Immunology

A

• ACE Inhibitor–Induced Angioedema

  ACE‑I angioedema is bradykinin‑mediated; stop ACE‑I permanently. Airway protection is paramount; icatibant or C1‑INH may help in severe cases; avoid ACE‑I/possibly caution with ARB.
• ACE-Inhibitor Angioedema — Airway First, Bradykinin-Targeted Options, and Disposition

  Non-histaminergic swelling (often lips/tongue) typically within months to years of ACEi use. Prioritize airway management; epinephrine/antihistamines/steroids may have limited effect. Consider icatibant or C1-INH in severe cases; avoid ACEi permanently.
• Acute Urticaria — ED Treatment

  Acute urticaria is sudden transient whealing, angioedema, or both lasting less than six weeks. The ED priority is to identify anaphylaxis or airway-threatening angioedema; isolated urticaria is treated primarily with a second-generation H1 antihistamine, while epinephrine is reserved for anaphylaxis rather than uncomplicated hives.
• Acute Urticaria & Angioedema — Evaluation

  Differentiate histaminergic from bradykinin‑mediated angioedema; identify triggers/medications; avoid unnecessary broad testing in acute urticaria.
• Allergic Contact Dermatitis — Patch Testing

  Suspect allergic contact dermatitis with well‑demarcated, patterned eczema. Patch testing identifies allergens; avoidance is primary therapy.
• Allergic Rhinitis–Asthma Link: Integrated Care

  Treating allergic rhinitis improves asthma control. Combine intranasal steroids/antihistamines, environmental control, and consider allergen immunotherapy in sensitized patients with symptoms.
• Allergy Testing — Skin Prick vs Serum IgE Interpretation

  Skin prick testing and serum specific IgE support diagnosis but must match clinical history; avoid testing large panels without pre‑test probability. Consider component‑resolved diagnostics for select foods/venoms.
• Anaphylaxis — Adult Recognition & Treatment

  Anaphylaxis is a rapidly evolving systemic hypersensitivity reaction that can cause fatal airway edema, bronchospasm, vasodilation, and shock. Intramuscular epinephrine in the anterolateral thigh is first-line treatment and should be given immediately when clinical criteria are met. Airway support, oxygen, rapid isotonic fluid resuscitation for hypotension, and repeated epinephrine are added as needed. Antihistamines and corticosteroids are adjuncts and must never delay epinephrine.
• Anaphylaxis — Epinephrine First and Observation

  Immediate intramuscular epinephrine in the lateral thigh is first line; add oxygen, IV fluids, and adjuncts; observe for biphasic reactions and discharge with auto injector and education.
• Anaphylaxis — Epinephrine First, Adjuncts Second, and Biphasic Risk Management

  Treat rapidly with IM epinephrine in the lateral thigh; repeat every 5–15 min as needed. Add oxygen, IV fluids, H1/H2 blockers, and corticosteroids as adjuncts; observe for biphasic reactions and prescribe an epinephrine auto‑injector with an action plan.
• Anaphylaxis — IM Epinephrine, Airway Preparedness, and Observation

  Acute, life-threatening allergic reaction with airway, breathing, or circulatory compromise. Give IM epinephrine 0.3–0.5 mg (1 mg/mL) in the lateral thigh immediately and repeat every 5–15 minutes as needed. Position patient supine, provide high-flow oxygen and IV fluids; add adjuncts after epinephrine.
• Anaphylaxis — Intramuscular Epinephrine First, Adjuncts, and Observation

  Anaphylaxis is a rapid, systemic hypersensitivity reaction. Inject IM epinephrine in the anterolateral thigh promptly; repeat every 5–15 min as needed. Position patient supine with legs elevated, give high-flow oxygen, IV fluids, H1/H2 blockers, bronchodilators, and steroids as adjuncts; observe for biphasic reactions.
• Anaphylaxis — Recognition & Treatment

  Anaphylaxis is a rapidly developing, potentially fatal systemic hypersensitivity reaction. Diagnosis is clinical and treatment must not wait for laboratory confirmation. Intramuscular epinephrine in the anterolateral thigh is first-line therapy for suspected anaphylaxis, including reactions dominated by airway compromise, bronchospasm, or hypotension even when skin findings are absent. Airway support, oxygen, rapid isotonic fluid resuscitation, and repeated epinephrine are added according to severity. Antih
• Anaphylaxis: Acute Management

  Immediate IM epinephrine in the mid‑anterolateral thigh is first‑line; support airway/breathing/circulation, identify trigger, and arrange observation with autoinjector and action plan at discharge.
• Aspirin Exacerbated Respiratory Disease — ED Care and Long Term Options

  Aspirin-exacerbated respiratory disease is the syndrome of asthma, chronic rhinosinusitis with nasal polyps, and respiratory reactions to aspirin or other strong COX-1-inhibiting NSAIDs. Acute reactions are treated according to airway and anaphylaxis severity, while long-term care combines asthma and sinus control, COX-1 NSAID avoidance unless desensitized, leukotriene-directed therapy, surgery or biologics when indicated, and aspirin desensitization with maintenance therapy in selected patients.
• Aspirin‑Exacerbated Respiratory Disease (AERD)

  Triad of asthma, nasal polyps, and respiratory reactions to NSAIDs. Manage with avoidance, optimal asthma/CRS control, and consider aspirin desensitization; biologics may help.
• Atopic Dermatitis — Step‑Up Treatment

  Emollients and trigger control are foundational; step‑up with topical steroids/calcineurin inhibitors, phototherapy, and systemic agents (dupilumab, JAK inhibitors) for moderate–severe disease.

B

• Beta Lactam Cross Reactivity — Practical Guide

  Beta-lactam cross-reactivity is driven mainly by shared side-chain structure rather than by the beta-lactam ring alone. A penicillin allergy label therefore does not require blanket avoidance of all cephalosporins, carbapenems, or monobactams. Safe selection depends on the culprit drug, reaction phenotype, severity, and side-chain relationship, with special caution after severe delayed immune reactions.
• Bradykinin Mediated Angioedema — Airway First and Targeted Therapy

  Bradykinin-mediated angioedema causes nonpruritic swelling without urticaria and can rapidly obstruct the upper airway. Epinephrine, antihistamines, and corticosteroids do not reliably reverse bradykinin disease, so airway planning comes first and targeted therapy with a C1 inhibitor concentrate, icatibant, or another approved hereditary-angioedema treatment should be given when available.

C

• Chronic Rhinosinusitis with Nasal Polyps (CRSwNP)

  CRSwNP is a Type 2‑skewed disease; treat with high‑volume saline rinses, intranasal steroids (sprays or irrigations with steroid), short steroid bursts for flares, ESS for refractory disease, and biologics for severe cases.
• Chronic Spontaneous Urticaria — Stepwise Therapy

  Chronic spontaneous urticaria is recurrent wheals, angioedema, or both for more than six weeks without a consistent external trigger. Diagnosis is clinical with limited targeted testing; treatment follows a stepwise pathway of second-generation H1 antihistamines, dose escalation when needed, biologic therapy such as omalizumab for antihistamine-refractory disease, and specialist-directed additional therapy while avoiding chronic systemic corticosteroids.
• Chronic Spontaneous Urticaria — Stepwise Therapy

  Treat with high‑dose second‑generation H1 antihistamines, then omalizumab, then cyclosporine for refractory cases; avoid chronic steroids.
• Common Variable Immunodeficiency — Diagnosis & Care

  CVID features low IgG with low IgA and/or IgM and impaired vaccine responses, causing recurrent sinopulmonary infections and autoimmunity. Treat with Ig replacement and targeted management of complications.
• Contrast Media Hypersensitivity — Acute Care and Pretreatment

  Prior allergic-like reaction to the same class of contrast medium is the strongest clinical predictor of another allergic-like reaction. Management starts by distinguishing allergic-like from physiologic reactions, considering an alternate study or alternate agent when feasible, and using evidence-based premedication only when the imaging benefit justifies residual risk. Shellfish allergy and povidone-iodine allergy do not confer special iodinated-contrast risk.

E

• Eosinophilic Esophagitis — Diagnosis & Treatment

  Chronic, immune‑mediated esophageal disease. Diagnose with symptoms and ≥15 eos/hpf on biopsy; treat with high‑dose PPI, swallowed topical steroids, and/or empiric elimination diet; dilate strictures.

F

• Food Allergy — ED Discharge and Prevention

  Discharge after food-triggered anaphylaxis is part of anaphylaxis treatment, not an administrative afterthought. The patient should leave only after clinical stability and individualized observation, with epinephrine access, device training, a written emergency plan, trigger-avoidance guidance, and allergy follow-up. Antihistamines and corticosteroids do not replace epinephrine and routine steroids are not proven to prevent biphasic anaphylaxis.
• Food Allergy: Selecting Candidates for Oral Immunotherapy

  OIT increases threshold to accidental exposures in select patients. Requires daily dosing, adherence, and management of adverse events including anaphylaxis and EoE risk.

H

• Hymenoptera Venom Allergy — Acute Care and Immunotherapy

  Hymenoptera venom allergy ranges from large local reactions to life-threatening anaphylaxis. Acute systemic reactions require intramuscular epinephrine and standard anaphylaxis care. After recovery, patients with systemic reactions should receive risk-based allergy evaluation, venom-specific IgE testing, epinephrine access, and consideration of venom immunotherapy, which markedly reduces the risk of severe reactions to future stings.
• Hymenoptera Venom Allergy — Anaphylaxis & Immunotherapy

  Venom immunotherapy (VIT) prevents life‑threatening anaphylaxis in patients with systemic sting reactions. Diagnose with history + testing; continue carry of autoinjector.

L

• Latex Allergy — Perioperative & Healthcare Settings

  Ensure latex‑free environments for sensitized patients and healthcare workers. Identify cross‑reactive foods (banana, avocado, kiwi) and manage perioperative exposure risks.
• Latex Allergy — Recognition and Management

  Latex allergy includes immediate IgE-mediated reactions to natural rubber latex proteins, delayed contact dermatitis to rubber-processing chemicals, and nonimmune irritant dermatitis. Immediate reactions can progress to anaphylaxis and require epinephrine. Long-term management centers on accurate phenotype diagnosis and a latex-safe environment, with individualized evaluation of latex-fruit cross-reactivity rather than blanket avoidance of every cross-reactive food.

P

• Pediatric PID — 10 Warning Signs & Initial Labs

  Use practical red flags to identify children at risk of PID and start an initial lab panel; refer early to Immunology for definitive testing and management.
• Penicillin Allergy — Delabeling Pathways

  Most penicillin allergy labels do not represent persistent clinically significant allergy. Delabeling begins with a detailed reaction history and risk stratification. Patients with remote benign or clearly nonallergic histories can often undergo a supervised direct oral amoxicillin challenge, while higher-risk immediate reactions may require skin testing first. Severe delayed immune-mediated reactions are not challenge candidates and require specialist-directed avoidance.
• Penicillin Allergy Delabeling in Clinic/Hospital

  Most patients labeled 'penicillin allergic' are tolerant. Use risk stratification to guide direct oral amoxicillin challenge vs skin testing, especially in stewardship programs and pre‑op clinics.
• Physical/Inducible Urticarias (Cold, Cholinergic, Pressure)

  Inducible urticarias (cold, cholinergic, delayed pressure, dermographism, heat, solar) are diagnosed with provocation testing; management centers on trigger avoidance and high‑dose second‑generation antihistamines.

R

• Recurrent Infections in Adults — PID Work‑up

  Adult PID work‑up starts with CBC with differential, quantitative immunoglobulins, specific antibody titers (pre/post immunization), and HIV testing; tailor further testing to pattern of infections.

S

• Selective IgA Deficiency — Practical Management

  Most are asymptomatic; some have recurrent infections, autoimmunity, or celiac disease. No routine Ig replacement; manage infections, vaccinate, and use washed/IgA‑depleted blood if anti‑IgA antibodies present.
• Severe Asthma — Phenotyping & Biologics

  Phenotype severe asthma (Type 2 high vs low) to select biologics (omalizumab, mepolizumab/benralizumab, dupilumab, tezepelumab). Optimize inhaled therapy and adherence first.
• Severe Cutaneous Adverse Reactions (SJS/TEN/DRESS) — Recognition & Initial Management

  Recognize and manage severe cutaneous adverse reactions (SJS/TEN, DRESS). Stop culprit drugs immediately, provide supportive care (burn unit for TEN), and consult dermatology/immunology early.