Endogenous intoxication syndrome

Local process formation and primary intoxication

The development of endogenous intoxication syndrome begins directly at the port of entry of the infection, which is typically the nasopharyngeal mucosa. The key pathogenetic link at this stage is damage to the vascular endothelium.

This damage is caused by the active release of a whole cascade of endogenous pro-inflammatory mediators. These include:

• Interleukins;
• Tumor necrosis factor (TNF);
• Prostaglandins;
• Leukotrienes;
• Reactive oxygen species.

The action of these biologically active substances naturally leads to increased vascular permeability and the initiation of a local inflammatory response. Even at the localized stage of infection (e.g., during the development of nasopharyngitis), short-term bacteremia occurs. Together with the developing endotoxemia, it forms the baseline intoxication syndrome that determines the primary deterioration of the condition.

Generalization of the process and systemic disorders

In some patients, the local inflammatory process is not resolved, and massive hematogenous dissemination of the pathogen occurs. At this stage, endogenous intoxication syndrome reaches its maximum severity, transitioning into a systemic form (e.g., in meningococcemia).

The foundation of the pathogenesis of severe systemic intoxication is the development of thrombohemorrhagic syndrome (also known as DIC syndrome). It occurs against the background of:

1. Massive destruction of circulating bacteria.
2. A sharp, avalanche-like release of huge doses of endotoxin into the systemic circulation.

As a result of these catastrophic processes in the vascular bed, severe hemodynamic shifts occur. Pronounced tissue hypoperfusion (reduced tissue blood supply) and venous stasis develop. Ultimately, these mechanisms of endogenous intoxication lead to the development of a life-threatening condition—shock.

Central nervous system involvement

A specific and extremely severe manifestation of endogenous intoxication syndrome is damage to brain structures (as occurs in the development of meningitis). The pathological process is triggered when the pathogen overcomes the blood-brain barrier (BBB).

The penetration of infection and toxins into the central nervous system causes intrathecal inflammation. The pathogenesis of cerebral disorders includes several parallel processes:

• Direct toxic effect on the brain parenchyma;
• A significant increase in the permeability of the blood-brain barrier itself;
• Pronounced disturbance of intracerebral hemodynamics.

The combination of these factors leads to excessive production of cerebrospinal fluid (CSF). As a result, the patient rapidly develops cerebral edema and a sharp increase in intracranial pressure, which is clinically defined as intracranial hypertension.

Class and exam questions

What else to study on this topic

• Mechanisms of increased vascular permeability under the action of prostaglandins and leukotrienes.
• Pathogenesis of thrombohemorrhagic syndrome (DIC syndrome) against the background of endotoxemia.
• Pathophysiology of tissue hypoperfusion and venous stasis in shock states.
• Mechanisms of overcoming the blood-brain barrier by bacterial agents.
• Impairment of intracerebral hemodynamics and the formation of intracranial hypertension.

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