Emergency care for allergic reactions

Pathogenesis and Major Triggers

Anaphylaxis represents the most severe form of immediate-type (type I) hypersensitivity reaction. Symptoms can develop either instantaneously or up to 5 hours after contact with the trigger. From a pathophysiological perspective, it is a vascular (distributional) shock. Due to the release of mediators, marked vasodilation occurs, arteriovenous shunts open, and capillary permeability increases. This leads to blood redistribution, a drop in total peripheral vascular resistance (TPVR), and relative hypovolemia.

At-risk individuals include those with a burdened medical history (asthma, drug dermatitis). Triggers depend on age and setting:

• In children: food allergens predominate (cow's milk proteins, eggs, peanuts, seafood).
• In adults and surgical practice: medications (penicillin antibiotics, protein volume expanders, sera, radiocontrast agents) and insect venoms (wasps, bees) come to the forefront.
• Rare factors: physical exertion, ethanol, latex contact.

Basic Emergency Care Algorithm

The success of resuscitation depends on the "golden hour" rule. Therapy is initiated immediately, relying on the ABC system (Airway, Breathing, Circulation). The core principle: epinephrine (adrenaline) is administered first.

1. Cessation of exposure: stop drug administration, remove the allergen.
2. Oxygen therapy: initiate oxygen delivery if equipment is available.
3. Epinephrine administration: standardly administered intramuscularly as a 0.1% solution. The dosage is 0.01 mg/kg of body weight (not exceeding 0.5 mg per single dose).
4. Dynamic monitoring: the effect is evaluated after 5 minutes. If hemodynamics do not stabilize, injections are repeated every 5–10 minutes.
5. Severe shock: slow intravenous administration of epinephrine is permitted, but strictly under cardiac monitoring due to the risk of arrhythmias.

Management of Hypovolemia and Adjunctive Therapy

All other medications do not replace adrenaline; rather, they prevent relapses and relieve local symptoms. If shock persists despite epinephrine, combating relative hypovolemia becomes the priority.

• Volume support: intravenous fluid infusion at 20 ml/kg. Colloid solutions, dextran (molecular weight 30,000–40,000), or gelatin are used.
• Glucocorticoids: dexamethasone or prednisolone administered IM or IV.
• Antihistamines (H1-blockers): administered systemically, but solely for relieving pruritus and skin manifestations.
• Bronchodilators: in case of severe dyspnea, salbutamol inhalations and topical steroids (budesonide) are added.
• Antigen inactivation: in penicillin-induced shock, administration of the enzyme penicillinase (beta-lactamase) may be indicated.

Relief of Allergic Laryngeal Edema

Laryngeal edema is another fatal manifestation of anaphylaxis, often accompanied by periorbital edema, lip swelling, and urticarial rash. The patient requires urgent hospitalization. Drug management is similar to shock therapy: epinephrine is administered first, followed by systemic glucocorticoids and antihistamines to achieve the fastest possible reduction in tissue edema and restoration of airway patency.

Class and exam questions

What else to study on this topic

• Pathogenesis of Gell and Coombs Type I hypersensitivity reactions.
• Mechanisms of relative hypovolemia development in distributive shock.
• Differences between IgE-dependent anaphylaxis and anaphylactoid reactions.
• Specifics of using volume expanders and colloid solutions in shock.
• Prevention measures and allergological history taking in surgical practice.

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Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.