Background: Osteoarthritis (OA) is the most widespread chronic joint disease worldwide. Symptomatic knee OA is observed in approximately 12% of individuals more than 60 years of age. Conservative treatments models may not be effective always, and that some of them have serious adverse effects that prompted the researchers to research different treatment methods. In this study, we investigated short-and mid-term effectiveness of intra-articular pulsed radiofrequency (PRF) applied in patients with chronic knee pain due to OA. Methods: This study was carried out in the pain management center of a university hospital between January 2009 and June 2009. The patient record files of 31 patients who received intra-articular PRF were retrospectively reviewed. The antero-lateral area of the knee, where the intervention would be applied, was anesthetized with 1% lidocaine. An introducer needle was placed intra-articularly. PRF was started as 42 C at 2 Hz for 15 minutes. The pain of the patients was evaluated by 10 cm Visual Analog Scale (VAS). Furthermore, the ages, the gender, the symptom duration of the patients, the side of the knee on which the intervention was applied, and the complications were collected for statistical evaluation. Results: Although the mean initial VAS scores of the patients were 6.1 AE 0.9 cm, it was found, respectively, to be 3.9 AE 1.9 cm and 4.1 AE 1.9 cm at the first-and sixth-month follow-ups. In general, a decrease of 32.8% in mean in the VAS scores was achieved in the last follow-up; whereas the rate of patients reporting a minimum decrease of 2 points in the VAS scores was 64.5% and the rate of patients reporting a decrease of !50% in their pain was calculated as 35.5%. Conclusion: PRF applied to the knee joint appears to be an effective and safe method.

It was seen that the cooled radiofrequency used for sacroiliac denervation was an effective and safe method in the short to intermediate term.

Purpose: This study was designed to assess the correlation between the neuroprotective effect of dexmedetomidine and oxidative stress, neural inflammation and mast cell stability in rats with bupivacaine-induced sciatic nerve toxicity. Methods: Forty adult Wistar Albino rats, eight rats per group, were used. Saline (0.3 ml of 0.9%), dexmedetomidine (20 µg/kg), 0.5% bupivacaine or 0.5% bupivacaine+dexmedetomidine (20 µg/kg) was injected into the sciatic nerve. A control group of rats received no injection. Fourteen days after injection, the sciatic nerves were harvested and total oxidant status, total anti-oxidant status, paraoxonase-1, galectin-3 and matrix metalloproteinase 2 and 9 levels were measured in the sciatic nerves. In addition, the presence and status of inflammation, edema, and mast cells were evaluated histopathologically. Results: The combination of dexmedetomidine and bupivacaine alleviated oxidative stress. In addition, it decreased matrix metalloproteinase 9 and galectin-3 levels and increased matrix metalloproteinase 2 levels. Moreover, it stabilized recruited mast cells at the injury site; however, it did not significantly decrease inflammation or edema. Conclusion: Dexmedetomidine may ameliorate bupivacaine-induced neurotoxicity by modulating mast cell degranulation. The neuroprotective effect of dexmedetomidine may make it a suitable adjuvant agent to local anesthetics in peripheral nerve blocks.

Zinc phosphide has been used widely as a rodenticide. Upon ingestion, it gets converted to phosphine gas in the body, which is subsequently absorbed into the bloodstream through the stomach and the intestines and gets captured by the liver and the lungs. Phosphine gas produces various metabolic and nonmetabolic toxic effects. Clinical symptoms are circulatory collapse, hypotension, shock symptoms, myocarditis, pericarditis, acute pulmonary edema, and congestive heart failure. In this case presentation, we aim to present the intensive care process and treatment resistance of a patient who ingested zinc phosphide for suicide purposes.

The antioxidant and anti-inflammatory effects of Dex and MgSO ameliorated the detrimental effects of HCI-induced ALI. However, adverse effects on hemodynamics and lung damage were observed when the two drugs were administered together.