Anaphylactic and Anaphylactoid Reactions During Anesthesia Flashcards
Anaphylaxis
Reproducible adverse reaction to extrinsic substance mediated by immune system
Type 1 (acute)
Atopy, urticaria, angioedema, anaphylaxis
Type II (cytotoxic)
Hemolytic transfusion rx, HIT
Type III (immune complex)
Serum sickness
Type IV (delayed)
Contact dermatitis (red weepy skin, Pruriti) erythema, crack, and fissures, pruritis or pain
Anaphylaxis
a severe, life-threatening, generalized or systemic hypersensitivity reaction, primarily mediated by type E immunoglobulins.?
Anaphylaxis
Type 1, incidence 1:2,500-20,000, Mortality 6%, brain damage 2%
Anaphylaxis (clinical features)
rapid onset, prior exposure, ab-ag rxn, affects CV,Pulmonary, and cutaneous sys, circulatory collapse
Grade 1
Cutaneous mucus signs: erythema, urticaria, angiodema
Grade 2
Moderate multi-visceral: grade 1+/- HypoTN, tachycardia. Dyspnea, GI issues
Grade 3
Life threatening mono-multivisceral: CV collapse, tachy/bradycardia, +/- dyrrthmias, bronchospasm, cutaneous mucous, and GI disturbances
Grade 4
Cardiac arrest
Anaphylaxis
Patients sensitivity and route of admin determine severity. IV and mucous membrane exposure fastest and most sever rx
Anaphylaxis (risk factors)
Hx univestigated life threatening event, mastocytosis, allergy to an anesthesia drug, latex allergies inc risk, hx of atopy
Mechanism
Exposure to ag, production of spscfc IgE ab, ab fix to mast cell or basophils, reexposure bing to ab and cross linking, release of chemical mediators
productos of human mast cells
Granule proteins, cytokines, leukotrines, chemokines
Important mediators
Histamines, LK, PG
Histamines
Inc cap perm, Peripheral vasodilation, Bronchoconstriction
Leukotrienes (LK)
Bronchconstriction, inc cap perm, negative ionotropy
Prostaglandins (PG)
Bronchconstriction, vasodilations
Anaphylactoid
Non IgE anaphylaxis
Anaphylactoid (clinical)
Direct action on mast cells, MASSIVE release of histamine, may occur on 1st exposure, clinically indistinguishable, life thret, PREDISPOSITION: pregnancy,youth, atopy
Anaphylaxis (diagnosis)
Periop - challenging, multiorgan effects, pt cannot complain, anesthetic drugs mimic
Anaphylaxis (diagnosis)
OR drapes, limited access delay Dx, variation in manifestations and course of rxn, spectrum of rxn from minor to CP collapse, lack of prior allergy hx
Signs under anesthesia
Sudden and profound HypoTN, Circu collapse, bronchospasm, flush, edema, Cardiac arrest
Circulatory collapse
profound vasodilation, HypoTN diff to tx, tachcardia, dysrrythmiasm Pulmonary vasoconstriction/HTN, cardiac arrest
Kounis Syndrome
Acute Coronary event related to hypersensitivity rxn, may or not have predisposing factors to CAD, CA spasm/Angina, acute MI
Pumonary Insults
wheezing, Bronchospasm difficult to tx, Increased PIP, Laryngeal edema/stridor, Acute pulmonary edema, acute respiratory failure/hypoxia
Cutaneous signs
Urticaria, flushing, edema (periorbital and perioral)
Differential DX
astma/ reactive airway, Cardiogenic shock, Tension pneumo, pericardial tamponade, pulmonary embolus, septic shock, vasovagal rxn, venous air embolism
Tx goals
immediate recognition and tx
Tx goals
stop ag admin, 100% O2 and PPv, stop volatile, IV volume expansion 1-4L, or 20mL/ kg boluses, Epi 100mcg, 0.1cc/kg IV, double and q3-5min, External cardiac massage
Epi
inc cAMP, stabilizing cell membranes and inhibiting mediator release (increase ca++) b2 agonist effect (bronchodilation), alpha agonist effects (vasoconstriction)
Anaphylatic shock refractory to catecholamines
due to desenstization of adrenergic receptors (beta blocker therapy), Inc dynthesis of NO contributes to HypoTN and resistance to pressors, NO and metabolic acidosis hyperpolarize K channels preventing Ca from entering cells NorEpi, glucago and neo helpful
Vasopressin
alternative therapy when Epi fails, causes vasoconstriction via V1 receptors, directly decreases intracellular conc of NO, detrimental if used to early (WAIT 10-20min after onset of shock)
Methylene blue
Interfere with NO mediated vascular smooth muscle relaxation, useful when catecholamin and vasopressin resitant anaphylaxis
secondary tx
diphenhydramine (1-2mg/kg), hydrocortisone 2mg/kg, Inhaled bronchodilators, Aminophylline-resitant bronchospasm, inotrope infusion to maintain BP, NaHCO3 for acidosis
Biologic assesment
assist in dx, biochemical tests in vivo and in vitro, inc in plasma histamin (drawn withn 30min short t1/2)
Histamines
inc in plasma histamin (drawn withn 30min short t1/2), indicates Mast cell/basophil activation, does NOT diff immune vs non immune cause
Tryptase- mast cell neutral serine protease
Preformed enzyme, elevated serum tryptase = mast cell/ basophil activation (peaks 15-60min) baseline tryptase (after 24hrs) determines immune and non immunologic mechanis
Immunologic anaphylaxis
Inc serum histamine and tryptase
Nonimmunologic
inc serum histamine NO CHANGE in tryptase
Po-op management
Clotting screen, ICU, airway eval before extubation, skin testing intradermal vs RAST, ELISA, patient ed furture prophylaxis
Intradermal Skin Test
Gold Std for IgE mediated rxns, ids culprit agentm proves mechanism allergic vs non allergic, safe alternative. Done 4-6wks after rxn
Coomon anes offenders
NMBs 69%, Latex 12-16% children 76%, antibiotics 8%, Opiods (morphine ann meperidine) PABA ester LA, hynotics,
NMB
Sux, atracurium, vecuronium, cross rxty btw sux and NMBAs, IgE type 1 and non IgE mivacurium
Hypnotics
Thiopental, propofol (other hx ex Egg) Anaphylaxis may occur after an uneventful previous exposure
Opiods
anaphylactoid more common due to direct histamine release, arterial and venodilation
LA
PABA ester Type 1 IgE or cross rxty, Amide LA preservative agent
Antibotics
PCN, cephalosporins (cross rxty 1-7%), PCN 50%. Vancomycin produces both rxn Redman syndrome-histamine release
Latex
true rxn, delayed onset, increasing incidence in children
High risk Latex
spina bifida, spinal cord injury, healthcare workers, allergy to bananas, avocado, kiwi
Others
Blood products, Plasma volume expanders, IV contrast dye, Protamine, halothane hepatitis (neoag stimulate abs, eosinophilia rash fever, prior exposure to halothane
Etiology and dx of periop anaphylaxis
Depends of clinical, biologic and allergologic evidence
Etiology and dx of periop anaphylaxis
severe rxn+serum tryptase+ pos skin test =anaphylaxis
Etiology and dx of periop anaphylaxis
suggestive clinical hx+ +/- serum histamine - serum tryptase+ neg skin test = non allergenic rxn
death prevention
High index of suspicion, prompt recognition+ prompt and aggressive tx