Overview of the Incidence and Etiology of Neurologic Complications of
Regional Anesthesia.
Introduction
Neurologic complications associated with regional anesthesia often
have a diverse and complex etiology. Following peripheral nerve
blockade (PNB), presenting features of potential nerve injury include
paresthesia, dysesthesia, neuropathic pain and weakness. Devastating
complications of neuraxial anesthesia such as epidural hematoma and
abscess have been subject to large series and its risk-benefit ratio
examined. In recent years, regional anesthesia and in particular PNB
has been increasingly utilized and evolved significantly with the use of
new procedures, technology and equipment.
Neuraxial anesthesia
Moen et al performed a comprehensive retrospective study on severe
complications following neuraxial blockade in Sweden.1 The
denominator was estimated from a postal survey to all anesthetic
departments, then modified according to commercial records of local
anesthetics. To validate the number of CNBs performed relevant
registers were consulted - the Swedish birth registry; the hip and knee
arthroplasty registers and a national audit of hip fractures. From a
denominator of 1,260,000 spinal and 450,000 epidural nerve blocks
there were 127 complications and permanent neurologic damage in 85
patients. Complications occurred more frequently in orthopedic patients
(47/127) and in patients who had received epidural anesthesia (EA). To
illustrate how infrequently major complications are published, only 17
from 127 complications were the subject of case reports. Hematoma in
obstetric cases only occurred with coexisting severe coagulopathy, for
example the HELLP (Hemolysis, Elevated Liver enzymes and Low
Platelets) syndrome. This resulted in a risk of hematoma following
obstetric epidural blockade of 1:200,000. The incidence of epidural
hematoma following total knee arthroplasty in female patients was
1:3,600. In the Moen study, in addition to coagulopathy (often
pharmacologically induced) osteoporosis was proposed as an important
risk factor (more common in females) and part of a degenerative
process contributing to spinal canal stenosis. Spinal canal stenosis
combined with continuous epidural blockade is a particular concern and
requires a high level of vigilance and postoperative neurologic
surveillance. The study detected iatrogenic meningitis (1:44,000) and
abscess rarely. In a 1-year nationwide survey in Denmark, Wang et al
estimated the incidence of spinal-epidural abscess after EA to be
1:1930.2 Risk factors were immunosuppression, prolonged duration of
catheterization (> 5 days) and delayed diagnosis. The most common
organism identified was staphloccocus aureus. The incidence of
abscess in this study was significantly higher than previously
appreciated. In a review of neuraxial morbidity at a single hospital,
Cameron et al published experience of over 8000 cases.3 Epidural site
infection and pyrexia were triggers for investigation with 20 MRIs
performed to diagnose 6 abscesses. The combined risk of abscess or
hematoma was 1:1026 patients (95% CI 0.04 – 019%), however only
one laminectomy was required and there were no cases of permanent
neurological deficits. Epidural abscess was associated with epidural site
infection and fever in 5 out of 6 cases. The low rate of surgical
intervention and lack of long-term sequelae were a distinguishing
feature of this series. For a comprehensive review of infectious
complications of regional anesthesia refer to a recent article by
Horlocker.4 A collaborative effort involving all hospitals in the United
Kingdom (UK) National Health Service, recently reported on serious
complications of CNB.5 The article and especially the accompanying
report contain substantial detail. The pessimistic and optimistic
incidences of paraplegia or death were 1.8 (1.0 – 3.1) and 0.7 (0 – 1.6),
n/100,000, 95% Confidence Interval (CI) respectively. The risk of
permanent injury following adult perioperative EA was 1:5,800 and
1:12,200 using pessimistic and optimistic incidences respectively. In a
large population-based cohort study, the incidence of decompressive
laminectomy at 30 days was unchanged if patients received EA
(8:44,094) compared to those receiving GA (7:44,094).6 This incidence
of laminectomy is similar to the abovementioned UK (1:8,100)5 and
single-center study (1:8,000).3
It is the author’s opinion that neuraxial anesthesia has been subject to
more intense scrutiny than any other anesthesia procedure. This
scrutiny is understandable given the potential devastating nature of
neurologic complications following neuraxial anesthesia. The incidence
of serious complications is consistently rare and clearly influenced by
patient morbidities with outcome influenced by practice location. A good
patient outcome following abscess and hematoma depend of a high
level of vigilance, early diagnosis and treatment. Neuraxial catastrophes
may be associated with organizational and professional failures. The
obstetric population is the safest, while the aged comorbid orthopedic
surgical population appears to represent a higher risk group.
Peripheral nerve blockade
Auroy and colleagues used voluntary reporting and a telephone hotline
service offering expert advice to estimate the incidence of major
complications of regional anesthesia in France.7 The incidences of
block related neuropathy were 2.9 (0 – 14.5), interscalene block; 1.8 (0
– 6.3), axillary block; 2.9 (0 – 7.8), femoral block and 2.4 (0 – 8.2),
sciatic block [n/10,000, 95% CI]. From a total of 50,000 PNB there were
12 neurologic complications and 7 had sequelae at 6 months. The
Australasian Regional Anaesthesia Collaboration collected data on a
total of 6950 patients who received 8189 PNB.8 Of the 6950 patients,
6069 patients were successfully followed up. In these 6069 patients,
there were a total of 7156 PNB forming the denominator for late
neurologic complications. Thirty patients (0.5%) had clinical features
(paresthesia 22, pain 4, motor 3 and none 1) meeting the criteria for
neurologic assessment. Three of the 30 patients had a block-related
nerve injury, giving an incidence of 0.4 per 1000 blocks (95%
confidence interval, 0.08-1.1:1000). The remainder of the 30 patients
had patient etiologies (cervical spine degeneration, ulnar entrapment,
carpal tunnel syndrome, lumbar canal stenosis, diabetic and peripheral
neuropathies, n = 9), surgical etiologies (swelling, direct trauma,
peroneal injury, n = 7) or anesthesia was excluded as the cause (n = 9).
Anatomical, patient, surgical and anesthetic factors
The brachial plexus is a long and complex structure that is tethered
medially to the vertebral transverse processes and laterally to the
axillary fascia. The attachments of the brachial plexus together with the
high ratio of neural to connective tissue in its proximal components may
place it at risk of stretch or compression injuries.9 It is therefore not
surprising, that neurological sequelae after interscalene block and
shoulder surgery are not uncommon, but fortunately most neurologic
features resolve with time.10,11 An editorial written by Hebl12 that
accompanied a case report of brachial plexopathy after ultrasoundguided interscalene block in a patient with multiple sclerosis highlighted
important factors relating to the neurologic complications associated
with PNB. The main message was that PNI often originate from multiple
sources and that patient, surgical and anesthetic factors may all be
contributory in determining outcome. In addition, distinguishing between
these factors may be difficult if not impossible for a given case. Of note
surgical patients may have a preoperative subclinical neuropathy that
becomes clinically evident in the postoperative period. Entrapment
neuropathies may involve the ulnar, median, lateral femoral cutaneous
nerves or proximal nerve roots. The ulnar nerve is particularly
vulnerable at the elbow and its course through the superficial
postcondylar groove and cubital tunnel place it at risk of compression.
When the elbow is extended the ulnar groove is smooth, round and
capacious. However, in flexion the nerve is flattened and tortuous in a
narrow canal with an aponeurosis pulled tightly across it. In elbow
flexion, the ulnar nerve can sublux across the medial humeral
epicondyle to wear the full brunt of the compression. A further dynamic
is supination/pronation and with a forearm supinated in a patient
positioned supine, the olecranon wears the pressure, but in pronation
the nerve in the groove is more exposed. Therefore flexion of the elbow
and pronation of the forearm places the nerve at increased risk.13 Risk
factors for ulnar neuropathy include male gender, extremes of body
habitus and prolonged admission.14 Postoperative forearm and wrist
swelling may induce an acute median nerve neuropathy or exacerbate
existing carpal tunnel syndrome. Spinal canal stenosis is relevant to PNI
in that its severity may be asymmetrical and may exaggerate what may
have otherwise been a mild deficit. Intrinsic peripheral neuropathies
may have many causes including diabetes, vascular disease,
chemotherapy and other metabolic etiologies.15 Familial peripheral
neuropathies may require only a mild insult such as pressure resulting
in PNI. Medical conditions that adversely impact on the caliber and
function of the small blood vessels that supply nerves are potential risk
factors. These include diabetes, cigarette smoking and hypertension. In
summary, surgical patients frequently have comorbidities that result in
preoperative neural compromise, theoretically placing them at increased
risk of PNI.
Surgical procedures have a native risk of nerve injury and this has been
highlighted in recent studies. Tourniquet neuropathy can cause nerve
damage either by ischemia or mechanical deformation with damage
greatest at the edge of the tourniquet and the fast conducting
myelinated fibers the most vulnerable. The main findings of tourniquet
neuropathy are motor loss, diminished touch, vibration and position
sense and preserved senses of heat, cold and pain. The risk of
tourniquet neuropathy is reduced by wider cuffs, inflation pressure just
adequate for arterial occlusion and reducing the total duration of
inflation. During major orthopedic surgery patients are placed in
positions they would not normally tolerate if not anesthetized. In addition
physical force, compression, contusion and stretch are additional
mechanisms of nerve injury. The risk of regional anesthesia has been
examined recently in the context of total knee arthroplasty in 20-year
cohort study.16 During the time period of the study, there was a
substantial increase in utilization of PNB, however there was no change
in the incidence of PNI. PNI within 3 months of TKA was not associated
with PNB or anesthesia type. PNI risk was increased with age and
tourniquet time.
Mechanisms of nerve injury related to regional anesthesia include direct
toxicity of local anesthetics (concentration and time dependent) and
mechanical trauma from the needle and/or injectate.17 A cadaver sciatic
nerve model has indicated that as few as 3% of fascicles may be injured
during deliberate intraneural injection.18 The clinical implications of this
and other experimental models (e.g. animal) are unknown and of note,
no deliberate human intraneural model incorporating histological
analysis will be possible. Peripheral nerve injection injury has been
studied recently in a rodent model and demonstrated that even
extrafascicular injection of ropivacaine caused marked histologic
abnormalities, although not as severe as intrafascicular injection.19
In summary, postoperative neurologic sequelae following PNB are not
infrequent and most resolve. The incidence of serious neurologic
complications related to PNB is infrequent or rare. Distinguishing and
determining the relative contribution of each of those factors is
challenging. PNI frequently have patient, anesthetic and surgical
etiologies with evidence mounting that support its complex and
multifactorial etiology.
1.
Moen V, Dahlgren N, Irestedt L: Severe neurological
complications after central neuraxial blockades in Sweden 1990-1999.
Anesthesiology 2004; 101: 950-9
2.
Wang LP, Hauerberg J, Schmidt JF: Incidence of spinal epidural
abscess after epidural analgesia: a national 1-year survey.
Anesthesiology 1999; 91: 1928-36
3.
Cameron CM, Scott DA, McDonald WM, Davies MJ: A review of
neuraxial epidural morbidity: experience of more than 8,000 cases at a
single teaching hospital. Anesthesiology 2007; 106: 997-1002
4.
Horlocker TT, Wedel DJ: Infectious complications of regional
anesthesia. Best Pract Res Clin Anaesthesiol 2008; 22: 451-75
5.
Cook TM, Counsell D, Wildsmith JA: Major complications of
central neuraxial block: report on the Third National Audit Project of the
Royal College of Anaesthetists. Br J Anaesth 2009; 102: 179-90
6.
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7.
Auroy Y, Benhamou D, Bargues L, Ecoffey C, Falissard B,
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8.
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9.
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after interscalene blockade in a patient receiving cisplatin
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intraneural needle insertion. Reg Anesth Pain Med 2009; 34: 201-5
19. Whitlock EL, Brenner MJ, Fox IK, Moradzadeh A, Hunter DA,
Mackinnon SE: Ropivacaine-induced peripheral nerve injection injury in
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