CASE presentation & TOPIC discussion

ANGIOEDEMA:ANGIOEDEMA:
CASE & DISCUSSIONCASE & DISCUSSION
Pathophysiology and ManagementPathophysiology and Management

CaseCase
 GMGM
 68 year old female68 year old female
 Presented to the casualty early hours of morningPresented to the casualty early hours of morning
on Saturday 6 April 2013on Saturday 6 April 2013
 C/o swelling in mouth and face with increasingC/o swelling in mouth and face with increasing
‘tightening’ of throat, progressively worsening‘tightening’ of throat, progressively worsening
over last 12hrsover last 12hrs
 No new medications, no medical or food allergyNo new medications, no medical or food allergy

PMHx:PMHx:
 HypertensionHypertension
 DMDM
 Current breast cancer patient on chemotherapyCurrent breast cancer patient on chemotherapy
 Had similar presentation one year ago, treated atHad similar presentation one year ago, treated at
hospitalhospital
 No known allergiesNo known allergies

Social Hx:Social Hx:
 Nil of noteNil of note
Surgical historySurgical history::
 Biopsy breast lump 3 years ago.Biopsy breast lump 3 years ago.

Meds:Meds:
 PerindoprilPerindopril
 HCTZHCTZ
 SimvastatinSimvastatin
 MetforminMetformin
 AspirinAspirin
 lasixlasix
 Chemotherapy (drug names unknown toChemotherapy (drug names unknown to
patient’s daugther)patient’s daugther)

sats 97% R/A, BP 150/90 regular pulsesats 97% R/A, BP 150/90 regular pulse
 tachycardiactachycardiac
 No stridorNo stridor
 Edema of lips and mainly of tongueEdema of lips and mainly of tongue
 Posterior pharyngeal wall not well visualizedPosterior pharyngeal wall not well visualized
 Flexible scope, larynx anatomically normal noFlexible scope, larynx anatomically normal no
oedema or impending airway obstructionoedema or impending airway obstruction

DDx:DDx:
 AngioedemaAngioedema
 Facial lymphedemaFacial lymphedema
 Autoimmune (Sjogren’s, SLE)Autoimmune (Sjogren’s, SLE)
 HypothyroidismHypothyroidism
 SVC syndromeSVC syndrome

Management:Management:
 Kept in casualty for initial treatmentKept in casualty for initial treatment
 Anti hypertensives given with omission of coversylAnti hypertensives given with omission of coversyl
 Lasix 20 mg iviLasix 20 mg ivi
 Decadron 8 mgDecadron 8 mg
 In 5 mins, the tongue almost halved in size andIn 5 mins, the tongue almost halved in size and
patient was much more comfortable and notpatient was much more comfortable and not
distresseddistressed
 Patient then admitted to ward for continuation ofPatient then admitted to ward for continuation of
corticosteroids and monitering of vitalscorticosteroids and monitering of vitals
 Patient discharged after 24 hours of monitering andPatient discharged after 24 hours of monitering and
getting dexamethasone in the wardgetting dexamethasone in the ward

Definition:Definition:
 Rapid nonpitting edema of the dermis, subcutaneousRapid nonpitting edema of the dermis, subcutaneous
tissue, mucosa and submucosal tissuestissue, mucosa and submucosal tissues

Areas of involvement:Areas of involvement:
 FaceFace
 LipsLips
 LarynxLarynx
 ExtremitiesExtremities
 GenitalsGenitals
 IntestinesIntestines
 If involvement of face/larynx = potentially life-If involvement of face/larynx = potentially life-
threateningthreatening
 94% of the time involves structures in the H&N94% of the time involves structures in the H&N

Epidemiology:Epidemiology:
 10% of Americans have an episode once in their10% of Americans have an episode once in their
lifetime (20% in south africa)lifetime (20% in south africa)
 Higher in hypertensive patients that are on ACEHigher in hypertensive patients that are on ACE
inhibitorsinhibitors
 Usually in 3Usually in 3rdrd
/4/4thth
decades of lifedecades of life
 M=FM=F
 Attacks usually self-limiting and resolve in 24-48Attacks usually self-limiting and resolve in 24-48
hourshours
 Principal cause of mortality is airway compromisePrincipal cause of mortality is airway compromise

Basic Pathophysiology:Basic Pathophysiology:
 Increased vascular permeability in theIncreased vascular permeability in the
submucosal, subcutaneous, and deep dermalsubmucosal, subcutaneous, and deep dermal
tissues.tissues.
 Mediated by vasoactive substances:Mediated by vasoactive substances:
• HistamineHistamine
• BradykininBradykinin
• Products of complement cascade: C3a, C5aProducts of complement cascade: C3a, C5a

5 Main Causes:5 Main Causes:
1.1. Hereditary C1INH deficiencyHereditary C1INH deficiency
2.2. Acquired C1INH deficiencyAcquired C1INH deficiency
3.3. ACE inhibitorsACE inhibitors
4.4. Allergic reactionsAllergic reactions
5.5. IdiopathicIdiopathic

Can sub-divide the causes of angioedema by mediatorsCan sub-divide the causes of angioedema by mediators
involved:involved:
BradykininBradykinin – Induced:– Induced:
 Hereditary or acquired C1 inhibitor deficiencyHereditary or acquired C1 inhibitor deficiency
 ACE inhibitorsACE inhibitors
HistamineHistamine – Induced:– Induced:
 Allergic angioedemaAllergic angioedema
UnknownUnknown
 IdiopathicIdiopathic

BradykininBradykinin
 Peptide in blood coagulation subsystemPeptide in blood coagulation subsystem
• ‘‘contact system’contact system’
 Release regulated by C1-INHRelease regulated by C1-INH
Stimulus for production:Stimulus for production:
 ToxinsToxins
 Injury/inflammationInjury/inflammation
 IschemiaIschemia
 Viral infectionsViral infections

Kinin-Kallikrein SystemKinin-Kallikrein System
 High molecular weight kininogen is combinedHigh molecular weight kininogen is combined
with prekallikreinwith prekallikrein
 Prekallikrein broken down by factor XIIa toPrekallikrein broken down by factor XIIa to
kallikreinkallikrein
 Kallikrein then breaks high molecular weightKallikrein then breaks high molecular weight
Aminogen to bradykininAminogen to bradykinin
 Bradkinin is main mediator of vasopermeabilityBradkinin is main mediator of vasopermeability

C1-INH inhibits the reaction cascade at two points:C1-INH inhibits the reaction cascade at two points:
 Prevents self-activation of factor XII (PreKPrevents self-activation of factor XII (PreKK)K)
 Inhibits release of bradykinin from HMW kininogenInhibits release of bradykinin from HMW kininogen

Support for Bradykinin as mediator:Support for Bradykinin as mediator:
 Cicardi (2003)Cicardi (2003): showed increased levels of: showed increased levels of
bradykinin in affected arms of patientsbradykinin in affected arms of patients
 BUT increased bradykinin levels in normal patientsBUT increased bradykinin levels in normal patients
taking ACEIs (prolongs survival of bradykinin)taking ACEIs (prolongs survival of bradykinin)

ACEi AngioedemaACEi Angioedema
 Recently become the leading cause of acquiredRecently become the leading cause of acquired
angioedemaangioedema
 Corresponds with increasingly widespread use ofCorresponds with increasingly widespread use of
ACEi to manage hypertension and CHFACEi to manage hypertension and CHF

Renin-Angiotensin-AldosteroneRenin-Angiotensin-Aldosterone
System (RAAS)System (RAAS)

Mechanism:Mechanism:
ACE inhibition:ACE inhibition:
 reduces the catabolism of bradykininreduces the catabolism of bradykinin
 increase the availability of bradykininincrease the availability of bradykinin
*BUT bradykinin elevated in ALL patients on*BUT bradykinin elevated in ALL patients on
ACEi’s and <1% develop angioedemaACEi’s and <1% develop angioedema

Incidence:Incidence:
 Can occur at ANY time during treatment.Can occur at ANY time during treatment.
 Most severe episodes occur within the first weekMost severe episodes occur within the first week
of treatment.of treatment.
 Some reports of incidence AFTERSome reports of incidence AFTER
discontinuation of therapy therefore may havediscontinuation of therapy therefore may have
latent effect.latent effect.

Large Trial - Determine Incidence:Large Trial - Determine Incidence:
Omapatrilat Cardiovascular Treatment versusOmapatrilat Cardiovascular Treatment versus
Enalipril (Enalipril (O.C.T.A.V.E.O.C.T.A.V.E.) trial Kostis et al (2004)) trial Kostis et al (2004)
• Double-blinded RCTDouble-blinded RCT
• N = 24,302N = 24,302
• Primary outcome: drug efficacy in cardiac settingPrimary outcome: drug efficacy in cardiac setting
• Secondary outcome – incidence of angioedemaSecondary outcome – incidence of angioedema
• 2.17% vs 0.68%2.17% vs 0.68%

 More common in Black populations thanMore common in Black populations than
Caucasian 3:1Caucasian 3:1
 Increased risk unrelated to dose, type of ACEiIncreased risk unrelated to dose, type of ACEi
or concomitant medicationsor concomitant medications
 Increased sensitivity to elevated bradykininIncreased sensitivity to elevated bradykinin
levelslevels

Other Risk Factors:Other Risk Factors:
 ImmunocompromisedImmunocompromised
 Prior history of idiopathic angioedemaPrior history of idiopathic angioedema
 Seafood allergySeafood allergy

Clinical presentation:Clinical presentation:
 Wide range of symptomsWide range of symptoms
• Life-threatening to minor swelling (may not reportLife-threatening to minor swelling (may not report
to health-care provider)to health-care provider)
• Can resolve spontaneouslyCan resolve spontaneously
 In severe cases:In severe cases:
• Swelling of lips, tongue, post pharynx, eyesSwelling of lips, tongue, post pharynx, eyes
• Dyspnea, dysphagia, dysphonia in up to 20%Dyspnea, dysphagia, dysphonia in up to 20%
patientspatients  a/w obstructiona/w obstruction

Treatment:Treatment:
*Difficult to tailor Rx as difficult to determine etiology*Difficult to tailor Rx as difficult to determine etiology
in acute scenarioin acute scenario
 ABCs always firstABCs always first
• establish a/westablish a/w
• Tongue edema is NON pitting therefore difficult orotrachealTongue edema is NON pitting therefore difficult orotracheal
intubationintubation
• May require nasotracheal intubation or trachMay require nasotracheal intubation or trach
 Secondary goal = prevent further edemaSecondary goal = prevent further edema

Treatment:Treatment:
 Antihistamines often used, but ~ no effectAntihistamines often used, but ~ no effect
 Corticosteroids – minimal/no benefitCorticosteroids – minimal/no benefit
 Epinephrine – works in non-specific mannerEpinephrine – works in non-specific manner
(vasoconstriction of leaky blood vessels)(vasoconstriction of leaky blood vessels)
 FFP (likely the effect of functional kininase II –FFP (likely the effect of functional kininase II –
breaks down bradykinin)breaks down bradykinin)

 Currently NO diagnostic test to determine whoCurrently NO diagnostic test to determine who
is at riskis at risk

ARB AngioedemaARB Angioedema
 Links have been made with ARBs and angioedemaLinks have been made with ARBs and angioedema
 Highly variable results depending on the studyHighly variable results depending on the study
 Controversial evidence for triggering angioedemaControversial evidence for triggering angioedema
 ARBs not supposed to be involved in kinin metabolismARBs not supposed to be involved in kinin metabolism
 Seen in patients who previously developed angioedemaSeen in patients who previously developed angioedema
with ACEiwith ACEi

 Also present in patients who never receivedAlso present in patients who never received
ACEi’sACEi’s
 Unknown mechanismUnknown mechanism
 Unknown incidenceUnknown incidence

Cicardi et al (2004):Cicardi et al (2004):
 2 of 26 patients with ACEi induced angioedema2 of 26 patients with ACEi induced angioedema
also had angioedema when placed on an ARBalso had angioedema when placed on an ARB
 Effect disappeared upon w/drawl of the ARBEffect disappeared upon w/drawl of the ARB
 Recommendations: use ARBs cautiously inRecommendations: use ARBs cautiously in
patients w/ history of ACEi angioedemapatients w/ history of ACEi angioedema

Hereditary Angioedema (HAE)Hereditary Angioedema (HAE)
 Rare (1:50 000-1:150 000)Rare (1:50 000-1:150 000)
 Autosomal dominantAutosomal dominant
 No ethnic or sexual predilictionNo ethnic or sexual prediliction
 Individuals affected = commonly heterozygousIndividuals affected = commonly heterozygous
 Disorder of C1 inhibitor (C1INH)Disorder of C1 inhibitor (C1INH)

Genetics - C1INH:Genetics - C1INH:
 C1 inhibitor – heavily glycosylated serine proteaseC1 inhibitor – heavily glycosylated serine protease
inhibitorinhibitor
 Chromosome 11q11-13.2Chromosome 11q11-13.2
 Single dysfunctional allele results in diseaseSingle dysfunctional allele results in disease

C1INH:C1INH:
 Only regulator of classical complement pathwayOnly regulator of classical complement pathway
activationactivation
Involved in:Involved in:
 Contact system (XII and kallikrein)Contact system (XII and kallikrein)
 Complement cascade (C1r,C1s, MASP 2)Complement cascade (C1r,C1s, MASP 2)
 Intrinsic coagulation cascade (XI, plasmin, tPA)Intrinsic coagulation cascade (XI, plasmin, tPA)
 Low levels C1INH OR dysfunctional C1INH =Low levels C1INH OR dysfunctional C1INH =
HAEHAE

2 types of HAE:2 types of HAE:
 Type IType I (85%)(85%)
 low levels of C1INH and functional deficiencylow levels of C1INH and functional deficiency
 Type IIType II (15%)(15%)
 Normal protein concentration but functional defectNormal protein concentration but functional defect

Diagnosis – Type I or II:Diagnosis – Type I or II:
 Measure C1INH antigen and functional levelsMeasure C1INH antigen and functional levels
 Type I – values <50% normalType I – values <50% normal
 Not specific asNot specific as::
 absolute C1INH level is NOT correlated with freqabsolute C1INH level is NOT correlated with freq
or degree of symptomsor degree of symptoms

 Onset of attacks usually w/in 2Onset of attacks usually w/in 2ndnd
decade of lifedecade of life
 Time of onset to diagnosis 3-8 yearsTime of onset to diagnosis 3-8 years

Clinical Presentation:Clinical Presentation:
 Repeated episodes of edema (NON pruritic andRepeated episodes of edema (NON pruritic and
NON pitting):NON pitting):
 FaceFace
 ExtremitiesExtremities
 GenitalsGenitals
 Intestines (w/ pain, N/V/D)Intestines (w/ pain, N/V/D)
 Larynx (less common)Larynx (less common)
**Combination and migratory attacks common**Combination and migratory attacks common

 Laryngeal edemaLaryngeal edema
 Usually in 3Usually in 3rdrd
 Lifetime incidence of 70%Lifetime incidence of 70%
 Retrospective review (Bork, 2000): 40% pt’s lostRetrospective review (Bork, 2000): 40% pt’s lost
family member to asphyxiationfamily member to asphyxiation

 Erythema marginatum and macular rash inErythema marginatum and macular rash in
SOME patientsSOME patients
 ***NO urticaria***NO urticaria
 Swelling increases over 24 hours then subsidesSwelling increases over 24 hours then subsides
over next 24-72 hoursover next 24-72 hours
 Frequency, duration and severity of symptomsFrequency, duration and severity of symptoms
VARIABLE even w/in same familyVARIABLE even w/in same family

 Recognized triggers:Recognized triggers:
 OCP (Estrogen – containing)OCP (Estrogen – containing)
 MensesMenses
 TraumaTrauma
 InfectionInfection
 StressStress
 Dental surgery(trigger for laryngeal attack)Dental surgery(trigger for laryngeal attack)

Labs:Labs:
1) C1INH - low levels, or elevated levels of1) C1INH - low levels, or elevated levels of
dysfunctional C1 esterase inhibitor (detected bydysfunctional C1 esterase inhibitor (detected by
an immune assay).an immune assay).
2) Between attacks, low levels of C4 are noted.2) Between attacks, low levels of C4 are noted.

Economic/Burden:Economic/Burden:
 Untreated patients lose up to 100-150 workUntreated patients lose up to 100-150 work
days/yeardays/year
 Morbidity ~50%Morbidity ~50%

Diagnostic Criteria:Diagnostic Criteria:
A)A) Clinical:Clinical:
 Self-limited, angioedema without urticaria,Self-limited, angioedema without urticaria,
recurrent and >12 hoursrecurrent and >12 hours
 Self-remitting abdo pain without clear organicSelf-remitting abdo pain without clear organic
etiology, recurrent and >6hrsetiology, recurrent and >6hrs
 Recurrent laryngeal edemaRecurrent laryngeal edema

Diagnostic Criteria:Diagnostic Criteria:
B)B) Laboratory:Laboratory:
 C1INH<50% at 2 sep determinations withC1INH<50% at 2 sep determinations with
patient at basal conditionpatient at basal condition
 C1INH function <50%C1INH function <50%
 Mutation in C1INH gene altering proteinMutation in C1INH gene altering protein
syn/functionsyn/function
*low C4 not mentioned in criteria although part of*low C4 not mentioned in criteria although part of
initial w/uinitial w/u

Supportive treatment:Supportive treatment:
Laryngeal edema:Laryngeal edema:
 Prudent use ETT intubationPrudent use ETT intubation
 Monitored setting until resolution of attackMonitored setting until resolution of attack
 Steroids/antihistamines NOT usefulSteroids/antihistamines NOT useful
 Adrenaline nebs may decrease the vascularAdrenaline nebs may decrease the vascular
component of edema but doesn’t change thecomponent of edema but doesn’t change the
underlying processunderlying process

Supportive treatment:Supportive treatment:
Intestinal edema:Intestinal edema:
 Aggressive replacement fluid losses (3Aggressive replacement fluid losses (3rdrd
spacingspacing
and V/D)and V/D)
 Pain managementPain management
 Non-sedating anti-emeticsNon-sedating anti-emetics
 Avoid interventional procedures unless unusualAvoid interventional procedures unless unusual
s/s (hematemesis, hematochezia)s/s (hematemesis, hematochezia)

Established Pharmacologic Treatments:Established Pharmacologic Treatments:
ProphalaxisProphalaxis::
1)1) Androgen derivativesAndrogen derivatives
2)2) Antifibrinolytic agentsAntifibrinolytic agents
Acute attacks:Acute attacks:
3) FFP (replacement)3) FFP (replacement)
4) Purified C1INH (not available in SA)4) Purified C1INH (not available in SA)

Mechanism of action:Mechanism of action:
1) Androgens (Danazol)1) Androgens (Danazol)
 Stimulate hepatocytes and other cells to secreteStimulate hepatocytes and other cells to secrete
more C1INHmore C1INH
2) Antifibrinolytics (2) Antifibrinolytics (Transexamic acid)Transexamic acid)
 Inhibits fibrinolysis and reduces consumption ofInhibits fibrinolysis and reduces consumption of
C1INHC1INH

Mechanism of action:Mechanism of action:
3) FFP3) FFP
 Replaces C1INH missing/dysfunctional inReplaces C1INH missing/dysfunctional in
recipientrecipient
4)4) Purified C1INHPurified C1INH
 Replaces C1INHReplaces C1INH

Recent Study (CSL Behring):Recent Study (CSL Behring):
TheThe I.M.P.A.C.TI.M.P.A.C.T. trial (International Multi-centre. trial (International Multi-centre
Prospective Angioedema C1-inhibitor TrialsProspective Angioedema C1-inhibitor Trials
 Phase III study conducted in N America and EuropePhase III study conducted in N America and Europe
 Comparing human pasteurized C1-INH vs placebo forComparing human pasteurized C1-INH vs placebo for
speed of relief of symptomsspeed of relief of symptoms
 Studying patients with acute abdominal or facial HAEStudying patients with acute abdominal or facial HAE

Future Therapies:Future Therapies:
2 Treatments Under Investigation:2 Treatments Under Investigation:
• DX-88DX-88
• Bradykinin Antagonist – IcatibantBradykinin Antagonist – Icatibant

DX-88DX-88
 binds and inhibits proteolytic activity ofbinds and inhibits proteolytic activity of
 300x more specific than C1INH300x more specific than C1INH
 Lumry et al (2006) showed successfulLumry et al (2006) showed successful
resolution symptoms in all 215 attacks treatedresolution symptoms in all 215 attacks treated
with DX-88with DX-88

Bradykinin antagonist – IcatibantBradykinin antagonist – Icatibant
 potent, selective bradykinin receptor antagonistpotent, selective bradykinin receptor antagonist
 Bork et al (2007) showed treatment considerablyBork et al (2007) showed treatment considerably
shortened duration of attacks compared withshortened duration of attacks compared with
untreated attacks (1.0 hr vs several hrs)untreated attacks (1.0 hr vs several hrs)

Resolution after attack - not well understoodResolution after attack - not well understood
Theories:Theories:
1)1) Consumption of available substrates forConsumption of available substrates for
2)2) Removal of triggerRemoval of trigger

Acquired Angioedema (AAE)Acquired Angioedema (AAE)
2 Types:2 Types:
1)1) Type I (AAE-I)Type I (AAE-I)
• associated with other diseases, most commonly B-associated with other diseases, most commonly B-
cell lymphoproliferative disorderscell lymphoproliferative disorders
1)1) Type II (AAE-II)Type II (AAE-II)
• an autoimmune process (autoantibody directedan autoimmune process (autoantibody directed
against the C1 inhibitor molecule (C1-INH).against the C1 inhibitor molecule (C1-INH).

Pathophysiology:Pathophysiology:
1)1) AAE-IAAE-I
• assoc disorders (usually lymphoproliferativeassoc disorders (usually lymphoproliferative
malignancies, most common – B cell lymphoma)malignancies, most common – B cell lymphoma)
• produce complement-activating factors, antibodies,produce complement-activating factors, antibodies,
or other immune complexesor other immune complexes
• destroy C1-INH functiondestroy C1-INH function

PathophysiologyPathophysiology
2)2) AAE-IIAAE-II
• normal C1-INH molecule is synthesized innormal C1-INH molecule is synthesized in
adequate amountsadequate amounts
• subpopulation of B cells secretes autoantibodies tosubpopulation of B cells secretes autoantibodies to
the C1-INH moleculethe C1-INH molecule
• autoantibody binds to the reactive center of C1-autoantibody binds to the reactive center of C1-
INH and its regulatory capacity isINH and its regulatory capacity is
diminished/destroyed.diminished/destroyed.

EpidemiologyEpidemiology
 Rare (150 cases reported in the literature)Rare (150 cases reported in the literature)
 ?M=F??M=F?
 Race?Race?
 Onset most common after 4Onset most common after 4thth

Clinical presentation:Clinical presentation:
 *no family history (distinguish from HAE)*no family history (distinguish from HAE)
 PainlessPainless
 Non-pruriticNon-pruritic
 Non-pittingNon-pitting
 Usually not assoc with urticariaUsually not assoc with urticaria
Edema of the skin and subcutaneous tissuesEdema of the skin and subcutaneous tissues

Labs:Labs:
 AAE-I and AAE-IIAAE-I and AAE-II
 Low C1-INH levelsLow C1-INH levels
 Low C1q levels (except 1 reported case)Low C1q levels (except 1 reported case)
 Low C4 levelsLow C4 levels
 Low C2 levelsLow C2 levels
 AAE-II - Positive immunoblot assay findings for 95-AAE-II - Positive immunoblot assay findings for 95-
kd C1-INH cleavage productkd C1-INH cleavage product

 Supportive (airway)Supportive (airway)
 AndrogensAndrogens
 may be beneficial in AAE-I but are of no value inmay be beneficial in AAE-I but are of no value in
AAE-IIAAE-II
 AntifibrinolyticsAntifibrinolytics
 more effective for long-term prophylaxis in thosemore effective for long-term prophylaxis in those
with AAE.with AAE.

 Immunosuppressive therapyImmunosuppressive therapy
 Direct toward decreasing autoantibody productionDirect toward decreasing autoantibody production
may be of value in patients with AAE-IImay be of value in patients with AAE-II

Allergic Angioedema/UrticariaAllergic Angioedema/Urticaria

 Reactions are induced by histamine andReactions are induced by histamine and
mediated by IgEmediated by IgE
 IgE mediated hypersensitivity reactionIgE mediated hypersensitivity reaction
 Reaction with allergen induces the release ofReaction with allergen induces the release of
histamine and other mediatorshistamine and other mediators
 Result: vasodilatation and edemaResult: vasodilatation and edema

Biochemistry:Biochemistry:
 Dependent on presence IgE molec sp toDependent on presence IgE molec sp to
proteins in causative agentproteins in causative agent
 IgE molec bind to patients mast cellsIgE molec bind to patients mast cells
 Trigger rxn upon re-exposure to antigenTrigger rxn upon re-exposure to antigen

Inciting Agents:Inciting Agents:
 MedicationsMedications
 FoodsFoods
 LatexLatex
 Environmental (includes insect bites)Environmental (includes insect bites)

 Highly variableHighly variable
 Depends on:Depends on:
 prev sensitizationprev sensitization
 type of allergentype of allergen
 +/- urticaria+/- urticaria
(pruritic)(pruritic)

 Often seen in patients with other allergicOften seen in patients with other allergic
conditions:conditions:
 Atopic dermatitisAtopic dermatitis
 Allergic rhinitisAllergic rhinitis
 AsthmaAsthma

 As always, airway firstAs always, airway first
 AAE does respond to:AAE does respond to:
 SteroidsSteroids
 H1 and H2 blockersH1 and H2 blockers
 subcutaneous epinephrinesubcutaneous epinephrine
 antihistamines.antihistamines.

Management AngioedemaManagement Angioedema

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