To the Editor:—

Arndt and Downey 1vividly convey a physician's dismay when motor, sensory, and bladder function are agonizingly slow to return after uneventful spinal block. The delayed recovery pattern described here is not unlike that seen when a potent vasoconstrictor such as neosynephrine is added to the local anesthetic solution to prolong deliberately the duration of sensory blockade. Because the patient remained painfree, pharmacologic or mechanical cauda equinopathy, 2fortunately, could be ruled out decisively in the differential diagnosis.

Although the authors postulate low spinal fluid volume as a contributing factor, that might be a rather slender straw to cling to in a healthy 20-yr-old young woman with freely aspirable spinal fluid. 3Instead (because a vasoconstrictor wasn't used), the addition of fentanyl to intensify and prolong bupivacaine block did achieve its intended purpose—albeit as a statistical outlier well beyond the expected norm of 4 ± 2 h. 1All told, this correspondent finds no compelling evidence to single out bupivacaine as the sole culprit for the protracted spinal analgesia. 4That is to say, the letter's title “Exceptionally Prolonged Anesthesia after a Small Dose of Intrathecal Bupivacaine” falls short. Rather, the title should have read “Prolonged Analgesia after Intrathecal Bupivacaine plus  Fentanyl.”


Arndt JA, Downey T: Exceptionally prolonged anesthesia after a small dose of intrathecal bupivacaine (letter). A nesthesiology 2002; 97: 1042
de Jong RH: The intrathecal lidocaine enigma: on the brink of cauda equinopathy, Annual of Anesthetic Pharmacology. Edited by Hines R, Bowdle TA. Philadelphia, Saunders, 1999, pp 287–98
Carpenter RL, Hogan QH, Liu SS, Crane B, Moore J: Lumbosacral cerebrospinal fluid volume is the primary determinant of sensory block extent and duration during spinal anesthesia. A nesthesiology 1998; 89: 24–29
Horlocker TT, Wedel D: Neurologic complications of spinal and epidural anesthesia (review). Reg Anesth Pain Med 2000; 25: 83–98