There have been few studies describing wound infiltration with additional intraarticular administration of multimodal analgesia for total knee arthroplasty (TKA). In this study, we assessed the efficacy of wound infiltration combined with intraarticular regional analgesia with epidural infusion on analgesic requirements and postoperative pain after TKA. 40 consecutive patients undergoing elective, primary TKA were randomized into 2 groups to receive either (1) intraoperative wound infiltration with 150 mL ropivacaine (2 mg/mL), 1 mL ketorolac (30 mg/mL), and 0.5 mL epinephrine (1 mg/mL) (total volume 152 mL) combined with intraarticular infusion (4 mL/h) of 190 mL ropivacaine (2 mg/mL) plus 2 mL ketorolac (30 mg/mL) (group A), or (2) epidural infusion (4 mL/h) of 192 mL ropivacaine (2 mg/mL) combined with 6 intravenous administrations of 0.5 mL ketorolac (30 mg/mL) for 48 h postoperatively (group E). For rescue analgesia, intravenous patient-controlled-analgesia (PCA) morphine was used. Morphine consumption, intensity of knee pain (0–100 mm visual analog scale), and side effects were recorded. Length of stay and corrected length of stay were also recorded (the day-patients fulfilled discharge criteria). The median cumulated morphine consumption, pain scores at rest, and pain scores during mobilization were reduced in group A compared to group E. Corrected length of stay was reduced by 25% in group A compared to group E. Peri- and intraarticular analgesia with multimodal drugs provided superior pain relief and reduced morphine consumption compared with continuous epidural infusion with ropivacaine combined with intravenous ketorolac after TKA.

Background: Patients with chronic myeloproliferative neoplasms (MPNs), including essential thrombocythemia (ET), polycythemia vera (PV), and primary myelofibrosis (PMF), are at high risk of vascular complications. However, the magnitude of this is risk not well known and the possible effect of comorbidity is poorly understood. Aim: Our aim was to compare the risk of vascular diseases in patients with MPNs and matched comparisons from the general population and to study the effect modification of comorbidity. Methods: We followed 3087 patients with ET, 6076 with PV, 3719 with PMF or unspecified MPN, and age- and sex-matched general population comparisons to estimate the risks of cardiovascular diseases such as myocardial infarction and stroke. We computed 5-year cumulative incidences (risks) for vascular disease in patients with MPNs and comparisons as well as 1-year and 5-year risks, risk differences, and hazard ratios (HRs) for vascular diseases comparing rates in each group of patients with their comparison cohort by level of comorbidity based on the Charlson Comorbidity Index (CCI) [score of 0 (low comorbidity), of 1–2 (moderate comorbidity), and of >2 (severe comorbidity)], as well as other comorbid conditions. Results: The overall 5-year risk of vascular disease ranged from 0.5% to 7.7% in patients with MPNs, which was higher than the risk in the general population. In the same period, the adjusted HRs for vascular disease were 1.3 to 3.7 folds higher in patients with MPNs compared to the general population. An increase in CCI score was associated with an equally increased rate of most types of vascular diseases during the first 5 years of follow-up in both MPN and comparisons. Conclusion: Patients with MPNs have a higher risk of vascular diseases during the first 5 years than that of the general population; however, comorbidity modifies the rates similarly in MPN and in the general population.

Background: Former studies on smoking as a risk factor for Philadelphia‐negative myeloproliferative neoplasms (MPNs) have mainly been carried out in women's cohorts and studies with various definitions of MPNs. Herein, we conducted a cohort study with register‐based follow‐up of a general population from Denmark, to validate and substantiate prior observations.Methods: In the Danish Health Examination Survey cohort, we used the Cox proportional‐hazards model adjusted for age, sex, body mass index, and level of education, to calculate hazard ratios (HRs), to investigate, whether daily smokers or occasional/ex‐smokers had an increased risk of MPNs compared to never‐smokers.Results: From the time of data collection (September 2007 to October 2008) until 1 January 2015, 70 individuals were diagnosed with MPNs among 75 896 study participants. Similar results were observed in both the age and sex adjusted analysis and the multivariable analysis. The multivariable HR of any MPN diagnosis for daily smokers was 2.5 (95% CI: 1.3‐5.0). For essential thrombocytosis, polycythemia vera, myelofibrosis, and MPN‐unclassified, the HRs were 1.8 (95% CI: 0.5‐5.8), 1.7 (95% CI: 0.5‐5.8), 4.3 (95% CI: 0.9‐19), and 6.2 (95% CI: 1.5‐25), respectively. Among occasional/ex‐smokers the corresponding HRs were 1.9 (95% CI: 1.1‐3.3), 1.5 (95% CI: 0.6‐3.7), 0.8 (95% CI: 0.3‐2.4), 0.9 (95% CI: 0.2‐4.4), and 6.2 (95% CI: 1.8‐21). Participants, who smoked >15 g/day, had an overall HR of 3.4 (95% CI: 1.4‐8.2) for any MPN diagnosis, while participants who smoked ≤15 g/day, had an overall HR of 2.1 (95% CI: 0.9‐4.7).Conclusion: Smoking was associated with MPN development when comparing smokers and never‐smokers. Further studies investigating smoking in MPNs are warranted to substantiate our findings.

Age-related macular degeneration (AMD) is a chronic progressive eye disease that affects the macular region of the retina.^1,2 The early and intermediate stages of the disease are characterized by drusen formation, with pigment changes also occurring in the intermediate stage. Patients may develop late-stage AMD, characterized by geographic atrophy or choroidal neovascularization (neovascular AMD), and some patients progress rapidly.³ Inflammation seems to be involved in the pathogenesis of AMD; recent studies have shown that systemic inflammation is also highly likely to be present.⁴ In addition, few studies have suggested an association between AMD and systemic diseases, in which chronic inflammation also plays a crucial role.^5-7