Volume 76, No. 5 THE JOURNAL May 1992 - Anesthesiology THE AMERICAN SOCIETY OF ANESTHESIOLOGISTS, INC. Anesthesiology "76:667-669, 1902 Spinal Anesthesia in Anesthesiologists have long considered sepsis to be a rel- ative contraindication to the administration of spinal anesthesia. The needle might introduce infected blood into the subarachnoid or epidural space and cause men- ingitis or epidural abscess, Some have speculated that performance of dural puncture alters the protection forded by the blood-brain barrier and allows infection by an unknown mechanism, In support of these concerns, several authors have ob- served the development of meningitis after performance of dural puncture in bacteremic laboratory animals.?* Furthermore, there are several published cases of patients who underwent either diagnostic dural puncture or spinal anesthesia during confirmed or presumed bacteremia and who subsequently developed meningitis. However, physicians often perform diagnostic lumbar puncture in patients with fever and/or bacteremia of unknown origin. If dural puncture during bacteremia results in meningitis, fone would expect that uneq . However, clinical stu and are limited primarily to pediatric patients at high risk for meningitis.!!°!® Wegeforth and Latham'® performed diagnostic lumbar puncture in 98 patients who were suspected of having meningitis. The diagnosis was confirmed in 38 patients. Of the remaining 55 patients with normal cerebrospinal Aluid, 6 were bacteremic at the time of lumbar puncture. ‘Of those 6 patients, 5 subsequently developed meningitis. It was implied, but not stated, that meningitis did not ‘occur in the remaining patients who had bothsterile blood cultures and normal cerebrospinal fluid. These lumbar ‘Accepted for publication January $1, 1992. Reprints will not be available. ‘Address correspondence to Dr. Chestnut: Department of Anesthesia, ‘The University of lowia Hospitals and Clinics, lowa City, Iowa 82242, Key words: Anesthesia techniques: spinal. Complications. 667 EDITORIAL VIEWS. the Febrile Patient punctures were performed during an epidemic of men- ingitis, and one wonders whether some or all of these patients would have developed meningitis without ante- cedent lumbar puncture. ‘Teele et al.'* reviewed the records of 277 children with bacteremia. They noted that meningitis occurred in 7 of 46 (15%) children who had normal cerebrospinal fluid. obtained during bacteremia, compared with only 2 of 231 (1%) children who did not undergo lumbar puncture (P < 0.001). All cases of meningitis after lumbar puncture occurred in infants less than 1 yr of age. Among bacter- emic infants who underwent lumbar puncture, only 2 of 17 infants who received antibiotic therapy developed meningitis, compared with 5 of 6 untreated infants (P = 0,008). (It was implied, but not stated, that these infants received antibiotic therapy aftr lumbar puncture.) In contrast, Smith et al'® reported diagnostic lumbar puncture in 11 preterm neonates with sepsis at 9-22 days after delivery. None of the infants developed meningitis. Pray! noted that 8 of 30 (27%) children with pneumo- coccemia developed meningitis after normal lumbar puncture, compared with 86 of 386 (22%) similar children who did not undergo lumbar puncture (P = not signifi- cant), Similarly, Eng and Seligman’? observed that the incidence of meningitis after lumbar puncture did not significantly differ from the incidence of spontaneous meningitis in bacteremic patients. Shapiro et al.' con- cluded: ‘The development of bacterial meningitis in children with occult bacteremia is strongly associated with the species of bacteria that ‘causes theinfection, but not witha lumbar puncture... Children ‘with high-density bacteremia may appear to be more severely il than children who have bacteremia with lower concentrations of | bacteria, and therefore may be more likely to undergo. lumbar puncture." Teele et al." acknowledged that clinical judgment might have enabled their pediatricians to perform lumbar668 puncture in children in whom meningitis was developing, before the cerebrospinal fluid was diagnostic. Thus, selec- tion bias clouds our interpretation of these retrospective epidemiologic studies. Some anesthesiologists have cited anecdotal cases of ‘meningitis as the basis for recommending that we avoid. spinal anesthesia not only in patients with existing infec- tion, but also in patients at risk for transient, intraoper- ative bacteremia.” However, few data suggest that spinal anesthesia before or during bacteremia isa risk factor for ‘meningitis in adults. Dripps and Vandam'® prospectively studied 8,460 patients who received 10,098 spinal anes- thetics between 1948 and 1951, and they reported no cases of central nervous system infection, Likewise, Phi lips et a."” reported their experience with 10,440 patients, who received spinal anesthesia between 1964 and 1966. None of these patients experienced central nervous system, infection, These authors!®"” did not state how many pa- tients were febrile during administration of spinal anes- thesia. However, a substantial number of these patients underwent obstetric or urologic procedures, and its likely, that some patients had bacteremia after, if not during, dural puncture. Similarly, two retrospective reviews of 27,000 and 505,000 obsteiric patients who received epi- dural anesthesia included no cases of meningitis and only two cases of epidural space infection."®'® This safety re- cord is remarkable, given the frequency with which par- turients develop chorioamnionitis, fever, and/or bacter- emia during labor. sue of ANESTHESIOLOGY, Carp and Bailey” report their observations of the association between men- and dural puncture in bacteremic rats. Briefly, 12 of 40 animals that underwent cisternal puncture during Excherichia coli bacteremia subsequently developed men- Bacteremic animals not undergoing dural puncture did not develop meningitis, and dural puncture in the absence of bacteremia also did not result in infection. ‘These results augment those from earlier laboratory studies in at least three ways. First, in the present study, the bacteremia was similar in magnitude to that which occurs clinically during the early phase of sepsis. Second, only animals with a circulating bacterial count of = 50 CFU/ml atthe time of dural puncture developed men- ingitis, Third, Carp and Bailey"? included a fourth group of bacteremic animals who received an intraperitoneal dose of gentamicin 15 min before performance of cisternal puncture. None of these 30 animals developed meningitis. Carp and Bailey® appropriately stated that one should not apply their observations to the performance of epi- dural anesthesia, which may incur a greater likelihood of venous injury and which typically includes the introduc- tion of an indwelling foreign body. (However, epidural anesthesia usually does not result in violation of the men- ingeal barrier to infection.) The authors also acknowl- EDITORIAL VIEWS edged several other limitations in the application of their study to clinical practice. First, although E. coli is a com- mon cause of bacteremia, it is an uncommon cause of ‘meningitis. Second, the relative size of the dural tear pro- duced by a 26-G needle in rats is greater than that which occurs in humans. Third, anesthesiologists perform spinal ferspace, in contrast to the cis- ternal site of dural puncture in the present study. Fourth, anesthesiologists inject a solution of local anesthetic, which is pethaps bacteriostatic and which may provide some protection against subsequent infection. I would add two additional limitations. First, the authors knew the identity of the bacterium (ie., E. coi), and also they knew that it ‘was susceptible to gentamicin. Second, in contrast to the transient, low-grade bacteremia encountered in many ob- stetric and urologic patients, animals in the present study likely had hemodynamic and metabolic derangements characteristic of early sepsis.2" Nonetheless, epidemiologic data and the present study together provide helpful guidelines for anesthesiologists who give spinal anesthesia in patients at risk for bacter- emia, First, one need not avoid spinal anesthesia in patients at risk for transient, low-grade, intraoperative bacteremia after dural puncture. Second, appropriate antibiotic ther- apy before anesthesia may lessen the risk of meningitis or epidural abscess in patients with established infection, Surgeons and obstetricians often begin antibiotic therapy before surgery o delivery in febrile patients. Heretofore, some obstetricians were reluctant to give antibiotics before delivery in patients with chorioamnionitis. However, sev- eral studies have recently suggested that antepartum an- tibiotic therapy reduces the risk of maternal and neonatal morbidity in patients with chorioamnionitis.~® I ac- knowledge that there are published cases of meningitis and epidural abscess after spinal anesthesia, despite pre- operative administration of antibiotics.°*° Nonetheless, I give spinal or epidural anesthesia to selected patients with evidence of systemic infection, provided that appropriate antibiotic therapy has begun, and the patient has shown a positive response to therapy (eg., a decline in temper- ature). We do not give regional anesthesia in the absence of other relevant information, Rather, we provide care for febrile patients who require anesthesia for labor, delivery, or emergency surgery. When one considers the risks of infection with regional anesthesia, one should ask: What are the alternatives? What are the consequences of with- holding regional anesthesia in a febrile patient? For ex- ample, what is the greater risk in a febrile parturient: meningitis or epidural abscess after spinal or epidural anesthesia, or failed intubation and aspiration during gen- eral anesthesia? Choice of anesthesia remains problematic in those cases when surgeons defer antibiotic therapy until they haveAvestelaor, eM ey 1992 obtained culture specimens at surgery. (It would have been interesting if Carp and Bailey had included a fifth ‘group of bacteremic animals who received gentamicin 15, min after dural puncture.) If the anesthesiologist believes that spinal anesthesia is the anesthetic technique of choice, there may be some cases when he or she should insist that, amtibioticsare given before anesthesia. Otherwise, it seems, prudent to avoid spinal or epidural anesthesia in untreated, patients with overt evidence of sepsis. Finally, in the rare cases when central nervous system infection occurs after regional anesthesia, one should not, assume a cause-and-effect relationship between the an- esthetic and the infection. Most cases of meningitis and epidural abscess occur spontaneously. Eng and Seligman"? stated: “Even if an appropriate temporal sequence isdocumented.. . ., one cannot differentiate spontaneous meningitis from lumbar puncture-induced meningitis in, vidual patient.”"* Davip H. CuestNuT, M.D. Professor of Anesthesia and Obstetrics and Gynecology University of Iowa College of Medicine Towa City, Iowa References 1, Pray LG: Lumbar puncture as a factor in the pathogenesis of ‘meningitis. Am J Dis Child 62:295-808, 1941 2. Weed LH, Wegefarth P, Ayer JB, Felton LD: The production of meningitis by release of cerebrospinal fluid during an experi ‘mental septicemia: Preliminary note. JAMA 72:190-193, 1919 8. Idzumi G: Experimental peumacoccus meningitis in rabbits and dogs. J Infect Dis 26:873-887, 1920 4, Petersdorf RG, Swarner DR, Garcia Me Studies onthe pathogenesis ‘of meningitis: Il. Development of meningis during pneumo- coceal bacteremia. J Clin Invest 41:320-327, 1962 5. Myers MG, Wright PF, Smith AL, Smith DH: Complications of ‘occult pneumococcal bacteremia in children. J Pediatrics 84: 656-860, 1974 6. Rapkin RH: Repeat lumbar punctures in the diagnosis of men- itis, Pediatrics 54:34-37, 1974 17. 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ANESTHESIOLOGY 76:000-000, 1992 21, MelaRiker L, Alexander P, Barts D, Bryant RE, Connell RS, Erwin L, Gilchrist B, Harrison M, Lualin D, Oh G, Widener LL Chroni hyperdynami sepsis inthe rat. Characterization ofthe animal model. Creulatory Shock 25:281-244, 1988 22. Spering RS, Ramamurthy RS, Gibbs RS: A comparison of nu partum versus immediate postpartum treatment of intra-am- oti infection. Obstet Gynecol 70:361-865, 1987 25, Gibbs RS, Dinsmeor MJ, Newton ER, Ramamorthy RS: Aran- domized ial of intrapartum versus immediate postpartum treatment of women with intrammniotic infection. Obstet Gy- necol 72:823-828, 1988 24, Gilsrap LC, Leveno KJ, Cox SM, Burrs JS, Mashburn M, Ro- senfld CR: Intrapartim treatment of seatechorioamnionit Tpact on neonatal sepsis, Am J Obstet Gynecol 169:579-588, 1988) 25, Mead PB: When to treat intraamniotc infection (editor, Obstet Gynecol 72:985-856, 1988 26, Loare Dj, Fsrley HB: Epidural abices following spinal anesthesia "ANESTHESIOLOGY 87:351-358, 1978