Cerebral complications

Cerebral edema and swelling (CES)

CES is the most dangerous complication of generalized forms of infections and meningitis. The pathology is based on a significant increase in the volume of intracellular and/or extracellular fluid. This inevitably leads to an increase in the total volume of brain tissue. Since the skull is a closed space, the additional volume leads to a progressive increase in intracranial pressure (ICP) and the escalation of acute cerebral insufficiency.

Morphologically, the affected tissue appears moist and shiny on cross-section. The relief of the cortex is smoothed out: the gyri become flattened and the sulci narrowed. Characteristic features include marked dilatation and venous congestion of the cortical vessels, loss of clear boundaries between the gray and white matter, and a decrease in the volume or complete compression of the lateral ventricles. Notably, in swelling, structural changes affect the white matter of the brain to a much greater extent.

Causes and forms of edema

The key triggers for the development of CES are intrathecal inflammation (in meningitis and encephalitis), as well as cerebral ischemia, hypoxia, and severe metabolic disorders accompanying severe meningococcemia with multiple organ failure.

Four main pathogenetic forms are distinguished, which in practice most often occur in combination:

1. Vasogenic — occurs due to disruption of the normal permeability of the blood-brain barrier (BBB) and cerebral capillaries.
2. Cytotoxic — caused by the direct damaging effect of bacterial toxins on cells.
3. Osmotic — associated with an increase in the total osmolarity of the brain tissue.
4. Hydrostatic — develops during occlusion of the cerebrospinal fluid pathways, which creates high hydrostatic pressure within the ventricular system.

Herniation syndrome (brain herniation syndromes)

If care is delayed, the rapid increase in ICP forces parts of the brain to shift (protrude) into natural openings of the skull or dural folds. This process is called herniation syndrome.

The most critical scenario is the displacement of the cerebellar tonsils into the foramen magnum. This entails entrapment of the structures of the medulla oblongata. Clinically, herniation manifests as profound impairment of consciousness, seizures, severe focal and general cerebral symptoms, as well as hemodynamic disorders. The presence of abnormal breathing patterns in the patient unequivocally indicates an extremely severe course of the process and impending herniation. The outcome is the patient's death from cardiac and respiratory arrest.

Ischemic, hemorrhagic, and systemic processes

In addition to edema, inflammation is frequently accompanied by vascular catastrophes. The development of phlebitis and venous thrombosis of the meningeal vessels provokes hemorrhagic cerebral infarction. Arterial thromboses causing focal symptoms, subarachnoid hemorrhages, and the accumulation of subdural effusion also occur.

The course of cerebral lesions is sharply aggravated by the development of infectious-toxic shock (ITS). In the decompensated stage of shock, profound hypoxemia occurs, consciousness is depressed down to coma, and hallucinations and delirium appear. Severe disorders of acid-base and electrolyte balance are formed, which closes the vicious circle of the pathogenesis of CES. In surviving patients, severe consequences often persist in the long-term period: symptomatic epilepsy, persistent central limb paresis, sensorineural hearing loss, aphasia, and severe cognitive impairment.

Class and exam questions

What else to study on this topic

• Criteria and stages of infectious-toxic shock (ITS)
• Waterhouse-Friderichsen syndrome in meningococcemia
• Purulent ventriculitis and secondary hydrocephalus
• Pathophysiology of acute respiratory distress syndrome (ARDS)

Other topics in the "Additional Topics" section

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