Discussion
Multimodal analgesia is currently a standard treatment for pain control. Nonsteroidal anti-inflammatory drugs play an essential role in reducing opioid consumption and acute postoperative pain management in orthopedic surgeries, including TKA. However, some patients are subject to the adverse effects of NSAIDs when prescribed systemically due to their potential side effects. Therefore, systemic NSAIDs are usually avoided in these patients, leading to inadequate pain control postoperatively. Our study aimed to focus on postoperative pain control following TKA in these challenging patients by adding SNB to ACB and PIA blocks. To our knowledge, this is the first study in TKA focusing on the NSAIDs susceptible patients.
In this study, pain scores (both at rest and on movement), as well as 24-h morphine consumption, were significantly lower in the SNB group compared to the control group. In the previous studies, SNB was an effective rescue block in patients with severe posterior knee pain.[9,19] However, adopting such a rescue block might be problematic at wards with limited medical personnel and equipment. To the best of our knowledge, only a few studies were published in the literature evaluating the addition of SNB to ACB and PIA in pain management after TKA. Kampitak et al. reported that SNB utilizing 0.25% levobupivacaine (15 ml) with an ACB and PIA decreased morphine consumption. Nevertheless, the SNB group demonstrated a statistical difference in its degree of pain reduction relative to an obturator-nerve-block group.[20] The other study from the same group of authors also compared SNB (0.25% levobupivacaine 15 ml) to the interspace between the popliteal artery and the capsule of the posterior knee (IPACK block) after TKA.[16] They reported a higher incidence of a motor blockade in the SNB group than IPACK, but the SNB group had a lower incidence of posterior knee pain. In both studies, SNBs were performed with a higher concentration of local anesthetic and included postoperative NSAIDs in the protocol. In comparison, our study used a low-dose SNB (20 ml of 0.125% bupivacaine) and dexamethasone (5 mg) combined with PIA and ACB and revealed the effectiveness for post-TKA pain control without motor weakness. Despite no systemic NSAIDs given, low-dose SNB was still significantly decreased pain scores at rest, on motion, and anterior knee up to 18–24 h following TKA.
Although we primarily hypothesized that pain would be alleviated in the SNB group due to the analgesia in the sciatic nerve distribution, mainly to reduce posterior knee pain. However, the median posterior knee pain score was reduced only at 12 h. One of the reasons would be our intention to use a low concentration of bupivacaine (0.125%) for SNBs to limit local anesthetic doses. With this concentration, the patients might not be able to characterize the specific area of pain, particularly if the pain was mild. Secondly, only 5 (20%) patients (1 in the SNB and 4 in the control group) reported moderate-severe posterior knee pain. Due to the small sample size, it might be challenging to demonstrate the statistical difference in posterior knee pain. The incidence of moderate-severe posterior knee pain in our study also correlates to the previous studies by Gi et al. and Kampitak et al. The authors reported that 10–30% of the patients underwent TKA with a femoral nerve block and PIA had posterior knee pain.[16,21] Therefore, the benefit from adding SNB to adductor canal block and PIA may not be solely explained by posterior knee pain reduction.
We also added dexamethasone 5 mg to the SNB, while the control group patients did not receive dexamethasone. It has been well-demonstrated that dexamethasone is an effective adjunct to other multimodal analgesia techniques for postoperative pain control in TKA, regardless of the routes of administration.[18,22–24] Although a meta-analysis by De Oliveira et al. had reported that low dose dexamethasone (< 0.1 mg/kg) did not provide opioid-sparing effect or analgesia during the early postoperative period (< 4 h), however, dexamethasone significantly reduced late pain scores (24 h) both at rest and on movement, even at low dose.[24] Since we compared pain scores at 6–24 h postoperatively, dexamethasone given in the SNB injections to prolong the duration of the block may potentially be a confounder in our study and caused better pain relief in the SNB group compared to the control.
Although the mean 24-h morphine consumption was statistically lower in the SNB group (1.96 ± 2 mg Vs. 3.80 ± 2.48 mg), the slight difference may have modest clinical effects. The overall morphine consumption in our study was relatively lower than that reported from the earlier studies in patients with TKA. The reason might be that the patient-controlled analgesia was not cooperated in our protocol for morphine administration. Additionally, in older studies, 24-h morphine consumption and pain score were relatively high because multimodal analgesia combined with ultrasound-guided peripheral nerve block technique had not yet been a standard of care.[19,25] Among newer studies in which multimodal analgesia was utilized with improvement in peripheral nerve block technique and PIA, average total doses of 24-h morphine consumption also ranged only between 2 and 10 mg.[9,16,26] In our study, overall 24-h morphine consumption was considered low in both groups, and the difference was only approximately 2 mg which may not have significant clinical effects. The combination of ACB and PIA had already provided substantial pain control for most patients even without the use of NSAIDs. Therefore, the further opioid-sparing benefit of SNB was not well determined.
The risks of bupivacaine toxicity when combining several blocks must be taken into account. We limited the total dose of bupivacaine for the peripheral nerve blocks not to exceed 1.7 mg/kg (75 mg for 45 kg patient). Also, 100 mg of PIA was a low range commonly used in other studies, 100–400 mg, due to minimal absorption at this injection site and was considered safe by several studies.[16,27,28] Additionally, the duration between performing the peripheral nerve blocks and the PIA was about 90–120 min, resulting in a mismatch of the peak plasma concentration of bupivacaine. The peak plasma concentration of peripheral nerve block is at 60 min,[29–31] while the peak plasma concentration of PIA is at 24–48 h.[32] Previous studies showed that the total plasma concentrations of the maximum recommended doses of bupivacaine used in the peripheral nerve block and the PIA remained below half of the described toxicity thresholds. The margin of safety was probably much broader than current standards or the manufacturer's recommended dose.[29–32] However, all patients were closely monitored for the local anesthetic systemic toxicity (LAST) because of high doses of the local anesthetic in this study, especially in low body weight patients.
There are some limitations to this study. First, this was a single-center study using a small sample size, which had led to limitations for the analysis of the difference in posterior knee pain. Secondly, we did not use patient-controlled analgesia for administering morphine postoperatively, therefore, it might underrepresent the 24-h morphine dose. Third, NSAIDs was still used in this study as a single dose of ketorolac in PIA. Only systemic NSAIDs was omitted. Finally, dexamethasone added into the SNB for an extended duration of analgesia may be a potential confounder for better pain control in the SNB group.
BMC Anesthesiol. 2021;21(282) © 2021 BioMed Central, Ltd.
