2.3 - Anaphylaxis and Angioedema in the Dental Office

Recognize anaphylaxis quickly, give IM epinephrine first, and distinguish histamine-mediated from bradykinin-mediated angioedema.

anaphylaxis

systemic type I hypersensitivity

• mechanism:

  1. first exposure → IgE produced to coat mast cells and basophils

  2. re-exposure → allergen cross-links IgE and causes mast cell degranulation within seconds

• mediators:

  • histamine → vasodilation, vascular leak, bronchospasm

  • leukotrienes → prolonged bronchoconstriction

  • PGD₂ + platelet activating factor → further vasodilation, further vascular leak

• reaction occurs throughout body at once

• occurs within minutes of an exposure

  • skin or mucosa → hives, flushing, swollen lips/tongue

  • breathing trouble or low blood pressure

anaphylaxis vs vasovagal syncope

• anaphylaxis — flushed skin, hives, swelling, fast pulse

  • wheeze or stridor

  • does not recover lying flat

  • treat with epinephrine

• vasovagal syncope — pale, cool, sweaty, slow pulse

  • breathing normal

  • recovers lying flat

  • treat with position and reassurance

anaphylaxis management

1. stop procedure, call for help, activate EMS

2. IM epinephrine into anterolateral thigh

   • 1 mg/mL concentration → adult (0.3-0.5 mg) and child (0.01 mg/kg, max 0.3 mg)

   • auto-injector → adult (0.3 mg) and child (0.15 mg), repeat every 5-15 minutes as needed

3. position → supine with legs raised, sitting up if breathing is main problem

4. oxygen and vital signs

5. adjuncts → antihistamine, corticosteroids, bronchodilators

epinephrine

only drug that treats anaphylaxis

• ⍺1 → raises BP, reduces airway swelling

• β1 → supports the heart

• β2 → opens the airway and stabilizes mast cells

• antihistamines are not enough

  • blocks one mediator slowly

  • leukotrienes and shock do not wait

• deaths are associated with delayed or absent epinephrine

• everyone receiving epinephrine goes to the hospital

  • symptoms can return later for biphasic reaction

kinds of angioedema

• histamine-mediated — IgE and mast cells

  • hives and itching

  • onset in minutes

  • allergens include drugs, latex, foods

  • responds to epinephrine

• bradykin-mediates — ACE inhibitors, C1 inhibitor deficiency

  • no hives, no itching

  • develops over hours, may last days

  • responds poorly to epinephrine

  • prioritize airway and hospital

ACE inhibitor angioedema

ACE makes angiotensin II and breaks down bradykinin, where inhibitors will cause bradykinin buildup

• angioedema occurs in 0.1-0.7% of patients on lisinopriol, enalapri, ramipril, and others

  • several times more common in black patients

• can start after years on the drug

• reaction favors lips, tongues, and floor of mouth; can be provoked by dental manipulation

• prioritize airway, then activate EMS and stop ACE inhibitor

  • notify physician about reaction

hereditary angioedema

C1 esterase inhibitor deficiency or dysfunction, usually autosomal dominant

• results in recurrent bradykinin-mediated edema of the skin, gut, or airway without hives

  • abdominal attacks can mimic a surgical emergency

• laryngeal swelling can be fatal

• dental trauma can trigger bradykinin release

  • contact physician about short-term prophylaxis of C1 inhibitor concentrate prior to treatment

  • keep procedures atraumatic