Intensive Care of Emergency Conditions - V. M. Zaporozhan 2006

Urgent Detoxification

Depending on the routes of entry and elimination of toxic substances from the body, the following emergency detoxification Methods are used: gastric lavage, enterosorption, Forced diuresis, hemoperfusion, hyperventilation, and washing of the Skin and mucous membranes.

When poison is ingested orally, the patient should be given a tablespoon of activated charcoal slurry before gastric lavage. Gastric lavage must be performed regardless of the time elapsed since poisoning or the dose of the toxic substance. The Stomach is washed through a large gastric tube using 15–20 L of room-Temperature tap Water (cooled water is advisable in cases of corrosive poisoning accompanied by gastrointestinal bleeding) in portions of no more than 300–500 ml, since an overfilled stomach can cause vomiting or regurgitation around the tube with a risk of vomit aspiration. After gastric lavage, a laxative—such as liquid paraffin or castor oil—can be administered through the tube.

In cases of corrosive poisoning, the gastric tube is generously lubricated with liquid paraffin or sunflower oil and inserted only after preliminary subcutaneous or intravenous administration of analgesics (morphine, promedol, omnopon, etc.). No laxatives are administered after lavage in such cases.

Burns of the digestive tract are not a contraindication for gastric lavage, as the risk of perforation is overstated.

It is strictly unacceptable to use acid or alkali solutions to neutralize acids or alkalis in the stomach, as this may cause gas formation resulting in acute gastric dilation and significantly worsen the patient's condition.

In addition to activated charcoal as a universal sorbent, other substances can be administered into the stomach for specific poisonings. For example, in barium chloride poisoning, magnesium sulfate is administered to form an insoluble barium sulfate salt. In silver nitrate poisoning, a sodium chloride solution is used to form insoluble and non-toxic silver chloride. In poisonings with chlorinated Hydrocarbons (dichloroethane, carbon tetrachloride, chloroform), up to 100 ml of liquid paraffin must be introduced into the stomach; it is practically unabsorbed in the digestive tract and, by dissolving the aforementioned poisons, prevents them from entering the bloodstream. For heavy metal and arsenic poisoning, 20–30 ml of unithiol solution is prescribed both before and after gastric lavage.

If tracheal intubation with a cuffed tube is feasible, it must be performed prior to gastric lavage in comatose patients lacking cough and laryngeal Reflexes to prevent aspiration of vomit and wash water.

In inhalation poisoning, the patient must first be removed from the contaminated area, airway patency ensured, and respiratory resuscitation performed using a manual resuscitator, avoiding "Mouth-to-mouth" and "mouth-to-Nose" breathing, but with mandatory oxygen inhalation. The person evacuating the patient from the hazardous area must wear a gas mask.

Toxic substances on the skin or in the eyes are removed by thorough rinsing, and those in cavities (rectum, Vagina, ear canals) by douching.

In injection-type poisoning, local cold application, injections of 0.1% adrenaline solution, and a circular novocaine block of the limb proximal to the injection site are used.

Elimination of toxic substances absorbed into the bloodstream should, whenever possible, be carried out in specialized intensive care units or toxicology centers. There, or even at the pre-hospital stage (at the scene or in an ambulance, if the patient's condition permits), early forced diuresis is urgently performed. Its methodology is as follows:

1. Preliminary water loading. Intravenous infusion lines are set up, and 500 ml of a 5% glucose solution is administered During the first hour.

2. Administration of Diuretics. Concurrently with water loading, 300–600 ml of a 20% mannitol solution (0.5–1 g of dry substance per 1 kg of the patient's body weight) is administered intravenously as a bolus over 10–15 minutes, or 20–40 mg (1–2 ampoules) of furosemide (lasix). Both drugs can be used simultaneously in the specified doses. The duration of action of such a dose is 3–4 hours, after which, if forced diuresis needs to be continued, the dose is repeated. Other diuretic agents may also be used, such as a 2.4% euphylline solution at 0.5 ml intravenously every 15 minutes during the first 3 hours.

3. Maintenance of diuresis. During forced diuresis, a urinary catheter is inserted into the bladder and left in place for several hours while the Procedure continues. This facilitates urine output monitoring and prevents urinary retention resulting from bladder atony. Forced diuresis is considered effective if it reaches 10 ml/min (normal is 1–1.5 ml/min). To maintain urine production rate, lost water and electrolytes must be continuously replenished by administering saline solutions (0.9% isotonic sodium chloride solution supplemented with 50 ml of 3% potassium chloride solution per 400 ml, Ringer's or Phillips' solutions). The volume of solutions administered in each subsequent hour must equal the volume of urine excreted in the preceding hour, averaging about 500 ml/h.

4. Plasma alkalinization. This is achieved by intravenous infusion of a 4% sodium bicarbonate solution at a rate of approximately 200 ml/h for the first 3 hours, and 100 ml/h thereafter. An indicator of effectiveness is a freshly voided urine pH of 7–8, determined using litmus paper. Plasma alkalinization is particularly recommended for poisonings with barbiturates, organophosphates, dichloroethane, quinine hydrochloride, and pachycarpine hydroiodide, as well as in cases of massive intravascular hemolysis.

The forced diuresis method is contraindicated in acute and chronic cardiovascular failure (persistent collapse, stage II–III circulatory failure) and Renal Dysfunction (oliguria, azotemia). In patients over 50 years of age, the method may be less effective due to age-related sclerotic Changes in the Kidneys.

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Fig. 28. USOK-100 P hemoperfusion system

Hemoperfusion is an effective detoxification method. To perform it in non-specialized medical facilities and at the pre-hospital stage, our department has developed the portable USOK-100 P hemoperfusion system (Fig. 28). Factory packaging of the hemosorbent into a sterile, single-use cartridge made of biocompatible polymers eliminates the need to assemble and sterilize the system prior to the hemoperfusion procedure. Furthermore, the inclusion of additional Dacron microfilters in the cartridge, capable of retaining the finest Blood clots and sorbent particles, makes it completely safe for the patient.

The cartridge is connected to two antecubital Veins via attached polymer tubing lines terminating in specialized needles for blood vessel puncture. One of the lines is equipped with a manual blood perfusion pump. The entire system is hermetically sealed and can remain sterile for at least two years after manufacture.

Syndromic therapy is carried out in accordance with the primary pathological syndromes that occur during poisonings.

Respiratory disorders:

The aspiration-obstructive form occurs As a result of Tongue fallback, vomit aspiration, salivation, bronchorrhea, or laryngeal edema. It is most frequently observed in comatose patients. Airway patency is restored according to resuscitation guidelines. If asphyxia due to laryngeal edema develops as a result of airway burns from acids or alkalis, emergency cricothyroidotomy or tracheotomy is required.

The central form is caused by respiratory center depression during coma, or impaired innervation of Respiratory Muscles in organophosphate or pachycarpine poisoning. Artificial pulmonary ventilation is recommended, preferably using basic devices (Ambu bag, RPA) via a face mask or endotracheal tube simultaneously with antidote therapy.

The pulmonary form results from toxic pulmonary edema or tracheobronchitis, most commonly following inhalation of chlorine, ammonia, acid, phosgene, or nitrogen oxide vapors. It develops immediately after inhaling the toxic substance or within 3–6 hours. Treatment involves intravenous administration of Hormones (prednisolone 60–90 mg, etc.), bronchodilators (ephedrine, euphylline), and antihistamines (diphenhydramine, suprastin, tavegil). Early administration of Antibiotics, inhalation of humidified oxygen, ethyl alcohol vapors to suppress foam in pulmonary edema, and diuretics (furosemide) are essential.

Hemic Hypoxia is caused by poisoning with substances that form carboxyhemoglobin or methemoglobin (carbon monoxide, nitrates, aniline), which disrupts Blood Oxygen transport.

Tissue hypoxia results from cyanide poisoning, which blocks respiratory Enzymes such as cytochrome oxidases.

Circulatory Disorders

Primary toxigenic collapse is characterized by the sudden and rapid development of circulatory failure, where compensatory mechanisms fail to engage in time, leading to sudden death. Such a scenario can occur in confined spaces with high concentrations of toxic vapors or gases, in oxygen-depleted atmospheres resulting from putrefaction, combustion, or grain germination, as well as in poisonings with extremely high doses of potent toxins. Primary toxigenic collapse accounts for 1–5% of all fatal poisoning cases. Treatment involves resuscitation.

Exotoxic Shock develops as a result of hypovolemia (due to poisoning with corrosive liquids or dichloroethane), decreased vascular tone (barbiturates, organophosphates), or cardiotoxic effects (veratrine, barium chloride, Manchurian aralia tincture, strophanthidin, organophosphates). It is noted in 65–70% of fatal poisoning cases. Treatment consists of anti-shock measures. In cases of poisoning by corrosive agents, relieving pain with analgesics is of paramount importance.

Secondary somatogenic collapse is a manifestation of non-specific toxic myocardial dystrophy against the Background of impaired Liver, Kidney, or respiratory function. It is the cause of death in 30–35% of fatal poisonings. Therapy is identical to that for cardiovascular failure.

Acute Liver failure occurs in poisoning with hepatotoxic agents (chlorinated and aromatic hydrocarbons, organochlorine pesticides, ethyl alcohol, phenols, aldehydes, amines, inorganic substances such as iron sulfate and phosphorus, plant toxins including death cap, ragwort, marsh-elder, heliotrope, etc.). It frequently accompanies renal failure resulting from nephrotoxic poisoning and shock. The foundation of preventing toxic hepatopathy is urgent detoxification coupled with hepatoprotective therapy—lipotropic agents, Choline chloride, vitamin complexes, and hormone therapy.

ACUTE RENAL FAILURE arises from poisoning with nephrotoxic agents (Ethylene glycol, heavy metal salts, dichloroethane, carbon tetrachloride, mushroom toxin) and hemolytic agents (acetic acid essence, copper sulfate, arsine), as well as from exotoxic shock caused by other intoxications. An essential factor in diagnosing and preventing this condition is monitoring hourly diuresis during the Treatment of exotoxic shock and the early use of mannitol and furosemide tests, while massive hemolysis requires forced diuresis with plasma alkalinization. Fluid intake restriction prior to hospitalization in facilities equipped for hemodialysis is crucial in treatment (400 mL/day + diuresis = losses from vomiting, diarrhea, etc.).

Specific (antidote) therapy. Indicated when relatively small amounts of toxic substances are present. Requires precise Diagnosis and is effective only during the early toxigenic stage. The main antidote therapy is summarized in Table 12.

Table 12 Specific (antidote) therapy

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