Recovery after cerebral edema
Edema of the brain - a pathological process characterized byexcessive accumulation of fluid in the brain tissue. Developing at the same time, an increase in the volume of the brain leads in most cases to an increase in intracranial pressure. For cerebral edema, accumulation is not so much extracellular fluid as an increase in the volume of water inside cells, primarily glial cells. In connection with this, the term "edema-swelling of the brain" is often used.
On the basis of etiologic signs, a tumor,traumatic, postoperative, toxic (intoxication), inflammatory, ischemic and hypertensive edema of the brain. Perhaps the development of cerebral edema with epileptic seizures, diseases of the blood and internal organs, endocrine disorders, hypoxia, exposure to ionizing radiation.
In the pathogenesis of cerebral edema mattercirculatory, vascular and tissue factors. Circulatory factors imply, on the one hand, a significant increase in blood pressure in the capillaries of the brain due to increased blood pressure and the expansion of the cerebral arteries: this increases the filtration of water from microvessels into the intercellular spaces of the brain and damages its tissue elements, on the other hand, with generalized or local circulatory insufficiency brain tissue its structural elements are damaged and become prone to the accumulation of water (ischemic and postischemic edema of the brain).
Vascular factors - permeability impairmentwalls of microvessels of the brain, as a result of which the molecules of the protein and other components of the blood plasma pass through the broken blood-brain barrier into the brain tissue spaces, which not only increases the osmolarity of the intercellular fluid, but also damages the cell membranes, disrupting the function of the neural elements of the brain. Tissue factors - primary damage to cell membranes and cytoplasm of neurons; This breaks the transport through the membranes of ions and water, which accumulates inside the cellular elements, primarily glial, causing them to swell.
By prevalence, local anda generalized (encompassing one or both hemispheres) edema of the brain. Macroscopically, with edema, the brain is moist, the turbidity of the surface of its hemispheres is marked, the boundaries between gray and white matter are not clear on the cut. When the edema is pronounced due to the increase in the volume of the brain, its areas are shifted to the sickle-like process of the dura mater, the papillae of the cerebellum or to the large occipital opening with the appearance of strangulation impressions in the corresponding regions. With predominantly edema, the brain tissue is flabby, excessively moist at the cut, with local fullness and swelling of the soft dura mater, from the surface of which a clear liquid flows. With a predominantly swelling of the brain substance is highly dense and dryish.
Clinical symptoms are secondary, because is associated with an increase in brain volume and an increase in intracranial pressure. There are paroxysmal headaches of a bursting nature, at the height of which there can be vomiting, a disorder of consciousness by the type of stunning, a change in the activity of the cardiovascular system. A common symptom is stagnant nipples of the optic nerves. Focal symptoms develop as a result of the growth of edema and dislocation of the brain, its wedging into the hole of the cerebellar nerve and a large occipital opening.
In this stage, stem symptoms appear: defeat of the oculomotor nerves (dilated pupils and decreased pupillary reactions), paresis or paralysis of the gaze upward, etc. When the posterior cerebral artery is compressed, visual impairment or homonymous hemianopsia may occur. In cases of severe dislocation of the brain, decerebral rigidity, hemiparesis, vestibular disorders, bradycardia, dysphagia develop. Often there is a sudden vomiting, there is rigidity of the occipital muscles. It is possible to stop breathing.
Diagnosis in outpatient settings is difficult inconnection with the absence of specific clinical and neurological symptoms. The diagnosis is based on data on the underlying disease, clinical manifestations and the results of additional studies (eg, the fundus). It should be remembered that in the early stages of ophthalmology may be asymptomatic.
If there is a suspicion of cerebral edema of the patientshould be urgently hospitalized in the neurosurgical or resuscitation department, where the question of indications for lumbar puncture, angiography, etc. can be solved. Direct diagnosis of cerebral edema is possible with computed tomography, which allows to detect a decrease in the density of the medulla, to assess the degree of edema, its prevalence . A valuable diagnostic method is nuclear magnetic resonance imaging, in which areas of hyperhydration of the brain substance are determined.
Treatment of edema and swelling of the brainis based on the elimination of the cause that caused it, as well as on the removal of excess fluid, normalization of cerebral circulation and permeability of the blood-brain barrier, correction of metabolic disorders. Conditionally it is possible to distinguish specific and nonspecific components of therapy. Nonspecific therapy is aimed at normalizing respiration, cardiac activity, central venous pressure, kidney function, etc. on the elimination of extracranial factors contributing to the development of cerebral edema.
Pathogenetic therapy is carried out with drugsglucocorticoid hormones (dexamethasone, etc.). Need for dehydration therapy, treatment aimed at improving microcirculation and cerebral blood flow. Apply diuretics, vitamins, ganglioblokatora, antihypoxants, sometimes conduct moderate hypothermia.
The prognosis is always serious and depends on the severityunderlying disease, timeliness and adequacy of treatment. With the progressive development of edema, the patient may die due to impairment of vital functions due to the infringement of the brainstem in the opening of the cerebellar nest or the dislocation of the hemispheres with an uneven increase in their volume.