ANAPHYLAXIS

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ANAPHYLAXIS:

ANAPHYLAXIS Dr Dineo Moiloa EM Registrar

LEARNING OBJECTIVES:

Knowledge of the different mechanisms which cause anaphylaxis and the agents which are most likely to cause it; Be able to recognize the signs and symptoms of anaphylaxis; Understand how to treat anaphylaxis LEARNING OBJECTIVES

LECTURE OBJECTIVES:

Definition Introduction Epidemiology Pathophysiology Aetiology Clinical presentation Management Prevention LECTURE OBJECTIVES

Case study:

You respond to an P1 call at an upmarket restaurant. Metro Control says there is a ‘collapsed’ patient. On arrival, a 25-year old tourist is unresponsive with an audible stridor . Her skin is red and blotchy, and feels cold and clammy. Her friend mumbles something about a ‘pen’ she uses when she gets very sick. What do you do? Case study

DEFINITION:

Ana (without); phylaxis (protection/guard) An acute multi-system severe Type I hypersensitivity reaction. Anaphylaxis is a life threatening condition. True vs pseudo-anaphylaxis. DEFINITION

Gell & Coombs:

Type I : Mediated by IgE Type II : Mediated by anti-tissue Ab IgG and IgM Type III : Mediated by immune complexes Type IV : Cell-mediated immune complexes Gell & Coombs

INTRODUCTION:

INTRODUCTION

INTRODUCTION:

Anaphylaxis – a syndrome with varied mechanisms, clinical presentations, and severity. An acute life-threatening reaction. Usually mediated by an immunologic mechanism, allergic anaphylaxis, but not always. Includes non-allergic anaphylaxis (formerly referred to as an anaphylactoid reaction). Results from the release of mast- basophil mediators. INTRODUCTION

ANAPHYLACTIC SHOCK:

Anaphylaxis asociated with systemic vasodilation ( Hypotension, fainting, collapse, LOC) and/or severe bronchoconstriction ( stridor , respiratory compromise). ANAPHYLACTIC SHOCK

Pseudoanaphylaxis:

Anaphylactoid reactions are caused by activation of mast cells and release of the same mediators, but without the involvement of IgE antibodies . Management is similar to anaphylaxis. Pseudoanaphylaxis

EPIDEMIOLOGY:

50/100 000 p/yr Young people and females high risk 1-15% at risk every year 1500 deaths p/yr Global increasing rates EPIDEMIOLOGY

PATHOPHYSIOLOGY:

PATHOPHYSIOLOGY

PATHOPHYSIOLOGY:

An allergic reaction results from the interaction of an allergen with specific IgE antibodies. IgE antibodies are bound to Fc receptors for IgE on mast cells and basophils . This leads to activation and degranulation of the mast cell PATHOPHYSIOLOGY

PATHOPHYSIOLOGY:

Release of preformed mediators stored in granules, e.g. Histamine, tryptase , heparin, cytokines, chymase,etc Other newly-formed mediators synthesised rapidly, e.g. prostaglandin D2, leukotriene B4, PAF, LTC4, LTD4, and LTE4. Eosinophils may play pro-inflammatory role (release of cytotoxic granule-associated proteins) or anti-inflammatory role (e.g., metabolism of vasoactive mediators). PATHOPHYSIOLOGY

PATHOPHYSIOLOGY:

These mediators are responsible for the clinical features in anaphylaxis. Rapid systemic release of large quantities of mediators will cause capillary leakage and mucosal oedema, resulting in shock and/or asphyxia. PATHOPHYSIOLOGY

PATHOPHYSIOLOGY:

PATHOPHYSIOLOGY

AETIOLOGY:

AETIOLOGY

AETIOLOGY:

Common causes of anaphylaxis ( IgE -mediated) Foods Bee and wasp stings Drugs Latex rubber AETIOLOGY

AETIOLOGY:

AETIOLOGY Foods that cause anaphylaxis Peanuts Fish Shelfish Eggs Milk Sesame

Causes of anaphylaxis:

Causes of anaphylaxis Direct activation of mast cells - opiates, tubocurare , dextran,radiocontrast dyes Mediators of arachidonic acid metabolism - Aspirin (ASA) - Nonsteroidal anti-inflammatory drugs (NSAIDs) Mechanism unknown - Sulphites

Other Causes of anaphylaxis:

Other Causes of anaphylaxis Exercise-induced cold-induced idiopathic

CLINICAL EFFECTS:

CLINICAL EFFECTS

Frequency of symptoms in Anaphylaxis:

Frequency of symptoms in Anaphylaxis

Effects of mast cell mediators:

PHYSIOLOGICAL EFFECT CLINICAL EFFECT DANGER Capillary leakage Urticaria Angioedema Laryngeal oedema Hypotension Asphyxia Hypotension Mucosal oedema Laryngeal oedema Rhinitis Asthma Respiratory arrest Smooth muscle contraction Asthma Abdominal pain Respiratory arrest Effects of mast cell mediators

CLINICAL EFFECTS:

Systemic effects of histamine release. Minutes to hours Type of allergen Mode of transmission Symptoms may recur within 72hrs with no further exposure to allergen : 1-20% (Biphasic anaphylaxis) CLINICAL EFFECTS

CLINICAL EFFECTS:

SKIN : Hives, Itchiness, flushing, swelling of lips, tongue or throat. RESP : SOB, wheeze, stridor , Hypoxia GIT : Abdo cramps, diarrhoea, vomiting CVS : Coronary artery spasm, MI, Dysrhytmia CNS : Light-headedness, LOC (Low BP) Loss of bladder control & muscle tone Anxiety CLINICAL EFFECTS

MANAGEMENT:

Case-specific Follow ACLS protocol Remove allergen DRUGS : Adrenaline Glucagon Anti-histamine Inotropes Corticosteroids Isoprotenerol B2 agonist (inhaled) IV fluids Racemic Adrenaline Oxygen MANAGEMENT

MANAGEMENT:

ABCDEFG Adrenaline Adrenaline Adrenaline Adrenaline alleviates bronchoconstriction through B2 adrenoR stimulation; helps prevent cardiovascular collapse through cardiac B1 R stimulation MANAGEMENT

PREVENTION:

Allergy tests Allergy ‘action plan’ : Education Medic-alert Epi -pen Avoid triggers Immunotherapy/ Desensitization PREVENTION

QUESTIONS:

? ? ? ? ? QUESTIONS

TAKE HOME POINTS:

Anaphylaxis is a life-threatening condition. Recognise Sx early ACLS guidelines Adrenaline for severe cases TAKE HOME POINTS

Thank you:

Thank you