Adverse events related to drugs are common in primary care, and many are preventable or ameliorable. Monitoring for and acting on symptoms are important. Improving communication between outpatients and providers may help prevent adverse events related to drugs.
Lorazepam administration is an important and potentially modifiable risk factor for transitioning into delirium even after adjusting for relevant covariates.
Older age is a strong predictor of hypoactive delirium in MICU patients, and this motoric subtype of delirium may be missed in the absence of active monitoring.
OBJECTIVE:To describe the incidence of adverse drug events (ADEs), preventable ADEs, and ameliorable ADEs occurring after hospital discharge and their associated risk factors.DESIGN: Prospective cohort study.SETTING: Urban academic health sciences center.PATIENTS: Consecutive patients discharged home from the general medical service.
INTERVENTIONS:We determined posthospital outcomes approximately 24 days following discharge by performing a chart review and telephone interview. Using the telephone interview, we identified new or worsening symptoms, the patient's health system use, and recollection of processes of care. Posthospital outcomes were judged by 2 internists independently.RESULTS: Four hundred of 581 potentially eligible patients were evaluated. Of the 400 patients, 45 developed an ADE (incidence, 11%; 95% confidence interval [CI], 8% to 14%). Of these, 27% were preventable and 33% were ameliorable. Injuries were significant in 32 patients, serious in 6, and life threatening in 7. Patients were less likely to experience an ADE if they recalled having side effects of prescribed medications explained (OR, 0.4; 95% CI, 0.2 to 0.8). The risk of ADE per prescription was highest for corticosteroids, anticoagulants, antibiotics, analgesics, and cardiovascular medications. Risk increased with prescription number. Failure to monitor was an especially common cause of preventable and ameliorable ADEs.
CONCLUSION:Following discharge, ADEs were common and many were preventable or ameliorable. Medication side effects should be discussed, and interventions should include better monitoring and target patients receiving specific drug classes or multiple medications.
INTRODUCTIONReporting and sharing pharmacogenetic test results across clinical laboratories and electronic health records is a crucial step toward the implementation of clinical pharmacogenetics, but allele function and phenotype terms are not standardized. Our goal was to develop terms that can be broadly applied to characterize pharmacogenetic allele function and inferred phenotypes.MATERIALS AND METHODSTerms currently used by genetic testing laboratories and in the literature were identified. The Clinical Pharmacogenetics Implementation Consortium (CPIC) used the Delphi method to obtain consensus and agree on uniform terms among pharmacogenetic experts.RESULTSExperts with diverse involvement in at least one area of pharmacogenetics (clinicians, researchers, genetic testing laboratorians, pharmacogenetics implementers, and clinical informaticians; n=58) participated. After completion of five surveys, consensus (>70%) was reached with 90% of experts agreeing to the final sets of pharmacogenetic terms.DISCUSSIONThe proposed standardized pharmacogenetic terms will improve the understanding and interpretation of pharmacogenetic tests and reduce confusion by maintaining consistent nomenclature. These standard terms can also facilitate pharmacogenetic data sharing across diverse electronic health care record systems with clinical decision support.
Studies of acute kidney injury (AKI) commonly lack data on pre-admission renal function, often substituting an inpatient or imputed serum creatinine (SCr) as an estimate for “baseline” renal function. We examined the error introduced when applying methods to estimate “baseline” on AKI classification and mortality. Within a cohort of 4863 adults with a known outpatient baseline admitted to Vanderbilt University Hospital between 10/07 and 10/08, the following surrogates were studied: (1) an eGFR of 75 ml/min/1.73m2 as suggested by the Acute Dialysis Quality Initiative (ADQI), (2) a minimum inpatient SCr, and (3) the first admission SCr. We calculated AKI incidence and mortality rates using each surrogate, and assessed their ability to correctly classify AKI incidence and mortality compared to the most recent outpatient SCr between 7-365 days before admission. Using both imputed and minimum baseline SCr values inflated AKI incidence (38.3% and 35.9% vs. 25.5%; p<0.001), reflecting low specificities of 77% and 80%, respectively. In contrast, using an admission SCr baseline underestimated AKI incidence (13.7% vs. 25.5%, p<0.001), demonstrating a low sensitivity of 39%. Using any surrogate led to frequent misclassification of patient deaths as following AKI and differences for both in-hospital and 60-day mortality rates. In summary, commonly used surrogates for baseline SCr result in bi-directional misclassification of AKI incidence and prognosis in a hospitalized setting.
SummaryBackground and objectives Inaccurate determination of baseline kidney function can misclassify acute kidney injury (AKI) and affect the study of AKI-related outcomes. No consensus exists on how to optimally determine baseline kidney function when multiple preadmission creatinine measurements are available.Design, setting, participants, & measurements The accuracy of commonly used methods for estimating baseline serum creatinine was compared with that of a reference standard adjudicated by a panel of board-certified nephrologists in 379 patients with AKI or CKD admitted to a tertiary referral center.Results Agreement between estimating methods and the reference standard was highest when using creatinine values measured 7-365 days before admission. During this interval, the intraclass correlation coefficient (ICC) for the mean outpatient serum creatinine level (0.91 [95% confidence interval (CI), 0.88-0.92]) was higher than the most recent outpatient (ICC, 0.84 [95% CI, 0.80-0.88]; P,0.001) and the nadir outpatient (ICC, 0.83 [95% CI, 0.76-0.87; P,0.001) serum creatinine. Using the final creatinine value from a prior inpatient admission increased the ICC of the most recent outpatient creatinine method (0.88 [95% CI,). Performance of all methods declined or was unchanged when the time interval was broadened to 2 years or included serum creatinine measured within a week of admission.
ConclusionsThe mean outpatient serum creatinine measured within a year of hospitalization most closely approximates nephrologist-adjudicated serum creatinine values.
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