Anaphylactic shock emergency care

General patient management principles

The strategy for combating anaphylaxis always involves two fundamental stages: emergency management of life-threatening manifestations and subsequent prevention of recurrent episodes. The cornerstone of therapy is the "golden hour" rule—medical care must be delivered immediately and directly at the site of the pathological reaction.

It is important to remember that epinephrine (Adrenalinum) is the only proven first-line agent. All other pharmacological agents play a purely adjunctive role. The administration of bronchodilators, diuretics, or antibacterial drugs cannot save a patient's life in the first minutes of anaphylaxis development.

Step-by-step emergency care algorithm

The physician's actions must be brought to automaticity and rely on a rapid assessment of vital functions.

Step 1. Recognition of the reaction Clinical markers help suspect anaphylaxis. These include a burdened allergic history and life-threatening symptoms: shock presentation, stridor, or respiratory distress syndrome. Skin reactions (e.g., urticaria) often accompany the attack, but their absence does not rule out the diagnosis.

Step 2. Basic measures

• Immediately stop the entry of the trigger (allergen) into the body, e.g., stop the administration of a medicinal product.
• Perform an assessment using the ABC system: check airway patency, adequacy of pulmonary ventilation, and hemodynamic parameters.
• Initiate oxygen therapy (delivery of 100% oxygen).

Step 3. Administration of epinephrine

• The standard route of administration is intramuscular (IM). A 0.1% solution is used.
• Dose calculation: 0.01 mg/kg of body weight, but not more than 0.5 mg per single administration.
• In extremely severe shock, slow intravenous (IV) administration is permitted.
• If asphyxia and bronchoconstriction come to the foreground, inhalation of bronchodilators (salbutamol) and topical glucocorticoids (budesonide) is added to the therapy.

Step 4. Dynamic monitoring The effectiveness of administered adrenaline is assessed after 5 minutes. If hemodynamics and breathing have not stabilized, the intramuscular injection is repeated (interval of 5–10 minutes). If the shock state persists, volume resuscitation is deployed—fluids are administered intravenously at 20 ml/kg.

Adjuvant pharmacotherapy

Symptomatic treatment aims to consolidate the effect and manage associated manifestations:

1. Glucocorticoids (GCS): prednisolone or dexamethasone are administered IV or IM to suppress systemic inflammation.
2. Antihistamines: systemic H1-receptor blockers are necessary to eliminate itching and skin elements, as their pathogenesis is directly linked to mast cell degranulation.
3. Bronchodilators: used for concomitant airway obstruction.

Within the framework of general anti-shock therapy (to restore microcirculation and circulating blood volume), colloidal solutions, gelatin, or dextran with a medium molecular weight of 30,000–40,000 are used. Vasopressors such as norepinephrine or ephedrine may be used. If the reaction is caused by penicillin, penicillinase (betalactamase) is administered to inactivate the antigen.

Special clinical situations

Allergic laryngeal edema Clinically manifests as urticarial rash, eyelid and lip edema. The algorithm requires cessation of contact with the allergen and mandatory hospitalization. Medicamentously, the condition is managed by administering adrenaline, systemic GCS, and antihistamines.

Severe and refractory reactions In such cases, examination by an anesthesiologist-resuscitator is mandatory. Strict sequence of actions: epinephrine first, followed by massive fluid loading, after which prednisolone or dexamethasone is administered. With any blood pressure fluctuations, administration of the triggering drug is stopped; the issue of resuming therapy is decided exclusively after the patient's complete stabilization.

Link to hypersensitivity reactions

Medicinal products (especially antibacterial chemotherapeutic agents) can trigger various types of hypersensitivity reactions. Immediate-type hypersensitivity manifests as anaphylaxis, urticaria, or pruritus. Delayed-type hypersensitivity (DTH) more frequently manifests as contact dermatitis. Broad-spectrum antibiotics also possess an immunosuppressive effect: they reduce the activity of T-lymphocytes and macrophages, which suppresses DTH and paves the way for opportunistic mycoses.

In a number of pathologies (rheumatic diseases, systemic vasculitides), reaction types can succeed one another. Thus, the exudative phase of rheumatism eventually transitions into the formation of specific granulomas (transition from immediate to delayed type). Atopic asthma may combine components of types I, III, and IV, and also proceed as heteroallergy (reaction to non-specific stimuli, e.g., cold).

Class and exam questions

What else to study on this topic

• Precise clinical stages of anaphylactic shock development.
• Detailed analysis of emergency care algorithms for specific types of shock.
• Mechanisms of autoimmune cytopenia development as a classic example of type II hypersensitivity.
• Features of using dextrans and colloidal solutions in shock states.
• Immunosuppressive action of antibiotics and the pathogenesis of opportunistic mycoses.

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