Introduction:Rhabdomyolysis (RM) is a condition where there is injury to striated muscle fibers causing release of myoglobin, creatine phosphokinase (CPK), and other intracellular contents into the circulation. High myoglobin levels cause acute kidney injury (AKI). Trauma is the most common cause of RM and development of complications related to the degree of myoglobin released. Currently, the degree of RM is assessed and treatment is instituted based on serum CPK. As myoglobin is the direct cause of AKI, we set out to determine if serum myoglobin is a more reliable predictor than CPK for the development of AKI in traumatic RM.Methodology:A prospective observational study of 90 patients was admitted to the surgical Intensive Care Unit/high dependency unit of a tertiary hospital with traumatic RM whose serum CPK >5000 U/L. Along with standard treatment including intravascular volume optimization and hemodynamic stabilization, they were treated with “crush protocol.” Daily/twice a day, serum CPK and myoglobin were estimated. Categorical data are expressed as frequency and percentage, and the continuous variables are presented as mean (standard deviation) or median (interquartile range) based on normality. Other statistical analyses were done using the Chi-square test, independent t-test, and rank sum test based on normality.Results:Fourteen out of 90 patients developed AKI and one patient required renal replacement therapy. CPK value of >12,000 U/l was identified to have 64% sensitivity and 56% specificity for developing AKI whereas serum myoglobin value of >5000 ng/ml was identified to have 78% sensitivity and 77% specificity for developing AKI.Conclusion:Following traumatic RM, in patients on “crush protocol,” serum myoglobin is a more sensitive and specific test than serum CPK, for predicting AKI.
Objective:Antimicrobial stewardship programs (ASPs) are effective in developed countries. In this study, we assessed the effectiveness of an infectious disease (ID) physician–driven post-prescription review and feedback as an ASP strategy in India, a low middle-income country (LMIC).Design and setting:This prospective cohort study was carried out for 18 months in 2 intensive care units of a tertiary-care hospital, consisting of 3 phases: baseline, intervention, and follow up. Each phase spanned 6 months.Participants:Patients aged ≥15 years receiving 48 hours of study antibiotics were recruited for the study.Methods:During the intervention phase, an ID physician reviewed the included cases and gave alternate recommendations if the antibiotic use was inappropriate. Acceptance of the recommendations was measured after 48 hours. The primary outcome of the study was days of therapy (DOT) per 1,000 study patient days (PD).Results:Overall, 401 patients were recruited in the baseline phase, 381 patients were recruited in the intervention phase, and 379 patients were recruited in the follow-up phase. Antimicrobial use decreased from 831.5 during the baseline phase to 717 DOT per 1,000 PD in the intervention phase (P < .0001). The effect was sustained in the follow-up phase (713.6 DOT per 1,000 PD). De-escalation according to culture susceptibility improved significantly in the intervention phase versus the baseline phase (42.7% vs 23.6%; P < .0001). Overall, 73.3% of antibiotic prescriptions were inappropriate. Recommendations by the ID team were accepted in 60.7% of the cases.Conclusion:The ID physician–driven implementation of an ASP was successful in reducing antibiotic utilization in an acute-care setting in India.
Background & objectives: Acinetobacter baumannii is an opportunistic pathogen responsible for causing nosocomial infections. A. baumannii develops resistance to various antimicrobial agents including carbapenems, thereby complicating the treatment. This study was performed to characterize the isolates for the presence of various β-lactamases encoding genes and to type the isolates to compare our clones with the existing international clones across five centres in India. Methods: A total 75 non-repetitive clinical isolates of A. baumannii from five different centres were included in this study. All the isolates were confirmed as A. baumannii by bla OXA-51-like PCR. Multiplex PCR was performed to identify the presence of extended spectrum β-lactamases (ESBL) and carbapenemases. Multilocus sequence typing was performed to find the sequence type (ST) of the isolates. e-BURST analysis was done to assign each ST into respective clonal complex. Results: bla OXA-51-like was present in all the 75 isolates. The predominant Class D carbapenemase was bla OXA-23-like followed by Class B carbapenemase, bla NDM-like . Class A carbapenemase was not observed. bla PER-like was the predominant extended spectrum β-lactamase. ST-848, ST-451 and ST-195 were the most common STs. Eight-novel STs were identified. e-BURST analysis showed that the 75 A. baumannii isolates were clustered into seven clonal complexes and four singletons, of which, clonal complex 208 was the largest. Interpretation & conclusions: Most of the isolates were grouped under clonal complex 208 which belongs to the international clonal lineage 2. High occurrence of ST-848 carrying bla OXA-23-like gene suggested that ST-848 could be an emerging lineage spreading carbapenem resistance in India.
We retrospectively studied the prevalence of the nasal carriage of methicillin-sensitive Staphylococcus aureus (MSSA) and methicillin-resistant Staphylococcus aureus (MRSA) on admission to a medical surgical intensive care unit (ICU). We also compared the intensive care survival of MSSA carriers with non-carriers. Records of 678 patients admitted over a 24-month period were retrospectively reviewed. Nasal swabs were taken from 565 patients on admission to the ICU. MSSA was isolated from the anterior nares of 126 (22%) patients, MRSA was isolated in 16 (3%) patients and 423 (75%) patients had no nasal carriage identified. MSSA carriers were more likely to have been admitted to the ICU after less than 24 h hospital stay (28% non-carriers, 44% MSSA carriers) and were significantly younger (mean age of 50 years) than non-carriers (mean age 55 years). The median survival (with confidence intervals (CI)) was 29 days (CI 14-44) in non-carriers, 16 days (CI 10-22) in MSSA carriers and 6 days (CI 4-8) for the MRSA carriers. This difference was significant when MSSA carriers were compared with non-carriers ( p=0.003). The ICU mortality was also significantly higher ( p=0.004) in MSSA carriers (88 of the 423 (21%) non-carriers and 40 of 126 (32%) MSSA carriers died prior to ICU discharge).
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