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 | ||
* | **Isolated uvular angioedema, or Quincke's disease, is a relatively rare presentation of angioedema of the upper airway | ||
* | [[File:Nejmicm020617 f1.jpg|thumb|Uvular Angioedema (Quincke's Disease)]] | ||
==Hereditary Angioedema== | ===Etiologies=== | ||
*'''Allergic angioedema:''' [[Allergic reaction|IgE–mediated type I]] [[Hypersensitivity Reaction|hypersensitivity reaction]] | |||
*'''Hereditary angioedema:''' Congenital or acquired loss of C1 esterase inhibitor | |||
*'''[[ACE inhibitor|ACE-I]] induced angioedema:''' ACEI adverse reaction from excessive bradykinin | |||
*'''Idiopathic angioedema''' | |||
[[File:Angioedema_post_lisinopril_use_2014-12-08_12-35.jpg|thumbnail|Angioedema]] | |||
[[File:Angioedema2013.jpg|thumbnail|Angioedema of tongue]] | |||
==Hereditary angioedema== | |||
===Background=== | ===Background=== | ||
*Due to C1 esterase inhibitor deficiency | *Due to C1 esterase inhibitor deficiency | ||
**Leads to unregulated activity of vasoactive mediators (bradykinin) associated with complement pathway | **Leads to unregulated activity of vasoactive mediators (bradykinin) associated with complement pathway | ||
**Autosomal dominant | **Autosomal dominant | ||
*Edema of face, extremities, bowel wall | |||
=== | ===Evaluation=== | ||
*Suspect in patients with history of recurrent peripheral angioedema and abdominal pain | *Suspect in patients with history of recurrent peripheral angioedema and abdominal pain | ||
**75% experience onset of symptoms before age 15yr | **75% experience onset of symptoms before age 15yr | ||
Line 20: | Line 27: | ||
*Decreased levels of C1 and C4 esterase inhibitors confirms diagnosis | *Decreased levels of C1 and C4 esterase inhibitors confirms diagnosis | ||
== | ==ACE inhibitor-induced angioedema== | ||
===Background=== | ===Background=== | ||
*Incidence is highest within the first month; however, may occur at anytime | *Incidence is highest within the first month; however, may occur at anytime | ||
*40% present months to years after initial dose<ref>Winters ME, et al. Emergency department management of patients with ACE-inhibitor angioedema. JEM. 2013; 45(5):775–780.</ref> | |||
*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 | ||
==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 beta-blockers and not responding to Epinephrine | |||
*[[FFP]] for possible etiology related to bradykinin<ref>Moellman, J.J., Bernstein, J.A., Lindsell, C., Banerji, A., Busse, P.J., Camargo, C.A., Collins, S.P., Craig, T.J., Lumry, W.R., Nowak, R., Pines, J.M., Raja, A.S., Riedl, M., Ward, M.J., Zuraw, B.L., Diercks, D., Hiestand, B., Campbell, R.L., Schneider, S. and Sinert, R. (2014) ‘A consensus parameter for the evaluation and management of Angioedema in the emergency department’, Academic Emergency Medicine, 21(4), pp. 469–484.</ref> | |||
**2 units | |||
*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 | |||
===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 | |||
**[[Methylprednisolone]] 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> | |||
**Note: control group did not receive FFP | |||
*Consider [[Ecallantide]] | |||
**10mg SQ x 3 in different anatomical locations (30mg in total) | |||
**A 2015 trial showed a non-statistically significant trend towards increased rate of ED discharge<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> | |||
**No benefit seen in mild-moderate cases in multi-center, double blind study<ref>Lewis, L.M., Graffeo, C., Crosley, P., Klausner, H.A., Clark, C.L., Frank, A., Miner, J., Iarrobino, R. and Chyung, Y. (2015) ‘Ecallantide for the acute treatment of angiotensin-converting enzyme Inhibitor–Induced Angioedema: A Multicenter, Randomized, controlled trial’, Annals of Emergency Medicine, 65(2), pp. 204–213.</ref> | |||
==Disposition== | ==Disposition== | ||
*Consider discharge after 4-6 hrs | *Consider discharge after 4-6 hrs observation if there is no airway edema and patient improves or swelling remains isolated to face and lips only | ||
*24 hrs obs if | *24 hrs obs if epinephrine given | ||
*Ishoo Staging (based on retrospective study) | *Ishoo Staging (based on retrospective study)<ref>Ishoo E, et al. Predicting airway risk in angioedema: staging system based on presentation. Otolaryngol Head Neck Surg. 1999; 121(3):263-268.</ref> | ||
**Stage 1 - face/lip | **Stage 1 - face/lip | ||
***48% outpatient, 52% floor, 0% ICU or advanced airway | ***48% outpatient, 52% floor, 0% ICU or advanced airway | ||
**Stage 2 - soft palate | **Stage 2 - soft palate | ||
***60% | ***60% outpatient, 40% floor, 0 ICU or advanced airway | ||
**Stage 3 - tongue | **Stage 3 - tongue | ||
***26% | ***26% outpatient, 67% ICU, 7% advanced airway | ||
**Stage 4 - larynx | **Stage 4 - larynx | ||
***100% ICU, 24% advanced airway | ***100% ICU, 24% advanced airway | ||
Line 64: | Line 89: | ||
*[[Tongue Diagnoses]] | *[[Tongue Diagnoses]] | ||
== | ==References== | ||
<references/> | |||
[[Category:ENT]] | [[Category:ENT]] |
Revision as of 17:38, 25 January 2019
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
- Isolated uvular angioedema, or Quincke's disease, is a relatively rare presentation of angioedema of the upper airway
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
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
Evaluation
- 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
- Allergic reaction/urticaria
- Anaphylaxis
- Angioedema
- Anxiety attack
- Asthma exacerbation
- Carcinoid syndrome
- Cold urticaria
- Contrast induced allergic reaction
- Scombroid
- Shock
- Transfusion 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 beta-blockers and not responding to Epinephrine
- FFP for possible etiology related to bradykinin[2]
- 2 units
- 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)[3]
- 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
ACE-I Induced Angioedema
- Typical anaphylaxis medications do not effect bradykinin levels[4], but consider:
- Epinephrine 0.3mg IM
- Diphenhydramine 50mg IV
- Methylprednisolone 125mg IV
- Icatibant
- 30mg SQ
- Significantly decreases time to complete resolution (8 hrs vs 27.1 hrs)[5]
- Note: control group did not receive FFP
- Consider Ecallantide
Disposition
- Consider discharge after 4-6 hrs observation if there is no airway edema and patient improves or swelling remains isolated to face and lips only
- 24 hrs obs if epinephrine given
- Ishoo Staging (based on retrospective study)[8]
- Stage 1 - face/lip
- 48% outpatient, 52% floor, 0% ICU or advanced airway
- Stage 2 - soft palate
- 60% outpatient, 40% floor, 0 ICU or advanced airway
- Stage 3 - tongue
- 26% outpatient, 67% ICU, 7% advanced airway
- Stage 4 - larynx
- 100% ICU, 24% advanced airway
- Stage 1 - face/lip
See Also
References
- ↑ Winters ME, et al. Emergency department management of patients with ACE-inhibitor angioedema. JEM. 2013; 45(5):775–780.
- ↑ Moellman, J.J., Bernstein, J.A., Lindsell, C., Banerji, A., Busse, P.J., Camargo, C.A., Collins, S.P., Craig, T.J., Lumry, W.R., Nowak, R., Pines, J.M., Raja, A.S., Riedl, M., Ward, M.J., Zuraw, B.L., Diercks, D., Hiestand, B., Campbell, R.L., Schneider, S. and Sinert, R. (2014) ‘A consensus parameter for the evaluation and management of Angioedema in the emergency department’, Academic Emergency Medicine, 21(4), pp. 469–484.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Lewis, L.M., Graffeo, C., Crosley, P., Klausner, H.A., Clark, C.L., Frank, A., Miner, J., Iarrobino, R. and Chyung, Y. (2015) ‘Ecallantide for the acute treatment of angiotensin-converting enzyme Inhibitor–Induced Angioedema: A Multicenter, Randomized, controlled trial’, Annals of Emergency Medicine, 65(2), pp. 204–213.
- ↑ Ishoo E, et al. Predicting airway risk in angioedema: staging system based on presentation. Otolaryngol Head Neck Surg. 1999; 121(3):263-268.