Anaphylactic shock management algorithm

Strategy and Recognition

The management of a patient with anaphylaxis is divided into two main stages: emergency treatment of the life-threatening condition and subsequent prevention of recurrences. It is critically important to follow the "golden hour" rule — act immediately wherever the reaction has developed.

Impending shock can be recognized by key clinical markers:

• Burdened allergic history.
• Life-threatening signs: appearance of stridor, respiratory distress syndrome, hemodynamic drop (classic picture of shock).
• Cutaneous manifestations such as urticaria or itching may be present, but their absence does not exclude the diagnosis under any circumstances.

In case of any severity of blood pressure changes, administration of the trigger drug (allergen) must be stopped immediately. The question of continuing therapy with this agent is decided solely after the patient has completely stabilized.

Step-by-step emergency care algorithm

The entire logic of actions is based on a rapid assessment of vital functions and the immediate administration of adrenaline. It is important to remember that antibiotics, diuretics (furosemide), or isolated inhalations are not life-saving measures in the first minutes.

1. Primary assessment and basic measures. Assessment is carried out using the ABC system (airway patency, adequacy of breathing, and hemodynamic parameters). Contact with the allergen is stopped immediately. If technically feasible, oxygen therapy is initiated immediately.
2. First-line pharmacotherapy. An intramuscular injection of epinephrine (0.1% solution) is performed. Dose calculation: 0.01 mg/kg of body weight, while the maximum single dose should not exceed 0.5 mg. In cases of extremely severe shock, slow intravenous administration is permitted.
3. Dynamic monitoring. Evaluation of the clinical effect is carried out in exactly 5 minutes. If there is no improvement, intramuscular epinephrine injections are repeated every 5–10 minutes until respiration and circulation are completely stabilized.
4. Therapy correction. If signs of shock persist, the patient requires volume support — intravenous fluid infusion is started at a rate of 20 ml/kg to normalize circulating blood volume.

Adjuvant therapy and management of laryngeal edema

After the administration of adrenaline and the start of infusion load (colloid solutions, dextran, gelatin), symptomatic treatment is initiated. The generalized algorithm includes the following drug groups:

• Glucocorticoids (GCs): dexamethasone or prednisolone administered intravenously or intramuscularly.
• Antihistamines: systemic H1-receptor blockers are used to relieve itching and skin manifestations.
• Bronchodilators: for severe asphyxia, inhalations of salbutamol and topical GCs (budesonide) are prescribed.
• Specific antigen inactivation: for example, the use of penicillinase (beta-lactamase) in shock caused by penicillin antibiotics.

Special attention requires allergic laryngeal edema. Its markers are concomitant symptoms: edema of the lips, eyelids, urticarial rash. In this case, after stopping contact with the allergen, mandatory hospitalization is indicated, and treatment is based on the triad: epinephrine, systemic GCs, and antihistamines. For severe or refractory reactions, an examination by an anesthesiologist-resuscitator is mandatory.

Pathogenetic features and hypersensitivity

Anaphylaxis is an extreme manifestation of immediate-type hypersensitivity (ITH) reactions. The pathogenesis of many concomitant symptoms, such as urticaria or rhinitis, is associated with massive mast cell degranulation. That is why antihistamines serve as the baseline therapy for skin manifestations.

Drugs acting as triggers (e.g., antibiotics) can cause various reactions:

• ITH (Type I): manifests with rash, itching, and anaphylaxis.
• Delayed-type hypersensitivity (Type IV): manifests with contact dermatitis.

In addition, broad-spectrum antibiotics can have an immunosuppressive effect, reducing the functional activity of macrophages and T-lymphocytes. This suppresses delayed-type hypersensitivity and promotes the development of opportunistic mycoses. In systemic vasculitis, rheumatism, and atopic asthma, the pathogenesis is often mixed: early exudative changes can transform into specific granulomas, involve type III and IV mechanisms, or manifest as heteroallergy (attacks triggered by non-specific stimuli, such as cooling).

Class and exam questions

What else to study on this topic

• Exact clinical stages of anaphylactic shock.
• Detailed characteristics of the mechanisms of development of autoimmune cytopenias (a classic example of Type II hypersensitivity).
• Morphological characteristics of delayed-type hypersensitivity (DTH).
• Mechanisms of specific granuloma formation in rheumatic diseases.

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