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Bee Sting Case Management: Emergency → IPD → Discharge

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1. TRIAGE & INITIAL ASSESSMENT (Emergency Department)

Classify the Reaction First

Serum tryptase measured early in the reaction provides evidence of anaphylaxis if levels are elevated or significantly increased from basal level (Stinging Insect Hypersensitivity, p. 13).

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2. EMERGENCY MANAGEMENT

A. Anaphylaxis Protocol (First Priority)

1. Remove stinger immediately — scrape, do not squeeze (reduces further venom injection)
2. Epinephrine (adrenaline) — FIRST-LINE, no contraindications
   • IM epinephrine 0.3–0.5 mg (0.3 mL of 1:1000) into anterolateral thigh
   • Repeat every 5–15 min if no improvement
   • If individual has a bee-sting kit, use subcutaneous epinephrine 0.3 mL of 1:1000, repeated every 20–30 min (Harrison's, p. 13104)
3. Position: Supine with legs elevated (unless respiratory distress → semi-recumbent)
4. IV access × 2 + O₂ (high-flow 10–15 L/min via non-rebreather mask)
5. Fluid resuscitation: IV crystalloid (Normal saline) 1–2 L bolus for hypotension/shock

B. Adjunct Pharmacotherapy

IV epinephrine and other vasopressors, intubation/supplemental oxygen, fluid resuscitation, bronchodilators, and parenteral antihistamines are the mainstay of profound shock management (Harrison's, p. 13104).

C. Airway Management

• Early intubation if stridor, voice change, or rapidly progressing angioedema
• Have surgical airway (cricothyrotomy) kit at bedside

D. Toxic / Massive Envenomation (>50–100 stings)

• Treat as medical emergency with full resuscitation
• Anticipate: haemolysis, rhabdomyolysis, AKI, DIC, hepatic injury, cardiac arrhythmias
• IV hydration: aggressive fluid loading (2–3 mL/kg/h) to maintain UO ≥1 mL/kg/h
• Urinary alkalinisation (sodium bicarbonate) if myoglobinuria present
• Monitor ECG continuously

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3. MONITORING IN EMERGENCY (Observation Period)

Patients should be observed for 24 h for recurrent anaphylaxis, renal failure, or coagulopathy (Harrison's, p. 13104).

Biphasic Anaphylaxis

• Occurs in 5–20% of cases, typically 1–8 hours after initial resolution
• Reason for mandatory observation even after clinical improvement

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4. CRITERIA FOR INPATIENT ADMISSION (IPD)

• Severe anaphylaxis requiring IV epinephrine or vasopressors
• Persistent bronchospasm or hypoxia despite treatment
• Angioedema of airway (actual or threatened)
• Cardiovascular compromise
• Multiple stings (toxic envenomation)
• Renal impairment (↑ creatinine, haematuria, oliguria)
• Suspected haemolysis or rhabdomyolysis
• Biphasic reaction
• Comorbidities: cardiac disease, COPD, elderly, on beta-blockers
• Inadequate home situation / inability to access emergency care

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5. IPD MANAGEMENT

A. Monitoring

B. Ongoing Pharmacotherapy

• Continue IV corticosteroids (methylprednisolone 1–2 mg/kg/day or hydrocortisone 100–200 mg QID) for 24–48 h to suppress biphasic and late-phase reactions
• Oral antihistamine continuation (cetirizine 10 mg OD or loratadine 10 mg OD)
• IV fluids — guided by renal function and UO
• If renal failure develops: nephrology consult, possible haemodialysis
• DIC: FFP, cryoprecipitate, platelets as indicated

C. Specific Organ Complication Management

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6. CRITERIA FOR DISCHARGE

• Haemodynamically stable ≥24 h off IV medications
• Airway clear, no stridor or bronchospasm
• Tolerating oral intake
• Renal function normal or improving/stable
• No active bleeding/coagulopathy
• Patient educated and has written action plan

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7. ON-DISCHARGE MANAGEMENT

A. Prescriptions at Discharge

B. Patient & Caregiver Education

1. Avoid bee/wasp habitats — disturbing hives, working in gardens without protection
2. Wear protective clothing outdoors; avoid floral perfumes
3. Carry 2 EpiPen auto-injectors at all times
4. How to use EpiPen — demonstrate and provide written instructions
5. When to call emergency services — any systemic symptoms after a sting
6. Stinger removal — scrape with a card, do not squeeze
7. Recognition of early anaphylaxis signs: urticaria, throat tightness, dizziness, vomiting

C. Follow-Up Plan

D. Venom Immunotherapy (VIT) — Discharge Counselling

• VIT is highly effective — reduces risk of systemic reaction on re-sting from ~60% to <5%
• Indicated after systemic anaphylaxis in adults; consider in children with severe reactions
• Not typically required for large local reactions alone
• Consists of subcutaneous venom injections over 3–5 years
• Referral to allergist at discharge is standard of care

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Summary Flow Chart

BEE STING
    │
    ▼
Classify Reaction
    ├── Local only ──► Analgesia, antihistamine, observe 30 min, discharge
    ├── Large local ──► Antihistamine + corticosteroid, observe 4–6 h, discharge with EpiPen
    │
    └── Systemic / Anaphylaxis / Toxic
              │
              ▼
         EMERGENCY
         IM Epinephrine → Fluids → O₂ → Adjuncts → Observe 24 h
              │
              ▼
         ADMIT (IPD) if criteria met
         Monitoring + IV corticosteroids + Organ support
              │
              ▼
         DISCHARGE when stable
         EpiPen × 2 + Prednisolone taper + Antihistamine
         Allergist referral → Venom Immunotherapy

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• Harrison's Principles of Internal Medicine, 21st Edition, p. 13104
• Stinging Insect Hypersensitivity (GLGCA), p. 13
• WAO/EAACI Anaphylaxis Guidelines; ASCIA Hymenoptera Venom Allergy Guidelines

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Why Both Inj. Dexamethasone AND Inj. Hydrocortisone in Bee Sting?

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The Core Concept: Speed vs. Duration

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Why Hydrocortisone First?

1. Structural Similarity to Endogenous Cortisol

• Rapidly replaces/supplements endogenous cortisol
• Provides both glucocorticoid AND mineralocorticoid effects — important for maintaining vascular tone and sodium/water retention in shock states
• Begins suppressing mast cell mediator release and inflammatory cascade within 1–2 hours

2. Immediate Haemodynamic Support

• Retain sodium and water → supports intravascular volume
• Works synergistically with epinephrine and IV fluids to reverse distributive shock

3. Bridges the Gap

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Why Dexamethasone Added?

1. Prevention of Biphasic Anaphylaxis

• Biphasic reactions occur in 5–20% of cases, typically 1–8 hours (up to 72 h) after the initial reaction resolves
• Hydrocortisone's duration (8–12 h) does not fully cover this window
• Dexamethasone's duration of 36–72 hours provides sustained suppression of the late-phase allergic response, covering the entire biphasic risk window

"Patients with severe allergic reactions or anaphylaxis are usually discharged with prescriptions for antihistamines and corticosteroids for 3 to 5 days" (Tintinalli's Emergency Medicine, p. 3804)

2. Superior Anti-inflammatory Potency

• Dexamethasone is 25–30× more potent than hydrocortisone per mg
• It more powerfully suppresses:
  • Cytokine release (IL-1, IL-6, TNF-α)
  • Phospholipase A₂ → reduced arachidonic acid → reduced prostaglandins + leukotrienes
  • Vascular permeability and capillary leak
  • Late-phase eosinophil and mast cell activation

3. No Mineralocorticoid Effects (Advantage Here)

• In the recovery phase, you don't want excessive sodium/water retention
• Dexamethasone's pure glucocorticoid activity gives anti-inflammatory effect without fluid retention — useful once haemodynamic crisis has resolved

4. Longer Dosing Interval

• A single dose of dexamethasone 8 mg provides 48–72 h of anti-inflammatory cover
• Reduces the need for multiple follow-up doses in the IPD setting

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The Pathophysiology They Are Targeting

BEE VENOM INJECTION
        │
        ▼
IgE-mediated / Direct mast cell degranulation
        │
        ▼
Release of: Histamine, Tryptase, Leukotrienes, Prostaglandins, PAF
        │
   ┌────┴─────────────────────────────┐
   ▼                                  ▼
EARLY PHASE (0–1 h)           LATE / BIPHASIC PHASE (1–72 h)
Vasodilation, bronchospasm,   Eosinophil recruitment, ongoing
urticaria, angioedema,        cytokine release, renewed
hypotension                   bronchoconstriction, serum sickness
        │                                  │
        ▼                                  ▼
  HYDROCORTISONE               DEXAMETHASONE
  (covers early phase,         (covers late phase,
   supports haemodynamics)      prevents biphasic reaction)

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Mechanism of Action (Both Drugs)

1. Enter cell → bind cytoplasmic glucocorticoid receptor
2. GR-drug complex translocates to nucleus
3. Binds glucocorticoid response elements (GREs) on DNA
4. Upregulates: lipocortin-1 (inhibits phospholipase A₂) → suppresses arachidonic acid cascade
5. Downregulates: NF-κB → reduces transcription of TNF-α, IL-1, IL-6, IL-8
6. Reduces vascular permeability, mast cell activity, eosinophil survival

This is why corticosteroids take 1–6 hours to show clinical effect — they work at the level of gene transcription, not receptor blocking.

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Clinical Rationale Summary Table

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In Simple Terms

Hydrocortisone = fast cortisol replacement + haemodynamic stability NOW Dexamethasone = powerful, long-lasting anti-inflammatory cover for the next 48–72 hours

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