Patellofemoral osteoarthritis does not influence clinical outcomes of fixed-bearing unicompartmental knee arthroplasty.

Unicompartmental knee arthroplasty (UKA) is an ideal surgical approach in treatment of end-stage knee osteoarthritis (KOA), however, indications of UKA have been controversial, and the radiographic and symptomatic patellofemoral osteoarthritis (PFOA) are often considered as a contraindication of medial UKA. 337 fixed bearing UKAs were retrospectively recruited in our joint center between January 1, 2011 and June 30, 2020. There were 105 patients accompanied by PFOA and 232 patients have normal PF joint. International Cartilage Repair Society (ICRS) system was introduced to quantify the degeneration degree of PF joint. Oxford Knee Score (OKS), Forgotten Joint Score (FJS), Kellgren-Lawrence (K-L) classifying system and visual analogue scale (VAS) were adopted to evaluate outcomes between with and without PFOA. There was no significant difference of age, BMI, gender, OKS, FJS and other variables between PFOA and Non-PFOA group. After more than 5 years follow-up, UKA patients with or without PFOA could all achieve a satisfactory improvement of OKS, VAS and FJS score. ROM of the replaced knee increased from preoperative 110° to 130°. 74.3% (78/105) and 75.0% (174/232) patients have no change of K-L grade in PFOA and Non-PFOA group, OKS, FJS, VAS score and ROM were also comparable in all patients and no significant outcomes difference were found between two group. The presence of patellofemoral joint osteoarthritis and anterior knee pain should not be considered to be contraindications to medial fixed-bearing UKA.

Peripheral patellar denervation has a better effect in reducing postoperative anterior knee pain than patellar resurfacing in TKA.

Patellar resurfacing (PR) and peripheral patellar denervation (PD) are common surgical treatments for knee osteoarthritis (KOA) in total knee arthroplasty (TKA). The aim of study was to compare preventive effect on postoperative anterior knee pain (AKP) between PR and peripheral PD in TKA. A total of 202 patients who underwent unilateral TKA were randomized into 3 groups: T, TPD, and TPR. Patients in T group received simple TKA, patients in TPD group received TKA combined PD while patients in TPR group received TKA combined PR. Incidence, intensity, and presentation time of AKP and clinical outcomes were evaluated at 3, 6, 9, 12, 18, and 24 months postoperatively. The incidence of AKP was significantly lower and the intensity of AKP and patients' satisfaction score were significantly better at 3 months after surgery in group TPD and TPR compared with group T. Compared with group TPR, the intensity of AKP was significantly better at 3 months after surgery in group TPD. There were no significant difference in Oxford knee score, range of motion (ROM), patellar score, knee society score (KSS) and activities of daily living (ADL) score among 3 groups in the follow-up period. Both PD and PR can effectively reduce the intensity and incidence of AKP after TKA and improve patients' satisfaction at 3 months after TKA. Additionally, PD is more effective on alleviating AKP than PR.

Beta-adrenergic activation induces cardiac collapse by aggravating cardiomyocyte contractile dysfunction in bupivacaine intoxication.

In order to determine the role of the adrenergic system in bupivacaine-induced cardiotoxicity, a series of experiments were performed. In an animal experiment, male Sprague-Dawley (SD) rats under chloral hydrate anesthesia received intravenous bupivacaine, followed by an intravenous injection of adrenalin or isoprenalin, and the electrocardiogram (ECG), left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), the maximum rate of rise of left ventricular pressure (+dP/dtmax) and the maximum rate of pressure decrease (-dP/dtmax) were continually monitored. In a cellular experiment, freshly isolated adult SD rat ventricular myocytes were perfused with bupivacaine at different concentrations in the presence or absence of isoprenalin, with or without esmolol. The percentage of the sarcomere shortening (bl% peak h), departure velocity (dep v) of sarcomere shortening and time to 50% of the peak speed of myocyte contraction (Tp50) was assessed by a video-based edge-detection system. In an additional experiment, Swiss mice pretreated with saline, isoprenalin, esmolol or dexmedetomidine received bupivacaine to determine the 50% lethal dose (LD50) of bupivacaine. Electron microscopy of myocardial mitochondria was performed to assess damage of these structures. To test mitochondrial reactive oxygen species (ROS) production, freshly isolated SD rat ventricular myocytes were incubated with bupivacaine in the presence of isoprenalin, with or without esmolol. First, our results showed that bupivacaine significantly reduced the LVSP and +dP/dtmax, as well as enhanced the LVEDP and -dP/dtmax (P < 0.05, vs. control, and vs. baseline). Adrenalin and isoprenalin induced a further reduction of LVSP and +dP/dtmax (P < 0.05, vs. before adrenalin or isoprenalin delivery, and vs. control). Second, bupivacaine induced a dose-dependent cardiomyocyte contractile depression. While 5.9 µmol/L or 8.9 µmol/L of bupivacaine resulted in no change, 30.0 µmol/L of bupivacaine prolonged the Tp50 and reduced the bl% peak h and dep v (P < 0.05, vs. control and vs. baseline). Isoprenalin aggravated the bupivacaine-induced cardiomyocyte contractile depression, significantly prolonging the Tp50 (P < 0.05, vs. bupivacaine alone) and reducing the dep v (P < 0.05, vs. bupivacaine alone). Third, esmolol and dexmedetomidine significantly enhanced, while isoprenalin significantly reduced, the LD50 of bupivacaine in mice. Fourth, bupivacaine led to significant mitochondrial swelling, and the extent of myocardial mitochondrial swelling in isoprenalin-pretreated mice was significantly higher than that compared with mice pretreated with saline, as reflected by the higher mitochondrial damage score (P < 0.01). Meanwhile, esmolol pretreatment significantly reduced the mitochondrial damage score (P < 0.01). Fifth, bupivacaine significantly increased the ROS in freshly isolated cardiomyocytes, and added isoprenalin induced a further enhancement of ROS production (P < 0.05, vs. bupivacaine alone). Added esmolol significantly decreased ROS production (P < 0.05, vs. bupivacaine + isoprenalin). Our results suggest that bupivacaine depressed cardiac automaticity, conductivity and contractility, but the predominant effect was contractile dysfunction which resulted from the disruption of mitochondrial energy metabolism. ß-adrenergic activation aggravated the cellular metabolism disorder and therefore contractile dysfunction.

NaHCO3-Buffered Lidocaine Gel for Outpatient Rigid Cystoscopy in Men.

PURPOSE: The purpose of this study was to explore the effect of NaHCO3-buffered lidocaine gel as a topical anesthetic agent for pain relief for rigid cystoscopy. DESIGN: Prospective randomized controlled trial. METHODS: ASA I-II male patients undergoing rigid cystoscopy randomly received 10 mL 2% Carbocaine lidocaine gel with 1 mL 0.9% saline (group 1) or 1 mL 5% NaHCO3 solution (group 2). After 3 minutes exposure, the cystoscope was inserted into the urethra. On receiving the gel, cystoscope insertion, and intravesical observation, pain score was recorded using the visual analog scale. FINDINGS: The gel pH with or without NaHCO3 was 7.20 and 6.41, respectively. The concentration of soluble lidocaine in the gel was stable for 24 hours or more. The visual analog scale score in group 2 was significantly lower (1.3 ± 0.9) than in group 1 (5.28 ± 1.99). No adverse effects were recorded. CONCLUSION: Alkalized lidocaine gel resulted in successful analgesia for rigid cystoscopy in men without adverse effects.

Effectiveness of retigabine against levobupivacaine-induced central nervous system toxicity: a prospective, randomized animal study.

PURPOSE: KCNQ2/3 channels play an important role in controlling neuronal excitability. Agents that decrease KCNQ2/3 current amplitudes are proconvulsant, whereas KCNQ2/3 current enhancers are anticonvulsant. Levobupivacaine is able to block the KCNQ2/3 channels and enhance neuronal excitation, whereas retigabine is able to reopen the channels and thus reduce overexcitation of neurons. In this study, we aimed to determine if retigabine is able to abolish local-anesthetic-induced seizures. METHODS: Twenty New Zealand rabbits were randomly divided into two groups of ten. Levobupivacaine (0.5 %) was infused into conscious rabbits via the marginal ear vein at 8 ml/kg/h until the rabbits seized, and 5 mg/kg of retigabine were injected intravenously to terminate the seizure. The corresponding volume of saline was used as a control. The behavior of and the electroencephalogram (EEG) for each rabbit were continually monitored. Before levobupivacaine infusion, the rabbits were placed in a prostrate position calmly on the experimental platform, and the EEG pattern exhibited ß waves. Intravenous levobupivacaine induced a typical EEG seizure characterized by multiple spike and slow wave complexes. The EEG changes were accompanied by behavioral convulsions which were characterized by clonic activity and opisthotonus. RESULTS: Retigabine effectively terminated the electrographic and behavioral seizures. After receiving 5 mg/kg of retigabine, the animals became drowsy, and the EEG changed to δ waves. CONCLUSIONS: We propose that KCNQ2/3 channels play an important role in levobupivacaine-induced central nervous system toxicity, and a KCNQ2/3 channel activator may be used to treat levobupivacaine-induced convulsions.

Inhibition of Kv7/M Channel Currents by the Local Anesthetic Chloroprocaine.

BACKGROUND: Chloroprocaine is a local ester anesthetic, producing excellent sensory block in clinical use. The Kv7/M potassium channel plays an important role in the control of neuronal excitability. In this study, we investigated the effects of the local anesthetic chloroprocaine on Kv7/M channels as well as the effect of retigabine on chloroprocaine-induced seizures. METHODS: A perforated whole-cell patch technique was used to record Kv7 currents from HEK293 cells and M-type currents from rat dorsal root ganglion (DRG) neurons. RESULTS: Chloroprocaine produced a number of effects on Kv7.2/Kv7.3 currents, including a lowering of current amplitudes, a rightward shift in the voltage-dependent activation curves, and a slowing of channel activation. Chloroprocaine had a more selective inhibitory effect on the homomeric Kv7.3 and heteromeric Kv7.2/Kv7.3 channels than on the homomeric Kv7.2 channel. Chloroprocaine also inhibited native M channel currents and induced a depolarization of the DRG neuron membrane potential. CONCLUSION: Taken together, the findings indicate that chloroprocaine concentration dependently inhibited Kv7/M channel currents.