Lipid emulsion injection-induced reversal of cardiac toxicity and acceleration of emergence from general anesthesia after scalp infiltration of a local anesthetic: a case report

This report describes a case of delayed emergence from anesthesia in a patient who received a scalp infiltration of ropivacaine at the end of brain surgery. After infiltration, the frequency of ventricular arrhythmias increased and respiration was suppressed. The administration of a 20% lipid emulsion mitigated these symptoms. Owing to the timing, we thought that LAST had occurred because delayed emergence from general anesthesia and the symptoms described above were seen even though the estimated target concentrations of propofol and opioids were presumably below subanesthetic levels.

Distinguishing between symptoms of postoperative LAST and brain damage is difficult because both may induce disturbance of consciousness, and delayed emergence from general anesthesia after a craniotomy is not unusual. However, the American Society of Regional Anesthesia (ASRA) Practice Advisory on Local Anesthetic Systemic Toxicity has stated that “The practitioner’s vigilance is of critical importance in recognizing early signs of LAST (CNS depression [coma, respiratory arrest] and cardiac excitation [PVCs and tachyarrythmias]), appreciating their variable presentation, and having a low threshold for considering LAST in patients that have received potentially toxic doses of local anesthetics and manifest atypical or unexpected signs and symptoms” [13]. Delayed emergence from general anesthesia, which was one of the symptoms of LAST in a previous study [9], may have been the cause of LAST in our case because the PVC rate increased during the observation period. Administration of a lipid emulsion resulted in the disappearance of the PVCs and the return of spontaneous breathing and consciousness.

Lipid rescue was first described by Weinberg et al. [6] in 1998. They showed that an intravenously administered lipid emulsion prevented cardiac arrest and increased the likelihood of resuscitation after a cardiac arrest induced by LAST. The ASRA currently recommends lipid rescue as a first-line therapy for LAST [14]. There are several theories as to how lipid rescue reverses LAST. The well-documented, experimentally tested lipid sink theory [6, 15] suggests that the lipid emulsion absorbs the local anesthetic from several tissues (e.g., myocardium, brain, and vascular smooth muscle), which increases the metabolic capacity of the liver and, consequently, the catabolism of the local anesthetic [16].

In our case, the blood ropivacaine concentrations were higher 30 min after administration of the emulsion when compared with before. This phenomenon is strange because “free” local anesthetics are thought to have unfavorable effects including CNS and cardiac toxicity, and increases in their amounts after lipid rescue appear to worsen LAST. However, if the intravenously injected lipid emulsion absorbs the local anesthetics from the intoxicated tissue, their concentrations in the blood would transiently increase. Such an increase was observed in our study and is consistent with the lipid sink theory.

Other mechanisms may account for the lipid rescue phenomenon in patients with LAST. A recent study showed that infusion of a lipid emulsion reduced the peak concentrations of local anesthetics by 26 to 30%, presumably by expediting their clearance [17]. The lipids may also serve as an energy source for mitochondria, thereby facilitating the restoration of cellular function in intoxicated tissues [6, 18]. Alternatively, the lipids may directly promote the recovery of sodium channel function [19].

In our patient, the dose of ropivacaine was less than 3 mg/kg, and the plasma concentration of ropivacaine when LAST was suspected was less than that in a previous report [2]. In a previous study, the maximum tolerated plasma concentrations of ropivacaine in the arterial blood of healthy volunteers were shown to be in the microgram per milliliter range [20]. However, our patient had an adverse cardiac reaction that included an increase in PVC frequency even though the plasma concentration of ropivacaine was below the microgram per milliliter range. A previous study reported that intravenous administration of a small dose of ropivacaine (36.9 ± 8.6) caused cardiac conduction disturbance (elongation of the PR interval, QRS width, and QT length) and CNS symptoms in healthy male volunteers [21], and the dose of ropivacaine in that study was less than half of the maximal tolerated dose in the study by Knudsen et al. [20]. Taken together, even a small dose of local anesthetic, which has been thought not to cause adverse effects, could potentially lead to CNS and cardiovascular symptoms. In our case, the PVCs disappeared and hypotension was alleviated after infusion of the lipid emulsion. These findings suggest that the PVCs were due to LAST.

The delayed emergence from anesthesia and accompanying PVCs in our case were unexpected because we had not encountered these phenomena in previous craniotomies, even when the wound was infiltrated with 20 mL of 0.75% ropivacaine. However, previous studies on healthy volunteers suggest that relatively small doses of local anesthetics can potentially cause CNS dysfunction [20, 21]. Thereafter, we recommend that neurosurgeons use ropivacaine or levobupivacaine at concentrations less than 0.75% (e.g., 0.375 to 0.5%) for wound infiltration.

We strongly recommend that LAST be considered in cases in which emergence from general anesthesia is delayed after a scalp block because overlooking this condition can result in circulatory collapse. On the basis of our own experience and previous reports, we suggest that lipid rescue is an effective and safe treatment for LAST. Lipid emulsions should be readily available in the operating room for timely treatment of LAST.