Anaphylaxis Secondary to Bee Sting (Hymenoptera Venom-Induced Anaphylaxis)
Jerome is experiencing anaphylaxis from a bee sting, a life-threatening IgE-mediated systemic allergic reaction requiring immediate epinephrine administration. 1, 2
What Leads to This Diagnosis
The clinical presentation demonstrates the classic triad of anaphylaxis involving multiple organ systems:
Cardiovascular Involvement (Most Critical)
- Hypotension (BP 69/45) with tachycardia (P 120) represents the most serious manifestation and is the most common cardiovascular reaction in Hymenoptera-induced anaphylaxis 1
- Weakness and dizziness reflect hemodynamic compromise from distributive shock 1
- The drowsiness indicates impending circulatory collapse 2
Cutaneous Manifestations
- Generalized urticaria (not contiguous with the sting site) confirms systemic rather than local reaction 1
- Pallor reflects peripheral vasoconstriction and poor perfusion 2
Respiratory Involvement
- Wheezing and mild respiratory distress indicate bronchospasm and lower airway obstruction 1
- Tachypnea (R 39) reflects respiratory compensation 1
- Notably, the absence of lip/tongue swelling and normal voice suggests laryngeal edema has not yet developed—a critical distinction, as laryngeal edema is the most common cause of death from Hymenoptera-induced anaphylaxis 1, 3
Temporal Pattern
- Symptom onset within 15 minutes of the sting is characteristic of anaphylaxis; the more rapidly anaphylaxis develops after exposure, the more likely the reaction is severe and potentially life-threatening 2
Pathophysiologic Basis
IgE-Mediated Mechanism
- Bee venom proteins trigger cross-linking of venom-specific IgE antibodies on mast cells and basophils, causing sudden massive mediator release (histamine, tryptase, leukotrienes, prostaglandins) 2, 4
- This is a Type I immediate hypersensitivity reaction 4, 5
Cardiovascular Collapse
- Increased vascular permeability is the hallmark pathophysiologic feature, allowing transfer of up to 50% of intravascular fluid into the extravascular space within 10 minutes 2
- This rapid fluid shift causes distributive shock with profound hypotension, explaining Jerome's BP of 69/45 2
- Compensatory tachycardia (P 120) attempts to maintain cardiac output despite reduced preload 1
Respiratory Manifestations
- Histamine and leukotrienes cause bronchial smooth muscle contraction, producing wheezing and bronchospasm 1
- Increased vascular permeability in airways can progress to laryngeal edema if untreated 1, 3
Cutaneous Findings
- Histamine release causes vasodilation and increased capillary permeability, producing generalized urticaria and erythema 1
- Peripheral vasoconstriction (pallor) occurs as a compensatory response to hypotension 2
Critical Management Points
Immediate intramuscular epinephrine 0.3-0.5 mg (anterolateral thigh) is mandatory and life-saving 3, 2, 6
Common Pitfalls to Avoid
- Do not delay epinephrine administration—when in doubt, it is better to give epinephrine; anaphylaxis is a clinical diagnosis that must be made rapidly, and confirmatory testing should never delay treatment 2
- The absence of lip/tongue swelling does NOT exclude anaphylaxis; cutaneous manifestations may be delayed or absent in rapidly progressive anaphylaxis, particularly with cardiovascular collapse 2
- Hypotension with tachycardia can be mistaken for vasovagal reaction, but vasovagal reactions typically present with bradycardia, not tachycardia 1
- Be prepared for rapid deterioration, as laryngeal edema can develop suddenly and is the most common cause of death 3
Post-Acute Management Requirements
- Prescribe epinephrine auto-injector for discharge 1, 3
- Refer to allergist-immunologist for venom-specific IgE testing 1, 3
- Venom immunotherapy (VIT) is indicated for adults with systemic reactions involving cardiovascular and respiratory systems who have positive venom-specific IgE antibodies; VIT reduces risk of future systemic reactions to as low as 5% 1