To the Editor:—
We would like to report an unusually long-lasting anesthetic after the administration of 7.5 mg of hyperbaric bupivacaine (Astra, Westborough, MA) and 25 μg of fentanyl (Abbott Laboratories, North Chicago, IL). The patient was a 20-yr-old female of average height and weight who was scheduled to have orthopedic hardware removed from her ankle. With the exception of a mild upper respiratory tract infection, she was otherwise healthy and had no significant past medical history. After all anesthetic options were discussed, the patient decided to be anesthetized with a spinal anesthetic. With the patient in the right lateral decubitus position, the spinal needle placement was performed with a 25-gauge pencil point needle (B. Braun Medical, Bethlehem, PA) via a midline approach. The L3–L4 interspace was used. The spinal agent consisted of 7.5 mg of hyperbaric bupivicaine (Astra, Westborough, MA) with 25 μg of fentanyl (Abbott Laboratories, North Chicago, IL). The injection of the spinal agent was uneventful and cerebrospinal fluid was aspirated before and after the injection. The direction and speed of the injection were not noted. The spinal needle and bupivacaine were obtained from an unexpired custom supplied spinal tray (B. Braun Medical, Bethlehem, PA). The fentanyl (Abbott Laboratories, North Chicago, IL) was preservative free and sterilely drawn up immediately before placing the block. The patient was positioned supine and the surgery proceeded as anticipated. The final cephalad level was T11 bilaterally. She remained hemodynamically stable throughout the procedure. At 8 h post-placement, the sensory level (to temperature) of the spinal had regressed approximately 3 dermatomal levels. The patient's condition was otherwise unremarkable; she had no back or lower extremity pain. The decision was made to observe her overnight. The next morning she began to experience pain at her operative site but still remained unable to void (requiring urinary catheterization). At this time (approximately 15 h post-placement) her dermatomal sensory level (to temperature) had only regressed a total of 5 levels. This, coupled with inability to void, made us concerned about the evolution of a serious neuraxial process. We obtained an emergent neurology consultation as well as a gadolinium enhanced MRI of the lumbar–sacral spine. The MRI ruled out an inflammatory process or compression of the spinal cord. During this evaluation, the patient's dermatomal level regressed another level. In light of these findings and evidence of a progressively resolving spinal, it was decided to continue observation and provide supportive care as needed (i.e., pain medication or catheterization). By approximately 36 h post-placement, the patient was able to void on her own and had resolution of her motor and sensory blockade. She was discharged later that day. No incontinence of stool was noted during this whole event.
It is tempting to classify this case as a presentation of cauda equina syndrome, transient radicular irritation, or anterior artery spinal syndrome. 1–4
Although these events are possible with hyperbaric bupivacaine, they are rare. 5–6
They also involve higher doses of bupivacaine than the one used in this case. 1–6
In addition, no other confounding variable that make cauda equina or transient radicular irritation more likely (such as advanced age, presence of vascular disease, use of epinephrine, use of hyperbaric lidocaine, lithotomy position, or performance of a knee arthroscopy) were present. 1–6
Our findings are interesting for at least two reasons. First, the time it took for the spinal to resolve was exceptionally prolonged. We expected the duration of the anesthetic to be 4 ± 2 h. 7
The duration of the spinal anesthetic presented in this case was approximately 36 h. Second, although the spinal lasted an unusual amount of time, there was no convincing evidence indicating a significant neurologic event such as cauda equina syndrome, transient radicular irritation, epidural hematoma or abscess, or anterior spinal artery syndrome.
We speculate that this presentation could have been the result of low cerebrospinal fluid volume. In a small study by Carpenter et al.
they demonstrated that low cerebrospinal fluid volume will cause increased sensory blockade. Unfortunately, this correlation was not true for motor blockade. The resolution of our patient's motor and sensory blockade were parallel throughout her presentation.
In conclusion, this case demonstrates that spinal bupivacaine can have an exceptionally prolonged effect in the absence of other confounding factors.
Joseph A. Arndt, M.D.
Tim Downey, C.R.N.A.
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6. Pleym H, Spigset O: Peripheral neurologic deficits in relation to subarachnoid or epidural administration of local anesthetic for surgery: A survey of 21 cases. Acta Anaesthesiol Scand 1997; 41: 453–60
7. Liu SS, Mc Donald SB: Current issues in spinal anesthesia. A nesthesiology 2001; 94 (5): 888–906
8. Carpenter RL, Hogan QH, Liu SS, Crane B, Moore J: Lumbrosacral cerebrospinal fluid volume is the primary determinant of sensory block extent and duration during spinal anesthesia. A nesthesiology 1998; 89 (1): 24–9
© 2002 American Society of Anesthesiologists, Inc.