Brain coma

Brain coma is of primary importance in the practice of a neurosurgeon. It develops with craniocerebral trauma (CCT), as well as inflammation of the substance of the brain and its membranes, ie, with meningitis and meningoencephalitis.

[1], [2], [3], [4]

Brain coma with head injury

Violation of brain function with development in cases of head injury may be caused by:

1. damage to the skull and secondary compression of the brain with bone fragments. The most serious is a fracture of the base of the skull, accompanied by blood and liquor circulation from the nose, throat, ears;
2. brain injury, i.e. Contusion damage of the brain substance in the place of impact and in the area of the counterblow. Upon impact (shaking), the brain moves in the cranial cavity in the direction of the impact. In addition to the cerebral hemispheres, the brain stem is damaged, it is often the stem symptoms that become leading in the clinical picture of the brain coma.

In the cases listed above, epi-, subdural, subarachnoid, intragastric, parenchymal hemorrhage is possible. More often there are subarachnoid hemorrhages and subdural hematomas that promote the dislocation of the brain and its compression, the development of the brain coma.

Circulatory disorders, hypercoagulation, hypoxia, lactic acidosis, and irritation of the brain's membranes with blood and detritus are the main causes of impaired consciousness and peculiarities of the clinical symptomatology of the cerebral coma.

Morphologically, hemorrhages and necrosis of brain tissue are detected, mainly in the place of direct damage. With the growth of edema-swelling of the brain, these phenomena can become diffuse up to complete aseptic or septic (with open trauma) melting.

Often the cranial cerebral coma develops gradually (after a light interval for several hours), which is associated with an increase in intracranial hematoma. At the same time complete loss of consciousness is preceded by doubt, stunnedness, and sopor. The most important clinical signs of increasing intracranial pressure are headache and a symptom of vomiting, which is part of the cerebral sinus syndrome.

Brain cerebral events are always accompanied by meningeal and focal symptoms. In craniocerebral trauma, the cranial nerves are affected, and paresis and paralysis develop in varying degrees. Violations of the rhythm of breathing and pulse can be a sign of damage to the trunk. The dislocation of the brain is accompanied by anisocoria, hyperthermia, bradycardia.

Diagnosis of TBI is based on an anamnesis, M-echography of the skull (echo deviation more than 2 mm from the axis), computer or nuclear magnetic tomography. Diagnostic spinal puncture should be carried out with great care. EEG and angiography complete the main survey methods.

Principles of treatment of cerebral coma with CCT:

• provision of vital functions from the moment of transportation of the patient is transferred to the position lying on his side or on his back, necessarily turning his head sideways (with the aim of preventing aspiration of vomit or blood and cerebrospinal fluid upon fracture of the base of the skull);
• Oxygen therapy while maintaining spontaneous ventilation or during ventilation;
• restoration of bcc and microcirculation in vessels with the help of plasma substitutes (albumin, rheopolyglucin);
• neurovegetative blockade;
• antibiotics of a wide spectrum of action (in some cases, dexazone - as a means of preventing swelling-swelling);
• Neurosurgical intervention is carried out urgently with the verification of hematoma, depressed or comminuted fractures of the bones of the skull.

[5], [6], [7], [8]

Brain coma due to inflammation

Primary brain inflammation in children can be in the form of meningitis (inflammation of the soft shell), encephalitis (parenchymal inflammation), meningoencephalitis, and meningoencephalomyelitis.

The causes of the cerebral coma of an inflammatory nature are very diverse. Their pathogens can be bacteria, viruses, fungi, rickettsia. Among the bacterial group, meningococcal, pneumococcal, staphylo- and streptococcal, as well as tuberculous meningitis or meningoencephalitis, meningitis caused by a hemophilic rod are most often observed in children. The enterovirus and parotitic etiology of serous meningitis has recently dominated viral meningitis.

The causative agents of meningitis penetrate the brain tissues mainly hematogenically, but also lymphogenous and perineural penetration is possible. As a rule, the inflammatory process develops rapidly, the clinical manifestations of meningitis often become maximum By the 3-4th day (except for tuberculosis).

The main pathogenetic factors that determine the symptoms of cerebral coma are edema-swelling of the brain, hypoxia, toxic-hypoxic damage to cells. Dystrophic and necrotic changes are observed at the site of inflammation. General cerebral and meningeal symptoms occur against a background of feverish reaction, external manifestations of a specific infectious disease. With encephalitis (meningoencephalitis), there is also a marked impairment of consciousness and the appearance of focal symptoms. The cranial nerves are more often affected.

When diagnosing a cerebral coma accompanied by brain damage, the entire spectrum of routine studies is used, including the mandatory conduct of a spinal puncture with microscopy, biochemical examination and culture of the cerebrospinal fluid.

The cerebral coma of this etiology is treated as follows:

• targeted antibiotic and antiviral therapy, the choice of which is determined by the diagnosis of the disease. Usually, intramuscular and intravenous routes of administration are used. The dose of antibiotics determines their ability to penetrate the blood-brain barrier in pathological conditions. In this regard, penicillins, for example, are administered in high doses;
• struggle with cerebral edema (diuretics, plasma substitutes, GCS) and its hypoxia (oxygen therapy, IVL);
• detoxification (infusion of liquids in the volume of 20-50 ml / kg per day);
• symptomatic therapy (anticonvulsant in the presence of seizures, neurovegetative blockade during excitation, antipyretic therapy, etc.). 

[9], [10], [11], [12], [13], [14]