ANAPHYLAXISANAPHYLAXISYOGESH NATALYYOGESH NATALY

AK EDAK ED

“ITS TYPICAL EXPLOSIVE ONSET AND UNFORESEEN

NATURE OF SEVERITY IS FRIGHTENING”

(Bochner B.S, Lichtenstein L.M. Anaphylaxis: Current Concepts. New England Journal of Medicine,1991. 324: 1785-1790)

ANAPHYLAXISANAPHYLAXIS

“IMMUNE-MEDIATED LIFE-THREATENING SYNDROME

RESULTING FROM THE SUDDEN RELEASE OF

MAST CELL AND BASOPHIL-DERIVED MEDIATORS

INTO THE CIRCULATION”

(Kemp S.F, Lockey R.F. Anaphylaxis: a review of causes and mechanisms.J Allergy Clin Immunol.2002 Sep;110(3):314-8)

ANAPHYLACTOID ANAPHYLACTOID

“CLINICALLY INDISTINGUISHABLE SYNDROME, INVOLVING SIMILAR MEDIATORS BUT NOT

MEDIATED BY IgE ANTIBODY AND NOT NECESSARILY REQUIRING PREVIOUS EXPOSURE

TO THE INCITING SUBSTANCE”

(Bochner B.S, Lichtenstein L.M. Anaphylaxis: Current Concepts. New England Journal of Medicine,1991. 324: 1785-1790)

EPIDERMIOLOGYEPIDERMIOLOGY

1 PER 1,500 PATIENT 154 FATAL CASES PER 1,000,000 HOSPITALISED CASES

USA 84,000 ANAPHYLAXIS AND 840 FATALITIESBETA-LACTAM

1 IN 5,000 EXPOSURES WITH 400 TO 600 FATALITIES

FOOD150 FATALITIES FOR 30,000 ANAPHYLACTIC REACTIONS.

COMMON CAUSESCOMMON CAUSES

• FOOD: peanuts, other nuts, fish, shellfish, egg, milk.

• INSECT VENOM: bee and wasp sting, fire ants, snake.

• DRUGS: antibiotics, iv anaesthetic drugs, aspirin, nsaids, opioids,

haemaccel.

• LATEX RUBBER.

• RARELY, exercise, vaccines, heat, cold, sunlight.

• IDIOPATHIC.

MECHANISM MECHANISM in ANAPHYLAXISin ANAPHYLAXIS

MECHANISM MECHANISM in ANAPHYLAXISin ANAPHYLAXIS

MECHANISM MECHANISM in ANAPHYLACTOID in ANAPHYLACTOID REACTIONREACTION

• COMPLEMENT FIXATION: release of anaphylatoxins (C3a, C5a) e.g. incompactible transfusions,

radioconstrast media.

• KININ PRODUCTION: ACE inhibitors.

• DIRECT RELEASE:HISTAMINE RELEASE: opioids, haemaccelARACHIDONIC METABOLISM: aspirin, nsaids

MEDIATORSMEDIATORS

A VARIETY OF CHEMOTACTIC, VASOACTIVE AND SPASMOGENIC COMPOUNDS MEDIATE THE ANAPHYLACTIC REACTION.

• IMMEDIATE (5-30 mins): histamines, leukotrienesIntense reaction characterised by oedema, mucus secretion, and smooth muscle

spasm.

• LATE (2-8 hours): leukotrienes, PAF, TNF-, cytokinesRecruit other inflammatory cells and release additional waves of mediators that

cause injury

EFFECTSEFFECTS

Ewan P.W. Anaphylaxis. BMJ May 1998; 7142: 1442-45

DIFFERENTIAL DIAGNOSISDIFFERENTIAL DIAGNOSIS

• Facial swelling or oedema

• Bronchial asthma, pulmonary oedema, chemical irritant

exposure, FB airway obstruction and tension pneumothorax

• Vasovagal reaction

• CASE PRESENTATION19 yo F 8 weeks pregnant presenting with hypotensionQuick history and examination were diagnostic

LABORATORY TESTINGLABORATORY TESTING

• NO SPECIFIC IMMEDIATE DIAGNOSTIC LAB TEST• NO REPLACEMENT FOR A BRIEF BUT SUCCINCT HISTORY

• FBC, GLUCOSE, ELECTROLYTES, LFTs, CXR, ECG, ABG

• MAST CELL TRYPTASE ASSAY– highly sensitive indicator of anaphylaxis– serum levels parallel histamine (half-life of mins.)– peaks in an hour following the reaction– elevated for 4 hours (half-life of 2 hours)– used more in postmortem diagnosis of anaphylaxis– $149.45 per test

TREATMENTTREATMENT

FIRST-LINE• O xygen

• Adrenaline (Dose: 0.3-0.5 ml im 1:1000 q5-10min)

-adrenergic

1-adrenergic

2-adrenergic

cAMP

• Fluids

colloids or crystalloids

SECOND-LINE

• Anti-histamines(H1 and H2)

promethazine

ranitidine

• Steroids

hydrocortisone

• Glucagon (in patients on -blockers)

• Nebulised salbutamol and other

bronchodilators

TREATMENTTREATMENT

Combined H1 and H2 receptor blocker use

“Consensus regarding the use of antihistamines in acute anaphylaxis now favours a combination of an H1 and H2 receptor blocker”

“Acute urticaria should now be given H1 receptor blocker together with H2 receptor blocker”

(Brown AFT 1998 Therapeutic controversies in the management of acute anaphylaxis. Journal of Accident and Emergency Medicine 15: 89-95)

DISCHARGEDISCHARGE• BIPHASIC ANAPHYLAXIS (5%)• DISCHARGE MEDICATION (3days)

prednisone 40mg daily ranitidine 150mg Bdloratidine 10mg daily

• INSTRUCTIONS TO RETURN• PROTECT AGAINST FURTHER

ATTACKS / EDUCATE• REFERAL TO AN ALLERGIST

ESSENTIALSESSENTIALS

• DIAGNOSIS IS ENTIRELY CLINICAL

• NEVER UNDERESTIMATE THE POTENTIAL FOR

DETERIORATION

• PARENTAL ADRENALINE IS SAFE AND EFFECTIVE

• 6-8 HOUR OBSERVATION IN PATIENTS RECEIVING

ADRENALINE

• CAREFUL DISCHARGE PLANNING