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

Main types of acute poisoning and their treatment
Poisoning by gunpowder (explosive) gases

The experience of past wars demonstrates the possibility of poisoning by propellant or explosive gases, which are formed and accompany the combustion and decomposition of specific chemical substances during a shot or explosion.

Propellant gases contain fairly toxic substances: carbon monoxide, nitrogen oxides, and carbon dioxide (СO₂), as well as less toxic ones, such as hydrogen and methane.

The complex of pathological phenomena observed after the inhalation of gases and fumes generated by explosions is referred to as propellant sickness. Its Clinical presentation is highly variable due to the simultaneous action of a mixture of toxic substances. However, the clinical picture is predominantly characterized by Carbon monoxide poisoning, and less frequently by nitrogen oxides and carbon dioxide.

The Toxic Effect of Carbon dioxide is primarily driven by the following pathophysiological changes. Hypercapnia, resulting from the inhalation of carbon dioxide, exacerbates Hypoxia due to more complete oxyhemoglobin dissociation and decreased synthesis in the Lungs; it leads to increased peripheral resistance and hemorheological Blood flow disorders, impairs pulmonary gas exchange, and reduces alveolar ventilation. Furthermore, respiratory acidosis causes paralytic vasodilation of cerebral vessels and cerebral Circulation disorders, decreases myocardial contractility (following an initial phase of enhancement), and impairs renal function, among other effects. The clinical course of carbon dioxide poisoning exhibits a distinct phased progression.

Clinical Presentation

At the onset of СO₂ intoxication, excitation, a state of euphoria, excessive talkativeness, and insomnia are observed. Objective Examination reveals flushing of the Skin, particularly the face, elevated skin Temperature, hyperhidrosis, dyspnea, tachycardia, as well as arterial and venous Hypertension. Subsequently, all these symptoms intensify: the skin acquires a cyanotic-purple hue, "acidotic coma" develops, and Reflexes are suppressed; the pupils, which were initially constricted, become markedly dilated, accompanied by diffuse cyanosis and profound hypotension. Death results from respiratory arrest.

Among the most clearly described Clinical symptoms of propellant sickness, the syndrome of "pseudo-intoxication" ("propellant intoxication" as defined by French authors) is most frequently encountered, caused by the combined effects of Carbon Monoxide and carbon dioxide. The victim's characteristic appearance includes a puffy, hyperemic face and conjunctival injection. Nausea and vomiting frequently occur. Victims present in a depressed or agitated state, gesticulating, talking excessively, and complaining of migrainous headaches, tinnitus, and dizziness. Subsequently, drowsiness or heavy Sleep with nightmares develops. The pulse, which may be slowed at the onset of intoxication, invariably becomes accelerated. Arterial hypertension is observed. As the intoxication progresses, cyanosis increases, and breathing becomes pathological—specifically Cheyne-Stokes Respiration. In extremely severe cases, death ensues from central respiratory paralysis.

Other forms of propellant sickness can be caused by various combinations of toxic gases and lack a definitive clinical picture, as the symptom complex varies depending on the type and Properties of the predominant gas. In particular, СО and СO₂, which practically always act simultaneously, lead to the aforementioned clinical picture of poisoning, whereas nitrogen oxides ("nitro-gases") induce pronounced irritation of the eyes and Upper Respiratory Tract, asphyxia, inflammation, and toxic pulmonary edema, coupled with methemoglobin formation and a depressive effect on circulation and the Central Nervous system.

Treatment

First aid and treatment are administered in accordance with the clinical manifestations of intoxication. Most often, these measures are aimed at treating carbon monoxide poisoning. Performing artificial respiration as a first-aid measure, which is essential in СО and СO₂ poisonings, can be dangerous in cases of nitrogen oxide poisoning. Given the difficulties in establishing a definitive Diagnosis during the Cytology/cytology/16.html">Early stages of poisoning, all victims with eye injuries showing no signs of exposure to irritant chemical warfare agents must be managed as casualties of "nitro-gases" and given first aid similar to those exposed to choking agents. If the clinical picture of intoxication clearly reveals symptoms of "nitro-gases" exposure, the full therapeutic protocol for such poisonings must be implemented, primarily focusing on the Prevention and treatment of toxic pulmonary edema, elimination of hypoxia, restoration of respiratory and cardiac Functions, reduction of methemoglobin formation, and detoxification.

Following exposure to explosive gases, post-intoxication complications frequently arise in the form of asthenic and astheno-vegetative syndromes, as well as respiratory and circulatory dysfunctions, which necessitate a comprehensive rehabilitation program both during the hospital stage and after discharge.