Integrating clinical communication with clinical reasoning and the broader medical curriculum

Objective

The objectives of this paper are to discuss the results of a workshop conducted at EACH 2012. Specifically, we will (1) examine the link between communication, clinical reasoning, and medical problem solving, (2) explore strategies for (a) integrating clinical reasoning, medical problem solving, and content from the broader curriculum into clinical communication teaching and (b) integrating communication into the broader curriculum, and (3) discuss benefits gained from such integration.

Methods

Salient features from the workshop were recorded and will be presented here, as well as a case example to illustrate important connections between clinical communication and clinical reasoning.

Results

Potential links between clinical communication, clinical reasoning, and medical problem solving as well as strategies to integrate clinical communication teaching and the broader curricula in human and veterinary medicine are enumerated.

Conclusion

Participants expressed enthusiasm and keen interest in integration of clinical communication teaching and clinical reasoning during this workshop, came to the idea of the interdependence of these skills easily, and embraced the rationale immediately.

Practice implications

Valuing the importance of communication as clinical skill and embracing the interdependence between communication and thought processes related to clinical reasoning and medical problem solving will be beneficial in teaching programs.     

UHMWPE Wear Debris and Tissue Reactions Are Reduced for Contemporary Designs of Lumbar Total Disc Replacements

Background

Lumbar total disc replacement (L-TDR) is a procedure used to relieve back pain and maintain mobility. Contemporary metal-on-polyethylene (MoP) L-TDRs were developed to address wear performance concerns about historical designs, but wear debris generation and periprosthetic tissue reactions for these newer implants have not been determined.

Questions/purposes

The purpose of this study was to determine (1) whether periprosthetic ultrahigh-molecular-weight polyethylene (UHMWPE) wear debris and biological responses were present in tissues from revised contemporary MoP L-TDRs that contain conventional cores fabricated from γ-inert-sterilized UHMWPE; (2) how fixed- versus mobile-bearing design affected UHMWPE wear particle number, shape, and size; and (3) how these wear particle characteristics compare with historical MoP L-TDRs that contain cores fabricated from γ-air-sterilized UHMWPE.

Methods

We evaluated periprosthetic tissues from 11 patients who received eight fixed-bearing ProDisc-L and four mobile-bearing CHARITÉ contemporary L-TDRs with a mean implantation time of 4.1 and 2.7 years, respectively. Histologic analysis of tissues was performed to assess biological responses and polarized light microscopy was used to quantify number and size/shape characteristics of UHMWPE wear particles from the fixed- and mobile-bearing devices. Comparisons were made to previously reported particle data for historical L-TDRs.

Results

Five of seven (71%) fixed-bearing and one of four mobile-bearing L-TDR patient tissues contained at least 4 particles/mm² wear with associated macrophage infiltration. Tissues with wear debris were highly vascularized, whereas those without debris were more necrotic. Given the samples available, the tissue around mobile-bearing L-TDR was observed to contain 87% more, 11% rounder, and 11% less-elongated wear debris compared with tissues around fixed-bearing devices; however, there were no significant differences. Compared with historical L-TDRs, UHMWPE particle number and circularity for contemporary L-TDRs were 99% less (p = 0.003) and 50% rounder (p = 0.003).

Conclusions

In this preliminary study, short-term results suggest there was no significant influence of fixed- or mobile-bearing designs on wear particle characteristics of contemporary L-TDRs, but conventional UHMWPE has notably improved the wear resistance of these devices compared with historical UHMWPE.     

Does Cyclic Stress Play a Role in Highly Crosslinked Polyethylene Oxidation?

Background

Minimizing the impact of oxidation on ultrahigh-molecular-weight polyethylene components is important for preserving their mechanical integrity while in vivo. Among the strategies to reduce oxidation in modern first-generation highly crosslinked polyethylenes (HXLPEs), postirradiation remelting was considered to afford the greatest stability. However, recent studies have documented measurable oxidation in remelted HXLPE retrievals. Biologic prooxidants and physiologic loading have been proposed as potential mechanisms.

Questions/purposes

In our pilot study, we asked: (1) Does cyclic stress induced by wear or (2) by cyclic compression loading increase oxidation and crystallinity of remelted HXLPE? (3) Does oxidative aging reduce the wear resistance of remelted HXLPE?

Methods

Remelted and annealed HXLPE prisms (n = 1 per test condition) were tested in a wear simulator for 500,000 cycles. After wear testing, some samples were subjected to accelerated aging and then wear-tested again. Wear track volumes were characterized by confocal microscopy. Thin films (200-μm thick) were microtomed from wear prisms and then used for Fourier transform infrared spectroscopy oxidation and crystallinity assessments. Remelted HXLPE compression cylinders (n = 1 per test condition) were subjected to fatigue experiments and similar oxidation characterization.

Results

Remelted HXLPE qualitatively showed low oxidation indices (≤ 1) when subjected either to cyclic loading or aging alone. However, oxidation levels almost doubled in near-surface regions when remelted HXLPE samples underwent consecutive cyclic loading, artificial aging, and cyclic loading steps. The type of loading (wear versus compression fatigue) appeared to not affect the oxidation behavior in the studied conditions. Annealed HXLPE showed higher oxidation (oxidation index > 3) than remelted HXLPE and delamination wear. No delamination wear was observed in remelted HXLPE in agreement with its comparatively low oxidation levels (oxidation index < 3).

Conclusions

With the numbers available in our pilot study, the findings suggest that cyclic stress arising from a wear process or from cyclic compression may trigger the loss of oxidative stability of remelted HXLPE and contribute to synergistically accelerate its progression. Further studies of the effect of cyclic stress on oxidation of remelted HXLPE are needed.

Clinical Relevance

Retrieval studies are warranted to determine the natural history of the in vivo oxidation and wear behavior of first-generation, remelted HXLPE.     

Rare complications of osteolysis and periprosthetic tissue reactions after hybrid and non-hybrid total disc replacement

Purpose

Few complications have been reported for lumbar total disc replacement (TDR) and hybrid TDR fixations. This study evaluated retrieved implants and periprosthetic tissue reactions for two cases of osteolysis following disc arthroplasty with ProDisc-L prostheses.

Methods

Implants were examined for wear and surface damage, and tissues for inflammation, polyethylene wear debris (polarized light microscopy) and metal debris (energy-dispersive X-ray spectroscopy).

Results

Despite initial good surgical outcomes, osteolytic cysts were noted in both patients at vertebrae adjacent to the implants. For the hybrid TDR case, heterotopic ossification and tissue necrosis due to wear-induced inflammation were observed. In contrast, the non-hybrid implant showed signs of abrasion and impingement, and inflammation was observed in tissue regions with metal and polyethylene wear debris.

Conclusions

In both cases, wear debris and inflammation may have contributed to osteolysis. Surgeons using ProDisc prostheses should be aware of these rare complications.

     

Kidney‐Induced Cardiac Allograft Tolerance in Miniature Swine is Dependent on MHC‐Matching of Donor Cardiac and Renal Parenchyma

Kidney allografts possess the ability to enable a short course of immunosuppression to induce tolerance of themselves and of cardiac allografts across a full‐MHC barrier in miniature swine. However, the renal element(s) responsible for kidney‐induced cardiac allograft tolerance (KICAT) are unknown. Here we investigated whether MHC disparities between parenchyma versus hematopoietic‐derived “passenger” cells of the heart and kidney allografts affected KICAT. Heart and kidney allografts were co‐transplanted into MHC‐mismatched recipients treated with high‐dose tacrolimus for 12 days. Group 1 animals (n = 3) received kidney and heart allografts fully MHC‐mismatched to each other and to the recipient. Group 2 animals (n = 3) received kidney and heart allografts MHC‐matched to each other but MHC‐mismatched to the recipient. Group 3 animals (n = 3) received chimeric kidney allografts whose parenchyma was MHC‐mismatched to the donor heart. Group 4 animals (n = 3) received chimeric kidney allografts whose passenger leukocytes were MHC‐mismatched to the donor heart. Five of six heart allografts in Groups 1 and 3 rejected <40 days. In contrast, heart allografts in Groups 2 and 4 survived >150 days without rejection (p < 0.05). These data demonstrate that KICAT requires MHC‐matching between kidney allograft parenchyma and heart allografts, suggesting that cells intrinsic to the kidney enable cardiac allograft tolerance.     

Insulin resistance is associated with increased serum levels of glycosylphosphatidylinositol-specific phospholipase D

The dyslipidemia of the metabolic syndrome is associated with alterations in triglyceride and high-density lipoprotein (HDL) metabolism. We examined the serum levels of glycosylphosphatidylinositol-specific phospholipase D (GPI-PLD), a minor HDL-associated protein, in a cohort with a wide range of insulin sensitivity. The mean serum GPI-PLD mass from 109 subjects was 58.9 +/- 18.4 microg/mL (mean +/- SD). GPI-PLD levels directly correlated with cholesterol, apolipoprotein AI, triglycerides, insulin, and homeostasis model assessment (HOMA) but not C-reactive protein. These results suggest that increased serum GPI-PLD is associated with the insulin resistance.     

Accuracy of supplementary serologic testing for human T-lymphotropic virus types I and II in US blood donors. Retrovirus Epidemiology Donor Study

Blood donations in the United States have been screened for antibody to human T-lymphotropic virus type I (HTLV-I) by HTLV-I enzyme immunoassay (EIA) since November 1988. Specimens repeatedly found to be reactive by EIA undergo confirmation by supplementary serologic tests. We assessed the accuracy of blood center testing of 994 HTLV-I EIA repeat-reactive specimens in five US blood centers between November 1988 and December 1991. Of 410 confirmed HTLV-I/II donations, 407 (99.3%) were infected with HTLV-I/II, as determined by polymerase chain reaction (PCR) (403 cases) and by repeat serologic testing (4 cases). The three false- positive results occurred in the first year of testing. Of 425 HTLV- indeterminate specimens, 6 (1.4%) were found to be infected by PCR (5 with HTLV-II and 1 with HTLV-I). None of 159 confirmatory test-negative donations was PCR positive. Of HTLV-I/II-seropositive specimens, 80.2% to 95.4% could be typed as HTLV-I or HTLV-II by type-specific serologic assays. These results support recommendations that HTLV-I/II- seropositive donors should be advised that they are infected with HTLV- I, HTLV-II, or HTLV-I/II (depending on results of type-specific assays). HTLV-indeterminate donors should be advised that their results only rarely indicate HTLV infection. HTLV confirmatory test-negative donors should be reassured that they are not infected with HTLV-I or HTLV-II.     

Atrial natriuretic peptide inhibits renin release from juxtaglomerular cells by a cGMP-mediated process.

We have examined the effect of a synthetic analogue of human alpha-atrial natriuretic peptide (ANP), APII, on renin release in cultured renal juxtaglomerular cells (JGA cells). Using cell cultures containing 80-90% renal juxtaglomerular cells, we found that ANP (10(-13)-10(-9) M) strongly inhibited renin release from the cells in a dose-dependent fashion (ki, 10 pM) to about 10% of control. Inhibition of renin release by ANP was paralleled by an increase in cellular cGMP levels; while in the presence of the cGMP-phosphodiesterase inhibitor M&B 22948 (1 mM), concentrations of ANP lower by a factor of 100 were required to obtain the same effects on renin release and cGMP levels. The guanylate cyclase inhibitor methylene blue (10 microM), on the other hand, shifted the dose-response curves for renin release and cGMP levels to 100-fold higher concentrations of ANP. Neither the influx of 45Ca into the cells nor the intracellular quin-2 signal, which is a measure for changes of intracellular Ca concentration, was in any way altered by ANP. Our results suggest that ANP inhibits renin release from juxtaglomerular cells by a cGMP-dependent process that does not involve changes in intracellular calcium.