Intensive Care of Acute Poisoning - A. V. Hovenko 2010

General Characteristics of Acute Poisoning
Exotoxic Shock
Impairment of Vital Organs and Systems in Exotoxic Shock

During Exotoxic Shock, the function of virtually all vital Organs and systems is impaired. The Pathogenesis of these disorders involves multiple factors: the general toxic and specific ("selective") effects of chemicals on various organs and systems, neuroendocrine regulation disorders, circulatory disturbances, as well as impaired oxygen delivery and utilization. These factors contribute to the rapid progression of exotoxic shock and worsen its prognosis.

In addition to the Circulatory system, the "shock organs" also include the Lungs, Kidneys, and Liver.

In severe acute poisonings accompanied by exotoxic shock, non-specific circulatory Hypoxia develops as a consequence of systemic Circulatory Disorders and Regional Blood Flow impairments in the Pulmonary Circulation. Low Cardiac Output syndrome, microcirculatory disturbances, and sluggish blood flow lead to an increased alveolar dead space and impaired pulmonary gas exchange.

In "shock lung," pulmonary elasticity progressively decreases, and p_aO₂ drops. During spontaneous breathing, this results in a continuous increase in respiratory effort. Subsequently, p_aCO₂ begins to rise, necessitating a progressively greater minute ventilation.

The "shock lung" syndrome in exotoxic shock is characterized by pronounced interstitial edema and Atelectasis with intra-alveolar edema leading to a loss of respiratory function. Over time, this results in ventilation-perfusion mismatch. On the one hand, ventilation suffers due to The Development of atelectasis; on the other hand, perfusion is impaired As a result of blood shunting, disseminated intravascular coagulation (DIC), and microcirculatory disorders.

In 15% of Acute Poisoning cases, central neurogenic disorders of respiratory regulation and respiratory Muscle Function occur; in 45%, aspiration-obstructive disorders associated with mechanical asphyxia are observed; in other cases, the cause of hypoxia is pathological processes in the lungs, such as atelectasis and Pneumonia (E. A. Luzhnikov, L. G. Kostomarova, 1989).

Two main mechanisms are distinguished in the pathogenesis of liver and Kidney dysfunction during exotoxic shock: a specific mechanism associated with their excretory and detoxifying Functions, and a non-specific mechanism dependent on The Role of these organs in maintaining Homeostasis. In specific-type injuries, direct contact of the toxic substance with The Liver and kidney parenchyma is of primary importance (the damaging effect of hepatotoxic and nephrotoxic poisons).

Non-specific toxic injuries to the liver and kidneys develop secondarily as a consequence of pathological Changes in the body during acute poisoning. One of these is the impairment of regional blood flow during exotoxic shock. Reduced blood supply leads to ischemic damage to the liver and kidneys.

Specific and non-specific injuries to these organs mutually exacerbate each other.

The surge in sympathoadrenal system activity, typical of shock states, causes an increase in portal pressure due to the constriction of portal Veins and a reduction in hepatic blood flow along with lower arterial and venous fractions. Reduced venous Blood flow through the liver, in turn, leads to blood retention and stasis within the portal system vessels, where up to 60–80% of the body's total blood volume can pool. Such massive pathological blood pooling not only exacerbates systemic hemodynamic disorders and impedes venous outflow from abdominal organs, but also leads to Functional and Structural damage, up to and including necrosis.

Furthermore, exotoxic shock impairs the functional state of the kidneys, particularly in poisonings involving nephrotoxic agents. As early as the first hours, a decrease in Glomerular Filtration, a reduction in effective renal plasma flow, impaired urinary concentration capacity, and a drop in urine output (oligoanuria) are observed.