Laminar flow reduces cases of surgical site infections in vascular patients

Introduction

Numerous strategies are employed routinely in an effort to lower rates of surgical site infections (SSIs). A laminar flow theatre environment is generally used during orthopaedic surgery to reduce rates of SSIs. Its role in vascular surgery, especially when arterial bypass grafts are used, is unknown.

Methods

A retrospective review of a prospectively maintained database was undertaken for all vascular procedures performed by a single consultant over a one-year period. Cases were performed, via random allocation, in either a laminar or non-laminar flow theatre environment. Demographic data, operative data and evidence of postoperative SSIs were noted. A separate subgroup analysis was undertaken for patients requiring an arterial bypass graft. Univariate and multivariate logistical regression was undertaken to identify significant factors associated with SSIs.

Results

Overall, 170 procedures were analysed. Presence of a groin incision, insertion of an arterial graft and a non-laminar flow theatre were shown to be predictive of SSIs in this cohort. In the subgroup receiving arterial grafts, only a non-laminar flow theatre environment was shown to be predictive of an SSI.

Conclusions

This study suggests that laminar flow may reduce incidences of SSI, especially in the subgroup of patients receiving arterial grafts.     

In the Experimental Model of Acute Mesenteric Ischemia,The Correlation of Blood Diagnostic Parameters with the Duration of Ischemia and their Effects on Choice of Treatment

ABSTRACT

Purpose/Aim: Acute mesenteric ischemia is a syndrome characterized by sudden onset abdominal pain followed by intestinal necrosis. Morbidity and mortality increase with delayed diagnosis. Even with the latest radiological diagnostic methods, early diagnosis and initiation of treatment can be delayed. Using an experimental model, here we aim to determine the relationship between the laboratory parameters used to detect acute mesenteric ischemia and the duration of irreversible ischemia. Materials and Methods: A total of 30 male Wistar albino rats were divided into five groups, all of which underwent general anesthesia: (i) Superior mesenteric artery (SMA) dissection with laparotomy was performed, and blood samples and intestinal segment samples were taken after 2 hr (Sham group); (ii) volvulus of one-third of the small intestines was performed manually by laparotomy, and blood samples and intestinal segment samples were taken after 2 hr (Volvulus group); (iii) SMA was ligated with laparotomy, and blood samples and intestinal segment samples were taken after 2 hr (SMA+ligated 2-hr group); (iv) SMA was ligated with laparotomy, and blood samples and intestinal segment samples were taken after 4 hr (SMA+ligated 4-hr group); and (v) SMA was ligated with laparotomy, and blood samples and intestinal segment samples were taken after 6 hr (SMA+ligated 6-hr group). Results: The mean lactate dehydrogenase (LDH) activities of the SMA+ligated 2-hr and SMA+ligated 6-hr groups were statistically higher than the control group (p = .004). Compared to the Sham and Volvulus groups, the mean lactate level of the SMA+ligated 6-hr group was significantly higher (p = .004). Compared to the Sham and Volvulus groups, the mean D-dimer levels of the SMA+ligated 4-hr and SMA+ligated 6-hr groups were significantly higher (p = .004 and .003, respectively). By histopathological evaluation, we found that pathological damage increased as the ischemia lengthened. Conclusions: Mesenteric ischemia leads to an irreversible loss of intestinal perfusion and an increase in parameters of ischemia. Irreversible tissue damage occurs after 4 hr of ischemia and peaks after 6 hr, whereas parameters of ischemia (D-dimer, LDH, and L-Lactate levels) are highest at 2 hr after the onset of ischemia.     

EFFECT OF CAST RECTIFIERS ON THE MARGINAL FIT OF UCLA ABUTMENTS

Objectives:

This study assessed the effect of cast rectifiers on the marginal misfit of cast UCLA abutments compared to premachined UCLA abutments. The influence of casting and porcelain baking on the marginal misfit of these components was also investigated.

Methods:

Two groups were analyzed: test group – 10 cast UCLA abutments, finished with cast rectifier and submitted to ceramic application; control group – 10 premachined UCLA abutments, cast with noble metal alloy and submitted to ceramic application. Vertical misfit measurements were performed under light microscopy. In the test group, measurements were performed before and after the use of cast rectifiers, and after ceramic application. In the control group, measurements were performed before and after casting, and after ceramic application. Data were submitted to statistical analysis by ANOVA and Tukey''s test (α= 5%).

Results:

The use of cast rectifiers significantly reduced the marginal misfit of cast UCLA abutments (from 25.68μm to 14.83μm; p<0.05). After ceramic application, the rectified cylinders presented misfit values (16.18μm) similar to those of premachined components (14.3 μm). Casting of the premachined UCLA abutments altered the marginal misfit of these components (from 9.63 μm to 14.6 μm; p<0.05). There were no significant changes after porcelain baking, in both groups.

Conclusion:

The use of cast rectifiers reduced the vertical misfit of cast UCLA abutments. Even with carefully performed laboratory steps, changes at the implant interface of premachined UCLA abutments occurred. Ceramic application did not alter the marginal misfit values of UCLA abutments.     

Fluorescence in situ hybridization mapping of translocations and deletions involving the short arm of human chromosome 12 in malignant hematologic diseases

Translocations and deletions of the short arm of chromosome 12 [t(12p) and del(12p)] are common recurring abnormalities in a broad spectrum of hematologic malignant diseases. We studied 20 patients and one cell line whose cells contained 12p13 translocations and/or 12p deletions using fluorescence in situ hybridization (FISH) with phage, plasmid, and cosmid probes that we previously mapped and ordered on 12p12-13. FISH analysis showed that the 12p13 translocation breakpoints were clustered between two cosmids, D12S133 and D12S142, in 11 of 12 patients and in one cell line. FISH analysis of 11 patients with deletions demonstrated that the deletions were interstitial rather than terminal and that the distal part of 12p12, including the GDI-D4 gene and D12S54 marker, was deleted in all 11 patients. Moreover, FISH analysis showed that cells from 3 of these patients contained both a del(12p) and a 12p13 translocation and that the affected regions of these rearrangements appeared to overlap. We identified three yeast artificial chromosome (YAC) clones that span all the 12p13 translocation breakpoints mapped between D12S133 and D12S142. They have inserts of human DNA between 1.39 and 1.67 Mb. Because the region between D12S133 and D12S142 also represents the telomeric border of the smallest commonly deleted region of 12p, we also studied patients with a del(12p) using these YACs. The smallest YAC, 964c10, was deleted in 8 of 9 patients studied. In the other patient, the YAC labeled the del(12p) chromosome more weakly than the normal chromosome 12, suggesting that a part of the YAC was deleted. Thus, most 12p13 translocation breakpoints were clustered within the sequences contained in the 1.39 Mb YAC and this YAC appears to include the telomeric border of the smallest commonly deleted region. Whether the same gene is involved in both the translocations and deletions is presently unknown.     

An endogenous glycosylphosphatidylinositol-specific phospholipase D releases basic fibroblast growth factor-heparan sulfate proteoglycan complexes from human bone marrow cultures

Basic fibroblast growth factor (bFGF) is a hematopoietic cytokine that stimulates stromal and stem cell growth. It binds to a glycosylphosphatidylinositol (GPI)-anchored heparan sulfate proteoglycan on human bone marrow (BM) stromal cells. The bFGF- proteoglycan complex is biologically active and is released by addition of exogenous phosphatidylinositol-specific phospholipase C. In this study, we show the presence of an endogenous GPI-specific phospholipase D (GPI-PLD) that releases the bFGF-binding heparan sulfate proteoglycan and the variant surface glycoprotein (a model GPI-anchored protein) from BM cultures. An involvement of proteases in this process is unlikely, because released proteoglycan contained the GPI anchor component, ethanol-amine, and protease inhibitors did not diminish the release. The mechanism of release is likely to involve a GPI-PLD and not a GPI-specific phospholipase C, because the release of variant surface glycoprotein did not reveal an epitope called the cross- reacting determinant that is exposed by phospholipase C-catalyzed GPI anchor cleavage. In addition, phosphatidic acid (which is specifically a product of GPI-PLD-catalyzed anchor cleavage) was generated during the spontaneous release of the GPI-anchored variant surface glycoprotein. We also detected GPI-PLD-specific enzyme activity and mRNA in BM cells. Therefore, we conclude that an endogenous GPI-PLD releases bFGF-heparan sulfate proteoglycan complexes from human BM cultures. This mechanism of GPI anchor cleavage could be relevant for mobilizing biologically active bFGF in BM. An endogenous GPI-PLD could also release other GPI-anchored proteins important for hematopoiesis and other physiologic processes.     

Modulation of in vitro eosinophil progenitors by hydrocortisone: role of accessory cells and interleukins

The growth of human eosinophil progenitors (CFU-Eo) and the modulation of growth by hydrocortisone were studied as functions of the presence of lymphocytes and monocytes in marrow cells under study; and the source of colony-stimulating factors, specifically, media conditioned by macrophage-like cell line, GCT; phytohemagglutinin-stimulated mononuclear cells (PHA-LCM); or the T cell line, MO. CFU-Eo growth was greatest in marrow containing accessory cells as compared to marrow depleted of accessory cells; and in marrow treated with phytohemagglutinin-stimulated leukocyte conditioned media (PHA-LCM) or MO (T cell line)-conditioned medium (MO-CM) as compared with GCT cell- conditioned medium (GCT-CM). Hydrocortisone reproducibly inhibited eosinophil progenitor growth in unfractionated marrow stimulated by GCT- CM. This effect was abrogated by admixing irradiated mononuclear cells or T lymphocytes with the target marrow or by adding interleukin 1 or interleukin 2 (IL-1, IL-2). Inhibition by hydrocortisone did not occur when monocyte and T lymphocyte depleted marrow was studied. Unlike GCT- CM, MO-CM and PHA-LCM stimulated equal proportions of eosinophil progenitors in nondepleted and accessory cell-depleted marrow and demonstrated less hydrocortisone inhibition. However, both GCT-CM and PHA-LCM produced in the presence of hydrocortisone stimulated significantly fewer CFU-Eos in both unfractionated and accessory cell- depleted marrow target populations. These results indicate that the growth of CFU-Eo and inhibition of growth by hydrocortisone is a direct function of a monocyte-T cell interaction and probably is mediated through effects on the production/release of eosinophil colony stimulating factor (Eo-CSF).