neuraxial blockade after spinal surgery

Neuraxial Blockade in Patients with PreexistingSpinal Stenosis, Lumbar Disk Disease, or Prior SpineSurgery: Efficacy and Neurologic ComplicationsJames R. Hebl, MD,* Terese T. Horlocker, MD,* Sandra L. Kopp, MD,* and Darrell R. Schroeder, MS†

BACKGROUND: Patients with spinal canal pathology, including spinal stenosis and lumbar diskdisease, are often not considered candidates for neuraxial blockade because of the risk ofexacerbating preexisting neurologic deficits or developing new neurologic dysfunction. In contrast, ahistory of spine surgery is thought to increase the likelihood of difficult or unsuccessful block. In thisretrospective study we investigated the risk of neurologic complications and block efficacy in patientswith preexisting spinal canal pathology, with or without a history of spine surgery, after neuraxialanesthesia.METHODS: During the 15-year study period, all patients with a history of spinal stenosis or lumbarradiculopathy undergoing a neuraxial technique were studied. Patient demographics, preoperativeneurologic diagnoses and neurologic findings at the time of surgery/neuraxial block, details of theneuraxial block including technique (spinal vs. epidural, single injection vs. continuous), injectate,technical complications (paresthesia elicitation, bloody needle/catheter placement, inability to advancecatheter, accidental dural puncture), and block success were noted. New or progressive neurologic deficitswere identified. All patients were followed until resolution or last date of evaluation.RESULTS: There were 937 patients included, 207 (22%) of whom had undergone spinal surgery. Ahistory of spinal stenosis was present in 187 (20%), lumbar radiculopathy in 570 (61%), and peripheralneuropathy in 210 (22%) patients; 180 patients (19%) had multiple neurologic diagnoses. A majority ofpatients had active but stable neurologic symptoms at the time of surgery. Overall block success was97.2%. A history of spine surgery did not affect the success rate or frequency of technical complications.Ten (1.1%; 95% confidence interval [CI] 0.5%–2.0%) patients experienced new deficits or worsening ofexisting symptoms. Three (1.4%) complications occurred in patients with a history of spinal surgery, andthe remaining 7 (1.0%) in patients without prior surgical decompression or stabilization (P � NS). Althoughan orthopedic procedure was not a risk factor, in 5 of the 6 patients in which the surgery was a unilaterallower extremity procedure, the postoperative deficit involved the operative side. Likewise, in both patientsundergoing bilateral orthopedic procedures who developed bilateral deficits, the outcome was worse onthe previously affected side. A surgical cause was presumed to be the primary etiology in 4 (40%) of 10patients. The primary etiology of the remaining 6 (60%) complications was judged to be nonsurgical(including anesthetic-related factors). The presence of a preoperative diagnosis of compressive radicu-lopathy (P � 0.0495) or multiple neurologic diagnoses (P � 0.005) increased the risk of neurologiccomplications postoperatively.CONCLUSIONS: We conclude that patients with preexisting spinal canal pathology have a higherincidence of neurologic complications after neuraxial blockade (1.1%; 95% CI 0.5%–2.0%) than thatpreviously reported for patients without such underlying pathology. However, in the absence of acontrol group of surgical patients with similar anatomic pathology undergoing general anesthesia, wecannot determine whether the higher incidence of neurologic injury is secondary to the surgicalprocedure, the anesthetic technique, the natural history of spinal pathology, or a combination offactors and the relative contributions of each. (Anesth Analg 2010;111:1511–9)

Patients with preexisting spinal canal pathology, in-cluding spinal stenosis and lumbar disk disease(with or without prior spine surgery), are often not

considered candidates for neuraxial blockade. For example,

previous case reports have specifically attributed the pres-ence of spinal stenosis or lumbar disk disease (with com-pressive radiculopathy) to an increased risk of neurologiccomplications. The mechanisms of injury are presumed tobe ischemic,1–3 mechanical trauma,4,5 local anesthetic tox-icity,6,7 or a multifactorial etiology. Large series and anincreasing number of case reports suggest that undiag-nosed spinal stenosis may be a significant contributor toneurologic complications after neuraxial block.3,5,6,8 Addi-tional surgical factors such as intraoperative positioning,prolonged tourniquet ischemia, or high tourniquet inflationpressure may contribute in a synergistic (rather than simpleadditive) manner.9–11 Furthermore, it is unclear whetherpatients who have undergone prior spine surgery (e.g.,laminectomy, diskectomy, spinal fusion) for these condi-tions are at additional risk of neurologic injury or blockfailure secondary to anatomic alterations or scarring of the

From the Departments of *Anesthesiology and †Health Sciences Research,Mayo Clinic College of Medicine, Rochester, Minnesota.

Accepted for publication July 30, 2010.

Terese T. Horlocker is section Editor of Regional Anesthesia for the Journal. Thismanuscript was handled by Gregory Crosby, section Editor of Neuroscience inAnesthesiology and Perioperative Medicine/Pediatric Neuroscience, and Dr.Horlocker was not involved in any way with the editorial process or decision.

Funding was provided by the Mayo Clinic Foundation.

Address correspondence to James R. Hebl, MD, Department of Anesthesi-ology, Mayo Clinic College of Medicine, 200 First Street, SW, Rochester, MN55905. Address e-mail to [email protected].

Copyright © 2010 International Anesthesia Research SocietyDOI: 10.1213/ANE.0b013e3181f71234

December 2010 • Volume 111 • Number 6 www.anesthesia-analgesia.org 1511

central canal. Previous investigations have included smallnumbers of patients, typically with a history of extensiveinstrumentation or fusion who underwent epidural cath-eter placement for labor analgesia.12–15 However, the ap-plicability of these results to other patient populations isunknown.

Therefore, the primary aim of this investigation was toexamine the overall success and neurologic complicationrates among patients with spinal stenosis or lumbar diskdisease, with or without a history of prior spinal surgery,undergoing neuraxial blockade.

METHODSAfter IRB approval and patient consent, the medicalrecords of all patients with a history of spinal stenosis orlumbar disk disease (i.e., compressive radiculopathy) whounderwent a subsequent spinal or epidural anestheticduring a 15-year study period were retrospectively re-viewed. Patients were identified if “spinal stenosis” or“lumbar disk disease” was entered on their Master Diag-nosis List within the Mayo Clinic database. Neurologicdiagnoses were limited to abnormalities of the spinal canaland did not include patients with primary central nervoussystems disorders such as multiple sclerosis, amyotrophiclateral sclerosis, or postpolio syndrome. All neurologicdiagnoses were confirmed by clinical examination andradiographic imaging by a neurologist or neurosurgeonbefore study inclusion. During the 15-year study period,multiple anesthesiologists (�15 faculty members) partici-pated in the care of all patients.

Demographic data including age, gender, height, andweight were collected. The date of each neurologic diagno-sis and details such as the presence of (1) motor deficits, (2)sensory deficits, (3) paresthesias or dysesthesias, or (4)hyperreflexia at the time of their spinal or epidural anes-thetic were collected for each patient. Neurologic symp-toms at the time of their procedure were further classifiedas (1) acute (exacerbation of symptoms within the last 30days), (2) subacute (exacerbation of symptoms within thelast 1 to 6 months), or (3) chronic/stable (no change insymptoms within the last 6 months).

Indications for neuraxial anesthesia or analgesia in-cluded surgical anesthesia, labor analgesia, or postopera-tive analgesia only. If a surgical indication occurred, itwas classified as (1) orthopedic, (2) urologic, (3)general/abdominal, (4) cesarean delivery, or (5) other.Neuraxial blockade was categorized as (1) epidural, (2)single-injection spinal, (3) continuous spinal, or (4) com-bined spinal– epidural. Details of each neuraxial tech-nique, including awake placement (yes or no), approach(midline, paramedian, both), number of attempts, and localanesthetic(s) used were collected. The use of epinephrine orother local anesthetic additives was also noted. Tech-nical complications occurring at the time of blockplacement—such as difficulty identifying the epiduralspace, difficulty advancing an epidural or subarachnoidcatheter, traumatic block placement (evidence of blood),unplanned dural puncture, difficulty obtaining cerebrospi-nal fluid, paresthesia elicitation, or unintended “total” or

“high” spinal—were identified. Block efficacy was catego-rized as (1) satisfactory (surgery performed without addi-tional intervention), (2) unilateral anesthesia or analgesia,(3) segmental or incomplete anesthesia or analgesia, or (4)no block/block failure.

New or progressive postoperative neurologic deficits(motor or sensory deficits, painful paresthesias, or bowel orbladder dysfunction) were identified in the daily progressnotes of the primary surgical service or the anesthesia acutepain service. Complications were also noted during thepatient’s 2-, 4-, or 6-week surgical follow-up visit. Thepresence of infectious (neuraxial abscess) or hematologic(neuraxial hematoma) complications was also documented.All complications were followed until complete resolutionor until the last documented date of evaluation.

Data are summarized using mean � sd for continuousvariables and percentages for categorical variables. Thepercentage of failed blocks and technical and neurologiccomplications was compared in patients with and withouta history of spine surgery using the �2 test or Fisher’s exacttest as appropriate. Patients with and without neurologiccomplications were compared to identify risk factors usingFisher’s exact test. P � 0.05 was considered statisticallysignificant.

RESULTSNine hundred thirty-seven (n � 937) patients were identi-fied as having spinal stenosis or lumbar disk disease andundergoing subsequent neuraxial anesthesia or analgesia;207 of these had a history of spinal surgery before under-going subsequent spinal or epidural anesthesia (Table 1).Of these, 210 (22%) patients had a coexisting peripheralneuropathy in addition to their spinal canal pathology. Atthe time of neuraxial blockade, painful paresthesias ordysesthesias were the most common neurologic deficit,followed by nonspecific sensory and motor deficits (Table1). The majority of patients (n � 335; 51%) had activeneurologic signs or symptoms (motor or sensory deficits,dysesthesias/paresthesias, or hyperreflexia) at the time ofsurgery and subsequent neuraxial blockade.

The type of neuraxial blockade included spinal anesthe-sia in 545 (58%) patients, epidural anesthesia or analgesia in358 (38%) patients, continuous spinal anesthesia in 24 (3%)patients, and a combined spinal–epidural technique in 10(1%) patients. Eighty of the patients undergoing epiduralanesthesia or analgesia noted above received postoperativeepidural analgesia with local anesthetic infusions.

One hundred ninety-three (24%) patients underwentblock placement precisely at the level of spinal canalpathology, and �75% of patients had block placementwithin 2 vertebral levels (Table 2). In addition, the majorityof patients with a history of spine surgery (n � 165; 83%)underwent subsequent neuraxial anesthesia or analgesiawithin 2 vertebral levels of their prior spinal surgery.

There was no significant difference in block efficacywhen comparing those patients with or without a historyof spinal surgery (Table 3). Nine hundred eleven (97.2%)patients had a satisfactory block, 10 (1.1%) patientsreported a patchy or segmental block, and 16 (1.7%)patients experienced complete block failure. Overall,there were 107 (11.4%) technical complications. There

Neuraxial Block and Spinal Canal Pathology

1512 www.anesthesia-analgesia.org ANESTHESIA & ANALGESIA

was no significant difference in technical complicationscomparing those patients with and without a history ofspinal surgery (Table 3).

There were 10 (1.1%; 95% confidence interval [CI]0.5%–2.0%) patients who experienced new deficits (3 pa-tients) or worsening of preexisting symptoms (7 patients)postoperatively [Table 4 (cases 1 to 4), and Table 5 (cases 5to 10)]. Three (1.4%) complications occurred in patientswith a history of spinal surgery, and the remaining 7 (1.0%)in patients without prior surgical intervention. Eight of 10patients with complications underwent an orthopedic sur-gical procedure; in 5 of the 6 cases in which the surgery wasa unilateral lower extremity procedure, the postoperativedeficit involved the operative side (cases 3, 4, and 8 to 10).Likewise, in both patients undergoing bilateral orthopedicprocedures who developed bilateral deficits, the outcomewas worse on the previously affected side (cases 2, 6). Fromexploratory analyses, the frequency of complications wasfound to be significantly higher in patients with a preop-erative diagnosis of compressive radiculopathy versusother neurologic diagnoses (9/530 vs. 1/407; Fisher exacttest P � 0.049) and also in patients with multiple versussingle preoperative neurologic diagnoses (6/180 vs. 4/757;Fisher exact test P � 0.005).

A surgical cause was presumed to be the primaryetiology in 4 (40%) of 10 patients (Table 4). Specifically,direct nerve trauma/stretch was the principal mechanismin 3 patients (cases 1, 2, 4), tourniquet ischemia in 2 patients(cases 2, 4), and ischemia from a popliteal cyst in 1 patient

(case 3). However, it is possible that neurotoxicity pro-duced by local anesthetic injection at the site of existing rootcompromise may have contributed in 3 cases (cases 2 to 4),because the postoperative deficits were a worsening ofexisting deficits. In 3 (75%) of the 4 patients, the neurologicdeficits returned to baseline (complete resolution did notoccur); in the remaining patient (25%), the symptomspersisted for 3 years (time of last patient follow-up).

The primary etiology of the remaining 6 (60%) com-plications was judged to be nonsurgical (includinganesthetic-related factors) (Table 5). Contributing factorswere identified in 3 of these patients and included apreviously undiagnosed L2 to L3 ependymoma thatbecame symptomatic after failed epidural anesthesia(likely resulting from needle trauma/bleeding of the neo-plasm or alterations in cerebrospinal fluid flow) (case 5),compartment syndrome (with a delay in the diagnosis and

Table 1. Neurologic History of Patients withSpinal Stenosis or Lumbar Disk Disease

Neurologic feature

Number ofpatients

(N � 937)Percentage

(%)a

Neurologic diagnosisSpinal stenosis 187 20Compressive radiculopathy 530 57Disk herniation (without radiculopathy) 40 4Peripheral neuropathy 210 22Multiple (�1) diagnoses 180 19

Neurologic historyMotor deficits 479 51Sensory deficits 568 61Pain/dysesthesias 882 94Hyperreflexia 74 8

History of prior spinal surgerys/p Laminectomy 193 21s/p Diskectomy 9 1s/p Spinal fusion or other 5 0.5

Disease status at time of block placementAcute exacerbation (�30 days) 32 3Subacute exacerbation (1–6 months) 69 8Chronic/stable (�6 months) 828 89Unknown 8 —

Disease progression within last 12 monthsYes 153 19No 632 81Unknown 152 —

Active symptoms at time of neuraxial blockYes 335 51No 323 49Unknown 279 —

a Percentages based upon those patients with available data.s/p � status post (previous condition).

Table 2. Block Characteristics of Patients withSpinal Stenosis or Lumbar Disk DiseaseUndergoing Subsequent Neuraxial Anesthesiaor Analgesia

Block characteristic

Number ofpatients

(N � 937)Percentage

(%)a

Neuraxial techniqueSpinal 545 58Continuous spinal 24 3Epidural 358 38Combined spinal–epidural 10 1

IndicationLabor analgesia 34 4Postoperative analgesia only 65 7Surgical 838 89

Orthopedic 535 64Urologic 192 23Intraabdominal 50 6Cesarean delivery 10 1Other 51 6

Block placement relative tospinal canal pathology

Precisely at the level 193 24Within 1–2 levels 430 52Within 3–4 levels 172 21More than 4 levels 26 3Unknown 116 —

Block placement relative to priorspinal surgery (if applicable)

Precisely at the level 26 13Within 1–2 levels 139 70Within 3–4 levels 28 14More than 4 levels 7 3Unknown 7 —

Number of attempts requiredOne 712 79Two 153 17Three or more 39 4Unknown 33 —

Local anesthetic useb

Intraoperatively 867 93Postoperatively 80 9

Epinephrine usedYes 422 46No 505 54Unknown 10 —

a Percentages based upon those patients with available data.b Ten patients received both intra- and postoperative local anesthetics.


worsening of outcome attributed to epidural infusion) (case6), and neuropathy of critical illness (case 10). The remain-ing 3 patients, each with a preoperative diagnosis of spinalstenosis, underwent an uneventful surgery under spinalanesthesia. In these 3 patients (cases 7 to 9), the spinalanesthetic, in the setting of a preexisting neurologic condition,was determined to be the primary etiology, because nopositioning or surgical factors were identified. Thus, in 5 of 6patients with a neurologic complication attributed to a non-surgical primary etiology, the neuraxial anesthetic was pre-sumed to be the primary mechanism (cases 7 to 9) or acontributing factor in the outcome (cases 5, 6). Decompressivelaminectomy was performed in 2 of 6 patients with deficitsassociated with a nonsurgical etiology (1 for ependymoma; 1for radiculopathy/spinal stenosis). However, complete reso-lution was documented in only 2 (33%) of the 6 patients (1 ofwhom underwent laminectomy; case 5).

DISCUSSIONPatients with preexisting neurologic conditions are typi-cally considered to be at increased risk of neurologiccomplications after spinal or epidural techniques. Previousstudies have investigated the risk associated with multiplesclerosis or polio16 or diabetic sensorimotor neuropathy17

and concluded that the risk of severe postoperative neuro-logic injury in these patients is relatively uncommon butappears to be higher than that reported for the generalpopulation.6,18 Our series is the first to characterize thefrequency and severity of neurologic events after neuraxialblockade in patients with previously diagnosed spinalstenosis or lumbar disk disease (with or without priorspinal decompressive surgery). Our major findings suggestthat this patient population is at increased risk for worsen-ing of preexisting or the development of new neurologicdeficits postoperatively when compared with the generalpopulation,6,18 and that the presence of multiple neurologicdiagnoses (radiculopathy, spinal stenosis, peripheral neu-ropathy) increases the risk.

Our results also demonstrated that a history of spinalsurgery did not increase the risk of technical or neurologiccomplications or affect block success. Previous spinal sur-gery has often been considered a relative contraindicationto the use of neuraxial blockade. Many of these patientsexperience chronic back pain and are reluctant to undergoepidural or spinal anesthesia, fearing exacerbation of theirpreexisting back complaints. Several postoperative ana-tomic changes make needle or catheter placement moredifficult and complicated after major spinal surgery. Thepresence of adhesions or obliteration of the epidural spacefrom scar tissue may increase the incidence of dural punc-ture or decrease the spread of local anesthetic within theepidural space, producing an incomplete or failed block.Needle placement in an area of the spine that has under-gone bone grafting and posterior fusion may not be pos-sible with midline or lateral approaches; needle insertioncan be accomplished only at unfused segments.

Previous series investigating the efficacy and safety ofneuraxial block after spinal surgery typically involvedparturients with a history of Harrington rod instrumenta-tion and fusion. For example, the largest series by Daley etal.19 included 18 patients with previous Harrington rodinstrumentation who underwent 21 attempts at epiduralanesthesia for obstetric analgesia. Continuous lumbar epi-dural anesthesia was successfully established in 20 of 21attempts, but only 10 procedures were performed easily onthe first attempt. The remaining 11 patients required largeramounts of local anesthetics or complained of a patchyblock or both. There were no side effects except for lowback pain in 2 patients with multiple attempts at catheterplacement. Similar results were reported by Crosby andHalpern12 and Hubbert.14 Thus, historically, it was con-cluded that epidural anesthesia may be successfully per-formed in patients who have had spinal surgery, butsuccessful catheter placement may be possible on the firstattempt in only 50% of patients, even by an experienced

Table 3. Outcomes of Neuraxial Blockade in Patients with Spinal Stenosis or Lumbar Disk Disease withor without Prior Spinal Surgery

Outcome

Patients without prior history ofspine surgery

Patients with prior history of spinesurgery

PvalueaN n % N n %

Block efficacy 730 207 0.72Satisfactory 709 97.1 202 97.6Unilateral 0 0.0 1 0.5Patchy or segmental 9 1.2 0 0.0No block (block failure) 12 1.7 4 1.9

Technical complicationsEpidural 285 73 0.88

Unable to reach epidural space 5 1.8 0 0.0Unable to advance catheter 14 4.9 3 4.1Unplanned dural puncture 8 2.8 2 2.7

Spinal 439 130 1.00Unable to obtain CSF 1 0.2 0 0.0

Epidural or spinal 730 207 0.91Traumatic (blood) 19 2.6 8 3.9Unintentional paresthesia 37 5.1 9 4.3Unintended “high” spinal 1 0.1 0 0.0

Neurologic complications 730 7 1.0 207 3 1.4 0.54

CSF � cerebrospinal fluid.a The percentage of patients experiencing one or more of the listed complications within the given category was compared between groups using the Chi-squaretest or Fisher’s exact test as appropriate.



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anesthesiologist. Although adequate epidural anesthesiawas eventually produced in 40% to 95% of patients, thereappeared to be a higher incidence of traumatic needleplacement, unintentional dural puncture, and unsuccessfulepidural needle or catheter placement, especially if spinalfusion extends to between L-5 and S-1. However, the smallnumbers of patients and an indication of “labor analgesia”made extrapolation to patients with other surgical indica-tions undergoing a nonepidural technique difficult.

A single study by Berkowitz and Gold20 evaluated thesuccess rate and complications in 33 patients with priorlaminectomy who underwent tetracaine spinal anesthesia.On the basis of their 100% success rate and lack of neuro-logic complications, including evidence of a prolongedblock, the authors concluded that there was “no logicalbasis for avoiding spinal anesthesia in postlaminectomypatients.” Our 97.6% block success rate, trauma frequencyof 3.9%, and paresthesia elicitation rate of 4.3% in patientswith prior spine surgery support the conclusions ofBerkowitz and Gold regarding block efficacy after laminec-tomy. Furthermore, their frequency of technical complica-tions was similar to those for patients in our series (Table 3)and previous series from our outcomes database.21 Unfor-tunately, the frequency of persistent postoperative neuro-logic deficits in the current retrospective series (1.1%; 95%CI 0.5%–2.0%) is much higher than was expected; prospec-tive epidemiologic investigations have reported frequen-cies between 1:1000 and 1:10,000.6,22 Although theneuraxial block was not the primary etiology of all 10neurologic deficits in our series, it may have been acontributing factor in nearly all the cases because of the“double crush” phenomenon.

The double crush syndrome, first proposed by Upton andMcComas11 in 1973, is a general term referring to thecoexistence of dual compressive lesions along the courseof a nerve, where the presence of a proximal lesionrenders the nerve vulnerable to further injury with amore distal compression. Importantly, the 2 minor (per-haps even subclinical) insults synergistically result in aclinical and potentially permanent nerve injury.23 Al-though initially described in patients with concomitantcervical radiculopathies and median or ulnar neuropathies,the term has been extended to include injury from noncom-pressive mechanisms, such as toxic (chemotherapeuticagents, local anesthetics),24 metabolic (aging, diabetic sen-sorimotor neuropathy),17,25,26 ischemic (tourniquet infla-tion),27 and traumatic (surgical traction, needle/catheterplacement)28 etiologies. The presence of a preexisting neu-rologic condition, whether neuraxial or peripheral in na-ture, would represent an additional mechanism by whichminor or subclinical symptoms may interact to result in anew or worsened neurologic deficit.6,17 Our results suggestan additive effect of multiple preexisting neurologic condi-tions; we reported that neuraxial block performed in pa-tients with a preoperative diagnosis of a compressiveradiculopathy or multiple neurologic diagnoses signifi-cantly increased the risk of neurologic complications post-operatively. Previous surgical treatment did not affect thefrequency.

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the patient to further functional worsening. The mecha-nism(s) of nerve injury after neuraxial block in patientswith spinal stenosis or lumbar disk disease is presumedto be the additive effects of local anesthetic toxicity andneural ischemia (from the volume effects of theinjectate/infusate)1,6,8,29 with epidural techniques andlocal anesthetic neurotoxicity with spinal blockade. Theneurotoxic effects may be enhanced by maldistributioncreated by degenerative changes within the spinal col-umn.30 Spinal cord ischemia from microcirculatory de-rangement has also been proposed.3,31 Perioperativepositioning may also contribute to injury; postoperativecauda equina syndrome and paresis have been reported inpreviously asymptomatic patients with spinal stenosis afteruneventful spinal6,8 or general anesthesia.32 Often thesecases involve an orthopedic procedure.8,32

Patients undergoing orthopedic surgical proceduresmay be especially prone to the double crush syndrome.Two or more insults along the course of a nerve mayreadily occur, because the surgical procedure is oftenassociated with a defined postoperative neuropathy (due tosurgical neurapraxia), and tourniquet inflation is routinelyused to assure a bloodless field. For example, total kneereplacement is associated with an overall 2.2% frequency ofperoneal nerve palsy (from surgical traction to the peronealnerve at the fibular head), which increases to 7.7% withprolonged tourniquet inflation (producing ischemia to boththe tibial and peroneal components of the sciatic nerve atthigh level).9,27 A preexisting L5/S1 radiculopathy mayrender the sciatic components even more sensitive toischemia and traction, as well as to local anesthetic neuro-toxicity. Although an orthopedic procedure was not a riskfactor in our series, in 7 of the 8 orthopedic cases withcomplications, surgery was to the previously affected ex-tremity. Although the relative roles of patient, surgicalfactors, and anesthetic factors remain undetermined, ourresults suggest that the overall risk may be high in thispatient population.

We conclude that patients with preexisting spinal canalpathology have a higher incidence of neurologic complica-tions after neuraxial blockade than that previously reportedfor patients without such underlying pathology. However,in the absence of a control group of surgical patients withsimilar anatomic pathology undergoing general anesthesia,we cannot determine whether the higher incidence ofneurologic injury is secondary to the surgical procedure,the anesthetic technique, the natural history of spinalpathology, or a combination of factors and the relativecontributions of each.

REFERENCES1. Usubiaga JE, Wikinski JA, Usubiaga LE. Epidural pressure and

its relation to spread of anesthetic solutions in epidural space.Anesth Analg 1967;46:440–6

2. Hooten WM, Hogan MS, Sanemann TC, Maus TJ. Acute spinalpain during an attempted lumbar epidural blood patch incongenital lumbar spinal stenosis and epidural lipomatosis.Pain Physician 2008;11:87–90

3. de Seze MP, Sztark F, Janvier G, Joseph PA. Severe andlong-lasting complications of the nerve root and spinal cordafter central neuraxial blockade. Anesth Analg 2007;104:975–9

4. Tetzlaff JE, Dilger JA, Wu C, Smith MP, Bell G. Influence oflumbar spine pathology on the incidence of paresthesia duringspinal anesthesia. Reg Anesth Pain Med 1998;23:560–3

5. Stambough JL, Stambough JB, Evans S. Acute cauda equinasyndrome after total knee arthroplasty as a result of epiduralanesthesia and spinal stenosis. J Arthroplasty 2000;15:375–9

6. Moen V, Dahlgren N, Irestedt L. Severe neurological compli-cations after central neuraxial blockades in Sweden 1990–1999.Anesthesiology 2004;101:950–9

7. Yuen EC, Layzer RB, Weitz SR, Olney RK. Neurologic compli-cations of lumbar epidural anesthesia and analgesia. Neurol-ogy 1995;45:1795–801

8. Kubina P, Gupta A, Oscarsson A, Axelsson K, Bengtsson M. Twocases of cauda equina syndrome following spinal–epidural anes-thesia. Reg Anesth 1997;22:447–50

9. Horlocker TT, Hebl JR, Gali B, Jankowski CJ, Burkle CM, BerryDJ, Zepeda FA, Stevens SR, Schroeder DR. Anesthetic, patient,and surgical risk factors for neurologic complications afterprolonged total tourniquet time during total knee arthroplasty.Anesth Analg 2006;102:950–5

10. Warner MA, Warner DO, Harper CM, Schroeder DR, MaxsonPM. Lower extremity neuropathies associated with lithotomypositions. Anesthesiology 2000;93:938–42

11. Upton AR, McComas AJ. The double crush in nerve entrap-ment syndromes. Lancet 1973;2:359–62

12. Crosby ET, Halpern SH. Obstetric epidural anaesthesia inpatients with Harrington instrumentation. Can J Anaesth1989;36:693–6

13. Feldstein G, Ramanathan S. Obstetrical lumbar epidural anes-thesia in patients with previous posterior spinal fusion forkyphoscoliosis. Anesth Analg 1985;64:83–5

14. Hubbert CH. Epidural anesthesia in patients with spinalfusion. Anesth Analg 1985;64:843

15. Kardash K, King BW, Datta S. Spinal anaesthesia for caesareansection after Harrington instrumentation. Can J Anaesth1993;40:667–9

16. Hebl JR, Horlocker TT, Schroeder DR. Neuraxial anesthesiaand analgesia in patients with preexisting central nervoussystem disorders. Anesth Analg 2006;103:223–8

17. Hebl JR, Kopp SL, Schroeder DR, Horlocker TT. Neurologiccomplications after neuraxial anesthesia or analgesia in pa-tients with preexisting peripheral sensorimotor neuropathy ordiabetic polyneuropathy. Anesth Analg 2006;103:1294–9

18. Auroy Y, Benhamou D, Bargues L, Ecoffey C, Falissard B,Mercier FJ, Bouaziz H, Samii K. Major complications of re-gional anesthesia in France: The SOS Regional AnesthesiaHotline Service. Anesthesiology 2002;97:1274–80

19. Daley MD, Rolbin SH, Hew EM, Morningstar BA, Stewart JA.Epidural anesthesia for obstetrics after spinal surgery. RegAnesth 1990;15:280–4

20. Berkowitz S, Gold MI. Spinal anesthesia for surgery in patientswith previous lumbar laminectomy. Anesth Analg1980;59:881–2

21. Horlocker TT, McGregor DG, Matsushige DK, Schroeder DR,Besse JA. A retrospective review of 4767 consecutive spinalanesthetics: central nervous system complications. AnesthAnalg 1997;84:578–84

22. Auroy Y, Narchi P, Messiah A, Litt L, Rouvier B, Samii K.Serious complications related to regional anesthesia: results ofa prospective survey in France. Anesthesiology 1997;87:479–86

23. Prielipp RC, Warner MA. Perioperative nerve injury: a silentscream? Anesthesiology 2009;111:464–6

24. Hebl JR, Horlocker TT, Pritchard DJ. Diffuse brachial plexopa-thy after interscalene block in a patient receiving cisplatinchemotherapy: the pharmacologic double crush syndrome.Anesth Analg 2001;92:249–51

25. Moghtaderi A, Izadi S. Double crush syndrome: an analysis ofage, gender and body mass index. Clin Neurol Neurosurg2008;110:25–9

26. Yee TC, Kalichman MW. Effects of aging on nerve conductionblock induced by bupivacaine and procaine in rats. J PeripherNerv Syst 1997;2:175–9



27. Horlocker TT, Cabanela ME, Wedel DJ. Does postoperativeepidural analgesia increase the risk of peroneal nerve palsyafter total knee arthroplasty? Anesth Analg 1994;79:495–500

28. Hebl JR, Horlocker TT, Sorenson EJ, Schroeder DR. Regionalanesthesia does not increase the risk of postoperative neurop-athy in patients undergoing ulnar nerve transposition. AnesthAnalg 2001;93:1606–11

29. Jacob AK, Borowiec JC, Long TR, Brown MJ, Rydberg CH,Wass CT. Transient profound neurologic deficit associatedwith thoracic epidural analgesia in an elderly patient. Anes-thesiology 2004;101:1470–1

30. Hampl KF, Schneider MC, Drasner K. Toxicity of spinal localanaesthetics. Curr Opin Anaesthesiol 1999;12:559–64

31. Markman JD, Gaud KG. Lumbar spinal stenosis in olderadults: current understanding and future directions. Clin Geri-atr Med 2008;24:369–88

32. Lewandrowski KU, McLain RF, Lieberman I, Orr D. Cord andcauda equina injury complicating elective orthopedic surgery.Spine 2006;31:1056–9

Denham S. Ward, MD, PhD, Named Next President of Foundation for Anesthesia Education and Research For Immediate Release

Rochester, MN, October 28, 2010 – At their annual fall meeting October 16, 2010, the Board of Directors of the Foundation for Anesthesia Education and Research (FAER) named Denham S. Ward, MD, PhD, as successor for long-time President, Alan D. Sessler, MD. Dr. Ward will begin his term as President in 2011.

“Dr. Ward is an accomplished physician scientist with a long history of leadership in anesthesiology,” said Dr. Sessler. “Over the months ahead, I will assume a support role in advocating for FAER’s mission, confident that my successor will act wisely to create new pathways to propel the specialty’s next generation to a new and higher level of patient care, innovation and discovery.”

Dr. Ward has been a member of the FAER Board of Directors since 2002 and is now serving as Board Chair. He is currently Professor of Anesthesiology and Biomedical Engineering at the University of Rochester, Rochester, NY, where he is also Chair of the Anesthesiology Department and Associate Dean for Faculty Development – Medical Education.

FAER is a 501(c)(3) organization whose mission is to advance medicine through education and research in anesthesiology. FAER provides research grants and career development opportunities for medical students, residents and anesthesiologists. Since it was founded by the American Society of Anesthesiologists in 1986, the foundation has awarded more than $20 million in research grants, and typically awards more than $1 million in research grants annually.

Contact:

Nicole Brudos Ferrara, Associate Director - Communications Foundation for Anesthesia Education and Research 507-538-7886 www.faer.org


neuraxial blockade after spinal surgery

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