Muscle relaxant anaphylaxis

Nybo M, Madsen JS Serious anaphylactic reactions due to protamine sulfate a systematic literature review. Basic Clin Pharmacol Toxicol 2008 103 192. Moneret-Vautrin DA, Kanny G Anaphylaxis to muscle relaxants rational for skin tests. Allerg Immunol (Paris) 2002 34 233. 

Mertes PM, Moneret-Vautrin DA Skin reactions to intradermal neuromuscular blocking agent injections a randomized multicenter trial in healthy volunteers. Anesthesiology 2007 107 245. Moneret-Vautrin DA, Gueant JL, Kamel L, Laxenaire MC, el Kholty S, Nicolas JP Anaphylaxis to muscle relaxants cross-sensitivity studied by radioimmunoassays compared to intradermal tests in 34 cases. J Allergy Clin Immunol 1988 82 745. 

Uses Severe, systemic fungal Infxns oral cutaneous candidiasis Action Binds ergosterol in the fungal membrane to alter permeability Dose Adults Peds. Test dose 1 mg IV adults or 0.1 mg/kg to 1 mg IV in children then 0.25-1.5 mg/kg/24 h IV over 2-6 h (range 25-50 mg/d or qod). Total dose varies w/ indication PO 1 mL qid Caution [B, ] Disp Inj SE -1- K /Mg from renal wasting anaphylaxis reported, HA, fever, chills, n hrotox, -1- BP, anemia, rigors Notes -1- In renal impair pre-Tx w/ APAP antihistamines (Benadryl) X SE Interactions T Nephrotoxic effects W/ antineoplastics, cyclosporine, furosemide, vancomycin, aminoglycosides, T hypokalemia W/ corticost oids, skeletal muscle relaxants EMS May cause electrolyte imbalances, monitor ECG OD May effect CV and resp Fxn symptomatic and supportive... 

Anaphylactic reactions result from the interaction of antigens with specific IgE antibodies, which have been formed by previous exposure to the antigen. Anaphylactoid reactions are clinically indistinguishable from anaphylaxis but do not result from prior exposure to a triggering agent and do not involve IgE. Intravenous anaesthetics and muscle relaxants can cause anaphylactic or anaphylactoid reactions and, rarely, they are fatal. Muscle relaxants are responsible for 70% of anaphylactic reactions during anaesthesia and suxamethonium accormts for almost half of these. 

The diagnosis of an allergic reaction to a muscle relaxant is based on clinical features, measurement of histamine and tryptase concentrations in the plasma during the reaction, and subsequent skin testing a few weeks later. However, during general anesthesia isolated sjmptoms can occur, most often hypotension or bronchospasm. Therefore, the clinical features of anaphylaxis may not be recognized as such. 

Leynadier F, Dry J. Anaphylaxis to muscle-relaxant drugs study of cross-reactivity by skin tests. Int Arch Allergy Appl Immunol 1991 94(l ) 349-53. 

Death caused by an anaphylactic reaction to a muscle relaxant seems to be rare, although mortality rates from intraoperative anaphylaxis in the range of 3.4-6% have been reported (28-31). The incidence of cardiac arrest was 4.9% among patients with anaphylactic reactions to muscle relaxants referred to the French GERAP centers for further testing, but these patients all survived (22). 

Baldo BA, Fisher MM. Anaphylaxis to muscle relaxant drugs Cross-reactivity and molecular basis of binding of IgE antibodies detected by radioimmunoassay. Mol Immunol. 1983b 20 1393-400. 

These mediators can produce a number of effects including bronchiolar constriction, capillary dilatation, or urticaria (i.e., hives). In severe episodes of type I reactions a life-threatening anaphylaxis can develop in humans due to extreme bronchoconstriction and precipitate hypotension. Epinephrine is the principal drug used in the acute management of these critical effects since it achieves (1) an elevated blood pressure via activation of alpha receptors in peripheral resistance blood vessels and (2) relaxation of bronchiolar smooth muscle via activation of (32 receptors in the lung. Relief from the dermatological problem (i.e., hives) is also achieved via vasoconstriction of capillaries in the skin that reduce permeability, and, hence, fluid accumulation. Penicillin is a classic example of a drug that can cause a type I reaction. 

The actions of prostaglandins on isolated pulmonary blood vessels were reviewed by Piper and Vane (1979). Usually, E-type PG relax pulmonary vascular smooth muscle but there is some species variation in the reaction of intrapulmonary blood vessels (Palmer et al. 1973, Kadowitz et al. 1975). The intrapulmonary vessels will be exposed to the prostaglandins released in the lung by agents such as bradykinin, slow-reacting substance of anaphylaxis or histamine. 

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