IV lipid emulsion increases the lethal threshold and decreases mortality after systemic overdose of local anesthetics in animals.1,2 Recent reports in humans suggest that Intralipid® may be an effective therapy for cardiac toxicity from high systemic concentrations of ropivacaine and bupivacaine, even in patients for whom conventional resuscitation is ineffective.3,4 We report the successful use of 20% lipid infusion to treat a ventricular arrhythmia after ropivacaine and lidocaine injection in a psoas compartment block in a child.
A 13-yr-old girl, weighing 55 kg, 162 cm tall, and ASA I physical status was scheduled for meniscectomy of her left knee. Her medical history was unremarkable. She was receiving no medication. The parents consented, and the child assented, to placement of a posterior lumbar plexus block under general anesthesia.
The patient was premedicated with oral hydroxysine 50 mg. General anesthesia was induced and maintained with sevoflurane (up to 3%) in oxygen and nitrous oxide (50/50) via a facemask. An IV catheter was placed and 0.9% saline was administered at 10 mL · kg−1 · h−1. Her heart rate, arterial blood pressure, oxygen saturation, and end-tidal carbon dioxide were continuously monitored and recorded. Her baseline heart rate was 84 bpm, arterial blood pressure was 88/45 mm Hg, pulse oximetry showed 99% saturation, and end-tidal carbon dioxide was 41 mm Hg. After anesthetic induction the child was placed in the right lateral decubitus position and a lumbar plexus block was performed as described by Dadure et al.5 The posterior lumbar plexus block was achieved with an 18-gauge insulated needle (Plexuolong®, Pajunk, Melsungen, Germany) using a neurostimulator (HNS 11®, Braun, Germany), with a starting output of 2 mA, 1 ms, and 1 Hz. We observed patellar movements elicited by impulses of 0.50 mA. After a negative aspiration test, a 2 mL mixture containing equal volumes of 1% lidocaine with added epinephrine 1/200,000 and 0.75% ropivacaine was injected through the needle. Although using the same intensity of impulse, muscular contractions disappeared, and reappeared by using 2 mA impulses. Vital signs remained unchanged throughout administration. A total volume of 20 mL of the same lidocaine/ropivacaine solution was administered in divided doses of 3 mL over a 2-min period. After administration a 20-gauge catheter was introduced through the needle, and positioned 3 cm distal to the needle tip. The needle was removed and the catheter fixed to the skin with a “U” stitch and covered by a transparent dressing. The patient was placed supine for the operation.
A ventricular tachycardia at 150 bpm wide with QRS complexes (Fig. 1A) spontaneously developed 15 min after the end of local anesthetic administration. Her arterial blood pressure was 120/92 mm Hg, and her arterial oxygen saturation decreased to 92%. There was no change in end-tidal carbon dioxide. The concentration of sevoflurane was decreased to 1%, nitrous oxide administration was discontinued, and the lungs were manually ventilated. Suspecting local anesthetic toxicity, 150 mL (3 mL/kg) of a 20% lipid emulsion (Medialipid 20%®, Braun, Germany) was rapidly injected over 3 min. During this infusion, we drew peripheral venous blood from the contralateral arm to measure plasma concentrations of local anesthetics and obtain blood chemistries.
Within 2 min after the lipid emulsion injection, her heart rate decreased to100 bpm, arterial blood pressure decreased to 100/48, arterial oxygen saturation increased to 97%, and the electrocardiogram (ECG) reverted to normal complex QRS with persistent ST depression (Fig. 1B). After 30 min the ST segment abnormalities disappeared and the decision was made to commence surgery. During surgery, no other analgesics were required because the lumbar plexus block was totally effective. After completion of surgery, and 2 h after lumbar injection, a second venous sample was obtained to measure local anesthetic concentrations. The plasma concentrations of ropivacaine and lidocaine were 872 and 648 ng/mL, respectively, at the time of the cardiac arrhythmia, and 494 and 360 ng/mL 2 h later.
After surgery, the perineural catheter was removed and systemic analgesics were administered. Her ECG and echocardiography on postoperative Day 1 were normal. The patient had no further arrhythmia and was discharged home on the second postoperative day without sequelae.
We report a case of ventricular dysrhythmia occurring a few minutes after injection of ropivacaine and lidocaine in a healthy child. The arrhythmia occurred despite a negative aspiration test and the use of divided doses. The first measured plasma local anesthetic concentrations are compatible with partial absorption. The 15 min delay between injection and arrhythmia is also more consistent with rapid absorption than direct IV injection.
Lumbar plexus block has been associated with a higher risk of systemic toxicity than other regional anesthetic techniques.6–8 Incomplete systemic absorption likely explains the relatively moderate cardiac toxicity, as the patient maintained arterial blood pressure despite a ventricular rhythm. We did not observe a seizure, but the patient was anesthetized with sevoflurane, which likely prevented any signs of central nervous system toxicity. Unremarkable oxygen saturation and end-tidal carbon dioxide suggest that hypoxemia and hypercapnia did not contribute to development of the cardiac arrhythmia.9 The drug concentrations are compatible with the development of systemic toxicity, similar to Knudsen et al.10 who documented wide interindividual variation in maximal tolerated plasma concentrations after IV ropivacaine administered alone in adult volunteers, with a threshold for minor neurological signs ranging from 0.5 to 3.2 μg/mL.
It is not clear how to interpret plasma concentrations after lipid administration, as the total plasma concentration might increase even as the lipid emulsion substantially reduces the unbound concentration of local anesthetic.
We decided to keep an emergency supply of lipid emulsion in the operating rooms after publication of two case reports describing its use in resuscitation from cardiac arrhythmias attributed to local anesthetic toxicity.3–4 In the previously published cases lipid emulsion was used after unsuccessful conventional resuscitation. In these articles, the authors recommended an initial bolus dose of 1–3 mL/kg of 20% lipid emulsion.3–4 We chose to start with the highest recommended dose. Within 2 min the heart rate and QRS on ECG tracing returned to nearly normal, except for ST depression, which persisted for approximately 30 min. In two previously reported cases, the authors suggested that the initial bolus be followed by a continuous infusion at 0.25–0.5 mL · kg−1 · h−1. We elected to not start an infusion because hemodynamic stability rapidly returned.
We administered Medialipid 20% (B Braun lab., Germany), a lipid emulsion used for IV nutrition of pediatric patients. This solution contains soya 10 g and medium chain fatty acids 10 g/100 mL. This solution differs from Intralipid (B Braun lab), which was used in the previous reports.1,3,4,11,12 Our experience suggests that the exact formulation of the 20% lipid emulsion may not matter.
In conclusion, we report a case of apparently effective lipid treatment of ventricular arrhythmia in a child after administration of a mixture of ropivacaine and lidocaine. We recommend that 20% lipid emulsion be stored with the other emergency drugs in operating rooms where local anesthetics are used.
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