Complication
Nerve localization technique
Nerve stimulation (N = 2507)
Ultrasound (N = 5141)
Other (N = 541)
Total (N = 8189)
Local anesthetic toxicity
1.2 (0.25–3.5)
0.8 (0.2–2.0)†
1.8 (0.05–10.3)
0.98 (0.42–1.9)
Inadvertent vascular puncture††
13.9 (8.2–21.9)
5.1 (3.0–8.1)*
2.3 (0.06–12.8)
7.2 (5.1–10.0)
Unintended paresthesia††
10.8 (5.9–18.1)
20.5 (15.9–25.9)†
2.3 (0.06–12.8)
16.8 (13.4–20.8)
Late neurologic deficit
0.8 (0.1–2.9)
0.2 (0.005–1.1)†
–
0.4 (0.08–1.1)
Long-term neurologic deficit
0.4 (0.01–2.2)
0.2 (0.05–1.1)†
–
0.2 (0.03–0.9)
Data quality control methods developed during this study period included hospital-specific random and systematic checks comparing database content with medical records and audits to ensure all cases were captured (e.g., operating list or notes compared with database entry). In addition, monthly audits (for follow-up rates and trends indicating data collection issues) and spot checks were performed to identify and correct missing data. Investigators received feedback regarding any data quality issues. Key project requirements were communicated regularly with investigators and data collectors using individual and conferences phone calls, emails, personal correspondence, newsletters, and written material. Other strengths of this project included:
- 1.
Systematic postoperative contact with patients, proactively seeking complications. A systematic approach to capturing complications is associated with more reliable capture of complications compared to a passive approach [7]. Without this approach, there is a risk of either over-diagnosing or missing complications.
- 2.
A defined follow-up and neurologic referral and investigative pathway [6]. The project also utilized a standardized questionnaire for detecting patients with potential complications.
- 3.
Clear definition and verification of all key outcomes—clear definitions for nerve injury due to PNB and other adverse events were utilized so as to improve reliability of the results.
- 4.
Robust neurologic evaluation —it was only by evaluating patients with a focused history and examination, electro diagnostic tests and imaging studies that we were able to separate PNB causes of injury from those unrelated to PNB. In total, 26 out of 30 patients had electro diagnostic tests and 10 patients had magnetic resonance imaging.
- 5.
Web-based central database—all practitioners utilized the same database with the same fields. In addition, the outcome definitions were readily available on the online interface using context-sensitive links.
- 6.
Anonymity—all results were presented without identifying the patient, anesthesiologist, or hospital.
Clearly, maintaining patient anonymity is essential in any case report. Maintaining anesthesiologist and hospital anonymity potentially improved compliance with the project.
This study had limitations and challenges that have been previously described [6]. Study limitations included the timing (1 week or 6 weeks) of and proportion of patient follow-up (87 %). Follow-up at 6 weeks, as occurred in 34 % of our patients, may have missed nerve injury presenting in the early postoperative period but had resolved by time of contact. The incidence and time course of neurologic features has been well studied following shoulder surgery and interscalene blockade where early in the postoperative period the proportion of patients with neurologic features was temporarily high, with almost all patients having complete recovery [8, 9] The significance of early postoperative neurologic symptoms is important because the results of these studies are often interpreted as being PNB-related nerve injury [10]. In one study, minimal attempt was made to determine etiology, for example, there was no standardized neurologic investigative pathway that included electro diagnostic tests [9]. Candido concluded that symptoms in the C5–6 distribution were likely to represent complications related to interscalene block; however, distal mononeuropathies (e.g., in the ulnar nerve distribution) were unlikely to represent PNB-related nerve injury . Regarding proportion of patients successfully contacted, the author believes that patients with complications would actually be more likely than not to present back to their original hospital with a complaint. In addition, the denominator for the incidence of nerve damage was only calculated from the number of PNB s performed in the number of patients successfully contacted. It is for these reasons that we consider the denominator calculation and incidence accurate [6]. The numbers of some block types are low, and therefore we cannot calculate the incidence of injury for individual PNB types. The reliance on phoning patients (most commonly) rather than direct physical evaluation to detect potential complications is a study limitation. However, the resources required to assess in person every patient would have been prohibitive.
Results from the Australian and New Zealand Registry of Regional Anaesthesia
An important objective of continuing and developing the registry project was to obtain results from a larger patient cohort providing a more accurate estimate of the range in which the true incidence of PNB-related nerve injury value is likely to be. During the period of study January 2006 to May 2012, a total of 63 patients met a trigger for referral to neurology (new onset of motor/sensory deficit, non-resolving paresthesia, allodynia/dysesthesia, surgical referral) [11]. The most common presenting feature was a sensory deficit (most commonly paresthesia, followed by dysesthesia, allodynia) in the distribution of the PNB in 48 (76 %), followed by pain in 8 (13 %) and motor deficit in 6 (9.5 %), and in one patient the finding was incidental. Foot drop associated with knee arthroplasty was the most common motor presentation. Nine out of 63 patients referred had a defined diagnosis of generalized preoperative neuropathy confirmed with electro diagnostic testing. Postoperative investigations revealed that 20 patients had a specific mononeuropathy diagnosed distal to the site of PNB . Examples of these mononeuropathies were ulnar neuropathy localized to the elbow, median neuropathy localized to the wrist, radial neuropathy localized at the humerus, and common peroneal neuropathy localized to the fibular head.
There were a total of 11 patients with PNB-related nerve injury . There were five patients who had a mild femoral neuropathy following total knee arthroplasty and 4/5 patients were designated as having a PNB-related injury. From the 11 patients diagnosed with PNB-related deficits, four patients had preoperative chronic pain issues, one had peripheral vascular disease, three had a defined peripheral neuropathy, and six required a pneumatic tourniquet for their surgery. Four patients had more than one intraoperative risk factor (neuropathic pain, positioning, preoperative neuropathy, spinal canal stenosis, tourniquet, chronic pain, diabetic neuropathy, microvascular disease). The duration of postoperative deficit in the 11 patients with PNB-related nerve injury was: less than 6 months (n = 5); 6–12 months (n = 1) and greater than 12 months (n = 4). One patient with a complex medical history including a likely preexisting vasculitic neuropathy had a persisting motor deficit. Table 27.2 presents incidences of late and long-term neurologic complications from ARAC, AURORA, and ARAC/AURORA combined. Table 27.3 presents incidences of neurologic complications for specific PNB types. When brachial plexus, femoral, and sciatic blocks are included as the denominator (19,353 PNB), the incidences of PNB-related late and long-term neurological deficits are 0.6 (0.28–1.01) and 0.30 (0.11–0.67) [n per 1000 PNB, 95 % Confidence Interval], respectively. Long-term neurologic deficit defined as the criteria for late neurologic deficit having been met, and with persistence of symptoms for greater than 6 months after onset [11]. At the time of writing this chapter, the author is analyzing a larger cohort including patients recruited to May 2014.
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Table 27.2
Incidences of late and long-term neurologic complications from ARAC, AURORA, and ARAC/AURORA combined
Late neurologic deficit | Long-term neurologic deficit | |
|---|---|---|
ARAC | ||
Ultrasound (N = 5141) | 1 | 1 |
0.2 (0.005–1.1) | 0.2 (0.005–1.1) | |
No ultrasound (N = 3048) | 2 | 1 |
0.7 (0.08–2.4) | 0.3 (0.008–1.8) | |
Total (N = 8189) | 3 | 2 |
0.4 (0.08–1.1) | 0.2 (0.03–0.9) | |
AURORA | ||
Ultrasound (N = 17,831) | 7 | 3 |
0.4 (0.16–0.8) | 0.2 (0.03–0.5) | |
No ultrasound (N = 3563) | 1 | 1 |
0.3 (0.007–1.6) | 0.3 (0.007–1.6) | |
Total (N = 21,646) | 8 | 4 |
0.4 (0.2–0.7) | 0.2 (0.05–0.5) | |
ARAC/AURORA combined | ||
Ultrasound (N = 22,972) | 8 | 4 |
0.3 (0.2–0.7) | 0.2 (0.05–0.4) | |
No ultrasound (N = 6611) | 3 | 2 |
0.5 (0.09–1.3) | 0.3 (0.04–1.1) | |
Total = 29,835 | 11 | 6 |
0.4 (0.2–0.7) | 0.2 (0.07–0.4) | |
ARAC indicates Australasian Regional Anaesthesia Collaboration (2006 to May 30 2008), AURORA Australian and New Zealand Registry of Regional Anesthesia (June 1 2008 to May 30 2012), PNB indicates peripheral nerve or plexus block, and N the total number in each PNB category. Results expressed as number of events, n per 1000, (95 % Confidence Interval). Late neurologic deficits related to anesthesia were defined as a new onset of sensory and/or motor deficit consistent with a nerve/plexus distribution without other identifiable cause, and one of the following: electrophysiological evidence of nerve damage; new neurologic signs; new onset of neuropathic pain in a nerve distribution area; paresthesia in relevant nerve/plexus distribution area. Long-term neurologic deficit was defined as the criteria for late neurologic deficit having been met, and with persistence of symptoms greater than 6 months after onset. No technology designated in 252. Source: Barrington, M. J. (2012). The quality and safety of peripheral regional anesthesia. Ph.D. thesis, Department of Anatomy and Neuroscience, Faculty of Medicine, Dentistry and Health Sciences, The University of Melbourne
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