Transcript Basics Anaphylaxis_New 2011 Dr Chow

Urticaria, Angioedema
and Anaphylaxis in the
Emergency Department
Back to Basics 2011
Jennifer Clow MD, CCFP (EM)
With slides by: Anita Pozgay, MD, FRCPC EM
Case One




A 7 year old comes in to the ED after an
possible exposure to peanut butter
He has a severe nut allergy for which he was
prescribed an EpiPen
He was recently admitted to PICU for a severe
asthma attack but was not intubated
Mom gave him some oral Benadryl and he is no
longer itchy but still has lip swelling
Case One continued



He is sent for a CXR due to decreased air entry
in the lower lobes
While in radiology, he becomes acutely SOB and
his lip becomes more swollen
What do you do now?
Case Two




A 45 y o woman involved in a MVC needs a CT
abdo after she is stabilized in the ED
She received 2 L NS for a hypotensive episode
and her BP is now 120/70
She has a positive FAST U/S
Although her CXR is normal she has palpable
lower rib fractures & a distended abdomen
Case Two continued

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She is given both oral and IV contrast for her
CT
She becomes hypotensive again!
What do you do now?
There is no rash
Case Three
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A 67 y o man is stung by an insect while
gardening
He developed pruritus, dizziness, and SOB 20
min later so he called 911
He self-treated with Benadryl po and was
given another 50 mg IV by EMS due to
persistent sx and rash
He is now asymptomatic and refusing
transport to hospital
Case Three: Do you transport?
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EMS convinced him to get “checked out” in the
hospital
On arrival, he becomes hypotensive, and his
hives reappeared, along with facial edema
An ECG shows T wave inversion in his lateral
leads
PHx: MI, HTN, IV contrast allergy
Meds: ASA, metoprolol, lisinopril
Allergic Reactions


Generalized: anaphylaxis/anaphylactic shock
Localized:
Skin – dermatitis, urticaria, angioedema
 Respiratory – rhinorrhea, angioedema, wheezing
 GI – food intolerance (as contrasted with food
allergy)

Definitions

Anaphylaxis: a severe systemic allergic reaction
involving 2 or more systems
* hives/angioedema NOT universally present!


Anaphylactic Shock: above, plus hypotension
and other signs of shock
Allergic reactions: localized reaction, involving
a single system; e.g. urticaria, angioedema,
contact dermatitis, rhinoconjunctivitis
Urticaria versus Angioedema

Both characterized by transient, pruritic, red
wheals on raised serpiginous borders

urticaria due to edema of dermis
angioedema due to edema of subcutaneous
tissues

Urticaria
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AKA Hives
Raised, well-circumscribed areas of edema and
erythema involving the dermis and epidermis
Intensely pruritic
May be acute or chronic (>6 weeks)
Multiple types: IgE-mediated, chemical-induced,
cholinergic, cold-induced, autoimmune, etc.
Pathophysiology

Mast cells and basophils release histamine,
bradykinin, leukotrienes, prostaglandins into the
dermis



Causes fluid extravasation… leads to lesion
Pruritis is due to histamine release into the
dermis
Multiple triggers: IgE mediated, others
Causes


Causes: found in 40-60% of acute urticaria, and
10-20% chronic urticaria
Include:
Infections, pregnancy, other medical conditions
 Foods, drugs, latex
 Environmental factors
 Stress
 Cold/heat, exercise

History

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Previous episodes/causative factors
Medical history, medications, allergies
Possible precipitants:
Recent illness or travel
 New medications or IV contrast
 Foods, pets, exposures
 Changes in perfumes, lotions, clothes
 Exercise, temperature extremes, stress

Physical Exam

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Identify and confirm urticarial diagnosis
Dermographism?
Look for precipitants/other illnesses:
Signs of infections: e.g. URTI, fungal infection
 Signs of liver/thyroid disease
 Angioedema, respiratory changes (edema, wheezes)
 Joint examination


Ensure no signs of anaphylaxis are present
Treatment


H1-blockers i.e. diphenhydramine, hydroxyzine
H2-blockers i.e. ranitidine



Act synergistically with H1 blockers
Doxepin 10-25mg tid-qid
Glucocorticoids e.g. prednisone
Stabilize mast cells, stopping histamine release
 Anti-inflammatory effect

Angioedema
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Deep, subcutaneous, submucosal edema due to
increased vascular permeability
May be episodic and self-limited, or recurrent
May involve skin, buccal mucosa/tongue, larynx
or GI mucosa
Usually presents with urticaria: mast-cell
mediated in these cases
Types
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Hereditary C1-esterase inhibitor deficiency
Acquired: autoimmune/lymphoprolif. disorders
Drug-induced (e.g. ACEI)
Urticaria-associated
Idiopathic (most cases)
Urticaria-associated is mast-cell mediated, all
others are kinin-mediated
History

Hereditary/idiopathic/drug-induced:
Episodic, self-limiting episodes of edema
 Skin swelling, tongue swelling, abdominal pain
 Look for triggers


Urticaria-associated:
Look for potential triggers: drugs, allergens, food
allergies, hymenoptera
 History of atopy

Physical Exam

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Acute onset of well-demarcated cutaneous
edema of distensible tissues
Usually face, limbs, genitals
Assess airway
Abdominal examination
Treatment

AIRWAY management


Mild Angioedema


Intubate early if any question
Remove offending agent; self-limited
Severe Angioedema
H1, H2 blockers, corticosteroids
 Epinephrine

Anaphylaxis
Definition



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Severe allergic reaction (IgE-mediated)
Requires prior-sensitization and re-exposure
Rapid in onset, may cause death
Usually includes prominent dermal and systemic
manifestations
Full syndrome involves urticaria/angioedema,
respiratory manifestations +/- GI upset
Anaphylactic shock: above + hypotension
Anaphylactic vs. Anaphylactoid

Anaphylactoid has the same clinical features as
anaphylaxis but is not IgE mediated

Instead it is due to direct mast cell degranulation
and thus, does not require prior sensitization
Pathophysiology

Sensitization occurs when IgE adheres to the
mast cell
Ag (allergen)

IgE specific
Degranulation of mast cell
mediators
Pathophysiology

Re-exposure leads to antigen binding, and rapid
release of mediators:


Histamines, leukotrienes, prostaglandins, tryptase
Leads to rapid onset of:
Increased secretion from mucus membranes
 Increased bronchial smooth muscle tone
 Decreased vascular smooth muscle tone
 Increased capillary permeability

Epidemiology

Likely under reported due to lack of recognition
or self treatment in the field

in Ontario: 4 cases/ 1 million
in Germany: 10 cases/100 000
in Minnesota, U.S.A.: 17/19,122 visits
in Brisbane, Australia: 1/440 visits
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Common Causative Agents
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Drugs: Antibiotics, ASA, NSAIDS, sulfa,
opioids, IV contrast dye
Foods: Peanuts, Seafood, Eggs, milk
Latex gloves
Insect Stings
Physical Factors: Exercise (FDEIA), Cold/Heat
Clinical Features
SMOOTH MUSCLE
CONTRACTION
CAPILLARY LEAK

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urticaria
angioedema
laryngeal edema
hypotension/syncope
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abdominal cramps
nausea
rhinitis
conjunctivitis
MUCOSAL SECRETIONS
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bronchospasm
diarrhoea
vomiting
DDx: Anaphylaxis
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MI/arrhythmia/cardiogenic shock
Airway obstruction due to other causes: FB
aspiration, asthma, COPD, epiglottitis, peritonsillar abscess, etc.
Flushing syndromes (eg: carcinoid)
Vasovagal syncope
Panic attack
Scombroid poisoning
Hereditary angioedema
History
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Skin: pruritis, edema
Respiratory: upper and lower tract symptoms
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GI complaints
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Rhinorrhea, congestion, dyspnea
Nausea, vomiting, diarrhea, abdominal pain
Try to elicit causes/triggers
PMHx, allergies, previous episodes
Physical Examination
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Vitals, ABC’s
General appearance
Skin
Respiratory
Cardiovascular
Grading of Anaphylaxis
Grade
1
Skin
GI tract
Resp
CV
Neuro
Local pruritus,
hives, mild lip
swelling
Oral “tingling”,
pruritus
2
Generalized
pruritus, hives,
flushing,
angioedema
Above plus
nausea +/emesis
Nasal
congestion/
sneezing
3
Any of above
Any of above
+ repetitive
vomiting
Rhinorrhea,
sensation of
throat
tightness
Tachy
( > 15 bpm)
Above plus
anxiety
4
Any of above
Any of above
+ diarrhea
Hoarseness
dysphagia,
SOB,
cyanosis
Above +
arrhythmia
+/- dec BP
dizziness
Feeling of
impending
doom
5
Any of above
Any above +
stool incont.
Any above +
resp arrest
Brady +/card arrest
LOC
Activity
change
Management Questions?
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What is the first line of therapy?
When do you give IV vs IM epi?
Do all patients need Epinephrine;
corticosteroids?
What is the role of combined H1 & H2
blockers?
Who needs to be monitored? Referred?
Who needs an EpiPen?
Key Management of Anaphylaxis
1st line of therapy:
AWARENESS
 RECOGNITION
 TREAT QUICKLY
 CALL FOR BACK-UP!

Anaphylaxis Algorithm
Most severe
Anaphylaxis:
(Hypotension with/without
respiratory obstruction)
Eg: SBP<90 +/- stridor,
tongue/laryngeal swelling
Least severe
Systemic Allergic Reaction:
(angioedema or
bronchospasm)
Simple Allergic Reaction:
(urticaria, GI upset,
contact dermatitis)
ABCs
Cardiac Monitor + 1 L NS bolus
0.3 mg (0.3 ml) 1: 1,000 epinephrine IM* (1mg/ml amp)
Hypotension persists
No or inadequate response
Repeat 1L NS bolus, if
no response
Repeat IM epinephrine &
add ventolin 2 cc via neb
CALL FOR BACK-UP!
• 0.1 mg epinephrine in 10 ml NS IV over 10
minutes! (Dilute 0.1 ml of 1:1,000 from 1mg/ml amp
in 10 ml NS or 1 ml of 1:10,000 from 1mg/10 ml in 10
ml NS & run @ 1 mcg/min; total 10 mcg)
* never use SC due to
inconsistent absorption
• In pts on Bblockers
beware of poor response
to epi; use Glucagon 1
mg IV/IM instead.
All three groups of patients receive the following:
Anita Pozgay, MD.
•
•
•
•
Benadryl 50 mg IV/PO &
Ranitidine 50 mg IV or 150 mg PO &
Prednisone 50 mg PO (or Solumedrol 125 mg IV)
+/- Ventolin 2cc nebulized q 5 min X 3 prn
Management: Adult Epi dosing

Epinephrine:
0.3 mg (0.3 ml) 1:1000 solution IM
(NOT SC or IV)
may repeat in 5 min X 1
(empirical only but safe)
Epi: Pediatric Dosing
(0.01 ml/kg)
Age (yrs)
1
2-3
>4
Volume of
1:1000(1mg/ml)
0.1 ml
0.2 ml
0.3 ml
Dose (mg)
0.1
0.2
0.3
EPI cautions: Co-morbidities
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Thyroid disease
Cocaine addicts
CAD on BBlockers, ACEi
Depression using MAOIs or TCAs
Mechanisms of Epinephrine

Alpha agonist effects increase peripheral
resistance, raise BP, reduce vascular leakage

Beta agonist effects cause bronchodilation,
positive cardiac inotropy/chronotropy (caution
in CAD pts!)
Dangers of Epinephrine IV
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Only use IV Epi if patient has refractory shock
not responding to fluid bolus first
dose 0.1 mg (10 ml) 1:100,000 dilution over 10
minutes
must be on cardiac monitor
caution in elderly or those with CAD
may cause supraventricular/ventricular
dysrhythmias!
Management
Do all patients need Epi?

Epinephrine reverses mediator release while
antihistamines (H1) do not

Epinephrine should be used for all systemic
signs of allergy: airway edema (includes
tongue/lips), SOB, cyanosis, hypotension
Management: Do all patients
need Corticosteroids?


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Corticosteroids take 4-6 hours to work
theoretically blunt the multi-phasic reaction of
anaphylaxis
the quicker the onset of anaphylaxis the worse
the reaction/quicker resolution less likely to
relapse
Caution in IV steroids esp if given in bolus
doses; case reports of anaphylaxis!
Oral form preferred if possible
Histamine Classes

H1 receptor: stimulates bronchial, intestinal,
smooth muscle contraction, vascular
permeability, coronary artery spasm

H2 receptor: increase rate & force of
ventricular & atrial contraction, gastric acid
secretion, airway secretions, vascular
permeability, bronchodilation, & inhibition of
histamine release
Management: What is the role of
combined H1 & H2 Antagonists?
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RCT, N=91 w/ allergic syndromes
50 mg Benadryl (H1) & saline vs. 50 mg Benadryl
& 50 mg Ranitidine (H2) IV
Endpoints of resolution of urticaria, angioedema,
or erythema
also measured subjective improvement & vitals
Lin et al., Improved outcomes in patients with acute allergic syndromes who are treated with combined H1
& H2 antagonists, Annals of Emergency Medicine 36(5) 2000.
Histamines: Results
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Statistically significant diminution of
angioedema and/or urticaria with addition of
H2 blocker
study too small to determine if H2 blockers
helpful in anaphylaxis (those with respiratory
compromise &/or hypotension)
also significant decrease in HR in Rx group
Back to Cases: Management Case 1
Case One: Peanut allergy in
asthmatic




A 7 year old comes in to the ED after an
possible exposure to peanut butter
He has a severe nut allergy for which he was
prescribed an EpiPen
He was recently admitted to PICU for a severe
asthma attack but was not intubated
Mom gave him some oral Benadryl and he is no
longer itchy but still has lip swelling
Case One continued



He is sent for a CXR due to decreased air entry
in the lower lobes
While in radiology, he becomes acutely SOB and
his lip becomes more swollen
What do you do now?
Case 1 Conclusion
He needs IM Epi!
(He weighs 30 kg and thus 0.3 mg IM is
fine.)

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O2, IV fluids, cardiac monitoring
Consider Ventolin neb (esp if concurrent
asthma)
Case Two : MVC Management




A 45 y o woman involved in a MVC needs a CT
abdo after she is stabilized in the ED
She received 2 L NS for a hypotensive episode
and her BP is now 120/70, HR 100
She has a positive FAST U/S
Although her CXR is normal she has palpable
lower rib fractures & a distended abdomen
Case Two continued




She is given both oral and IV contrast for her
CT
She becomes hypotensive again!
What do you do now?
There is no rash
Case 2: Conclusion
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Is she in hypovolemic shock or anaphylactic?
doesn’t matter b/c both require IV crystalloids!
There may be no rash initially
Look for airway compromise/swelling: intubate?
IV contrast reactions are anaphylactoid and so
prior sensitization not necessary (thus may be no
prior hx of anaphylaxis)
If no response to fluids give IV epi 1st via slow
infusion, except if pulseless then may give IV
bolus
Anaphylaxis Algorithm
Most severe
Anaphylaxis:
(Hypotension with/without
respiratory obstruction)
Eg: SBP<90 +/- stridor,
tongue/laryngeal swelling
Least severe
Systemic Allergic Reaction:
(angioedema or
bronchospasm)
Simple Allergic Reaction:
(urticaria, GI upset,
contact dermatitis)
ABCs
Cardiac Monitor + 1 L NS bolus
0.3 mg (0.3 ml) 1: 1,000 epinephrine IM* (1mg/ml amp)
Hypotension persists
No or inadequate response
Repeat 1L NS bolus, if
no response
Repeat IM epinephrine &
add ventolin 2 cc via neb
CALL FOR BACK-UP!
• 0.1 mg epinephrine in 10 ml NS IV over 10
minutes! (Dilute 0.1 ml of 1:1,000 from 1mg/ml amp
in 10 ml NS or 1 ml of 1:10,000 from 1mg/10 ml in 10
ml NS & run @ 1 mcg/min; total 10 mcg)
* never use SC due to
inconsistent absorption
• In pts on Bblockers
beware of poor response
to epi; use Glucagon 1
mg IV/IM instead.
All three groups of patients receive the following:
Anita Pozgay, MD.
•
•
•
•
Benadryl 50 mg IV/PO &
Ranitidine 50 mg IV or 150 mg PO &
Prednisone 50 mg PO (or Solumedrol 125 mg IV)
+/- Ventolin 2cc nebulized q 5 min X 3 prn
Case 3: Gardener Management
Case Three
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


A 67 y o man is stung by an insect while
gardening
He developed pruritus, dizziness, and SOB 20
min later so he called 911
He self-treated with Benadryl po and was
given another 50 mg IV by EMS due to
persistent sx and rash
He is now asymptomatic and refusing
transport to hospital
Case Three: Do you transport?





EMS convinced him to get “checked out” in the
hospital
On arrival, he becomes hypotensive, and his
hives reappeared, along with facial edema
An ECG shows T wave inversion in his lateral
leads
PHx: MI, HTN, IV contrast allergy
Meds: ASA, metoprolol, lisinopril
Case 3 Management: Refractory
Anaphylaxis



Biphasic (multi?) reactions can occur typically
after 3-4 hours but as late as 72 hours later!
Beware of the patient with increased age and comorbidities (eg. CAD) b/c anaphylaxis can
cause cardiac ischemia
B-Blockers & ACEi blunt the catecholamine
response
Management Refractory
Anaphylaxis: Glucagon
Glucagon: increases inotropy/chronotropy &
causes smooth muscle relaxation independent of
B receptors
Dose: 1-5 mg in adults (0.5 - 1 mg in kids)
IV/IM
Management: Disposition &
Follow-up


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
Inquire about possible antigen exposure
Those with systemic reactions require a
prescription for and instruction on how to use a
EpiPen
A Medic Alert Bracelet is useful
Follow-up with an allergist for skin testing
should be arranged particularly if the allergen is
unknown
EpiPen
Summary




Acute anaphylaxis is often poorly recognized
& treated due to the protean clinical features
and variation in the speed of onset
a trigger is often not found
Pruritis is a universal feature and should
differentiate anaphylaxis from asthma
Expedious treatment w/ epi is necessary &
thus patient education on its use is essential
Anaphylaxis Algorithm
Most severe
Anaphylaxis:
(Hypotension with/without
respiratory obstruction)
Eg: SBP<90 +/- stridor,
tongue/laryngeal swelling
Least severe
Systemic Allergic Reaction:
(angioedema or
bronchospasm)
Simple Allergic Reaction:
(urticaria, GI upset,
contact dermatitis)
ABCs
Cardiac Monitor + 1 L NS bolus
0.3 mg (0.3 ml) 1: 1,000 epinephrine IM* (1mg/ml amp)
Hypotension persists
No or inadequate response
Repeat 1L NS bolus, if
no response
Repeat IM epinephrine &
add ventolin 2 cc via neb
CALL FOR BACK-UP!
• 0.1 mg epinephrine in 10 ml NS IV over 10
minutes! (Dilute 0.1 ml of 1:1,000 from 1mg/ml amp
in 10 ml NS or 1 ml of 1:10,000 from 1mg/10 ml in 10
ml NS & run @ 1 mcg/min; total 10 mcg)
* never use SC due to
inconsistent absorption
• In pts on Bblockers
beware of poor response
to epi; use Glucagon 1
mg IV/IM instead.
All three groups of patients receive the following:
Anita Pozgay, MD.
•
•
•
•
Benadryl 50 mg IV/PO &
Ranitidine 50 mg IV or 150 mg PO &
Prednisone 50 mg PO (or Solumedrol 125 mg IV)
+/- Ventolin 2cc nebulized q 5 min X 3 prn
Case of EIA





28 year old male, after eating spaghetti and
then playing soccer 1 hr later, developed
urticaria & dizziness
attempted to drive to hospital but pulled over
because worse
EMS vitals: BP 80/42, HR 90, RR 24
Rx: w/ epi and 1 litre NS
In ED: BP 130/85, chest was clear and
“hives” gone but skin still edematous
Exercise Induced Anaphylaxis



Clinical features indistinguishable from allergen
induced anaphylaxis
food dependent & food independent forms (also
cholinergic urticaria)
mechanism not fully known, but thought
exercise lowers threshold for mast cell
degranulation esp after a food allergen triggers
an IgE response
Exercise-Induced Allergic
Syndromes
Cholinergic
Urticaria
Heat, stress
Exercise
EIA
FDEIA
Exercise
Only
Food &
Exercise
Skin effects
Hives <4mm
Hives
10-15mm
Hives
10-15mm
Vascular
Collapse
Resp effects
Rare
Yes
Yes
Rare
Present
Present
Reproducible
Yes
Variable
Yes
Stimuli
Natural History of EIA
N= 365 respondents with 10 yr hx of
EIA to 75 item questionaire
 EIA if anaphylactic Sx with exercise but
not with passive warming

Shadick, Nancy A., et al. The Natural History of Exercise-Induced Anaphylaxis:
Survey results from a 10-year follow-up study, J Allergy Clin Immunol 1999;
104: 123-7.
Results of Survey


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

frequency of attacks lesson over time
a wide range of activities associated but more
CV demand more likely
70% had atopy or family hx of it
subjects avoided attacks by not exercising in
humid weather or high allergy seasons
no single trigger identified; most common food
H1 blockers/ epi were used by 30% emergently;
Role of prophylaxis?