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REGIONAL ANESTHESIA

Transient Neurological Symptoms After Subarachnoid Meperidine

Department of Anesthesiology, VA Connecticut Healthcare System, West Haven, Connecticut, Yale University School of Medicine, New Haven, Connecticut

Address correspondence to Wilfred R. Lewis, MD, Anesthesia Service (186), VA Connecticut Health Care System, 950 Camp- bell Avenue, West Haven, CT 06516. Address e-mail to Wilfred.Lewis{at}med.va.gov

	Abstract

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Subarachnoid injection of lidocaine and other local anesthetics has been implicated in the syndrome of transient neurological symptoms (TNS). This syndrome has been well documented in a number of case reports and prospective, randomized controlled trials (1–8). The relatively frequent incidence of this complication with subarachnoid lidocaine has led to the search for alternative local anesthetics, including meperidine.

Although meperidine, an opioid with local anesthetic properties, has not been approved for subarachnoid administration, it has been used in varying degrees for clinical anesthesia over the last 50 yr (9,10). Reported side effects from subarachnoid meperidine have included nausea and vomiting, itching, urinary retention, respiratory depression, and hypotension (11,12). TNS after subarachnoid meperidine has not been reported. We describe a case of TNS after spinal anesthesia with meperidine for a urological procedure.

IMPLICATIONS: The syndrome of transient neurological symptoms (TNS) after subarachnoid use of local anesthetics, particularly lidocaine, has been well described. This syndrome has not been reported with the subarachnoid use of opioids. This case report describes TNS that occurred after administration of subarachnoid meperidine, an opioid with local anesthetic properties.

	Case Report

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A 70-yr-old male patient scheduled for transurethral resection of a bladder tumor underwent spinal anesthesia in the sitting position at the L3-4 interspace. A 22-gauge Quincke needle was used for dural puncture and clear cerebrospinal fluid was obtained on the first attempt. Meperidine 50 mg (Demerol, preservative free, 50 mg/mL, Abbott Laboratories, North Chicago, IL) mixed with 0.5 mL of 10% dextrose (final concentration of dextrose, 3.3%) was injected into the subarachnoid space. No paresthesia was elicited and the patient was placed in the lithotomy position for the procedure. A peak sensory level of T7 by pinprick was obtained. Intraoperatively, a total of 20 mg of ephedrine was required to treat mild hypotension and nausea. The surgical procedure was completed in 45 min. Complete resolution of the sensory and motor block occurred in 150 min after subarachnoid injection. The patient was discharged home after he was able to ambulate.

Ten hours after subarachnoid injection, the patient developed severe sharp back pain radiating to the posterior aspects of both buttocks and thighs, severe in intensity (Verbal Numeric Scale [VNS] of 8/10; 0 = no pain; 10 = worst pain imaginable) with no other associated sensory, motor or autonomic symptoms. The patient was unable to sleep the night after surgery and returned to the emergency room (ER) in the morning. Evaluation by the ER physician and an anesthesiologist revealed no sensory or motor deficits, normal deep tendon reflexes, and no paraspinal muscle spasm. There was no erythema or discharge at the site of the spinal puncture. He was treated with IV ketorolac 30 mg and IM meperidine 50 mg with marked improvement in his symptoms (VNS of 1–2). He had no difficulty in micturition. His back pain required oral ibuprofen 600 mg every 6 h. Complete resolution of back pain did not occur until the fourth postoperative day. The patient, who did not have any prior history of back pain, remains pain free 6 mo after the episode.

	Discussion

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TNS, previously referred to as transient radicular irritation, was first reported in 1993 after spinal anesthesia with lidocaine (13). The syndrome is characterized by pain or dysesthesias in the buttocks or lower extremities after otherwise full recovery from single-shot spinal anesthesia. The pain typically resolves within 1 week without lasting sequelae (14). The postoperative course in this report is consistent with TNS. We were unable to account for our patient’s symptoms by other conditions that mimic TNS, such as paraspinal muscle spasm and degenerative disk disease. After over 50 years of clinical use, this is the first report of TNS in a patient after spinal meperidine.

Although the most frequent incidence of TNS has been associated with spinal lidocaine at various concentrations, it has also been documented to occur after spinal anesthesia with several local anesthetics, including mepivacaine (15,16), procaine (17), bupivacaine (18), and ropivacaine (19). Meperidine, like fentanyl, is a phenylpiperidine derivative with strong opioid agonist effects. In contrast to other opioids, subarachnoid meperidine has been used for many years as the sole drug for spinal anesthesia, providing segmental sensory and motor blockade (10,20–22). Meperidine blocks conduction in myelinated and unmyelinated dorsal root axons, whereas fentanyl and sufentanil do not (9). The hypothesis that meperidine has local anesthetic properties is supported by Wagner et al. (23), who demonstrated that at concentrations achieved during typical clinical dosing for subarachnoid administration, meperidine blocks sodium channels to a degree comparable with lidocaine. Interestingly, meperidine shares several structural features that are the hallmark of local anesthetics, including a protonated tertiary amine (pKA 8.5), an ester group and a phenyl group, which serves as a lipophilic tail (23,24). This report alerts anesthesiologists that TNS can follow spinal anesthesia with meperidine, a complication meperidine shares with other local anesthetics.

The etiology of TNS remains elusive. Transient neural toxicity has been proposed as a causative factor. Stretching of nerve roots has been suggested as a contributing factor. A recent editorial has suggested that TNS may represent myofascial pain resulting from musculoskeletal strain (25). Regardless of the etiology, the symptoms of TNS are often severe and disabling. Our patient responded well to empiric treatment with a nonsteroidal antiinflammatory drug. Until etiology or preventative measures for TNS are identified and characterized, development of effective treatment protocols remains a priority.

	References

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