Edema of the brain with coma

Pathogenesis com. Mechanisms of development of coma.

Initial mechanisms of different types of com are different. For example: ketoacidosis, hyponatremia and hyperglycemia, as well as dehydration in diabetic coma; hypoglycemia - with hypoglycemic coma; Hyperazotemia and hypochloraemia - with uremic coma; acute increase in intracranial content - with apoplectic coma (cerebral hemorrhage), etc. In all cases, the most important resultant pathogenetic factor is the alteration (damage) of the cell membranes of neurons. The main pathogenetic mechanisms are as follows:

1. Depletion of the energy substrate (ATP) in connection with the overexcitation of neurons. This leads to the inactivation of an ion pump operating on ATP energy. The result: the inability to maintain the polarization of the cell - the potential difference on both sides of the cell membrane, ie, depolarization.

2. Rapid accumulation in brain cells excitatory amino acids - glutamate and aspartate.

3. Persistent cell depolarization. Occurs in connection with the abovedisorders, and is also provided by another mechanism: the excitatory amino acids bind to the surface receptors of the cell - calcium channel agonists and thus open the nonspecific ion channels, promoting the Ca ++, Na + and C1- invader to the cell and the exit of K. It also favors penetration into the cell of water, i.e., intracellular edema.

4. Increase intracellular concentration of Ca ++. which leads to a new allocation of excitatory amino acids and excessive consumption of ATP, that is, a vicious circle is created.

5. The consequence of a breakdown in the calcium homeostatic mechanism is the activation of phospholipases and proteases with subsequent degradation of cell membranes - the so-called "calcium cell death".

6. An important role in coma plays a violation of lipid peroxidation. Normally, lipid peroxidation and its control system (antioxidant system) form an important homeostatic mechanism of protection from activated oxygen (superoxide-sidant, anion-radical O2, hydrogen peroxide H2O2 hydroxyl radical OH-). Violation in this system is the most important component of cerebral metabolic disorders in coma. In the mechanism of this pathology, many factors are important, including cerebral hypoxia, destabilization of membranes, calcium homeostatic mechanism disorder, intoxication, etc. Combined insufficiency is increased - lipid peroxidation is increased and the antioxidant system is insolvent: antiradical, responsible for inhibition of peroxidation processes lipids, and an-ti-peroxide, which ensures the metabolization of peroxides that have already formed.

7. The underlying pathogenetic factor. combining comatose states, - alterationcell membranes, which is the most important mechanism of cerebral edema in comatose states. This mechanism becomes leading in a chain of a number of pathogenetic links in a destructive coma. Edema - swelling of the brain - a universal reaction to its damage. In destructive coma in its pathogenesis, other factors, in particular anoxo-ischemic, increase in intracranial pressure and a drop in perfusion pressure, are important. However, with any coma, the associated disorders of breathing and hemodynamics can be accompanied by anoxic and ischemic disorders, which usually causes vasogenic brain edema.

With local brain damage (non-extensive cerebral infarction, light bruisebrain, etc.) edema can be local. For large lesions (extensive infarction, severe brain contusion, etc.), edema spreads to the entire hemisphere. With generalized brain damage (acute hypertensive encephalopathy, diffuse brain contusion, etc.), cerebral edema can be total. The dramatic consequence of cerebral edema is a sharp increase in intracranial pressure, a reduction in cerebral perfusion pressure followed by secondary cerebral ischemia, that is, the emergence of a new vicious circle. The tragic consequence of cerebral edema is the dislocation of the brainstem with the development of a secondary stem syndrome (strabismus, anisocoria, reduction and loss of root and pupillary reactions, etc.), including respiratory and hemodynamic disorders.

Anoxic-ischemic disorders in the brain tissue (local or more generalized) withThe destructive coma is accompanied by a cascade of adverse disorders described above. In addition, cerebral hypoxia leads to the switching of aerobic respiration to anaerobic, resulting in lactate acidosis. The latter is accompanied by vasoparesis, which, in turn, leads to brain edema. With vasoparesis in the lesion, the phenomenon of "luxurious perfusion of the brain" arises: the cerebral blood flow, including volumetric flow, increases, but this is not accompanied by a useful metabolic effect due to depletion of the energy substrate and enzymes of membrane transport.