SCHNEIDER et al. 1initially described transient neurologic symptom (TNS) in 1993 after hyperbaric lidocaine spinal anesthesia. The reported incidence varies from 0–37% based on the drug used and surgical position, with hyperbaric 5% lidocaine resulting in the highest incidence of TNS and bupivacaine resulting in the lowest incidence. 2Lithotomy position and flexion of knee are associated with a higher incidence. 2Ropivacaine, an enantiomerically pure local anesthetic has been documented to produce less motor blockade than other local anesthetics. Van Kleef et al. 3documented the efficacy of ropivacaine as a spinal anesthetic. Gautier et al. 4used it for outpatient arthroscopy and report no TNS in 90 patients. We have used low-dose ropivacaine (10 mg) intrathecally for knee arthroscopy in a small number of patients. We report one patient who received 10 mg hyperbaric ropivacaine and in whom TNS developed, lasting 3 weeks.
A 38-yr-old woman scheduled to undergo elective knee arthroscopy underwent spinal anesthesia while in the right lateral decubitus position at L2–L3, with 10 mg ropivacaine, 1% (Naropin; AstraZeneca, Mississauga, Ontario, Canada), and was made hyperbaric with addition of 0.5 ml dextrose, 10%. Spinal puncture was accomplished during the second attempt using a 25-gauge Whitacre needle, and the cerebrospinal fluid (CSF) was clear. There was no paresthesia. The patient remained in a lateral position until the sensory block to pin prick reached the T12 level during testing 1 min after the drug delivery. Soon after turning supine the patient reported severe low backache in the sacral area even before surgery started, which she attributed to the position. She refused administration of sedation or other analgesics because she wanted to observe surgery. Discomfort was present throughout surgery. Vital signs remained stable throughout the procedure. The sensory block reached a level of T4 bilaterally. Surgical duration was 41 min and the patient reported no pain or nausea in the postanesthesia care unit. The backache resolved during assumption of the supine position. She had no motor block in both legs on arrival in the postanesthesia care unit and the sensory block receded more than 75 min completely. She could pass urine 25 min after complete recession of sensory block.
At follow-up the morning after surgery, she reported moderate to severe headache and nausea, which improved when lying down. She also had neck pain but no auditory symptoms. She had severe backache, which worsened during coughing but denied having “sciatica” pain. She experienced some disequilibrium when she stood up. She gave a verbal reporting score of 30–40 for wound pain (on a scale of 0–100, 100 being the worst pain). She was afebrile and denied having any sensory motor disturbances in her lower limbs, blurring of vision, or photophobia. A provisional diagnosis of postdural puncture headache was made and she was advised to take regular doses of acetaminophen with codeine and Keterolac and drink lots of coffee. The follow-up on the second postoperative day revealed that her wound pain was 50–60 out of 100. The headache was moderate. She continued to have backache that worsened during coughing. On the third postoperative day, headache and surgical pain improved but she reported continuing backache that radiated to her buttocks, the back of both thighs, and her calves with no fever. On the fifth postoperative day she had significant pain radiating to her thighs and a severe ache in her calves and noted some numbness on the inner aspect of her soles. She was still afebrile. She had no bladder or bowel disturbance. A detailed examination was performed the following day and a neurosurgical consult was obtained to rule out disk herniation, epidural abscess, or epidural hematoma.
At examination she had no fever or photophobia and did not look ill. She had driven to the hospital herself. The straight leg-raising test was restricted to 45° because of pain in the back, thighs, and legs. Her neck was supple and cranial nerves were intact. Sensory examination showed normal sensation, except for the inner aspect of soles for which it was slightly reduced. Tendon reflexes were preserved; however, the left ankle was sluggish. Motor power was normal. A rectal examination was not performed. Magnetic resonance imaging of the spine showed mild bulging of the T10–T11 and L4–L5 disks, but protrusion or encroachment of neural structures was not obvious. There was no entrapment or abnormality noted in the L5 root. Therewas no evidence of epidural or spinal hematoma or abscess. A provisional diagnosis of TNS was determined. No therapeutic interventions were performed. The patient gradually recovered, and at 20 days after spinal anesthesia, she had only a mild ache in the sacrum with no radicular pain. This ache improved over a period of 6 weeks. The sensation in her foot returned to normal.
Schneider et al. 1initially brought TNS to the attention of the anesthesia community in 1993. Although the highest incidence was reported in patients who received spinal anesthesia with lidocaine (4–33%), it has been documented to occur after spinal anesthesia using bupivacaine (1.3%), mepivacaine, and tetracaine (1.6%). This incidence varies with the type of surgical procedure but is unaffected by baricity and concentration. 5TNS is considered to be a manifestation of neurotoxicity of some local anesthetics. Therefore, many anesthesiologists use procaine for ambulatory anesthesia, the duration of which can sometimes be inadequate if the surgery proceeds more than 1 h. Ropivacaine is less potent than bupivacaine, resulting in a lower incidence of motor blockade 6and thus may be an optimal anesthetic for ambulatory surgery. TNS has not been described after ropivacaine administration; however, McDonald et al. 6reported a higher incidence of backache in volunteers after administration of intrathecal ropivacaine. Unfortunately, this subset of volunteers were administered two spinal anesthetics 1 week apart, which could have contributed to backache. Gautier et al. 4used 0.2–0.35% ropivacaine for intrathecal administration, with no report of TNS, and we used a 1% solution diluted with dextrose to yield a final concentration of 0.66%. Whether this higher concentration is neurotoxic is not established.
The TNS symptoms in our patient were bilateral and of the same severity on both sides. Development of backache as soon as the drug was delivered intrathecally has not been reported in association with TNS. Larger studies are needed to determine the incidence of TNS after administration of intrathecal ropivacaine.
A number of clinical conditions can mimic TNS. Paraspinal muscle spasm caused by trauma potentially could mimic TNS but usually occurs early in the recovery period. Degenerative disk disease and postdural puncture headache can confound the clinical course, and the diagnosis of TNS seems to be one of exclusion. Although a majority of patients improve spontaneously, the symptoms can be significant enough to delay recovery from minor surgical procedures. In conclusion, we report the first case of TNS after administration of intrathecal ropivacaine, and only ongoing use of this drug will provide the true incidence of this complication after intrathecal ropivacaine administration.