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

Main types of acute poisoning and their treatment
Chemical poisoning
Poisoning by rocket propellant components

Two MAIN TYPES OF propellants are used in rocket propulsion systems: liquid and solid. Liquid propellants are of primary toxicological concern.

The most common type of liquid rocket propellant is bipropellant, consisting of an oxidizer and the fuel proper. The oxidizers include nitrogen tetroxide (NTO or amyl) and nitric acid (NA), while the fuel proper is unsymmetrical dimethylhydrazine (UDMH or heptyl). Upon contact, these components form a self-igniting composition that simplifies the rocket engine's ignition system and reduces the risk of explosion in the combustion chamber.

5.4.3.1. Oxidizer Poisoning

Oxidizers of the NTO and NA types. Physicochemical properties. The NTO oxidizer (nitrogen tetroxide, or amyl) consists of 99% nitrogen tetroxide (N₂O₄) and is a volatile liquid with a characteristic sweetish-pungent odor. The color of the liquid and its vapor changes with Temperature from nearly colorless at t° -40 °C, through yellow and red-brown, to nearly black at t° +180 °C. The density of nitrogen tetroxide is 1.447 g/cm³, the freezing (melting) point is -11.2 °C, and the boiling point is +21.5 °C. At a temperature of +40 °C, nitrogen tetroxide dissociates almost completely into NO₂ and NO. Chemical Equilibrium in the mixture of nitrogen oxides is established almost instantaneously upon temperature changes. Amyl is readily miscible with organic Solvents, forming explosive mixtures with A number of organic substances (such as kerosene, gasoline, and benzene). When interacting with Water, NTO undergoes Hydrolysis to form nitric and nitrous acids.

Oxidizers of the NA type are multicomponent formulations in which nitric acid accounts for about 70% of the volume, nitrogen tetroxide for 24-28%, water for 0.7-3%, and corrosion inhibitors for 0.15-1.3%. The vapor of NA oxidizers has a yellow-brown or orange color.

Toxicological properties. Nitrogen dioxide—the primary toxicologically significant gaseous component of amyl oxidizer—is a highly hazardous compound.

The odor detection threshold for nitrogen dioxide is 10 mg/m³, the threshold for irritant effects is 150 mg/m³ for a 4-minute exposure and 90 mg/m³ for a 15-minute exposure. Concentrations of nitrogen dioxide above 400 mg/m³ induce toxic pulmonary edema.

The levels of nitrogen dioxide in ambient air and in the work zone air of industrial facilities are strictly regulated.

Pathogenesis of poisoning. Inhalation is the primary route by which the NTO oxidizer enters the victim's body. In the presence of moisture on the mucous membranes of the respiratory tract and on the Skin of the torso and extremities, NTO vapors may form nitric and nitrous acids, though this does not significantly impact the clinical picture of the injury.

The Nature of the Toxic Effect of nitrogen oxides on the victim's body depends on the COMPOSITION OF THE gas mixture. When NO predominates, poisoning proceeds via a resorptive (nitrite) type; when NO₂ predominates, it proceeds via an irritant type. Unlike other irritating gases, NO₂ does not trigger a strong reflex reaction because it is a relatively poorly soluble compound that readily penetrates through the Airways into the Lungs. Consequently, the largest areas of damaged lung tissue are the alveolar epithelium and the terminal portion of the respiratory bronchioles.

The Mechanism of the toxic action of NO₂ on the lungs is largely similar to the damaging action of phosgene and is based on three key links: a) destructive Changes in the alveolar-capillary membrane, b) Hypoxia, and c) elevated pressure in the Pulmonary Circulation.

The severity of hypoxia in nitrogen dioxide poisoning is significantly influenced by: 1) marked bronchospasm and 2) edema and Swelling of the bronchial mucosa caused by arachidonic acid metabolites (Prostaglandins, Leukotrienes, prostacyclins, and thromboxane) generated under the action of NO₂. Hemodynamic disturbances and microthrombosis in the pulmonary Blood Vessels exacerbate damage to the alveolo-capillary membranes and accelerate The Development of toxic pulmonary edema.

An important factor in the pathogenesis of nitrogen dioxide intoxication is the pronounced local effect of the poison on the Upper Respiratory Tract, leading to severe toxic pharyngolaryngitis and tracheobronchitis.

The resorptive action of NO is determined by the level of nitrites formed in the blood, resulting in marked methemoglobinemia, hemic hypoxia, vasodilation, lowered blood pressure, and cerebral disorders.

Contact of NA-type oxidizers with the skin or eyes causes coagulation of tissue Proteins (coagulation necrosis) and first- to fourth-degree chemical Burns. The latter are characterized by significant depth, delayed repair processes, and a reduced capacity for damaged tissue regeneration.

Clinical picture of Acute Poisoning. Clinical manifestations of inhalation injury caused by amyl and nitric acid vapors are variable. There are 4 possible variants of poisoning: 1) irritant, 2) reversible, 3) asphyctic, and 4) combined. It is generally not possible to clearly isolate these forms, but the dependence of the clinical course on the composition of the gas mixture, The ratio of its main components—NO and NO₂—and their concentration is undeniable.

If nitrogen oxide (NO) predominates in the inhaled air, cerebral and cardiovascular disorders as well as methemoglobin formation come to the fore in the clinical picture (reversible type). Exposure to nitrogen dioxide (NO₂) damages the respiratory Organs, leading to pulmonary edema (irritant type). Inhalation of high concentrations of nitrogen dioxide rapidly induces asphyxia, convulsions, respiratory arrest, and death (asphyctic type). The combined action of NO and NO₂ is characterized by the very rapid development of dynamic cerebral disorders and cyanosis, followed—after a multi-hour latent period—by toxic pulmonary edema (combined type).

The irritant and combined types of intoxication, involving damage to the respiratory mucous membranes and lung tissue with the development of pulmonary edema, are the most characteristic of acute poisonings by amyl and nitric acid vapors.

Five stages are distinguished in the clinical course of toxic pulmonary edema: 1) reflex, 2) latent, 3) clinically overt symptoms of pulmonary edema, 4) lesion regression, and 5) complications and long-term sequelae.

1. The reflex stage is characterized by symptoms of irritation of THE EYE AND respiratory mucous membranes. A dry, painful cough appears. Breathing is accelerated and shallow. High concentrations of NTO or NA vapors may cause reflex laryngospasm and reflex respiratory arrest.

2. The latent stage (the period of apparent well-being, or latent period) varies in duration depending on the severity of the injury, lasting from 30 minutes to 24 hours, and averages 4–6 hours. Physical exertion and the intake of large amounts of fluids contribute to shortening the latent period and accelerating the development of toxic pulmonary edema. Careful examination during this stage may reveal tachypnea with relative bradycardia, alongside clinical and radiological signs of acute pulmonary emphysema.

3. The stage of clinically overt symptoms of toxic pulmonary edema is characterized by a deterioration in general condition, the onset of cough, dyspnea, acute weakness, chest pain, difficulty breathing, facial cyanosis, and distension of the neck Veins. Respiration is rattling, with significant amounts of frothy pink sputum. Changes in cardiovascular activity occur (increased pulse rate and Heart rate, muffled heart sounds), along with elevated body temperature. Auscultation of the lungs reveals coarse, medium, and fine moist rales, as well as dry rales. Blood tests show marked neutrophilic leukocytosis with a left shift, as well as erythrocytosis resulting from hemoconcentration.

4. The stage of regression (recovery) becomes apparent within 3 to 4 days if the toxic pulmonary edema follows a favorable course.

5. The stage of long-term sequelae is associated with the development of bacterial Pneumonia and neuropsychiatric alterations in the victims.

Alongside the severe injuries described above, moderate and mild cases of poisoning may also be registered.

Moderate poisoning most frequently manifests as toxic bronchopneumonia and toxic Bronchitis. Primary and secondary pneumonias are distinguished. Primary toxic pneumonia (pneumonitis) is characterized by a gradual onset and a mild Clinical presentation. Typically, in such victims, well within the first 24 hours following the period of autonomic disorders, their condition continues to deteriorate: coughing intensifies, breathing rate increases, dyspnea and cyanosis appear, and body temperature rises. Very similar clinical manifestations also develop in severe tracheobronchitis, which significantly complicates Differential Diagnosis. Persistent moist rales, strictly localized and auscultated in limited areas of the lungs, along with occasional changes in the Percussion sound over them, suggest the presence of pneumonia, which can be confirmed by radiological findings.

Secondary pneumonia is usually bacterial in nature and develops several days after the victim's poisoning and the subsiding of clinical symptoms. Unlike primary pneumonia, its onset is acute, accompanied by symptoms of general intoxication, cough, dyspnea, cyanosis, and frequently hemoptysis. Body temperature rises. Distinct moist rales are auscultated in the lungs. Blood tests show high leukocytosis, sometimes with eosinophilia. X-ray Examination reveals multiple small opacities in various PARTS OF THE lungs. The course of the pneumonia is severe, characterized by extremely slow resolution and a tendency to relapse.

Respiratory tract alterations are prominent even in mild inhalation poisonings, manifesting as mild to moderate toxic laryngitis and tracheobronchitis. At the same time, signs of the resorptive action of the poison are quite frequently observed, such as stupor, dizziness, general weakness, brief loss of consciousness, and lability of pulse and blood pressure.

The duration of inhalation injuries caused by oxidizer vapors ranges from 3 to 5 days in mild cases, and from 2 to 6 weeks in moderate cases.

Emergency care and Treatment. The Scope of medical care depends on the stage of the pathological process. Measures are aimed at preventing the development or relieving hypoxia, as well as preventing or reducing the severity of pulmonary edema.

The treatment strategy for individuals affected by nitrogen oxides and nitric acid is similar to the therapeutic measures for poisonings by suffocating agents (such as phosgene); however, there are a number of specific features determined by the peculiarities of the pathogenesis. First, among the mechanisms of the NEGATIVE IMPACT OF oxidizers on the victim's body, a prominent role is played by sharply pronounced activation of Lipid Peroxidation (LPO) processes; therefore, in the Cytology/cytology/16.html">Early stages of medical care, the administration of antioxidants in high doses is mandatory (Vit E and B6 at a dose of 15–20 ml; 5% ascorbic acid solution - Vit C). Second, in poisonings by nitrogen oxides, the local action of the poison is of significant importance, involving burns of the upper respiratory tract and the development of bronchospasm and laryngeal edema. To eliminate these manifestations, it is advisable to prescribe bronchodilators, decongestants, and desensitizing agents. Subsequently, prolonged treatment of purulent tracheobronchitis with a torpid course should be anticipated. Third, in the early period of oxidizer poisoning, there are relative contraindications to prescribing Oxygen therapy, since oxygen exerts a local pro-oxidant effect. It should be used only upon the appearance of pronounced signs of hypoxia and at later stages of intoxication, during the Development of the alveolar phase of pulmonary edema. The fourth feature of the therapeutic strategy is the mandatory prescription of anticoagulants (heparin) due to marked disturbances in the Blood Coagulation and anticoagulation systems (tendency toward thrombosis) throughout the intoxication caused by nitrogen oxides and nitric acid.

First aid and pre-medical care consist of evacuating the victim from the contaminated room, ensuring rest and warmth. The victims should be placed in a sitting or semi-sitting position. If necessary, rinse the eyes with water or a 2% sodium bicarbonate solution. In case of coughing and difficult breathing, inhalation of an anti-smoke mixture, intramuscular administration of 1.0 ml of a 0.1% atropine solution, 1.0 ml of a 2% diphenhydramine (dimedrol) solution, and 1.0 ml of a 2% promedol solution are indicated. For progressive laryngeal edema, intramuscular administration of 10 ml of a 10% calcium gluconate solution is recommended.

Initial medical care. For the purpose of preventing the development of toxic pulmonary edema, intravenous administration of 15-20 ml of 5% ascorbic acid solution, 10 ml of 5% unithiol solution, and 40 mg of furosemide, 2-3 puffs of Beclometasone (becotide) per os, and parenteral administration of 60-90 mg of prednisolone are indicated. In case of laryngobronchospasm, subcutaneous administration of 1 ml of 0.1% atropine sulfate solution and intravenous administration of 10 ml of 2.4% aminophylline (euphylline) solution are performed.

Individuals who have been evacuated from a contaminated area, even in the absence of Clinical symptoms of intoxication, must remain under constant medical observation for at least 24 hours. During this period, their water and food intake should be restricted. Every 2-3 hours throughout the observation period, percussion and auscultation of the lungs must be performed. A chest X-ray examination is mandatory. Early signs of incipient edema include the lowering of the lower lung borders (diaphragmatic domes), decreased mobility of the lung edges, the appearance of a tympanitic percussion sound, and fine moist rales in the posterior-inferior lung regions.

Upon the appearance of the first signs of edema, intravenous administration of corticosteroid drugs (prednisolone 150-200 mg or hydrocortisone 200-250 mg), 40 mg of furosemide, and heparin 5000 IU 4 times a day is indicated. Phlebotomy (200-300 ml) and the application of venous tourniquets to the extremities (provided the pulse is preserved) are carried out to reduce blood inflow to the lesser circulation. This method is effective only in the initial period of pulmonary edema. Humidified oxygen inhalations should be administered with caution and only in the presence of obvious signs of hypoxia, with an oxygen concentration in the gas-air mixture not exceeding 30%, since oxygen enhances the Toxic effects of nitrogen oxides (pro-oxidant action of oxygen).

Qualified and specialized care. At the stage of pronounced symptoms of toxic pulmonary edema (alveolar phase), medical measures should be aimed at ensuring upper airway patency, reducing fluid transudation, correcting cardiovascular disorders, eliminating oxygen starvation, normalizing disturbed metabolic processes, preventing thromboembolism, and preventing and treating infectious complications. To this end, intravenous administration of 10-20 ml of 2.4% aminophylline solution is indicated, which reduces bronchospasm, improves coronary and cerebral circulation, exerts a diuretic effect, and lowers pressure in the pulmonary artery system. Dehydration therapy should be continued (furosemide 40 mg 3–4 times a day), along with the administration of 100-150 mg of prednisolone or 200-250 mg of hydrocortisone, and 5000-10000 IU of heparin (total heparin dose on the first day of edema treatment up to 30-40 thousand IU). When cyanosis appears, the victim must be provided with inhalation of 40% oxygen with an antifoaming agent (20-30% ethyl alcohol) in sessions of 40-45 minutes with 10-15 minute intervals, tracheal intubation, and mechanical ventilation.

To unload the lesser circulation, ganglion blockers, alpha- and beta-blockers, or nitrates can be used. At the same time, strict monitoring of blood pressure levels is necessary due to the possible development of collapse-like reactions.

In case of vascular tone disturbances and the onset of Heart Failure resulting from low Cardiac Output, dopamine is the drug of choice for cardiotropic support. The Use of norepinephrine or phenylephrine (mesaton) is acceptable, but epinephrine is contraindicated, and its administration must be avoided. To eliminate metabolic acidosis, trisamin or sodium bicarbonate is administered.

For the Prevention of infectious complications, the complex therapy of toxic pulmonary edema includes the use of Antibiotics (ampicillin, amoxiclav, fourth-generation Cephalosporins). Early administration of antibiotics not only prevents secondary infection but also limits the development of pulmonary edema. Vascular wall-stabilizing agents and the administration of Vitamins P, C, and nicotinic acid are recommended.

With the progression of pulmonary edema, ineffectiveness of ongoing therapy, increasing hypoxia, disruption of respiratory rhythm and frequency, and loss of consciousness, tracheal intubation and transferring the victim to mechanical ventilation with positive end-expiratory pressure are necessary. All victims with this type of poisoning are not indicated for hyperbaric oxygen therapy (oxygen therapy under elevated pressure).

5.4.3.2. Fuel Poisoning

Unsymmetrical dimethylhydrazine (heptyl). Physicochemical properties. Unsymmetrical dimethylhydrazine (UDMH), or heptyl, is a colorless, transparent, highly volatile liquid with a sharp, unpleasant odor. The liquid is hygroscopic and readily soluble in water, Hydrocarbons, alcohols, and ethers. The molar mass is 60.1 g/mol.

Toxicological properties. Heptyl is a highly hazardous compound with sharply pronounced irritant properties. Its vapors irritate the mucous membranes of the eyes and respiratory tract. Exposure to heptyl at a concentration of 400 mg/m³ causes fatal poisoning in the victim.

The sharp odor of unsymmetrical dimethylhydrazine is perceptible at air concentrations exceeding 5.0 mg/m³ During the first minutes of contact. Olfactory adaptation to this odor may subsequently occur.

In the development of acute poisoning, the inhalation route of entry of the poison plays a leading role; however, percutaneous penetration of heptyl through exposed areas of the body presents an equal toxicological hazard, as it is rapidly absorbed through intact skin.

Pathogenesis of poisoning. Heptyl is a poison with neuro- and hepatotropic action. By interacting with Pyridoxal phosphate (vitamin B₆), heptyl blocks the Transamination and decarboxylation processes of Amino Acids, which are vital for the METABOLISM of Brain and Liver Tissues. This leads to a sharp decrease in the gamma-aminobutyric acid content in brain tissue due to the inhibition of its formation from glutamic acid. As a result, the ratio of Excitation and Inhibition processes in the Central Nervous system is disrupted. Severe neurological disorders developing during hydrazine poisoning and the onset of seizure syndrome are associated with these disturbances. Furthermore, UDMH suppresses The oxidation of catecholamines and serotonin, as it is an active monoamine oxidase inhibitor. This contributes to the accumulation of Neurotransmitters in biological fluids and the enhancement of their physiological effects.

In the development of hydrazine-induced liver damage, along with the aforementioned disorders, a significant role is played by The stimulation of lipid peroxidation, suppression of antioxidant defense, inhibition of Protein Synthesis, etc.

In the pathogenesis of UDMH poisonings, its local irritant properties are of certain importance. The development of acute inflammatory changes in the respiratory tract and toxic pulmonary edema is associated with them. Hypoxia arising from respiratory failure may be exacerbated due to methemoglobin formation and hemolysis.

Clinical picture of acute poisoning. The clinical manifestations of inhalation poisonings with heptyl are characterized by symptoms of upper respiratory tract irritation, general cerebral disorders, and signs of liver damage. The severity of these manifestations depends on the degree of intoxication. In cases of mild heptyl poisoning, a burning sensation in the eyes, dryness and tickling in the throat, cough, headache, dizziness, nausea, sweating, and general weakness appear. Gradually, usually within the first 24 hours after poisoning, these signs of intoxication intensify. Objectively, functional Changes in the central nervous system state and vegetative-vascular instability are noted. These phenomena resolve within a week.

The clinical picture in moderate poisoning proceeds with more pronounced symptoms of intoxication. Vomiting is noted, frequently recurrent. A brief loss of consciousness is possible. Body temperature rises. Stage I-II toxic hepatopathy develops. Complications in the form of bronchitis or pneumonia are possible. The duration of the poisoning course is 2 to 4 weeks or more.

Severe heptyl poisoning is accompanied by seizures, which typically develop 1.5–2 hours after exposure. The seizures manifest as acute episodes, usually combined with altered mental status. Repeated vomiting, asphyxia, and retrosternal pain are observed. Bronchitis, bronchiolitis, and pneumonia develop from the first days. Pulmonary edema may also occur. After a few days, yellowish discoloration of the skin and sclera appears, the liver enlarges, and symptoms of general intoxication increase, indicating the development of grade II–III toxic hepatopathy.

Contact of heptyl droplets with the eyes causes a burning sensation, blepharospasm, edema, and conjunctival inflammation. Skin contact results in erythematous dermatitis.

First aid and pre-medical care. If heptyl gets on the skin or into the eyes, the victim must be immediately removed from the danger zone, using personal protective equipment for both the rescuer and the victim. Then, flush the eyes with cold water and instill a 1% dicaine solution. Contaminated skin areas should be thoroughly washed for an extended period with cold water and soap.

In case of inhalation poisoning, remove or carry the victim out of the contaminated area. Remove any clothing contaminated with heptyl or its vapors. Rinse the eyes and Nose with water, and rinse the Mouth. Transport the victim to a medical aid station or a specialized toxicology department on a stretcher.

Initial medical care. At the medical aid station, regardless of the route of heptyl entry into the body, immediately administer intravenously (preferred) or intramuscularly 5–10 mL of a 5% solution of vitamin B₆ (pyridoxine), which has an antidote effect and blocks (stops) convulsive syndrome manifestations. Oxygen therapy using KI-4 or KI-3M apparatuses is indicated. In case of reflex respiratory arrest, Artificial ventilation is performed using an Ambu bag or portable mechanical ventilators.

Qualified and specialized care. Depending on the severity of intoxication, the administration of pyridoxine is continued at a rate of 0.5 mL of a 5% solution per 1 kg of body weight. If seizures persist, additionally administer intramuscularly 1.0 mL of a 1% phenazepam solution, 2 mL of sibazone, barbiturates, or MgSO₄. The administration of pyridoxine is repeated after 2 hours if psychomotor agitation increases or seizures recur.

Intravenous administration of 10–15 mL of 5% ascorbic acid in a 40% glucose solution is indicated, along with Forced diuresis to enhance the elimination of the poison from the body. Extracorporeal techniques may be employed both to remove the absorbed toxicant and to treat hepatopathy.

Treatment of toxic lesions of the eyes, skin, respiratory organs, and liver is carried out according to standard clinical guidelines.