P068: ANAPHYLAXIS FOLLOWING INDUCTION OF GENERAL ANESTHESIA
Matthew D Witkin, MD; Arnaldo Rafael Jose Vera-Arroyo, MD
University of Miami/Jackson Health System/Bruce W Carter Department of VAMC
Introduction/Background: Recognition of anaphylaxis in a patient under GA is critical to optimize patient safety but can be clouded by the masking effects of anesthetics and patient comorbidities. The incidence of periprocedural anaphylaxis in the US is 1 in 6531 procedures of which 7% are fatal/near-fatal (1). Anaphylactic reactions can occur via IgE-receptor cross-linking by an allergen or by IgE-independent processes with direct mast cell activation via MRGPRX2 receptor stimulation and degranulation of pro-inflammatory mediators/cytokines (2). Tryptase levels appear to be the most specific and reliable biomarker for anaphylaxis. Because tryptase levels can be elevated at baseline, the 20% + 2 formula (1.2 x baseline + 2ng/mL) is the gold standard for mast cell activation confirmation (3). Common culprits of perioperative anaphylaxis are antibiotics, NMBAs, dyes, and chlorhexidine. When anaphylaxis is suspected, initial management consists of discontinuation of the suspected allergen, calling for help, maintaining the airway with FiO2 100%, administration of epinephrine, and intravascular volume expansion (4).
Methods: A 76-year-old male with a PMH significant for ESRD, CAD s/p multiple PCI’s, HFpEF, pAFib, MAT, HTN, HLD, T2DM, COPD, OSA, RUL adenocarcinoma, TIA’s/CVA, achalasia, NAFLD, Crohn’s disease, PTSD, chronic IDA, obesity, and cervical stenosis/myelopathy s/p C4-C7 ACDF was scheduled to undergo a second stage AV fistula creation. His documented allergies were aspirin, iodine, mercaptopurine, and nifedipine. His course was complicated by hemodynamic collapse shortly following induction of GA with fentanyl, lidocaine, propofol, and cisatracurium. After an uncomplicated intubation, cefazolin was administered. Preoperatively, his vitals were unremarkable. Within 5 minutes following induction, he became severely hypotensive with SBP’s in the 60s and tachycardic with HR 97-112 (AFib). Initially, he was easy to ventilate but began showing evidence of obstruction with an upsloping capnograph and increased PIP from 28 cmH2O to 38 cmH20. Wheezing was also appreciated bilaterally on auscultation. Our initial differential diagnoses included a thromboembolic event, AECOPD, and anaphylactic reaction.
Initial attempts to treat his hypotension with boluses of calcium chloride, ephedrine, phenylephrine, and vasopressin were ineffective. Treatment for anaphylaxis ensued with administration of diphenhydramine, hydrocortisone, famotidine, albuterol, and epinephrine boluses (20-30mcg). A TEE was also performed which demonstrated hyperdynamic biventricular systolic function with mildly underfilled LV and no evidence of thrombi. He responded to epinephrine boluses and required volume resuscitation with crystalloids and colloids as well as pressor support with norepinephrine 12mcg/min and epinephrine 3mcgm/min. A serum tryptase level was collected during this acute event.
Results: His serum tryptase level was elevated at 35.9ng/mL during the acute event compared to a baseline level at 9.3ng/mL which is consistent for anaphylaxis with the most likely causative agent being cisatracurium or possibly cefazolin. The surgical procedure was aborted, and he remained intubated with a left IJ CVC and right radial arterial line placed prior to transport to the SICU.
Discussion/Conclusion: Our patient clinically demonstrated signs of anaphylaxis with severe hypotension, tachycardia, dysrhythmia (AFib), bronchospasm, increased inspiratory pressure, and erythema. The most important aspects of management are to cease the suspected offending agent, administer FiO2 100%, and provide early administration of epinephrine.