Regional Anesthesia and Pain Medicine • Volume 39, Number 6, November-December 2014

TABLE 1. Primary Anesthesia, Visual Analog Scale Score, and Nerve Blocks VAS Score Primary Anesthesia ± Nerve Block GA GA + FNB GA + FNB + SNB Spinal Spinal + FNB Spinal + FNB + SNB Total

No. Mild Moderate Severe No. Patients Receiving Patients (VAS 0–3) (VAS 4–6) (VAS >6) Rescue Analgesia 1 85 5 2 81 2 176

0 52 4 2 68 1 127

One hundred seventy-six patients scheduled for TKA received the anesthesia and nerve blocks shown in Table 1 and as follows: GA alone (1), GA + FNB (85), GA + FNB + SNB (5), spinal alone (2), spinal + FNB (81), spinal + FNB + SNB (2). General anesthesia–alone patient had no nerve block and required patient-controlled analgesia with morphine. Sixteen percent (GA + FNB) had VAS score of more than 6, which received rescue analgesia. None of the patients (GA + FNB + SNB) required further analgesia. Surprisingly, 2 spinal (no nerve block) patients did not require further analgesia. Eleven percent of patients (spinal + FNB) required rescue analgesia. Two patients (spinal + FNB + SNB) did not require further analgesia. We are aware that sciatic nerve injury after TKA is a well-established complication with an overall incidence of 0.2% to 2.4%.3–5 Some risk factors, such as valgus deformity of more than 10 degrees, total tourniquet time of more than 120 minutes, preexisting neuropathy, and postoperative bleeding, have been described.4 The surgical procedure also places significant stress on the sciatic nerve, and the blood supply to the nerve can be decreased by additional perioperative factors such as tourniquet, vasoconstrictor use, and accidental intraneural injection.5 Preoperative SNB not only increases the risk of neural injury theoretically but also could delay diagnosis and treatment of that injury. An electromyographic study done before and after TKA shows that almost 30% of neural damage is undetectable clinically; furthermore, half of the sciatic nerve injuries show incomplete recovery after 5 years.5 Although improvement in analgesia by adding sciatic nerve does not justify the above risks, nevertheless, some patients suffer from severe pain in the distribution of the sciatic and obturator nerves. Based on our experience, we advocate SNB by the anterior approach as a rescue block rather than performing it preoperatively in all patients with FNB, thus sparing 87% patients from potential ill effects of SNB.

1 17 1 0 4 1 37

0 16 0 0 9 0 26

1 (100%) 14 (16%) 0 0 9 (11%) 0 24 (13%)

Joselo Macachor, MD, DPBA Uday Ambi, MD Mary J. Baula, MD, DPBA Bin Wern Hsien, MBBS, MMed Chandra M. Kumar, MBBS, MSc, FFARCS, FRCA, EDRA Department of Anesthesia Khoo Teck Puat Hospital 90 Yishun Central Singapore

The authors declare no conflict of interest. REFERENCES 1. Sato K, Adachi T, Shirai N, Naoi N. Continuous versus single-injection sciatic nerve block added to continuous femoral nerve block for analgesia after total knee arthroplasty: a prospective, randomized, double-blind study. Reg Anesth Pain Med. 2014;39:225–229. 2. PROSPECT. Overall recommendations for postoperative pain management for total knee arthroplasty. Web site. Available at: Accessed June 24, 2014. 3. Mariano ER, Cheng GS, Choy LP, et al. Electrical stimulation versus ultrasound guidance for popliteal-sciatic perineural catheter insertion: a randomized controlled trial. Reg Anesth Pain Med. 2009;34:480–485. 4. Horlocker T, Cabanela ME, Wedel DJ. Does postoperative epidural analgesia increase the risk of peroneal nerve palsy after total knee arthroplasty? Anesth Analg. 1994;79:495–500. 5. Engerlhardt P, Roder R, Kohler M. Neurologic complications in implantation of knee endoprostheses: a clinical and GMG-documented study. Z Orthop Ihre Grenzgeb. 1987;125:190–193.

Reply to Dr Kumar Accepted for Publication: August 12, 2014. To the Editor: e thank Kumar and colleagues for their comments on our study, which have given us an opportunity to contribute


© 2014 American Society of Regional Anesthesia and Pain Medicine

Letters to the Editor

additional thoughts on sciatic nerve block (SNB) in patients undergoing total knee arthroplasty (TKA).1 Sciatic nerve injury, especially peroneal nerve injury, is a well-recognized and potentially devastating complication of TKA, although this complication is rare. Kumar et al pointed out 2 disadvantages of performing SNB preoperatively. First, SNB may increase the risk of peroneal nerve injury. Second, SNB may delay the diagnosis and treatment of that injury. We should consider carefully the major cause of sciatic nerve injury as a complication of TKA and the treatment strategies when it occurs. Although the definite cause of sciatic nerve injury after TKA remains uncertain, the theory most accepted is that the surgical correction of the malalignment, which stretches the sciatic nerve, contributes to the development of sciatic nerve injury.2 Patients with valgus deformity or flexion contracture were described to be predisposed to sciatic nerve injury because of this mechanism.3 Other additional factors are previous neuropathy, the pressure from soft tissue swelling, compressive dressings after surgery, hematoma, and prolonged tourniquet time. Does SNB really increase the risk of sciatic nerve injury by TKA? In our study, patients with valgus deformity, flexion contracture, and previous neuropathy were excluded, in order to avoid the potential sciatic nerve injury. We believe that preoperative SNB is beneficial in the selected patients. Once sciatic nerve injury occurs, immediate removal of any constrictive dressing and flexion of the knee are recommended.3 In our study, if we could not confirm the normal sciatic motor function postoperatively, we checked the pressure of dressings and kept the knee flexed not to stretch the sciatic nerve. It is recommended that patients with symptoms of peroneal nerve dysfunction who are having difficulty achieving an acceptable range of motion 4 weeks after TKA be considered for the surgical release of the peroneal nerve.4 We believe that SNB cannot delay the treatment of potential sciatic nerve injury. However, transient sciatic motor dysfunction by continuous SNB is common in our study, which inhibits early rehabilitation after TKA. We have to say that continuous SNB is problematic from the point of view of rehabilitation, and we agree that there are many institutions where SNB is not applied to patients undergoing TKA on this account. Unless SNB is performed, moderate to severe pain after TKA is common even if multimodal analgesia system is provided. The experiences of Kumar and colleagues showed 36% of patients felt moderate to severe pain after surgery, and


Copyright © 2014 American Society of Regional Anesthesia and Pain Medicine. Unauthorized reproduction of this article is prohibited.

Letters to the Editor

this may be underestimated because of the nature of retrospective study. Selective tibial nerve block may be a good way to balance the peroneal motor function and postoperative analgesia.5 Keita Sato, MD Department of Anesthesiology Tokyo Women’s Medical University Tokyo, Japan

Takehiko Adachi, MD, PhD Department of Anesthesiology Kitano Hospital Osaka, Japan

The authors declare no conflict of interest. REFERENCES 1. Sato K, Adachi T, Shirai N, et al. Continuous versus single-injection sciatic nerve block added to continuous femoral nerve block for analgesia after total knee arthroplasty: a prospective, randomized, double-blind study. Reg Anesth Pain Med. 2014;39:225–229. 2. Krackow KA, Maar DC, Mont MA, et al. Surgical decompression for peroneal nerve palsy after total knee arthroplasty. Clin Orthop Relat Res. 1993;292:223–228. 3. Nercessian OA, Ugwonali OF, Park S. Peroneal nerve palsy after total knee arthroplasty. J Arthroplasty. 2005;20:1068–1073. 4. Zywiel MG, Mont MA, McGrath MS, et al. Peroneal nerve dysfunction after total knee arthroplasty: characterization and treatment. J Arthroplasty. 2011;26:379–385.

Regional Anesthesia and Pain Medicine • Volume 39, Number 6, November-December 2014

to present for surgical procedures. The patient and her family consented to the presentation of this case. A 22-year-old, 5-ft-2-in, 59-kg woman with PA was scheduled for an outpatient calcaneal osteotomy, lateral column lengthening, and tendon transfer of the left foot. Her medical history was also significant for dilated cardiomyopathy with an ejection fraction of 45%. Before surgery, ultrasoundguided popliteal and adductor canal saphenous blocks were performed using an inplane technique with a 100-mm Stimuplex needle (B. Braun Medical, Melsungen, Germany). A SonoSite S-Nerve ultrasound system (Bothell, Washington) was used for the block procedure, and 30 and 10 mL of 0.5% ropivacaine were injected around the sciatic and saphenous nerves, respectively. The patient underwent an uneventful surgery with dexmedetomidine sedation. No narcotics or additional analgesics were given in the operating room or the postanesthesia care unit. She was pain-free in the postanesthesia care unit and at home until block resolution the following morning. The patient was contacted 1 week later, and she denied any symptoms of nerve injury. Mitochondrial diseases are a heterogeneous group of disorders that result in patients having abnormal cellular energy metabolism. Propionic acidemia is a rare, life-threatening, autosomal recessive, mitochondrial disease affecting fewer than 1 in 100,000 live births.1 A genetic mutation results in a deficiency of propionyl-CoA carboxylase, an enzyme responsible for

catalyzing propionyl-CoA to methylmalonylCoA inside the mitochondria (Fig. 1) before entering the Krebs cycle, which is essential for ATP formation. The decision to perform peripheral nerve blocks on a patient with a known mitochondrial disorder is controversial because of the theoretical concern for an increased risk of local anesthetic systemic toxicity. Local anesthetics are known inhibitors of mitochondrial ATP production,2,3 and depending on the type and severity of the disorder, this inhibition may be deleterious in patients with preexisting mitochondrial dysfunction. Despite this, it has been reported that local anesthetics have been used safely (presumably via infiltration) in patients with mitochondrial disorders.2 Our patient reported that her wisdom teeth were uneventfully extracted under local anesthesia, and this was at least partly reassuring with respect to her ability to tolerate local anesthetics. Anesthesiologists should be cautious with local anesthetic doses to minimize the risk of local anesthetic systemic toxicity, particularly because the effects of intralipid rescue in this patient population are unknown. Because metabolism of fatty acids is known to contribute to the reversal of bupivacaine cardiac toxicity by lipid emulsion infusion, it is possible that lipid emulsion’s benefits are reduced when fatty acids are metabolized less efficiently.4 Our limited but favorable experience in a patient with PA suggests that regional anesthesia may be safe in select patients with mitochondrial disorders.

5. Sinha SK, Abrams JH, Arumugam S, et al. Femoral nerve block with selective tibial nerve block provides effective analgesia without foot drop after total knee arthroplasty: a prospective, randomized, observer-blinded study. Anesth Analg. 2012;115:202–206.

Peripheral Nerve Block in a Patient With Propionic Acidemia Accepted for publication: July 30, 2014. To the Editor: e would like to relate our experience with the use of peripheral nerve blocks in a patient with propionic acidemia (PA). We believe that this is the first reported use of ultrasound-guided peripheral nerve blocks as a primary anesthetic in a patient with a mitochondrial disorder. As increasing numbers of patients with this and other uncommon metabolic disorders are living to adulthood, they are more likely



FIGURE 1. Metabolic pathway. Propionyl-CoA carboxylase (PCC) catalyzes the conversion of propionyl-CoA to methylmalonyl-CoA, which enters the Krebs cycle via succinyl-CoA. Sources of propionate include valine, isoleucine, threonine, methionine, odd-chain fatty acids, and cholesterol. Deficiency of PCC results in PA and accumulation of 3-OH propionate, methylcitrate, and glycine, among other metabolites. PCC is located inside the mitochondrion. PCC, a heterododecamer (α6β6), comprises 6 α-subunits (orange) and 6 β-subunits (purple). Biotin (blue), bicarbonate, and ATP have binding sites in the α-subunit. The β-subunits form a central core. Reprinted with permission from Carrillo-Carrasco N, Venditti C. Propionic Acidemia. In: Pagon RA, Adam MP, Bird TD, Dolan CR, Fong CT, Stephens K, eds. GeneReviews™ [Internet]. Seattle (WA): University of Washington, Seattle; 1993–2013. 2012 May 17. © 2014 American Society of Regional Anesthesia and Pain Medicine

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