Brain edema: causes, symptoms, diagnosis, treatment

Cerebral edema is a universal non-specific reaction of the brain, characterized by disturbances in the water-ion balance in the neuron-glia-adventitia system.

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Causes of cerebral edema

Cerebral edema may be accompanied by neurotoxicosis, neuroinfections, brain injuries, and metabolic disorders. The main causes of cerebral edema are hypoxia and hypoxemia, especially in combination with increased carbon dioxide levels. Metabolic disorders (hypoprogenemia), ionic balance, and allergic conditions play an important role. In children, cerebral edema is caused by arterial hypertension and increased body temperature, since they promote vasodilation.

Many authors characterize cerebral edema-swelling as a universal non-specific reactive process, the clinical expression of which is general cerebral disorders. The various pathogenetic factors leading to cerebral edema-swelling can be reduced to 2 main ones: vascular and tissue. With increased vascular permeability, interstitial edema develops, with parenchymatous damage - brain swelling.

Cerebral edema is an accumulation of free fluid in the brain tissue and intercellular space.

Brain swelling is characterized by increased water binding by biocolloids of the structural elements of the brain. The essence of the parenchymatous mechanism is the occurrence of metabolic shifts that promote the accumulation of water in biocolloids.

The pathogenetic scheme of cerebral edema-swelling is as follows:

• toxic or hypoxic effects on the receptors of the vascular plexus of the brain and increased vascular permeability lead to hyperproduction of cerebrospinal fluid;
• an increase in intracranial pressure to a level higher than arterial pressure leads to brain hypoxia;
• compression of the brainstem is accompanied by suppression of the reticular formation and its activating effect on the cerebral cortex, loss of consciousness is observed; -
• hypoxia leads to energy deficiency, metabolic disorders in brain cells, acidosis, accumulation of metabolites, various biologically active substances (histamine, kinins, adenosine, etc.), which further damage brain tissue;
• tissue catabolism is accompanied by an increase in the osmotic potential of tissue colloids and the amount of water associated with them. Tissue breakdown and accumulation of metabolites are accompanied by an increase in osmotic pressure inside cells and in the interstitium, and an influx of free water to them.

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Symptoms of cerebral edema

The development of cerebral edema in children is indicated by symptoms of increased intracranial pressure (manifested as a general cerebral syndrome). increasing severity of neurological changes and the degree of impaired consciousness, as well as the syndrome of dislocation of brain structures. Against the background of clinical manifestations of the underlying disease, weakness, lethargy, headache increase. Paresis and paralysis occur or intensify, edema of the optic nerve occurs. As the edema spreads, convulsions develop, lethargy, drowsiness, cardiovascular and respiratory disorders increase, pathological reflexes appear.

Cerebral edema in infants is characterized by agitation, headache, piercing "brain" cry, intractable hyperthermia, bulging of the large fontanelle, rigidity of the occipital muscles, stupor, coma, and convulsions. The first signs of cerebral edema development in Reye's syndrome and acute renal failure include the appearance of decerebrate rigidity with dilated pupils.

In the case of dislocation syndrome of brain structures, symptoms of temporoparietal or occipital herniation of the brain develop: the appearance of convergent strabismus, anisocoria, and worsening of vital function disorders. Compression of the midbrain is characterized by oculomotor crises with pupil dilation and fixation of the gaze, increased muscle tone, tachycardia, fluctuations in blood pressure, and hyperthermia. When the brainstem is compressed, loss of consciousness occurs, mydriasis, anisocoria, and vomiting are observed. Symptoms of cerebellar infringement: bradycardia, bradypnea, vomiting, dysphagia, paresthesia in the shoulders and arms, rigidity of the occipital muscles that occurs before other symptoms appear, and respiratory arrest.

Diagnosis of cerebral edema

The possibility of developing cerebral edema should be taken into account with any unclear loss of consciousness, convulsions, hyperthermia, especially against the background of any disease. Repeated, even short-term, hypoxic conditions are of significant importance. CT or MRI of the brain, as well as X-ray of the skull help diagnose edema. Spinal puncture should be performed only in a hospital setting.

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Emergency medical care for cerebral edema

In case of cerebral edema in children, the upper respiratory tract is inspected and their patency is ensured. 50% oxygen is given via a mask or nasal catheters. Artificial ventilation in the mode of moderate hyperventilation is carried out in a hospital setting. Mannitol is prescribed intravenously every 6-8 hours, followed by the introduction of furosemide (lasix). Magnesium sulfate can be used to reduce intracranial pressure.

To provide neuroplegia, reduce the need for oxygen and in case of convulsive syndrome, diazepam, droperidol or sodium oxybate (sodium oxybutyrate) are used. It is recommended to administer dexamethasone and anesthesia with barbiturates - hexobarbital (hexenal), phenobarbital. Infusion therapy is carried out in the volume of daily fluid requirements. To improve microcirculation in the brain, pentoxifylline (trental) is used intravenously by drip. On the 2nd-3rd day of treatment of cerebral edema, but not in the acute period, piracetam may be prescribed.

When transporting a patient with cerebral edema and acute increase in intracranial pressure, he or she should lie on his or her back with the head end raised.

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