Johnson, Margaret M.

Abstract Rationale Studies have shown the importance of simulation-based training on the outcomes of central venous catheter (CVC) insertion by trainees. Objectives To compare the performance of internal medicine trainees who underwent standardized simulation training of CVC insertion with that of internal medicine trainees who had traditional CVC training and were already deemed competent to perform the procedure during a proficiency evaluation using a training mannequin. Methods Trainees who perform CVC insertion were enrolled in the institutional Central Line Workshop, which includes both an online and an experiential simulation component. The training is followed by a certification station proficiency assessment. Residents and fellows previously certified competent to perform CVC placement without supervision completed the online module, but they could opt out of the experiential component and proceed directly to the evaluation. Results Forty-eight trainees participated in the study. Twenty-one (44%), 15 (31%), 6 (13%), 1 (2%), 2 (4%), and 3 (6%) were in postgraduate year 1 (PGY1), PGY2, PGY3, PGY4, PGY5, and PGY6, respectively. Twenty-nine completed the hands-on instruction, 28 (97%) of whom successfully passed the simulation-based assessment on their first attempt. Nineteen trainees previously credentialed to perform CVC placement without supervision opted out of the simulation-based experiential training. Of these, five (26%) failed in their first attempt (P = 0.02 vs. trainees who completed the simulation training). Conclusions Standardized simulation-based training can improve CVC insertion proficiency, even among trainees with previous experience sufficient to have been deemed competent in the procedure. Improved performance at simulation-based testing may translate to improved outcomes of CVC placement by trainees.

A 62-year-old male presented with productive cough, weight loss, and night sweats. CXR revealed a right upper lobe cavitary lesion. Evaluation was negative forMycobacterium tuberculosis, and sputum revealedMycobacterium avium intracellulare(MAI). Since his clinical course was atypical for MAI, further investigations were pursued which identifiedMycobacterium interjectumin lung specimens, a very rarely described etiology of pulmonary disease. Appropriate therapy with rifampin, intravenous amikacin, trimethoprim/sulfamethoxazole (TMP/SMX), and ethambutol resulted in clinical and radiographic improvement. This is the third case described over a period of 20 years of destructive lung disease in an immunocompetent adult due toM. interjectum.

Abstract Increasing evidence suggests that the subcellular and glycerolipid localization of esterified arachidonic acid (AA) is a key factor in regulating its availability to lipases. The goal of the current study was to determine the potential of AA stored in triglycerides (TG) to serve as a substrate for lipases and 5-lipoxygenase during neutrophil (polymorphonuclear leukocytes, PMN) activation. PMN containing high concentrations of AA in TG were generated by culturing PMN in vitro with high concentrations of exogenous AA (eAA) for 12 h. Cellular AA increased 2- and 4-fold in PMNs incubated with 5 and 20 μM AA, respectively, and this increase was almost exclusively observed in neutral lipids (NL). Further analysis revealed that 88% of the AA in the NL fraction was associated with TG. Subsequent experiments were designed to determine whether this AA in TG could be mobilized and metabolized to eicosanoids during cell activation. TG pools of AA were increased as previously described and then PMN were stimulated with ionophore, A23187. In contrast to the 43-fold increase in TG AA after eAA loading (20 μM), free AA increased by only 1.9-fold after cell stimulation. Similarly, leukotriene (LT)B4 production increased only 2-fold after loading TG with large quantities of AA. The magnitude of increase in free AA released and in LTB4 formation was similar to the magnitude of increase in AA mass in phospholipase (PL), suggesting that PL, and not TG, served as the source of released AA and subsequent product generation. To confirm that AA in TG did not serve as a source for eicosanoid production, cellular pools of AA were differentially labeled with [14C]AA and [3H]AA, and the [3H]AA–to–[14C]AA ratio of LTB4 and 20-hydroxyl LTB4 produced during cell stimulation was measured. The [3H]AA/[14C]AA ratios of LTs were markedly different from the ratios in TG, thus providing further evidence that AA pools in TG are not a major source of AA for LT generation.

Pulmonary embolic disease is most commonly a manifestation of venous thromboembolism (VTE). However, fat, tumor, and air may all embolize to the pulmonary vasculature and lymphatics resulting in various clinical manifestations. Tumor emboli to small pulmonary vessels and lymphatics can lead to hypoxemic respiratory failure and shock. We present a 62-year-old male with history of mild COPD and end-stage liver disease secondary to hepatitis C admitted due to progressive shortness of breath and hypoxemia who developed shock and right ventricular failure. After a negative evaluation for venous thromboembolic disease, he had progressive respiratory and hemodynamic deterioration despite mechanical ventilation, renal replacement therapy, and vasopressive/inotropic support. Postmortem examination revealed diffuse micronodular moderately differentiated hepatocellular carcinoma (HCC) without a discrete mass, as well as numerous HCC tumor emboli to the lung and focally to the heart, consistent with disseminated hepatocellular tumor microembolism.