Anaphylactic shock- a systemic generalized allergic reaction of an immediate type to repeated administration of an allergen as a result of a rapid massive immunoglobulin-E mediated release of mediators from tissue basophils (mast cells) and peripheral blood basophils. In drug-induced anaphylactic shock (LAS), the allergen is the drug. Anaphylactic shock is the most severe manifestation (variant) of a drug disease.

Classification
According to the pathogenetic basis, anaphylactic shock (true allergic or immunoglobulin-E-dependent) and anaphylactoid shock (pseudo-allergic or immunoglobulin-E - independent) are distinguished. Clinically, anaphylactic shock can proceed according to the classical, cerebral, hemodynamic, asphyxic and abdominal variants. There are acute malignant, acute benign, protracted, recurrent and abortive course of LASH.

Risk factors
The likelihood of developing anaphylactic shock is associated with external and internal factors. The main external factors of Anaphylactic shock:

• a sharp increase in the number of allergens in the environment,
• expansion of the spectrum and simultaneous exposure to several allergens and irritating substances in domestic and professional conditions,
• the prevalence of aerosol intake of foreign substances (xenobiotics) into the body,
• contributes to an increase in the number of sensitized individuals,
• polypharmacy,
• self-treatment of patients
• widespread use of vaccination,
• unfavorable social factors.

Among the internal causes of anaphylactic shock, the leading place is occupied by constitutional and genetic predisposition. External factors contributing to the development of anaphylactic shock are not mandatory. The action of allergens is realized only in an organism with an allergic phenotype.

Etiology
Anaphylactic shock can be caused by almost all drugs, including corticosteroids and antihistamines. Some of them, being proteins, glycoproteins, complex molecules of foreign origin (vaccines, sera, immunoglobulins) or hormones (insulin), easily induce an immune response and an anaphylactic reaction. Others - simple chemical molecules of small molecular weight (haptens) - are not able to independently trigger an immune response and participate in the immunological stage of LASH when combined with proteins, lipids, polysaccharides, being modified into the form of a highly immunogenic complex (full-fledged hapten). The development of an immunological reaction to the complex occurs when the drug enters the body again. Anaphylactic shock can be induced not only by drugs, but also by their impurities (low molecular weight substances, antigenic divalent and polyvalent conjugates). The purity and quality of the drug becomes clear.
The sensitization activity of a drug depends on the number and position of atoms in its structure. Medicines can give cross-reactions. For their occurrence, it is necessary to have a geometric similarity with the structure of the original antigen and the ability to form complex antigens. The first form of polyvalence of anaphylactic shock is the presence of sensitization in one person to several drugs that are similar in chemical structure or method of pharmacological action. The second form is manifested by sensitization to many drugs of various chemical structures and pharmacological actions. In the third form (in persons with a constitutional genetic predisposition), hypersensitivity to one or more drugs in the same patient may be combined with the presence of sensitization to infectious or non-infectious allergens.
Pathogenesis.
The development of true anaphylactic shock, as well as a drug disease, is based on immunological mechanisms. In its course, immunological, pathochemical and pathophysiological (clinical manifestations) stages are distinguished. Features of Anaphylactic shock appear only in the immunological stage. At this stage of anaphylactic shock, the hapten drug is converted into a full-fledged antigen, against which B-lymphocytes begin to produce large amounts of IgE. In morphological and functional terms, sensitized cells do not differ from normal ones, and a sensitized person is practically healthy until the allergen enters the body again and antigen-antibody reactions develop. IgE-dependent degranulation is initiated only by specific allergens, which in the body bind to IgE molecules fixed on the surface of basophils and mast cells. In the process of degranulation of peripheral blood basophils and mast cells, which coincides with the pathochemical stage of an allergic reaction, mediators - histamine, bradykinin, serotonin, and various cytokines - are released in large quantities. Depending on the localization of antigen-antibody complexes on one or another shock organ, various clinical manifestations of anaphylactic shock may develop.
With pseudo-allergic (anaphylactoid) shock, there is no immunological stage, and the pathochemical and pathophysiological stages proceed without the participation of allergic IgE with excessive release of mediators in a non-specific way. Three groups of mechanisms take part in the pathogenesis: histamine; disturbances in the activation of the complement system and disturbances in the metabolism of arachidonic acid. In each case, the leading role is assigned to one of the mechanisms. In the pathochemical stage of both anaphylactic and anaphylactoid shock, the same mediators are released, which determines similar clinical manifestations and makes their differential diagnosis extremely difficult. Mediators released in large quantities in LASH increase vascular permeability, cause contraction of the smooth muscles of the bronchi and blood vessels, etc. The most important are hemodynamic disorders that can cause death.

Clinic
The clinic of anaphylactic shock is characterized by diversity and is due to the interaction of such factors as the number of organs involved in the pathological process, the number of mediators released, the reactivity of perceiving receptors, etc. Most patients develop the classic clinical form of anaphylactic shock. Acutely there is a state of discomfort with feelings of anxiety, fear of death. Against the background of sudden onset of weakness, tingling and itching of the skin, a feeling of heat or chills, heaviness and tightness in the chest, pain in the heart, difficulty breathing or inability to breathe can be felt. Patients also note dizziness or headache, blurred vision, hearing loss. Nausea and vomiting follow. Objectively noted tachycardia and lowering blood pressure. In more severe cases, loss of consciousness occurs. Dry and wet rales are heard over the lungs. Further, convulsions, foam at the mouth, involuntary urination and defecation, dilated pupils, swelling of the tongue, larynx may appear. Death occurs within 5-30 minutes. with symptoms of asphyxia or after 24-48 hours or more due to severe irreversible changes in vital organs. In addition to the classic, 4 more options are distinguished according to the leading clinical syndrome: hemodynamic, asphyxic, cerebral, abdominal. Each of the variants of anaphylactic shock can occur with allergic skin manifestations (urticaria, Quincke's edema, etc.). Even with a favorable course and the reverse development of all threatening signs in patients, residual effects in the form of weakness, fever, weakness remain for a long time. During this period, the onset of relapses is not ruled out. That is why patients after the disappearance of the clinical manifestations of anaphylactic shock for another 10-12 days should remain under the supervision of a doctor in a hospital. An unfavorable outcome of anaphylactic shock may be due to an acute malignant course, as well as improper treatment management. The most common causes of errors: ignoring and lack of data on allergic and pharmacological anamnesis, use of drugs without indications, incorrect diagnosis, delayed or inadequate anti-shock therapy, insufficient recommendations for prevention.

Diagnostics
The presence of several clinical variants of anaphylactic shock requires differential diagnosis with myocardial infarction, pulmonary embolism, acute cerebral pathology, intestinal obstruction, perforated gastric or duodenal ulcer. As for the differential diagnosis of true and pseudo-allergic (anaphylactoid) anaphylactic shock, it is carried out mainly in patients with a history of drug disease. With pseudo-allergic shock, it is not possible to establish the presence of a period of sensitization, repeated reactions to the use of drugs similar in chemical or antigenic terms. The duration of pseudo-allergic shock is short-term, and the results of test-tube specific immunological tests are negative.

In favor of anaphylactic shock testify:

• previously used drug, "suspected" in the development of an allergic condition (unless the patient is not aware of the onset of sensitization, for example, penicillin, possibly contained in cow's milk),
• no dependence of an allergic reaction on the dose of the drug,
• reverse development of shock after the withdrawal of the "guilty" drug,
• allergic diseases in the present or past, as well as in blood relatives,
• occupational contact with drugs as a possible cause of sensitization,
• fungal diseases of the skin and nails, sensitizing to non-synthetic antibiotics.

Treatment
First aid involves mandatory anti-shock measures at the site of anaphylactic shock. All injections are performed intramuscularly so as not to waste time looking for veins. If shock occurs during intravenous administration of an allergen drug, the needle is left in the vein and drugs are injected through it.

At the same time, the administration of the drug that caused anaphylactic shock is stopped and the following is administered:

• adrenergic drugs at the injection site of the drug allergen (epinephrine 1 ml - 0.1% solution),
• glucocorticoids (prednisolone at the rate of 1-2 mg / kg of the patient's weight or dexamethasone 4-20 mg, hydrocortisone 100-300 mg),
• antihistamines (promethazine 2-4 ml - 2.5% solution, chloropyramine 2-4 ml - 2% solution, diphenhydramine 5 ml - 1% solution),
• xanthines for bronchospasm and difficulty breathing (aminophylline 1-2 ml 24% solution),
• cardiac glycosides (digoxin 0.025% -1 ml in 20 ml saline intravenously),
• respiratory analeptics (cordiamin 1 ml subcutaneously),
• highly active diuretics (furosemide 0.02 - 0.04 g 1 time per day intravenously or intramuscularly) with pulmonary edema.

In the absence of a therapeutic effect after 10-15 minutes, the introduction of these drugs is repeated. When an allergen drug is injected, a tourniquet is applied to the area of ​​\u200b\u200bthe extremities above the injection site and this place is chipped with epinephrine diluted with saline 1:10. In the event of anaphylactic shock from penicillin after epinephrine and glucocorticoids, rapid intramuscular administration of 1 million units is indicated. penicillinase dissolved in 2 ml of saline or distilled water. When taking an allergen drug orally, the stomach is washed, if the patient's condition allows. Intensive therapy for anaphylactic shock is carried out in a specialized department in the absence of the effect of mandatory anti-shock measures. It involves venipuncture (venesection), if the latter has not been done earlier, and intravenous administration of drugs, moreover, together with solutions of dextrose, isotonic sodium chloride solution or plasma-substituting fluids. At the same time, mucus is sucked off, the airways are freed from possible retraction of the tongue by unbending the head backwards, and humidified oxygen passed through the defoamer (alcohol) is introduced using a catheter inserted into the lumen of the trachea. In the absence of a therapeutic effect, the administration of the above drugs is repeated every 10-15 minutes. In the asphyxic form of LASH, drugs with a bronchodilating effect are additionally administered (aminophylline 2-3 ml of a 24% solution or 20 ml of a 2.4% solution, diprofillin 5 ml - 10% solution, isadrin 2 ml - 0.5%, orciprenaline 1-2 ml 0.05%).

In the absence of the effect of intensive therapy proceed to resuscitation. They involve closed heart massage, intubation, or tracheostomy. In acute asphyxia, ventilation of the lungs is carried out with the help of breathing apparatus. In cardiac arrest, epinephrine is administered intracardiac. With epileptic status and normal blood pressure, 1-2% chlorpromazine solution (or 2-4 ml of 0.5% diazepam solution) is administered. Resuscitation measures are carried out by a specialized team or doctors who have undergone special training. After relief of acute symptoms within 1-2 weeks, additional treatment is carried out with desensitizing, dehydrating, detoxifying and corticosteroid agents.

Prevention
Prevention of Anaphylactic shock is no less relevant than diagnosis and treatment. The best method of prevention is the reasonable prescription of drugs. A certain role in the prevention of anaphylactic shock is played by sanitary education among the population.
To prevent the development of anaphylactic shock, medication is recommended.

Anaphylactic shock is an immediate type of allergic reaction that occurs when an allergen is repeatedly introduced into the body.

Causes of occurrence. Anaphylactic shock can develop with the introduction of drugs into the body, the use of specific diagnostic methods. In very rare cases, shock can develop as a manifestation of a food allergy or as a reaction to insect bites. As for drugs, almost any of them can sensitize the body and cause anaphylactic shock. Most often, such a reaction appears on antibiotics, especially penicillin. The resolving dose of the drug that causes anaphylactic shock can be negligible.

Development. The rapid development of general manifestations (decrease in blood pressure and body temperature, dysfunction of the central nervous system, increased vascular permeability) is characteristic of anaphylactic shock. The time of development of a shock state and the frequency of occurrence depend on the route of introduction of the allergen into the body. With parenteral administration (with injections), anaphylactic shock is observed more often and proceeds more rapidly. Especially dangerous is the intravenous administration of the drug, in which anaphylactic shock can occur immediately ("at the tip of the needle"). Usually, anaphylactic shock occurs within 1 hour, and with rectal (through the anus), external skin and oral (through the mouth) use of the drug after 1-3 hours (as the allergen is absorbed). As a rule, anaphylactic shock is the more severe, the less time has passed from the moment the allergen was introduced to the development of the reaction. The incidence of anaphylactic shock and its severity increase with age.

Symptoms. The first symptoms of an incipient anaphylactic shock are anxiety, a feeling of fear, a throbbing headache, dizziness, tinnitus, and cold sweat. In some cases, there is a pronounced pruritus followed by Quincke's edema or urticaria. There is shortness of breath, a feeling of tightness in the chest (a consequence of bronchospasm or allergic laryngeal edema), as well as symptoms of dysfunction of the gastrointestinal tract in the form of paroxysmal pain in the abdomen, nausea, vomiting, and diarrhea. The following phenomena are also possible: foam from the mouth, convulsions, involuntary urination and defecation (stool), bloody discharge from the vagina. The arterial pressure decreases, the pulse is filiform.

In cases of anaphylactic shock occurring with loss of consciousness, the patient may die within 5-30 minutes from suffocation or after 24-48 hours or more due to severe irreversible changes in vital organs. Sometimes death can occur much later due to changes in the kidneys (glomerulonephritis), in the gastrointestinal tract (intestinal bleeding), in the heart (myocarditis), in the brain (edema, hemorrhage) and other organs. Therefore, patients who have undergone anaphylactic shock should be in the hospital for at least 12 days.

Treatment. Emergency care should be provided immediately from the moment the first clinical signs of anaphylactic shock appear. The first urgent measure is to stop the administration of the drug or limit its entry into the bloodstream (apply a tourniquet above the injection site of the drug or bite). At the site of injection or bite, 0.5 ml of 0.1% adrenaline solution should be injected (subcutaneously or intramuscularly and the same dose in another area. In severe cases, 0.5 ml of 0.1% adrenaline solution should be injected intravenously with 20 ml of 40% glucose solution In the absence of a therapeutic effect, it is recommended to repeat the injection of 0.5 ml of a 0.1% solution of adrenaline subcutaneously or intramuscularly.If this still fails to increase blood pressure, then intravenous drip infusion of norepinephrine should be used (5 ml of a 0.2% solution of norepinephrine in 500 ml 5 % glucose solution).
If there is no effect, pathogenetic therapy is carried out to restore the volume of circulating blood using colloid solutions, Ringer's solutions, isotonic solutions, etc., in combination with glucocorticoids. In complex therapy, antihistamines, heparin, sodium oxybuterate are used. Additionally, cordiamine, caffeine, camphor are administered, and in case of severe bronchospasm - intravenously 10 ml of a 2.4% solution of aminophylline with 10 ml of a 40% glucose solution. Since laryngeal edema and bronchospasm are often prolonged, repeated use of bronchodilators in combination with antihistamines and diuretics is often required. In the absence of an effect on vital indications, tracheal inturbation, artificial ventilation of the lungs, along with a complex of resuscitation measures, are necessary.

The prognosis depends on the timeliness of therapeutic measures and the severity of shock. A short-term increase in blood pressure is not a reliable sign of removing the patient from a state of shock. Anti-shock measures should be continued until the effective tissue blood flow is fully restored.

Prevention. It is not yet possible to predict the development of anaphylactic shock. Therefore, it is necessary to prescribe medicines with pronounced antigenic properties as carefully as possible. Persons prone to allergies or having other risk factors (professional contact with antibiotics, fungal skin lesions, etc.) are recommended to make the first injection of an antibiotic in the lower part of the body so that in case of anaphylactic shock a tourniquet can be applied above the injection site. Have at the ready a set of medicines and tools for immediate assistance.

Definition. Anaphylaxis is an acute systemic reaction of a sensitized organism to repeated contact with antigen, which develops according to type I allergic reactions (immediate type allergic reaction).

Anaphylactic shock (AS) is an acute systemic reaction of a sensitized organism to repeated contact with an allergen, which is based on an immediate allergic reaction.

Anaphylactic shock is a life-threatening acutely developed condition, accompanied by hemodynamic disturbances and leading to circulatory failure and hypoxia of all vital organs.

Epidemiology. In the entire spectrum of anaphylactic reactions AS is 4.4%. AS develops in patients suffering from allergic diseases. Among people with atopic diseases, the incidence of AS is higher.

Risk factors and primary prevention

The development of AS can be caused by drugs (up to 20.8%; in women, AS on NSAIDs develops 5 times more often than in men), heterologous (obtained from animal blood) sera, vaccines, hymenoptera venom (from 0.8 to 3, 3% of cases in the general population and from 15 to 43% in bees

lovodov), food and pollen allergens, some bacterial allergens, latex allergens (up to 0.3% in the general population).

AS can be a complication or a consequence of improper allergen-specific immunotherapy with the introduction of pollen, household, epidermal and insect allergens, as well as the use of these allergens for diagnostic purposes.

Etiology and pathogenesis. Anaphylactic shock, like other allergic diseases, is caused by non-dangerous substances in themselves - allergens. Allergens are usually divided into two groups: endoallergens, which are formed in the body itself, and exoallergens, which enter the body from outside. In the case of anaphylactic shock, exogenous allergens are the most common cause, while a significant part is drug allergy when using analgesics, sulfonamides and antibiotics from the penicillin group, less often cephalosporins (this should take into account the risk of cross-sensitization to penicillin and cephalosporins, which is from 2 to 25% ).

Endoallergens (autoallergens) are components of cells of human body tissues (thyroglobulin of the thyroid gland, myelin of muscle fibers, lens of the eye, etc.) changed under the influence of various factors (viruses, bacteria and other agents), which are normally isolated from systems that produce antibodies, and sensitized lymphocytes. Under the conditions of the pathological process, physiological isolation is violated, which contributes to the formation of endo (auto) allergens and the development of an allergic reaction.

Exogenous allergens are divided into allergens of non-infectious and infectious origin. Non-infectious exogenous allergens (Table 1, in the photographs below) differ in the way they enter the human body: inhalation (allergens that enter the body during breathing), enteral (allergens that enter through the digestive tract), parenteral (with subcutaneous, intramuscular or intravenous introduction of an allergen) Infectious exoallergens:

Bacterial (non-pathogenic and pathogenic bacteria and their metabolic products);

Fungal (non-pathogenic and pathogenic fungi and their metabolic products);

Viral (various types of rhinoviruses and products of their interaction with body tissues);

In addition to the so-called "full-fledged" allergens, there are haptens - substances that do not have the properties of themselves to cause an allergic reaction, but when they enter the body and combine with plasma proteins, they trigger the allergy mechanism. Relative to haptens

many micromolecular compounds (some drugs), simple chemicals (bromine, iodine, chlorine, nickel, etc.), more complex protein-polysaccharide complexes of plant pollen and other environmental factors of natural or anthropogenic origin, haptens can even be part of the chemical substances. Haptens, connecting with plasma proteins, form conjugates that cause sensitization of the body. When re-entering the body, these haptens can often combine with the formed antibodies and/or sensitized lymphocytes independently, without prior binding to proteins, provoking the development of an allergic reaction.

Pathogenesis: Allergens, getting on the skin and mucous membranes, are absorbed by macrophages. Macrophages process the allergen and present it to T helpers. T-helpers produce cytokines that trigger a number of reactions: 1) proliferation of B-lymphocytes and their differentiation into plasma cells, 2) production of IgE antibodies. Antigen-specific IgE antibodies are fixed on the membranes of mast cells, basophils, etc. (primary immune response). When the allergen enters the body again, the allergen cross-links the IgE antibodies fixed on the cell and the cellular receptors of this immunoglobulin. Cross-linking of two surface IgE molecules activates mast cells (secondary immune response), which triggers the synthesis of allergy mediators, causing the clinical manifestations of allergy (early phase: occurs within a few minutes after exposure to the allergen): contraction of smooth muscles, changes in local microcirculation, increased vascular permeability , tissue edema, irritation of peripheral nerve endings, hypersecretion of mucus by the mucous glands.

Mast cells secrete two types of mediators: 1) precursors (those that existed in the cell before activation) are histamine, eosinophilic factors, tryptase), 2) mediators after activation (prostaglandins D2, leukotrienes C4, D4, E4, platelet activation factor and other). Among the mediators secreted from mast cells, there are those that have a very pronounced effect on cells of the immune system interested in an IgE-mediated response: interleukins (IL) 4 and 13, as well as IL-3, -5, granulocyte-macrophage colony-stimulating factor , tumor necrosis factor. These mediators can maintain the IgE response or enhance it with additional allergenic stimulation of the body. Along with the effects that occur in the early phase of an allergic reaction, individual mediators cause migration and chemotaxis of other cells participating in the reaction: eosinophils, T cells (Th2 cells), basophils, monocytes, neutrophils, which, being activated by accumulating mediators and possibly , an IgE-mediated mechanism, also secrete mediators that complement the external manifestations of the tissue reaction with their action. Since it takes a relatively long time to attract these cells, the reaction they cause is delayed in relation to the time of the allergen action (late or delayed phase, occurs 6-8 hours or more after the allergen action). The mediators released from the cells involved in the late phase are for the most part the same mediators that are released in the early phase. However, new mediators also join their action, in particular, from among the mediators secreted by activated eosinophils: eosinophilic proteins with the properties of bases. These mediators have cytotoxic, damaging activity, which is associated with elements of tissue damage (for example, the epithelium of the mucous surface) in severe, often recurring and maintained allergic reactions.

Diagnostics. Clinical examination data

The initial examination of the patient should include:

Complaints and anamnesis (in a serious condition - according to relatives): the presence of a connection between the intake of a medicinal substance or other allergen with the onset of symptoms, the presence of a history of allergic reactions

Visual examination: assessment of the level of consciousness, the condition of the skin (the presence of elements of a rash or angioedema), the color of the skin (hyperemia, pallor)

Pulse study

Measurement of heart rate - bradytachycardia, arrhythmias, absence of heart beats

Blood Pressure Measurement - Hypotension

Airway patency (presence of stridor, dyspnea, wheezing, shortness of breath or apnea);

The presence of gastrointestinal manifestations (nausea, abdominal pain, diarrhea).

Temperature

Obligatory examination by an ENT doctor to exclude stenosis of the larynx with swelling of the face and neck

When taking anamnesis, the following mandatory questions should be asked:

Have you had allergic reactions before?

What caused them?

How did they show up?

What drugs were used for treatment (antihistamines, glucocorticosteroids, adrenaline, etc.)?

What preceded the development of an allergic reaction this time (food not included in the usual diet, insect bite, medication, etc.)?

What measures were taken by the patient on their own and their effectiveness?

The most common is a generalized (typical) form of anaphylactic shock, during which three periods are conditionally distinguished: the period of precursors, the peak period and the period of recovery from shock. The period of precursors, as a rule, develops within 3-30 minutes after the action of the allergen (medication, food, sting or bite by insects, etc.). In some cases (for example, with injections of deposited drugs or intake of allergens through the mouth), it develops within 2 hours after the introduction of the antigen. This period is characterized by the occurrence in patients of internal discomfort, anxiety, chills, weakness, dizziness, tinnitus, blurred vision, numbness of the fingers, tongue, lips, pain in the lower back and abdomen.

Patients often develop itching, shortness of breath, urticaria and Quincke's edema. With a high degree of sensitization of patients, this period may be absent (lightning shock).

The peak period is characterized by loss of consciousness, a drop in blood pressure (less than 90/60 mm Hg), tachycardia, pallor of the skin, cyanosis of the lips, cold sweat, shortness of breath, involuntary urination and defecation, and a decrease in urine output. In 5-20% of patients, the symptoms of anaphylaxis can recur after 1-8 hours (biphasic anaphylaxis) or persist for 24-48 hours (prolonged anaphylaxis) after the onset of its first symptoms.

The period of recovery from shock lasts, as a rule, 3-4 weeks. Patients have weakness, headache, memory impairment.

Classification. Depending on the severity of clinical manifestations, four degrees of AS severity are distinguished (see below). According to the nature of the flow, they distinguish:

1) acute malignant course;

2) acute benign course;

3) protracted course;

4) recurrent course;

5) abortive course.

Depending on the manifestations of anaphylaxis that accompany the main (hemodynamic) disorders, there are five forms of AS:

1) hemodynamic; 2) asphyxia; 3) abdominal; 4) cerebral; 5) AS with lesions of the skin and mucous membranes.

Depending on the rate of development of the reaction to the allergen, the following forms of anaphylactic shock are distinguished:

1. Lightning - shock develops within 10 minutes;

2. Immediate - the pre-shock period lasts up to 30-40 minutes;

3. Slow - shock manifests itself after a few hours.

The severity of anaphylactic shock is determined by the time interval from the moment the allergen enters to the development of a shock reaction (Table 2 in the photographs under the text).

The fulminant form develops 1-2 minutes after the allergen enters. Sometimes the patient does not even have time to complain. Lightning shock can occur without precursors or with their presence (feeling hot, throbbing in the head, loss of consciousness). On examination, pallor or sharp cyanosis of the skin, convulsive twitches, dilated pupils, and their lack of reaction to light are noted. The pulse on the peripheral vessels is not determined. Heart sounds are sharply weakened or not heard. Breathing is difficult. With swelling of the mucous membranes of the upper respiratory tract, there is no breathing.

A severe form of anaphylactic shock develops 5-7 minutes after the introduction of the allergen. The patient complains of a feeling of heat, lack of air, headache, pain in the region of the heart. Then cyanosis or pallor of the skin and mucous membranes, difficulty breathing,

arterial pressure is not determined, the pulse is only on the main vessels. Heart sounds are weakened or not heard. The pupils are dilated, their reaction to light is sharply reduced or absent.

Anaphylactic shock of moderate severity is observed after 30 minutes. after exposure to the allergen. Allergic rashes appear on the skin. Depending on the nature of the complaints and symptoms, 4 variants of moderate anaphylactic shock are distinguished.

The cardiogenic variant is the most common. The symptoms of cardiovascular insufficiency (tachycardia, thready pulse, low blood pressure, weakened heart sounds) come to the fore. Sometimes - a pronounced sharp pallor of the skin (the cause is a spasm of peripheral vessels), in other cases, marbling of the skin is noted (the reason is a violation of microcirculation). The electrocardiogram shows signs of cardiac ischemia. Respiratory dysfunction is not observed.

Asthmoid, or asphyxic variant. Respiratory failure is manifested by bronchospasm. Edema of the alveolocapillary membrane may develop, gas exchange is blocked. Sometimes suffocation is caused by swelling of the larynx, trachea with partial or complete closure of them.

lumen.

cerebral variant. Observed: psychomotor agitation, fear, severe headache, loss of consciousness, tonic-clonic convulsions, accompanied by involuntary urination and defecation. At the time of convulsions, respiratory and cardiac arrest may occur.

Abdominal option. There is a sharp pain in the upper part of the abdominal cavity, symptoms of irritation of the peritoneum. The picture resembles a perforated ulcer or intestinal obstruction.

Slow form - can develop within a few hours. The severity of AS is determined by the severity of hemodynamic disorders.

I degree - a slight violation of hemodynamics. Blood pressure is below the norm by 30 - 40 mm Hg. Art. The disease can begin with the appearance of precursors: rashes, sore throat, etc. The patient is conscious, anxiety, agitation, depression, fear of death are possible. There may be complaints of a feeling of heat, chest pain, tinnitus. Other manifestations of anaphylaxis are sometimes noted: urticaria, Quincke's edema, cough, etc. AS I degree of severity is easily amenable to antishock therapy.

At II degree, the violations are more pronounced, systolic blood pressure is 90-60 mm Hg. Art., diastolic blood pressure - 40 mm Hg. Art. Loss of consciousness does not occur immediately or does not occur at all. Sometimes there is a prodromal period with the presence of other symptoms of anaphylaxis.

Asphyxia due to laryngeal edema and bronchospasm, vomiting, involuntary defecation and urination may occur. On examination, pallor of the skin, shortness of breath are detected, on auscultation - wheezing in the lungs, stridor breathing. Heart sounds are muffled, register tachycardia, tachyarrhythmia.

In grade III AS, the symptoms are more severe. Note the convulsive syndrome. Systolic blood pressure is 60-40 mm Hg. Art., diastolic blood pressure may not be determined. Characterized by cyanosis of the lips, mydriasis. Pulse irregular, thready. Antishock therapy is ineffective.

AS IV severity develops rapidly, the patient loses consciousness immediately. BP is not determined, breathing in the lungs is not heard. The effect of antishock therapy is practically absent.

Data of laboratory and instrumental research methods.

Simultaneously with therapy aimed at stopping shock, the following laboratory tests are carried out.

Complete blood count, study of acid-base status, pH, pa CO2, pa O2 in order to assess the severity of respiratory and metabolic acidosis and the adequacy of therapy, water and electrolyte balance.

Study of the blood coagulation system.

It is possible to conduct an allergic examination: determination of the content of tryptase, histamine, interleukin-5, general and specific Ig E in the blood. In more detail, an allergological examination is carried out (according to various sources) 1-6 months after the reaction has stopped.

In addition to laboratory studies, the patient's condition is constantly monitored: physical examination, ECG, blood pressure control, auscultation, if necessary, determination of central venous pressure or pulmonary artery wedge pressure and other instrumental methods.

Differential diagnosis. Differential diagnosis is carried out with all acutely developing diseases accompanied by arterial hypotension, respiratory failure and impaired consciousness: acute cardiovascular failure, myocardial infarction, syncope, pulmonary embolism, epilepsy, sun and heat stroke, hypoglycemia, hypovolemia, drug overdose, aspiration, septic shock and etc.

Anaphylactoid reaction. AS must be differentiated from a systemic anaphylactoid reaction (it is based on a non-immune mechanism). The main difference is that an anaphylactoid reaction can occur already at the first injection of certain drugs (polymyxins, opioids, iodine-containing radiopaque substances, blood components, etc.). Anaphylactoid reactions require the same complex of therapy as AS, however, they are more amenable to antishock therapy and require other preventive measures.

Treatment. The goal of treatment is complete recovery or restoration of working capacity. AS of any severity is an absolute indication for hospitalization and treatment in the intensive care unit. The implementation of the main anti-shock measures should be urgent and, if possible, one-stage.

Non-pharmacological treatment

Stop the intake of the allergen into the body (stop the administration of drugs, remove the sting of an insect, etc.)

Lay the patient down, turn his head to the side and push the lower jaw.

Apply a tourniquet above the injection or sting site.

When breathing and blood circulation stop, cardiopulmonary resuscitation is performed.

Pharmacological treatment

Stopping the entry of the allergen into the body. Anti-shock measures. In case of anaphylactic shock, the patient should be laid down (head below the legs), turn his head to the side (to avoid aspiration of vomit), extend the lower jaw, remove removable dentures. Adrenaline is injected intramuscularly at a dose of 0.3-0.5 ml of a 0.1% solution (drug of choice, class of evidence A) in children 0.01 mg / kg of body weight, maximum 0.3 mg, if necessary, injections are repeated every 20 minutes. within 1 hour under the control of blood pressure.

With unstable hemodynamics with the development of an immediate threat to life, intravenous administration of adrenaline (leave) is possible while monitoring heart rate, blood pressure, oxygen saturation. At the same time, 1 ml of a 0.1% solution of adrenaline is diluted in 100 ml of isotonic sodium chloride solution and administered at an initial rate of 1 μg / min (1 ml / min).

If necessary, the speed can be increased to 2-10 mcg/min. Intravenous administration of adrenaline is carried out under the control of heart rate, respiration, blood pressure (systolic blood pressure must be maintained at a level of more than 100 mm Hg in adults and more than 50 mm Hg in children). Antiallergic therapy: prednisolone is administered intravenously (adults 60-150 mg, children at the rate of 2 mg / kg of body weight).

Symptomatic therapy: Correction of arterial hypotension and replenishment of circulating blood volume is carried out by introducing saline solutions (isotonic sodium chloride solution 0.9% 500-1000 ml). The use of vasopressor amines (dopamine 400 mg per 500 ml of 5% glucose, the dose is titrated until a systolic blood pressure of 90 mm Hg is reached) is possible only after replenishment of the BCC. With bradycardia, atropine is administered at a dose of 0.3-0.5 mg subcutaneously (if necessary, the administration is repeated every 10 minutes). With cyanosis, dyspnea, dry wheezing, oxygen therapy is also indicated. In case of respiratory arrest, artificial lung ventilation is indicated.

With swelling of the larynx and the absence of the effect of the therapy - conicotomy. In case of clinical death - artificial respiration and chest compressions.

Patient management tactics - can be removed, however, this section was among the mandatory when compiling the book.

Observation plan: the patient is observed in the intensive care unit or intensive care until the normalization of vital signs: consciousness, respiratory rate (RR), heart rate (HR) and blood pressure. After stabilization, the patient can be transferred to the department of therapy or allergology (if there is such a department in a medical institution). After discharge, the patient should be referred to an allergist at the place of residence.

Indications for referral to a specialist: the patient should be referred after suffering anaphylactic shock to an allergist at the place of residence.

Indications for hospitalization: After emergency care, patients with anaphylactic shock should be hospitalized for further observation.

Secondary prevention: The prevention of anaphylactic shock includes the elimination of the conditions and causes of the disease: elimination of allergens, drug treatment of chronic allergic diseases, improvement of ASIT, self-education of patients with a high risk of developing acute allergies and education of medical workers; elimination of unfavorable environmental factors.

Patient education is an important aspect of prevention. To this end, the most effective measures are the creation of allergy schools, where the patient can learn about the causes and mechanisms of the development of allergic diseases, the principles of emergency care,

learning how to control your condition.

For secondary prevention of anaphylactic shock, it is necessary to rationally use antibiotic therapy that promotes sensitization of the body, it is imperative to indicate the spectrum of drug intolerance on the outpatient card of the patient and the medical history in the hospital, do not prescribe drugs that were previously allergic, as well as drugs from the group of the "guilty" drug . In addition, ASIT should be performed only by an immunologist in specialized and equipped allergological rooms. A patient suffering from an allergic disease. should be informed how to avoid an allergic reaction and what steps he should take for first aid.

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Volgograd State Medical University.

Department of Immunology and Allergology.

Independent work of a student in immunology on the topic:

"Anaphylactic shock. Etiology, pathogenesis, classification, diagnosis, treatment".

Prepared by: 4th year student of group 1

Faculty of Medicine and Biology

Busarova Kristina

Volgograd 2015

Content

• Introduction
• 3. Clinical picture
• 5. Prevention

Introduction

At first, anaphylaxis was considered a purely experimental phenomenon. It was first described by P. Portier and S. Richet in 1902, observing in dogs an unusual, sometimes fatal reaction to repeated administration of an anemone tentacle extract; they also gave the name of this reaction - "anaphylaxis" (from the Greek. ana - reverse and philaxis - protection). Somewhat later, in 1905, the Russian scientist G.P. Sakharov described the development of a similar reaction in guinea pigs upon repeated administration of horse serum. Subsequently, similar reactions began to be described in humans and called them "anaphylactic shock." The term "anaphylactoid reaction" is used in cases where the release of mediators from both types of basophils is not associated with the formation of a specific IgE-allergen complex, but is due to the effect of histamine liberators on cells. Thus, we can say that anaphylactic shock is a systemic manifestation of anaphylaxis, which is based on an allergic reaction of an immediate type.

anaphylactic shock anaphylaxis diagnosis

1. Anaphylactic shock. Definition, epidemiology, etiology, classification

Anaphylactic shock (anaphylaxis, anaphylactic reaction, systemic anaphylaxis) is an immediate type of systemic allergic reaction that occurs as a result of a rapid massive IgE-mediated release of mediators from tissue basophils (mast cells) and peripheral blood basophils upon repeated contact of the body with an antigen (allergen).

Epidemiology.

Anaphylactic shock occurs in people of any age, equally common in men and women. According to foreign data, its prevalence is as follows: 0.7-10% among patients receiving penicillin injections; in 0.5-5% of those bitten or stung by insects; 0.22-1% among patients who received injections of radiopaque drugs; in 0.004% of patients with food allergies; 1 in 3,500-20,000 general anesthetic injections; 1 in 3,500-20,000 allergen injections during allergen-specific immunotherapy (ASIT). It occurs in 1 in 2,700-3,000 hospitalized patients. It is assumed that the prevalence of anaphylaxis in the population is from 1.21 to 15.04%, the incidence is 10-20 per inhabitant per year.

Etiology

Most often, anaphylactic shock is caused by drugs, hymenoptera stings (wasps, bees, hornets, etc.) and food products. Less commonly, it occurs when in contact with latex, performing physical activity, as well as during ASIT. In some cases, it is not possible to identify the etiological factor.

The most common causes of anaphylactic shock.

Anaphylactic shock can develop as a result of stings by hymenoptera (bees, bumblebees, hornets, wasps). It has been established that the allergenic activity of their venom is due to its constituent enzymes (phospholipase A1, A2, hyaluronidase, acid phosphatase, etc.). In addition to them, the composition of the poison includes peptides (melittin, apamin, a peptide that causes degranulation of mast cells) and biogenic amines (histamine, bradykinin, etc.), which probably determine its toxic effect and pseudo-allergic reactions.

Of the foods most common causes of anaphylactic shock in children are nuts, peanuts, crustaceans, fish, milk and eggs, in adults - crustaceans. Cases of anaphylaxis have been described with the use of soy protein in patients with hypersensitivity to peanuts. One should be aware of the possibility of developing shock when chick embryo cultured viral vaccines are administered to people who are sensitized to chicken protein.

In recent years, it has been established that in some cases latex, which is part of gloves, catheters, drains, fillings, bandages and other medical and household products, can be the cause of anaphylactic shock. Systemic reactions develop with inhalation or contact (with skin damage) routes of antigens. It is important to remember that the latter have common antigenic determinants with some foods (nuts, kiwi, avocados, bananas, mangoes, celery, papaya, etc.), which can cause the development of anaphylaxis in latex-sensitized patients. Risk groups for developing latex allergy are medical workers, children with developmental anomalies, who have a history of numerous operations, work in the production of rubber products and have professional contact with latex.

Cases of anaphylactic shock that occurs during physical activity (running, brisk walking, cycling, skiing, etc.) are described. The causes and mechanisms of its development are not well understood. It is noted that approximately 50% of these patients developed anaphylaxis after eating certain foods (shrimp, celery, etc.) and drugs (non-steroidal anti-inflammatory drugs). Apparently, in some cases it is due to food allergies and drug intolerances, in which exercise is the resolving factor. The study of changes in the structure of mast cells during provocative tests with dosed physical activity showed the possible role of these cells in the development of this type of anaphylaxis. It is known that it develops more often in patients suffering from atopic diseases and / or having a burdened heredity for these diseases.

Anaphylactic shock may develop during ASIT. As a rule, this complication occurs as a result of errors in the dosing of allergens, a high degree of sensitization of patients, during treatment in the acute phase of an allergic disease, with poorly controlled bronchial asthma, the use of systemic and local β-blockers that potentiate hypersensitivity reactions.

In some cases, the cause of anaphylactic shock cannot be determined. It is shown that approximately 50% of such patients suffer from atopic diseases. Idiopathic anaphylaxis often recurs and is characterized by refractoriness to ongoing therapy.

Classification of anaphylactic shock:

Anaphylactic shock pathogenetically can develop as an allergic reaction of type I (IgE-dependent), and non-allergic (involving other mechanisms).

Depending on the severity of the course of anaphylactic shock, which is determined by the severity of hemodynamic disorders, 4 degrees are distinguished. The severity of anaphylactic shock is determined by the severity of hemodynamic disorders:

1 degree of severity: Hemodynamic disturbances are minor, blood pressure is reduced by 30-40 mm Hg. Art. from the original values.

Grade 2: Hemodynamic disturbances are more pronounced. The decrease in blood pressure below 90-60/40 mm Hg continues. Art.

Grade 3: Loss of consciousness, BP 60-40/0 mm Hg. Art.

4 degree of severity: blood pressure is not determined.

Depending on the dominant clinical symptoms of anaphylactic shock:

1. A typical variant - hemodynamic disorders are often combined with damage to the skin and mucous membranes (urticaria, angioedema), bronchospasm.

2. Hemodynamic variant - hemodynamic disorders come to the fore.

3. Asphyxic variant - symptoms of acute respiratory failure predominate.

4. Abdominal variant - symptoms of damage to the abdominal organs prevail.

5. Cerebral variant - symptoms of damage to the central nervous system predominate.

Depending on the nature of the course of anaphylactic shock:

1. An acute malignant course is characterized by an acute onset with a rapid drop in blood pressure (diastolic - to 0 mm Hg), impaired consciousness and an increase in symptoms of respiratory failure with symptoms of bronchospasm. This form is quite resistant to intensive care and progresses with the development of severe pulmonary edema, a persistent drop in blood pressure and a deep coma. The faster anaphylactic shock develops, the more likely it is to develop severe anaphylactic shock with a possible fatal outcome. Therefore, this course of anaphylactic shock is characterized by an unfavorable outcome.

2. An acute benign course is characteristic of a typical form of anaphylactic shock. The disorder of consciousness is in the nature of stupefaction or soporosity, accompanied by moderate functional changes in vascular tone and signs of respiratory failure. The acute benign course of anaphylactic shock is characterized by the presence of a good effect from timely and adequate therapy and a favorable outcome.

3. The protracted nature of the course is detected after active anti-shock therapy, which gives a temporary or partial effect. In the subsequent period, the symptoms are not as acute as in the first two varieties of AS, but are resistant to therapeutic measures, which often leads to the formation of complications such as pneumonia, hepatitis, encephalitis. This course is typical for anaphylactic shock developed as a result of the introduction of long-acting drugs.

4. The relapsing course is characterized by the occurrence of a recurrent state of shock after the initial relief of its symptoms. Often develops after the use of drugs of prolonged action. Relapses according to the clinical picture may differ from the initial symptoms, in some cases they have a more severe and acute course, and are more resistant to therapy.

5. Abortive course is the most favorable. Often proceeds in the form of an asphyxic variant of the typical form of AS. Purchased fairly quickly. Hemodynamic disturbances in this form of AS are minimally expressed.

2. Pathophysiological basis of anaphylactic shock

The pathophysiological mechanisms of anaphylactic shock are mainly due to the physiological and pharmacological effects of rapid and abundant release of preformed and newly synthesized mediators from tissue basophils (mast cells) and blood basophils. There are two main mechanisms of degranulation of a large number of mast cells:

1) IgE-dependent (true allergic);

2) Independent of IgE (pseudo-allergic);

IgE-dependent degranulation is initiated by specific allergens, which, upon entering the body, bind to IgE molecules fixed on the surface of both types of basophils. As is known, IgE fixation occurs due to the existence on the surface of a special high affinity receptor for the IgE Fc fragment (FceRI). Below are examples of allergens, the role of which in the development of true allergic anaphylactic shock has been proven.

Allergens, the role of which in the development of true allergic (IgE-dependent) anaphylactic shock has been proven.

Complete protein antigens

1. Food - eggs, cow's milk, nuts, crustaceans, shellfish, legumes

2. Poisons - bees, wasps, etc.

3. Vaccines - measles, influenza, tetanus

4. Hormones - insulin, corticotropin, thyrotropin

5. Antisera - horse, antithymocyte, antilymphocyte globulin, against poisons

6. Enzymes - streptokinase, chemopapains

7. Latex - surgical gloves, endotracheal tubes

8. Allergenic extracts - house dust, animal dander, grass pollen

Haptens

1. Antibiotics - penicillin, cephalosporins, muscle relaxants

2. Vitamins - thiamine

3. Cytostatics - cisplatin, cyclophosphamide, cytosine arabinoside

4. Opiates

Polysaccharides

1. Dextran

2. Iron dextran

3. Polygemin

Binding of a specific allergen to IgE generates a signal that is transmitted through FCERI and includes a biochemical mechanism of activation of membrane phospholipids with the production of inositol triphosphate and diacylglycerol, activation of phosphokinase, followed by phosphorylation of various cytoplasmic proteins that change the ratio of cAMP and cGMP, which leads to an increase in the content of cytosolic Ca2+. As a result of the described changes, the granules of both types of basophils move to the cell surface, the membranes of the granules and the cell membrane merge, and the contents of the granules are ejected into the extracellular space, i.e. at this stage, the degranulation of the so-called preformed biologically active substances contained in the granules, which have pro-inflammatory properties, occurs. The main one is histamine, which causes vasodilation, an increase in vascular permeability with the release of plasma from the vascular bed into the tissues and the development of edema, bronchospasm, hypersecretion of mucus in the bronchi and hydrochloric acid in the stomach, increased intestinal motility, increased activity of the parasympathetic nervous system. In addition, under the influence of histamine, the expression of adhesive molecules, in particular P-selectin, on the surface of endothelial cells is enhanced.

Other preformed factors found in the granules of both types of basophils include tryptases, chymases, carboxypeptidase A, heparin, and chemotactic factors. There is evidence that granules of tissue basophils (mast cells) and blood basophils may contain tumor necrosis factor and IL-4 as preformed factors.

After the release of preformed factors, activated tissue basophils and blood basophils begin to synthesize and release new factors, which primarily include products derived from membrane phospholipids (prostaglandins, leukotrienes and platelet-activating factor), as well as a large number of different cytokines - IL-3 , IL-4, IL-5, IL-10, granulocyte-monocyte colony-stimulating factor (GM-CSF), IL-6, etc. It should be remembered that biologically active substances secreted by other cells of the immune system also take part in the pathogenesis of anaphylactic shock .

Cells and their mediators involved in the pathogenesis of anaphylactic shock.

As for the IgE-independent degranulation of mast cells (pseudo-allergic mechanism), it is known that a wide variety of factors take part in its implementation. The factors leading to the activation of both types of basophils are summarized below.

I. IgE-Dependent (True Allergic) Factors

Binding of a specific allergen to IgE on the surface of mast cells and basophils, followed by transmission of an activation signal into the cell through a high affinity receptor for the IgE Fc fragment (FceRI).

II. IgE independent (pseudo-allergic) factors

1. Complement products - C3a, C5a

2. Chemokines - MSR-1, MIP-1A, RANTES, IL-8

3. Interleukins - IL-3, GM-CSF4. Drugs - opiates, cytostatics, aspirin, non-steroidal anti-inflammatory drugs.

5. Autoantibodies to IgE

6. Autoantibodies to FceRI

7. Physical factors

8. Cold, ultraviolet radiation, physical activity.

The main mediators of an anaphylactic reaction and their action

3. Clinical picture

The most common is a generalized (typical) form of anaphylactic shock, during which three periods are conditionally distinguished: the period of precursors, the peak period and the period of recovery from shock.

The period of precursors, as a rule, develops within 3-30 minutes. after the action of an allergen (taking medication, food, sting or bite by insects, etc.). In some cases (for example, with injections of deposited drugs or intake of allergens through the mouth), it develops within 2 hours after the introduction of the antigen. This period is characterized by the occurrence in patients of internal discomfort, anxiety, chills, weakness, dizziness, tinnitus, blurred vision, numbness of the fingers, tongue, lips, pain in the lower back and abdomen. Patients often develop itching, shortness of breath, urticaria and Quincke's edema. With a high degree of sensitization of patients, this period may be absent (lightning shock).

The peak period is characterized by loss of consciousness, a drop in blood pressure (less than 90/60 mm Hg), tachycardia, pallor of the skin, cyanosis of the lips, cold sweat, shortness of breath, involuntary urination and defecation, and a decrease in urine output.

It is important to remember that in 5-20% of patients, the symptoms of anaphylaxis may recur after 1-8 hours (biphasic anaphylaxis) or persist for 24-48 hours (protracted anaphylaxis) after the onset of its first signs.

The period of recovery from shock lasts, as a rule, 3-4 weeks. Patients have weakness, headache, memory impairment. During this period, acute myocardial infarction, cerebrovascular accident, allergic myocarditis, glomerulonephritis, hepatitis, damage to the nervous system (meningoencephalitis, arachnoiditis, polyneuritis), serum sickness, urticaria and Quincke's edema, hemolytic anemia and thrombocytopenia can develop.

Depending on the severity of clinical symptoms, hemodynamic, asphyxic, abdominal and cerebral forms (variants of the course) of anaphylactic shock are conventionally distinguished. Their symptoms are always present to a certain extent in the generalized form of shock.

In the hemodynamic form of shock in patients, the clinical picture, along with hypotension, is dominated by pain in the heart area, arrhythmias. Perhaps the development of acute myocardial infarction (in 25%) and acute left ventricular failure. Most often, patients have supraventricular tachycardia, less often - sinus bradycardia, ventricular fibrillation and asystole. This form is more common in drug-induced anaphylactic shock.

The asphyxic form is characterized by the appearance of shortness of breath (bronchospasm, pulmonary edema) or hoarseness and stridor breathing (laryngeal edema). These symptoms are more common in patients with bronchial asthma. The severity of the patient's condition and the prognosis are determined by the degree of acute respiratory failure. In the abdominal form in patients, as a result of spasm of the smooth muscles of the intestine and the formation of erosions, the clinical picture is dominated by epigastric pain, symptoms of peritoneal irritation, involuntary defecation, and melena. This form is more common in food allergies.

The cerebral form is characterized by the occurrence of psychomotor agitation, stupor, convulsions and meningeal symptoms, which are caused by swelling of the brain and meninges.

Anaphylactic shock can develop in patients during intubation during surgical interventions. It is manifested by hypotension, tachycardia, shortness of breath, cyanosis. It is difficult to notice the appearance of skin changes (urticaria, Quincke's edema, hyperemia, etc.) during intubation, since the patient is covered with surgical linen.

4. Diagnosis and treatment

Manifestations of anaphylaxis (anaphylactoid reaction) that require immediate diagnosis and appropriate treatment include cardiovascular symptoms (dizziness, fainting and palpitations), abdominal symptoms (bloating, nausea, vomiting and tenesmus), upper respiratory symptoms (nasal congestion, rhinorrhea and sneezing). It is known that in terms of the frequency of deaths in AS, respiratory causes are in first place (74%), and cardiovascular causes are in second place (24%).

When examining a patient, it is necessary to pay attention to the following signs: reddening of the face, urticaria, swelling of the lips, uvula, tongue or other areas, wheezing on exhalation and / or on inspiration, cyanosis and arterial hypotension. Of particular importance to the clinician is the immediate evaluation of the cardiac and respiratory systems for airway obstruction, bronchospasm, or shock.

Additional studies are important for the differential diagnosis of anaphylactic shock and the establishment of its cause in difficult cases, as well as the early diagnosis of complications observed during recovery from anaphylactic shock. In the clinical analysis of blood in patients, leukocytosis with eosinophilia is noted, less often - anemia and thrombocytopenia. In a biochemical blood test, with the development of appropriate complications, an increase in the concentration of creatinine, potassium, bilirubin, transaminases (ALT, AST), creatine phosphokinase, alkaline phosphatase, and a decrease in the prothrombin index can be observed. Chest x-rays may show signs of interstitial pulmonary edema. The electrocardiogram reveals supraventricular arrhythmias, T wave inversion. Approximately a quarter of patients may develop acute myocardial infarction (deep Q wave, elevation of the S-T segment in the corresponding leads). According to the indications, consultations are carried out by narrow specialists (ophthalmologist, neuropathologist, etc.). To establish the cause of shock in difficult cases, allergen-specific IgE to suspected allergens is determined using radioallergosorbent, enzyme immunoassay, or chemiluminescent analysis.

Laboratory indicators used for the differential diagnosis of anaphylactic shock.

In recent years, a method for determining the level of β-tryptase has been used to confirm anaphylaxis.

β-tryptase is a neutral protease stored in the secretory granules of human tissue basophils (mast cells) and released by them during degranulation. In normal blood, β-tryptase is not detected (< 1 нг/мл). Повышенные уровни в-триптазы в крови показывают, что происходит, активация тканевых базофилов с выделением медиатора либо под влиянием IgE (и тогда это анафилаксия), либо под влиянием либераторов (и тогда это анафилактоидная реакция). Чем тяжелее клинически протекает реакция, тем больше вероятность, что уровень в-триптазы сыворотки возрастет. Триптаза сыворотки не повышается при некоторых анафилактоидных реакциях, не сопровождающихся активацией тканевых базофилов (например, при активации комплемента). Уровень в-триптазы сыворотки достигает пика через 1-2 ч после начала анафилаксии, а затем снижается с периодом полураспада около 2 ч. Повышенный уровень в-триптазы можно использовать для дифференциации анафилаксии от других явлений с подобными клиническими характеристиками, особенно при наличии артериальной гипотензии. Наиболее информативным является определение уровня триптазы сыворотки через 1-1,5 ч после появления симптомов, но, в зависимости от максимального уровня триптазы, повышенное количество ее иногда выявляется через 6-12 ч после эпизода.

Each institution that works with drugs that can cause an anaphylactic reaction (primarily drug allergy) should have at its disposal the following equipment and medicines to provide assistance:

1. Stethoscope and sphygmomanometer;

2. Tourniquets, syringes, needles for hypodermic and intravenous injections;

3. A solution of adrenaline hydrochloride 0.1%;

4. Oxygen and equipment for its supply;

5. Solutions for intravenous infusions and related equipment;

6. Oral ducts;

7. Diphenhydramine (diphenhydramine);

8. Bronchodilators for intravenous or inhalation administration;

9. Corticosteroids for intravenous administration;

10. Vasoconstrictors.

11. Means for maintaining cardiac activity.

It is generally accepted that the correct use of the above equipment and drugs by professionally trained personnel will provide effective primary treatment in most (if not all) cases of acute anaphylactic reactions occurring in hospitals.

1. Diagnose the presence or suspicion of anaphylactic shock;

2. Put the patient in a horizontal position and raise the lower limbs;

3. Frequently check vital signs (every 2-5 minutes) and stay with the patient;

4. Inject a 0.1% solution of adrenaline hydrochloride: adults - 0.01 ml / kg up to a maximum dose of 0.2-0.5 ml every 10-15 minutes if necessary; children - 0.01 ml / kg up to a maximum dose of 0.2-0.5 ml subcutaneously or intramuscularly, and if necessary, repeat every 15 minutes, up to two doses. Adrenaline, being an activator of b- and b-adrenergic receptors, remains the first drug of choice in the treatment of anaphylactic shock. The effect of adrenaline on β-adrenergic receptors contributes to vasoconstriction and a decrease in the permeability of the capillary membrane. In turn, by acting on β-adrenergic receptors, adrenaline eliminates the spasm of the smooth muscles of the respiratory tract. In addition, by increasing the level of cyclic AMP in cells, adrenaline thereby suppresses the process of degranulation of tissue basophils (mast cells);

5. Give oxygen - usually 8-10 l / min; lower concentrations may be sufficient in patients with chronic obstructive pulmonary disease;

6. Maintain an open airway;

7. Introduce antihistamines: 25-50 mg of diphenhydramine (diphenhydramine) (children - 1-2 mg / kg), usually parenterally;

8. If anaphylactic shock has developed after the injection of the drug, inject 0.15-0.3 ml of a 0.1% solution of adrenaline hydrochloride at the site of the previous injection to inhibit further absorption of the injected drug;

9. In the presence of uncontrolled arterial hypotension or persistence of bronchospasm, when providing assistance on an outpatient basis, the patient must be hospitalized;

10. In case of arterial hypotension, administer replenishing solutions intravenously, use vasoconstrictors;

11. In the treatment of bronchospasm, it is preferable to use a 2-agonist at intervals or continuously; it is possible to use aminophylline intramuscularly (24% solution 1-2 ml) or slowly intravenously (2.4% solution - 10 ml);

12. Administer 5mg/kg hydrocortisone (or about 250mg) intravenously (in mild cases, 20mg oral prednisolone may be given). The main goal is to reduce the risk of recurrence or prolongation of an anaphylactic reaction. If necessary, these doses can be repeated every 6 hours;

13. In refractory cases that do not respond to adrenaline, for example, due to the fact that the patient received a β-adrenergic blocker, it is recommended to administer intravenously a single dose of 1 mg of glucagon; if necessary, you can enter continuously 1-5 mg of glucagon per hour;

14. Patients receiving a β-blocker who do not respond to epinephrine, glucagon, intravenous fluids, and other therapies are sometimes given isoproterenol (a β-agonist with non-β-agonist characteristics). It should be borne in mind that although isoproterenol is able to overcome the decrease in myocardial contractility caused by β-blockers, however, it can increase arterial hypotension, causing peripheral vasodilation, and also cause the development of cardiac arrhythmias and myocardial infarction. In this regard, it is necessary to control the activity of the heart;

15. Medical institutions where patients may develop anaphylactic shock should conduct periodic training sessions for medical personnel on the diagnosis and treatment of this condition;

5. Prevention

Measures to prevent anaphylactic shock can be divided into three groups:

1) public;

2) general medical;

3) individual.

Public events include:

1. Improving the technology for the manufacture of medicines and preparations for immunization (vaccines, sera, g-globulins, etc.)

2. The fight against environmental pollution by products of production of enterprises of the chemical and pharmaceutical industries.

3. Strict regulation or prohibition of the use of drug additives as preservatives in food products (penicillin, acetylsalicylic acid), vaccines (kanamycin, gentamicin) and blood products (levomycetin).

4. Dispensing antibiotics from pharmacies only by prescription.

5. Informing the population and the medical community about adverse reactions, including allergic ones, to medicines.

General medical prevention of shock consists of the following measures:

1) reasonable prescribing of drugs to patients;

2) the fight against polypharmacy, i.e. simultaneous administration of a large number of medications to the patient; in this case, potentiation of their effect and the transformation of therapeutic doses into toxic ones can be observed;

3) an indication of intolerable drugs on the title page of the case history or outpatient card in red ink;

4) use for injections only disposable syringes and needles;

5) observation of patients after injection for at least or within 30 minutes;

6) providing each treatment room with an anti-shock kit.

Individual prevention of drug anaphylactic shock includes:

1. Careful collection of allergic anamnesis. When talking with a patient, it is important to pay attention to the following circumstances:

a) whether the patient and his relatives suffer from allergic diseases;

b) whether the patient has received the prescribed drug before;

c) what drugs the patient was treated for a long time and a lot;

d) whether allergic reactions were noted after taking the medicines. Be sure to specify adverse reactions when prescribing antibiotics, sulfonamides, analgesics, local anesthetics, iodine preparations, blood substitutes, vitamins;

e) whether the patient has fungal diseases of the skin and its appendages;

e) whether there is professional contact with drugs. As a rule, it occurs in workers of pharmaceutical enterprises, warehouses, pharmacies, medical institutions;

g) whether the patient has signs of epidermal sensitization. Patients with hypersensitivity to animals may develop severe allergic reactions to injections of preparations containing heterologous proteins (serums: antitetanus, antidiphtheria, antistaph. Kilococcal, antilymphocytic, etc., anti-rabies gamma globulin, etc.);

h) whether the patient had previously received vaccines and sera and what was their tolerability. When drug intolerance is detected, it is impossible to administer to the patient not only the “guilty” drug, but also drugs that have common antigenic determinants with it.

List of used literature

1. Immunology, Khaitov R.M., Ignatieva G.A., Sidorovich I.G.

2. Yarilin - Immunology - 2010 - GEOTRA-MEDIA

3. Drannik G.N. - Clinical Immunology and Allergology

4. Kovalchuk - Clinical immunology and allergology.

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Acute allergic reactions (anaphylactic shock, anaphylaxis). Study of anaphylaxis by Charles Richet. The frequency of episodes of anaphylaxis. Causes of anaphylactic reactions in children. Clinic of anaphylactic shock. The urgency of a complex of therapeutic measures.

presentation, added 02/11/2014


Normal immune response to antigenic substances. The mechanism of development of anaphylactic shock, its clinical manifestations. Causes of angioedema. Types and forms of drug allergy. Diagnosis of multiform exudative erythema.

presentation, added 02/09/2013


Stages of development and severity of hemorrhagic shock, its clinical picture and pathogenesis. Causes of acute blood loss: various injuries and diseases. Compensatory reactions of the functional systems of the body. Diagnosis and treatment of hemorrhagic shock.

abstract, added 10/17/2013


The main pathogenetic mechanisms of shock states in trauma. Clinical picture of traumatic shock. Diagnosis of the amount of blood loss according to the Algover index. Emergency assistance at the scene of the incident, measures during transportation and in the hospital.

test, added 02/27/2010


Anaphylactic shock of drug etiology caused by the administration of antibiotics, novocaine, aspirin and thiamine is a severe general reaction of the body that develops in response to the administration of substances to which patients have hypersensitivity.

1. Anaphylactic- antigen-antibody reaction.

2. Anaphylactoid- non-immune, without the participation of the antigen-antibody complex, direct destruction of mast cells and release of inflammatory mediators.

clinical picture. Manifestations of anaphylactic shock are due to a complex set of symptoms and syndromes. Shock is characterized by rapid development, rapid manifestation, severity of the course and consequences.

Conventionally, 5 variants of clinical manifestations of anaphylactic shock can be distinguished

- With predominant lesion of the cardiovascular system - the patient suddenly develops a collapse, often with loss of consciousness. Of particular danger in terms of prognosis is the clinical variant of loss of consciousness with involuntary urination and defecation. At the same time, other manifestations of an allergic reaction (skin rashes, bronchospasm) may be absent.

- With a predominant lesion of the respiratory system in the form of acute bronchospasm (asphyxic or asthmatic variant). This option is often combined with sneezing, coughing, a feeling of heat throughout the body, reddening of the skin, hives, and heavy sweat. Be sure to join the vascular component (decrease in blood pressure, tachycardia). In this regard, the color of the face changes from cyanotic to pale or pale gray;

- With predominant damage to the skin and mucous membranes. The patient experiences severe itching followed by the development of urticaria or angioedema. At the same time, symptoms of bronchospasm or vascular insufficiency may occur. Of particular danger is the angioedema of the larynx, which is manifested first by stridor breathing, and then by the development of asphyxia.

With the above clinical variants of anaphylactic shock, symptoms may appear that indicate involvement in the process of the gastrointestinal tract: nausea, vomiting, acute colicky abdominal pain, bloating, diarrhea (sometimes bloody);

- with a predominant lesion of the central nervous system (cerebral variant). Neurological symptoms come to the fore - psychomotor agitation, fear, severe headache, loss of consciousness and convulsions, reminiscent of status epilepticus or cerebrovascular accident. Respiratory arrhythmia is noted;

- With predominant lesion of the abdominal organs (abdominal). In these cases, the symptoms of an "acute abdomen" (sharp pain in the epigastric region, signs of peritoneal irritation) are characteristic, leading to an incorrect diagnosis of perforated ulcer or intestinal obstruction. Painful abdominal syndrome usually occurs 20-30 minutes after the first signs of shock appear. In the abdominal variant of anaphylactic shock, there are shallow disorders of consciousness, a slight decrease in blood pressure, the absence of severe bronchospasm and respiratory failure.

There is a certain pattern: the less time has passed from the moment the allergen enters the body, the more severe the clinical picture of shock. The highest percentage of deaths is observed with the development of shock after 3-10 minutes from the moment the allergen enters the body, as well as with a fulminant form.

Although in most cases the diagnosis of anaphylactic shock is not difficult, sometimes it is necessary to differentiate it from acute cardiovascular insufficiency, myocardial infarction, epilepsy, sun and heat stroke, pulmonary embolism, etc.

Thus, given the acute course and severe condition of patients with anaphylactic shock, the need for emergency intensive care and the lack of specific laboratory data available for use in wide practice, it should be stated that diagnostics shock is based on the main typical clinical manifestations and anamnestic data.

Clinical variants of the course of anaphylactic shock.

1. Acute malignant- no complaints, pronounced collapse, resistant to therapy, poor prognosis, retrospective diagnosis.

2. Acute benign- stunning, moderate respiratory and circulatory disorders, effective therapy.

3. Abortive- symptoms disappear quickly, the most favorable course.

4. lingering― more than 6 hours, allergen of the prolonged action.

5. Acute relapsing course- repeated shock after 4-5 to 10 days, an allergen of prolonged action.

Treatment of anaphylactic shock consists in providing urgent assistance to the patient, since minutes and even seconds of delay and confusion of the doctor can lead to the death of the patient from asphyxia, severe collapse, cerebral edema, pulmonary edema, etc.

It must be remembered that injections of all drugs should be made with syringes that have not been used to administer other medications. The same requirement applies to the drip infusion system and catheters in order to avoid recurrent anaphylactic shock.

The complex of therapeutic measures should be absolutely urgent, carried out in a clear sequence (about the possibilities at the same time) and have certain patterns:

First of all, it is necessary to lay the patient down, turn his head to the side, push the lower jaw to prevent retraction of the tongue, asphyxia and to prevent aspiration of vomit. If the patient has dentures, they must be removed. Provide fresh air to the patient or inhale oxygen;

immediately introduce a 0.1% solution adrenaline. If there is no venous access and it is not possible to quickly catheterize a vein, adrenaline should be administered intramuscularly at an initial dose of 0.3-0.5 ml. Intramuscular injection can be performed as quickly as possible. It was noted that in many cases of anaphylactic shock, even intramuscular administration of mandatory anti-shock agents is enough to completely normalize the patient's condition. It is impossible to inject more than 1 ml of adrenaline into one place, since, having a large vasoconstrictor effect, it also inhibits its own absorption. The drug is injected fractionally by 0.3-0.5 ml into different parts of the body every 10-15 minutes until the patient is removed from the collaptoid state or vein catheterization. Mandatory control indicators for the introduction of adrenaline should be indicators of pulse, respiration and blood pressure;

If possible, it is necessary to stop the further intake of the allergen into the body - stop the administration of the drug, carefully remove the sting with a poisonous sac if a bee has stung. In no case should you squeeze out the sting or massage the bite site, as this enhances the absorption of the poison. Apply a tourniquet above the injection (stinging) site, if localization allows. Prick the injection site (stings) with a 0.1% solution of adrenaline in an amount of 0.3-1 ml and apply ice to it to prevent further absorption of the allergen. When instilling an allergenic medication, the nasal passages or the conjunctival sac must be washed with running water. It must be remembered that if anaphylactic shock occurs in a treatment room or dressing room, the air of which is saturated with vapors of various drugs, the patient after an injection of adrenaline, hormones and cordiamine must be urgently placed in a separate ward or other room, and then continue intensive therapy. When taking the allergen orally, the patient's stomach is washed, if his condition allows;

In parallel with the initial measures, it is advisable to puncture the vein and insert a catheter for infusion of fluids and drugs;

In case of hypotension (immediately - with intravenous access or after the initial intramuscular injection), adrenaline is administered intravenously slowly at a dose of 0.25 to 0.5 ml, previously diluted in 10 ml of isotonic sodium chloride solution, or as an infusion of 1- 4 µg/min. in adults (in children - 0.1 mcg / kg / min.). Perhaps endotracheal administration - 1 ml of solution 1:1000 per 10 ml of 0.9% solution of sodium chloride. It is necessary to control blood pressure, pulse and respiration. If persistent hypotension persists against the background of severe tachycardia, it is necessary to establish a drip injection of 1-2 ml of a 0.2% norepinephrine solution in 300 ml of a 5% glucose solution;

· For restoration of BCC and improve microcirculation, crystalloid and colloid solutions must be administered intravenously. An increase in BCC is the most important condition for the successful treatment of hypotension. Infusion therapy can be started with the introduction of isotonic sodium chloride solution, Ringer's solution or lactosol in an amount up to 1000 ml. In the future, it is advisable to use colloidal solutions: 5% albumin solution, dextrans (rheopolyglucin), hydroxyethyl starch. The amount of injected fluids and plasma substitutes is determined by the value of blood pressure, CVP and the patient's condition;

· corticosteroid drugs used from the very beginning of anaphylactic shock, since it is impossible to predict the severity and duration of an allergic reaction. Initial doses of hormones in the acute period: hydrocortisone 100 mg IV or methylprednisolone 40-250 mg (1-2 mg/kg), IV every 6 hours. The drugs are administered intravenously. The duration of treatment and the final dose of the drug depend on the patient's condition and the effectiveness of the relief of an acute reaction;

with bronchospasm that does not respond to adrenaline - inhaled β-agonists. To stop bronchospasm against the background of stopped hypotension, intravenous administration of a 2.4% solution is also recommended. eufillina with 10 ml of isotonic sodium chloride solution or 40% glucose solution. With persistent bronchospasm, the dose of eufillin is 5-6 mg / kg of body weight;

In the event of stridor breathing and the absence of the effect of complex therapy, it is necessary to immediately intubate. In some cases, according to vital indications, they do conicotomy;

It is necessary to ensure adequate pulmonary ventilation: be sure to suck out the accumulated secret from the trachea and oral cavity, and also, until the relief of a serious condition, carry out oxygen therapy; if necessary - IVL or IVL;

· antihistamines it is better to enter after the restoration of hemodynamic parameters, since they do not have an immediate effect and are not a means of saving lives. Some of them may themselves have a hypotensive effect, especially pipolfen (diprazine).

It should be noted that suprastin should not be administered in case of allergy to aminophylline. The use of pipolfen is contraindicated in anaphylactic shock caused by any drug from the group of phenothiazine derivatives.

Antihistamines can be administered intramuscularly or intravenously: 1% diphenhydramine solution up to 5 ml or tavegil solution - 2-4 ml; every 6 hours. The introduction of H 2 blockers of histamine receptors (famotidine, ranitidine) is also shown.

In case of convulsive syndrome with strong excitation, 5-10 mg of diazepam should be administered intravenously.

If, despite the therapeutic measures taken, hypotension persists, the development of metabolic acidosis should be assumed and an infusion of sodium bicarbonate solution should be started at the rate of 0.5-1 mmol / kg of body weight, control of CBS;

With the development of acute pulmonary edema, which is a rare complication of anaphylactic shock, it is necessary to carry out specific drug therapy. The clinician must necessarily differentiate hydrostatic pulmonary edema, which develops in acute left ventricular failure, from edema due to increased membrane permeability, which occurs most often in anaphylactic shock. The method of choice in patients with pulmonary edema that has developed as a result of an allergic reaction is mechanical ventilation with positive pressure (+5 cm of water column) at the end of exhalation (PEEP) and the simultaneous continuation of infusion therapy until hypovolemia is completely corrected

In case of cardiac arrest, the absence of a pulse and blood pressure, urgent cardiopulmonary resuscitation is indicated.

SEPTIC SHOCK

Patients with septic shock represent a special category, clinically and pathophysiologically significantly different from the category of patients with cardiogenic and hemorrhagic shock. The hemodynamic status in septic shock is significantly different from the hemodynamic changes characteristic of other categories of shock. Under normal conditions, microvascular perfusion is regulated in such a way that more intense blood flow is maintained in tissues with a higher level of metabolism. At rest, only 25-30% of the capillaries function, in which 5-10% of the BCC is located. In the early stages of septic shock, TPVR is often reduced, and MOS is increased. The degree of peripheral vasodilation is closely correlated with the severity of the septic process and depends on the intensity of the release of various mediators.

In this case, the distribution of blood flow is disturbed: despite increased cardiac output, due to damage to autoregulation of the peripheral circulation, the perfusion of tissues with a high level of metabolism is insufficient to cover metabolic needs, while tissues with a lower level of metabolism are overperfused. A characteristic feature of septic shock is damage to the mechanism of oxygen extraction by tissues. The development of a systemic inflammatory response (SYR-syndrome) leads to an increase in the energy needs of tissues and an increasing oxygen debt. Violation of tissue oxygen supply, in addition to disorders of autoregulation, is also associated with microaggregation, endothelial and perivascular edema, and damage to intracellular transport mechanisms. Decompensation of septic shock is characterized by the addition of hypovolemia due to leakage of fluid from the vascular bed into the tissues and heart failure. Myocardial depression, on the one hand, is caused by a decrease in coronary blood flow, and, on the other hand, by the influence of various mediators circulating in the blood of septic patients, including tumor necrosis factor (TNF) and myocardial depressant factor (MDF).

As defined by the ACCP/SCCM Consensus Conference:

Septic shock (SS) -this is sepsis with signs of tissue and organ hypoperfusion and arterial hypotension, not eliminated by infusion therapy and requiring the appointment of catecholamines.

Sepsis is a syndrome of systemic inflammatory response to microorganism invasion.

Extended diagnostic criteria for sepsis

General Criteria

• Fever temperature >38°C
• Hypothermia temperature<36°С
• Heart rate >90/min (>2 standard deviations from normal age range)
• Tachypnea
• Disturbance of consciousness
• Edema or the need to achieve positive fluid balance (>20 ml/kg in 24 hours)
• Hyperglycemia (>7.7 mmol/L) in the absence of diabetes

Inflammatory changes

• Leukocytosis >12×109/l
• Leukopenia<4×109/л
• Shift towards immature forms (>10%) with a normal content of leukocytes
• C-reactive protein >2 standard deviations from N
• Procalcitonin>2 standard deviations from N

Hemodynamic changes

• Arterial hypotension: BPsyst<90 мм.рт.ст., АДср < 70 мм.рт.ст., или снижение АДсист более, чем на 40 мм.рт.ст. (у взрослых) или снижение АДсист как минимум на 2 стандартных отклонения ниже возрастной нормы
• SpO2 saturation< 70%
• Cardiac index >3.5 l/min/m3

Manifestations of organ dysfunction

• Arterial hypoxemia PaO2/FiO2<300
• Acute oliguria<0,5 мл/кг/ч
• Increase in creatinine by more than 44 mmol / l (0.5 mg%)
• Thrombocytopenia<100х109/л
• Coagulation disorder: APTT >60 sec or INR >1.5
• Hyperbilirubinemia >70 mmol/l
• Intestinal obstruction (lack of bowel sounds)

Indicators of tissue hypoperfusion

• Hyperlactatemia >1 mmol/l
• Delayed capillary refill syndrome, marbling of extremities

Principles of treatment

1. Sanitation of the focus of infection and antimicrobial therapy
2. Restoration of perfusion and tissue oxygenation
3. Immunomodulation
4. Antitoxic and anticytokine therapy
5. Substitution, symptomatic, maintenance therapy for polyorthane insufficiency

1. Pathogenetic therapy of septic shock is reduced to the rehabilitation of foci of infection, the appointment of broad-spectrum antibiotics. Sanitation of the infectious focus is the cornerstone of the treatment of septic shock. Even the most powerful antibiotics and other methods of detoxification therapy are ineffective in the absence or insufficient sanitation of the focus. Targeted antibiotic therapy is possible after the isolation of the pathogen and the determination of its sensitivity to antibiotics, that is, at best, not earlier than 48 hours. At the same time, early antibiotic therapy (within 30 minutes from fasting) significantly reduces mortality in this category of patients. Therefore, it seems appropriate to use the so-called de-escalation principle of antibiotic therapy with the initial prescription of antibiotics of the broadest possible spectrum of action (carbopenems, fluoroquinolones, 4th generation cephalosporins) followed by replacement, if possible, with an antibiotic of a certain (as a result of bacteriological examination) spectrum.

2.1 hemodynamic support. Infusion therapy belongs to the initial measures to maintain hemodynamics and, above all, cardiac output. According to the American College and the American Association of Critical Medicine, approximately 50% of septic patients can achieve normal hemodynamic parameters with adequate fluid therapy. The main objectives of infusion therapy in patients with sepsis are: restoration of adequate tissue perfusion, normalization of cellular metabolism, correction of homeostasis disorders, reduction in the concentration of septic cascade mediators and toxic metabolites

Infusion therapy is started with the introduction of crystalloids - a bolus of 20 ml / kg for 20-30 minutes, then, after assessing the state of hemodynamics, again, at a rate of about 20-30 ml / kg / hour under the control of CVP and hemodynamic parameters up to a total dose of 4 liters (60 ml /kg)

For infusion therapy in the framework of targeted IT of sepsis and SS, crystalloid and colloid infusion solutions are used with almost the same result.

All infusion media have both their advantages and disadvantages. Taking into account the available results of experimental and clinical studies, today there is no reason to give preference to any of the infusion media. However, it should be borne in mind that adequate correction of venous return and the level of preload requires significantly larger volumes (2–4 times) of infusion of crystalloids than colloids, which is associated with the peculiarities of the distribution of solutions between different sectors. In addition, infusion of crystalloids is more associated with the risk of tissue edema, and their hemodynamic effect is less long-lasting than colloids. At the same time, crystalloids are cheaper, do not affect the coagulation potential and do not provoke anaphylactoid reactions. In this regard, the qualitative composition of the infusion program should be determined by the characteristics of the patient: the degree of hypovolemia, the phase of the DIC syndrome, the presence of peripheral edema and the level of blood albumin, the severity of acute pulmonary injury.

Plasma substitutes (dextrans, gelatinol, hydroxyethyl starches) are indicated for severe BCC deficiency. Hydroxyethyl starches (HES) with a molecular weight of 200/0.5 and 130/0.4 have a potential advantage over dextrans due to a lower risk of membrane leakage and the absence of a clinically significant effect on hemostasis. The use of albumin in critical conditions may contribute to increased mortality. The increase in COD during albumin infusion is transient, and then, under the conditions of the “capillary leakage” syndrome, further albumin extravasation (rebound syndrome) occurs. Albumin transfusion may be useful only if the albumin level is below 20 g/l and there is no evidence of "leakage" into the interstitium. The use of cryoplasma is indicated for coagulopathy of consumption and a decrease in the coagulation potential of the blood. According to most experts, the minimum concentration of hemoglobin for patients with severe sepsis should be in the range of 90–100 g/l. In sepsis and SS, it is necessary to strive for rapid achievement (the first 6 hours after admission) of the target values ​​of the following parameters: CVP 8–12 mm Hg. Art., GARDEN>65 mm Hg. Art., diuresis 0.5 ml/kg/h, hematocrit over 30%, blood saturation in the superior vena cava or right atrium at least 70%.

Low perfusion pressure requires the immediate inclusion of drugs that increase vascular tone and / or inotropic function of the heart. Dopamine and/or norepinephrine are the drugs of first choice for the correction of hypotension in patients with SS. Norepinephrine (at an initial rate of 1 µg/min (in adults) titrated to achieve a systolic pressure of 90 mmHg) increases SBP and increases glomerular filtration. Optimization of systemic hemodynamics under the action of norepinephrine leads to an improvement in renal function without the use of low doses of dopamine. Recent studies have shown that the use of norepinephrine compared with the combination of dopamine in high doses ± norepinephrine leads to a statistically significant decrease in mortality.

Adrenalin- an adrenergic drug with the most pronounced side hemodynamic effects. Adrenaline has a dose-dependent effect on heart rate, blood pressure, cardiac output, left ventricular function, oxygen delivery and consumption. However, this action of adrenaline is accompanied by tachyarrhythmias, deterioration of splanchnic blood flow, and hyperlactatemia. Therefore, the use of epinephrine should be limited to cases of complete refractoriness to other catecholamines.

dobutamine should be considered as the drug of choice for increasing cardiac output and oxygen delivery and consumption at normal or elevated levels of preload. Due to the predominant action on  1 receptors, dobutamine, to a greater extent than dopamine, contributes to an increase in these indicators.

Catecholamines, in addition to supporting blood circulation, can interfere with the course of systemic inflammation by influencing the synthesis of key mediators that have a long-term effect. Under the action of adrenaline, dopamine, norepinephrine and dobutamine, the synthesis and secretion of TNF- by activated macrophages decreased. Cardiocirculatory support drugs should be canceled 24-36 hours after stabilization of central hemodynamics.

Refractory septic shock- persistent arterial hypotension, despite adequate infusion, the use of inotropic and vasopressor support. In the case of the development of refractory septic shock, the introduction of glucocorticosteroids is indicated - hydrocortisone 240-300 mg on the first day. After stabilization of the pressure, the dose can be reduced to 50 mg every 8 hours for the next 48 hours. The duration of therapy is 5-7 days.

2.2 Respiratory support. The lungs very early become one of the first target organs involved in the pathological process in sepsis. Acute respiratory failure (ARF) is one of the leading components of multiple organ dysfunction. Clinical and laboratory manifestations of ARF in sepsis correspond to the syndrome of acute pulmonary injury, and with the progression of the pathological process, to acute respiratory distress syndrome (ARDS). Oxygen inhalation is carried out, and, according to indications, tracheal intubation and mechanical ventilation.

3. The expediency of including intravenous immunoglobulins (IgG and IgG + IgM) is associated with their ability to limit the excessive action of pro-inflammatory cytokines, increase the clearance of endotoxin and staphylococcal superantigen, eliminate anergy, enhance the effect of -lactam antibiotics. The most optimal results with the use of immunoglobulins are obtained in the early phase of shock ("warm shock") and in patients with severe sepsis. Pentaglobin (IgG and IgM), intraglobin (IgG), ronleukin are used.

4. In order to prevent the formation of kinin-like peptides and the accumulation of MDF, the use of protease inhibitors is indicated: contrical at 80000-150000 IU per day or Gordox at a dose of 200-400 CIE, pentoxifylline at a dose of 100-300 mg potentiates the anti-inflammatory effect of adenosine, prostacyclin and class E prostaglandins due to synergy when exposed to cyclic AMP.

5. Prevention and treatment of multiple organ failure, incl.

· correction of microcirculation disorders and systemic coagulation disorders - rheopolyglucin; heparin therapy (unfractionated heparin, low molecular weight heparins) in combination with fresh frozen plasma; activated protein C (drotrecogin-a activated).

· glycemic control

· prevention of the formation of stress ulcers of the gastrointestinal tract.

In conclusion, it should be said that the clinical criteria for the adequacy of antishock therapy are:

1). stabilization of central hemodynamic parameters (SBP 60-100 mm Hg, CVP 60-100 mm water column, heart rate 60-100 bpm);

2). normalization of hemic parameters (Hb 100 g/l, Ht 0.3);

3). restoration of diuresis (0.5-1 ml / min).

It should be remembered that the way out of the state of shock implies not only the restoration of normal blood circulation, but also the absence of persistent multiple organ disorders.

Independent work of students

Task number 1

Examine a patient admitted to the ICU with a diagnosis of gastrointestinal bleeding. Determine the amount of blood loss. For this:

Determine blood pressure, pulse, respiratory rate, diuresis, CVP, symptom of "white spot";

Calculate the shock index (Algover);

Determine the amount of the BCC deficit in% of the due;

Calculate the amount of blood loss using the Moore formula.

Task number 2

Analyze the medical history of a patient with severe nosocomial pneumonia, systemic inflammatory response syndrome, who is in the intensive care unit. For this:

Analyze the degree of hemodynamic disorders and their correction;

Evaluate the severity of respiratory failure in the patient according to the diaries of dynamic observation; evaluate the proposed method of treatment of respiratory failure, if necessary, make adjustments and justify them;

IX. Clinical tasks

Task #1

In a patient admitted to the hospital with a diagnosis of intra-abdominal bleeding, pulse 112 per minute, BP system. 90 mmHg Determine the level of blood loss and evaluate it according to P.G. Bryusov?

Task #2

A 34-year-old patient was taken to the hospital after a fire. There is no thermal damage to the skin, there are traces of soot in the area of ​​the nose and lips. Objectively - shortness of breath up to 28 per minute, noisy breathing, auscultatory - hard, a large number of wheezing. What is your presumptive diagnosis? Should the patient be admitted to the ICU?

Test control:

1) Criteria for hospitalization in the ICU for adults:

a) 3rd degree burn more than 5% BSA.*

b) 3rd degree burn more than 15% BSA.

c) Isolated thermal injury.*

d) Second degree burn more than 10% BSA.

e) Burns around the circumference of the torso.*

f) Facial burns.*

2) What is the main pathogenetic link in burn disease?

a) Impaired lung function.

b) Impaired kidney function.

c) Hypovolemia.*

d) Impaired function of the respiratory system.

3) Intensive care measures for septic shock:

a) Sanitation of inflammation*

b) Infusion therapy*

c) Oxygen therapy*

d) Use of vasoactive drugs*

e) Antibiotic therapy*

f) Epidural blockade,

g) Immunocorrective therapy*

4) Indications for the use of corticosteroids in sepsis:

a) The initial stage of septic shock with a simultaneous entry of the infection into the blood*

b) Always indicated in sepsis

c) Refractory septic shock*

5) In type 1 allergy, released inflammatory mediators after degranulation of mast cells and basophils primarily affect the following target organs, with the exception of:

a) Smooth muscles of the bronchi

b) Vascular smooth muscle

c) Skeletal muscles*

d) Endothelium of postcapillary venules

e) Peripheral nerve endings

6) The clinical picture of immediate type hypersensitivity is least of all due to the following inflammatory mediator released during degranulation of mast cells and basophils:

a) Histamine

b) Prostaglandins

c) Catecholamines*

d) Heparin

7) During an anaphylactic reaction, the following substances are released except:

a) Histamine

b) Slow-reacting anaphylaxis substance

c) Heparin

d) Adrenaline*

8) The symptom of the "white spot" is normally:

a) 2 seconds.*

b) No more than 3 seconds.

c) 1 second.

d) No more than 4 seconds.

9) Normally, hourly diuresis is:

a) 0.5-1 ml/kg.*

b) 1-2 ml/kg.

c) 0.1-0.3 ml/kg.

d) 2-3 ml/kg.

10) In young men, the BCC is equal to:

a) 60 ml/kg.

b) 50 ml/kg.

c) 70 ml/kg.*

d) 80 ml/kg.

Answers:

Task #1

The data obtained is sufficient to determine the Algover shock index. SI is equal to 112/90 = 1.2, which corresponds to blood loss of 40% of the BCC, which is pathological in appearance, large in volume and severe in the degree of hypovolemia.

Task #2

The patient has a thermal inhalation injury, which is an indication for hospitalization in the intensive care unit.

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