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Asphaltene deposition is an increasing problem in many oil fields around the world. One of the most common strategies to mitigate asphaltene deposition is based on the continuous injection of asphaltene inhibitors. These chemicals are usually screened in the laboratory following one or more of the many techniques available to evaluate their performance, such as precipitation tests or deposition tendencies, using various setups, such as a Taylor–Couette cell, flow loop, capillary tube, or packed-bed column. The performance ranking of chemicals for a given crude oil sample depends upon the type of test used. There are cases where chemicals that perform well in the laboratory are not as effective in the field, as a lab to field correlation for asphaltene inhibitor screening is still being developed. In this work, we investigate the case of a commercial asphaltene inhibitor that shows adequate performance in a deepwater–oil well. We analyze its behavior in the laboratory using a series of tests on treated and untreated oil samples collected from the field. Depostion behavior of model oils prepared from the deposits retrieved from this field has also been studied. Moreover, we have put special attention on the effect of asphaltene polydispersity on the performance of the chemical and track the performance of the product over a period of several years. The results and analyses presented in this work aim to expand our knowledge on this topic and provide some best practices for testing the performance of asphaltene inhibitors in the laboratory, with the ultimate objective of establishing a series of laboratory tests and a workflow to correlate laboratory and field performance of these chemicals.

Background: Immunocompromised hematologic malignancy (HM) patients experience high mortality after respiratory syncytial virus (RSV) lower respiratory tract infection (LRTI). We measured radiologic severity to determine whether it could improve the performance of 60-day mortality models based only upon immunodeficiency severity. Methods:We studied 155 HM patients, including 84 hematopoietic cell transplant recipients, who developed RSV LRTI from 2001 to 2013. We measured immunodeficiency using lymphopenia (lymphocyte count <200 cells/mm 3 ), Immunodeficiency Severity Index (ISI), and Severe Immunodeficiency (SID) criteria. Radiologic severity was measured by the Radiologic Severity Index (RSI, range 0-72) at time of LRTI (baseline-RSI) and peak severity (peak-RSI). Delta-RSI was defined as the difference between baseline-RSI and peak-RSI. We used logistic regression models to measure the association of immunodeficiency and RSI with 60-day all-cause mortality, and measured model discrimination using areas under the receiver-operating characteristics curves, calibration using Brier scores, and explained variance using pseudo-R 2 values.Results: Forty-one patients died within 60 days of RSV LRTI. Severe immunodeficiency was associated with higher mortality. Peak-RSI (odds ratio [OR] 1.06/point, 95% confidence interval [CI] 1.04-1.08), and delta-RSI (OR 1.07/point, 95% CI 1.05-1.10) were associated with 60-day mortality after RSV LRTI, but not baseline-RSI. Addition of peak-RSI or delta-RSI to baseline immunodeficiency improved the discrimination, calibration, and explained variance (P < 0.001) of 60-day mortality models. Conclusions:Although baseline immunodeficiency in HM patients helps predict 60day mortality after RSV LRTI, mortality risk estimates can be further refined by also measuring LRTI progression using RSI. RSI is well-suited as a marker of LRTI severity in RSV infection.