Brian J. Anderson
· MD MSCEVerifiedUniversity of Pennsylvania · Rehabilitation Medicine
Active 1979–2026
About
Brian J. Anderson, MD, MSCE, is an Associate Professor of Clinical Medicine specializing in Pulmonary, Allergy, and Critical Care at the Perelman School of Medicine at the University of Pennsylvania. He serves as the Physician Lead for the Critical Care Clinical Effectiveness Team and Medical Director for the Founders Medical Intensive Care Units (MICUs) at the Hospital of the University of Pennsylvania. His clinical expertise includes sepsis and septic shock, mechanical ventilation, acute respiratory failure, delirium, and post-intensive care syndrome. Dr. Anderson attends on critical care services, including the Medical Intensive Care Units, Critical Care Outreach and Procedure Service, and Nocturnal Intensive Care Outreach Service at HUP. His research and quality improvement efforts focus on enhancing ICU outcomes through reducing delirium, preventing hospital-acquired infections, prompt recognition and treatment of sepsis, and implementing care pathways aimed at ventilator liberation. He also collaborates on molecular studies related to sepsis-induced cognitive dysfunction, acute respiratory distress syndrome, and acute kidney injury. Dr. Anderson is involved as a site co-investigator for clinical trials in critically ill patients, contributing to advancing critical care practices and patient outcomes.
Research topics
- Internal medicine
- Virology
- Medicine
- Demography
- Emergency medicine
Selected publications
Whole blood transcriptomics reveals sepsis mortality-associated changes in neutrophil degranulation
American Journal of Respiratory Cell and Molecular Biology · 2026-02-10
articleOpen accessTranscriptomic analysis of blood cells can reveal key elements of the dysregulated host response in sepsis and spur biomarker and mechanism identification. We hypothesized that sepsis nonsurvivors exhibit a distinct transcriptional signature in whole blood that reflects insights to sepsis mortality. We conducted a prospective observational cohort study of 161 critically ill sepsis patients. Whole blood RNA was collected within 24 hours of intensive care unit admission. Gene expression levels were measured using microarrays and changes in gene levels were compared between 30-day nonsurvivors and survivors, adjusting for age, sex, and neutrophil count. Pathway overrepresentation analysis and weighted gene co-expression analysis were performed to identify biological pathways and gene co-expression groups, respectively, associated with sepsis mortality. Gene- and pathway-based results were compared to findings in an independent cohort of 479 sepsis patients with 28-day mortality data. Thirty-day mortality in the enrolled sepsis cohort was 37% (60 of 161 patients). We identified 1,106 differentially expressed genes in nonsurvivors (Benjamini-Hochberg-adjusted p-value <0.05), including several neutrophil-related genes (CEACAM8, ELANE, PRTN3, MPO, CEACAM6, DEFA4, MS4A3) with expression levels over 1.8 times higher in nonsurvivors despite adjusting for neutrophil counts. The neutrophil degranulation pathway was prominent based on its overrepresentation in 1) differentially expressed genes in both cohorts, 2) overrepresentation by gene set enrichment analysis, and 3) four of the six gene co-expression groups correlated with sepsis mortality. Our findings highlight the involvement of neutrophil degranulation genes in sepsis mortality, prompting further study to better understand whether they constitute a modifiable target.
Identifying a Unique Signature of Sepsis in Patients With Pre-existing Cirrhosis
American Journal of Respiratory and Critical Care Medicine · 2025-05-01 · 1 citations
articleAbstract Rationale: A pre-existing diagnosis of cirrhosis is clinically recognized as a risk factor for sepsis and sepsis-associated complications. However, the unique epidemiology, sepsis characteristics, and underlying mechanisms of immune dysregulation in sepsis among patients with cirrhosis remain incompletely understood. Comorbid conditions, including cirrhosis, may influence sepsis biology and host response, and thus identify specific subgroups with sepsis that may benefit from a personalized approach. Our primary objective was to identify clinical and biological characteristics that differ between patients with and without cirrhosis among patients presenting to the ICU with sepsis. Methods: We analyzed data from a prospective cohort of patients presenting to our center's ICU with sepsis, according to Sepsis-3 criteria. Pre-existing diagnosis of cirrhosis and other detailed comorbidity data were extracted from the electronic medical record. Subjects were followed for 6 days for the development of acute respiratory distress syndrome (ARDS) adjudicated according to the Berlin definition and acute kidney injury (AKI) adjudicated according to KDIGO creatinine and dialysis criteria, and for mortality at 30 days. Inflammatory, endothelial, and vascular injury proteins were measured via electrochemiluminescence multiplex array in plasma collected at ICU admission in a subset of patients. We determined associations of cirrhosis with ARDS, AKI, and mortality using multivariable logistic regression adjusting for pre-specified confounders. We tested differences in plasma protein levels by cirrhosis diagnosis using the Wilcoxon Rank-sum test. Results: We enrolled 2,692 subjects between 2008 and 2022, 371 (13%) of whom had a pre-existing diagnosis of cirrhosis. Patients with cirrhosis had higher severity of illness scores, were more likely to have an abdominal source of sepsis, and had more significant coagulation abnormalities relative to patients without cirrhosis (Table). In multivariate analysis, cirrhosis was associated with higher AKI risk (adjusted OR 1.92; 95% CI 1.43 to 2.53; P&lt;0.001) and 30-day mortality (adjusted OR 1.39; 95% CI 1.09 to 1.78; P=0.007), but not ARDS risk (adjusted OR 1.15; 95% CI 0.82 to 1.61; P=0.42). Cirrhosis was associated with higher plasma levels of angiopoietin-2 (P&lt;0.001), von Willebrand factor (P&lt;0.001), and soluble thrombomodulin (P&lt;0.001), as well as lower levels of interleukin (IL)-10 (P&lt;0.001), IL-1β (P=0.008), and IL-1RA (P=0.036) (Table). There were no significant differences in levels of IL-6 (P=0.30). Conclusions: We identified associations between pre-existing cirrhosis and endothelial biomarker concentrations, AKI, and mortality in sepsis. Patients with pre-existing cirrhosis who develop sepsis may display a unique signature of endothelial dysfunction that requires targeted approaches.
Critical Care Explorations · 2025-08-01
articleOpen accessIMPORTANCE: The vascular endothelial growth factor (VEGF) signaling pathway is important in the pathogenesis of acute respiratory distress syndrome (ARDS) with supportive genetic and proteomic evidence. Genetic polymorphisms within FLT1, which encodes VEGF receptor 1, associate with risk of ARDS in sepsis. Soluble Fms-like tyrosine kinase-1 (sFlt-1) is a secreted splice variant of FLT1 that acts as a potent antagonist to circulating VEGF. OBJECTIVES: To assess the association between early plasma concentrations of sFlt-1 and risk of ARDS and to determine if ARDS mediates the relationship between sFlt-1 and mortality during sepsis. DESIGN, SETTING, AND PARTICIPANTS: In a prospective cohort study, we enrolled 198 critically ill patients with sepsis per Sepsis-2 criteria. ARDS was defined per Berlin criteria. MAIN OUTCOMES AND MEASURES: Levels of sFlt-1 were quantified using electrochemiluminescence on plasma collected in the emergency department upon admission. We tested the association between plasma levels of sFlt-1 with ARDS and mortality using logistic regression adjusting for age, sex, and pulmonary versus nonpulmonary source of sepsis. We applied causal mediation analysis to determine the percentage of the total effect of sFlt-1 on mortality that was mediated by ARDS. RESULTS: We enrolled 198 patients; ARDS developed within 6 days in 29%. Plasma levels of sFlt-1 were significantly associated with risk of ARDS in sepsis (odds ratio [OR], 1.91 per log increase; 95% CI, 1.31-2.76 per log increase; p < 0.01). Plasma sFlt-1 levels were also associated with mortality (OR, 2.19 per log increase; 95% CI, 1.57-3.08 per log increase; p < 0.01). ARDS mediated 20.3% (95% CI, 6.9-98.1%) of the total effect of sFlt-1 on mortality (p < 0.01). CONCLUSIONS AND RELEVANCE: Higher plasma levels of sFlt-1 were associated with an increased risk of ARDS and ARDS mediated a significant proportion of the sFlt-1-associated mortality observed during sepsis. Our findings further implicate dysregulated VEGF signaling in ARDS and suggest that plasma sFlt-1 merits further investigation as an early endothelial therapeutic target for sepsis-associated ARDS and mortality.
CHEST Critical Care · 2025-07-30 · 1 citations
articleOpen access<h3>Background</h3> Mechanically ventilated (MV) patients undergoing a transfer to a higher-resourced hospital have variable outcomes. We aimed to evaluate patient outcomes by transfer status and timing. <h3>Research Question</h3> What are the characteristics and outcomes of mechanically ventilated patients who are transferred from 1 ICU to another? Does timing of transfer affect these outcomes? <h3>Study Design and Methods</h3> In a retrospective observational study, we identified patients admitted on a ventilator to a Midwestern health system (7 local hospitals, 1 tertiary hospital) from March 2018 to December 2021. Exposures were transfer status (being transferred to a tertiary hospital or retained at a local hospital) and transfer timing (early transfers if transferred ≤ 2 days after admission or late transfers). Propensity score weighting was used to balance patient characteristics (age, sex, race/ethnicity, insurance, comorbidity, and primary diagnosis) and baseline clinical factors (admission Sequential Organ Failure Assessment score, COVID-19 test, days on mechanical ventilation, major surgery, and ICU use of dialysis, tracheostomy, and vasopressors). Associations with exposures were estimated through multinomial logistic regression for discharge destination or negative binomial regression for total length of stay (LOS). <h3>Results</h3> Of a total of 5,883 adult MV patients, 5,719 were retained and 164 were transfers (80 early transfers and 84 later transfers). Transfers were associated with longer LOS (33.4 days vs 10.2 days; incident rate ratio [IRR] = 3.11; 95% CI, 2.53-3.82; <i>P</i> < .001) and had an increased likelihood of discharge to other facilities (rehabilitation and nursing facilities) (OR = 2.62; 95% CI, 1.51-4.56; <i>P</i> < .01) than retained patients at the local hospitals. Additionally, early transfer was found to be associated with a shorter LOS than late transfers (19.6 days vs 47.7 days; IRR=0.41; 95% CI, 0.33-0.51; <i>P</i> < .01). <h3>Interpretation</h3> Our results show that MV patient transfers within our health system have lower likelihood of discharge to home and longer LOS when compared with MV patients retained at local hospitals. However, the time to transfer may be an important contributor to better outcomes.
Identifying a unique signature of sepsis in patients with pre-existing cirrhosis
Critical Care · 2025-05-19 · 4 citations
articleOpen accessBACKGROUND: The pre-existing diagnosis of cirrhosis is a complicating factor in the progression and prognosis of sepsis; however, the unique epidemiology, sepsis characteristics, and underlying mechanisms of immune dysregulation in sepsis among patients with cirrhosis remain incompletely understood. Our primary objective was to identify clinical outcomes and biological characteristics that differ between patients with and without cirrhosis among critically ill patients with sepsis. METHODS: We analyzed data from a prospective cohort of critically ill patients presenting to single center with sepsis. Subjects were followed for 6 days for the development of acute respiratory distress syndrome (ARDS) and acute kidney injury (AKI), and 30 days for mortality. Inflammatory, endothelial, and coagulopathic proteins were measured in plasma collected at ICU admission in a subset of patients. We determined associations of cirrhosis with outcomes using multivariable logistic regression adjusting for pre-specified confounders. We tested differences in plasma protein levels by cirrhosis diagnosis using the Wilcoxon Rank-sum test. RESULTS: We enrolled 2962 subjects, 371 (13%) of whom had a pre-existing diagnosis of cirrhosis. Patients with cirrhosis had higher severity of illness scores, were more likely to have an abdominal source of sepsis, and had more significant clinically measured coagulation abnormalities relative to patients without cirrhosis. In multivariate analysis, cirrhosis was associated with higher AKI risk (adjusted OR 1.65; 95% CI 1.21 to 2.26; P = 0.002), and 30-day mortality (adjusted OR 1.38; 95% CI 1.05 to 1.82; P = 0.022). There was no significant difference in risk for ARDS (adjusted OR 1.02; 95% CI 0.69 to 1.50; P = 0.92). Cirrhosis was associated with higher plasma levels of angiopoietin-2 (P < 0.001), von Willebrand factor (P < 0.001), and soluble thrombomodulin (P < 0.001), as well as lower levels of interleukin (IL)-10 (P < 0.001), IL-1β (P = 0.008), and IL-1RA (P = 0.036). There were no significant differences in levels of IL-6 (P = 0.30). CONCLUSIONS: We identified associations between pre-existing cirrhosis and endothelial injury, AKI, and mortality in sepsis. Patients with pre-existing cirrhosis who develop sepsis may display a unique phenotype of endothelial dysfunction that requires unique targeted approaches.
Genome-wide Association Between LRRK2 Variants and Risk for Acute Respiratory Distress Syndrome
2024-04-30
articleThe Journal of Cardiovascular Nursing · 2024-03-21 · 1 citations
articleOpen accessBACKGROUND: Sleep disruption, a common symptom among patients requiring cardiovascular surgery, is a potential risk factor for the development of postoperative delirium. Postoperative delirium is a disorder of acute disturbances in cognition associated with prolonged hospitalization, cognitive decline, and mortality. OBJECTIVE: The aim of this study was to evaluate the feasibility and acceptability of using polysomnography (PSG) to capture sleep in patients with scheduled cardiothoracic surgery. METHODS: Wireless limited PSG assessed sleep at baseline (presurgery at home), postoperatively in the intensive care unit, and at home post hospital discharge. Primary outcomes were quality and completeness of PSG signals, and acceptability by participants and nursing staff. RESULTS: Among 15 patients, PSG data were of high quality, and mean percentage of unscorable data was 5.5% ± 11.1%, 3.7% ± 5.4%, and 3.7% ± 8.4% for baseline, intensive care unit, and posthospitalization measurements, respectively. Nurses and patients found the PSG monitor acceptable. CONCLUSIONS: Wireless, limited PSG to capture sleep across the surgical continuum was feasible, and data were of high quality. Authors of future studies will evaluate associations of sleep indices and development of postoperative delirium in this high-risk population.
2024-04-30
articleAmerican Journal of Respiratory and Critical Care Medicine · 2023-03-31 · 82 citations
articleOpen accessAbstract Background Sleep and circadian disruption (SCD) is common and severe in the ICU. On the basis of rigorous evidence in non-ICU populations and emerging evidence in ICU populations, SCD is likely to have a profound negative impact on patient outcomes. Thus, it is urgent that we establish research priorities to advance understanding of ICU SCD. Methods We convened a multidisciplinary group with relevant expertise to participate in an American Thoracic Society Workshop. Workshop objectives included identifying ICU SCD subtopics of interest, key knowledge gaps, and research priorities. Members attended remote sessions from March to November 2021. Recorded presentations were prepared and viewed by members before Workshop sessions. Workshop discussion focused on key gaps and related research priorities. The priorities listed herein were selected on the basis of rank as established by a series of anonymous surveys. Results We identified the following research priorities: establish an ICU SCD definition, further develop rigorous and feasible ICU SCD measures, test associations between ICU SCD domains and outcomes, promote the inclusion of mechanistic and patient-centered outcomes within large clinical studies, leverage implementation science strategies to maximize intervention fidelity and sustainability, and collaborate among investigators to harmonize methods and promote multisite investigation. Conclusions ICU SCD is a complex and compelling potential target for improving ICU outcomes. Given the influence on all other research priorities, further development of rigorous, feasible ICU SCD measurement is a key next step in advancing the field.
2023-05-01
article
Recent grants
NIH · $64k · 2016
NIH · $959k · 2018–2024
NIH · $1.5M · 2004
Frequent coauthors
- 59 shared
Michael G. S. Shashaty
University of Pennsylvania
- 47 shared
Jason D. Christie
University of Pennsylvania
- 46 shared
John P. Reilly
- 45 shared
Nuala J. Meyer
University of Pennsylvania
- 39 shared
C.A.G. Ittner
University of Pennsylvania
- 31 shared
Thomas Dunn
Mayo Clinic Hospital
- 28 shared
Tiffanie K. Jones
University of Pennsylvania
- 24 shared
Todd A. Miano
University of Pennsylvania
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