Vancomycin-resistant Enterococcus outbreak in a pre- and post-cardiothoracic transplant population: Impact of discontinuing multidrug-resistant organism surveillance during the coronavirus disease 2019 pandemic.

INTRODUCTION: Many institutions suspended surveillance and contact precautions for multidrug-resistant organisms (MDROs) at the outset of the coronavirus disease 2019 (COVID-19) pandemic due to a lack of resources. Once our institution reinstated surveillance in September 2020, a vancomycin-resistant Enterococcus (VRE) faecium outbreak was detected in the cardiothoracic transplant units, a population in which we had not previously detected outbreaks. METHODS: An outbreak investigation was conducted using pulsed-field gel electrophoresis for strain typing and electronic medical record review to determine the clinical characteristics of involved patients. The infection prevention (IP) team convened a multidisciplinary process improvement team comprised of IP, cardiothoracic transplant nursing and medical leadership, environmental services, and the microbiology laboratory. RESULTS: Between December 2020 and March 2021, the outbreak involved thirteen patients in the cardiothoracic transplant units, four index cases, and nine transmissions. Of the 13, seven (54%) were on the transplant service, including heart and lung transplant recipients, patients with ventricular assist devices, and a patient on extracorporeal membrane oxygenation as a bridge to lung transplantation. Four of 13 (31%) developed a clinical infection. DISCUSSION: Cardiothoracic surgery/transplant patients may have a similar risk for VRE-associated morbidity as abdominal solid organ transplant and stem cell transplant patients, highlighting the need for aggressive outbreak management when VRE transmission is detected. Our experience demonstrates an unintended consequence of discontinuing MDRO surveillance in this population and highlights a need for education, monitoring, and reinforcement of foundational infection prevention measures to ensure optimal outcomes.

Pulse pressure and perioperative stroke.

PURPOSE OF REVIEW: Central pulse pressure (PP), a marker of vascular stiffness, is a novel indicator of risk for perioperative morbidity including ischemic stroke. Appreciation for the mechanism by which vascular stiffness leads to organ dysfunction along with understanding its clinical detection may lead to improved patient management. RECENT FINDINGS: Vascular stiffness is associated with increased mortality and neurologic, cardiac, and renal injury in nonsurgical and surgical patients. Left ventricular hypertrophy and diastolic dysfunction along with microcirculatory changes in the low vascular resistance, high blood flow, cerebral and renal vasculature are seen in patients with vascular stiffness. Pulse wave velocity and the augmentation index have higher sensitivity for detecting of vascular stiffness than peripheral PP as the hemodynamic consequences of vascular stiffness are secondary to alterations in the central vasculature. Vascular stiffness alters cerebral autoregulation, resulting in a high likelihood of having a lower limit of autoregulation more than 65 mmHg during surgery. Vascular stiffness may predispose to cerebral hypoperfusion, increasing vulnerability to ischemic stroke, postoperative delirium, and acute kidney injury. SUMMARY: Vascular stiffness leads to alterations in cerebral, cardiac, and renal hemodynamics increasing the risk of perioperative ischemic stroke and neurologic, cardiac, and renal dysfunction.

Extracorporeal Membrane Oxygenation Can Successfully Support Patients With Severe Acute Respiratory Distress Syndrome in Lieu of Mechanical Ventilation.

OBJECTIVES: Extracorporeal membrane oxygenation is increasingly used in the management of severe acute respiratory distress syndrome. With extracorporeal membrane oxygenation, select patients with acute respiratory distress syndrome can be managed without mechanical ventilation, sedation, or neuromuscular blockade. Published experience with this approach, specifically with attention to a patient's respiratory drive following cannulation, is limited. DESIGN: We describe our experience with three consecutive patients with severe acute respiratory distress syndrome supported with right jugular-femoral configuration of venovenous extracorporeal membrane oxygenation without therapeutic anticoagulation as an alternative to lung-protective mechanical ventilation. Outcomes are reported including daily respiratory rate, vital capacities, and follow-up pulmonary function testing. RESULTS: Following cannulation, patients were extubated within 24 hours. During extracorporeal membrane oxygenation support, all patients were able to maintain a normal respiratory rate and experienced steady improvements in vital capacities. Patients received oral nutrition and ambulated daily. At follow-up, no patients required supplemental oxygen. CONCLUSIONS: Our results suggest that venovenous extracorporeal membrane oxygenation can provide a safe and effective alternative to lung-protective mechanical ventilation in carefully selected patients. This approach facilitates participation in physical therapy and avoids complications associated with mechanical ventilation.

Cerebral Small Vessel, But Not Large Vessel Disease, Is Associated With Impaired Cerebral Autoregulation During Cardiopulmonary Bypass: A Retrospective Cohort Study.

BACKGROUND: Impaired cerebral blood flow (CBF) autoregulation during cardiopulmonary bypass (CPB) is associated with stroke and other adverse outcomes. Large and small arterial stenosis is prevalent in patients undergoing cardiac surgery. We hypothesize that large and/or small vessel cerebral arterial disease is associated with impaired cerebral autoregulation during CPB. METHODS: A retrospective cohort analysis of data from 346 patients undergoing cardiac surgery with CPB enrolled in an ongoing prospectively randomized clinical trial of autoregulation monitoring were evaluated. The study protocol included preoperative transcranial Doppler (TCD) evaluation of major cerebral artery flow velocity by a trained vascular technician and brain magnetic resonance imaging (MRI) between postoperative days 3 and 5. Brain MRI images were evaluated for chronic white matter hyperintensities (WMHI) by a vascular neurologist blinded to autoregulation data. "Large vessel" cerebral vascular disease was defined by the presence of characteristic TCD changes associated with stenosis of the major cerebral arteries. "Small vessel" cerebral vascular disease was defined based on accepted scoring methods of WMHI. All patients had continuous TCD-based autoregulation monitoring during surgery. RESULTS: Impaired autoregulation occurred in 32.4% (112/346) of patients. Preoperative TCD demonstrated moderate-severe large vessel stenosis in 67 (25.2%) of 266 patients with complete data. In adjusted analysis, female sex (odds ratio [OR], 0.46; 95% confidence interval [CI], 0.25-0.86; P = .014) and higher average temperature during CPB (OR, 1.23; 95% CI, 1.02-1.475; P = .029), but not moderate-severe large cerebral arterial stenosis (P = .406), were associated with impaired autoregulation during CPB. Of the 119 patients with available brain MRI data, 42 (35.3%) demonstrated WMHI. The presence of small vessel cerebral vascular disease was associated with impaired CBF autoregulation (OR, 3.25; 95% CI, 1.21-8.71; P = .019) after adjustment for age, history of peripheral vascular disease, preoperative hemoglobin level, and preoperative treatment with calcium channel blocking drugs. CONCLUSIONS: These data confirm that impaired CBF autoregulation is prevalent during CPB predisposing affected patients to brain hypoperfusion or hyperperfusion with low or high blood pressure, respectively. Small vessel, but not large vessel, cerebral vascular disease, male sex, and higher average body temperature during CPB appear to be associated with impaired autoregulation.

Pharmacokinetic Assessment of Pre- and Post-Oxygenator Vancomycin Concentrations in Extracorporeal Membrane Oxygenation: A Prospective Observational Study.

BACKGROUND: Extracorporeal membrane oxygenation (ECMO) is a form of cardiopulmonary life support frequently utilized in catastrophic lung and or cardiac failure. Patients on ECMO often receive vancomycin therapy for treatment or prophylaxis against Gram-positive organisms. It is unclear if ECMO affects vancomycin pharmacokinetics, thus we modeled the pharmacokinetic behavior of vancomycin according to ECMO-specific variables. METHODS: Adult patients receiving vancomycin and Veno-Arterial-ECMO between 12/1/2016 and 10/1/2017 were prospectively enrolled. Extracorporeal membrane oxygenation settings and four sets of pre- and post-oxygenator vancomycin concentrations were collected for each patient. Compartmental models were built and assessed ECMO flow rates on vancomycin clearance and potential circuit sequestration. Bayesian posterior concentrations of the pre- and post-oxygenator concentrations were obtained for each patient, and summary pharmacokinetic parameters were calculated. Simulations were performed from the final model for efficacy and toxicity predictions. RESULTS: Eight patients contributed 64 serum concentrations. Patients were a median (interquartile range) age of 58.5 years (50.8-62.3) with a calculated creatinine clearance of 39 mL/min (29.5-62.5) and ECMO flow rates of 3980 mL/min (interquartile range = 3493.75-4132.5). A three-compartment model best fit the data (Bayesian: plasma pre-oxygenation R2 = 0.99, post-oxygenation R2 = 0.99). Vancomycin clearance was not impacted by ECMO flow rate (p = 0.7). Simulations demonstrated that vancomycin 1 g twice daily was rarely sufficient for minimum inhibitory concentrations > 0.5 mg/L. Doses ≥ 1.5 g twice daily often exceeded toxicity thresholds for exposure. CONCLUSIONS: Extracorporeal membrane oxygenation flow rates did not influence vancomycin clearance between flow rates of 3500 and 5000 mL/min and vancomycin was not sequestered in ECMO. Common vancomycin regimens resulted in suboptimal efficacy and/or excessive toxicity. Individual therapeutic drug monitoring is recommended for patients on ECMO.

Fulminant myocarditis in a patient with coronavirus disease 2019 and rapid myocardial recovery following treatment.

Coronavirus disease 2019 (COVID-19) is a global pandemic increasingly encountered in the clinical setting. It typically manifests as a respiratory illness, although cardiac involvement is common and portends a worse prognosis. We present the case of a 56-year-old male admitted with COVID-19 fulminant myocarditis and cardiogenic shock. We discuss important aspects of the multidisciplinary and interventional care involved in treating cardiogenic shock as well as the likely mechanisms of, and potential treatment for, COVID-19 myocarditis. The various pathways of myocardial injury, including direct viral damage, macrophage activation, and lymphocytic infiltration, are outlined in detail in addition to associated pathology such as cytokine release syndrome. COVID-19 is a complex and multisystem disease process; in addition to supportive care, specific consideration should be given to the underlying mechanism of injury for each patient.

Repeated episodes of respiratory distress in an obese parturient after cesarean delivery.

A 25-yr-old obese parturient with mild asthma underwent an uneventful spinal anesthetic for primary cesarean delivery. Within 4 h after delivery, the patient twice developed acute shortness of breath, inspiratory stridor, and hypoxemia that required intubation. A battery of blood tests revealed no evidence of an allergic reaction. She had a normal echocardiogram and chest computed tomography, but her neck computed tomography showed an enlarged left thyroid lobe asymmetrically compressing the endotracheal tube cuff. We hypothesized that, after delivery, decreased maternal vascular capacitance increased central venous pressure such that venous engorgement of an undiagnosed goiter may have caused symptomatic tracheal compression.

Analysis of prostate-specific antigen rebound interval in patients with prostate cancer receiving hormonal therapy and external-beam radiation therapy.

The goal of this investigation is to characterize the clinical significance of the rebound interval (RI) after neoadjuvant short-course hormonal therapy (HT) and external-beam radiation therapy (RT), during which the prostate-specific antigen (PSA) may rise because of hormone withdrawal prior to full RT efficacy. The charts of 257 consecutive patients with localized prostate cancer who received short-course neoadjuvant HT and RT were reviewed. A piecewise-linear log PSA versus time curve was generated for each patient and averaged over the population to facilitate identification of the RI start and end dates. Existing definitions of biochemical failure--American Society for Therapeutic Radiology and Oncology (ASTRO), Vancouver and Houston--were applied, as were these same definitions modified to exclude failures during the RI. Sensitivity and specificity were analyzed, using no evidence (by digital rectal examination or radiology) of disease failure as the gold standard. The 5-year biochemical survival with different failure definitions were ASTRO versus ASTRO-modified: 81.6% versus 86.7%; Houston versus Houston-modified: 71.4% versus 76.7%; and Vancouver versus Vancouver-modified: 83.5% versus 85.6%. The sensitivity and specificity comparisons were ASTRO versus ASTRO-modified 58.3% versus 33.3%; 91.4% versus 94.3%, Vancouver versus Vancouver-modified: 50% versus 50%; 92.7% versus 95.5%, Houston versus Houston-modified: 100% versus 66.7%; 90.6% versus 92.2%. The RI after HT and RT is likely not merely an artifact of hormone withdrawal but is correlated with ultimate clinical outcome. Excluding RI failures can marginally improve specificity but may possibly have an unacceptable risk of lowering sensitivity. Further work is needed to design and validate definitions of failure, which account for the RI.