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

General Characteristics of Acute Poisoning
Exotoxic Shock

Exotoxic Shock (from Greek exō outside, toxikon poison) is a clinical syndrome resulting from the acute chemical impact on the body, characterized by impaired METABOLISM, nervous regulation, and the functioning of all vital Organs and systems accompanied by signs of shock. It can be triggered by any severe acute exogenous poisoning.

Exotoxic shock develops within the first few hours following Acute Poisoning and accounts for 65–70% of fatal cases. The incidence of shock in acute poisonings varies, reaching 30.5% for corrosive substances, 86.5% for chlorinated Hydrocarbons, 27% for organophosphorus insecticides, and 16.9% for psychopharmacological agents (Luzhnikov E. A., 1989, 2000).

Exotoxic shock in acute poisoning is a specific variant of hypovolemic shock. It is driven either by absolute hypovolemia resulting from external and internal plasma loss, or relative hypovolemia resulting from vascular regulation disorders of various origins. Absolute hypovolemia (associated with poisonings by corrosives, chlorinated hydrocarbons, death cap mushrooms, etc.) is linked to damage to The Cell membranes of the digestive tract mucosa and the walls of microcirculatory vessels. Relative hypovolemia (caused by organophosphorus insecticides or OPIs) occurs As a result of pathological peripheral vasodilation driven by cholinesterase inhibition and the accumulation of large amounts of endogenous acetylcholine, or by the suppression of the vasomotor center and the direct action of chemical compounds and their metabolites on vascular receptors (in poisonings by hypnotics and psychotropic drugs).

In OPI poisoning, alongside the aforementioned primary mechanism of shock development, a direct toxic effect on the myocardium is observed, leading to reduced contractility. Consequently, shock in acute OPI poisoning frequently exhibits cardiogenic features and occurs against a backdrop of life-threatening cardiac rhythm and conduction disorders.

The developing hypovolemia leads to reduced venous return to The Heart, the onset of low Cardiac Output syndrome, and a decrease in stroke volume.

Clinically, shock in acute poisoning is characterized by: a severe General condition of the patient, altered mental status with preserved consciousness, cold and cyanotic Skin, cold sweat, dyspnea, tachycardia, hypotension, and oliguria. Although Functions of virtually all vital body systems are impaired, ACUTE CIRCULATORY FAILURE comes to the fore. Pronounced disorders of central, peripheral, and regional hemodynamics (especially in the portal system and Kidneys) manifest within the very first hours post-poisoning. Metabolic disturbances, as well as changes in Blood hemocoagulation and rheological properties, develop rapidly, compounded by the specific toxic action of chemical compounds (additional factors in the Pathogenesis of acidosis in poisonings by corrosive liquids, toxic coagulopathy).

The most critical features of exotoxic shock include:

1. Early involvement of metabolic links in the pathogenetic chain—virtually simultaneous with The entry of the toxic substance into the victim's body—which in Other types of shock typically represents the end result of a long sequence of pathological reactions.

Some authors (Golikov S. N. et al., 1980) suggest that these severe Homeostasis disorders are rooted in the biochemical (molecular) interaction of the toxicant with receptors and enzyme systems. This precise mechanism determines the primary feature of the pathogenesis of exotoxic shock.

2. Selective toxicity of specific chemical compounds toward particular organs and Tissues—hepatotoxicity, nephrotoxicity, cardiotoxicity, and the early onset of decompensated metabolic acidosis.

3. Prolonged action of the toxic substance and the repeated entry of the chemical compound or its metabolites into the victim's body. This leads to the repeated Formation of the vicious circle typical of shock states.