Brain coma

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

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Cerebral coma in traumatic brain injury

Impaired brain function that develops with traumatic brain injury can be caused by:

1. damage to the skull and secondary compression of the brain by bone fragments. The most serious is a fracture of the base of the skull, accompanied by bleeding and cerebrospinal fluid from the nose, throat, and ears;
2. contusion of the brain, i.e. contusive damage to the brain tissue at the site of the blow and in the area of the counterblow. During a blow (concussion), the brain is displaced in the cranial cavity in the direction of the blow. In addition to the cerebral hemispheres, the brain stem is damaged, and it is often the brain stem symptoms that become the leading ones in the clinical picture of cerebral coma.

In the above cases, epi-, subdural, subarachnoid, intraventricular, parenchymatous bleeding is possible. Subarachnoid bleeding and subdural hematomas are more common, contributing to the dislocation of the brain and its compression, the development of cerebral coma.

Circulatory disorders, hypercoagulation, hypoxia, lactic acidosis and irritation of the meninges by blood and detritus are the main causes of impaired consciousness and the characteristics of the clinical symptoms of cerebral coma.

Morphologically, hemorrhages and necrosis of brain tissue are detected, mainly at the site of direct injury. With increasing edema-swelling of the brain, these phenomena can become diffuse up to complete aseptic or septic (in case of open injury) melting.

Often, craniocerebral coma develops gradually (after a lucid interval of several hours), which is associated with the growth of intracranial hematoma. In this case, complete loss of consciousness is preceded by somnolence, stupor, and stupor. The most important clinical signs of increased intracranial pressure are headache and the symptom of vomiting, which is part of the general cerebral syndrome.

General cerebral phenomena in cerebral coma are always accompanied by meningeal and focal symptoms. In TBI, cranial nerves are affected, paresis and paralysis develop to varying degrees. Disturbances in the rhythm of breathing and pulse may be a sign of damage to the brainstem. Dislocation of the brain is accompanied by anisocoria, hyperthermia, bradycardia.

Diagnosis of TBI is based on anamnesis, M-echography of the skull (echo signal deviation of more than 2 mm from the axis), computed tomography or nuclear magnetic resonance imaging. Diagnostic spinal puncture should be performed with great caution. EEG and angiography complement the main examination methods.

Principles of treatment of cerebral coma in TBI:

• to ensure vital functions, starting from the moment of transportation, the patient is placed in a lying position on his side or on his back, with his head necessarily turned to the side (in order to prevent aspiration of vomit or blood and cerebrospinal fluid in the event of a fracture of the base of the skull);
• oxygen therapy while maintaining spontaneous ventilation or during mechanical ventilation;
• restoration of circulating blood volume and microcirculation in vessels using plasma substitutes (albumin, rheopolyglucin);
• neurovegetative blockade;
• broad-spectrum antibiotics (in some cases, dexazone - as a means of preventing edema and swelling);
• Neurosurgical intervention is performed urgently upon verification of a hematoma, depressed or comminuted fractures of the skull bones.

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Cerebral coma due to inflammation

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

Causes of cerebral coma of inflammatory nature are very diverse. Their pathogens can be bacteria, viruses, fungi, rickettsia. Among the bacterial group, meningococcal, pneumococcal, staphylococcal and streptococcal, as well as tuberculous meningitis or meningoencephalitis, meningitis caused by Haemophilus influenzae are most often observed in children. Enterovirus and mumps etiology of serous meningitis has recently dominated among viral meningitis.

Meningitis pathogens penetrate into brain tissues mainly hematogenously, but lymphogenous and perineural penetration is also possible. As a rule, the inflammatory process develops rapidly, clinical manifestations of meningitis often become maximal by the 3rd-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 the background of a febrile reaction, external manifestations of a specific infectious disease. In encephalitis (meningoencephalitis), there is also a pronounced impairment of consciousness and the appearance of focal symptoms. Cranial nerves are most often affected.

In diagnosing cerebral coma accompanied by brain damage, a full range of standard studies is used, including mandatory spinal puncture with microscopy, biochemical examination and cerebrospinal fluid culture.

Cerebral coma of this etiology is treated as follows:

• targeted antibacterial and antiviral therapy, the choice of which is determined by the diagnosis of the disease. Intramuscular and intravenous routes of drug administration are usually used. The dose of antibiotics is determined by their ability to penetrate the blood-brain barrier under pathological conditions. In this regard, penicillins, for example, are administered in high doses;
• combating cerebral edema (diuretics, plasma substitutes, GCS) and its hypoxia (oxygen therapy, artificial ventilation);
• detoxification (infusion of fluids in a volume of 20-50 ml/kg per day);
• symptomatic therapy (anticonvulsants in the presence of convulsions, neurovegetative blockade in case of agitation, antipyretic therapy, etc.).

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