BACKGROUND Peripherally inserted central catheters (PICCs) are increasingly utilized. Patient and system factors that increase risk of complications should be identified to avoid preventable patient harm. METHODS A case control analysis of adult inpatients who underwent PICC placement from January 2009 to January 2010 at Scott & White Memorial Hospital was conducted to determine the incidence and risk factors for complications. One hundred seventy cases of inpatients who experienced PICC‐related complications were identified. Age‐ and gender‐matched controls were randomly selected among patients who underwent PICC placement without documented complications during this time. RESULTS A total of 1444 PICCs were placed, with a complication rate of 11.77% (95% confidence interval: 10.11%‐13.44%). Complications included catheter‐associated thrombosis (3%), mechanical complications (4%), catheter‐associated bloodstream infections (2%), and cellulitis (1%). In multivariable logistic regression analyses, malnutrition and after‐hours placement were significantly associated with increased risk of complications, as was body mass index (BMI) >30 after adjusting for anticoagulation and time of placement. In a secondary multivariable logistic regression analysis, after‐hours placement and malnutrition were significantly associated with increased risk of nonmechanical complications. Additionally, in conditional univariate analyses, length of stay, malnutrition, and after‐hours placement were associated with increased risk of catheter‐associated thrombosis. In our multivariable logistic regression analyses, use of anticoagulation/antiplatelet agents was associated with decreased risk of all‐cause complications, nonmechanical complications, and catheter‐associated thrombosis. CONCLUSIONS Screening of patients undergoing PICC placement with attention to malnutrition, BMI >30, and length of stay may reduce the risk of PICC‐associated complications. Use of anticoagulation/antiplatelet agents and avoiding after‐hours placement may reduce complications and enhance patient safety. Journal of Hospital Medicine 2014;9:481–489. © 2014 Society of Hospital Medicine
Coxiella burnetii, the etiological agent of Q fever, is a gram-negative obligate intracellular bacterium. Two striking characteristics of this microorganism are its ability to thrive within a phagolysosome and its ability to persist in the environment outside a host cell. These abilities have been attributed to the existence of C. burnetii developmental cycle variants: large-cell variants (LCV), small-cell variants (SCV), and small dense cells (SDC). Variants differ in protein profiles, including differential expression of a major outer membrane protein (MOMP) of C. burnetii, designated P1. The ϳ29-kDa MOMP is highly expressed in LCV, downregulated in SCV, and not apparent in SDC. We sought to characterize P1 through purification of native protein for N-terminal analysis, cloning, and functional studies. Highly purified P1, extracted from C. burnetii membranes by using the zwitterionic detergent Empigen, allowed the determination of N-terminal and internal peptide sequences. The entire P1 coding locus was cloned by PCR amplification based upon these peptide sequences, followed by inverse PCR. Comparison of the predicted P1 amino acid sequences among the C. burnetii isolates Nine Mile, Koka, Scurry, and Kerns indicated a high degree of conservation. Structural prediction suggests that the peptide has a predominantly -sheet conformation, consistent with bacterial porins. Typical porin characteristics were observed for native P1, including detergent solubilization properties, heat modification of purified protein, and channel formation in a planar lipid bilayer. Characterization of differentially expressed P1 as a porin increases our understanding of the function of morphological variants and their role in pathogenesis.
The agent of acute and chronic Q fever, Coxiella burnetii, occupies a unique niche among intracellular pathogens. The mechanisms the organism employs to cause disease are unclear but involve persistence in a parasitophorous vacuole and the subsequent host response. Studies designed to model molecular mechanisms of pathogenesis have relied upon indirect evidence for testing the role of virulence factors since methods for generation of defined mutations have not been developed. Evidence suggests replication involving a developmental lifecycle is critical for intra- and extracellular survival but this cycle is incompletely defined. It has been proposed that survival in the phagolysosomal-like parasitophorous vacuole requires specific iron uptake systems, secretion of enzymes to detoxify the compartment (catalase and SOD), and down-regulation of an oxidative burst (acid phosphatase). Studies to test these potential virulence mechanisms can be accelerated with the recent development of the complete genome sequence for the prototype acute disease isolate, Nine Mile. Proteins differentially expressed during the developmental cycle can more readily be identified with MALDI-TOF description of proteomic profiles. Genes encoding secreted Cu/Zn SOD, catalase, and acid phosphatase are predicted and can be tested for function and expression. An iron regulon is predicted based upon Fur-regulated open reading frames. The specific role the iron-regulated genes play in iron acquisition can be tested. Confirmation of the iron regulon and others can be tested using microarrays based upon the genomic ORF predictions. These are examples of how we are rapidly changing the experimental approaches used to investigate C. burnetii to improve our understanding of the biology of this unusual and highly adapted organism.
In recent years, there has been increased interest in stemming the tide of hospital readmissions in an attempt to improve quality of care. This study presents the Phase I results of a resident-led quality improvement initiative to determine the percentage of and risk factors for same-cause readmissions (SCRs; defined as hospital readmission within 30 days of hospital discharge for treatment of the same condition) to the internal medicine service of a multispecialty teaching hospital in central Texas. Results indicate that patients diagnosed with chronic obstructive pulmonary disease/asthma or anemia may be at increased risk for SCRs. Those patients who are insured by Medicaid and those who require assistance from social services also demonstrated an increased risk for SCRs. This study appears to be the first resident-led initiative in the field to examine 30-day SCRs to an internal medicine service for demographic and clinical risk factors.
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