Anesth Analg 2001;93:1534-1536

Timothy B. Gilbert, MD FACC

Divisions of Cardiothoracic Anesthesiology and Cardiology, University of Maryland School of Medicine, Baltimore, Maryland

 

	Abstract

 An overdose of the antiarrhythmic drug, lidocaine hydrochloride, was inadvertantly administered to a patient through an arterial pressure monitoring apparatus, resulting in cardiac asystole. This medication error demonstrates to all anesthesia care team members the importance of preventing similar occurrences.

 

	Introduction

 Errors in administration of IV drugs continue to plague medical care and in particular, anesthesiology. Even when the desired medication is properly chosen, errors may occur because many drugs are packaged in widely differing concentrations. This is particularly true for medications that can be given by both IV bolus and infusion (e.g., cardiovascular drugs). Further compounding such errors, technicians assisting health care personnel may contribute indirectly to the problem by inadvertent handling of these drugs, as this case highlights.

 

	Case Report

 An otherwise healthy elderly male patient with known coronary artery disease and moderate left ventricular dysfunction presented for routine elective coronary artery bypass grafting (CABG). His preoperative medications included a ß-blocker and aspirin. He had no known drug allergies and weighed approximately 70 kg. In addition to standard monitoring, systemic (right radial artery) and pulmonary arterial catheters were placed before anesthetic induction and attached to fluid transducers (Model #PX272; Baxter Healthcare Company, Irvine, CA). Additionally, transesophageal echocardiography (TEE) was used—per institution routine—for monitoring of cardiac performance throughout the intended procedure. After uneventful anesthetic induction, maintenance, and cardiopulmonary bypass (CPB) for CABG, the patient was quickly weaned from CPB before chest closure.

Per our routine perfusion protocol, lidocaine hydrochloride 100 mg (1.5 mg/kg) was administered into the CPB apparatus at the time of cross-clamp removal; an additional 100 mg was given near the separation from CPB for frequent ventricular ectopy. Shortly after CPB separation, prominent damping of the radial arterial pressure line was noted; the anesthesiology resident subsequently flushed the line repeatedly over approximately 5 min (including several 10-mL aliquots via syringe attached at the transducer) in an attempt to resolve the observed monitor malfunction. After this repetitive flushing of the line, the patient became asystolic. TEE examination revealed no apparent cardiac function with spontaneous contrast noted in all chambers. As the chest remained open, cardiopulmonary resuscitation (CPR) was begun by the surgical team, and the administration of atropine and epinephrine and epicardial pacing were quickly performed. Because the CPB cannulae had not yet been removed nor had protamine sulfate been administered for heparin reversal, CPB was reinitiated rapidly. After these brief maneuvers, the rhythm returned to sinus bradycardia with an adequate blood pressure and cardiac output. He required only a short period of epicardial pacing before his transfer to the intensive care unit and had an otherwise uncomplicated recovery. His hand distal to the arterial pressure catheter remained neurovascularly intact.

Because of the temporal relationship between the repetitive flushing of the arterial line and the occurrence of asystole, the anesthesia team carefully inspected the operating room (OR) environment, and, in particular, the pressure transducer set-up . Before the patient’s entry into the OR, an anesthesia technician had inadvertently spiked the flush system with a 500-mL intravenous bag containing 4 gm of lidocaine hydrochloride (8 mg/mL) intended for antiarrhythmic maintenance infusions, instead of the usual normal saline solution. As the medication bag was partially obscured within an outer cover semiopaque pressurized bag , the anesthesia team had been unaware of this potential complication before its bolus administration—via repetitive flushing of the arterial (and possibly other) catheters—and eventual asystolic arrest of the patient. Fortunately for this patient, his chest remained open and he was still connected to the CPB apparatus, affording a rapid return of circulation while the cause of the arrest was determined and effectively treated. No apparent sequelae were noted from this massive local anesthetic bolus. Although no drug level was available postarrest for this patient (as a sample drawn postarrest was not able to be processed), no other cause for the arrest was apparent from review of the case.
Assuming that three transducers (systemic and pulmonary arterial pressures and central venous pressure) continuously flush at approximately 3 mL/h each, the dose of lidocaine excluding boluses was at least 288 mg (i.e., 8 mg/mL · 3 mL/h · 3 transducers · 4 h). Each 10 mL manual flush through the arterial catheter supplied an additional 80-mg dose added to the intended 200 mg given through the CPB apparatus, and if at least three manual flushes were performed (i.e., 240 mg), the total dose of lidocaine administered to this patient was at least 728 mg (or 10.4 mg/kg).

 

	Discussion

 Large systemic concentrations of local anesthetics can cause refractory cardiac dysrhythmias by their adverse effects on cardiac sodium channels. Drug overdosing does not necessarily occur via the IV route but can arise from any delivery device attached to a given patient. Lidocaine toxicity via an indwelling arterial line has not been reported previously. Typical of many drug errors, a cascade of system mishaps occurred before the actual administration of the drug. A novice technician performing his routine duties was unaware of the existence of concentrated lidocaine in the area. The OR normally did not stock such lidocaine bags in the cardiac suites, but apparently one remained from a previous procedure. The use of a semiopaque pressure infusion bag, as well as its placement below and behind the pressure transducers, obscured the anesthesiologists’ view of the flush solution. The concurrent administration of additional lidocaine for therapy likely compounded the error. Toxicity can be further enhanced from decreased hepatic clearance, often seen in patients with reduced cardiac output, liver dysfunction, advanced age, and/or under general anesthesia (1). Fortunately for our patient, the overdose became manifest while he was still cannulated to the CPB apparatus, affording rapid resuscitation and support while the error was diagnosed and treated. The management of acute lidocaine toxicity is purely supportive care, including CPR, vasopressors, fluid infusions, and ventricular pacing, as needed (2).

Central nervous system effects of lidocaine (e.g., altered consciousness, seizures, dizziness, tinnitus) usually presage frank cardiovascular collapse; the so-called "CC/CNS ratio" for lidocaine is 7.1 ± 1.1,¹ with drug levels in excess of 12 and 24 µg/mL concentration required for significant central nervous system and cardiovascular collapse symptoms, respectively (3). These signs and symptoms of lidocaine toxicity may be difficult to ascertain under general anesthesia, particularly if neuromuscular blockade is used (2,4). Therefore, cardiovascular instability, arrhythmias, and frank asystole are commonly described manifestations in such patients (4,5). Lidocaine toxicity can also be responsible for delayed emergence in the absence of other more ominous signs (6).

Assuming a volume-of-distribution of 1.5 L/kg, a total lidocaine bolus of 540 mg (i.e., ignoring the basal transducer infusions) should result in an instantaneous blood concentration of approximately 4.2 µg/mL–a level unexpected to produce asystole. It is possible that in this patient the repetitive flushing of large boluses through the arterial transducer apparatus could result in drug traveling retrograde from the radial artery to the aortic arch rather than traversing the capillary beds (7). Furthermore, the threshold concentration at which toxicity occurs may be more related to the rate of increase of serum concentration than to the total amount of drug injected (8). If so, it is conceivable that transarterial passage of undiluted lidocaine reached the coronary arteries directly and rapidly, causing the events seen.

Errors in medication administration can easily occur when drugs are marketed in similar packaging (9). Lidocaine overdosing by syringe is one of the more common drug errors, owing to its packaging in both bolus and concentrated (e.g., for infusion preparation) forms (10). Some authors have actually advocated using premixed bags of lidocaine for infusion to prevent similar overdosing errors (11,12). Use of lidocaine diluted in glass bottles could potentially reduce the chance of a similar error as occurred in this patient (13). However, as this case readily demonstrates, such overdosing can and does occur despite changes in the stocking of medications.

Ultimately, this case report should reinforce to those supervising an anesthetic that every team member–including residents and technicians–can contribute to system errors and that heightened vigilance must be maintained to prevent similar errors in the future. We have since modified our training of technicians with respect to IV and other line set-ups in the OR.

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