Difference between revisions of "Angioedema"

(Reformat of treatment with added ace treatments)
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===Etiologies===
 
===Etiologies===
*Congenital or acquired loss of C1 esterase inhibitor
+
*Allergic angioedema: [[Allergic reaction|IgE–mediated type I]] [[Hypersensitivity Reaction|hypersensitivity reaction]]  
*IgE–mediated type I [[Hypersensitivity Reaction|hypersensitivity reaction]] ([[Allergic reaction]])
+
*Hereditary angioedema: Congenital or acquired loss of C1 esterase inhibitor
*ACEI adverse reaction from excessive bradykinin
+
*ACE-I induced angioedema: ACEI adverse reaction from excessive bradykinin
*Idiopathic
+
*Idiopathic angioedema
  
 
[[File:Angioedema_post_lisinopril_use_2014-12-08_12-35.jpg|thumbnail|Angioedema]]
 
[[File:Angioedema_post_lisinopril_use_2014-12-08_12-35.jpg|thumbnail|Angioedema]]
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*C4 level screens for HAE (suspect if low)  
 
*C4 level screens for HAE (suspect if low)  
 
*Decreased levels of C1 and C4 esterase inhibitors confirms diagnosis
 
*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==
 
==ACE inhibitor-induced angioedema==
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*Incidence is 0.1-2.2% (more common in blacks)
 
*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
 
*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==
 
==Differential Diagnosis==
 
{{Template:Acute Allergic DDX}}
 
{{Template:Acute Allergic DDX}}
 +
 +
==Management==
 +
===General===
 +
*Consider [[Epinephrine]] 0.3mg IM if there is any concern this could be allergic in nature
 +
*Consider [[Glucagon]] 1-5mg IV if patient is on B-blockers and not responding to Epinephrine
 +
*Consider definitive airway if voice change, hoarseness, stridor, dyspnea
 +
**Prepare for a [[difficult airway]] which can include need for fiberoptics, ENT/anesthesia assistance, [[surgical airway]], or transfer to the OR
 +
 +
===Hereditary Angioedema===
 +
====First-Line Therapies====
 +
*C1 inhibitor (C1INH)<ref>Craig TJ, Levy RJ, Wasserman RL, et al. Efficacy of human C1 esterase inhibitor concentrate compared with placebo in acute hereditary angioedema attacks. J Allergy Clin Immunol. 2009; 124(4):801.</ref>
 +
**1000 units if ≤50kg
 +
**1500 units if >50-75kg
 +
**2000 units if >75-100kg
 +
**2500 units if >100kg
 +
*[[Ecallantide]]
 +
**10mg SQ x 3 in different anatomical locations (30mg in total)
 +
*[[Icatibant]]
 +
**30mg SQ
 +
====First-Line Therapies====
 +
*[[FFP]]
 +
**2 units
 +
 +
===ACE-I Induced Angioedema===
 +
Typical anaphylaxis medications do not effect bradykinin levels<ref>Bas M, Greve J, Stelter K, et al. Therapeutic efficacy of icatibant in angioedema induced by angiotensin-converting enzyme inhibitors: a case series. Ann Emerg Med. 2010; 56(3):278-282.</ref>, but consider:
 +
**[[Epinephrine]] 0.3mg IM
 +
**[[Diphenhydramine]] 50mg IV
 +
**[[Methyprednisolone]] 125mg IV
 +
*[[Icatibant]]
 +
**30mg SQ
 +
**Significantly decreases time to complete resolution (8 hrs vs 27.1 hrs)<ref>Baş M, Greve J, Stelter K, et al. A randomized trial of icatibant in ACE-inhibitor-induced angioedema. N Engl J Med. 2015; 372(5):418-25.</ref>
 +
*Consider [[Ecallantide]]
 +
**10mg SQ x 3 in different anatomical locations (30mg in total)
 +
**A 2015 trial showed a non-statistically significant trend towards benefit<ref>Bernstein JA, Moellman JJ, Collins SP, et al. Effectiveness of ecallantide in treating angiotensin-converting enzyme inhibitor-induced angioedema in the emergency department. Ann Allergy Asthma Immunol. 2015; 114(3):245.</ref>
  
 
==Disposition==
 
==Disposition==

Revision as of 18:03, 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

  • Allergic angioedema: IgE–mediated type I hypersensitivity reaction
  • Hereditary angioedema: Congenital or acquired loss of C1 esterase inhibitor
  • ACE-I induced angioedema: ACEI adverse reaction from excessive bradykinin
  • Idiopathic angioedema
Angioedema
Angioedema of tongue

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

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

Differential Diagnosis

Acute allergic reaction

Management

General

  • Consider Epinephrine 0.3mg IM if there is any concern this could be allergic in nature
  • Consider Glucagon 1-5mg IV if patient is on B-blockers and not responding to Epinephrine
  • Consider definitive airway if voice change, hoarseness, stridor, dyspnea

Hereditary Angioedema

First-Line Therapies

  • C1 inhibitor (C1INH)[2]
    • 1000 units if ≤50kg
    • 1500 units if >50-75kg
    • 2000 units if >75-100kg
    • 2500 units if >100kg
  • Ecallantide
    • 10mg SQ x 3 in different anatomical locations (30mg in total)
  • Icatibant
    • 30mg SQ

First-Line Therapies

ACE-I Induced Angioedema

Typical anaphylaxis medications do not effect bradykinin levels[3], but consider:

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)[6]
    • 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

See Also

References

  1. Winters ME, et al. Emergency department management of patients with ACE-inhibitor angioedema. JEM. 2013; 45(5):775–780.
  2. Craig TJ, Levy RJ, Wasserman RL, et al. Efficacy of human C1 esterase inhibitor concentrate compared with placebo in acute hereditary angioedema attacks. J Allergy Clin Immunol. 2009; 124(4):801.
  3. Bas M, Greve J, Stelter K, et al. Therapeutic efficacy of icatibant in angioedema induced by angiotensin-converting enzyme inhibitors: a case series. Ann Emerg Med. 2010; 56(3):278-282.
  4. Baş M, Greve J, Stelter K, et al. A randomized trial of icatibant in ACE-inhibitor-induced angioedema. N Engl J Med. 2015; 372(5):418-25.
  5. Bernstein JA, Moellman JJ, Collins SP, et al. Effectiveness of ecallantide in treating angiotensin-converting enzyme inhibitor-induced angioedema in the emergency department. Ann Allergy Asthma Immunol. 2015; 114(3):245.
  6. Ishoo E, et al. Predicting airway risk in angioedema: staging system based on presentation. Otolaryngol Head Neck Surg. 1999; 121(3):263-268.