Anaphylaxis

ANAPHYLAXIS
Liza Stefanie Peña-Sulay, M.D., DPPS, DPSAAI

Pediatric / Adult Allergy, Asthma & Immunology
General Pediatrics
OUTLINE
 What is anaphylaxis?
 How is anaphylaxis diagnosed?
 How does anaphylaxis occur?
What are the causes?
 What are the effects of anaphylaxis?
 How is anaphylaxis treated?
OBJECTIVES
1. Diagnose anaphylactic/ anaphylactoid

reactions
2. Analyze the event as to the most
probable cause
3. Institute immediate proper treatment
4. Educate the patient on post-
anaphylaxis care
WHAT IS ANAPHYLAXIS?
 1902: Portier & Richet were attempting

to immunize dogs to the venom of the
sea anemone
 [Dogs were sensitized]
 Dogs unexpectedly reacted fatally to a
previously non-lethal dose
 “anaphylaxis”: against or w/o protection
WHAT IS ANAPHYLAXIS?
 Immediate
 Systemic
 Hypersensitivity reaction
caused by
 Release of mediators from mast cells &
basophils
HOW IS ANAPHYLAXIS DIAGNOSED?
CLINICALLY
 (Immediate): Exposure to allergen w/in 1 hour
OR
 (Hypersensitivity reaction):
Urticaria/angioedema (90%)
PLUS
 (Systemic): 1 systemic symptom or sign
“sense of impending doom”

SYSTEMIC SYMPTOMS & SIGNS:
 Respiratory (60%)---major shock organ
-Upper airway: includes nose; ear/ throat

pruritus/ “tightness”, dysphagia, hoarseness,
stridor; “staccato” dry cough may herald
upper airway obstruction!
-Lower airway: chest tightness, “deep” cough,

dyspnea, wheezing
CASE of the “WHEEZING w/o ASTHMA”
 P.S., 8/M
 2 hrs PTC, ate dinner
 30 mins later: (+) abdominal pain,
(+) vomiting 2x, 10 mins apart
CASE of the “WHEEZING w/o ASTHMA”
 ER: (+) wheezing, “asthma”

 Mother: “No asthma”
 X-ray
While at the x-ray room, (+) urticaria
SYSTEMIC SYMPTOMS & SIGNS:
 CVS (50%): tachycardia, palpitations, chest

pain, arrythmia, feeling of faintness, syncope,
hypotension
 GIT (45%): nausea, pain, vomiting, diarrhea
 Others: eye ssxs, oral pruritus/ edema

DIFFERENTIAL DIAGNOSES: (“Flush”)
 “Restaurant syndromes”: MSG, sulfites (found

in wine, shellfish, sausage, pickles, dried
fruits)
 Scombroid poisoning: tuna, mackerel,

“tulingan”
-spoiled fish Kleb pneumo & Proteus
decarboxylate histidine saurine
“THE CASE OF THE UNFRESH FISH”:
 B.G., 40/F
 Well, no history of atopy/ allergy
 Ate fish soup in restaurant
 Within 30 minutes, (+) rash & dyspnea
 Demanded reimbursement from restaurant
for all hosp expenses and was rewarded
DIFFERENTIAL DIAGNOSES:
(Pulmonary)
 Foreignbody aspiration
 Severe asthma attack
 Pulmonary embolus
(Sudden collapse)
 Vasovagal response: pallor,

diaphoresis, bradycardia
 Arrythmia/ MI
 Seizure/ CVA
 Hypoglycemia
 Drug overdose
“THE CASE OF THE PENADUR”:
 M.G., 16/M
 Severe mitral stenosis secondary to RHD
 Came in for his usual Penadur injection
 Few minutes after: cardiorespiratory arrest
 Panicattacks
 Hyperventilation syndrome
-No objective findings

HOW DOES ANAPHYLAXIS OCCUR/
WHAT ARE THE CAUSES?
I. IMMUNOLOGIC MECHANISMS
A. Type I reaction: “ANAPHYLAXIS”
B. Type II reaction
C. Type III reaction
II. NON-IMMUNOLOGIC MECHANISMS

A. Direct release of mediators
B. Disturbed arachidonic acid metabolism
C. Unknown
IMMUNOLOGIC MECHANISMS
 Type I: IgE-mediated, “true” anaphylaxis
-FOOD
-DRUGS (Penicillins & related antibiotics,
insulin, immunoglobulins, muscle relaxants,
some local anesthetic reactions), latex
-venoms of Hymenoptera (bees, yellow

jackets, hornets, wasps, fire ants)
 Type II: cytotoxic reactions
-blood products
-dialysis membranes
 Type III: Ag-Ab complexes
-albumin, some immunoglobulin rxns,

dextran
 Type II: cytotoxic reactions

 Type III: Ag-Ab complexes
-complement system C3a, C5a

(“anaphylatoxins”)
 interact directly w/ mast cell & basophil
surface, and
 directly induce vascular permeability &
contract smooth muscles
NON-IMMUNOLOGIC MECHANISMS
(Non Ag-Ab mediated)
 Direct
activation of mast cells
-DRUGS: radiocontrast media, opiates,
local anesthetics,
some muscle relaxant
reactions
 Disturbed
arachidonic acid metabolism
-DRUGS: ASA, NSAIDs
 Unknown
-many DRUGS
-exercise
-physical factors
-idiopathic
H1 Smooth muscle constriction of
receptor bronchi, GIT, coronary arteries
Inc. release of inflammatory
mediators & recruitment of cells;
Dec. AV node conduction time
H2 Inc. mucus production in airway
receptor Inc. chronotropy & inotropy
Both H1 Vasodilation & inc. vascular
& H2 permeability (flushing, headache,
receptors edema, hypotension)
WHAT ARE THE EFFECTS OF
ANAPHYLAXIS?
FINAL COMMON PATHWAYS:
 Inc. vascular permeability, vasodilation

fluid shifted to extravascular space can result
in a 50% loss of vascular volume within 10
minutes
compensatory vasoconstriction
myocardial ischemia
 Spasm: respiratory & GI tracts,
coronary arteries
HOW IS ANAPHYLAXIS TREATED?
Regardless of mechanism
(whether anaphylactic or anaphylactoid):
CLINICAL MANIFESTATIONS &

EMERGENCY TREATMENT
ARE THE SAME!
 EPINEPHRINE
 Airway
 Breathing
 Circulation
 Drugs
 Monitoring
 Education
 EPINEPHRINE:
-direct acting adrenergic agonist
In the initial treatment of anaphylaxis:

-alpha-1: dec. mucosal edema,
vasoconstriction, inc. PVR
-beta-2: dec. mediator release,
bronchodilation
 “EPINEPHRINE should be given
promptly in anaphylaxis treatment, as
achieving high plasma & tissue
concentrations rapidly is crucial to
survival. In an animal model,
epinephrine given at the nadir of shock
failed to produce recovery, despite
elevated plasma epinephrine
concentrations.”
Bautista et al, Am J Respir Crit Care Med 2000
 EPINEPHRINE 1:1000 (1 mg/ml)
-0.01 ml/kg up to 0.5 ml IM

- if necessary, repeat q15 up to 2x
then q4
 AIRWAY
-endotracheal intubation/
tracheostomy if needed
 BREATHING
-O2 at 4-6 LPM

 O2 sat >90%, PO2>60 mm Hg,
PCO2<65
-B2 agonist nebulization if needed
 CIRCULATION
-recumbent, feet elevated (unless wheezing)

-if BP post-Epinephrine:
 NSS/ pLR 30 cc/kg in the 1st hour then
titrate according to vital signs, degree
of hypovolemia, urine output,
pulmonary exam
-maintain SBP =/> 90 mm Hg
 CIRCULATION
Refractory hypotension/ frank shock:

-CVP monitoring
-colloids
-Epinephrine IV bolus followed by drip
-Dopamine 2-20 mcg/kg/min
 DRUGS
-Diphenhydramine 1-2 mg/kg/dose IM/

IV up to 50 mg q4-6
-Ranitidine 1-2 mg/kg/day up to 50 mg IV
q6-8
-Hydrocortisone 5-10 mg/kg/dose up to
100-500 mg IV q4-6
COURSE
-usually begins within minutes

-peaks within 15-30 minutes
-complete within hours
COURSE
 Delayed
-the more rapid the onset, the more severe
 Biphasic
-quiescent period 1-3 hours
-2nd phase 8-24 hours later, usually w/
severe respiratory symptoms/
bronchospasm
-may occur despite treatment
 Protracted: 1 day- 3 weeks
 MONITOR VITAL SIGNS

 Observe for at least 8-12 hours after
signs & symptoms abate, and
 For at least 24 hours after stabilization
for severe/ life-threatening reactions
 Watch out for arrhythmias & treat
accordingly
1. EDUCATION OF PATIENT ON
EMERGENCY MANAGEMENT
*Note Epinephrine expiry or renew yearly
*D/C B-blockers
2. AVOIDANCE
3. REFERRAL
SUMMARY
CLINICAL DIAGNOSIS
 Exposure to allergen within 1 hour

OR urticaria/ angioedema
PLUS
1 systemic symptom/ sign

SUMMARY
USUAL CAUSES
 FOOD
 DRUGS
 Others
SUMMARY
TREATMENT
 EPINEPHRINE!!!
 ABCs of resuscitation
 Drugs: H1 & H2 antagonists, steroid
 Close monitoring
SUMMARY
POST-ANAPHYLAXIS CARE
 EDUCATION OF PATIENT ON
EMERGENCY TREATMENT
 AVOIDANCE
 REFERRAL
SUMMARY
IMPORTANT IMPLICATIONS FOR
CLINICAL PRACTICE:
1. Always ask on ALLERGIES, esp. to

DRUGS.
2. Always bring EPINEPHRINE with you
whenever & wherever you plan to inject.
3. Keep patients in clinic 20-30 mins after
injection.
THANK YOU!

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What is anaphylaxis?

What is anaphylaxis?

How is anaphylaxis diagnosed clinically and systemically?

How is anaphylaxis diagnosed clinically and systemically?

ANAPHYLAXIS

Liza Stefanie Peña-Sulay, M.D., DPPS, DPSAAI

1. Diagnose anaphylactic/ anaphylactoid

 1902: Portier & Richet were attempting

“sense of impending doom”

-Upper airway: includes nose; ear/ throat

-Lower airway: chest tightness, “deep” cough,

 ER: (+) wheezing, “asthma”

 CVS (50%): tachycardia, palpitations, chest

 Others: eye ssxs, oral pruritus/ edema

 “Restaurant syndromes”: MSG, sulfites (found

 Scombroid poisoning: tuna, mackerel,

 Vasovagal response: pallor,

“THE CASE OF THE PENADUR”:

-No objective findings

II. NON-IMMUNOLOGIC MECHANISMS

-venoms of Hymenoptera (bees, yellow

 Type II: cytotoxic reactions

 Type III: Ag-Ab complexes

-albumin, some immunoglobulin rxns,

 Type II: cytotoxic reactions

-complement system C3a, C5a

 Inc. vascular permeability, vasodilation

CLINICAL MANIFESTATIONS &

In the initial treatment of anaphylaxis:

-0.01 ml/kg up to 0.5 ml IM

-O2 at 4-6 LPM

-recumbent, feet elevated (unless wheezing)

Refractory hypotension/ frank shock:

-Diphenhydramine 1-2 mg/kg/dose IM/

-usually begins within minutes

 MONITOR VITAL SIGNS

 Exposure to allergen within 1 hour

1 systemic symptom/ sign

1. Always ask on ALLERGIES, esp. to

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