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Perencevich E.N.,Iowa City Veterans Affairs Health Care System | Bailey G.,Iowa City Veterans Affairs Health Care System | Winokur P.L.,Iowa City Veterans Affairs Health Care System | Schweizer M.L.,Iowa City Veterans Affairs Health Care System
Antimicrobial Agents and Chemotherapy | Year: 2013

While numerous studies have assessed the outcomes of methicillin-resistant S. aureus (MRSA) colonization over the short term, little is known about longer-term outcomes after discharge. An assessment of long-term outcomes could provide information about the utility of various MRSA prevention approaches. A matched-cohort study was performed among Veterans Affairs (VA) patients screened for MRSA colonization between the years 2007 and 2009 and followed to evaluate outcomes until 2010. Cox proportional-hazard models were used to evaluate the association between MRSA colonization and long-term outcomes, such as infection-related readmission and crude mortality. A total of 404 veterans were included, 206 of whom were MRSA carriers and 198 of whom were noncarriers. There were no culture-proven MRSA infections on readmission among the noncarriers, but 13% of MRSA carriers were readmitted with culture-proven MRSA infections on readmission (P<0.01). MRSA carriers were significantly more likely to be readmitted, to be readmitted more than once due to proven or probable MRSA infections, and to be readmitted within 90 days of discharge than noncarriers (P<0.05). Infection-related readmission (adjusted hazard ratio [HR] = 4.07; 95% confidence interval [CI], 2.16 to 7.67) and mortality (adjusted HR=2.71; 95% CI, 1.87 to 3.91) were significantly higher among MRSA carriers than among noncarriers after statistically adjusting for potential confounders. Among a cohort of VA patients, MRSA carriers are at high risk of infection-related readmission, MRSA infection, and mortality compared to noncarriers. Noncarriers are at very low risk of subsequent MRSA infection. Future studies should address whether interventions such as nasal or skin decolonization could result in improved outcomes for MRSA carriers. Copyright © 2013, American Society for Microbiology.


News Article | October 31, 2016
Site: www.eurekalert.org

Study in mice suggests that protecting axons may prevent development of neurological problems associated with TBI More than 200,000 U.S. soldiers serving in the Middle East have experienced a blast-related traumatic brain injury, making it a common health problem and concern for that population. Traumatic brain injury (TBI) can have various harmful long-term neurological effects, including problems with vision, coordination, memory, mood, and thinking. According to the Centers for Disease Control and Prevention, TBI from a head injury is a leading cause of death and disability in the United States, and close to 5 million Americans--soldiers and non-soldiers alike--are currently living with a TBI-related disability. Current therapy for these patients involves supportive care and rehabilitation, but no treatments are available that can prevent the development of chronic neurological symptoms. Researchers from the University of Iowa believe they may have identified a potential approach for preventing the development of neurological problems associated with TBI. Their research in mice suggests that protecting axons--the fiber-like projections that connect brain cells--prevents the long-term neuropsychiatric problems caused by blast-related traumatic brain injury. In a recent study, the UI team, led by Andrew Pieper, MD, PhD, professor of psychiatry at the UI Carver College of Medicine, investigated whether early damage to axons--an event that is strongly associated with many forms of brain injury, including blast-related TBI--is simply a consequence of the injury or whether it is a driving cause of the subsequent neurological and psychiatric symptoms. To answer that question, the researchers used mice with a genetic mutation that protects axons from some forms of damage. The mutation works by maintaining normal levels of an important energy metabolite known as nicotinamide adenine dinucleotide (NAD) in brain cells after injury. When mice with the mutation experienced blast-mediated TBI, their axons were protected from damage, and they did not develop the vision problems or the thinking and movement difficulties that were seen when mice without the mutation experienced blast-related TBI. The findings were published Oct. 11 in the online journal eNeuro. "Our work strongly suggests that early axonal injury appears to be a critical driver of neurobehavioral complications after blast-TBI," says Pieper, who also is a professor of neurology, radiation oncology, and a physician with the Iowa City Veterans Affairs Health Care System. "Therefore, future therapeutic strategies targeted specifically at protecting or augmenting the health of axons may provide a uniquely beneficial approach for preventing these patients from developing neurologic symptoms after blast exposure." In confirming the critical relationship between axon degeneration and development of subsequent neurological complication, the new study builds on previous work from Pieper's lab. The researchers also have discovered a series of neuroprotective compounds that appear to help axons survive the kind of early damage seen in TBI. These compounds activate a molecular pathway that preserves neuronal levels of NAD, the energy metabolite that has been shown to be critical to the health of axons. Pieper's team previously demonstrated that these neuroprotective compounds block axonal degeneration and protect mice from harmful neurological effects of blast-TBI, even when the compound are given 24 to 36 hours after the blast injury. In addition to Pieper, the research team included Terry Yin, Jaymie Voorhees, Rachel Genova, Kevin Davis, Ashley Madison, Jeremiah Britt, Coral Cinton, Latisha McDaniel, and Matthew Harper. Pieper also is a member of the Pappajohn Biomedical Institute at the UI. The research was supported by funds from Calico LLC (California Life Company) and the Mary Alice Smith Fund for Neuropsychiatry Research.


Morgan D.J.,University of Maryland Baltimore County | Morgan D.J.,Veterans Affairs Maryland Health Care System | Pineles L.,University of Maryland Baltimore County | Pineles L.,Veterans Affairs Maryland Health Care System | And 9 more authors.
Infection Control and Hospital Epidemiology | Year: 2013

Background and objective. Conta ctprecautions are a cornerstone of infection prevention but have also been associated with less healthcare worker (HCW) contact and adverse events. We studied how contact precautions modified HCW behavior in 4 acute care facilities. Design. Prospective cohort study. Participants and setting. Four acute care facilities in the United States performing active surveillance for methicillin-resistant Staphylococcus aureus. Methods. Trained observers performed "secret shopper" monitoring of HCW activities during routine care, using a standardized collection tool and fixed 1-hour observation periods. Results. A total of 7,743 HCW visits were observed over 1,989 hours. Patients on contact precautions had 36.4% fewer hourly HCW visits than patients not on contact precautions (2.78 vs 4.37 visits per hour; P <.001) as well as 17.7% less direct patient contact time with HCWs (13.98 vs 16.98 minutes per hour; P =.02). Patients on contact precautions tended to have fewer visitors (23.6% fewer; P =.08). HCWs were more likely to perform hand hygiene on exiting the room of a patient on contact precautions (63.2% vs 47.4% in rooms of patients not on contact precautions; P <.001). Conclusion. Contact precautions were found to be associated with activities likely to reduce transmission of resistant pathogens, such as fewer visits and better hand hygiene at exit, while exposing patients on contact precautions to less HCW contact, less visitor contact, and potentially other unintended outcomes. © 2012 by The Society for Healthcare Epidemiology of America. All rights reserved.


News Article | March 2, 2017
Site: www.eurekalert.org

Researchers from the University of Iowa Carver College of Medicine and the University of Miami Miller School of Medicine have shown that a neuroprotective compound tested in rats provides two-pronged protection for brain cells during stroke and improves physical and cognitive outcomes in the treated animals. Every year, nearly 800,000 Americans have a stroke and almost 130,000 die. Survivors often are left with long-term physical and cognitive disability that significantly alters their lives. When a stroke interrupts the brain's blood supply, mature brain cells (neurons) die. In addition, reestablishing blood flow, known as reperfusion, also leads to processes that cause cell death. A part of the brain's natural response to stroke injury is to increase production of new brain cells in two specific regions (the subgranular zone of the hippocampal dentate gyrus and the subventricular zone of the lateral ventricles), which normally make a smaller number of new brain cells every day. Unfortunately, the vast majority of these newborn cells die within one to two weeks, limiting the benefit of this potential repair process. Minimizing the loss of brain cells is a primary goal for new stroke therapies. "If we could prevent the mature brain cells from dying that would be beneficial," says Andrew Pieper, MD, PhD, professor of psychiatry in the UI Carver College of Medicine and co-senior study author. "But if we could also support or enhance this surge in neurogenesis (birth of new neurons), we might be able to further foster recovery, especially in terms of cognitive function, which is critically dependent on the hippocampus." Using rats, Pieper and his colleagues Zachary B. Loris and W. Dalton Dietrich, PhD, tested the effects of a compound called P7C3-A20 on these two aspects of neuroprotection following ischemic stroke. Blood flow to the rats' brains was interrupted for 90 minutes and then the blockage was cleared allowing reperfusion. One group of rats was given the P7C3-A20 compound twice daily for seven days following the stroke. P7C3-A20 has previously been shown to prevent brain cell death in other animal models of neurologic injury, including Parkinson's disease, amyotrophic lateral sclerosis, stress-associated depression, and traumatic brain injury. In terms of the brain itself, the P7C3-A20 compound reduced loss of brain tissue (atrophy) and increased survival of newborn neurons six weeks after stroke. In addition to the improved survival of both mature and newborn neurons, rats that received the P7C3-A20 compound for seven days after stroke also had better physical and cognitive outcomes than untreated rats. Treated rats had improved balance and coordination one week after stroke, and improved learning and memory one month after stroke. The findings were published recently in the journal Experimental Neurology. "There is no previous demonstration of a pharmacologic agent that both protects mature neurons from dying and also boosts the net magnitude of neurogenesis," Pieper says. "Our compound is beneficial in this animal model of stroke, and we're hopeful that it might eventually benefit patients." "Currently there are limited treatments for acute stroke that make a real difference in patient's lives. There is an urgent need to identify, test, and translate new therapies to the clinic," adds Dietrich, co-senior study author and Scientific Director of The Miami Project to Cure Paralysis, professor of neurological surgery, neurology, biomedical engineering and cell biology at the University of Miami where the studies were conducted. "The ability to both protect and repair the injured nervous system has major implications on how we think about improving outcomes in millions of people each year with acute neurological injuries." The neuronal protection provided by the P7C3-A20 compound was also associated with a boost in the levels of a substance called nicotinamide adenine dinucleotide (NAD) in the rats' brains. NAD is emerging as an important player in neuronal health and survival. Levels of this substance are depleted during stroke, and it has been proposed that increasing NAD levels may be a therapeutic target for treating stroke. In this study, P7C3-A20 treatment restored NAD to normal levels in the rats' cortex after a stroke. Importantly, the study examined the effects of P7C3-A20 on cognitive and physical outcomes well beyond the time of the initial stroke. The sustained physical and cognitive improvement seen in the rats up to one month after the stroke suggests that the P7C3-A20 compound provides a long-term benefit. "We found we can give the compound in this critical period immediately after the stroke and it has a lasting effect," notes Pieper, who also is a professor of neurology, radiation oncology, and a psychiatrist with the Iowa City Veterans Affairs Health Care System. In recent years, advances in treatments that break up or remove stroke-causing blood clots have reduced the death rate for stroke and are improving outcomes for patients. The researchers hope that a treatment based on P7C3-A20 used in addition to the clot-clearing therapies might further improve outcomes by protecting brain cells during the traumatic ischemia/reperfusion period. The research was supported by funding from the American Heart Association, The Miami Project to Cure Paralysis, the Mary Alice Smith Fund for Neuropsychiatry Research, the Titan Neurologic Research fund, and the University of Iowa and the Department of Veterans Affairs.


News Article | November 2, 2016
Site: www.sciencedaily.com

More than 200,000 U.S. soldiers serving in the Middle East have experienced a blast-related traumatic brain injury, making it a common health problem and concern for that population. Traumatic brain injury (TBI) can have various harmful long-term neurological effects, including problems with vision, coordination, memory, mood, and thinking. According to the Centers for Disease Control and Prevention, TBI from a head injury is a leading cause of death and disability in the United States, and close to 5 million Americans -- soldiers and non-soldiers alike -- are currently living with a TBI-related disability. Current therapy for these patients involves supportive care and rehabilitation, but no treatments are available that can prevent the development of chronic neurological symptoms. Researchers from the University of Iowa believe they may have identified a potential approach for preventing the development of neurological problems associated with TBI. Their research in mice suggests that protecting axons -- the fiber-like projections that connect brain cells -- prevents the long-term neuropsychiatric problems caused by blast-related traumatic brain injury. In a recent study, the UI team led by Andrew Pieper, professor of psychiatry at the UI Carver College of Medicine, investigated whether early damage to axons -- an event that is strongly associated with many forms of brain injury, including blast-related TBI -- is simply a consequence of the injury or whether it is a driving cause of the subsequent neurological and psychiatric symptoms. To answer that question, the researchers used mice with a genetic mutation that protects axons from some forms of damage. The mutation works by maintaining normal levels of an important energy metabolite known as nicotinamide adenine dinucleotide (NAD) in brain cells after injury. When mice with the mutation experienced blast-mediated TBI, their axons were protected from damage, and they did not develop the vision problems, or the thinking and movement difficulties that were seen when mice without the mutation experienced blast-related TBI. The findings were published Oct. 11 in the online journal eNeuro. "Our work strongly suggests that early axonal injury appears to be a critical driver of neurobehavioral complications after blast-TBI," says Pieper, who also is a professor of neurology, radiation oncology, and a physician with the Iowa City Veterans Affairs Health Care System. "Therefore, future therapeutic strategies targeted specifically at protecting or augmenting the health of axons may provide a uniquely beneficial approach for preventing these patients from developing neurologic symptoms after blast exposure." In confirming the critical relationship between axon degeneration and development of subsequent neurological complication, the new study builds on previous work from Pieper's lab. The researchers also have discovered a series of neuroprotective compounds that appear to help axons survive the kind of early damage seen in TBI. These compounds activate a molecular pathway that preserves neuronal levels of NAD, the energy metabolite that has been shown to be critical to the health of axons. Pieper's team previously demonstrated that these neuroprotective compounds block axonal degeneration and protect mice from harmful neurological effects of blast-TBI, even when the compound are given 24 to 36 hours after the blast injury.


Waters T.M.,University of Tennessee Health Science Center | Daniels M.J.,University of Texas at Austin | Bazzoli G.J.,Virginia Commonwealth University | Perencevich E.,University of Iowa | And 8 more authors.
JAMA Internal Medicine | Year: 2015

IMPORTANCE In 2008, Medicare implemented the Hospital-Acquired Conditions (HACs) Initiative, a policy denying incremental payment for 8 complications of hospital care, also known as never events. The regulation's effect on these events has not been well studied. OBJECTIVE To measure the association between Medicare's nonpayment policy and 4 outcomes addressed by the HACs Initiative: central line-associated bloodstream infections (CLABSIs), catheter-associated urinary tract infections (CAUTIs), hospital-acquired pressure ulcers (HAPUs), and injurious inpatient falls. DESIGN, SETTING, AND PARTICIPANTS Quasi-experimental study of adult nursing units from 1381 US hospitals participating in the National Database of Nursing Quality Indicators (NDNQI), a program of the American Nurses Association. The NDNQI data were combined with American Hospital Association, Medicare Cost Report, and local market data to examine adjusted outcomes. Multilevel models were used to evaluate the effect of Medicare's nonpayment policy never events. EXPOSURES United States hospitals providing treatment for Medicare patients were subject to the new payment policy beginning in October 2008. MAIN OUTCOMES AND MEASURES Changes in unit-level rates of HAPUs, injurious falls, CLABSIs, and CAUTIs after initiation of the policy. RESULTS Medicare's nonpayment policy was associated with an 11% reduction in the rate of change in CLABSIs (incidence rate ratio [IRR], 0.89; 95%CI, 0.83-0.95) and a 10% reduction in the rate of change in CAUTIs (IRR, 0.90; 95%CI, 0.85-0.95), but was not associated with a significant change in injurious falls (IRR, 0.99; 95%CI, 0.99-1.00) or HAPUs (odds ratio, 0.98; 95%CI, 0.96-1.01). Consideration of unit-, hospital-, and market-level factors did not significantly alter our findings.CONCLUSIONS AND RELEVANCE The HACs Initiative was associated with improvements in CLABSI and CAUTI trends, conditions for which there is strong evidence that better hospital processes yield better outcomes. However, the HACs Initiative wanot associated with improvements in HAPU or injurious fall trends, conditions for which there is less evidence that changing hospital processes leads to significantly better outcomes. © 2015 American Medical Association. All rights reserved.


Bernardy N.C.,National Center for PTSD | Lund B.C.,Comprehensive Care | Alexander B.,Iowa City Veterans Affairs Health Care System | Friedman M.J.,National Center for PTSD
Pain Medicine (United States) | Year: 2014

Background: Posttraumatic stress disorder (PTSD) treatment is often complicated in veterans by co-occurring conditions including pain, insomnia, brain injury, and other mental disorders. Pharmacologic approaches to these conditions can produce an accumulation of sedating medications with potential for safety concerns. Objective: The objective of this study was to characterize polysedative prescribing among veterans with PTSD over an 8-year period. Design: National Department of Veterans Affairs (VA) data were used to identify veterans with PTSD using International Classification of Diseases, Ninth Revision codes among regular medication users. Prescribing of benzodiazepines, hypnotics, atypical antipsychotics, opioids, and muscle relaxants was determined annually. Prevalence and incidence rates were determined for each medication class from 2004 through 2011. Polysedative use was determined from longitudinal refill patterns that indicated concurrent use across sedative classes. Results: In 2004, 9.8% of veterans with PTSD concurrently received medications from three or more sedative classes. By 2011, the prevalence of concurrent use involving three or more classes increased to 12.1%. Polysedative use varied across demographic subgroups, with higher rates observed among women, rural residents, younger adults, Native Americans and Whites. The most common combination was an opioid plus a benzodiazepine, taken concurrently by 15.9% of veterans with PTSD. Conclusions: Important trends in polysedative use among veterans with PTSD illustrate the complexity of treating an intersecting cluster of symptoms managed by sedative medications. As the VA seeks to improve care by focusing on non-pharmacologic options, our findings emphasize the need for a comprehensive approach that encompasses overlapping conditions of relevance to veterans with PTSD. © 2014 Wiley Periodicals, Inc.


Skoff R.A.,Iowa City Veterans Affairs Health Care System | Waterbury N.V.,Iowa City Veterans Affairs Health Care System | Shaw R.F.,Iowa City Veterans Affairs Health Care System | Egge J.A.,University of Iowa | Cantrell M.,University of Iowa
Journal of Managed Care Pharmacy | Year: 2011

Background: In 2009, the Veterans Health Administration (VHA) released a national bulletin regarding the risk of hypoglycemia associated with the use of glyburide in elderly patients with renal dysfunction. Providers were encouraged to avoid glyburide and use glipizide in patients with a calculated creatinine clearance (CrCl) of less than 50 mL per minute. Since this initiative, many veterans were converted by their providers from glyburide to glipizide regardless of renal impairment. Objectives: To (a) identify whether hemoglobin A1c remained equivalent in patients converted from glyburide to glipizide, (b) evaluate the prevalence of hypoglycemia during treatment with glyburide or glipizide, © compare change in glycemic control for renally impaired versus nonimpaired patients, and (d) analyze dosage conversion ratios selected by providers and measures of patient follow-up after conversion including time until A1c measurement and number of glipizide dose titrations. Methods: This was a single-center, retrospective analysis of veterans converted from glyburide to glipizide from January 1, 2008, through May 31, 2010, who had documented A1c values concurrent with glyburide and glipizide use. A 2-sided equivalence analysis was used for the primary outcome. Equivalence was defined as a change in mean A1c of ± 0.2. Hypoglycemia was defined as blood glucose of less than 70 mg per dL, symptoms of hypoglycemia, or hypoglycemia that led to a fall, loss of consciousness, emergency room visit, hospitalization, or death. The pre- to post-conversion change in rates of hypoglycemia was tested for significance using a McNemar's test. Results: In the 141 (99.3% male, 53.9% CrCl < 50 mL per minute, mean age = 74.0 years) patients meeting inclusion criteria between 2008-2010, the average change in A1c (+ 0.34) was nonequivalent after conversion from glyburide to glipizide (7.08% vs. 7.42%, respectively). Hypoglycemia occurred more frequently during treatment with glyburide than glipizide (31.2% vs. 12.8%, respectively, P < 0.001). Mean dose conversion ratios were consistent with VHA recommendations (1 mg per day glyburide = 1.26-1.55 mg per day glipizide). Conclusions: Conversion from glyburide to glipizide was associated with an increase in A1c, but the incidence of hypoglycemia was reduced. Results of this study are consistent with the recommendation of the American Diabetes Association and European Association for the Study of Diabetes to use second-generation sulfonylureas other than glyburide. Patients converted to glipizide should be monitored closely to adjust therapy as appropriate to maintain glycemic control. © 2011, Academy of Managed Care Pharmacy.


Nuno D.W.,Iowa City Veterans Affairs Health Care System | Nuno D.W.,University of Iowa | England S.K.,University of Iowa | England S.K.,Washington University in St. Louis | And 2 more authors.
American Journal of Physiology - Regulatory Integrative and Comparative Physiology | Year: 2012

Vascular smooth muscle contraction occurs following an initial response to an increase in intracellular calcium concentration and a sustained response following increases in the sensitivity of contractile proteins to calcium (calcium sensitization). This latter process is regulated by the rhoA/ rho kinase pathway and activated by serotonin. In multiple cell types, signaling molecules compartmentalize within caveolae to regulate their activation. We hypothesized that serotonin differentially compartmentalizes rhoA within caveolar versus noncaveolar lipid rafts to regulate sustained vascular contractions. To test this hypothesis, we measured aortic contractions in response to serotonin in wild-type (WT) and cav-1-deficient mice (cav-1 KO). RhoA-dependent contractions in response to serotonin were markedly augmented in arteries from cav-1 KO mice despite a modest reduction in rhoA expression compared with WT. We found that under basal conditions, rhoA in WT arteries was primarily localized within high-density sucrose gradient fractions but temporally shifted to low-density fractions in response to serotonin. In contrast, rhoA in cav-1 KO arteries was primarily in low-density fractions and shifted to high-density fractions in a similar timeframe as that seen in WT mice. We conclude that localization of rhoA to caveolar versus noncaveolar lipid rafts differentially regulates its activation and contractions to rhoA-dependent agonists with greater activation associated with its localization to noncaveolar rafts. Disruption of rhoA localization within caveolae may contribute to increased activation and enhanced vascular contractions in cardiovascular disease. © 2012 the American Physiological Society.


Chiang H.-Y.,University of Iowa | Herwaldt L.A.,University of Iowa | Blevins A.E.,University of Iowa | Cho E.,University of Iowa | And 2 more authors.
Spine Journal | Year: 2014

Background context Some surgeons use systemic vancomycin to prevent surgical site infections (SSIs), but patients who do not carry methicillin-resistant Staphylococcus aureus have an increased risk of SSIs when given vancomycin alone for intravenous prophylaxis. Applying vancomycin powder to the wound before closure could increase the local tissue vancomycin level without significant systemic levels. However, the effectiveness of local vancomycin powder application for preventing SSIs has not been established. Purpose Our objective was to systematically review and evaluate studies on the effectiveness of local vancomycin powder for decreasing SSIs. Study design Meta-analysis. Sample We included observational studies, quasi-experimental studies, and randomized controlled trials of patients undergoing surgical procedures that involved vancomycin powder application to surgical wounds, reported SSI rates, and had a comparison group that did not use local vancomycin powder. Outcome measures The primary outcome was postoperative SSIs. The secondary outcomes included deep incisional SSIs and S. aureus SSIs. Methods We performed systematic literature searches in PubMed, the Cochrane Database of Systematic Reviews, the Database of Abstracts of Reviews of Effects, the Cochrane Central Register of Controlled Trials via Wiley, Scopus (including EMBASE abstracts), Web of Science, ClinicalTrials.gov, BMC Proceedings, ProQuest Dissertation, and Thesis in Health and Medicine, and conference abstracts from IDWeek, the Interscience Conference on Antimicrobial Agents and Chemotherapy, the Society for Healthcare Epidemiology of America, and the American Academy of Orthopedic Surgeons annual meetings, and also the Scoliosis Research Society Annual Meeting and Course. We ran the searches from inception on May 9, 2013 with no limits on date or language. After reviewing 373 titles or abstracts and 22 articles in detail, we included 10 independent studies and used a random-effects model when pooling risk estimates to assess the effectiveness of local vancomycin powder application for preventing SSIs, the outcome of interest. We used the I2-index, Q-statistic, and corresponding p value to assess the heterogeneity of the risk estimates, and funnel plots to assess publication bias. Results We included seven quasi-experimental studies, two cohort studies, and one randomized controlled trial, encompassing 5,888 surgical patients. The pooled effects showed that applying local vancomycin powder was significantly protective against SSIs (pooled odds ratio [pOR] 0.19; 95% confidence interval [CI] 0.09-0.38), deep incisional SSIs (pOR 0.23; 95% CI 0.09-0.57), and SSIs caused by S. aureus (pOR 0.22; 95% CI 0.08-0.58). However, significant heterogeneity was present for studies evaluating all SSIs or deep incisional SSIs. When we pooled the risk estimates from the eight studies that assessed patients undergoing spinal operations, vancomycin powder remained significantly protective against SSIs (pOR 0.16; 95% CI 0.09-0.30), deep incisional SSIs (pOR 0.18; 95% CI 0.09-0.36), and SSIs caused by S. aureus (pOR 0.11; 95% CI 0.03-0.36). The pooled ORs from studies of spinal operations were lower than those for all studies and the estimates from spinal operation studies were homogeneous. However, there was evidence of publication bias. Conclusions Local administration of vancomycin powder appears to protect against SSIs, deep incisional SSIs, and S. aureus SSIs after spinal operations. Large, high-quality studies should be performed to evaluate this intervention before it is used routinely. © 2014 Elsevier Inc. All rights reserved.

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