AVOIDING COMPLICATIONS IN REGIONAL ANESTHESIA: PART 2
From Sleepless in Seattle, Hold the Mayo: Regional Anesthesia 2006, August 4-6, 2006
| NEURAXIAL COMPLICATIONS OF SPINAL AND EPIDURAL ANESTHESIA—Denise J. Wedel, MD, Professor
of Anesthesiology, Mayo Clinic College of Medicine, Rochester, MN
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| Introduction: infectious complications of regional anesthesia increasing; renaissance in regional anesthesia in past decade
(reasons include innovative techniques and equipment, surgical enthusiasm, and training emphasis); rare complications
in earlier studies included seizure with peripheral nerve blockade, minor peripheral nerve injury, and cardiac
arrest (with spinal anesthesia); other major complications “were just not big issues”
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| Intraoperative technical problems: learning curve important part of clinical practice; needle trauma can occur
with regional anesthesia; contraindications to regional anesthesia—patient refusal; local anesthetic allergies (rare);
ongoing progressive neurologic disease (relative contraindication); infection at needle insertion site; possibly systemic
infection; coagulopathies
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| Coagulopathy: Vandermeulen 1994—review of 61 cases of spinal hematoma related to central neural blockade; majority
had hemostatic abnormalities, and most of these related to thrombolytic agents; needle placement difficult or
bloody in 50% of cases; most were epidural anesthetics with continuous catheters; spinal bleeding occurred at time of
catheter removal in ≈50% of cases; necessary to manage patient throughout duration and during removal of catheter;
early intervention necessary or complete recovery unlikely; Moen 2004—reviewed large number of spinal and epidural
blocks and found low incidence of spinal hematoma; labor analgesia low risk; elderly women undergoing total knee
arthroplasty highest risk; suggested differences dependent on spinal anatomy or response to thromboprophylaxis;
American Society of Regional Anesthesia and Pain Medicine—publishes consensus statements to keep anesthesia
provider abreast of new anticoagulants and suggestions to avoid problems
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| Infectious complications: until recently, long history of spinal and epidural anesthesia with few infectious complications;
original concerns focused on faulty sterilization of reusable equipment, break in aseptic technique, preexisting
sepsis in patient, and other factors, eg, hematoma that subsequently became infected; historically, risk of central
neuraxial needle placement in infected individual unproven
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 | Meningitis: dural puncture considered risk factor for meningitis because of introduction of blood into intrathecal space
and disruption of blood-brain barrier; however, lumbar puncture (LP) often performed in patients with fever of unknown
origin, so cause and effect unclear; Weed et al (1919)—demonstrated dural puncture in bacteremic rats resulted
in meningeal irritation, but no meningitis developed in patients who had intravenous (IV) bacterial
inoculation; Carp et al (1992)—repeated Weed’s study using rats with Escherichia coli bacteremia and found that
appropriate antibiotic treatment before dural puncture prevented onset of meningitis; thus, risk of dural puncture in
presence of septicemia reasonably low in human receiving appropriate antibiotics; another 1919 study—described
patients suspected of having meningitis who had diagnostic LP and blood cultures; 38 patients had proven meningitis;
other 55 patients had normal cerebrospinal fluid (CSF) evaluation at time of LP; 5 of 6 patients with positive
blood culture at time of LP developed meningitis; question whether they would have developed meningitis had they
not had LP; subsequent clinical studies suggest “it’s probably not important” that they had LP; 1941 study—reported
incidence of meningitis in children who underwent diagnostic LP during pneumococcal sepsis same as in
children who contracted spontaneous meningitis
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| Modern data on incidence of postspinal meningitis: “overall it’s pretty low,” historically, ≈1 in 22,000; European studies
show similar low incidence; in future, gowning and gloving may need to be considered for placement of epidural
or spinal anesthetic (already in use for placement of central lines), perhaps because of nosocomial infections and increased
rate of immunocompromise in patient population; agents used for epidural and spinal anesthetics have antimicrobial
properties; these problems easily diagnosed with magnetic resonance imaging (MRI)
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| Epidural abscess: usually hematogenous spread; may be direct extension, but that usually involves osteomyelitis; neural
compression or circulatory changes can cause neurologic symptoms; study—looked at incidence up to 1975;
showed low incidence (0.2-1.0 in 10,000 admissions); 39 cases between 1947 and 1974; most had Staphylococcus
aureus, suggesting skin pathogens, or gram-negative bacilli; etiology generally osteomyelitis or bacteremia; only 1
case in series related to epidural catheter placement; “perhaps that’s changed” (between 1974 and 1996, one author
reported 42 cases related to epidural anesthesia); Danish survey (1999)—found 9 epidural abscesses in ≈17,000
epidural catheters (included thoracic and lumbar catheters); mean catheter duration 11 days, median duration 6
days; most placed for postoperative pain management; localized back pain, local infection at site of catheter insertion,
and neurologic changes common; majority had S aureus infection and were immunocompromised; possible
risk factors include anticoagulation, immunosuppression, and duration of catheter (extremely common in hospitalized
patients); MRI sensitive, even for small epidural abscesses; Moen et al (2004)—found time from catheter insertion
to symptoms (fever and backache) 2 days to 5 wk; 70% of patients immunocompromised (eg, diabetic,
heavy alcohol use); found epidural abscess and meningitis combined accounted for 46% of obstetric neuraxial complications;
treatment—epidural abscesses usually progress slowly; look for back pain and fever; patient should not
be managed over telephone by obstetrician or surgeon, but should be examined for localized signs of infection by
anesthesia provider; progression can occur rapidly; obtain emergency neurosurgical consultation; treat with antibiotics
and surgical drainage if needed; injection of central neuraxial steroids may increase risk
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| Summary: despite conflicting data, many experts suggest avoiding central neuraxial blocks in patients with untreated
systemic infection; speaker considers clinical situation; appropriate antibacterial therapy with observed response appears
to provide some safety; continue routine postoperative neurologic evaluation; be involved if patient develops
problems; if suspicious, early use of MRI recommended; timing of diagnosis and early surgical intervention affect
outcome
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| TRANSIENT NEUROLOGIC COMPLICATIONS—Julia E. Pollock, MD, Staff Anesthesiologist, Virginia Mason
Medical Center, Seattle, WA
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| History: lidocaine introduced in 1948 as spinal anesthetic; Phillips et al (1969)—first safety study; looked at >10,000
patients (>90% obstetric) undergoing spinal anesthesia with lidocaine (85% received ≤50 mg); reported no major neurologic
complications; however, data show 284 patients complained of significant back pain, and of these, 91 refused
subsequent spinal anesthesia because of postspinal back pain; reported 38 transient other peripheral neurologic symptoms
(all but 8 resolved; 2 due to spinal anesthetic; unable to determine whether related to drug or technique); spinal
microcatheter and continuous spinal anesthesia—introduced in 1991; Rigler and others reported on 11 patients with
cauda equina syndrome after continuous spinal anesthesia (10 involved lidocaine); Food and Drug Administration
(FDA) determined cause to be maldistribution of initial spinal dose on cauda equina, followed by redosing; lowest-
amount patients received >300 mg; because of propensity for maldistribution, FDA removed microcatheters from
market in United States; neurotoxicity not considered problem because patients had received such large doses of
lidocaine; Schneider et al (1993)—case report of 4 gynecologic patients in lithotomy position who postoperatively
experienced transient back pain radiating down leg after single injection of lidocaine spinal anesthesia; “transient
radicular irritation” term used initially; subsequently, terminology changed to “transient neurologic symptoms” (TNS;
but etiology not proven, “so this is not a great name either”); symptoms include pain or dysesthesia occurring within
24 hr after spinal anesthesia, that usually resolves within ≈72 hr; no permanent neurologic sequelae
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| Incidence: studies show remarkable variability in incidence of TNS among patients undergoing spinal anesthesia with
lidocaine; incidence of TNS seems to vary with type of surgery performed; gynecologic patients in high lithotomy position
have incidence of 30% to 40%; knee arthroscopy (stretching of operative and nonoperative extremity) has incidence
of 18% to 25%; in patients in supine position for duration of surgery, incidence 3% to 8%
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| Etiology: possible causes include local anesthetic neurotoxicity, neural ischemia secondary to stretching of sciatic
nerve in extremes of position, and muscle spasm (or extreme muscle relaxation); early ambulation, needle trauma,
and maldistribution refuted as major etiologies
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| Local anesthetic neurotoxicity: Ready et al (1985)—looked at intrathecal injections in rabbits; found that in greater
than clinically used concentrations, all local anesthetics neurotoxic; tetracaine and lidocaine appear more neurotoxic
than chloroprocaine or bupivacaine; Lambert et al (1994)—found clinically used concentrations of local anesthetic
(eg, 5% lidocaine or 0.5% tetracaine) can cause irreversible conduction defects in isolated frog sciatic nerve; subsequent
study (Bainton et al [1994]) showed irreversible loss of conduction with concentrations of 1% lidocaine in
same model; speaker’s study—used lidocaine, 50 mg, in patients undergoing knee arthroscopy; randomized patients
to receive either 2%, 1%, or 0.5% lidocaine; showed equal incidence of TNS in each group; indicates decreasing concentration
does not decrease incidence of TNS (with 50 mg); Drasner 1997—found area of local anesthetic neurotoxicity
causes damage to posterior nerve roots, rather than spinal cord; another study by speaker—used 50-mg 5%
lidocaine spinals and measured nerve conduction in posterior nerve root (H reflex); found patients experiencing TNS
acutely do not appear to have alterations in nerve conduction at time of TNS; cauda equina syndrome—incidence
increased by 1) increasing local anesthetic concentration, 2) increasing dose of local anesthetic, and 3) use of vasoconstrictors;
factors that increase incidence of cauda equina syndrome not same as factors that increase incidence of
TNS; probable causes of TNS—surgical position one of few things known to increase incidence of TNS; lidocaine,
<30 mg, causes no TNS (but also provides questionable anesthesia); speaker suspects combination of neural ischemia
secondary to sciatic stretching makes nerve more susceptible to some elements of neurotoxicity
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| Risk factors: Freedman et al (1998)—found risk factors for TNS in their patient population were use of lidocaine,
ambulatory surgery status, use of lithotomy position, and obesity; subsequent studies show ambulatory patients probably
not at increased risk, compared to inpatients
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| Diagnosis: TNS usually presents 12 to 24 hr after surgery; average duration, 6 hr to 4 days; speaker finds average verbal
pain rating score 6.2 on scale of 1 to 10; no patient has asked to be readmitted; statistically significant incidence of
increased functional impairment in sitting, walking, and sleeping in patient with TNS; most have no symptoms at 2 wk
postoperatively; no reported patients with TNS have had motor weakness; if patient complains of motor weakness,
other possible etiologies, eg, epidural hematoma and abscess, must be eliminated; chloroprocaine back pain after epidural
completely different phenomenon; differential diagnosis includes neuropathy, anterior spinal artery syndrome,
adhesive arachnoiditis, and cauda equina syndrome
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| Treatment: TNS does not respond well to opioids, but does appear to respond to nonsteroidal anti-inflammatory drugs
(NSAIDs); may respond to muscle relaxants, symptomatic therapy, and trigger point injections
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| Prevention: bupivacaine excellent for inpatient anesthesia (low incidence of complications); outpatients—none of
currently available spinal anesthetics short-acting, so unable to provide adequate anesthesia, and get patient home
quickly with minimum complications; procaine not as reliable as lidocaine (problems include TNS and nausea);
lidocaine, 25 mg, combined with fentanyl, 20 mg, does not provide much motor block (other complications, including
fairly high incidence of pruritus and nausea); mepivacaine also has reported incidence of TNS (4%-18%) and longer-
acting than lidocaine; bupivacaine also longer-acting (even with low dose; higher degree of variability per dose than
lidocaine); prilocaine agent of choice in Europe; chloroprocaine— if considering, “you must use the preservative-
free solution that is found in the brown bottle”; laboratory studies on toxicity confusing; block regression times and
patterns of chloroprocaine spinal anesthesia similar to those of lidocaine, but probably ≈15 min less; produces spinal
anesthesia that starts to wear off at ≈100 min, and “virtually gone” in 2 hr; Virginia Mason Medical Center has performed
>1700 procedures using chloroprocaine as spinal anesthetic; only 2 known reports of TNS and no major neurologic
complications; however, speaker has no data on safety of chloroprocaine given intrathecally; no incidence of
TNS in knee arthroscopy with chloroprocaine, compared to 22% incidence with lidocaine
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| Summary: speaker believes “TNS and cauda equina syndrome are not the same thing”; consider alternative agents;
TNS distressing to patients and physicians; results in functional impairment of daily life and fairly high verbal pain
rating score; however, when patients call and do not have symptoms of motor weakness and “you’re fairly sure that
they have TNS”, you can be reassuring (suggest NSAIDs, and assure patient symptoms will resolve completely)
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Suggested Reading
Bainton CR et al: Concentration dependence of lidocaine-induced irreversible conduction loss in frog nerve. Anesthesiology
81:657, 1994; Carp H et al: The association between meningitis and dural puncture in bacteremic rats. Anesthesiology
76:739, 1992; de Jong RH: Last round for a "heavyweight"? Anesth Analg 78:3, 1994; Drasner K:
Lidocaine spinal anesthesia: a vanishing therapeutic index? Anesthesiology 87:469, 1997; Freedman JM et al: Transient
neurologic symptoms after spinal anesthesia: an epidemiologic study of 1,863 patients. Anesthesiology 89:633,
1998; Erratum in: Anesthesiology 89:1614, 1998; Hampl KF et al: A similar incidence of transient neurologic symptoms
after spinal anesthesia with 2% and 5% lidocaine. Anesth Analg 83:1051, 1996; Hampl KF et al: Transient neurologic
symptoms after spinal anesthesia: a lower incidence with prilocaine and bupivacaine than with lidocaine.
Anesthesiology 88:629, 1998; Horlocker TT et al: Anticoagulation and neuraxial block: historical perspective, anesthetic
implications, and risk management. Reg Anesth Pain Med 23:129, 1998; Horlocker TT et al: Regional anesthesia
in the anticoagulated patient: defining the risks (the second ASRA Consensus Conference on Neuraxial
Anesthesia and Anticoagulation). Reg Anesth Pain Med 28:172, 2003; Kane RE: Neurologic deficits following epidural
or spinal anesthesia. Anesth Analg 60:150, 1981; Kindler CH et al: Epidural abscess complicating epidural anesthesia
and analgesia. An analysis of the literature. Acta Anaesthesiol Scand 42:614, 1998; Lambert LA et al:
Irreversible conduction block in isolated nerve by high concentrations of local anesthetics. Anesthesiology 80:1082,
1994; Moen V et al: Severe neurological complications after central neuraxial blockades in Sweden 1990-1999. Anesthesiology
101:950, 2004; Narchi P et al: Ventilatory effects of epidural clonidine during the first 3 hours after caesarean
section. Acta Anaesthesiol Scand 36:791, 1992; Phillips et al: Neurologic complications following spinal
anesthesia with lidocaine: A prospective review of 10,440 cases. Anesthesiology 30:284, 1969; Pollock JE et al: Dilution
of spinal lidocaine does not alter the incidence of transient neurologic symptoms. Anesthesiology 90:445, 1999;
Ready LB et al: Neurotoxicity of intrathecal local anesthetics in rabbits. Anesthesiology 63:364, 1985; Rigler ML
et al: Cauda equina syndrome after continuous spinal anesthesia. Anesth Analg 72:275, 1991; Schneider M et al:
Transient neurologic toxicity after hyperbaric subarachnoid anesthesia with 5% lidocaine. Anesth Analg 76:1154, 1993;
Vandermeulen EP et al: Anticoagulants and spinal-epidural anesthesia. Anesth Analg 79:1165, 1994; Wang LP
et al: Incidence of spinal epidural abscess after epidural analgesia: a national 1-year survey. Anesthesiology 91:1928,
1999; Wang LP et al: Long-term outcome after neurosurgically treated spinal epidural abscess following epidural analgesia.
Acta Anaesthesiol Scand 45:233, 2001.
Educational Objectives
| The goal of this program is to avoid neuraxial complications of spinal and epidural anesthesia and to improve the
diagnosis and management of transient neurologic symptoms. After hearing and assimilating this program, the participant
will be better able to:
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| Eliminate intraoperative technical problems associated with neuraxial complications of spinal and epidural anesthesia.
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| Identify neuraxial hematoma as a complication of spinal and epidural anesthesia.
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| Explain infectious complications occurring with spinal and epidural anesthesia.
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| Recognize transient neurologic symptoms (TNS) and provide a history of TNS in spinal anesthesia.
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| Summarize the incidence, etiology, risk factors, evaluation, prevention, and treatment of TNS after spinal anesthesia.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty members to disclose relevant
financial relationships within the past 12 months that might create any personal conflicts of interest. Any identified
conflicts were resolved to ensure that this educational activity promotes quality in health care and not a proprietary business
or commercial interest. For this program, the faculty reported nothing to disclose.
Acknowledgements
Drs. Wedel and Pollock spoke at Sleepless in Seattle, Hold the Mayo: Regional Anesthesia 2006, held August 4-6,
2006, in Seattle, WA, and sponsored by Virginia Mason Medical Center, Seattle, WA, and the Mayo Clinic, Rochester,
MN. The Audio-Digest Foundation thanks the speakers, Virginia Mason Medical Center, and the Mayo Clinic for their
cooperation in the production of this program.
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