffuse low density area of the two hemispheres; no change 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 cerebral sulcus and the disappearance of the brain pool are cytotoxic cerebral edema, which is common in cerebral ischemia, cerebral hypoxia and toxic encephalopathy.

Interstitial cerebral edema: more common in infarcted hydrocephalus, because cerebrospinal fluid can not be absorbed by researchers through normal channels, this type of edema mainly occurs in the surrounding white matter of the ventricles, also known as hydrocephalus edema, due to ventricular enlargement, chamber tube Membrane expansion, changes in cerebral surface structure and permeability, part of the cerebrospinal fluid escapes into the cerebral ventricle and squeezes into the nearby white matter. Therefore, the level of cerebrospinal fluid pressure in the ventricle can directly affect the degree of such cerebral edema. CT scan can be seen in the ependymal membrane to absorb a large amount of cerebrospinal fluid. The white matter around the ventricle, especially around the forehead, is a butterfly-like low-density area.

Osmotic cerebral edema: experimental and clinical findings have found that such cerebral edema and acute water intoxication, insufficient secretion of antidiuretic hormone, comprehensive abdominal cavity sign, plasma low Na + low osmotic pressure is closely related.

The main features are:

1 gray matter, white matter has edema, white matter is more obvious;

2 edema fluid is mainly known to accumulate in glial cells;

3 The extracellular space does not expand, and the blood-brain barrier is not destroyed;

4 edema fluid osmotic pressure is low, Na+, K+ concentration is low, K+ concentration is more obvious (cells rely on K+ to maintain intracellular osmotic pressure), this type of edema is mainly caused by hypotonic pressure of extracellular fluid, blood Osmotic imbalance caused by dialysis can also cause such cerebral edema.

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