Angioedema: Difference between revisions
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==Background== | ==Background== | ||
*Angioedema is paroxysmal, nondemarcated swelling of dermal or submucosal layers of skin or mucosa | *Angioedema is paroxysmal, nondemarcated swelling of dermal or submucosal layers of skin or mucosa | ||
**Swelling is asymmetric, nonpitting, and nonpruritic | **Swelling is asymmetric, nonpitting, and nonpruritic, however can be associated with allergic features depending on cause | ||
===Etiologies=== | ===Etiologies=== | ||
*Congenital or acquired loss of C1 esterase inhibitor | *Congenital or acquired loss of C1 esterase inhibitor | ||
*IgE–mediated type I [[Hypersensitivity Reaction|hypersensitivity reaction]] | *IgE–mediated type I [[Hypersensitivity Reaction|hypersensitivity reaction]] ([[Allergic reaction]]) | ||
*ACEI adverse reaction | *ACEI adverse reaction from excessive bradykinin | ||
*Idiopathic | *Idiopathic | ||
Revision as of 17:25, 1 July 2016
Background
- Angioedema is paroxysmal, nondemarcated swelling of dermal or submucosal layers of skin or mucosa
- Swelling is asymmetric, nonpitting, and nonpruritic, however can be associated with allergic features depending on cause
Etiologies
- Congenital or acquired loss of C1 esterase inhibitor
- IgE–mediated type I hypersensitivity reaction (Allergic reaction)
- ACEI adverse reaction from excessive bradykinin
- Idiopathic
Hereditary angioedema
Background
- Due to C1 esterase inhibitor deficiency
- Leads to unregulated activity of vasoactive mediators (bradykinin) associated with complement pathway
- Autosomal dominant
- Edema of face, extremities, bowel wall
Diagnosis
- Suspect in patients with history of recurrent peripheral angioedema and abdominal pain
- 75% experience onset of symptoms before age 15yr
- C4 level screens for HAE (suspect if low)
- Decreased levels of C1 and C4 esterase inhibitors confirms diagnosis
Treatment
- Strongly consider definitive airway if voice change, hoarseness, stridor, dyspnea - arrange transfer to OR if not crashing
- Epinephrine can produce some improvement in early acute attacks associated with anaphylaxis, however, HAE is bradykinin mediated and the role of steroids and H1/H2 blockers is limited
- If available - C1 esterase inhibitors (Berinert 20u/kg IV), kallikrein/bradykinin inhibitors (ecallantide 30mg SQ), or bradykinin receptor antagonist (icantibant 30mg SQ)
- FFP
- Replaces the missing inhibitor protein
- Not recommended in life-threatening laryngeal edema (some patients may become more edematous)
- Instead, pt should undergo fiberoptic intubation w/ preparation for surgical airway
ACE inhibitor-induced angioedema
Background
- Incidence is highest within the first month; however, may occur at anytime
- 40% present months to years after initial dose[1]
- Incidence is 0.1-2.2% (more common in blacks)
- Physiology more closely related to bradykinin-mediated pathway than IgE-mediated pathway, therefore current treatments may be insufficient
Treatment
- Airway management as above, consider awake fiberoptic intubation
- Epinephrine 0.3mg IM q15-20min prn
- Consider glucagon 1-5mg IV if pt on B-blockers and not responding to epi
- Diphenhydramine 50mg IV OR cetirizine 10mg PO
- Methylprednisolone 125mg IV
- H2 blocker IV or PO
Differential Diagnosis
Acute allergic reaction
- Allergic reaction/urticaria
- Anaphylaxis
- Angioedema
- Anxiety attack
- Asthma exacerbation
- Carcinoid syndrome
- Cold urticaria
- Contrast induced allergic reaction
- Scombroid
- Shock
- Transfusion reaction
Disposition
- Consider discharge after 4-6 hrs obs if there is no airway edema and pt improves
- 24 hrs obs if epi given
- Ishoo Staging (based on retrospective study)[2]
- Stage 1 - face/lip
- 48% outpatient, 52% floor, 0% ICU or advanced airway
- Stage 2 - soft palate
- 60% outpt, 40% floor, 0 ICU or advanced airway
- Stage 3 - tongue
- 26% outpt, 67% ICU, 7% advanced airway
- Stage 4 - larynx
- 100% ICU, 24% advanced airway
- Stage 1 - face/lip