Now to the Scary — ANGIOEDEMA

Background — Angioedema is a paroxysmal, non-demarcated swelling of dermal or submucosal layers of skin / mucosa. Swelling is typically asymmetric, non-pitting and nonpruritic but can be associated with allergic features. 

  • isolated uvular angioedema (Quincke’s disease) is a rare presentation
    • causes: trauma, inhalation, general anesthesia, meds (ACEI), infections, hereditary

Etiologies 

  • ACE-I (bradykinin) 
  • Hereditary 
    • Autosomal Dominant
    • C1 esterase deficiency –> unregulated bradykinin associated with compliment pathway
  • Allergic (IgE, Type 1 Hypersensitivity reaction)
  • Idiopathic 

Clinical — Areas of swelling

  • Face, lips, tongue
  • Upper airway  = respiratory distress, stridor
  • Hands, genitals
  • Intestines = N/V, abdominal pain, diarrhea

Differentials

  • Allergic reaction / urticaria
  • Anaphylaxis
  • Angioedema
  • Anxiety ?
  • Asthma
  • Carcinoid
  • Cold urticaria
  • Scombroid
  • Shock
  • Transfusion Rxn
  • Infection
  • Foreign body

General Management

  • AIRWAY AIRWAY AIRWAY — take it if you have to; stridor, voice change, hoarseness, dyspnea
    • Don’t be an egomaniac — involve anesthesia / surgery as soon as you think about intubating these patients
    • ALL airway adjuncts at bedside — boujie, glide, our new fiberoptic toy!, cric set up, etc
  • Consider Epi 0.3 mg IM if thought to be allergic
  • Consider glucagon 1-5 mg IM if patient on BB and not responsive to Epi
  • Consider TXA 1g IV for bradykinin-mediated AE
  • FFP for possible C1-esterase or bradykinin (2 units)

Specific Cases

ACEI – Induced 

Highest incidence within the first month, but may occur at any time; 40% present months – years after initial doses

  • Epi/Benadryl/Methylpred
  • Icatibant 30 mg SubQ
  • Ecallantide 30 mg SQ (10 mg three separate sites)

Hereditary AE

  • C1 Inhibitor based on weight
  • Ecallantide 30 mg SQ (10 mg three separate sites)
  • Icatibant 30 mg SQ

Some Evidence

Both patients in our ED were ACE-I induced and both received TXA and both improved. Not sure if you guys saw the EMDOCs post concerning this but success seems pretty 50-50 reading the comments. TXA is the new haldol, it might fix everything.

Are these patients that can be on an OBS status in our ED if they show clinical improvement and no signs of airway compromise? Do we admit them all? What say you?

Comprehensive Guide with some flow charts from EMCRIT

https://emcrit.org/ibcc/angioedema/#bradykinin_angioedema:_treatment

References

https://www.wikem.org/wiki/Angioedema

https://rebelem.com/?s=angioedema

https://www.ncbi.nlm.nih.gov/m/pubmed/29735174/?fbclid=IwAR3-xVYmW7AZ6o_kiIvv_Cgh1QR-rXn80Oj81WxdB-COtz-_-reSK8KYuUM

Author