1/31/17 Resident Morning Report – Angioedema

CC: tongue swelling, drooling

ID: 40 yo woman with HTN, GERD, anxiety disorder presents with throat swelling, subjective fevers, and drooling for 3 days.  She presented to an urgent care clinic 2 days ago with the same complaints and was given clindamycin without any improvement in her symptoms.  Home medications included amlodipin, omeprazole, and paroxetine.  She denied a family history of any swelling.  A thorough workup, including C4, auto-antibodies, C1 esterase inhibitor levels and function all returned normal.  She was finally deemed to have idiopathic angioedema after extensive evaluation for underlying rheumatologic and malignant disease

angioedema

Don’t forget:

  • Anaphylaxis can be diagnosed if any of the following 3 clinical criteria are met (this confers 95% specificity for anaphylaxis).  Remember that respiratory compromise or hypotension are notable features in anaphylaxis.
    1. acute onset skin/mucosal involvement AND respiratory compromise or hypotension
    2. exposure to a likely allergen AND 2 of the following 4
      • skin/mucosal involvement
      • respiratory compromise
      • hypotension
      • persistent GI symptoms
    3. exposure to a known allergen AND hypotension
  • Urticaria is localized areas of edema associated with pruritis and affects the superficial dermis.  It is usually transient and evanescent (< 24 hrs).  Angioedema is a deeper form of localized urticaria and affects the subcutaneous tissue, typically lasting slightly longer (48-72 hrs).

Pearls from morning report:

  • Mast cell mediated angioedema is associated with urticaria, pruritis, flushing, bronchospasm, throat tightness and hypotension.  Bradykinin mediated angioedema is NOT associated with urticaria or pruritis.
  • Initial laboratory workup for angioedema should include: CBC, CMP, CRP, ESR, C4.  Decreased C4 levels should prompt evaluation for C1 inhibitor deficiency – consider measuring levels of C1 inhibitor antigen and C1 inhibitor functional levels.
  • Early complement deficiencies (C1, C2, C3) can predispose to autoimmune disease.  Late complement deficiencies (C5 – C9) cause recurrent bacterial infections.

Random trivia:

Trauma can sometimes precipitate angioedema in a patient taking ACEi by way of direct tissue injury activation of bradykinin.  Angioedema was first described by Dr. Heinrich Quincke (of “Quincke’s pulse” – a sign of aortic insufficiency) in 1882 and was postulated to have a hereditary basis by Sir William Osler in 1888.


Want to read more?

Urticaria and angioedema (Allergy, Asthma, & Clinical Immunology)
Urticaria and angioedema: A practical approach (American Family Physician)


References: 

Zuraw BL. Clinical practice: Hereditary angioedema. N Engl J Med. 2008;359(10):1027-36.

Zuraw B, Bingham CO. An overview of angioedema: Pathogenesis and cause. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. (Accessed on February 1, 2017)

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