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Anaphylactic shock in dogs treatment. Anaphylaxis

The pathological reaction of the body to the ingress of a foreign substance of a protein nature manifests itself in the form of anaphylactic shock. In recent years, due to widespread use feed additives, protein substitutes, flavorings, new medications, dogs often exhibit hypersensitivity in the form of anaphylactic shock. The serious condition of the body requires immediate qualified assistance. Delay can cost your pet's life.

The reasons for the body’s increased reaction to a particular substance are both external and internal factors.

External factors

Veterinary specialists distinguish following reasons, leading to sensitization of the body:

Insect bites (bees, wasps, hornets, poisonous spiders and other arthropods). The most dangerous thing for a dog is anaphylactic shock caused by the bite of a poisonous snake, such as a viper.

Medications. In very rare cases, a pathological reaction of the body manifests itself when antibacterial, hormonal drugs, muscle relaxants, enzyme preparations. Among antibiotics, penicillin and tetracycline agents can cause anaphylactic shock.

Often an individual is found severe allergies for the administration of cephalosporins, chloramphenicol. There is a risk of developing a pathological reaction when using a radiopaque contrast agent for diagnostic purposes. Opiates and anesthetics can lead to a state of shock when putting a pet into a narcotic sleep.

Biological drugs. In treatment and prevention infectious diseases In veterinary medicine, ready-made immunoglobulins or vaccines are used. The main components of these products are protein substances, which the dog’s body often perceives aggressively.
Shock due to transfusion of incompatible blood group. Collapse occurs due to the development of hemolytic processes when the blood used does not match the antigenic composition of the affected animal.
Shock may be caused by trauma. Fractures of the limbs, spine, internal bleeding, ruptures of organs during car collisions, intestinal volvulus and other emergencies are accompanied by a severe reaction of the body.

Spinal after surgery

A special type of collapse in animals is spinal shock. Pathology occurs due to complete transverse damage (transection) spinal cord and is accompanied by a sharp drop in excitability below the damaged area. The disease can be caused by a fracture of the spine or be a consequence of surgery.

The animal experiences loss of function of organs located below the injury spinal column(violation of the act of defecation and urination, paresis and paralysis of the limbs, etc.). For example, an injury to the cervical vertebrae is accompanied by paralysis of all limbs, pathology of breathing and heartbeat. If nerve conduction is disrupted in the lumbosacral region, the prognosis is more favorable.

Spinal shock is a peculiar reaction of the body to overstimulation nerve cells. Arose as a result pathological condition functional disorders partially or completely reversible. Veterinary practice shows that the average duration of spinal collapse in four-legged pets is 7 - 10 days.

First symptoms

Clinical manifestations of anaphylactic shock are varied. Veterinary specialists distinguish the following variants of manifestation of sensitization of the body:

Asphyxial. As a rule, the pathology begins with the development of redness, rash, and skin itching. The reaction to a foreign substance quickly develops from local to general. The animal has swelling of the mucous membrane of the nose, mouth, and larynx. These phenomena make breathing difficult. The dog's barking becomes hoarse. Spasm respiratory tract leads to blue discoloration of the mucous membranes.

Hemodynamic shock. Collapse is caused by a violation blood pressure(hypotension). Indicators blood pressure can fall to critical levels, causing cardiac arrest, heart attack or stroke. Against the background of impaired blood supply during anaphylactic shock, pulmonary edema develops, which has dangerous consequences for the animal.
Cerebral. The symptomatic complex includes deep lesions of the central nervous system. A sick animal experiences fear, hides in a corner, whines, and reacts inadequately to external stimuli. Often the dog may act aimlessly circular movements, stand with your head against the wall. With the cerebral variant, manifestations of sensitization are observed, often ending in the death of the pet.
Thromboembolic The nature of the symptoms of anaphylactic shock is life-threatening for the dog. The animal instantly develops cyanosis associated with blockage of the lumen of large arteries by a thrombus. There is shortness of breath, suffocation and rapid death.
Abdominal option the owner often mistakes the course of collapse for symptoms of acute enteritis. The dog has severe vomiting and pain in the abdominal area. The animal whines in pain. Visible mucous membranes quickly turn pale.

Veterinary specialists distinguish between the early and deep phases of anaphylactic shock. During the early phase of collapse, the dog exhibits the following signs:

tachycardia, rapid and confused breathing;
anemia of the mucous membranes;
change in the pet’s behavior: the dog is worried, whines, shows fear of familiar objects and people;
depression, apathy, lethargy;
increased salivation;
aimless movements, sometimes the animal moves in an imaginary circle;
body temperature is within the physiological norm.

With deep collapse, a dog may experience the following symptoms:

lack of reaction of the body to external stimuli (sound, light), empty, meaningless look;
rare and shallow breathing, bradycardia, arrhythmia;
Body temperature can drop to 36 C.

With the development of anaphylactic shock due to the ingestion of a foreign protein (pollen, antibiotic, vaccine, etc.) into the body, itching, skin rashes, and urticaria are most often observed. In the absence of help, sensitization quickly leads to generalization of the pathological process.

As a result of the development of traumatic shock, the owner more often encounters such phenomena as lethargy, apathy, hypothermia, and disorders of the central nervous system.

About Quincke's edema in dogs, watch this video:

Help an animal

Detection of clinical signs of the development of anaphylactic or traumatic collapse is a reason for urgent contact with a veterinary specialist. While traveling to a specialized facility or while waiting for a doctor to be called to your home, the owner can take the following steps:

free the oral cavity from mucus, vomit, foamy secretions;
if bitten by a poisonous insect or snake, apply a tourniquet (belt, leash, belt) above the area of injury;
remove the sting (for a bee or hornet sting);
apply cold to the bite site;
wrap your pet in a warm blanket or blanket.

Further actions to save the life of your four-legged friend should be carried out by a veterinary specialist. It is important to take a sick pet to a specialized facility within an hour after symptoms develop. In the clinic, a dog undergoing anaphylactic shock undergoes the following procedures:

Intravenous injections of Adrenaline or Epinephrine. In some cases, these drugs are used to inject the site of a poisonous insect or snake bite.

In case of difficulty breathing due to swelling of the larynx, the dog undergoes tracheal intubation.
Diphenhydramine, Dexamethasone, Suprastin, Tavegil are used to relieve tissue edema.
In order to normalize blood pressure, the pet is given intravenous infusions isotonic solutions, injections of vasoconstrictor drugs are used.
An oxygen cushion is an integral part of complex therapy for anaphylactic shock.

As a rule, the animal is left in veterinary clinic before full recovery, since a recurrence of sensitization of the body is possible.

A state of collapse in a dog can occur as a result of a wide variety of reasons (administration of medications, poisonous insect bites, spinal injuries). The symptoms of the pathological reaction are quite varied and usually develop at lightning speed. To save lives four-legged friend the owner must deliver it to a specialized facility within an hour.

Anaphylaxis - immediate (first) type hypersensitivity, one of the types allergic reaction. This reaction is a pathological variant of the immune response to a foreign agent (allergen). The consequence of this reaction is tissue damage in the body.

IN normal conditions When an antigen first enters the body, it provokes a reaction from the immune system. She recognizes it, analyzes its structure, which is then memorized by memory cells. In response to the antigen, antibodies are produced, which remain in the blood plasma in the future. So, the next time an antigen enters the body, antibodies immediately attack and neutralize it, preventing the disease from developing.

An allergy is the same response of the immune system to an antigen, with the only difference that in a pathological reaction there is a disproportionate ratio of the strength of the reaction to the cause that provoked it.

There are 5 types of allergic reactions:

I type – anaphylactic or immediate allergic reactions. They arise due to the interaction of antibodies of group E (IgE) and G (IgG) with the antigen and the sedimentation of the resulting complexes on membranes mast cells. As a result of this interaction, a large amount of histamine is released, which has a pronounced physiological effect. The time for the reaction to occur ranges from a couple of minutes to several hours after the antigen enters the animal’s body. These include anaphylactic shock, urticaria, allergic rhinitis, atopic bronchial asthma, Quincke's edema.

Type II – cytotoxic(or cytolytic) reactions.

III type – immune complex reactions(Arthus phenomenon).

IV type – late hypersensitization, or delayed-type allergic reactions that develop 24 hours or more after the antigen enters the body.

V type – stimulating reactions hypersensitivity.

Among the reliably confirmed causes of anaphylaxis in dogs are:

Insect bites of the family Hymenoptera - four-winged (bees, wasps, hornets, fire ants)
Some chemotherapy agents, contrast agents, and antibiotics
Blood transfusion

Symptoms

In anaphylaxis, the skin, respiratory, cardiovascular and gastrointestinal systems are most often involved. The skin and mucous membranes are involved in 80-90% of cases. Most adult patients have some combination of urticaria, erythema, itching, and edema—increased porosity of the vessel wall. However, for reasons that are still poorly understood, some dogs are more likely to exhibit respiratory symptoms of anaphylactic shock accompanied by skin symptoms. It is also important to note that some of the most severe cases of anaphylaxis occur in the absence of skin manifestations. Initially, as a rule, itching and redness occur. Then, over a short period of time, other symptoms develop:

Dermatological/ocular: lacrimation, urticaria, increased vascular reaction (vessels are sharply injected), itching, hyperthermia and edema.
Respiratory: Nasal congestion, runny nose, rhinorrhea (nasal discharge), sneezing, shortness of breath, cough, hoarseness.
Cardiovascular reactions: dizziness, weakness, fainting, chest pain, convulsions, tachycardia.
Gastrointestinal tract: dysphagia, nausea, vomiting, diarrhea, bloating,
Neurological: headache, dizziness, blurred vision, (very rare and often associated with hypotension)

Manifestation of anaphylactic reactions

In dogs, histamine is primarily released from the gastrointestinal tract into portal vein, which leads to hepatic arterial vasodilation and increased hepatic arterial blood flow. In addition, the release of histamine into the portal system creates significant venous outflow obstruction, which leads to increased resistance vascular wall up to 220% of normal within a few seconds. As a result, venous blood flow to the heart is reduced. Decreased venous return of blood from the liver to the heart reduces cardiac output and therefore contributes to hypovolemia and decreased oxygen delivery to tissues. Due to decreased oxygen delivery and hypovolemic shock, common clinical signs include collapse and acute occurrence gastroenteritis (sometimes hemorrhagic in nature).

General principles of anaphylaxis treatment

Anaphylactic shock in dogs is emergency, requiring immediate recognition and intervention. Patient management and prognosis depend on the severity of the initial reaction and response to treatment. Patients with refractory or very severe anaphylaxis (with cardiovascular and/or severe respiratory symptoms) should be observed for more than long period time in the intensive care unit.

Supportive care for patients with suspected anaphylaxis includes the following:

Airway management (eg, bag or mask ventilation support, endotracheal intubation, tracheostomy if necessary)
Oxygen therapy with high-flow concentrated oxygen
Cardiac monitoring and/or pulse oximetry
Providing intravenous access (large channel)
Intravenous stress bolus fluid administration

Drug therapy: primarily, within emergency assistance for the treatment of acute anaphylactic reactions, adrenaline 0.2-0.5 ml intramuscularly and antihistamines, for example, diphenhydramine 1-4 mg/kg intramuscularly, are administered.

intensive care veterinarian at MEDVET
© 2018 SEC "MEDVET"

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.

The most typical is the generalized form of drug-induced anaphylactic shock.

This form is characterized by the sudden appearance feelings of anxiety, fear, severe general weakness, widespread skin itching, skin hyperemia. Possible appearance of urticaria, angioedema various localizations, including in the larynx area, which is manifested by hoarseness of voice, up to aphonia, difficulty swallowing, and the appearance of stridor breathing. Animals are disturbed by a pronounced feeling of lack of air, breathing becomes hoarse, wheezing can be heard at a distance.

Many animals experience nausea vomit, abdominal pain, cramps, involuntary act of urination and defecation. The pulse in the peripheral arteries is frequent, thread-like (or not detectable), the blood pressure level is reduced (or not detected), and objective signs of shortness of breath are detected. Sometimes, due to pronounced edema of the tracheobronchial tree and total bronchospasm, there may be a picture of a “silent lung” on auscultation.

In animals suffering from pathology of cardio-vascular system , the course of drug-induced anaphylactic shock is quite often complicated by cardiogenic pulmonary edema.

Despite the generalization clinical manifestations drug anaphylactic shock, depending on the leading syndrome, there are five variants: hemodynamic (collaptoid), asphyxial, cerebral, abdominal, thromboembolic.

In different animal species, the development of anaphylactic shock is accompanied by various disorders blood circulation and respiration. Based on the nature of the disorders of these functions, some researchers (N. N. Sirotinin, 1934; Doerr, 1922) identify several types of anaphylactic shock in animals. Tract of anaphylactic shock in guinea pigs can be called asphyxial, since the earliest and leading symptom of anaphylactic shock in these animals is bronchospasm, causing asphyxia; Against the background of the latter, circulatory disorders of the asphyxial type develop secondarily. Blood pressure first rises sharply due to excitation of the bulbar, vasomotor center during hypercapnia. Subsequently, paralysis of this center develops, blood pressure drops catastrophically and death occurs. In guinea pigs and rabbits, during anaphylactic shock, excitation of the respiratory center is observed, the motor center radiating to the vessel; subsequently, inhibition of these centers occurs, which is expressed in respiratory depression and a drop in blood pressure.

In dogs, anaphylactic shock develops according to a different type; it can be characterized as anaphylactic shock of the collapse type. This is where the name anaphylactic collapse, used by some authors, came from. The leading manifestation of anaphylactic shock in dogs is circulatory disorders in organs abdominal cavity. arise congestion in the liver, spleen, kidneys and intestinal vessels.

Circulatory disorders in the abdominal organs are a consequence of the effect of antigen on nervous mechanisms regulation of vascular tone in the abdominal organs. The antigen also has a direct effect on the smooth muscle of the wall of the hepatic veins and some other blood vessels abdominal cavity. In many wild animals - bears, wolves, foxes - anaphylactic shock, like in dogs, occurs through the mud of collapse. In rabbits with anaphylactic shock, the leading symptoms are circulatory disorders in the pulmonary circulation. There is an increase in blood pressure in the pulmonary artery, caused by spasm of the pulmonary arteries.

In rats and mice, anaphylactic shock is characterized by circulatory disorders in the systemic and pulmonary circulation. Anaphylaxis in these animal species is discussed in a special section.

In cats and wild animals of the feline order (lions, tigers, leopards, panthers, etc.), anaphylactic shock approaches the type of shock in dogs. However, due to the high excitability of the autonomic nervous system and its parasympathetic department, one of the primary signs of anaphylactic shock in these animals is a sharp slowdown in heart contractions up to short-term cardiac arrest.

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Introduction

Anaphylactic shock (French shoc - blow, push, shock) - general state organism of an animal, 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. Similar anaphylactic reaction the repeated administration of horse serum to 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 a mild course of 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, intestinal smooth muscles 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 over the lungs.

With moderate anaphylactic shock, certain symptoms occur - precursors: general weakness, anxiety, fear, vomiting, suffocation, urticaria, often - convulsions, and then loss of consciousness occurs. On the forehead - cold sticky sweat. There is pallor of the skin and cyanosis of the lips. 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 provided immediate emergency assistance, sudden death. There is a sharp pallor of the skin, cyanosis, dilated pupils, foam at the mouth, tonic and clonic convulsions, wheezing, audible at a distance, the exhalation is lengthened. Heart sounds are not heard, blood pressure is not 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 coagulation.

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 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 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 recovery of an individual from shock with compensation from the body over the next 3-4 weeks. However, during this period patients may develop acute heart attack myocardium, disorder cerebral circulation, 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, cramps 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.

Algorithm therapeutic measures when emergency assistance help 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 soft tissues remove the latter and put ice on this place.

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 negative consequences for anaphylactic shock, intravenous or intramuscular injection is recommended antihistamines, the purpose 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 at the stage of an individual’s recovery from shock include continued assistance according to the algorithm described above, intensive care with rehydration of the body by administering saline, glucose solution, etc. intravenously quickly for 5 minutes, and then slowly intravenously.

6. Forecast

anaphylactic shock animal allergic

The prognosis for anaphylactic shock is cautious. This is explained by 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 chemicals, - 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.

Bibliography

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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Definition 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.

Etiology and pathogenesis

The pathogenesis of anaphylactic shock is based on the reagin mechanism. As a result of the release of mediators, the vascular tone and collapse develops. The permeability of microcirculatory vessels increases, which contributes to the release of the liquid part of the blood into the tissues and thickening of the blood. The volume of circulating blood decreases. The heart is involved in the process a second time. The result of these disorders is a decrease in venous return, a drop in stroke volume and the development of profound hypotension. The second leading mechanism in the pathogenesis of anaphylactic shock is a violation of gas exchange against the background of the development of bronchospasm or obstruction of the upper respiratory tract (larynx stenosis). Usually the animal recovers from shock on its own or with medical help. If homeostatic mechanisms are insufficient, the process progresses, metabolic disorders in tissues associated with hypoxia occur, and a phase of irreversible changes in shock develops

Clinical picture of anaphylactic shock

The most typical is the generalized form of drug-induced anaphylactic shock.

This form is characterized by the sudden onset of feelings of anxiety, fear, severe general weakness, widespread skin itching, and skin hyperemia. Urticaria, angioedema of various localizations, including in the larynx, may appear, which is manifested by hoarseness, even aphonia, difficulty swallowing, and the appearance of wheezing. Animals are disturbed by a pronounced feeling of lack of air, breathing becomes hoarse, wheezing can be heard at a distance.

Many animals experience nausea, vomiting, abdominal pain, convulsions, and involuntary urination and defecation. The pulse in the peripheral arteries is frequent, thread-like (or not detectable), the blood pressure level is reduced (or not detected), and objective signs of shortness of breath are detected. Sometimes, due to pronounced edema of the tracheobronchial tree and total bronchospasm, there may be a picture of a “silent lung” on auscultation.

In animals suffering from pathology of the cardiovascular system, the course of drug-induced anaphylactic shock is quite often complicated by cardiogenic pulmonary edema.

Despite the generalized clinical manifestations of drug-induced anaphylactic shock, depending on the leading syndrome, five variants are distinguished: hemodynamic (collaptoid), asphyxial, cerebral, abdominal, thromboembolic.

The hemodynamic variant is characterized by the prevalence in the clinical picture of hemodynamic disorders with the development of severe hypotension, vegetative-vascular changes and functional (relative) hypovolemia.

In the asphyxial variant, the dominant development is broncho- and laryngospasm, laryngeal edema with the appearance of signs of severe acute respiratory failure. The development of respiratory distress syndrome with severe hypoxia is possible.

Cerebral option. Distinctive feature This clinical variant is the development of convulsive syndrome against the background of psychomotor agitation, fear, and impaired consciousness. Quite often this form is accompanied by respiratory arrhythmia, vegetative-vascular disorders, meningeal and mesencephalic syndromes.

The abdominal variant is characterized by the appearance of symptoms of the so-called “false acute abdomen” ( sharp pains in the epigastric region and signs of peritoneal irritation), which often leads to diagnostic errors.

The thromboembolic variant resembles the picture of pulmonary embolism.

The severity of the clinical picture of drug-induced anaphylactic shock is determined by the degree and rate of development of hemodynamic disorders, as well as the duration of these disorders.

Drug-induced anaphylactic shock has three degrees of severity.

Mild degree - the clinical picture is not sharply characterized severe symptoms shock: pale skin, dizziness, itching, urticaria, hoarseness appear. Signs of bronchospasm and cramping abdominal pain are often observed. Consciousness is preserved, but the animal may be inhibited (nubilation). There is a moderate decrease in blood pressure, the pulse is frequent and threadlike. The duration of mild drug-induced anaphylactic shock ranges from several minutes to several hours.

Moderate severity is characterized by a detailed clinical picture: the animal develops general weakness, anxiety, fear, visual and hearing impairment, and skin itching.

There may be nausea, vomiting, coughing and choking (often wheezing). The animal's consciousness is depressed. When examining the skin, urticaria is detected, angioedema Quincke.

Characterized by a sharp change from hyperemia of the mucous membranes to pallor. The skin is cold, the lips are cyanotic, the pupils are dilated. The appearance of seizures is often noted. From the cardiovascular system, tachycardia is detected, the pulse is threadlike (or not detected), blood pressure is not determined. There may be involuntary urination and defecation, foam in the corner of the mouth.

Severe severity accounts for 10-15% of all cases of anaphylactic shock. The process develops at lightning speed and is characterized by the absence of prodromal phenomena, sudden loss consciousness, convulsions and rapid onset of death.

Clonic and tonic convulsions, cyanosis, involuntary urination and defecation appear, foam in the corner of the mouth, blood pressure and pulse are not determined, the pupils are dilated. Death occurs within 5-40 minutes.

After leaving state of shock in animals, dysfunctions persist for some time various organs and systems for 3-4 weeks (most often renal and liver failure). Due to the possibility of developing post-shock complications, such animals require medical supervision.

With age, anaphylactic shock becomes more severe because compensatory possibilities organism decrease, and usually the organism acquires chronic diseases. Severe anaphylactic shock in combination with cardiovascular disease- a potentially lethal combination. In cats, anaphylactic shock occurs faster and more intensely, due to increased metabolism.

Risk factors for drug-induced anaphylactic shock

History of drug allergies.

Long-term use of medications, especially repeated courses.

Use of depot drugs.

Polypharmacy (use of a large number of drugs).

High sensitizing activity of the drug.

History of allergic diseases.

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.

Most often, drug-induced anaphylactic shock occurs with the administration of antibiotics, especially penicillin. Drug anaphylaxis often develops with the use of pyrazolone analgesics, local anesthetics, vitamins, mainly group B, and radiocontrast agents. In highly sensitized animals, neither the dose nor the route of administration of the drug plays a decisive role in the occurrence of shock. However, the most rapid (lightning-fast) development of LAS occurs with parenteral administration of drugs.

Some drugs can promote the release of histamine and other biologically active substances from cells not through the immune system, but directly pharmacological action on them. These drugs are called histamine liberators. These include radiocontrast agents, some plasma-substituting solutions, polymyxin antibiotics, proteolytic enzymes, antienzyme drugs (contrical), general anesthetics, morphine, codeine, promedol, atropine, phenobarbital, thiamine, D-tubocurarine, etc. In the event of an immediate reaction due to liberation histamine or activation of the complement system under the influence medicinal substance the condition is regarded as anaphylactoid shock. In this case, there is no immunological stage, and a reaction can develop after the first administration of the drug.

Thus, drug-induced anaphylactic shock, regardless of pathogenesis, has the same clinical symptoms and treatment tactics. Currently, clinicians do not yet have effective and simple express methods for diagnosing pathology that characterizes the mechanisms of drug shock. In this regard, in clinical practice one can only assume the likelihood of their development by analyzing anamnestic information and the allergen drug.

Treatment of anaphylactic shock

Therapy for anaphylactic shock includes a set of emergency measures aimed at eliminating the main disorders caused by an allergic reaction:

Elimination of acute disturbances of vascular tone;

Blocking the release, neutralization and inhibition of allergic reaction mediators;

Compensation for the resulting adrenocortical insufficiency;

Maintaining the functions of various vital organs and systems

When treating anaphylactic shock, doctors advise using the following groups of drugs:

Catecholamines (Adrenaline)

Glucocorticoids (Prednisolone, Dexamethasone, Methylprednisolone)

Bronchodilators (Eufillin)

Antihistamines (Diphenhydramine, Tavegil, Suprastin)

Adequate fluid therapy

What to do if your animal shows signs of anaphylactic shock:

1. CONSULT A DOCTOR IMMEDIATELY

2. Place cold on the site of the bite or injection of the drug and pull it higher with a tourniquet (if there was an insect bite or injection of the drug)

3. Inject intramuscularly Prednisolone - 0.3 - 0.6 mlkg

4. Inject intramuscularly Diphenhydramine 0.1 - 0.3 mlkg

Unfortunately, you can’t do anything else (if you don’t have special knowledge and skills); all other therapy and observation should be carried out by a doctor.