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Anaphylaxis Treatments - #PHARMFAX

You’d actually be surprised how many people die each year from bee stings and peanuts.

 

You’d actually be surprised how many people die each year from bee stings and peanuts. Anaphylactic shock is derived from mast cells, basophils, and histamanergic-mediated acute onset of hypersensitivity and inflammation. This will progress to profuse vasodilation, decreased venous return/CO, and eventual shock. Around 90% of patients will present with angioedema, which is inflammation of the throat, tongue, and lips. If left untreated, patients can rapidly progress to acute cardiopulmonary arrest. If there is one thing I hope you take from this segment, grab epinephrine if you are limited on time. Epinephrine agonizes alpha and beta receptors, leading to bronchodilation, increased inotropy, and vasoconstriction. Give 0.3 to 0.5 mg IM q 5 min up to three doses, then transition to IV epinephrine for refractory shock. Thigh is preferable given the vasculature provides a faster onset compared to the deltoid. Consider glucagon when patients are on beta blockers. Glucagon is indicated given it will promote inotropy/chronotropy via increased cAMP and bybassing adrenergic receptors. Everything we give is considered to be symptomatic and only given after epinephrine has been given (when indicated). Diphehydramine (H1-antihistamine) addresses symptomatic control of urticuria. Famotidine (H2 receptor antagonist) has minimal acute effect given H2 receptors are primarily in gut. Steroids have limited acute benefit since their onset is 4 to 6 hours their biphasics prevention is questionable. For more PHARMFAX in the drug bank, let me know what you want to learn about next on my poll, link in my bio.


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