gavin burgess em rounds 22 november 2007 thanks dr t vander leek

Gavin Burgess

EM Rounds

22 November 2007

Thanks Dr T Vander Leek

Anna Phil

Axis

IntroductionIntroduction

““Anaphylaxis” coined in 1902 Anaphylaxis” coined in 1902 (Portier + Richet)(Portier + Richet)

Experimented with dogs and sea Experimented with dogs and sea anemone venom immunisationsanemone venom immunisations

Dogs unexpectedly died after Dogs unexpectedly died after previously tolerated dosespreviously tolerated doses

Lieberman in Allergy: Principles and Practice Lieberman in Allergy: Principles and Practice v.5, 1079-92v.5, 1079-92

Definition?Definition?

DefinitionDefinition

A Severe, potentially fatal, systemic A Severe, potentially fatal, systemic allergic reaction that occurs suddenly allergic reaction that occurs suddenly after contact with an allergy-causing after contact with an allergy-causing substancesubstance

Sampson Sampson et alet al JACI 2006;117:391-7 JACI 2006;117:391-7


A severe allergic reaction to any A severe allergic reaction to any stimulus, having sudden onset, stimulus, having sudden onset, involving one or more body systems involving one or more body systems with multiple symptomswith multiple symptoms

Canadian Anaphylaxis Guidelines Canadian Anaphylaxis Guidelines www.allergysafecommunities.cawww.allergysafecommunities.ca

http://www.allergysafecommunities.ca/


An acute, life-threatening reaction An acute, life-threatening reaction mediated by IgEmediated by IgE

IgE-mediated Type I hypersensitivityIgE-mediated Type I hypersensitivity Release of Mast cell and Basophil Release of Mast cell and Basophil

contentscontents

What’s in the cells?What’s in the cells?

Biochemical Mediators Biochemical Mediators and Chemotactic Substancesand Chemotactic Substances

Degranulation of mast cells and Degranulation of mast cells and basophils.basophils.

PreformedPreformed granule-associated granule-associated substances, e.g., histamine, tryptase, substances, e.g., histamine, tryptase, chymase, heparin, histamine-releasing chymase, heparin, histamine-releasing factor, other cytokines.factor, other cytokines.

Newly generatedNewly generated lipid-derived lipid-derived mediators, e.g., prostaglandin Dmediators, e.g., prostaglandin D22, , leukotriene Bleukotriene B44, PAF, LTC, PAF, LTC44, LTD, LTD44, and LTE, and LTE44..

Biochemical Mediators Biochemical Mediators and Chemotactic Substancesand Chemotactic Substances

Eosinophils may play pro-Eosinophils may play pro-inflammatory role (release of inflammatory role (release of cytotoxic granule-associatedcytotoxic granule-associated proteins) or anti-inflammatory role proteins) or anti-inflammatory role (e.g., metabolism of vasoactive (e.g., metabolism of vasoactive mediators)mediators)

IncidenceIncidence

Analysis of published studies of most Analysis of published studies of most common causescommon causes

3.3 to 4 million Americans at risk.3.3 to 4 million Americans at risk. 1,433 to 1,503 at risk for fatal 1,433 to 1,503 at risk for fatal

reaction.reaction. Neugut, Ghatak, Miller Arch Int Med 2001 Neugut, Ghatak, Miller Arch Int Med 2001

Incidence Based on Incidence Based on Epinephrine Rx for Epinephrine Rx for Out-of-Hospital UseOut-of-Hospital Use

From Canada and Wales.From Canada and Wales. 0.95% of population in Manitoba, Canada.0.95% of population in Manitoba, Canada. 0.2 per 1000 in Wales.0.2 per 1000 in Wales. Incidence increased in Wales between Incidence increased in Wales between

1994 & 1999.1994 & 1999.

Simons, Peterson, BlackSimons, Peterson, Black JACI 2002JACI 2002

Rangaraj, Tuthill, Burr, AlfahamRangaraj, Tuthill, Burr, Alfaham JACI 2002JACI 2002

Case 1Case 1

6y at friend’s birthday party, ate 6y at friend’s birthday party, ate peanut-containing peanutspeanut-containing peanuts

Tingling around mouth, thick tongue, Tingling around mouth, thick tongue, lip swellinglip swelling

In ED, urticaria, swollen lips and In ED, urticaria, swollen lips and tongue, flushingtongue, flushing

Vitals: P120, RR 35-40, afebrile, BP Vitals: P120, RR 35-40, afebrile, BP 70/4070/40

Signs of anaphylaxis….Signs of anaphylaxis….

Case 1Case 1

Signs of anaphylaxisSigns of anaphylaxis

Loss of consciousnessLoss of consciousness

““sense of impending doom”sense of impending doom”


Cutaneous – urticaria, angioedema, Cutaneous – urticaria, angioedema, pruritis, erythema/flushingpruritis, erythema/flushing

Oral – tingling lips/tongue/palate, Oral – tingling lips/tongue/palate, swollen tongue/lipsswollen tongue/lips

Ocular – periocular oedema, Ocular – periocular oedema, erythema, conjunctival injection, erythema, conjunctival injection, tearingtearing


Respiratory Respiratory Upper airway – voice change, throat Upper airway – voice change, throat

clearing, airway obstruction (tongue, clearing, airway obstruction (tongue, laryngeal or oropharyngeal oedema), laryngeal or oropharyngeal oedema), sneezing, nasal pruritis, rhinorrhea, sneezing, nasal pruritis, rhinorrhea, congestioncongestion

Lower airway - wheeze, cough, tight Lower airway - wheeze, cough, tight chestchest


Gastrointestinal – nausea, vomiting, Gastrointestinal – nausea, vomiting, cramps, diarrhea, urgency, cramps, diarrhea, urgency, incontinenceincontinence

Genitourinary – uterine cramps, Genitourinary – uterine cramps, urgency, incontinenceurgency, incontinence

Cardiovascular – hypotension, Cardiovascular – hypotension, arrhythmia, shock, syncope, chest arrhythmia, shock, syncope, chest painpain


Signs/symptomsSigns/symptoms %%

Urticaria and angiooedemaUrticaria and angiooedema 8888

Dyspnoea, wheezeDyspnoea, wheeze 4747

Dizziness, syncope, hypotensionDizziness, syncope, hypotension 3333

N,V+D, crampsN,V+D, cramps 3030

FlushingFlushing 4646

Upper airway oedemaUpper airway oedema 5656

HeadacheHeadache 1515

RhinitisRhinitis 1616

Substernal painSubsternal pain 66

Itch without rashItch without rash 4.54.5

SeizureSeizure 1.51.5

Lieberman in Allergy: Principles and practice v.5 1079-92

Case 2Case 2

25y F, known ED, stands, has 25y F, known ED, stands, has syncopal event, diaphoresis, nauseasyncopal event, diaphoresis, nausea

Looks pale, P110, BP (L) 110/70, BP Looks pale, P110, BP (L) 110/70, BP (s) 90/50, RR18(s) 90/50, RR18

Differential DiagnosisDifferential Diagnosis

Anything can resemble anaphylaxisAnything can resemble anaphylaxis Vasovagal, globus hystericus, status Vasovagal, globus hystericus, status

asthmaticus, hereditary angioedema, asthmaticus, hereditary angioedema, hypoglycaemia, FB aspiration, hypoglycaemia, FB aspiration, seizures, seizures, etc.etc.

HypersensitivityHypersensitivity

Type I – immediate, preformedType I – immediate, preformed Almost all <60minAlmost all <60min Can skin test, IgE-mediated ONLYCan skin test, IgE-mediated ONLY

Type II – cytotoxic, IgM, IgG on cell Type II – cytotoxic, IgM, IgG on cell surfacesurface

<72hours<72hours

HypersensitivityHypersensitivity

Type III – immune complex, serum Type III – immune complex, serum sickness, IgGsickness, IgG

1-3 week delay LN, arthritis1-3 week delay LN, arthritis

Type IV – T-cell mediated, NO Type IV – T-cell mediated, NO antibodiesantibodies

>48 hours>48 hours

Adverse reactionsAdverse reactions

Reactions

Unpredictable (20-30%) Predictable(75-80%)

Non immune mediated (15-20%) Immune mediated (5-10%)

Mixed

Adverse ReactionsAdverse Reactions

Mixed reactionsMixed reactions Erythema multiforme -> Stevens-Johnson, Erythema multiforme -> Stevens-Johnson,

fixed drug reactionfixed drug reaction

Unpredictable, non immune Unpredictable, non immune mediated “pseudo allergic”mediated “pseudo allergic”

Red man, morphine, ACEI, G6PDRed man, morphine, ACEI, G6PD

Predictable reactionsPredictable reactions

CausesCauses

CausesCauses

Food Food VaccinesVaccines MedicationsMedications Blood productsBlood products LatexLatex

Drugs and Drugs and biologicalsbiologicals

ExerciseExercise Insect venomInsect venom Idiopathic Idiopathic

SignificanceSignificance

Food allergy is now the most Food allergy is now the most common cause of anaphylaxis in the common cause of anaphylaxis in the ED.ED.

>1/3 of presentations>1/3 of presentations Sampson HA. Pediatrics 2003;111:1601-8Sampson HA. Pediatrics 2003;111:1601-8

Risk FactorsRisk Factors

TomKat's Craziest TomKat's Craziest Comments:Comments: "She "She trusts me. She trusts me. She loves me. We show loves me. We show her the cut footage her the cut footage of my stunts and of my stunts and she digs it. She's she digs it. She's fun. That's why I'm fun. That's why I'm marrying her," Tom marrying her," Tom Cruise says he Cruise says he cleared his "MI:3" cleared his "MI:3" stunts with Katie. stunts with Katie.

Risk FactorsRisk Factors

Injected material vs ingested Injected material vs ingested materialmaterial

AtopyAtopy Asthma (even if well controlled)Asthma (even if well controlled) Failure to identify proper triggerFailure to identify proper trigger Previous reactions to triggerPrevious reactions to trigger Less risk at extremes of ageLess risk at extremes of age

Risk FactorsRisk FactorsFactorFactor PoorPoor GooGoo

dd

DoseDose LargeLarge SmalSmalll

Onset of symptomsOnset of symptoms EarlyEarly LateLate

Initiation of treatmentInitiation of treatment LateLate EarlyEarly

Route of exposure (drugs, not Route of exposure (drugs, not food)food)

IVIV Oral*Oral*

ΒΒ-blocker use-blocker use YesYes NoNo

Presence of underlying Presence of underlying diseasedisease

YesYes NoNo

Risk Factors for severe Risk Factors for severe anaphylaxisanaphylaxis

Prev anaphylaxisPrev anaphylaxis AsthmaAsthma Failure to identify Failure to identify

triggertrigger

TeensTeens ΒΒ-blockers/ ACEI-blockers/ ACEI Failure to Failure to

administer administer epinephrine epinephrine immediatelyimmediately

Case 1 cont.Case 1 cont.

Symptoms worsening. Wheezing, Symptoms worsening. Wheezing, lethargic.lethargic.

Sats 89%, prolonged expiration Sats 89%, prolonged expiration phase, Little air movement on phase, Little air movement on auscultationauscultation

Management?Management?

ManagementManagement

Failure to administer epinephrine Failure to administer epinephrine early is the early is the single most important single most important risk factorrisk factor for fatal or near fatal for fatal or near fatal reactionsreactions

Bock, SA J. Allergy Clin Immunol 2001;107:191-3Bock, SA J. Allergy Clin Immunol 2001;107:191-3

ManagementManagementI. Immediate InterventionI. Immediate Intervention a)a) Assessment of airway, breathing, Assessment of airway, breathing,

circulation, and mentation.circulation, and mentation.

b) Administer EPI, 1:1000 dilution, b) Administer EPI, 1:1000 dilution, 0.3 - 0.3 - 0.5 ml (0.01 mg/kg in 0.5 ml (0.01 mg/kg in children, max children, max 0.3 mg dosage) IM, 0.3 mg dosage) IM, to control SX and to control SX and BP. Repeat, as BP. Repeat, as necessary.necessary.

Kemp and Lockey JACI Kemp and Lockey JACI 20022002

Simons et al JACI 1998Simons et al JACI 1998

Simons, Gu, Simons JACI 2001Simons, Gu, Simons JACI 2001


c) IM into the anterolateral thigh c) IM into the anterolateral thigh produces higher & more rapid produces higher & more rapid peak peak plasma level versus SQ & IM in plasma level versus SQ & IM in arm. With moderate, severe, or arm. With moderate, severe, or progressive ANA, EPI IM into progressive ANA, EPI IM into anterolateral thigh. Alternatively, an anterolateral thigh. Alternatively, an EPI autoinjector given through clothing EPI autoinjector given through clothing in same manner. Repeat, as necessaryin same manner. Repeat, as necessary

Epinephrine route of Epinephrine route of administrationadministration

Simons JACI 1998;101:33-7

Simons JACI 2001;108:871-3

ManagementManagementd) Aqueous EPI 1:1000, 0.1- 0.3ml in d) Aqueous EPI 1:1000, 0.1- 0.3ml in

10ml NS (1:100,000 to 1:33,000 10ml NS (1:100,000 to 1:33,000 dilution), IV over several minutes prn.dilution), IV over several minutes prn.

e) For potentially moribund subjects, e) For potentially moribund subjects, tubercular syringe, EPI 1:1000, 0.1 ml, tubercular syringe, EPI 1:1000, 0.1 ml, insert into vein (IV), aspirate 0.9 ml of insert into vein (IV), aspirate 0.9 ml of blood (1:10,000 dilution). Give as blood (1:10,000 dilution). Give as necessary for responsenecessary for response


II. General measuresII. General measures

a) Place in recumbent position a) Place in recumbent position and and elevate lower extremities. elevate lower extremities. Up to Up to 35% of intravascular 35% of intravascular fluid may be fluid may be lost in 10 min! lost in 10 min! Pressors may fail Pressors may fail to workto work

b) Maintain airway (endotracheal b) Maintain airway (endotracheal tube or cricothyrotomy).tube or cricothyrotomy).


c) Oc) O22, 6 - 8 liters/minute., 6 - 8 liters/minute.

d) NS, IV. If severe hypotension, d) NS, IV. If severe hypotension, give give volume expanders volume expanders (colloid (colloid solution) – 35% of solution) – 35% of blood volume blood volume can be lost in 20 can be lost in 20 min.min.

e) Venous tourniquet above e) Venous tourniquet above

reaction reaction site. ? if decreases site. ? if decreases absorption of absorption of

allergen.allergen.


III. Specific Measures that Depend III. Specific Measures that Depend onon

Clinical ScenarioClinical Scenario

a) Aqueous EPI 1:1,000, ½ dose a) Aqueous EPI 1:1,000, ½ dose (0.1- (0.1- 0.2 mg) at reaction site.0.2 mg) at reaction site.


b) Diphenhydramine, 50 mg or more in b) Diphenhydramine, 50 mg or more in divided doses orally or IV, maximum divided doses orally or IV, maximum daily dose 200 mg (5 mg/kg) for daily dose 200 mg (5 mg/kg) for children and 400 mg for adults.children and 400 mg for adults.

c) Ranitidine, 50 mg in adults and 12.5 - c) Ranitidine, 50 mg in adults and 12.5 - 50 mg (1 mg/kg) in children, dilute 50 mg (1 mg/kg) in children, dilute

in in D5W, total 20 ml, inject IV, over 5 D5W, total 20 ml, inject IV, over 5 minutes. (Cimetidine 4 mg/kg OK for minutes. (Cimetidine 4 mg/kg OK for adults, not established for pediatrics).adults, not established for pediatrics).

ManagementManagementd) Bronchospasm, nebulized d) Bronchospasm, nebulized salbutamolsalbutamol

e) Aminophylline, 5mg/kg over 30 e) Aminophylline, 5mg/kg over 30 min IV min IV may be helpful. Adjust dose may be helpful. Adjust dose based on based on age, age, medications, medications, disease, current use.disease, current use.

f) Refractory hypotension, give f) Refractory hypotension, give dopamine, 400 mg in 500 ml G/W IV dopamine, 400 mg in 500 ml G/W IV 2 2 - 20 - 20 μμg/kg/min more or less.g/kg/min more or less.


g) Glucagon, 1- 5 mg (20 - 30 g) Glucagon, 1- 5 mg (20 - 30 μμg/kg g/kg [max 1 mg] in children), [max 1 mg] in children),

administered administered IV over 5 minutes IV over 5 minutes followed with IV followed with IV infusion 5-15 infusion 5-15 μμgg/min. /min.

h) Methylprednisolone, 1- 2 mg/kg per h) Methylprednisolone, 1- 2 mg/kg per 24 hr; prevents prolonged reactions 24 hr; prevents prolonged reactions and relapses- no studies, thoughand relapses- no studies, though

i) Cetirizinei) Cetirizine


Biphasic response in some Biphasic response in some individuals, unpredictableindividuals, unpredictable

Recommended observation for 4hRecommended observation for 4h

EpipensEpipens

0.15mg or 0.3mg doses available0.15mg or 0.3mg doses available Adult 0.3mgAdult 0.3mg PaedsPaeds

0.15mg (10-25kg)0.15mg (10-25kg) 0.3mg (>25kg)0.3mg (>25kg)

EpipensEpipens

Simons JACI 2000;105:1025-30

Case 3Case 3

70y obese hypertensive, started on 70y obese hypertensive, started on ACEI (captopril).ACEI (captopril).

Prev. ETT, thyroid surgeryPrev. ETT, thyroid surgery To ED with swollen face and lips. No To ED with swollen face and lips. No

largyneal involvementlargyneal involvement

Upper Airway OedemaUpper Airway Oedema

Life-threatening oedemaLife-threatening oedema Hereditary angioedemaHereditary angioedema Aquired oedemaAquired oedema ACEI induced oedemaACEI induced oedema

AngioedemaAngioedema

First described by Quincke in 1882First described by Quincke in 1882 Well-demarcated non-pitting oedemaWell-demarcated non-pitting oedema Caused by same pathological factors Caused by same pathological factors

that cause urticariathat cause urticaria Reaction occurs deeper in dermis and Reaction occurs deeper in dermis and

subcutaneous tissuessubcutaneous tissues Face, tongue, lips, eyelids most Face, tongue, lips, eyelids most

commonly affectedcommonly affected May cause life-threatening respiratory May cause life-threatening respiratory

distress if larynx involveddistress if larynx involved


HereditaryHereditary Type 1: CType 1: C11 esterase inhibitor esterase inhibitor

deficiencydeficiency Type 2: functional abnormality of CType 2: functional abnormality of C11

esterase inhibitoresterase inhibitor


AcquiredAcquired IdiopathicIdiopathic IgE-mediatedIgE-mediated Non-IgE-mediatedNon-IgE-mediated Systemic diseaseSystemic disease Physical causesPhysical causes OtherOther


IgE-mediatedIgE-mediated DrugsDrugs FoodsFoods StingsStings Infections (eg viral, helminthic)Infections (eg viral, helminthic)


Non-IgE-mediatedNon-IgE-mediated Cyclooxygenase inhibition (ASA and Cyclooxygenase inhibition (ASA and

other NSAIDS)other NSAIDS) Angiotensin converting enzyme Angiotensin converting enzyme

inhibitioninhibition


Systemic diseasesSystemic diseases Systemic lupus erythematosisSystemic lupus erythematosis HypereosinophiliaHypereosinophilia Lymphoma: Lymphoma:

abnormal antibodies activate abnormal antibodies activate complement systemcomplement system

AngioedemaAngioedemaPhysical causesPhysical causes ColdCold CholinergicCholinergic SolarSolar VibratoryVibratory

OtherOther Some contact reactionsSome contact reactions Autoantibodies to CAutoantibodies to C11-esterase inhibitor-esterase inhibitor Unopposed complement activationUnopposed complement activation


Angioedema occurs most commonly Angioedema occurs most commonly with with

urticaria (40% cases)urticaria (40% cases)

May occur in isolation (10% cases)May occur in isolation (10% cases)

Hereditary Angioedema (HAE)Hereditary Angioedema (HAE)

Type 1Type 1**

Autosomal dominantAutosomal dominant Markedly suppressed CMarkedly suppressed C11 esterase esterase

inhibitor protein levelsinhibitor protein levels

* Accounts for 85% cases* Accounts for 85% cases


Type 2Type 2**

Autosomal dominant, with a point Autosomal dominant, with a point mutation leading to synthesis of a mutation leading to synthesis of a dysfunctional proteindysfunctional protein

Functional assay required for Functional assay required for diagnosis as level may be normaldiagnosis as level may be normal

* Accounts for 15% cases* Accounts for 15% cases


EpidemiologyEpidemiology

1:10,000 - 1:150,000 with no racial 1:10,000 - 1:150,000 with no racial or gender predilectionor gender predilection


Clinical manifestationsClinical manifestations Usually manifests in 2nd decadeUsually manifests in 2nd decade May be seen in young childrenMay be seen in young children Oedema may develop in one or several Oedema may develop in one or several

organsorgans Presentation depends upon site of Presentation depends upon site of

swellingswelling Attacks last 2- 5 days before Attacks last 2- 5 days before

spontaneous resolutionspontaneous resolutionNzeako Arch Intern Med, 2001


Angioedema may develop in Angioedema may develop in subcutaneous tissues of extremities, subcutaneous tissues of extremities, genitalia, face, trunk.genitalia, face, trunk.

Oedema of wall of intestine may Oedema of wall of intestine may present as an acute abdominal present as an acute abdominal emergency.emergency.

Submucosal oedema of larynx or Submucosal oedema of larynx or pharynx may cause asphyxiation – pharynx may cause asphyxiation – this may occur on first presentationthis may occur on first presentation

Hereditary Angioedema (HAE)Hereditary Angioedema (HAE)Laryngeal oedemaLaryngeal oedema

Commonest cause of mortality in HAECommonest cause of mortality in HAE Time from onset of swelling to death 1- 14 Time from onset of swelling to death 1- 14

hours (mean 7 hours)hours (mean 7 hours) May be presenting featureMay be presenting feature Death may occur in those with no previous Death may occur in those with no previous

laryngeal oedema episodeslaryngeal oedema episodes Increased risk within certain familiesIncreased risk within certain families Early symptoms - lump in throat, tightness Early symptoms - lump in throat, tightness

in throatin throat Hoarseness, dysphagia, progressive Hoarseness, dysphagia, progressive

dyspnoeadyspnoea


DiagnosisDiagnosis

Clinical presentationClinical presentation For screening - quantitative and For screening - quantitative and

functional assays of Cfunctional assays of C11 inhibitor inhibitor CC44 and C and C22 levels reduced in acute levels reduced in acute

attackattack CC4 4 persistently low in most patientspersistently low in most patients


CC11 inhibitor inhibitor

Single chain glycoprotein; molecular Single chain glycoprotein; molecular weight 104,000; serine protease familyweight 104,000; serine protease family

Important regulatory protein of Important regulatory protein of complement cascadecomplement cascade

Inactivates CInactivates C11 esterase complex esterase complex Regulates coagulation, fibrinolytic, Regulates coagulation, fibrinolytic,

kinin, complement systemskinin, complement systems

Hereditary Angioedema (HAE)Hereditary Angioedema (HAE) Lack of CLack of C11 inhibitor leads to abnormal inhibitor leads to abnormal

activation of complement pathway, activation of complement pathway, reduced Creduced C22 and C and C44 levels levels

Hageman factor induces formation of Hageman factor induces formation of kallikrein from prekallikrein kallikrein from prekallikrein

Bradykinin is released from high Bradykinin is released from high molecular weight kininogenmolecular weight kininogen

All these mediators increase capillary All these mediators increase capillary permeability and are responsible for permeability and are responsible for attacks of angioedemaattacks of angioedema

Hereditary Angioedema (HAE)Hereditary Angioedema (HAE) Autosomal dominant; all patients Autosomal dominant; all patients

heterozygousheterozygous 25% no prior family history - 25% no prior family history -

spontaneous mutationsspontaneous mutations More than 100 different mutations More than 100 different mutations

reportedreported Varied clinical pattern may be Varied clinical pattern may be

explained by variable effect of explained by variable effect of mutations on Cmutations on C1 1 inhibitor synthesisinhibitor synthesis


Acute attacksAcute attacks

Treatment of choice is CTreatment of choice is C11 inhibitor concentrate, inhibitor concentrate, 500 - 1,000U intravenous infusion500 - 1,000U intravenous infusion Safe and effective - no long term side effects Safe and effective - no long term side effects

reportedreported Excellent and prompt response in most Excellent and prompt response in most

patientspatients Not available in USA, but in clinical trialsNot available in USA, but in clinical trials

Hereditary Angioedema (HAE)Hereditary Angioedema (HAE)Acute attacks when CAcute attacks when C11 inhibitor inhibitor

concentrate not availableconcentrate not available Intubation and respiratory support may Intubation and respiratory support may

be necessary when laryngeal oedema be necessary when laryngeal oedema present present

Fresh frozen plasma (FFP) has been Fresh frozen plasma (FFP) has been used successfully for acute attacks. used successfully for acute attacks. Exacerbation of symptoms by supplying Exacerbation of symptoms by supplying more kallikrein substrate is a theoretical more kallikrein substrate is a theoretical consideration but is rarely seenconsideration but is rarely seen


Avoid oral contraceptive pill, ACE Avoid oral contraceptive pill, ACE inhibitor medicationinhibitor medication

Premedicate before procedures Premedicate before procedures requiring radiocontrast media or requiring radiocontrast media or streptokinase as they may decrease streptokinase as they may decrease CC11 inhibitor levels inhibitor levels

Angioedema (ACEI)Angioedema (ACEI) Angioedema develops in 0.1% to 0.5% of Angioedema develops in 0.1% to 0.5% of

those receiving the drugthose receiving the drug Onset from 1st week of use to 2 - 3 years of Onset from 1st week of use to 2 - 3 years of

useuse Symptoms resolve within 24 - 48 hours of Symptoms resolve within 24 - 48 hours of

cessation of drugcessation of drug Most commonly seen with captopril and Most commonly seen with captopril and

enalopril but described with all in classenalopril but described with all in class Genetic factors may be important Genetic factors may be important Subjects with a history of angioedema from Subjects with a history of angioedema from

other causes are more susceptible to ACE-other causes are more susceptible to ACE-induced angioedemainduced angioedema


Most often occurs in association with Most often occurs in association with urticariaurticaria

When angioedema occurs alone, consider When angioedema occurs alone, consider HAE, AAEHAE, AAE

HAE is a rare disease but must be HAE is a rare disease but must be identified as it can be life-threateningidentified as it can be life-threatening

Refer to appropriate specialist for ongoing Refer to appropriate specialist for ongoing managementmanagement

ACE-inhibitor induced angioedema is an ACE-inhibitor induced angioedema is an important cause in older peopleimportant cause in older people

“There are no contraindications to the use of epinephrine for a life-threatening allergic reaction”

AAAAI board of Directors JACI 1998;102:173-76

ReferenceReference

GLORIA - world allergy congress GLORIA - world allergy congress 20062006

Ann Allergy 1993 May; 70(5): 396-8Ann Allergy 1993 May; 70(5): 396-8Myocardial infarction induced by coronary vasospasm after Myocardial infarction induced by coronary vasospasm after self-administration of epinephrine.self-administration of epinephrine.Saff R, Nahhas A, Fink JN.Saff R, Nahhas A, Fink JN.Department of Medicine, Medical College of Wisconsin, Department of Medicine, Medical College of Wisconsin, Milwaukee.Milwaukee.

"A case of a 30-year-old man who developed a myocardial "A case of a 30-year-old man who developed a myocardial infarction after self-administering an Epi-Pen for an episode infarction after self-administering an Epi-Pen for an episode of idiopathic anaphylaxis is reported. The patient had of idiopathic anaphylaxis is reported. The patient had numerous risk factors for coronary artery disease, and it numerous risk factors for coronary artery disease, and it was suspected that epinephrine-induced coronary spasm was suspected that epinephrine-induced coronary spasm caused the infarct. The Epi-Pen Junior may be indicated in caused the infarct. The Epi-Pen Junior may be indicated in such adults with numerous risk factors for coronary artery such adults with numerous risk factors for coronary artery disease who are at risk for recurrent anaphylaxis."disease who are at risk for recurrent anaphylaxis."

gavin burgess em rounds 22 november 2007 thanks dr t vander leek

Documents

fatal reaction

airway obstruction tongue

biochemical mediators

lifethreatening reaction

systemic allergic reaction

thick tongue

alfaham jaci

black jaci