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

Shock

METABOLISM/2.html">THE CONCEPT OF "shock" is constantly evolving along with our understanding of the body's vital processes. In the not-too-distant past, shock was simply defined as a specific reaction to extraordinary stimuli accompanied by arterial hypotension. Today, shock is understood as a symptom complex of vital organ dysfunctions resulting from a mismatch between tissue Blood flow and metabolic demand.

Emphasizing this hallmark feature of Circulatory Disorders, shock is also referred to as a "microcirculatory crisis." However, even this definition is not exhaustive. Given that hypoperfusion leads to tissue Hypoxia, P. L. Marino (1998) considers inadequate tissue oxygenation to be the central problem in shock. Taking this reasoning a step further, it is logical to conclude that the ultimate endpoint of shock—following central hemodynamic disturbances and tissue hypoperfusion—is the disruption of tissue metabolism.

The Etiology of shock can be diverse, based on which several types are distinguished: traumatic, hemorrhagic, burn-induced, hypochloremic, exotoxic, cardiogenic, septic, anaphylactic, etc.

Initially, the Pathogenesis of shock varies significantly depending on its etiology, but over time, the pathophysiological changes of its various forms converge, and in the final stages, shock acquires quite similar features. For instance, the triggering event in dehydration shock is a deficit in circulating blood volume (primary hypovolemic shock). In cardiac and Pulmonary Embolism, the Pumping Function of The Heart is impaired (cardiogenic shock). Septic and anaphylactic shock arise from a decrease in peripheral and venous vascular tone (vascular or vasogenic shock).

However, such a pathogenetic Classification of shock is rather schematic. In practice, etiologically diverse forms of shock often have a mixed pathogenesis. For example, Traumatic shock can simultaneously be primary hypovolemic (blood loss, plasma loss), cardiogenic (cardiac contusion, The Effect of the "myocardial depressant factor," endogenous intoxication in Crush syndrome), and vascular (pain reflex, The Influence of kinins).

Subsequently, all types of shock merge in their pathogenesis because a decrease in venous return to the heart or impaired pumping function leads to a reduction in cardiac output. The body responds to this decrease with a protective reaction known as adrenergic centralization of Circulation. This response is most pronounced in primary hypovolemic shock, less so in cardiogenic and septic shock, and is practically absent in anaphylactic shock.

The purpose of this reaction is to maintain cardiac output, blood pressure, and preferential Blood supply to Organs that are vital for immediate survival. This special adaptive mechanism is triggered by signals from baroreceptors and volume receptors located in the aortic arch.

These receptors react to the decrease in cardiac output via the Hypothalamus and neurohypophysis, which produce corticotropic hormone, increasing The activity of the sympathetic Nervous system and releasing catecholamines into the bloodstream.

By acting on cardiac ß-adrenergic receptors and vascular wall a-adrenergic receptors, adrenaline and noradrenaline increase heart rate and peripheral resistance, thereby temporarily maintaining normal cardiac output and blood pressure. However, vasoconstriction does not affect all peripheral vessels uniformly, but only those possessing a-receptors. As a result, centralization of circulation occurs—meaning the redistribution of the remaining blood volume with preferential flow to The Heart and Brain at the expense of organs less critical for acute survival (Liver, Pancreas, intestines, Kidneys, Skin, and Muscles). Initially, this sympathoadrenal reaction is purposeful, as it ensures normal BLOOD FLOW IN the coronary and cerebral vessels. However, if the circulating blood volume is not rapidly restored, There is a looming threat of ischemic damage to the organs supporting this circulatory centralization.

The pathogenesis of cardiogenic shock differs from primary hypovolemic shock in that the primary issue is not hypovolemia, but an acute failure of the heart's pumping function. This can be caused by myocardial damage resulting from inflammation and endotoxicosis. Stroke volume and cardiac output decrease, leading to blood stasis at the microcirculatory level. The Circulatory system's response to reduced blood volume mirrors that of hypovolemia: heart rate and peripheral vascular resistance increase due to a sympathoadrenal reaction.

Shock resulting from hypovolemia or impaired cardiac pumping function is classified as a hypodynamic form, which differs in the filling state of the microcirculatory bed. In hypovolemic shock, microcirculatory filling is reduced, whereas in cardiogenic shock, it is increased due to the heart's pumping failure and the pooling of blood outflowing from the organs.

The underlying factor causing shock in anaphylaxis and Sepsis is the primary disruption of vascular regulation. However, the mechanisms driving these disorders differ.

Septic shock was previously associated with the direct action of Bacterial toxins and breakdown products generated under their influence. It is now universally recognized that only bacterial exotoxins—protein toxins such as diphtheria or botulinum toxin—can directly cause irreversible necrotic cellular damage in the patient. Endotoxins, which are lipopolysaccharides from the Introduction/37.html">Bacterial Cell wall, do not cause cell necrosis on their own. Instead, they stimulate the patient's Cells (primarily macrophages) to produce substances known as cytokines—inflammatory mediators that lead to self-inflicted cellular damage (a form of cellular "cannibalism"). Cytokines trigger the systemic inflammatory response syndrome (SIRS), characterized by vasodilation and a drop in blood pressure. Vasodilation is mediated by nitric oxide (NO), one of the most potent vasodilators.

A generalized bodily reaction in the form of SIRS, accompanied by a clinical picture resembling septic shock, can also develop in response to massive tissue necrosis and damage, as seen in Burns, pancreatic necrosis, severe trauma, or Hemorrhage. It turns out that clinically, it is impossible to differentiate pathological states caused by infection from changes driven by tissue breakdown products. Evidently, the mechanisms of septic shock development described here are also characteristic of other shockogenic factors, notably anaphylaxis.

In anaphylactic shock, the release of histamine and histamine-like substances into the bloodstream causes a loss of tone in both peripheral and capacitance venous vessels. Peripheral resistance drops sharply, and blood pressure plummets. A mismatch arises between the available circulating blood volume and the vascular capacity, drastically reducing venous return. The myocardial contractile force declines, causing blood pressure to fall further. The sympathoadrenal reaction fails to manifest because the response to sympathetic stimuli is impaired. Only later, if the patient survives, does vasodilation give way to vasoconstriction.

Regardless of the etiopathogenetic features of shock, capillary blood flow inevitably decreases. Consequently, the delivery of oxygen and energy substrates to Tissues is disrupted, Cellular metabolism is impaired, and lactic acid accumulates, leading to acidosis. Acidosis causes precapillary vessels to dilate, decentralizes circulation, and increases blood coagulability. Blood flow slows down even further, blood pools in the capillaries, hydrostatic pressure within them rises, and plasma shifts into the interstitium.

In sluggish and hemoconcentrated blood, cellular aggregation and increased viscosity occur. All of this leads to an almost insurmountable resistance to blood flow, followed by microthrombus formation. In extreme cases, tissue blood flow ceases entirely—a process of disseminated intravascular coagulation. Such microcirculatory failure is characteristic of all types of shock and, regardless of the cause, leads to cellular dysfunction. Energy production within cells declines, cellular membrane function deteriorates, and specific organ Functions decrease or cease altogether.

The Lungs, kidneys, and liver are particularly sensitive to shock. Functional disorders of these organs (referred to as "shock organs"—"shock lung," "Shock Kidney," "shock liver") are reversible once shock is resolved. However, if the shock state affecting these organs is prolonged, necrotic changes set in, manifesting as organ failure or dysfunction after resuscitation. In such cases, clinicians speak of "shock lung," "shock kidney," and "shock liver," collectively termed "multiple organ dysfunction syndrome." Clinical signs of shock are best examined according to its etiological variety.

Hemorrhagic shock develops as a result of primary hypovolemia. Shock resulting from burns and dehydration is also primarily hypovolemic in nature.

The Specific features of its pathogenesis lie in the body's adaptation to hypovolemia through alterations in the capacity of the Venous system, which in a healthy individual holds about 75% of the circulating blood volume. However, the capacity to mobilize blood from venous reservoirs is limited. When 10% or more of the blood volume is lost, central venous pressure begins to fall, venous return to the heart decreases, and a "low output syndrome" ensues, leading to reduced tissue perfusion. In response, circulation becomes centralized: less vital organs (skin, muscles, the splanchnic bed—intestines, kidneys, liver) are excluded from active circulation, while blood supply to vital organs (brain, heart, lungs) is preserved. Vasoconstriction leads to tissue hypoxia and The Development of acidosis. Under these conditions, pancreatic Proteolytic Enzymes enter the bloodstream and stimulate The production of kinins, which increase vascular permeability, causing Water and electrolytes to shift into the interstitium. As a result, Blood Cells aggregate in the capillaries, creating conditions conducive to thrombosis. This process directly precedes the irreversibility of shock.

The clinical signs of shock depend on the critical reduction of capillary blood flow across various organs and tissues. Since the time of Pirogov, erectile and torpid phases have been distinguished, with Central Nervous System activity serving as the primary criterion. Admittedly, this general trajectory of shock development is correctly identified and remains utilized in modern classifications of clinical shock stages. However, such a division lacks sufficient Specificity regarding the pathophysiological changes occurring within the body during shock. Phase-based central nervous system disorders are rather integrative indicators of shock depth and are inadequate for guiding specific intensive care tactics for trauma victims. For practical purposes, given the concept of shock as a "microcirculatory crisis," three stages are distinguished:

I. Compensated reversible shock. Blood volume deficit does not exceed 25% (700–1300 ml in an adult). Moderate tachycardia, blood pressure remains normal or slightly decreased. Subcutaneous Veins collapse, central venous pressure drops. Signs of peripheral vasoconstriction appear—cold extremities, delayed capillary refill time ("pale spot" sign), and urine output (normally 1–1.2 ml/min) drops by half.

II. Decompensated reversible shock. Blood volume deficit is 25–45% (1300–1800 ml). Tachycardia reaches 120–140 bpm, systolic blood pressure is < 100 mm Hg, and pulse pressure decreases. Pronounced dyspnea develops, which partially compensates for metabolic acidosis via respiratory alkalosis, though it may also signal "shock lung." Cooling of the extremities and acrocyanosis worsen. Cold sweat appears. Urine output is 0.3 ml/min.

III. Irreversible shock. Blood volume deficit is < 50% (2000–2500 ml), with circulatory decompensation lasting over 12 hours. Pulse exceeds 140 bpm, systolic blood pressure is below 60 mm Hg or undetectable. Consciousness is absent. Oliguria develops.

Treatment for dehydration shock involves sequentially performing the following Procedures:

1. Vein catheterization, preferably central (most commonly subclavian or jugular via the Seldinger technique) if conditions permit.

2. Restoration of circulating blood volume (CBV) via rapid or drip intravenous administration of blood substitutes and blood components. Recently, it has been recommended to initiate emergency infusion therapy with small volumes at the scene and at the onset of shock treatment in the hospital: intravenous administration of 4 ml/kg of 7.5% NaCl solution (in 50 ml doses). This rapidly generates a transmembrane osmotic gradient. Water is immediately redistributed from the interstitial and intracellular spaces into the vascular bed, thereby increasing CBV and mitigating the risk of cellular edema and multiple organ dysfunction syndrome (MODS). The effect manifests within 1 min and persists for about 30 min (U. Kreimeier, 1997).

Even more effective is the combination of a 7.5% NaCl solution with colloid plasma expanders (e.g., 6% polyglucin or 6% hydroxyethyl starch), which facilitate fluid retention within the vasculature. To this end, specialized hypertonic-hyperoncotic solutions have been recently developed; administering 4–6 ml/kg of these solutions into a peripheral vein over 2–5 min rapidly increases blood pressure and cardiac output while concurrently decreasing peripheral resistance by reducing external vascular pressure caused by endothelial edema. This lowers the risk of MODS—specifically, enhancing diuresis. Furthermore, bacterial translocation from the intestine and the incidence of anaphylactic reactions associated with colloid plasma expanders are diminished.

Table 10 outlines a tentative infusion therapy plan for volume resuscitation based on blood loss estimates evaluated using the Allgower shock index (The ratio of pulse rate to systolic blood pressure).

3. Management of metabolic acidosis. Administer 150–300 ml of a 4% sodium bicarbonate solution.

4. Administration of glucocorticoids (0.7–1.5 g of hydrocortisone or equivalent doses of other corticosteroid agents). These not only enhance myocardial contractility but also alleviate peripheral vascular spasm and increase membrane density, safeguarding Cellular Structures and preserving their function during shock. A contraindication to their administration is suspected hemorrhage from an Acute gastric ulcer.

Class="center">Table 10 Transfusion replacement of blood loss (after P. G. Bryusov, 1997, with modifications)

5. Relief of peripheral vasospasm. Neuroleptics (e.g., droperidol 2–4 ml slowly intravenously) or even ganglion blockers, provided that infusion therapy is reliably established and blood pressure is monitored to prevent circulatory collapse.

6. Administration of pancreatic Enzyme Inhibitors—30,000–60,000 IU of Trasylol or Contrical in saline to reduce The rate of pathological kinin formation.

7. Humidified oxygen inhalation.

8. Management of hyperthermia through both physical cooling (applying ice packs) and pharmacological intervention (50% analgin solution 2 ml or rheopyrin 5 ml deeply intramuscularly).

9. Administration of broad-spectrum Antibiotics, as shock induces suppression of The Immune System.

10. Maintenance of adequate diuresis (50–60 ml/h). Against the Background of appropriate infusion therapy, when central venous pressure (CVP) reaches 120–150 mm H₂O, if diuresis remains low, osmotic Diuretics are prescribed (mannitol as a 10–15% solution in 5% glucose—300 ml intravenously as a bolus). If mannitol is ineffective, Lasix (furosemide) is administered at 40–160 mg intramuscularly or intravenously, with a total dose of up to 2000 mg During the first day of treatment for the initial period of ACUTE RENAL FAILURE (ARF).

11. Support of cardiac function with cardiotonic agents. Contraindications to cardiac Glycosides include complete or partial atrioventricular block and The Emergence of ectopic pacemaker foci. If bradycardia develops, ß-adrenoreceptor stimulants are prescribed (isadrine sublingual tablets, 0.005 g). For ventricular arrhythmias, cordarone (150–300 mg) or lidocaine (0.1–0.2 g) is administered intravenously.

Traumatic shock. A distinctive feature of its pathogenesis is multifactoriality: pain, toxemia, hemorrhage, and subsequent hypothermia. In crush syndrome and extensive soft tissue injuries, the primary pathogenic factor is early toxicosis. ARF arises as a result of toxic damage to the renal epithelium and obstruction of the convoluted tubules by Myoglobin casts. In some cases, oliguria and anuria, even in the presence of satisfactory blood pressure, serve as indicators of shock severity. In burn trauma, alongside pain and toxemia, plasma loss from the affected surface is a critical pathogenetic factor accompanied by the development of Protein deficiency.

The clinical picture clearly exhibits the phased progression of shock, first noted in the time of Pirogov, who provided a classic Description of the erectile phase (excitation, normotension or even Hypertension, pallor without cyanosis) and the torpid phase (lethargy, hypodynamia, oliguria, dyspnea, pallor with an earthy hue and cyanosis, cold clammy sweat). Modern systematization of traumatic shock phases involves the same three stages as hemorrhagic shock.

The treatment of traumatic shock employs the same Methods as that of hemorrhagic shock. At the scene and during transport, prompt emergency measures are of paramount importance: ensuring airway patency and adequate pulmonary ventilation, restoring and supporting hemodynamics through rapid infusion of blood substitutes (specifically, 7.5% NaCl solution, polyglucin, Stabizol, or Refortan), applying aseptic wound dressings, immobilizing fractures, proper stretcher positioning (semi-sitting for chest injuries, Fowler's position for traumatic brain injury, horizontal for abdominal injuries, and the "frog position" for pelvic trauma), analgesia (analgesics combined with antihistamines), and cardiac glycosides.

Septic shock (toxico-infectious, endotoxic, bacteremic) develops in cases of Peritonitis, urinary and biliary tract infections, Pneumonia, pancreatic necrosis, septic labor, and abortions, among others. It most commonly arises from Gram-negative Bacteria, though it may also be triggered by other agents (Gram-positive bacteria, anaerobes, Viruses, Fungi, Protozoa).

The features of pathogenesis largely depend on the causative agents of sepsis. Specifically, Gram-negative flora release endotoxins upon disintegration, which stimulate The adrenal medulla to release catecholamines, causing vasoconstriction. Gram-positive flora release exotoxins that induce proteolysis followed by The formation of plasma kinins, which lead to vascular paralysis. Myocardial contractility is impaired under the influence of toxins and hypoxia, while hemoconcentration further exacerbates hemodynamic deterioration. Acute Respiratory Failure (ARF) develops due to "shock lung," impaired function of Respiratory Muscles, tachypnea (as a compensation for metabolic acidosis), hyperthermia, and the Direct impact of bacterial toxins on the respiratory center. Tissue ischemia and toxemia frequently precipitate hepatic failure, causing coagulation disorders characteristic of disseminated intravascular coagulation (DIC), ARF secondary to necronephrosis, pancreatic injury resulting in subsequent hyperglycemia, excessive kinin activation—which increases vascular wall permeability and lowers blood pressure—and hemorrhagic gastroenterohemorrhage (gastroenterocolitis). Secondary immunodeficiency ensues.

The clinical picture combines symptoms of infection (hyperthermia, chills, bacteremia, changes in white and red blood cells), neuropsychiatric, hemodynamic, and respiratory disorders, parenchymal organ damage (kidneys, liver, pancreas), and Homeostasis disturbances (coagulation of the thrombohemorrhagic syndrome type, acid-base balance and water-electrolyte balance disorders, dysproteinemia).

Treatment of septic shock involves the elimination—preferably surgical—of the infection focus, correction of hemodynamic disorders (glycosides, e.g., digoxin 0.025% solution 1 ml diluted in 10 ml of 5% glucose slowly intravenously; dopamine, which at a dose of 0.5–2.0 µg/(kg·min) induces renal vasodilation and enhances renal function, at 2.0–10.0 µg/(kg·min) improves cardiac performance and reduces vascular resistance, and at 10.0 µg/(kg·min) and above causes vasoconstriction, tachycardia, and arrhythmias; coronarodilators and antiplatelet agents [dipyridamole 0.5% 2 ml and isoptin 0.25% 2 ml diluted in 150 ml of 5% glucose as an intravenous drip]; rheological agents [reopolyglucukin up to 1500 ml, neohaemodez up to 500 ml as an intravenous drip]), heparin (5000 IU every 4 h or continuously as an infusion up to 30,000 IU per day)—strictly in the absence of bleeding risk, or heparin fractions (nadroparin 0.3 ml, enoxaparin 40 mg, or dalteparin 5000 IU daily), which are safe even when a bleeding risk exists.

Adequate pulmonary ventilation, fluid loss replacement, and high-calorie (at least 4000 kcal) parenteral Nutrition via Amino Acids and CARBOHYDRATES are ensured (fat emulsions are avoided due to the threat of reticuloendothelial system [RES] blockade).

Metabolic shifts are meticulously corrected by administering glucose at a rate of 1 g/(kg·h) supplemented with Insulin at 1 IU per 2.5–3 g of glucose, anabolic Hormones (testosterone propionate 2 ml every other day, retabolil 1 ml every 7–10 days), a glucose-alcohol mixture to suppress antidiuretic hormone (ADH), the release of which increases in septic shock; protease inhibitors (Contrical up to 60,000 IU per day); and high doses of Vitamins C, B₁, B₆, B₁₂, cocarboxylase (0.05–1.00 g daily intramuscularly or intravenously), and phosphaden (2% solution, 2 ml 3–4 times daily).

Treatment is administered for acute renal failure and intestinal paresis (correction of water-electrolyte balance, stimulation of motility via hypertonic enemas, diadynamic currents, and subcutaneous administration of a 0.05% neostigmine solution, 1 ml twice daily).

Immune modulation (antistaphylococcal immunoglobulin up to 4 doses every other day for 5 days intramuscularly, antistaphylococcal plasma intravenously, biological agents—pentaglobin, sandoglobulin, Monoclonal Antibodies).

Administration of antibiotics with predominantly bactericidal action (Penicillins, including semisynthetic ones, Aminoglycosides, Cephalosporins), fluoroquinolone derivatives, high-dose carbapenems (gentamicin up to 240-400 mg/day, cephalosporins up to 12 g/day).

Bacteriostatic agents (Tetracyclines, chloramphenicol, macrolides) are not recommended. For superinfection Prevention—antifungal drugs (oral nystatin 500,000 IU 3-4 times daily, levorin 500,000 IU 2-4 times daily), intestopan 1-3 tablets 4-6 times daily, amphotericin B, diflucan. Biological agents are prescribed to prevent dysbiosis.

Cardiogenic shock occurs in myocardial infarction, pulmonary embolism, cardiac contusion, pericardial tamponade, and acute myocarditis.

The pathogenetic features include impaired myocardial contractility and the pain factor in myocardial infarction and pulmonary embolism.

Depending on pathogenetic and Clinical Features, the following forms of cardiogenic shock are distinguished:

— reflex shock—vascular tone, which changes reflexively, plays a crucial role;

— true cardiogenic shock—impaired myocardial contractility is decisive;

— arrhythmic shock—caused by cardiac rhythm disorders;

— areactive shock—cardiogenic shock refractory to drug therapy.

Clinical manifestations are characterized by a sharp drop in blood pressure against the background of symptoms typical of myocardial infarction. Adynamia and severe weakness are present; facial features are sharp, and the skin is pale, covered with cold, sticky sweat. Breathing is frequent and shallow; the pulse is rapid, sometimes arrhythmic, and of low volume. Oliguria or anuria. In extremely severe shock—loss of consciousness. Pulmonary edema is possible.

Treatment of the underlying condition that caused the shock (myocardial infarction, pulmonary embolism, pericardial tamponade, acute myocarditis, etc.), including surgical interventions—coronary angiography with coronary stenting, coronary artery bypass grafting, pericardial drainage for tamponade, pulmonary embolectomy, etc.

In reflex shock, analgesia is recommended: 2% promedol solution — 1 ml, 50% analgin solution — 2-4 ml, potentiated with antihistamines (1% diphenhydramine — 1 ml or 2.5% pipolfen — 1 ml), neuroleptanalgesia; fibrinolytics are advisable in the first 6-12 hours: kabikinase (streptokinase) 1.5 million IU in 100 ml of saline intravenously at a rate of 30 drops per minute, actilyse 100 mg in 100 ml, first 10 ml as a bolus, then 40 ml at 15 drops per minute, then 50 ml at 10 drops per minute; anticoagulants: heparin 10,000 IU intravenously, then 5,000 IU every 6 hours under Blood Coagulation monitoring, or fraxiparine (fragmin) 0.3-0.6 ml every 12 hours for 5-7 days.

In true cardiogenic shock, cardiac glycosides are used (0.5% strophanthin 0.5-1.0 ml in 20 ml of saline intravenously slow bolus); potassium preparations (3% KCl 30 ml or panangin 10-20 ml in 100-150 ml of 5% glucose with 8-10 IU of insulin—the so-called "polarizing solution"); rheological agents (reopoliglukin 400 ml or reosorbilact 250 ml intravenously dropwise); corticosteroids (hydrocortisone up to 500 mg or other adequate doses intravenously); management of metabolic acidosis (4% soda solution — 200 ml).

In areactive shock, the same agents are used as in true cardiogenic shock, along with circulatory support (counterpulsation using a special balloon catheter inserted into the aorta, which rapidly inflates at the beginning of each systole and deflates from mid-systole to the onset of diastole).

In arrhythmic shock, antiarrhythmic agents are recommended (cordarone 150 mg in 20 ml of 5% glucose, or 12% lidocaine 10 ml, or 10% novocainamide 5-10 ml intravenously); potassium preparations (see above); electrical cardioversion and cardiac pacing with electrodes inserted via central veins or the Esophagus.

Anaphylactic shock occurs as a severe manifestation of anaphylaxis (an immediate-type allergic reaction upon parenteral administration of an allergen) or atopy (an allergic disease with a hereditary predisposition to sensitization).

The feature of pathogenesis lies in the presence of reaginic antibodies in the body that promote the release of histamine from mast cells, under the influence of which severe disorders of Respiration and vascular tone develop.

True anaphylactic shock is preceded by sensitization—an immune reaction resulting in the appearance of reaginic antibodies, meaning the patient must have contacted the allergen at least once before the shock occurs. However, sometimes shock develops even upon first contact, as certain substances can trigger histamine release without the participation of antibodies (e.g., iodine-containing radiopaque agents), although the treatment methods for such shock do not differ from true anaphylactic shock.

The Clinical presentation of anaphylactic shock distinguishes the following forms:

— fulminant form characterized by the sudden onset of pallor or cyanosis, dilated pupils, agonal breathing, and clinical death ensuing within the next 10 minutes;

— severe form with precursors of impending catastrophe (Complaints of difficulty breathing and circulation), followed by the Development of the same symptoms as in the fulminant form;

— moderate shock occurs in several variants:

a) cardiac (most common)—spasm or dilation of peripheral vessels impairs peripheral and subsequently central hemodynamics with a drop in blood pressure; respiration is unaffected;

b) asphyctic—suffocation due to laryngeal or tracheal edema, or bronchospasm;

c) cerebral — presenting with symptoms resembling status epilepticus or acute cerebrovascular accident;

d) abdominal — presenting with symptoms of hollow viscus perforation or intestinal obstruction.

The identification of moderate anaphylactic shock is aided by the skin rash that typically appears in this form of the condition.

The management of anaphylactic shock depends on its clinical presentation. In fulminant and severe forms, resuscitation must be initiated immediately, including mechanical ventilation and closed-chest cardiac massage, along with the administration of appropriate medications. Once Cardiac Activity is restored in fulminant and severe cases—as well as in other variants of moderate anaphylactic shock—fractionated (bolus) administration of 0.1–0.2 ml of 0.1% adrenaline diluted in saline is recommended every 5–10 minutes until hemodynamics stabilize, since adrenaline acts as an antagonist to the humoral factors driving the development of anaphylactic shock. The adrenaline mixture may also be administered via continuous intravenous infusion.

Following adrenaline, antihistamines are administered (diphenhydramine, suprastin, diprazine, or tavegil at a dose of 0.5–1.0 mg/kg intravenously). Corticosteroids are then administered (hydrocortisone 125–500 mg or other agents in equivalent doses), keeping in mind that their onset of action is not immediate.

In the cardiac variant, In addition to the measures outlined above, circulating blood volume (CBV) is restored via crystalloid infusion. Colloidal solutions should be avoided due to their potential allergic risks.

In the asphyctic variant, due to laryngeal and tracheal edema, the administration of antihistamines, adrenaline, and corticosteroids is strongly recommended to combat the edema; in the event of bronchospasm, aminophylline (euphylline) 2.4% is also administered at a dose of 5 mg/(kg·h) (20 ml for adults) over 15 minutes, followed by 0.5 mg/(kg·h) (15 ml/h for adults). If drug therapy yields no effect, tracheal intubation or tracheostomy is performed.

In the cerebral variant, alongside adrenaline, antihistamines, and corticosteroids, diazepam 0.5% (2–3 ml) is administered and repeated after 8 hours, along with Lasix (furosemide) 2% (2–3 ml) intravenously.

In the abdominal variant, a thorough Differential Diagnosis is performed to prevent unnecessary surgical intervention.

After the symptoms of shock are resolved, the administration of antihistamines and corticosteroids is continued for 2–3 days, and the causative allergen is definitively identified to prevent future exposure for the patient.

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