C53-34 Local Anesthetic Systemic Toxicity Identified and Treated in the ICU: A Confluence of Risk Factors

Abstract Introduction Local anesthetic systemic toxicity (LAST) is a rare but serious adverse event possible with injected or topical lidocaine. While most common intraoperatively, we present a case of LAST treated in the ICU underscoring how multiple factors collectively lower the threshold for toxicity. Case Patient is a 57 y.o. female, past medical history of cT4bN3bMx Squamous cell carcinoma of the right hypopharynx, HFrEF (20-25%), and alcohol use presented with worsening dyspnea after radiation therapy. Recent CT neck showed a large invasive centrally necrotic mass within the right posterior neck, right carotid, parapharyngeal space, and mass effect upon the trachea. Labs on admission notable for AKI (BUN/Cr 33/0.92; 0.48/32 6 weeks prior), elevated transaminases (AST/ALT 33/27; 21/11 6 weeks prior), albumin 3.1, INR 1.2, bilirubin 1.1. Laryngoscopy revealed acute airway concerns leading to urgent tracheostomy in the OR. 4mL of 1% lidocaine was injected, and 3mL of 4% lidocaine was used topically. No immediate complications, but during transport back to ICU they developed bradycardia and hypotension. Arterial lines placed confirmed highly erratic blood pressures. Patient did not respond to phenylephrine, but a 10mcg push of epinephrine caused prompt increases in heart rate to 80s-90s and blood pressure to SBPs 220s. Shortly after, patient BPs and HR decreased again before an epinephrine drip yielded improvement. Meanwhile, the patient had rapidly fluctuating levels of consciousness between alertness and stupor. EKG showed 1st degree AV block, new ST depressions and T-wave inversions. POCUS showed globally reduced LV function. The patient remained on epinephrine until a lipid emulsion with a 1.5mL/kg IV bolus followed by a 0.25mL/kg/min infusion. Shortly afterwards BP, HR, and mental status stabilized, and epinephrine was weaned. She returned to baseline and discharged days later. Discussion This case highlights features of LAST, including CNS inhibition, cardiotoxicity, and prompt resolution following lipid infusion. Multiple risk factors contributed, one being the adjacency of lidocaine application to a vascular tumor, significantly increasing entry of lidocaine into circulation.Lidocaine undergoes hepatic metabolism into active metabolites MEGX (mono-ethyl-glycine-xylidide) then GX (glycine xylidine), both renally excreted. Our patient’s history of heavy alcohol consumption upregulated CYPs and accelerated hepatic metabolism. Increased production of active metabolites coupled with decreased renal clearance likely caused this toxicity. Moreover, CHF leads to decreased lidocaine clearance via decreased hepatic perfusion. Whereas most cases occur soon after injection, the dependence of this toxicity on metabolism explains latent onset of LAST in our patient. This abstract is funded by: None