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Departments of *Anesthesiology and Orthopedic Surgery, Hospital for Special Surgery, Weill Medical College of Cornell University, New York, New York
Address correspondence and reprint requests to Gregory A. Liguori, MD, Department of Anesthesia, Hospital for Special Surgery, 535 East 70th Street, New York, New York, 10021.
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Abstract |
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IMPLICATIONS: We report a case of possible bupivacaine toxicity after intraarticular injection during knee arthroscopy. The importance of the specific type of surgical procedure performed during arthroscopy and its relationship to potential local anesthetic toxicity are highlighted.
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Introduction |
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Case Report |
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waves. Upon arrival in the operating room, a noninvasive blood pressure cuff, three-lead ECG, and pulse oximeter were applied. Midazolam (Versed, Roche, Manati PR) 5 mg IV in divided doses was given over several minutes. An uneventful spinal anesthetic (3 mL of 1.5% mepivacaine (Polocaine, Astra, Westborough, MA)) was administered. During the course of the procedure, the patient received an additional 2 mg of midazolam and 60 mg of propofol (Diprivan, Zeneca, Wilmington, DE), and was awake and drowsy for most of the operation. Blood pressure and heart rate varied <10% from baseline, and SpO2 was 100% throughout the procedure.
The patient underwent a knee arthroscopy in the supine position. Neither a leg holder nor tourniquet was used. Arthroscopic irrigation consisted of normal saline with 0.33 µg/mL of epinephrine at variable flow rates. Superolateral, anteromedial, and anterolateral portals were used. After diagnostic arthroscopy, several small loose bodies were removed from the posteromedial aspect of the joint. Subsequent to this, a lateral retinacular release was performed using an arthroscopic electrocautery device. Attention was then turned to the femoral sulcus, where a 2 cm x 3 cm full-thickness cartilage defect was identified. A microfracture technique was used in an effort to treat this. Several (5–10) small holes were made into the subchondral plate in the area of the defect with awls designed for such a purpose. The entire arthroscopic time was less than 1 h.
On completion of the procedure, bupivacaine 0.25% (Sensorcaine, Astra, Westborough, MA) 20 mL with 40 mg of methylprednisolone (Depomedrol, Pharmacia Upjohn, Kalamazoo, MI) was injected percutaneously into the knee joint in a single bolus via a 20-gauge needle. Epinephrine was not included in the injectate. Within 1–2 min, the patient complained of chest heaviness, nausea, and lightheadedness. He was noted to be pale and diaphoretic. He did not exhibit seizure activity and did not lose consciousness. Simultaneously, his ECG revealed a junctional, wide complex tachycardia at 110 bpm. Blood pressure was 100/60 mm Hg and SpO2 was 99%. Metoprolol (Abbott Laboratories, North Chicago, IL) 5 mg IV was administered. The heart rate slowed and converted to normal sinus rhythm. The QRS complex remained prolonged and T-wave inversions were noted on the monitor.
At arrival in the postanesthesia care unit, the patient remained hemodynamically stable, with slow resolution of his symptoms. A 12-lead ECG revealed T-wave inversions in leads III and aVF with a normal QRS complex. The T- waves reverted to normal over the next several hours. The patient was discharged home later that day and had an uneventful postoperative course.
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Discussion |
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When noted, the arthroscopic procedures performed in the aforementioned investigations included medial and lateral meniscectomies, meniscal repairs, diagnostic arthroscopies, and removal of loose bodies. No complications of local anesthetic toxicity were described in any of these reports. However, it is important to consider the tissue upon which the arthroscopic procedure is being performed. The meniscus is a very avascular structure; hence its inability to heal when traumatized. Loose bodies are avascular. During operations on these tissues, there is little opportunity for entry of local anesthetics into vascular beds.
Sullivan and Abbott (16) published two cases of bupivacaine toxicity after intraarticular injection. The first case involved a preoperative injection of 60 mL 0.25% bupivacaine with epinephrine. The signs and symptoms experienced by that patient were similar to our case. In addition, the dysrhythmia reported, "a wide QRS with inverted T waves.... with tachycardia" was identical to the rhythm observed in our patient.
The second case also involved a preoperative injection of 30 mL 0.25% bupivacaine with epinephrine. Intraoperatively, a fracture of the lateral femoral condyle was noted. The authors speculate that this fracture provided access to the systemic circulation.
Several studies have evaluated blood levels of bupivacaine after intraarticular injection after knee arthroscopy (4,17). Meinig et al. (17) measured venous samples of plasma bupivacaine levels after intraarticular instillation of 30 mL of 0.5% bupivacaine and found mean plasma levels to be <650 ng/mL with a peak level occurring at 20 min after injection. Kaeding et al. (4) reported peak bupivacaine levels of 480 ng/mL occurring at 43 min after instillation. These levels are 8 to 10 times less than those reported to cause convulsions in humans (18). It is very unlikely that without a direct intravascular route, toxicity from intraarticular instillation of local anesthetic can occur. The arthroscopic procedures performed during these studies included meniscectomies, meniscal repairs, abrasion chondroplasty, plicectomy, and debridement. Again, these procedures involve surgical manipulation of relatively avascular structures within the knee joint.
The microfracture technique used for this patient has been previously described as a treatment for full-thickness cartilage injuries of the knee (19). Awls are used to create holes in the subchondral bone plate in the area of the cartilage defect. The overall integrity of the subchondral bone is maintained. The holes allow for the intraarticular release of marrow elements, which presumably enhance tissue regeneration. The holes, however, also allow intraarticular fluids to pass into the marrow cavity, and subsequently, into the systemic circulation. We postulate this to be the mechanism for the proposed intravascular uptake of local anesthetic. In addition, the performance of a lateral release traumatizes highly vascularized tissues and exposes the vasculature to intraarticular fluids. This mechanism is similar to that described by Sullivan and Abbott (16), except that the "chondral fracture" they reported was made intentionally in this case. We believe that a reaction such as this has never been reported despite the use of intraarticular local anesthetic in hundreds of patients in the previously referenced studies. As noted, these studies did not involve the microfracture technique or lateral release during arthroscopy.
The reaction experienced by our patient occurred one to two minutes after the local anesthetic injection. A toxic reaction caused by an increased blood level of local anesthetic taken up by a normal knee joint would not normally occur so quickly (4,17). Therefore, this episode may be similar to an intravascular injection of local anesthetic. Furthermore, the fact that the reaction occurred within 1 to 2 minutes of injection gives further support to the hypothesis that inadvertent intravascular uptake of the local anesthetic is the most likely etiology.
Other explanations for this reaction may include a coincidental wide complex tachycardia on the basis of preexistent cardiac pathology. Examples of underlying cardiac pathology that would present as a wide complex tachycardia include long QT syndrome and Wolff-Parkinson-White (WPW) syndrome (20). The long QT syndrome can either be acquired or congenital. Acquired forms are caused by several classes of antiarrhythmics, phenothiazines, tricyclic antidepressants, IV erythromycin, and organophosphate insecticides. In addition, altered nutritional states and electrolyte abnormalities may precipitate long QT syndrome-induced tachyarrhythmias.
Congenital forms are associated with enhanced adrenergic responsiveness. These patients often present with syncope during childhood in the setting of heightened sympathetic tone.
WPW syndrome is associated with young healthy patients experiencing episodes of tachycardia because of multiple atrioventricular (AV) connections. ECG characteristics include a short PR interval and a broad QRS complex with an abnormal initial deflection. The tachycardia is initiated by a properly timed atrial or ventricular premature beat that is blocked in one of the two AV connections.
Although these or other preexistent syndromes may be responsible for those experienced by our patient, there is no evidence to support this conclusion. The patient has previously been, and continues to be asymptomatic, and without invasive electrophysiologic testing these syndromes can neither be implicated nor eliminated.
Epinephrine was used in very dilute concentrations in the irrigating solution only; it was not used in the injectate. If this dysrhythmia was an exogenous catecholamine reaction from the epinephrine in the irrigating solution, one would expect the reaction to occur during the course of the arthroscopic procedure while the solution is pressurized in the knee joint. Therefore, an exogenous catecholamine reaction causing these symptoms could likely be excluded.
This event was not a prototypical local anesthetic reaction characterized by central nervous system toxicity and progressing to cardiovascular collapse. The patient did not have an overt seizure despite experiencing lightheadedness, pallor, and diaphoresis. The use of benzodiazepines as sedation may have altered the seizure threshold, thereby masking a clinically apparent seizure. The patient’s symptoms were more consistent with a vasovagal type reaction that has been reported after spinal (21) or epidural (22) anesthesia. The most common dysrhythmia associated with spinal anesthesia is bradycardia. Risk factors for the development of bradycardia during spinal anesthesia include a baseline heart rate <60 bpm, ASA physical status I, ß blocker usage, sensory level above T6, age <50 years, and prolonged PR interval (23). The mechanism is thought to be related in part to heightened vagal tone. However, the wide complex tachycardia is not consistent with increased vagal activity and therefore supports local anesthetic toxicity as the mechanism of this event.
Brown (24) describes three cardiovascular phases during a systemic toxic reaction to local anesthetics. First, an excitatory phase associated with sympathetic discharge and tachycardia occurs. This may be a response to central nervous system toxicity. The second phase is characterized by myocardial depression and decreased cardiac output. The final phase is associated with conduction abnormalities and cardiovascular collapse. The reaction experienced by our patient was most consistent with the sympathetic discharge phase (25) and responded to IV beta blockade. However, we believe that the widening of the QRS complex and T-wave inversions were reflective of bupivacaine’s effects on the conduction system.
The use of ß blockers is not the standard treatment for local anesthetic-induced conduction abnormalities. Although ß blockers may be useful in treating the excitatory cardiovascular phase, the potential to progress to the second and third phases with myocardial depression and collapse precludes their routine use. The treatment for local anesthetic-induced cardiac toxicity is generally supportive, and may include amrinone, closed chest cardiac massage, and cardiopulmonary bypass. In addition, effective ventilation with oxygen is essential (26). In this case, the relationship between the cardiovascular symptoms and the injection of bupivacaine was not immediately recognized. Therefore metoprolol was used to treat the tachycardia. In retrospect, metoprolol was effective in this case; however, the routine use of ß blockers as a treatment for local anesthetic toxicity is not advocated.
In conclusion, we have reported a case of presumed local anesthetic toxicity after intraarticular injection of 0.25% bupivacaine after arthroscopic knee surgery using a microfracture technique for repair of a cartilage defect, as well as an arthroscopic lateral release. Anesthesiologists and orthopedic surgeons should bear in mind the surgical procedure performed during knee arthroscopy and the potential for intravascular uptake of local anesthetic. When the meniscus, loose bodies, or other relatively avascular structures are being manipulated, there seems to be a body of evidence supporting the safe instillation of intraarticular bupivacaine. However, procedures such as the microfracture technique and lateral release involve invasion into more vascular structures within the knee joint. Intraarticular instillation of bupivacaine in these patients may carry an increased risk of intravascular injection of local anesthetic. Clinicians should carefully consider the risks and benefits of this practice in this surgical population.
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Acknowledgments |
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This article has been cited by other articles:
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  C. R. Chu, N. J. Izzo, C. H. Coyle, N. E. Papas, and A. Logar The in vitro effects of bupivacaine on articular chondrocytes J Bone Joint Surg Br, June 1, 2008; 90-B(6): 814 - 820. [Abstract] [Full Text] [PDF]
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