C53-32 Severe Systemic Lidocaine Toxicity Following Tumescent Liposuction

Abstract With the growing popularity of cosmetic surgery, liposuction has become one of the most commonly performed outpatient procedures. The tumescent technique—the most widely used approach—involves infiltration of large volumes of a dilute local anesthetic solution, often referred to as Klein’s solution. This formulation typically contains 400-1000 mg of lidocaine, 0.5-1.0 mg of epinephrine, and 10 mEq of sodium bicarbonate per liter of normal saline. While this method allows liposuction under local anesthesia with reduced bleeding and postoperative discomfort, the large cumulative doses of lidocaine required can increase the risk of systemic toxicity, particularly in the setting of dosing errors, rapid absorption, or impaired hepatic metabolism. Despite its widespread use, many clinicians remain unfamiliar with the potentially life-threatening complications of lidocaine toxicity during tumescent liposuction. Here we report a 43-year-old woman with obesity who developed recurrent seizures during outpatient liposuction after receiving a tumescent solution of unknown lidocaine concentration. Shortly after the procedure, she developed seizure-like activity initially treated with temazepam. As the episodes recurred, she was transferred to the emergency department for further management. On arrival, she experienced recurrent one- to two-minute generalized seizures that transiently improved after intravenous midazolam. She was intubated after receiving a total of 10 mg of midazolam and was started on continuous midazolam and propofol infusions. A loading dose of levetiracetam (1.5 g) was administered, after which seizure activity resolved under sedation. Communication with the aesthetic surgical team revealed that approximately 2 liters of infiltrate solution had been administered. Given concern for local anesthetic systemic toxicity (LAST), intravenous lipid emulsion therapy was promptly initiated, resulting in sustained seizure resolution. Head CT was negative for acute intracranial pathology. The patient was successfully extubated the following day and discharged home neurologically intact two days later. LAST results from excessive plasma concentrations of local anesthetics, leading to neuronal hyperexcitability and, at higher levels, cardiovascular instability. Toxicity often presents with neurologic manifestations—such as perioral numbness, metallic taste, tinnitus, agitation, and seizures—followed by hypotension, arrhythmias, and cardiac arrest. Lipid emulsion therapy, the cornerstone of management, functions via a “lipid sink” mechanism that sequesters lipophilic anesthetic molecules from plasma and tissues, reducing their bioavailability and toxic effects. This case underscores the risk of systemic lidocaine toxicity associated with high-volume tumescent infiltration. Enhanced recognition of this rare but serious presentation among critical care clinicians is essential for timely diagnosis, resuscitation, and recovery. This abstract is funded by: none