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Anaphylaxis PowerPoint Presentation

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Description : This medical presentation titled ""Anaphylaxis"" is about anaphylaxis which is a systemic, immediate hypersensitivity reaction caused by IgE-mediated release of histamine and other mediators from mast cells and basophils. The presentation provides epidemiology of anaphylaxis, its risk factors, respiratory symptoms and more.

Tags : Allergy, Portier, Richet, Clinical syndrome, multi-organ symptoms, Anaphylactoid, Epidemiology, Risk factors, Mediators, Nasal congestion, sneezing, rhinorrhea, GASTROINTESTINAL SYMPTOMS, CARDIOVASCULAR, BIPHASIC, PROTRACTED ANAPHYLAXIS, Self-injectable Epinephrine, Differential Diagnosis, FOOD SKIN TESTING, CLASSIFICATION, IgE Mediated, Complement, Immune Complex Activation, Direct Histamine Release, Unknown Mechanisms

Published on : Apr 24, 2021 | Views : 3651 | Downloads : 16

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Slide 1-

Anaphylaxis Scot A. Laurie, MD Dallas Allergy and Asthma Center Clinical Assistant Professor, Division of Allergy & Immunology University of Texas Southwestern Medical Center
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Historical Background Discovered by Portier and Richet in 1902 While attempting to immunize dogs to the venom of a sea anemone, they unknowingly sensitized the dogs Dogs unexpectedly reacted to a previously nonlethal dose Coined the term “anaphylaxie”, meaning without, or against, protection
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DEFINITIONS Anaphylaxis Systemic, immediate hypersensitivity reaction caused by IgE-mediated release of histamine and other mediators from mast cells and basophils Clinical syndrome with multi-organ symptoms cutaneous respiratory cardiovascular gastrointestinal Anaphylactoid Identical symptoms as anaphylaxis Non-IgE-mediated mechanism
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EPIDEMIOLOGY Hospitalization for Anaphylaxis 13 yr retrospective review of anaphylactic shock from a hospital in Denmark incidence of 3.2 cases per 100,000 inhabitants per year mortality rate of these 20 cases was 5% Sørensen H et al. Allergy 1989;44:288. ER Visits for Anaphylaxis Klein individually reviewed all 19,122 ER records during a 4 month period from St. Mary’s Hospital in Rochester, MN Incidence of anaphylaxis was 17 per 19,122 emergency visits or 0.09% Only 4/17 had ICD-9 codes for anaphylaxis most were simply classified as having an “allergic reaction” Klein J, Yocum M. J Allergy Clin Immunol 1995;95:637-8.
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Epidemiology of Anaphylaxis Retrospective review of 1255 cases of “anaphylaxis” identified in Olmsted County from 1983-1987 133 residents met criteria for anaphylaxis and had 154 reactions 116 single episode 13 had 2 episodes 4 had 3 episodes Anaphylaxis occurrence rate 30/100,000 person years Suspect allergen found 68% Allergy consultation in only 52% 1 patient died 0.65% fatality rate Yocum MW et al. J Allergy Clin Immunol 1999;104:452-6.
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Anaphylaxis: Risk factors Age More common in adults Atopy Foods Exercise Latex RCM Idiopathic Exposure route Oral less likely Gender Males Hymenoptera Females Latex Muscle relaxant Idiopathic
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Mediators of Anaphylaxis
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“SHOCK” ORGANS IN ANAPHYLAXIS Skin Respiratory tract Cardiovascular system Gastrointestinal tract
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CUTANEOUS SYMPTOMS Pruritus initially palms, soles, groin, and axilla Urticaria & Angioedema most common finding usually resolves within 24 hours angioedema may persist for 2-3 days Warmth Flushing Erythema
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RESPIRATORY SYMPTOMS Lower respiratory symptoms Dyspnea, wheezing, and chest tightness Upper respiratory symptoms Nasal congestion, sneezing, rhinorrhea Laryngeal edema often begin with a sensation of a “lump in the throat” may progress to: dysphonia hoarseness drooling due to inability to swallow secretions stridor asphyxia
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GASTROINTESTINAL SYMPTOMS Abdominal cramping Nausea Vomiting Diarrhea
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CARDIOVASCULAR Symptoms lightheadedness tachycardia bradycardia hypotension vascular collapse Signs Arrhythmias premature atrial contractions atrial fibrillation bundle branch block peaked P waves and right axis deviation ventricular premature contractions ventricular fibrillation asystole myocardial infarction
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FREQUENCY OF ANAPHYLACTIC SYMPTOMS
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BIPHASIC & PROTRACTED ANAPHYLAXIS Stark & Sullivan Prospective study of 25 patients with anaphylaxis at PMH 5 (20%) had " biphasic anaphylaxis" 6 had "protracted anaphylaxis" Risk Factors oral agent anaphylaxis began > 30 minutes after exposure Stark B, Sullivan T. J Allergy Clin Immunol 1986;78:76-83. Douglas et al. Biphasic anaphylaxis in only 5% of 44 inpatients Douglas D et al. J Allergy Clin Immunol 1994;93:977-85. Both Studies Glucocorticoid therapy did not prevent either recurrent or prolonged anaphylaxis Patients without hypotension or laryngeal edema did not have biphasic reactions
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Fatal Anaphylaxis Pumphrey RSH Clin Exp Allergy 2000:30:1144-50.
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Pumphrey RSH Clin Exp Allergy 2000:30:1144-50. Timing of Epinephrine in Fatal Anaphylaxis
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Pumphrey RSH Clin Exp Allergy 2000:30:1144-50. Self-injectable Epinephrine Use in Fatal Anaphylaxis
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Differential Diagnosis of Anaphylaxis and Anaphylactoid Reactions Vasodepressor reactions Flush syndromes- carcinoid “Restaurant syndromes”- scombroidosis Excessive endogenous production of histamine- mastocytosis Nonorganic disease- panic disorder, vocal cord disorder, undifferentiated somatoform anaphylaxis Chronic idiopathic urticaria/angioedema
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EVALUATION OF PATIENTS WITH ANAPHYLAXIS Working definition of anaphylaxis Either Airway obstruction such as laryngeal, pharyngeal, or glossal edema or severe bronchospasm Or Documented hypotension or syncope Plus Symptoms of generalized mediator release urticaria, angioedema, pruritus, or flushing Review ER records for objective findings
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DETERMINING THE ETIOLOGY OF ANAPHYLAXIS Detailed History Time of day Relationship to exercise, meals, and medications Prescribed medications different formulations or lots of medications Non-prescribed ingestants vitamins, health food supplements, laxatives, and suppositories specific ingredients of meals within 4 hours of episode(s) Women menses or intercourse
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SPECIFIC IgE in ANAPHYLAXIS Skin testing Accuracy > RAST Risk of fatal reactions Allergens medications, anesthetics, venoms, foods, insulin, latex heterologous sera, vaccines, and other foreign proteins Specificity fairly good Sensitivity of many tests is ? Some drugs can cause direct histamine release opiates, RCM , some muscle relaxants RAST testing Without risk Limited applicability due to lower accuracy Few allergens available venoms, foods, latex, and the major determinant of penicillin
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FOOD SKIN TESTING IN ANAPHYLAXIS Stricker et al Panel of 79 antigens Identified 7 food-induced anaphylaxis of 102 patients with IA Stricker W et al. J Allergy Clin Immunol 1986;77:516-519. Patients frequently unaware of foods that caused reactions Food allergic patients failed to identify causative food in 67% of positive DBPCFC Atkins F. J Allergy Clin Immunol 1985;75:348-355. Most all patients with fatal food-induced anaphylaxis unknowingly ingested their fatal food Skin testing with fresh foods Commercial food extracts may lack antigenic epitopes
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MEDIATOR MEASUREMENT IN ANAPHYLAXIS
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TRYPTASE Neutral protease in secretory granules of mast cells Specific for mast cells very minimal amounts in basophils a-tryptase predominant form of tryptase in circulation in both normals and mastocytosis patients b-tryptase released from secretory granules with systemic mast cell activation
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TRYPTASE MEASUREMENTS Total tryptase measured with mAb B12 measures both a & b-tryptase normal values < 15 ng/ml increases detectable earlier than G5 assay available through commercial labs b-tryptase measured with mAb G5 normal values < 1 ng/ml undetectable within 30 minutes peaks in 1-2 hours available through Dr. Schwartz’s lab at MCV
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CLASSIFICATION OF ANAPHYLAXIS IgE Mediated Complement/Immune Complex Activation Direct Histamine Release Unknown Mechanisms
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IgE MEDIATED ANAPHYLAXIS Antibiotics Penicillin, Cephalosporins, Sulfamethoxazole Proteins Venoms, Heterologous sera, Latex, Seminal fluid Hormones: ACTH, Insulin, PTH, GnRH Enzymes: Chymopapain, Streptokinase Foods Peanut, Tree nuts, Crustaceans, Fish, Seeds, Spices Milk, Egg, Soy, Many others Therapeutics Allergen extracts Vaccines - including fillers (gelatin) Intraoperative agents Thiopental, Muscle relaxants, ?Protamine, Fentanyl Chemotherapeutics, Ethylene oxide gas, Psyllium Local anesthetics, ?Corticosteroids, ?NSAID’s
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LOCAL ANESTHETIC ALLERGY Allergy rare and anaphylaxis extremely rare allergy to parabens also rare Non-cross-reacting local anesthetic groups defined based on patch testing for contact dermatitis unclear if any relevance to anaphylaxis Skin testing & incremental challenge validated method recommended for evaluation of possible allergy
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IMMUNE COMPLEX/COMPLEMENT ACTIVATION ? Radiocontrast Media Blood/Blood products Plasma, Serum, cryoprecipitate IgE mediated anaphylaxis passive sensitization IgE anti-IgA in IgA deficient patients FVIII Hemodialysis membranes IVIG
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THE MYTH OF SEAFOOD ALLERGY & RCM REACTIONS Despite the common belief that individuals with seafood allergy have a higher risk of RCM reactions, there is no data to support this and it has no theoretical basis Shellfish allergic patients are allergic to muscle proteins, not iodide RCM reactions are not caused by iodide Low-ionic RCM have a lower incidence of anaphylactoid reactions despite containing more iodide per particle than traditional RCM
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DIRECT HISTAMINE RELEASE Hypertonic Solutions RCM, Mannitol Plasma Expanders Dextran, Hydroxyethyl starch Drugs Opiates, Vancomycin, Curare, Fluoroscein
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Anaphylaxis with Unknown Mechanism Exercise Induced Anaphylaxis Idiopathic Anaphylaxis Progesterone Anaphylaxis
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ACUTE TREATMENT OF ANAPHYLAXIS Early recognition and treatment delays in therapy are associated with fatalities Assessing the nature and severity of the reaction Brief history identify allergen if possible initiate steps to reduce further absorption medications (especially -blockers) General Therapy supplemental oxygen, IVF, vital signs, cardiac monitoring Goals of therapy ABC’s
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EPINEPHRINE First-line drug of choice in anaphylaxis Mechanisms of action agonist increase BP by peripheral vasoconstriction -agonist reverse bronchoconstriction positive ionotropic and chronotropic activity increases cyclic AMP levels inhibit further mediator release from mast cells and basophils Subcutaneous administration dose: 0.3 to 0.5 mg of a 1:1,000 dilution prn q 10-15 min IV epinephrine for cardiovascular collapse Side effects severe hypertension, arrhythmias, myocardial ischemia and infarction DO NOT WITHHOLD EPINEPHRINE BECAUSE OF CARDIAC HISTORY
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Simons FER et al. J Allergy Clin Immunol 1998;101:33-7. Epinephrine Absorption: SQ vs. IM
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Epinephrine Subcutaneous Epinephrine Intramuscular Simons FER et al. J Allergy Clin Immunol 1998;101:33-7.
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Epinephrine Subcutaneous Epinephrine Intramuscular Simons FER et al. J Allergy Clin Immunol 1998;101:33-7.
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Simons FER et al. J Allergy Clin Immunol 1998;101:33-7. Outdated EpiPens
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Simons FER et al. J Allergy Clin Immunol 2000;105:1025-30.
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Use of EpiPen in Children with Anaphylaxis Retrospective survey of children with anaphylaxis who attended an allergy clinic in North Adelaide Australia 45 episodes of anaphylaxis EpiPen given 13 (29%) EpiPen not given 32 (71%) Hospitalization for anaphylaxis EpiPen given 2 (14%) p< .05 EpiPen not given 15 (47%) Gold MS, Sainsbury R. J Allergy Clin Immunol 2000;106:171-6.
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ANTIHISTAMINES IN ANAPHYLAXIS Not a substitute for epinephrine H1-antagonists useful for cutaneous symptoms H2-antagonists somewhat controversial combination of H1 and H2 antagonists was required for optimal prevention of hypotension in studies of histamine infusions overall evidence favors the addition of H2-antagonists especially in the presence of hypotension
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 -BLOCKED ANAPHYLAXIS Beta blockade increase release of mediators enhance the responsiveness of pulmonary, cardiovascular, and cutaneous systems to mediators paradoxical responses to epinephrine bronchoconstriction and bradycardia unopposed -adrenergic and reflex vagotonic effects May be especially refractory to therapy Treatment high doses of isoproterenol or dopamine atropine glucagon increases c-AMP independent of -receptor nausea and vomiting common
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PREVENTION OF ANAPHYLAXIS Referral to BC/BE allergist Determine an etiology skin testing challenges desensitization. Educate the patient on avoidance proper use and indications of injectable epinephrine when to seek medical attention obtain a Medic-Alert® bracelet Develop a management plan prevent and reduce further anaphylactic episodes Select an alternative drug if on -blocker
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ACUTE DESENSITIZATION Indications Patients allergic to an essential therapeutic agent Systemic reactions to venoms (optional) Technique Escalating doses of antigen administered over a brief period Oral route preferred when possible Desensitization procedures are dangerous Mechanism of desensitization Unknown Desensitized state is antigen specific not due to tachyphylaxis to mediators, mast cell depletion, or unresponsiveness to any IgE signal
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CASE REPORT LB is a 62 yo WM who presented with recurrent syncopal episodes. These episodes were associated with pruritus, urticaria, lightheadedness, and syncope with urinary & fecal incontinence and occurred after playing basketball or ping-pong. However, he has performed more vigorous exercise without reactions. An echocardiogram, Holter monitor and head CT were all normal. Physical examination was unremarkable
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EXERCISE-INDUCED ANAPHYLAXIS Classification Food dependent EIA Specific food dependent EIA occurs only if exercise after eating specific food(s) implicated foods shellfish, wheat, celery, tomato, apple, grapes, litchi, hazlenut, chestnut, peanut, milk, rice, potato Non-specific food dependent EIA occurs if exercising after eating any food Food independent EIA
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POSSIBLE MECHANISMS OF EIA Subthreshold amount of mast cell associated IgE cross-linking Endogenous opioid stimulus can trigger primed mast cells to degranulate Increases in codeine skin test reactivity after exercise Increased wheal response to compound 48/80 in individuals with food-dependent EIA, but only after challenges with specific foods and exercise. Gastrin can stimulate mediator release from mast cells Abnormal responses of the autonomic nervous system Increases in parasympathetic responses Decreases in sympathetic activity
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CLINICAL FEATURES OF EIA 7% of anaphylaxis due to EIA Symptoms & signs of EIA similar to other forms of anaphylaxis premonitory symptoms generalized warmth, pruritus urticaria are usually 10-15 mm in diameter angioedema of face, palms, and soles reactions occur while exercising or shortly thereafter duration of 0.5 to 4 hours Exercise triggers Tennis, warmups, dancing, soccer, basketball, running vaginal delivery Predisposing factors personal or family history of atopy familial EIA has been reported aspirin ingestion prior to exercise may trigger 30% exercising in warm or humid weather menses
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THERAPY OF EIA Acute treatment epinephrine available while exercising Prevention exercise with a partner limiting or discontinuing exercise at the first sign of prodromal symptoms avoid NSAID’s avoiding foods for 4-5 hours prior to exercise antihistamines - unable to totally prevent attacks oral disodium cromoglycate “exercise desensitization”
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Natural History of EIA 279 EIA patients completed mailed survey Clinical course Attacks/yr decreased from 14.5 to 8.3 47% decrease in attacks 46% same 7% increased Food Associated EIA 37% patients Shellfish, alcohol, tomato most common triggers Avoidance behaviors Avoid exercise in extreme hot/cold or allergy season Avoid eating before exercise Shadick NA et al. J Allergy Clin Immunol 1999;104:123-7.
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Case Report CW is a 14 yo WF with a history of large local reactions to “bees”. 3 weeks prior to evaluation she was bit in the forehead by an ant and within 5 minutes developed facial urticaria, chest tightness, and throat tightness which improved with H1 & H2 antagonists administered by her father a cardiologist. Prick testing to imported fire ants was positive
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IMPORTED FIRE ANTS IFA most common cause of anaphylaxis to stinging insects in this area Imported fire ant species Solenopsis richteri introduced from Uruguay or Argentina accidentally into the USA through the port of Mobile, Alabama in 1918 localized to northeastern Mississippi and northwestern Alabama Solenopsis invicta Brazilian species introduced later between 1933-1941
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Fire Ant Anaphylaxis 0.6% to 2% of patients requiring medical treatment for stings Texas has the 2nd highest number of IFA sting fatalities Diagnosis anaphylaxis history after sting with development of a pustule fire ant-specific IgE by skin tests 25% of nonallergic individuals in endemic areas have IFA specific IgE Immunotherapy Indicated for patients with systemic reactions, especially anaphylaxis IFA whole body immunotherapy efficacy field re-stings 2.1% risk of anaphylaxis intentional sting challenge 0/30 reactions Optimal duration of immunotherapy unknown
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CASE REPORT 34 yo BF with recurrent episodes of pruritus, urticaria, angioedema, chest tightness, and syncope. One episode required ER treatment and hypotension was documented. All episodes occurred shortly after sexual intercourse. She was seen initially by a neurologist who thought she was having hypoglycemic attacks and recommended eating prior to intercourse which did not help. She also had an ETT performed and the cardiologist thought she “was crazy”. Skin testing with her partners semen at 1:1,000 dilution was markedly positive while her partner was skin test negative Condom use was recommended and prevented the attacks
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HUMAN SEMINAL PLASMA ANAPHYLAXIS First reported by Specken in 1958 Pathogenesis Halpern et al. (1967) Evaluated a woman with anaphylaxis occurring 15-30 minutes after coitus Scratch tests were positive to husband’s whole sperm & seminal fluid devoid of spermatozoa donor seminal fluid devoid of spermatozoa Scratch tests negative to husband’s serum semen from rabbit, guinea-pig, horse and bull Passive transfer (Prausnitz-Küstner reaction) positive in 5 female controls as well as in monkeys Chromatography and electrophoresis of seminal fluid identified basic protein fractions that were the most antigenic
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HUMAN SEMINAL PLASMA ANAPHYLAXIS Antigens Isolated to seminal plasma reactions can occur with vasectomized partners only one case reported of a women reactive to spermatozoa and HSP canine sperm can also induce anaphylaxis due to bestiality Antigenic fraction of seminal fluid MW of 20,000 to 30,000 daltons heat stable prostatic origin prostate specific antigen (PSA) may be a major allergen
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THERAPY OF HSP ANAPHYLAXIS Condoms universally successful may induce remission if used for prolonged periods Prophylactic antihistamines may control local HSP reactions ineffective for systemic reactions Pregnancy successful impregnation may be achieved using artificial insemination with isolated spermatozoa Immunotherapy extracts of antigenic fractions of HSP most successful Immunologic changes variable decrease in IgE progressive rise in IgG rapid desensitization parenteral and local (intravaginal) long term success up to 8 years after immunotherapy maintaining sexual activity 2-3 times per week
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Idiopathic Anaphylaxis Diagnosis of exclusion Careful evaluation for known causes should be performed Mechanism is unknown Patients present with the same constellation of symptoms as others with anaphylaxis Treatment approach is the same Preventative therapy with qd or qod prednisone may be required Patients require education and support as part of their disease management
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CONCLUSIONS Anaphylaxis is the most dramatic and potentially fatal manifestation of immediate hypersensitivity Majority of reactions are due to medications, insect stings, radiocontrast media and food, however many are idiopathic Most anaphylactic reactions respond to aggressive therapy, but fatalities still occur, especially if treatment is delayed Epinephrine is still underutilized in many patients Almost all cases of anaphylaxis should be referred to an allergist