The Surgical Options and Clinical Evidence for Treatment of Wear or Corrosion Occurring With THA or TKA

Background

Wear and corrosion occurring in patients with hip and knee arthroplasty are common causes of failure leading to revision surgery. A variety of surgical approaches to these problems have been described, with varying efficacy. Polyethylene wear, metal-on-metal (MoM) hip bearing wear, and problems associated with modular taper corrosion are the areas of greatest clinical impact; results of revisions for these problems are likely to dictate a large portion of revision resources for the foreseeable future, and so they call for specific study.

Questions/purposes

We identified the most frequently reported procedures to treat hip polyethylene wear, knee polyethylene wear, MoM wear after THA, and modular taper corrosion and determined the timing and reasons these failed.

Methods

We performed systematic reviews of the published literature on the four topics using MEDLINE^® and Embase in October 2013; searches were supplemented by hand searches of bibliographies. Prespecified criteria resulted in the identification of 38 relevant articles, of which 33 were either case reports or Level IV evidence. Followup was generally at short term and ranged from 0.2 to 8 years.

Results

The most frequently reported procedures for treating clinically important wear were a partial or complete revision. When treating polyethylene wear, the more frequently reported reasons for hip and knee rerevisions were loosening, continued wear, and instability. Soft tissue reactions were more common and occasionally extensive in patients with MoM or modular taper corrosion. Patients with soft tissue reactions had more complications and higher rerevision rates.

Conclusions

Studies with longer followup and higher levels of evidence are needed to direct the treatment of wear and corrosion. When soft tissue damage secondary to MoM wear or taper corrosion is present, the results of treatment can be poor. There is an urgent need to better understand these two mechanisms of failure.     

Feeding jejunostomy during Whipple is associated with increased morbidity

Background

Placement of a feeding jejunostomy tube (FJ) is often performed during pancreaticoduodenectomy (PD). Few studies, however, have sought to determine whether such placement affects postoperative outcomes after PD.

Materials and methods

This is a retrospective analysis of the National Surgical Quality Improvement Program (NSQIP) database to determine the 30-d-postoperative mortality rate, major complication rate, and overall complication rate of jejunostomy tube placement at the time of PD. Univariate and multivariate comparison of postoperative outcomes between patients with and without FJ placement during PD was performed on a total of 4930 patients.

Results

Thirty-day-postoperative mortality did not differ between the two groups (4.0% for patients with FJ versus 2.7% without, P = 0.13), whereas overall morbidity (43.3% with FJ versus 34.6% without, P < 0.0001) and serious morbidity (29.5% with FJ versus 22.8% without, P < 0.0001) were significantly higher in patients undergoing FJ placement during PD. The specific complications that occurred more frequently in FJ patients than patients without FJ included deep space surgical site infection, pneumonia, unplanned reintubation, acute renal failure, and sepsis.

Conclusion

Although FJ placement during PD is considered to be routine at many institutions, our analysis of data from NSQIP suggest that FJ placement may be associated with increased postoperative morbidity.     

Molecular determinants of susceptibility to oncolytic vesicular stomatitis virus in pancreatic adenocarcinoma

Background

M protein mutant vesicular stomatitis virus (M51R-VSV) has oncolytic properties against many cancers. However, some cancer cells are resistant to M51R-VSV. Herein, we evaluate the molecular determinants of vesicular stomatitis virus (VSV) resistance in pancreatic adenocarcinoma cells.

Methods

Cell viability and the effect of β-interferon (IFN) were analyzed using 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium assay. Gene expression was evaluated via microarray analysis. Cell infectability was measured by flow cytometry. Xenografts were established in athymic nude mice and treated with intratumoral M51R-VSV.

Results

Four of five pancreatic cancer cell lines were sensitive to M51R-VSV, whereas Panc 03.27 cells remained resistant (81 ± 3% viability 72 h after single-cycle infection). Comparing sensitive MiaPaCa2 cells with resistant Panc 03.27 cells, significant differences in gene expression were found relating to IFN signaling (P = 2 × 10⁻⁵), viral entry (P = 3 × 10⁻⁴), and endocytosis (P = 7 × 10⁻⁴). MiaPaCa2 cells permitted high levels of VSV infection, whereas Panc 03.27 cells were capable of resisting VSV cell entry even at high multiplicities of infection. Extrinsic β-IFN overcame apparent defects in IFN-mediated pathways in MiaPaCa2 cells conferring VSV resistance. In contrast, β-IFN decreased cell viability in Panc 3.27 cells, suggesting intact antiviral mechanisms. VSV-treated xenografts exhibited reduced tumor growth relative to controls in both MiaPaCa2 (1423 ± 345% versus 164 ± 136%; P < 0.001) and Panc 3.27 (979 ± 153% versus 50 ± 56%; P = 0.002) tumors. Significant lymphocytic infiltration was seen in M51R-VSV–treated Panc 03.27 xenografts.

Conclusions

Inhibition of VSV endocytosis and intact IFN-mediated defenses are responsible for M51R-VSV resistance in pancreatic adenocarcinoma cells. M51R-VSV treatment appears to induce antitumor cellular immunity in vivo, which may expand its clinical efficacy.