Otitis

What to do if your dog has anaphylactic or painful shock? Anaphylactic shock and its symptoms in various animal species Treatment of anaphylactic reaction from vaccination in a dog.

Anaphylactic shock is a condition in a dog’s body that is caused by the introduction of a permissive dose of an antigen.

Manifests itself as a rapid and generalized hypersensitivity reaction.

Causes of anaphylactic shock in dogs

The most significant causes of anaphylaxis in dogs are exposure to animal and insect poisons and medications. Shock can occur from bites:

bumblebees,
bees,
hornets,
tarantulas,
spiders,
snake.

Any medicine can cause the development of anaphylactic shock, but antibiotics (cephalosporins, penicillins, tetracyclines, vancomycin, chloramphenicol, etc.) come first. They are followed by nonsteroidal anti-inflammatory drugs, radiocontrast agents, general anesthetics, and muscle relaxants.

Such a reaction is also possible from the administration of serums, hormones (ACTH, insulin, progesterone and others), enzymes (penicillinase, streptokinase, trypsin, chymotrypsin, asparaginase), vaccines, chemotherapeutic agents (cyclosporine, vincristine, methotrexate, etc.), sodium thiosulfate, local anesthetics.

Development of anaphylactic shock: first symptoms

Regardless of the cause, shock always develops in the same way. The first to occur is the immunological reaction of the dog’s body. Anaphylaxis can be local or systemic. Local manifestations are angioedema and urticaria. With urticaria appears:

redness,
rashes and blisters,
itching occurs.

With angioedema, swelling forms in the subcutaneous tissues and deep layers of the skin. Various gastrointestinal reactions also occur: tenesmus, nausea, vomiting and diarrhea. Sometimes urticaria can progress to systemic anaphylaxis.

Systemic anaphylaxis is the most severe form of shock and is life-threatening. Most often, it affects the dog's liver. The first signs of anaphylaxis are agitation with vomiting. As it progresses, breathing becomes impaired, reactions are inhibited, or muscle or cardiovascular collapse develops. Death can occur literally within an hour.

What to do if your dog is in shock?

If the described symptoms appear after bites or the administration of any drugs, urgent anti-shock measures are necessary. If the cause of shock is a bite or intramuscular or intravenous administration of medication, then it is necessary:

apply a venous tourniquet to the limb above the site of antigen entry,
inject this place with a 0.1% solution of adrenaline,
When an insect bites, the sting must be removed, ice or a cloth soaked in cold water should be applied to the area, and a 0.1% solution of adrenaline should be injected intramuscularly.

To prevent relapse, glucocorticoids (methylprednisolone, prednisolone, dexamethasone) are administered intravenously or intramuscularly. Thus, to save an animal in case of anaphylactic shock, the dog owner must urgently call veterinary help or try to take the animal to a veterinary clinic. After resuscitation, further treatment is prescribed only by a doctor.

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Introduction

Anaphylactic shock (French shoc - blow, shock, shock) is a general condition of the animal’s body caused by the introduction of a resolving dose of antigen and manifested by the development of a generalized immediate hypersensitivity reaction, resulting from the accelerated massive release of mediators from mast cells and basophils.

All organisms that have an immune system capable of storing in their memory the information of a single encounter with a foreign peptide agent are susceptible to the development of anaphylactic shock.

The term "anaphylaxis" (Greek: ana-reverse and phylaxis-protection) was coined by P. Portier and C. Richet in 1902 to refer to an unusual, sometimes fatal reaction in dogs to repeated administration of an extract from sea anemone tentacles. A similar anaphylactic reaction to repeated administration of horse serum in guinea pigs was described in 1905 by the Russian pathologist G.P. Sakharov. At first, anaphylaxis was considered an experimental phenomenon. Similar reactions were then discovered in humans. They began to be referred to as anaphylactic shock.

1. Reasonssoccurrence of anaphylactic shock

There are many causes of anaphylactic shock in animals. The most significant of them include the effects on the body of various medicines and poisons of animals and insects.

Any medications, regardless of route of administration (parenteral, inhalation, oral, cutaneous, rectal, etc.) can cause the development of anaphylactic shock. In the first place among the drugs that initiate anaphylaxis are antibiotics (penicillins, cephalosporins, tetracyclines, chloramphenicol, vancomycin, etc.). Next, in descending order of incidence of anaphylaxis, are nonsteroidal anti-inflammatory drugs (mainly pyrazolone derivatives), general anesthetics, radiocontrast agents, and muscle relaxants. The literature contains data on cases of the development of anaphylaxis with the administration of hormones (insulin, ACTH, progesterone, etc.), enzymes (streptokinase, penicillinase, chymotrypsin, trypsin, asparaginase), serums (anti-tetanus, etc.), vaccines (anti-tetanus, anti-rabies, etc. .), chemotherapeutic agents (vincristine, cyclosporine, methotrexate, etc.), local anesthetics, sodium thiosulfate.

Anaphylactic shock can develop as a result of animal bites from hymenoptera (bees, bumblebees, hornets, wasps), arthropods (spiders, tarantulas), and snakes. The reason for this is the presence in their venom of various enzymes (phospholipase A1, A2, hyaluronidase, acid phosphatase, etc.), as well as peptides (melittin, apamin, peptides that cause degranulation of mast cells) and biogenic amines (histamine, bradykinin, etc. ).

2. Degreesseverity of anaphylactic shock

Depending on the severity of clinical manifestations, there are three degrees of severity of anaphylactic shock:

· light,

medium-heavy

· heavy.

With mild anaphylactic shock, a short (within 5-10 minutes) prodromal period is often observed - a harbinger of anaphylactic shock: skin itching, skin rashes such as urticaria, erythema, and sometimes skin hyperemia. In this case, the skin of the face becomes pale, sometimes cyanotic. Sometimes bronchospasm occurs with difficulty exhaling and wheezing in the chest. Distant dry rales are often heard. Mail in all sick animals, even with mild anaphylactic shock, vomiting, sometimes loose stools, involuntary defecation and urination are observed due to anaphylactic contracture, smooth muscles of the intestine and bladder. As a rule, even with mild shock, patients lose consciousness. Blood pressure is sharply reduced, heart sounds are muffled, pulse is thready, tachycardia. Dry whistling rales are heard above the lungs.

In moderate cases of anaphylactic shock, certain symptoms occur - precursors: general weakness, anxiety, fear, vomiting, suffocation, urticaria, often - convulsions, and then loss of consciousness occurs. There is cold sticky sweat on the forehead. Pallor of the skin and cyanosis of the lips are noted. The pupils are dilated. Heart sounds are muffled, the pulse is threadlike, of irregular rhythm, with a tendency to tachycardia and, less often, to bradycardia, blood pressure is not determined. Involuntary urination and defecation, tonic and clonic convulsions, and in rare cases, uterine bleeding due to spasm of the uterine muscles are observed. Due to the activation of the fibrinolytic system of the blood and the release of heparin by mast cells of the lungs and liver, nasal and gastrointestinal bleeding may occur.

The severe course of anaphylactic shock is characterized by lightning-fast development of the clinical picture and, if the patient is not immediately provided with emergency assistance, sudden death may occur. There is a sharp pallor of the skin, cyanosis, dilated pupils, foam at the mouth, tonic and clonic convulsions, wheezing, audible at a distance, and prolonged exhalation. Heart sounds cannot be heard, blood pressure cannot be determined, and the pulse is almost not palpable. In severe cases of shock, sick animals usually die.

3. Mechanism of development of anaphylactic shock

However, regardless of the factors influencing the initiation of anaphylactic shock, the classical mechanism of its development appears to be a cascade of successive stages - immunological reactions > pathochemical reactions > pathophysiological changes.

The first stage in the development of anaphylactic shock is immunological reactions of the body. Initially, primary contact of the body with the antigen occurs, in other words, its sensitization. At the same time, the body begins to produce specific antibodies (IgE, less often IgG), which contain high-affinity receptors for the Fc fragment of antibodies and are fixed on mast cells and basophils. A state of immediate hypersensitivity develops after 7-14 days and persists for months and years. No more pathophysiological changes occur in the body.

Since anaphylaxis is immunologically specific, shock is caused only by the antigen to which sensitization has been established, even when received in negligible quantities.

Re-entry of the antigen (allowing the entry of the antigen) into the body leads to its binding to two antibody molecules, which entails the release of primary (histamine, chemoattractants, chymase, tryptase, heparin, etc.) and secondary (cysteine leukotrienes, prostaglandins, thromboxane , platelet activation factor, etc.) mediators from mast cells and basophils. The so-called “pathochemical” stage of anaphylactic shock occurs.

Pathophysiological stage anaphylactic shock is characterized by the effect of released mediators (histamine, serotonin) on vascular, muscle and secretory cells due to the presence of special receptors on their surface - G1 and G2. Attack by the above mediators of “shock organs”, which in mice and rats are the intestines and blood vessels; in rabbits - pulmonary arteries; in dogs - the intestines and hepatic veins, causes a decrease in vascular tone, a decrease in coronary blood flow and an increase in heart rate, a decrease in the contraction of smooth muscles of the bronchi, intestines, and uterus, an increase in vascular permeability, redistribution of blood and impaired coagulability.

The clinical picture of typical anaphylactic shock is very clear. It can be divided into three stages - the stage of harbingers, the stage of height and the stage of recovery from shock. In the case of a high degree of sensitization of the body during the fulminant development of anaphylactic shock, the precursor stage may be absent. It should be noted that the severity of anaphylactic shock will be determined by the characteristics of the first two stages - the precursor and peak stages.

The precursor stage changes stage of the height of the development of anaphylactic shock. During this period, patients experience loss of consciousness, a drop in blood pressure, tachycardia, cyanosis of the mucous membranes, shortness of breath, involuntary urination and defecation.

The completion of the development of anaphylactic shock is stage of an individual coming out of shock with compensation from the body over the next 3-4 weeks. However, during this period, patients may develop acute myocardial infarction, cerebrovascular accident, allergic myocarditis, glomerulonephritis, hepatitis, meningoencephalitis, arachnoiditis, polyneuritis, serum sickness, urticaria, Quincke's edema, hemolytic anemia and thrombocytopenia.

4. Variants of the course of anaphylactic shock

Depending on which vascular, muscle and secretory cells of which “shock organs” were more exposed to the released mediators, the symptoms of anaphylactic shock will depend. It is conventionally accepted to distinguish hemodynamic, asphyxial, abdominal and cerebral variants of the course of anaphylactic shock.

In the hemodynamic variant, hypotension, arrhythmias and other vegetative-vascular changes predominate.

In the asphyxial variant, the main development is shortness of breath, broncho- and laryngospasm.

In the abdominal variant, spasms of intestinal smooth muscles, epigastric pain, symptoms of peritoneal irritation, and involuntary defecation are noted.

In the cerebral variant, the dominant manifestation is psychomotor agitation, convulsions and meningeal symptoms.

Diagnosis of anaphylactic shock is not difficult and, as a rule, relies on the characteristic, pronounced clinical picture of the disease observed after an individual has been bitten by stinging hymenoptera insects, poisonous arthropods, animals, as well as during the administration of drugs.

5. Treatment

The principles of treatment of anaphylactic shock provide for the mandatory implementation of anti-shock measures, intensive care and therapy in the stage of recovery of the individual from shock.

The algorithm of treatment measures in case of emergency assistance is presented as follows.

In the event of a bite from poisonous animals, insects, or ingestion of allergenic medications for the individual, apply a venous tourniquet to the limb above the site of entry of the antigen. Inject this area with a 0.1% solution of adrenaline. If there is an insect sting in the soft tissues, remove the latter and put ice on the area.

Then inject a 0.1% solution of adrenaline intramuscularly. If necessary (at the discretion of the attending physician), repeat the injection of a 0.1% adrenaline solution after 5 minutes.

In order to prevent relapse of anaphylactic shock, administer glucocorticoids (prednisolone, methylprednisolone, dexamethasone) intravenously or intramuscularly. They can be administered again after 4-6 hours.

To reduce the negative consequences of anaphylactic shock, intravenous or intramuscular injection of antihistamines is recommended, the administration of which helps to level out skin manifestations of allergies.

In the asphyxial variant of anaphylactic shock, when bronchospasm and/or laryngospasm develops, in addition to the above medications, drugs that improve pulmonary ventilation are prescribed, for example, euphilin in combination with oxygen therapy. In more severe cases or if the therapy provided is ineffective, tracheostomy is resorted to.

Activities in the stage of an individual recovering from shock include continuing to provide assistance according to the algorithm described above, intensive therapy with rehydration of the body by administering saline, glucose solution, etc. intravenously quickly for 5 minutes, and then intravenously slowly.

6. Forecast

anaphylactic shock animal allergic

The prognosis for anaphylactic shock is cautious. This is explained by the fact that this pathology is caused by immunocompetent memory cells that live in the individual’s body for months and years. In this regard, in the absence of desensitization of the body, there is a constant probability of developing anaphylactic shock. This is confirmed by the results of L. Dowd and B. Zweiman, who indicated that in patients, symptoms of anaphylaxis can recur after 1-8 hours (biphasic anaphylaxis) or persist for 24-48 hours (protracted anaphylaxis) after the appearance of its first signs.

7. Prevention

In terms of preventing anaphylactic shock, there are three directions.

The first direction involves excluding the individual’s contact with the permitting agent.

The second direction is based on testing the tolerability of drugs in animals before providing medical care. For this purpose, 2-3 drops of the solution intended for use are applied to the animal in the sublingual space or it is injected intravenously in a volume of 0.1-0.2 ml, followed by observation for 30 and 2-3 minutes, respectively. The appearance of swelling of the mucous membrane, itching, urticaria, etc. indicates sensitization of the body and, as a consequence, the impossibility of using the test drug.

Conclusion

Anaphylactic shock is a type of immediate allergic reaction that occurs when an allergen is reintroduced into the body. Anaphylactic shock is characterized by rapidly developing predominantly general manifestations: a decrease in blood pressure (blood pressure), body temperature, blood clotting, central nervous system disorder, increased vascular permeability and spasm of smooth muscle organs. Most often, symptoms of anaphylactic shock occur 3-15 minutes after the body comes into contact with the drug. Sometimes the clinical picture of anaphylactic shock develops suddenly (“on the needle”) or several hours later (0.5-2 hours, and sometimes more) after contact with the allergen.

Almost all drugs can cause anaphylactic shock. Some of them, having a protein nature, are complete allergens, others, being simple chemical substances, are haptens. The latter, combining with proteins, polysaccharides, lipids and other macromolecules of the body, modify them, creating highly immunogenic complexes. The allergic properties of the drug are affected by various impurities, especially those of a protein nature.

List of used literature

1. ed. Zaiko N.N. “Pathological physiology” Higher school, 1985

2. Bezredka A. M., “Anaphylaxis”, M., 1928.

3. Lyutinsky. S.I. “Pathological physiology of farm animals.”, M., 2002

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First aid for anaphylactic shock

Treatment should be comprehensive and lightning fast. It is necessary to provide rest to the animal. Place your head on a pillow or towel cushion to ensure normal breathing.
Decide on the type of pathogenic agent - an insect bite, poisoning or another factor. This will make it easier to provide etiotropic and pathogenetic responses, otherwise it will only be possible to neutralize the symptoms.
First of all, we try to relieve the swelling:

cardiac medications - sulfocamphocaine, atropine, caffeine;
cold - apply to the throat;
prednisolone, suprastin, diphenhydramine.

specialists should carry out the following treatment measures:

adrenaline injections;
ensuring respiratory function - artificial ventilation, tracheotomy;
infusion therapy.

An anaphylactic reaction or anaphylactic shock is a hypersensitive reaction to a foreign substance, especially a protein.

What causes anaphylactic shock?

Before anaphylactic shock occurs, the animal must be under the influence of the allergen. A common example is a dog stung by a bee, who subsequently develops hypersensitivity to bee stings. After the first sting, there is usually a local reaction to the sting, also called a humoral reaction. This reaction causes the immune system to produce immunoglobulin E, which binds to mast cells. Massive cells are responsible for the redness and swelling (hives) you see at the site of the bite. The patient is also said to be sensitive to bee toxins. After the dog's second sting, sensitive mast cells recognize the foreign protein (bee toxins) and initiate a process called degranulation. In mild cases of anaphylactic shock, there is a local reaction, such as severe swelling at the site of the bite. In severe cases, large numbers of mast cells are released throughout the body, leading to systemic anaphylactic shock. As a rule, local anaphylaxis reactions are observed; severe anaphylactic shock is extremely rare.

Theoretically, any foreign substance can lead to an anaphylactic reaction. The most common are food proteins, insect bites, medications, vaccines, polluted environments and various chemicals.

It is important to note that this is not a normal reaction of the body. The immune system overreacts to a foreign substance or protein, resulting in a reaction. In most cases, anaphylaxis is believed to be hereditary.

What are the clinical symptoms of anaphylactic shock?

Clinical symptoms depend on the route of exposure (oral, skin, injection, etc.), the amount of antigen, and the level of immunoglobulin in the animal.

The most common symptoms of anaphylactic shock are itching, red swelling, blistering of the skin, blisters, swelling of the face or muzzle, excessive salivation, vomiting and diarrhea. In a severe anaphylactic reaction, the dog will have trouble breathing and its tongue and gums will turn blue.

How to diagnose anaphylaxis?

Anaphylactic shock is diagnosed by identifying recent exposure to an allergen and by characteristic clinical symptoms. Intradermal testing and immunoglobulin blood tests are also performed to identify specific allergens.

How is anaphylactic shock treated?

An anaphylactic reaction requires emergency medical attention and treatment. The first step is to remove the foreign substance, if possible. Next, to stabilize the animal, minimize the likelihood of severe anaphylaxis and control the airway and blood pressure. Drugs such as adrenaline, corticosteroids, atropine or aminophylline are often used. In mild cases, antihistamines and possibly corticosteroids may be sufficient, followed by monitoring the dog for 24 or 48 hours.

What are the forecasts?

The initial forecast is always reserved. There is no way to know whether the reaction will be localized or progress to severe.

An anaphylactic reaction worsens with each subsequent exposure to an allergen, so the main goal should be to prevent repeated exposure.

Anaphylaxis(anaphylaxia from the Greek ana - reverse action + phylaxis - protection, self-defense) - a state of increased sensitivity of the body to the repeated introduction of a foreign protein (antigen).

Anaphylactic shock(French shoc - blow, push, shock) - the general state of the animal’s body, caused by the introduction of a resolving dose of antigen and manifested by the development of a generalized immediate hypersensitivity reaction, resulting from the accelerated massive release of mediators from mast cells and basophils. All organisms that have an immune system capable of storing in their memory the information of a single encounter with a foreign peptide agent are susceptible to the development of anaphylactic shock.

Reasons

There are many reasons that provoke anaphylactic shock in animals. The most significant of them include the effects on the body of various medicines and poisons of animals and insects.

Any medications, regardless of route of administration (parenteral, inhalation, oral, cutaneous, rectal, etc.) can cause the development of anaphylactic shock. In first place among the drugs that initiate anaphylaxis are antibiotics (penicillins, cephalosporins, tetracyclines, chloramphenicol, vancomycin, etc.). Next, in descending order of incidence of anaphylaxis, are nonsteroidal anti-inflammatory drugs (mainly pyrazolone derivatives), general anesthetics, radiocontrast agents, and muscle relaxants. The literature contains data on cases of the development of anaphylaxis with the administration of hormones (insulin, ACTH, progesterone and others), enzymes (streptokinase, penicillinase, chymotrypsin, trypsin, asparaginase), serums (for example, anti-tetanus), vaccines (anti-tetanus, anti-rabies, etc.) , chemotherapeutic agents (vincristine, cyclosporine, methotrexate, etc.), local anesthetics, sodium thiosulfate.

Anaphylactic shock in dogs and cats can develop as a result of animal bites from hymenoptera (bees, bumblebees, hornets, wasps), arthropods (spiders, tarantulas), and snakes. The reason for this is the presence in their venom of various enzymes (phospholipase A1, A2, hyaluronidase, acid phosphatase, etc.), as well as peptides (melittin, apamin, peptides that cause degranulation of mast cells) and biogenic amines (histamine, bradykinin, etc. ).

Development mechanism

However, regardless of the factors that influence the occurrence of anaphylactic shock, the classical mechanism of its development appears to be a cascade of successive stages:

immunological reactions → pathochemical reactions → pathophysiological changes

The first stage in the development of anaphylactic shock is the body's immunological reactions. Initially, primary contact of the body with the antigen occurs, in other words, its sensitization. At the same time, the body begins to produce specific antibodies (IgE, less often IgG), which contain high-affinity receptors for the Fc fragment of antibodies and are fixed on mast cells and basophils. A state of immediate hypersensitivity develops after 7-14 days and persists for many months, or even several years. No more pathophysiological changes occur in the body. Since anaphylaxis is immunologically specific, shock is caused only by the antigen to which sensitization has been established, even when received in negligible quantities.

Re-entry of the antigen (allowing the entry of the antigen) into the body leads to its binding to two antibody molecules, which entails the release of primary (histamine, chemoattractants, chymase, tryptase, heparin, etc.) and secondary (cysteine leukotrienes, prostaglandins, thromboxane, factor activation of platelets, etc.) mediators from mast cells and basophils. The so-called “pathochemical” stage of anaphylactic shock occurs.

The pathophysiological stage of anaphylactic shock is characterized by the effect of released mediators (histamine, serotonin) on vascular, muscle and secretory cells due to the presence of special receptors on their surface - G1 and G2. Attack by the above mediators of “shock organs”, which in mice and rats are the intestines and blood vessels; in rabbits - pulmonary arteries; in dogs - the intestines and hepatic veins, causes a decrease in vascular tone, a decrease in coronary blood flow and an increase in heart rate, a decrease in the contraction of smooth muscles of the bronchi, intestines, and uterus, an increase in vascular permeability, blood redistribution and impaired coagulation.

Clinical picture

The clinical picture of typical anaphylactic shock in cats and dogs is very clear. It can be divided into three stages - the stage of harbingers, the stage of height and the stage of recovery from shock. In the case of a high degree of sensitization of the body during the fulminant development of anaphylactic shock, the precursor stage may be absent. It should be noted that the severity of anaphylactic shock will be determined by the characteristics of the first two stages - the precursor and peak stages.

The development of the precursor stage occurs within 3-30 minutes after parenteral entry into the body of the resolving antigen or within 2 hours after its oral penetration or its release from deposited injectable preparations. At the same time, individuals involved in the development of anaphylactic shock experience internal discomfort, anxiety, chills, weakness, blurred vision, weakened tactile sensitivity of the skin of the face and limbs, pain in the lower back and abdomen. Often there is the appearance of skin itching, difficulty breathing, urticaria and the development of Quincke's edema. The stage of precursors is replaced by the stage of the height of the development of anaphylactic shock. During this period, patients experience loss of consciousness, a drop in blood pressure, tachycardia, cyanosis of the mucous membranes, shortness of breath, involuntary urination and defecation.

The completion of the development of anaphylactic shock is the stage of the individual emerging from shock with compensation of the body over the next 3-4 weeks. However, during this period, patients may develop acute myocardial infarction, cerebrovascular accident, allergic myocarditis, glomerulonephritis, hepatitis, meningoencephalitis, arachnoiditis, polyneuritis, serum sickness, urticaria, Quincke's edema, hemolytic anemia and thrombocytopenia.

With hemodynamic variant hypotension, arrhythmias and other vegetative-vascular changes predominate.

With asphyxial variant the main one is the development of shortness of breath, broncho- and laryngospasm.

In the abdominal version spasms of intestinal smooth muscles, epigastric pain, symptoms of peritoneal irritation, and involuntary defecation are noted.

With cerebral variant the dominant manifestation is psychomotor agitation, convulsions and meningeal symptoms.

Diagnostics

Treatment

The principles of treatment of anaphylactic shock provide for the mandatory implementation of anti-shock measures, intensive care and therapy in the stage of recovery of the individual from shock.

The algorithm of treatment measures within the framework of emergency care is presented as follows. In the event of a bite from poisonous animals, insects, or ingestion of allergenic medications for an individual, a venous tourniquet must be applied to the limb above the site of entry of the antigen and the area injected with a 0.1% solution of adrenaline. If there is an insect sting in the soft tissues, remove the latter and put ice on this place, and then inject a 0.1% solution of adrenaline intramuscularly. If necessary (at the discretion of the attending physician), repeat the injection of a 0.1% adrenaline solution after 5 minutes. In order to prevent relapse of anaphylactic shock, administer glucocorticoids (prednisolone, methylprednisolone, dexamethasone) intravenously or intramuscularly. They can be administered again after 4-6 hours.

Activities in the stage of recovery of an individual from shock include continuing assistance according to the algorithm described above, intensive therapy with rehydration of the body by administering saline, glucose solution, etc. intravenously quickly over 5 minutes, and then intravenously slowly using a drip.

Forecast

The prognosis for anaphylactic shock is cautious. This is explained by the fact that this pathology is caused by immunocompetent memory cells that live in the individual’s body for months and years. In this regard, in the absence of desensitization of the body, there is a constant probability of developing anaphylactic shock. This is confirmed by the results of L. Dowd and B. Zweiman, who indicated that in patients, symptoms of anaphylaxis can recur after 1–8 hours (biphasic anaphylaxis) or persist for 24–48 hours (protracted anaphylaxis) after the appearance of its first signs.

Prevention

In terms of preventing anaphylactic shock, there are three directions. The first direction involves excluding the individual’s contact with the permitting agent. The second direction is based on testing the tolerability of drugs in animals before providing medical care. For this purpose, 2-3 drops of the solution intended for use are applied to the animal in the sublingual space or it is injected intravenously in a volume of 0.1-0.2 ml, followed by observation for 30 and 2-3 minutes, respectively. The appearance of swelling of the mucous membrane, itching, urticaria, etc. indicates sensitization of the body and, as a consequence, the impossibility of using the test drug.

Veterinary center "DobroVet"