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Portier and Richet first coined the term anaphylaxis.

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Portier and Richet first coined the term anaphylaxis. - PowerPoint PPT Presentation


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Portier and Richet first coined the term anaphylaxis. In 1902 when a second vaccinating dose of sea anemone toxin caused a dog's death. The response was the opposite of prophylaxis and thus was referred to as anaphylaxis, meaning without protection. . Phylaxis = protection.

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slide1
Portier and Richet first coined the term anaphylaxis.

In 1902 when a second vaccinating dose of sea anemone toxin caused a dog's death. The response was the opposite of prophylaxis and thus was referred to as anaphylaxis, meaning without protection.

Phylaxis= protection

slide2
Anaphylaxis- is an acute life-threatening reaction caused by an IgE-mediated reaction and results from the sudden systemic release of mast cells and basophil mediators .
slide3
Anaphylactoid reaction- reaction that produce the same clinical picture as anaphylaxis but are not IgE mediated.

Anaphylactic – this term has been used to describe the clinical reaction (not the mechanism).

slide6
PATHOPHYSIOLOGY OF ANAPHYLAXIS

Allergen crosses an epithelial and/or endothelial barrier

Access to the reactive, sensitized cells –mast cells, basophils

Release of cellular mediators leads to end-organ response in the skin, respiratory tract , cardiovascular system , gastrointestinal tract, nervous system.

slide7
Histamine

H3 receptor

H1 receptor

H1,H2 receptors

Pruritus

Rhinorrhea

Tachycardia

Bronchospasm

Headache

Flushing

Hypotension

Left ventricular function

slide8
Effects of histamine on airways

Histamine

Bronchoconstriction by stimulation of H1 receptors on smooth muscles.

Mucosal edema from increased microvascular permeability (H1) leading to

transudation of fluid and macromolecules through wide intercellular

gaps (> 12 nm).

Direct stimulation of vagal (cholinergic) nerves can induce airway smooth

muscle contraction

Stimulation of H1 receptors increases mucus secretions, and

stimulation of H2 receptors increases mucus viscosity.

slide9
Effects of histamine on the heart

H1 receptors mediate coronary artery vasoconstriction and increased vascular permeability.

H2 receptors mediate atrial and ventricular contractile forces, atrial rate, and coronary artery vasodilation.

Decreased diastolic pressure and increased pulse pressure

slide10
Histamine

H1 receptor on

endothelial cell

L-arginine

Nitric oxide

Decreases venous return

slide11
Pathologic features of anaphylaxis

Laryngeal edema

Pulmonary hyperinflation

Myocardial edema

Visceral congestion or hemorrhage

Eosinophilic infiltration

Elevated tryptase levels

Death from cardiovascular collapse or respiratory obstruction

slide14
The more rapidly anaphylaxis occurs after exposure to an offending stimulus the more likely the reaction is to be severe and potentially life-threatening.

Anaphylaxis often produces signs and symptoms within minutes typically 5-30 minutes , but some reaction , such as aspirin, might develop after 30 minutes .

Late-phase or biphasic reactions, which occur 8-12 hours after the initial attack.

slide16
The average annual incidence of anaphylaxis is 10-20 cases per 100,000 person-years.

Fatalities from anaphylaxis range from 0.65-2% of patients with anaphylaxis

The annual incidence of fatal anaphylaxis among hospitalized subjects is estimated to be 154 per 1,000,000.

ß-lactam antibiotics are tought to cause 400-800 fatal anaphylactic episodes per year.

An estimated 150 fatalities from food-induced anaphylaxis occur each year in the united states.

Allergen immunotherapy 1 per 2,000,000 injections.

Insect stings probably cause at least 50 fatalities annually in USA .

slide17
Risk factors

Atopy

Route and timing of administration

The longer the interval between exposures, the less likely an anaphylactic (IgE-mediated) reaction will recur.

Asthma

Delay in administration of epinephrine

slide21
IgE specific - RAST

Radio-AllergoSorbent Test

slide27
The first documented case of a food fatal reaction was described in 1926 by a pediatrician. A 1 -year-old boy with atopic eczema experienced three episodes of generalized allergic reactions at home after intake of a few spoons of mashed peas. In the hospital setting an oral challenge with carrots/mashed peas was performed under the supervision of a chief nurse. Immediately after the intake of the test meal the child developed angioedema, cyanosis and collapsed. He died despite emergency treatment.
slide29
Clinical aspects and allergenic foods in life-threatening food anaphylaxis

Moneret-Vautrin, D. A., Morisset, M., Flabbee, J., Beaudouin, E. & Kanny, G.Epidemiology of life-threatening and lethal anaphylaxis: a review.Allergy60 (4), 443-451.

slide30
Anaphylactic reactions to foods almost always occur immediately.

The majority of reactions are not fatal.

In general, reactions worsen with the development of asthma and as children get older.

The most useful diagnostic tests: SPT and food challenges

Epinephrine should be available for use

slide34
Exercise-induced anaphylaxis
  • This is a rare syndrome that can take one of two forms:
  • The first form is food-dependent, requiring both exercise and the recent ingestion of particular foods to cause an episode of anaphylaxis ~ 50%.
  • The second form is characterized by intermittent episodes of anaphylaxis during exercise, independent of any food ingestion. Anaphylaxis will not necessarily occur during every episode of physical exertion
slide35
Premonitory symptoms can include: diffuse warmth, itching and erythema, urticaria generally ensues and progress to angioedema. Episodes can include gastrointestinal symptoms, laryngeal edema, and/or vascular collapse.

Delaying exercise for about 5 hours after eating will prevent reaction in food related exercise-induced anaphylaxis.

Carry Epipen,

should wear alert identification denoting their condition,

have a companion with them when exercising.

slide36
idiopathic anaphylaxis

The diagnosis of idiopathic anaphylaxis a diagnosis of exclusion.

Nearly 20% of cases of anaphylaxis are idiopathic.

There are no clinically distinguishing features, and it may be fatal.

Management often consists of prophylactic corticosteroid and antihistamine therapy.

slide39
Etiologies of 100 cases of life-threatening drug anaphylaxis

Moneret-Vautrin, D. A., Morisset, M., Flabbee, J., Beaudouin, E. & Kanny, G.Epidemiology of life-threatening and lethal anaphylaxis: a review.Allergy60 (4), 443-451.

slide40
Penicillin and its metabolites are haptens, small molecules that only elicit an immune response when conjugated with proteins.

95%

5%

Benzylpenicilloyl (BPO)

Major determinant

Pre-Pen

Benzylpenicilloate , Benzylpeniloate

Minor determinant

Most severe allergic reaction

slide41
Other beta-lactam antibiotics may cross-react with penicillins or may have unique structures that also act as haptens. The incidence rate of anaphylaxis to cephalosporins in penicillin-anaphylactic patients appears to be much less than the 10% frequently quoted.
  • Patients with less well-defined reactions to penicillin have a very low risk (1-2%) of developing anaphylaxis to cephalosporins. The rate of skin-test reactivity to imipenem in patients with a known penicillin allergy is almost 50%.
slide42
The use of BPO and Penicillin G 10000 unit ( without minor determinants) can detect 97%-99% of potential life threatening reactions.

Skin test positive

To BPO and Penicillin G

Skin test negative to

BPO and Penicillin G

1.Give alternative drug

2. Desensitize to penicillin

History of mild

reaction

History of immediate

or severe reaction

Graded challenge given

1/100th of dose followed in

30 min by full dose

1.Graded challenge given

1/1000th of dose followed in

30 min by full dose.

2. desensitize

slide43
NSAIDs ALLERGY

Aspirin (ASA), by irreversibly inhibiting platelet cyclooxygenase-1 enzyme (COX-1), prevents platelet aggregation

slide45
ASA can also cause a hypersensitivity reaction:
  • respiratory sensitivity (asthma and/or rhinitis)-These patients have marked cross-reactivity between aspirin and most NSAIDs.
  • Arachidonic acid
  • cutaneous sensitivity (urticaria and/or angioedema)
  • systemic sensitivity (anaphylactoid reaction) mechanism that is more consistent with IgE-mediated anaphylaxis. With true anaphylaxis, the different cyclooxygenase inhibitors do not appear to cross-react.

cyclo-oxygenase pathway

lipoxygenase pathway

leukotrienes

slide49
3 groups are at higher risk:

health care workers: 4.5-14.4% sensitivity. ,

children with spina bifida and genitourinary abnormalities: 34-100% sensitivity.

workers with occupational exposure to latex.

Dig : SPT better than RAST

Patients with spina bifida – regardless of a HISTORY OF LATEX ALLERGY should have all medical-surgical-dental procedures performed in a latex-safe environment.

slide50
Hymenoptera sting anaphylaxis

Yelow jacket

Anaphylaxis occur with 0.5-1.5% of stings.

Vespa orientalis

Wasp

slide53
Diagnosis : Skin test

RAST

Sting Challenge test

Treatment : immunotherapy

Epipen

slide55
Epinephrine is the medication of choice for treating an anaphylactic episode .

The recommended dose of epinephrine is 0.01 mg/kg I.M to as much as 0.3 mg-in children, and it may be repeated within 5 minutes if symptoms worsen or severe symptoms persist. (1:1,000 aqueous solution (1 mg/mL) ).

The lateral aspect of the thigh appears to be the optimal location of administration.

There are 2 doses of self –injectable epinephrine : Epipen jr 0.15mg , Epipen 0.3mg.

Use of I.V should be reserved for the most extreme conditions ( more adverse reaction).

The more advanced the anaphylactic reaction- development of hypotension- the less likely epinephrine is to reverse the reaction.

slide56
.

Epinephrine should be administered I.V only during cardiac arrest or to profoundly hypotensive subjects who have failed to respond to intravenous volume replacement and several injected doses of epinephrine.

Epinephrine administered during anaphylaxis to patients taking ß-adrenergic antagonist might be ineffective . In this situation both glucagon administration and isotonic volume expansion is needed. Glucagon causes bronchodilatation and reverses anaphylaxis by increasing intracellular cAMP and release of catacholimies.

Glucagon 20-30 µg/kg –maximum 1mg in children , in adults up to 5mg; administrated i.v over 5 minutes followed by infusion 5-15 µg/min.

slide58
Fluid resuscitation

Changes in vascular permeability during anaphylaxis might permit transfer of 50% of the intravascular fluid into the extravascular space within 10 minutes.

The patients whose hypotension persists despite epinephrine should receive intravenous crystalloid solutions (saline) or colloid volume expanders.

Adults – 1-2 liters ; 5-10ml/kg in 5 minutes.

Children- up to 30ml/kg in the first hour.

slide59
Corticosteroids :

systemic corticosteroids have no role in the acute management of anaphylaxis because they might have no effect for 4-6 hours.

They might potentially prevent protected or biphasic anaphylaxis.

They provide additional benefit for patients with asthma.

If given , Corticosteroids should be administered early in the treatment of anaphylaxis at a dosage equivalent to 1-2 mg /kg/d of methylprednisolone every 6 hours. Oral prednisone 0.5 mg/kg is sufficient for milder attacts.

slide60
H1 and H2 antagonists

Antihistamines are supportive in the treatment of anaphylaxis.

Antihistamines use in anaphylaxis should be considered second line treatment after the adminstration of epinephrine.

They are useful in the treatment of urticaria or pruritus .

The role of H2 antagonist is more controversial , but some reports ghave demonstrated that H1+H2 are more effective than H1.

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