Compounding of nonsterile amino acid components of PN was initiated due to a manufacturer shortage. Failure to follow recommended compounding standards contributed to an outbreak of S. marcescens BSIs. Improved adherence to sterile compounding standards, critical examination of standards for sterile compounding from nonsterile ingredients, and more rigorous oversight of compounding pharmacies is needed to prevent future outbreaks.

BackgroundHeart failure is one of the most costly diagnosis‐related groups, largely because of hospital readmissions. Objective assessment of volume status to ensure optimization before hospital discharge could significantly reduce readmissions. We previously demonstrated an ultrasound method of quantifying percentage of cross‐sectional area (CSA) change of the right internal jugular vein with Valsalva that reliably estimates central venous pressure.Methods and ResultsPatients admitted with acute decompensated heart failure (ADHF) underwent ultrasound measurements of the right internal jugular vein at end‐expiration and during the strain phase of Valsalva to determine a percentage of CSA change. An initial subgroup of patients with right heart catheterization and accompanying ultrasound measurements of the right internal jugular vein identified a percentage of CSA change predictive of right atrial pressure (RAP) ≥12 mm Hg. Images of admitted ADHF patients were obtained at admission and discharge for final analysis. Simultaneous right heart catheterization and right internal jugular vein ultrasound measurements demonstrated that a <66% CSA change predicted RAP ≥12 mm Hg (positive predictive value: 87%; P<0.05, receiver operating characteristic curve). Elevated admission RAP by percentage of CSA change normalized by discharge (P<0.05), indicating that this test is significantly responsive to therapeutic interventions. Using the cutoff value of 66% CSA change, normal RAP at discharge had 91% predictive value for patients avoiding 30‐day readmission (P<0.05).ConclusionsThis bedside ultrasound technique strongly correlates to invasive RAP measurement in ADHF patients, identifies restoration of euvolemia, and is predictive of 30‐day ADHF readmission. This tool could help guide inpatient ADHF treatment and may lead to reduced readmissions.

Distal embolization of microthrombi during stenting for myocardial infarction (MI) causes microvascular obstruction (MVO). We have previously shown that sonoreperfusion (SRP), a microbubble (MB)-mediated ultrasonic (US) therapy, resolves MVO from venous microthrombi in vitro in saline. However, blood is more viscous than saline and arterial thrombi that embolize during stenting are mechanically distinct from venous clot. Therefore, we tested the hypothesis that MVO created with arterial microthrombi are more resistant to SRP therapy compared with venous microthrombi and higher viscosity further increases the US requirement for effective SRP in an in vitro model of MVO. Lipid MB suspended in plasma with adjusted viscosity (1.1 or 4.0 cP) were passed through tubing bearing a mesh with 40 μm pores to simulate a microvascular cross-section; upstream pressure reflected thrombus burden. To simulate MVO, the mesh was occluded with either arterial or venous microthrombi to increase upstream pressure to 40±5 mmHg. Therapeutic long-tone-burst US was delivered to the occluded area for 20 min. MB activity was recorded with a passive cavitation detector (PCD). MVO caused by arterial microthrombi at either blood or plasma viscosity resulted in less effective SRP therapy, compared to venous thrombi. Higher viscosity further reduced the effectiveness of SRP therapy. PCD showed a decrease in inertial cavitation when viscosity was increased while stable cavitation was affected in a more complex manner. Overall, these data suggest that arterial thrombi may require higher acoustic pressure US than venous thrombi to achieve similar SRP efficacy, increased viscosity decreases SRP efficacy, and both inertial and stable cavitation are implicated in observed SRP efficacy.