Emergency Medicine · Shock
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Intramuscular epinephrine in the mid-outer thigh is the first-line, life-saving treatment for anaphylaxis and should never be delayed.
Anaphylaxis is a clinical diagnosis. It is highly likely when: (1) two or more organ systems (skin, respiratory, cardiovascular, or GI) are involved after exposure to a likely allergen, or (2) hypotension, bronchospasm, or laryngeal involvement alone occurs after exposure to a known or highly probable allergen for that patient. Skin findings are absent in up to 10-20% of cases and are not required.
Biphasic reactions can occur hours after the initial resolution of symptoms, necessitating a period of observation in the emergency department.
Hypotension in anaphylactic shock results from systemic vasodilation and increased capillary permeability, leading to a decrease in systemic vascular resistance.
Urticaria, angioedema, and pruritus are the most common cutaneous manifestations, but their absence does not rule out anaphylaxis.
Airway compromise due to laryngeal edema or bronchospasm is the primary cause of mortality in anaphylactic patients.
H1 and H2 antihistamines and corticosteroids are considered adjunctive therapies and have no role in the acute resuscitation of anaphylactic shock.
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A 28-year-old male presents to the emergency department 20 minutes after eating a meal containing peanuts. He reports diffuse pruritus, hives, and a sensation of his throat closing. On physical exam, he is tachypneic with audible wheezing and has a blood pressure of 82/50 mmHg. He is currently tachycardic and appears diaphoretic. No prior history of similar reactions is noted.
What is the most appropriate next step in the management of this patient?
Intramuscular epinephrine
The patient is exhibiting signs of anaphylactic shock (hypotension, respiratory distress, and cutaneous involvement), and immediate administration of IM epinephrine is the definitive first-line treatment to reverse vasodilation and bronchoconstriction.
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Etiology / Epidemiology
Systemic IgE-mediated hypersensitivity reaction to allergens (foods, drugs, stings). Rapid onset distributive shock.
Clinical Manifestations
Rapid onset urticaria, angioedema, and hypotension. Look for stridor or wheezing.
Diagnosis
Clinical diagnosis. Serum tryptase levels (drawn 1-2 hours post-event) confirm mast cell degranulation.
Treatment
Immediate Epinephrine (IM). Do not delay for imaging or labs.
Prognosis
Risk of biphasic reaction (up to 12+ hours later); observation duration should be individualized by severity — as brief as ~1 hour for mild, single-dose-epinephrine-responsive reactions, longer (4-6h+) for severe or multi-dose reactions.
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Epidemiology & Etiology
Triggered by exposure to antigens such as penicillin, Hymenoptera stings, or food allergens (peanuts/shellfish). Occurs within minutes to hours of exposure. Rapid progression to cardiovascular collapse is the primary concern.
Pertinent Anatomy
Systemic vasodilation occurs due to massive release of mediators from mast cells and basophils. Upper airway angioedema causes mechanical obstruction, while systemic capillary leak leads to profound hypovolemia.
Pathophysiology
Antigen-specific IgE binds to mast cells, triggering massive release of histamine, leukotrienes, and prostaglandins. This causes systemic vasodilation (distributive shock) and increased capillary permeability. Airway compromise results from mucosal edema.
Clinical Manifestations
Patients present with urticaria, pruritus, and angioedema. Respiratory distress manifests as stridor or wheezing. Hypotension and tachycardia are signs of impending cardiovascular collapse. Look for laryngeal edema as a life-threatening red flag.
Diagnosis
Diagnosis is clinical. Do not wait for labs. Serum tryptase is the gold standard for retrospective confirmation of mast cell degranulation. Levels are best drawn 15 minutes to 3 hours after symptom onset; a normal tryptase does not exclude anaphylaxis, especially food-triggered reactions.
Treatment
Administer Epinephrine (1 mg/mL concentration, 0.3-0.5 mg IM) in the mid-outer thigh immediately. Do not use subcutaneous route due to poor absorption. Repeat every 5-15 minutes if response is inadequate, and keep the patient supine with legs elevated unless vomiting or in respiratory distress. Follow with IV fluids for hypotension and H1/H2 blockers/steroids as adjuncts.
Prognosis
Most patients recover with prompt treatment. Monitor for biphasic reaction (recurrence of symptoms) for a period individualized to severity: about 1 hour of symptom-free observation is reasonable for mild reactions that resolve promptly after a single dose of epinephrine, while extended observation is advised for severe anaphylaxis or reactions requiring more than one epinephrine dose. Discharge with an epinephrine autoinjector and strict allergen avoidance education.
Differential Diagnosis
Vasovagal syncope: bradycardia present
Hereditary angioedema: no urticaria/pruritus
Asthma exacerbation: no hypotension/skin findings
Scombroid poisoning: mimics anaphylaxis but history of fish ingestion
Carcinoid syndrome: chronic flushing/diarrhea