anaphylaxis in general anesthesia

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    Anaphylaxis in General

    AnesthesiaFredric M. Hustey, MD

    Associate Professor

    Cleveland Clinic Lerner College of MedicineCase Western Reserve University

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    Objectives

    Discuss challenges in the diagnosis ofallergic reactions/anaphylaxis during general

    anesthesiaList common precipitants of allergic and

    anaphylactic reactions in the OR

    Discuss management strategies for patientswith anesthesia induced anaphylaxis

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    Not Uncommon

    1/13,000 to as much as 1/3,180

    mortality ranges between 3 and 9%

    Moneret-Vaultrin et al. Anaphylaxis to General Anesthetics. ChemImmunology and Allergy 2010; 95:180-189.

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    Mechanisms

    IgE (cross-linked by allergen/drug)

    Cardiovascular collapse and bronchospasmmore frequent in IgE-dependent rx

    Complement activation via IgG or IgMbinding to antigen/drug

    Direct complement activation via alternate

    pathwayDirect activation of mast cells or basophils

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    Leading Causes

    Neuromuscular blocking agents (50-70% ofcases) IgE-dependent reactions predominant

    Cross-reactions not uncommon

    Second: latex allergy

    Third: antibiotics (beta-lactams in general)

    Anaphylaxis to intravenous hypnotics,plasma substitutes, aprotinin, protamineand other drugs can occur

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    Diagnosis

    90% of reactions appear at induction

    Within seconds or minutes after IVadministration

    Reactions appearing later (duringanesthesia maintenance

    Latex

    Volume expanders

    Dyes

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    Challenges in Diagnosis

    Patient under general anesthesia cannotcomplain

    Miss early warning signs Pruritis

    Malaise

    Dyspnea

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    Challenges in Diagnosis

    Draping

    Difficult to appreciate skin manifestations suchas uriticaria

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    Challenges in Diagnosis

    Tachycardia, increased airway resistance,hypotension

    Dose related side effects of drugs Inadequate depth of anesthesia

    Surgical complications

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    Challenges in Diagnosis

    Clinical features can vary widely b/wpatients

    May also occur in isolation Bronchospasm, hypotension with tachycardia

    Mild cases (single symptom) may resolvedspontaneously without specific tx

    Not recognized as allergic

    Fatal re-exposure

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    Most Commonly Reported Initial

    FeaturesDifficulty ventilating

    Desaturation

    Pulselessness

    Whittington et al. Anaphylactic and anaphylactoid reactions. ClinAnaesthesiol B Clin Anaesthesiol 1998; 12:301-323

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    Management: Three Principles

    Interrupt contact with offending agent

    Modulate effect of released mediators

    Inhibit further mediator production andrelease

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    Primary Treatment

    Cease all drugs/surgery when possible

    Often difficult to identify precipitant

    Multiple exposures in short timeframe

    Fluids

    Epinephrine

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    Ring and Messmer Severity Scale

    Grade I: cutaneous with or w/o angioedema

    Grade II: moderate multi-organ involvement

    Hypotension, tachycardia

    Difficulty ventilating, bronchial hyper-reactivity

    Grade III: Severe life threatening MOSinvolvement

    Grade IV: Cardiac and/or respiratory arrest

    Brown, SGA. Clinical features and severity grading of anaphylaxis. J AllergyClin Immunol 2004;114(2):371-376

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    Epinephrine

    Initial adult dosing depends on severity Grade I generally not necessary

    Grade II 10-20 ug IV boluses

    Grade III 100-200 ug IV boluses

    Grade IV: ACLS (1mg IV bolus)

    Titrate according to severity and responseRepeat q1-2 minutes as necessary

    IV qtt

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    Resistant to Epinephrine?

    Norepinephrine qtt

    Consider glucagon for patients on B-

    blockers Initial dose of 3-5mg IV

    *Vasopressin (2-10 unit increments IV)

    *Methylene blue (inhibits NO mediation ofvascular smooth muscle relaxation)

    *some data exists on these therapies but value is not

    completely clear

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    Secondary Treatment

    Antihistamines

    H1 and H2 blockers

    CorticosteroidsB2 agonists for persistent bronchospasm

    Observation

    *Relapse can occur up to 24 hours later

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    Neuromuscular Blocking Agents

    Higher risk

    *Succinylcholine 33.4%

    *Rocuronium 29.3% *Atracurium 19.3%

    *Vecuronium 10.2%

    Lower risk

    Pancuronium

    Cisatracurium

    *Mertes PM et al. Anaphylaxis during anesthesia in France: an 8 year nationalsurvey. J Allergy Clin Immunol 2011;128(2):366-373

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    Neuromuscular Blocking Agents

    Can occur during first administration fromcross sensitization via similar quaternaryammonium ions

    Cosmetics

    Toothpastes, soaps, shampoos

    Foods

    Drugs (cough suppressants)

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    Neuromuscular Blocking Agents

    Cross sensitization b/w NMBs is common

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    Latex

    Second most common cause of anaphylaxis

    Risk increases with increased exposure

    Health care workers Multiple surgeries

    Primary cause of anaphylaxis in children subjected tomultiple surgeries (especially spina bifida)

    Cross sensitization from food allergensAvocado, banana, kiwi, chestnut

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    Antibiotics

    Third most common etiology

    Penicillins and cephalosporins account for

    up to 70%Quinolones also common

    Vancomycin allergy rare

    Rxs related to basophil degranulation associatedwith rapid administration (red-man syndrome)

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    Hypnotics

    Less common

    Propofol in patients with egg/soy allergy

    Insufficient evidenceMidazolam, etomidate, ketamine

    Rare

    Isoflurane, desflurane, sevoflurane Exceedingly rare

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    Colloids

    All can precipitate but low incidence (.03-.2%)

    Gelatins and dextrans > Albumin orhetastarch

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    Post Anaphylaxis Analysis

    Challenges

    Was this a true allergic response?

    What was the precipitating agent?

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    Was This a True Allergic Response?

    Analyze the clinical data (hx, timing, sxs,response to tx)

    Serum markers of mast cell activation canbe sent intraoperatively

    Triptase levels within 30-120 minutes ofsymptom onset

    Serum histamine degraded quickly and may notbe reliable

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    What was the Precipitating Agent?

    Immunological assessment of suspectedallergen should be based on more than onetest

    Avoid single test - no test is perfect

    False positives exclude otherwise useful agent

    False negatives can result in potential fatal re-

    exposure

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    What was the Precipitating Agent?

    Referral for Allergy/Immunology testing

    Quantification of specific IgE (best during thefirst 6 months after the event)

    Skin testing (best within the first year after theevent)

    Other biologic assays

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    What was the Precipitating Agent?

    AVOID RE-EXPOSURE

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    Conclusion

    Anaphylaxis in general anesthesia is rarebut life threatening

    Diagnosis can be challenging in the ORenvironment

    Early recognition and management is criticalto prevent morbidity and mortality

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    Questions?