Anaphylaxis and anaphylactic shock

Questions about anaphylaxis are answered by Michaet S. Lagutchik, D.V.M.

1. What is systemic anaphylaxis?

Systemic anaphylaxis is an acute, life-threatening reaction resulting from the formation and release of endogenous chemical mediators and the action of these mediators on various systems organs (mainly the cardiovascular and pulmonary systems).

2. Name the forms of anaphylaxis. Which of them causes the most severe emergency condition?

Anaphylaxis can be systemic or local. The term anaphylaxis is usually used to describe three separate clinical conditions: systemic anaphylaxis, urticaria and angioedema. Systemic anaphylaxis resulting from generalized massive release of neurotransmitters mast cells, represents the most severe form. Urticaria and angioedema - local manifestations immediate hypersensitivity reactions. Urticaria is characterized by the formation of blisters or rashes, involvement of superficial dermal vessels and varying degrees itching. With angioedema, the deep vessels of the skin are involved in the process with the formation of edema in the deeper layers of the skin and subcutaneous tissues. Although uncommon, urticaria and angioedema may progress to systemic anaphylaxis.

3. What are the main mechanisms of development of anaphylaxis?

Two main mechanisms cause mast cell and basophil activation and hence anaphylaxis. Anaphylaxis is most often caused by immune processes. Not immune mechanisms lead to anaphylaxis much less frequently, and this syndrome is called anaphylactoid reaction. There is essentially no difference in treatment, but recognition of the mechanism allows for a better understanding of potential causes and leads to faster diagnosis.

4. What is pathophysiological mechanism immune (classical) anaphylaxis?

At the first contact of sensitive individuals with an antigen, immunoglobulin E (IgE) is produced, which binds to the surface receptors of effector cells (mast cells, basophils). Upon repeated exposure to an antigen, the antigen-antibody complex causes a calcium current into the effector cell and an intracellular cascade of reactions, leading to degranulation of previously synthesized mediators and the formation of new mediators. These mediators are responsible for the pathophysiological reactions in anaphylaxis.

5. What is the pathophysiological mechanism of non-immune anaphylaxis?

The development of anaphylactoid reactions occurs by two mechanisms. In most cases, there is direct activation of mast cells and basophils by drugs and other chemicals(i.e. idiosyncratic pharmacological or drug reactions). Subsequent effects are similar to classic anaphylaxis described above. With this form of anaphylaxis, prior exposure to the antigen is not required. Less commonly, activation of the complement cascade leads to the formation of anaphylatoxins (C3a, C5a), which cause degranulation of mast cells with the release of histamine, increase smooth muscle contraction and promote the release of hydrolytic enzymes from polymorphonuclear leukocytes.

6. Tell us about the mediators of pathophysiological reactions in anaphylaxis.

Mediators of anaphylaxis are divided into: 1) primary (pre-synthesized) and 2) secondary. Primary mediators include histamine (vasodilation; increased vascular permeability; contraction of smooth muscle of the bronchi, gastrointestinal tract and coronary arteries); heparin (anticoagulation; bronchospasm, urticaria, fever and anticomplementary activity are possible); chemotactic factors of eosinophils and neutrophils (chemotactic for eosinophils and neutrophils); proteolytic enzymes (formation of kinins, initiation of disseminated intravascular coagulation; activation of the complement cascade); serotonin (vascular reactions) and adenosine (bronchospasm, regulation of mast cell degranulation).

Secondary mediators are produced by eosinophils and neutrophils and through other mechanisms after activation by primary mediators. The main secondary mediators are arachidonic acid metabolites (prostaglandins and leukotrienes) and platelet activating factor. These mediators include prostaglandins E2, D2 and I2 (prostacyclin); leukotrienes B4, C4, D4 and J4; thromboxane A2 and platelet activating factor. Most of these mediators cause vasodilation; increase vascular permeability; enhance the formation of histamine, bradykinin, leukotrienes and chemotactic factors; lead to bronchospasm; promote platelet aggregation; stimulate the chemotaxis of eosinophils and neutrophils; cause cardiodepression; increase education bronchial mucus; cause platelet release; enhance the release of granules of polymorphonuclear cells. Some mediators (prostaglandin D2, prostaglandin I2 and eosinophil products) limit the hypersensitivity reaction.

7. What are the most common causes of anaphylaxis in dogs and cats?

8. What are the target organs of an anaphylactic reaction in cats and dogs?

The main target organs depend on the type of anaphylaxis. Local anaphylaxis (urticaria and angioedema) usually causes skin and gastrointestinal reactions. The most common skin symptoms- itching, swelling, erythema, characteristic rash and inflammatory hyperemia. Most frequent gastrointestinal symptoms- nausea, vomiting, tenesmus and diarrhea. The main target organs for systemic anaphylaxis in cats are the respiratory and gastrointestinal tract; in dogs - liver.

9. What are the clinical symptoms of an anaphylactic reaction in dogs and cats?

The clinical manifestations of systemic anaphylaxis vary significantly between dogs and cats.

In dogs, the earliest signs of anaphylaxis are agitation with vomiting, defecation, and urination. As the reaction progresses, breathing is inhibited or impaired, and collapse associated with muscle weakness, And cardiovascular collapse. Death can occur quickly (within approximately 1 hour). Autopsy reveals severe liver congestion with portal hypertension, since the liver is the main target organ in dogs. It is rarely possible to conduct an appropriate liver test before death to identify this symptom.

Cats have the most early sign anaphylaxis - itching, especially on the face and head. Typical manifestations of anaphylaxis in cats are bronchospasm, pulmonary edema and subsequent severe respiratory distress. Other symptoms include laryngeal swelling and upper airway obstruction, excessive salivation, vomiting and loss of coordination. Severe impairment of respiratory and cardiac activity leads to collapse and death.

10. What is anaphylactic shock?

Anaphylactic shock- this is the terminal phase of anaphylaxis, developing as a result of neurogenic and endotoxic changes in many organ systems, especially the cardiovascular and pulmonary. Primary and secondary mediators cause changes in microcirculation, which leads to accumulation of 60-80% of blood volume in the peripheral bloodstream. Important factor with anaphylaxis - increased vascular permeability and the release of fluid from the vessels. Mediators also cause hypovolemia, arrhythmias, decreased myocardial contractility and pulmonary hypotension, which ultimately lead to tissue hypoxia, metabolic acidosis and cell death. Clinical signs of anaphylactic shock are not pathognomonic; they are similar to symptoms of severe cardiopulmonary collapse due to any other cause.

11. How quickly does anaphylaxis develop?

Usually almost immediately or within a few minutes of exposure to the causative agent. However, the reaction may be delayed for several hours. In humans, anaphylaxis reaches its maximum severity within 5-30 minutes.

12. How to diagnose systemic anaphylaxis?

Diagnosis is based on history, physical examination and clinical presentation. Constant vigilance for anaphylaxis is necessary to quick diagnostics and starting treatment. The key point in the diagnosis of systemic anaphylaxis are rapid progression clinical signs target organ damage in animals of each species and history of recent contact of the animal with a substance that causes anaphylaxis.

13. Immediate recognition and treatment - criterion successful therapy anaphylaxis. What is the differential diagnosis?

Conditions that should be excluded as quickly as possible when evaluating animals with symptoms of severe systemic anaphylaxis include acute diseases respiratory systems s (asthma attack, pulmonary edema, pulmonary embolism, spontaneous pneumothorax, aspiration foreign body and laryngeal paralysis) and acute cardiac problems (supraventricular and ventricular tachyarrhythmias, septic and cardiogenic shock).

14. What does it feel like initial treatment systemic anaphylaxis?

Emergency treatment of anaphylaxis includes airway and vascular access, intensive fluid therapy, and epinephrine. Depending on the severity of the condition, respiratory care ranges from face mask oxygen therapy to orotracheal intubation; sometimes a tracheostomy is required. IN artificial ventilation Animals with severe respiratory tract disease, pulmonary edema and bronchospasm may need it. For the administration of solutions and medications, it is important to provide vascular access, preferably central venous. Infusion therapy are prescribed based on the severity of shock, but the veterinarian must be prepared to administer shock doses of isotonic crystalloid solutions and, possibly, colloid solutions. The use of adrenaline is the cornerstone in the treatment of anaphylaxis, as it eliminates bronchospasm and supports arterial pressure, inhibits further degranulation of mast cells, increases myocardial contractility and heart rate and improves coronary blood flow. The recommended dose is 0.01-0.02 mg/kg intravenously. This corresponds to 0.01-0.02 ml/kg of a 1:1000 solution of adrenaline hydrochloride. If venous access cannot be ensured, a double dose can be administered intratracheally. IN severe cases with persistent hypotension and constriction of the bronchi, the dose is repeated every 5-10 minutes or adrenaline is administered by continuous infusion at a rate of 1-4 mcg/kg/min.

15. What is adjuvant therapy with systemic anaphylaxis?

Adjuvant therapy for anaphylaxis includes the use of antihistamines, glucocorticoids and, if necessary, additional supportive measures to treat hypotension, pulmonary edema, bronchoconstriction and arrhythmias. Although antihistamines and glucocorticoids act rather slowly and may not be useful in the initial period of treatment of anaphylaxis, they do help important role in the prevention of late reactions and complications caused by secondary mediators. The most commonly used antihistamine is diphenhydramine (5-50 mg/kg, slowly intravenously 2 times a day). Some authors recommend the competitive use of H2 antagonists (eg, cimetidine 5-10 mg/kg orally every 8 hours). The most commonly prescribed glucocorticoids are dexamethasone sodium phosphate (1-4 mg/kg intravenously) and prednisolone sodium succinate (10-25 mg/kg intravenously). Cdopamine (2-10 mcg/kg/min) is often used to support blood pressure and cardiac function. Aminophylline (5-10 mg/kg intramuscularly or slowly intravenously) is recommended in cases of persistent bronchoconstriction.

16. If initial treatment of systemic anaphylaxis is successful, does this mean that the animal has escaped the threat of death?

Of course, it is not safe to let the animal go home. Animals that experience the immediate effects of systemic anaphylaxis often experience delayed reactions. These conditions are caused by secondary mediators and occur 6-12 hours after the first attack. To prevent these potentially fatal reactions, it is usually recommended to carefully monitor the animal, intensively treat shock and pulmonary complications, and use antihistamines and glucocorticoids. We advise you to hospitalize the animal for at least for 24 hours and monitor closely for signs of possible complications.

Unfortunately, it is almost impossible to predict the allergenic substance. And if anaphylaxis, rash or angioedema has already occurred in a dog, all that remains is to be observant and notice what substances caused these phenomena. It is especially important to cooperate with a veterinarian regarding the use of drugs and vaccines that caused allergies in the dog. Information about this should be included in her treatment record.

A dog may experience discomfort during vaccination. And if, in addition, an allergic reaction is observed, then a specialist needs to take the situation under increased control. If your dog needs to be vaccinated, an antihistamine should be administered first. And only then, after the vaccine is administered, you can observe the reaction for about 20-30 minutes. IN in some cases You can replace certain vaccines with others.

Do you know that…
Vaccines sometimes contain antibiotics as preservatives. And if your dog is allergic to any antibiotics, it is worth checking the vaccines for their presence. If you do this in advance, before use, you can avoid problems.

Situation. Your pet is not suffering from food and medicine, but is too sensitive to insect bites. What to do?

• 1. First of all, before a critical problem arises due to the bite, consultation with a veterinarian will be required. He will tell you options operational assistance in case of development of Quincke's edema or acute form anaphylactic reaction.

• 2. You may be advised to have a disposable syringe with a dose of adrenaline. If a reaction begins to develop, you can use it as first aid before the veterinarian arrives. Since it is sold by prescription only, you cannot buy it without a doctor's recommendation.

It is especially important to have a plan emergency care during a trip when prompt veterinary intervention is not possible. It is also impossible to completely protect your pet from bites.

NOTE! An anaphylactic reaction sometimes occurs not after the first, but after repeated administration of the vaccine. Therefore, if everything went well the first time, this does not mean that there will be no allergies. Even after 3, 5 or 10 injections of the vaccine, an anaphylactic reaction may appear for the first time.

The intensity of the anaphylactic reaction does not depend on how old the animal is. However, the dog's general predisposition to allergies should prompt owners to special attention treat possible manifestations anaphylaxis. If skin rashes or swelling have already appeared, an anaphylactic reaction to medications can occur at any time.

Continuing the articles on allergies: anaphylactic shock in dogs - symptoms and emergency care, including at home.

Continuing the series of articles on allergies, today we will talk about the topic: anaphylactic shock in dogs - symptoms and first aid. Anaphylaxis is a serious, usually spontaneous and fairly active allergic reaction of the body to any foreign substance, often of protein origin. Such substances are called allergens.

The danger of anaphylactic shock lies in the too rapid, almost lightning-fast development of the pathological process, which, if left untreated, can be fatal.

Anaphylaxis, as a clinical type of allergy, can be provoked by different allergens, depending on the state of the immune system of a particular animal. These include veterinary drugs, bites from venomous animals, diagnostic tools, mold, pollen, some food ingredients and even flea and tick saliva. An anaphylactic reaction usually develops suddenly, literally within the first minutes after a dog touches, inhales, ingests or is otherwise exposed to an allergen. Without prompt emergency treatment, anaphylactic shock in dogs almost always causes convulsions, collapse, coma, and often results in death.

Owners who know that their pet has allergies should always be ready to provide first aid to the animal when the first signs of anaphylaxis appear. Let's talk about this in more detail.

What is the essence of allergies?

The immune system is designed to protect a living organism from foreign elements that have entered the blood. Immune cells in their predominant composition consist of protein molecules that are capable of recognizing other proteins in a manner very reminiscent of “friend or foe.” If an unfamiliar protein structure gets in the way of a protective cell, a kind of identification is carried out at the molecular level. If the encountered elements are identified as “self,” there is no response from the immune system. If it is a “foreign” protein, a huge number of other immune bodies are delivered to the localization site, which actually eat the foreign protein and neutralize it. Such neutralization is organized through the development of the inflammatory process, which is a protective reaction stimulated by the so-called inflammatory mediators. The latter are released due to the activity of the immune cells themselves. This is the normal situation.

An allergy develops when even a slight ingress of a foreign protein into the body produces too much a large number of inflammatory mediators that stimulate disproportionate inflammatory process. As a result, it develops.

What is anaphylactic shock?

The severity of the allergic reaction depends on the amount of inflammatory mediators released into the blood. In some cases, it can resolve quickly, showing only minor itching in the dog's abdominal area, and in others, it can cause anaphylactic shock.

Among other things, it is worth noting such a phenomenon as sensitization. As a rule, dog owners may not suspect for some time that their pet is allergic to, say, some ingredient in a food additive until it enters the dog’s body. The first intake of the allergen can occur unnoticed and harmless. At this moment, immune cells first detect a foreign allergenic protein and produce antibodies against it, which absorb the foreign protein structure without releasing inflammatory mediators in excess. After the fight is completed, the immune system “remembers” the structure of the foreign protein molecule, which is expressed by the constant presence of antibodies against it in the dog’s blood. They say that the body has become sensitized against a specific allergen.

The next time a similar foreign allergen protein enters the body, this leads to an immediate release of an excess amount of inflammatory mediators due to the antibodies that are already ready to be killed, which stimulates the development of a sensitized allergic reaction.

It should be noted that allergies, that is, increased sensitivity the body to a specific allergen – the condition is abnormal. Such pathology in a particular animal depends on individual characteristics immunity, and therefore from hereditary factors. Although in some cases an acquired allergy may develop when too much of a foreign allergen protein enters the body.

What happens in a dog's body during anaphylaxis?

Anaphylactic shock in dogs, like other species of living organisms, should be distinguished from allergies in its classical definition. If, in case of allergies, an excessive amount of inflammatory mediators cause, as a rule, local reactions, more often - on the skin and mucous membranes, then with anaphylaxis there is a generalized - overall impact mediators throughout the body, which is expressed in the following clinical manifestations:

• Expansion (stretching beyond normal sizes) blood vessels.
• An increase in porosity (permeability) of the walls of blood vessels, which leads to the leakage of the liquid part of the blood into the intercellular space - edema.
• Dangerously low blood pressure (hypotension).
• Respiratory disorders associated with pulmonary edema.

• Accumulation of fluid in the bronchi.
• Violation heart rate due to the accumulation of wildness in the cardiac lining - the pericardium and low blood pressure.
• Gastrointestinal disorders.
• Severe skin itching.
• General severe pain.

It is worth recalling that all of these signs develop at lightning speed and against the background sharp deterioration conditions cause a shock-like state. It is for this reason that this pathological process is called anaphylactic shock.

Owners need to remember that there is only one step from minor manifestations of allergies to the development of anaphylactic shock in a dog. At any time on substances that cause mild local allergic reaction, anaphylaxis may develop if too much of the allergen is ingested.

Prevention of anaphylaxis

The best way to prevent allergies and anaphylactic shock in your dog is to avoid exposing your dog to allergens to which they are known to be hypersensitive. Unfortunately, other options do not yet exist completely in veterinary medicine.

Features of anaphylaxis in dogs

Anaphylactic reactions in humans typically manifest as choking because anaphylaxis primarily affects the upper Airways, trachea, bronchi and lungs. In dogs, this condition occurs somewhat differently. Pathological process focused primarily on cardiovascular system and gastrointestinal tract. Respiratory symptoms develop secondarily.

Symptoms

As noted above, anaphylaxis in dogs develops almost immediately after contact with the allergen - within the first minutes. Initial symptoms anaphylactic shock often includes a complex of the following manifestations:

• Cyanosis and pallor of the visible mucous membranes, which is clearly visible in the oral cavity.
• Increased heart rate - tachycardia.
• Weak pulse.
• Extremities are cold to the touch.
• The animal is lethargic and tends to sit or lie down.
• Involuntary acts of defecation and urination.
• Diarrhea.
• Vomit.
• Increased salivation – hypersalivation. Often expressed as foam.
• Shortness of breath in the form of an increase in the frequency of respiratory movements.

If left untreated, the end result of anaphylactic shock is almost always alternating between seizures, loss of consciousness, coma and death.

It is worth noting that the dog will not have obvious swelling around the circumference of the throat or in any area of ​​the facial part of the skull if the allergen has not come into contact in these places. In animals sensitized to insect bites or medicines administered by injection, mild to moderate swelling may develop at the site of allergen exposure.

Dogs at high risk

Allergies and anaphylactic shock affect any breed of dog, regardless of gender and age. It is believed that Boxers and Pit Bull Terriers are the most likely to show vascular reaction skin in the form of blisters and severe itching under the influence of an allergen.

Animals that spend a lot of time outdoors warm time spring and summer months, are exposed increased risk insect or snake bites are the most common reason development of anaphylactic shock.

First aid

Treatment of anaphylactic shock in dogs consists of providing emergency assistance, which is achieved by restoring the activity of the cardiovascular and respiratory systems. In the future, measures should be taken to prevent further release of inflammatory mediators and general support for the animal's body.

Delivery mechanism

The algorithm of actions in case of development of anaphylactic shock is developed in the form therapeutic regimens and should be followed step by step in any veterinary clinic:

• Intravenous administration of adrenaline or its synthetic analogue epinephrine. The hormone causes stabilization of the frequency and strength of heart contractions, narrows blood vessels and is involved in blocking further release of inflammatory mediators.
• Tracheal intubation. It is carried out if necessary when the dog has swelling of the larynx that interferes with breathing.

• Intravenous loading of fluids to increase blood volume to compensate for low blood pressure.
• If it is not possible to raise blood pressure, small doses are administered sequentially vasoconstrictor drugs, for example, dobutamine under regular blood pressure monitoring.
• Dexamethasone and diphenhydramine are administered intravenously to reduce swelling, if any, in the larynx.

Oxygen therapy is given if necessary. Antibiotics wide range actions are often given in an attempt to prevent the development of secondary bacterial infections which may develop after an anaphylactic episode.

As a rule, the dog is kept in the clinic until the symptoms of anaphylactic shock disappear. However, if the situation allows, it is better to leave her under the supervision of specialists for 1-2 days. A positive sign exit from serious condition is the volitional urination of the animal, which proves the balancing of the functionality of the cardiovascular system.

How to help a dog at home?

In some cases, it is not always possible to seek first aid in a timely manner. veterinary clinic. Despite the complexity of the manipulations in saving a dog from anaphylaxis, the main support, which will increase the time before contacting specialists, and, sometimes, completely rescue the animal, can be provided independently.

As a rule, a loading dose of adrenaline or epinephrine is enough to make the dog feel much better, but not all owners will be able to carry out the procedure on their own intravenous administration. In addition, the veins in a dog, due to low blood pressure may be extremely poorly accessible. The emergency method in this case is intratracheal administration. Stepping back from the dog's throat to the thickness of your little finger, you can feel the cartilage of the tracheal rings, between which the needle is inserted. Of course, in home medicine cabinet, which is taken with you into nature, there must be a dose of the drug calculated by the veterinarian for a particular dog.

Hormonal drugs have a fairly short shelf life, even if all storage conditions are met. The expiration date should be monitored and the dose promptly replaced with a fresh one. Using an expired product will not have a therapeutic effect.

Forecast

Prompt veterinary intervention is key factor for the successful recovery of a dog after anaphylactic shock. Most animals in this case recover completely, usually within 24 to 72 hours from the moment of exacerbation.

It is believed that first aid should be provided to the animal within the first hour. If this is not done, the probability fatal outcome is approaching 100%. Therefore, owners of hypersensitive dogs should be aware of the symptoms of anaphylactic shock in dogs and be alert if circumstances increase the risk of exposure to an allergen.

If you have any questions about the topic of the article, welcome to the comments below. Join

Anaphylaxis(from the Greek ana - a prefix meaning the opposite, opposite action, and phylaxis - protection, protection), a state of increased sensitivity of the body to the repeated introduction of a foreign substance of a protein nature - anaphylactogen; one of the types of allergies.

To induce anaphylaxis, animals are first sensitized with a certain anaphylactogen (blood serum, egg white, extracts of bacteria and animal organs, vegetable proteins and etc.). The size of the sensitizing dose of anaphylactogen depends on its quality, the type of animal, the individual properties of the organism, as well as the method of administration. The most effective method of administering anaphylactogen is parenteral; it can be administered through the gastrointestinal tract and mucous membranes of the upper respiratory tract. The state of hypersensitivity (sensitization) begins to appear 6-12 days after the administration of anaphylactogen and reaches its maximum after 3 weeks; proceeds without visible clinical signs. Then the strength of the reaction gradually decreases; however, increased sensitivity may persist for many months or even years. When a healthy animal is injected with serum from a sensitized animal, passive anaphylaxis. With it, the body’s reaction occurs within 24-48 hours and lasts 3-4 weeks. Passive anaphylaxis can be transmitted from mother to fetus through the placenta. When the same anaphylactogen is repeated, the sensitized animal quickly develops an anaphylactic reaction (anaphylactic shock, Arthus phenomenon, etc.). Anaphylactic shock occurs upon repeated parenteral administration of the same protein substance in the form of a violent, rapidly occurring reaction, sometimes 2-3 minutes after the administration of anaphylactogen. Clinical picture anaphylactic shock depends on the type of animal, the route of administration and the dose of the antigen and can vary significantly. Acute anaphylactic shock is characterized by pronounced anxiety of the animal, increased breathing and heart rate, decreased blood pressure, the appearance of tonic and clonic convulsions, and involuntary separation of feces and urine; changes in the morphological and biochemical composition of blood. The animal may die due to suffocation due to paralysis respiratory center or quickly comes to normal condition. When autopsying the corpses of animals that died from shock, hyperemia is detected internal organs, hemorrhages on the mucous membrane gastrointestinal tract, in the liver and kidneys. On histological examination they show protein dystrophy and fatty infiltration. After anaphylactic shock, the number of protective antibodies in the body decreases, serum complement decreases, the phagocytic ability of macrophages decreases, and the body’s susceptibility to infectious diseases. Animals that survive anaphylactic shock become resistant to the same substance. A. M. Bezredka called this phenomenon antianaphylaxis, or desensitization. It occurs 10-20 minutes after clinical manifestations shock and continues guinea pigs up to 40 days, and in rabbits up to 9 days. The state of sensitization can be reduced or eliminated if small doses of the same antigen are administered to the animal several hours before the permissive dose of the antigen is administered. This method, proposed by A. M. Bezredka, is used to prevent anaphylactic reactions, in particular serum sickness.

The Arthus phenomenon is local anaphylaxis - an inflammatory process that develops in a sensitized animal at the site of repeated administration of anaphylactogen. In this case, a general sensitization of the body is observed; If such an animal is given anaphylactogen intravenously, anaphylactic shock may occur. There are several theories that explain the mechanism of A formation. According to the hypothesis of humoral factors, during sensitization, antibodies are formed that circulate in the blood. When the antigen is reintroduced, it reacts with the antibody; the resulting protein complex is broken down by proteolytic enzymes, resulting in the formation of intermediate breakdown products, including anaphylotoxin, which causes the picture of an anaphylactic reaction (anaphylotoxin in pure form could not be identified). According to other sources, anaphylactic shock occurs as a result of the formation of substances such as histamine in the blood. Some researchers associate the cause of anaphylactic shock with profound changes in the colloid composition of the blood. Representatives of the cellular theory believe that antibodies react with antigens in cells. When they combine, the vital activity of cells is disrupted, which leads to anaphylactic shock. A. M. Bezredka was the first to point out the importance of the nervous system in the development of A., proving this by the fact that in an experiment A. can be prevented by introducing narcotic drugs. During hibernation, it is also very rare to cause anaphylactic shock in animals. The phenomenon of A. should be interpreted as a complex of reactions of the body in which the central nervous system, endocrine glands, immune mechanisms. Antihistamines, hormones, and ephedrine are used to treat A.

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

What causes anaphylactic shock?

Before anaphylactic shock occurs, the animal must be under the influence of the allergen. A typical 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, vaccine, contaminated environment and various chemicals.

It is important to note that this is not a normal reaction of the body. The immune system reacts too strongly to a foreign substance or protein, causing 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, your dog will have trouble breathing and his tongue and gums will turn blue.

How to diagnose anaphylaxis?

Anaphylactic shock is diagnosed by identifying recent contact with 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 immediate attention medical care 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, application may be sufficient. antihistamines, and possibly corticosteroids, with the dog observed 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.