Early-Onset Intraoperative Anaphylaxis Requiring VA-ECMO Volume 37 | Issue 1 | April 2026
Written by Katy Anderson   

Early-Onset Intraoperative Anaphylaxis Requiring VA-ECMO

by Adam Feigenbaum; Brooke Juszczak, MD; Steven McAfee, MD

Volume 37 | Issue 1 | April 2026

Abstract

Background: Perioperative anaphylaxis (POA) occurs in up to 1 in 6,531 anesthetics and carries a higher risk of cardiovascular collapse and mortality than anaphylaxis in nonoperative settings [1]. Diagnosis is challenging due to simultaneous administration of multiple agents and limited visibility of cutaneous signs. Early recognition and prompt initiation of epinephrine and advanced circulatory support, including veno-arterial extracorporeal membrane oxygenation (VA-ECMO), may be lifesaving [2]. 

Case Presentation: We report a case of severe intraoperative anaphylaxis in a 54-year-old woman undergoing elective microvascular decompression, resulting in refractory hypotension, cardiac arrest, and cardiogenic shock requiring VA-ECMO. Elevated serum tryptase confirmed anaphylaxis, and subsequent allergy testing identified chlorhexidine as the offending agent. 

Conclusion: This case underscores the atypical presentation of POA and highlights the importance of maintaining a high index of suspicion for anaphylaxis in rapidly deteriorating intraoperative patients. Early initiation of epinephrine and VA-ECMO may significantly improve outcomes in refractory cases.

Keywords: Perioperative anaphylaxis, chlorhexidine, cardiogenic shock, VA-ECMO

Introduction

Anaphylaxis is defined as an acute, potentially fatal systemic hypersensitivity reaction characterized by airway compromise, hypotension, or end-organ dysfunction. Anaphylaxis frequently presents atypically in the operating room and may rapidly progress to cardiovascular collapse. Perioperative anaphylaxis (POA) has a higher associated mortality rate than traditional anaphylaxis, emphasizing the need for early recognition and decisive management [3]. 

Approximately 95% of POA cases occur within 30 minutes of anesthetic induction, and neuromuscular blocking agents (NMBAs) are the most implicated agents in the United States [4,5]. Both IgE-mediated and non–IgE- mediated mechanisms contribute to POA, with the latter often occurring in patients without prior exposure or known risk factors [6]. Given these diagnostic challenges, anesthesiologists must rely on clinical suspicion and rapid physiologic deterioration rather than classic diagnostic criteria alone. 

Case Presentation

A 54-year-old woman (ASA II) with trigeminal neuralgia presented for elective microvascular decompression after failure of conservative therapy. Her medical history was notable only for vitamin D deficiency and a nonspecific aspirin allergy. She had previously tolerated general anesthesia without complication. Preoperative examination and laboratory studies were unremarkable. 

Following standard monitoring and intravenous access, anesthesia was induced with lidocaine (80mg), fentanyl (100mcg), propofol (160mg), and rocuronium (50mg), followed by uncomplicated endotracheal intubation. Anesthesia was maintained with sevoflurane, dexmedetomidine, and remifentanil infusions. Cefazolin (2 g) was administered for surgical prophylaxis. Approximately 10 minutes later, the patient was positioned laterally, and chlorhexidine was applied to the lumbar region in preparation for lumbar drain placement. 

Shortly thereafter, the patient developed abrupt hypotension and bradycardia refractory to fluid resuscitation, phenylephrine, glycopyrrolate, vasopressin, ephedrine, and escalating doses of epinephrine. Airway pressures were initially stable, though oxygen saturation and end-tidal CO2 subsequently declined. Electrocardiography demonstrated diffuse ST-segment elevation followed by ventricular tachycardia, ventricular fibrillation, and asystole. Cardiopulmonary resuscitation was initiated per ACLS guidelines. 

After 17 minutes of resuscitation, return of spontaneous circulation was achieved. Given persistent hemodynamic instability, VA-ECMO was initiated in the operating room, and the patient was transferred to the cardiac catheterization laboratory. Coronary angiography revealed no obstructive disease, and transesophageal echocardiography demonstrated global biventricular hypokinesis without focal structural abnormalities.

The patient was admitted to the cardiovascular intensive care unit with a diagnosis of cardiogenic shock secondary to suspected anaphylaxis. She was treated with an epinephrine infusion, corticosteroids, and antihistamines. Initial serum tryptase was markedly elevated at 104.0 ng/ mL, confirming severe anaphylaxis, with normalization on repeat testing. Ventricular function improved rapidly and she was successfully decannulated from ECMO on postoperative day (POD) 1. 

Her subsequent hospital course was notable for delayed extubation due to suspected angioedema which resolved with corticosteroid therapy. She was extubated on POD 4, transferred to the general cardiology service on POD 6, and discharged home on POD 8 with mild residual cognitive impairment but no focal neurologic deficits. Outpatient allergy evaluation revealed positive skin testing to chlorhexidine and negative testing to all other perioperative agents.

Discussion

POA may result from IgE-mediated hypersensitivity or non-IgE-mediated mast cell activation, frequently involving the Mas-related G protein–coupled receptor X2 (MRGPRX2) [7]. These mechanisms produce clinically indistinguishable syndromes, complicating diagnosis. Hypotension is the most common presenting sign of POA while bronchospasm and cutaneous findings may be absent or masked intraoperatively. In this case, profound vasoplegia and myocardial depression led to cardiac arrest, a rare but recognized manifestation of severe POA. The markedly elevated tryptase level supported the diagnosis, though normal tryptase values do not exclude anaphylaxis [8]. Early administration of epinephrine remains the cornerstone of treatment in conjunction with aggressive fluid resuscitation to counteract capillary leak and vasodilation. Adjunctive therapies, including corticosteroids and antihistamines, have limited evidence for acute benefit. VA-ECMO provided critical circulatory support during refractory shock and likely contributed to the patient’s favorable neurologic outcome. This case also highlights chlorhexidine as an underrecognized but clinically significant cause of POA, particularly given its widespread use and potential for repeated exposure during invasive procedures.

Conclusion 

Perioperative anaphylaxis may present abruptly with isolated hypotension and rapid cardiovascular collapse, often without classic mucocutaneous signs. Failure to respond to escalating vasopressors should prompt immediate consideration of anaphylaxis and early epinephrine administration. In cases of refractory cardiogenic shock or cardiac arrest, VA-ECMO can be lifesaving. This case emphasizes the need for heightened awareness of POA, including chlorhexidine hypersensitivity, and readiness to deploy advanced resuscitative strategies to reduce morbidity and mortality.

References

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