| Overview of the Incidence and Etiology of Neurologic Complications of Regional Anesthesia.
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.
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 ultrasound-guided 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.
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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
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15. Hebl JR, Horlocker TT, Pritchard DJ: Diffuse brachial plexopathy after interscalene blockade in a patient receiving cisplatin chemotherapy: the pharmacologic double crush syndrome. Anesth Analg 2001; 92: 249-51
16. Jacob AK, Mantilla CB, Sviggum HP, Schroeder DR, Pagnano MW, Hebl JR: Perioperative nerve injury after total knee arthroplasty: regional anesthesia risk during a 20-year cohort study. Anesthesiology 2011; 114: 311-7
17. Hogan QH: Pathophysiology of peripheral nerve injury during regional anesthesia. Reg Anesth Pain Med 2008; 33: 435-41
18. Sala-Blanch X, Ribalta T, Rivas E, Carrera A, Gaspa A, Reina MA, Hadzic A: Structural injury to the human sciatic nerve after 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 the rodent model. Anesth Analg 2010; 111: 214-20