Human immunodeficiency virus infection is associated with greater risk of pneumonia and readmission after cardiac surgery.

Objective: Human immunodeficiency virus infection (HIV+) is associated with a 2-fold increased risk of cardiovascular disease. Increasingly, patients who are HIV + are being evaluated to undergo cardiac surgery. Current risk-adjusted scoring systems, including the Society of Thoracic Surgeons Predicted Risk of Mortality score, fail to stratify HIV + risk. Unfortunately, there exists a paucity of cardiac surgery outcomes data in modern patients who are HIV+. Methods: We conducted a retrospective review of PearlDiver, an all-payer claims administrative database. In total, 14,714,743 patients were captured between 2010 and 2020. Of these, 59,695 (0.4%) of patients had a history of HIV+, and 1759 (2.95%) of these patients underwent cardiac surgery. Patients who were HIV+ were younger, more often male, and had greater comorbidity, history of hypertension, chronic obstructive pulmonary disease, chronic liver disease, chronic kidney disease, chronic lung disease, and heart failure. Results: Postoperatively, patients who were HIV + had significantly greater rates of pneumonia (relative risk, 1.70; P = .0003) and 30-day all-cause readmission (relative risk, 1.28, P < .0001). After linear regression analysis, these results remained significant. Data also show that a lesser proportion of patients with HIV + underwent coronary artery bypass grafting, aortic valve replacement, and any cardiac surgery compared with controls. Conclusions: Patients who are HIV + undergoing cardiac surgery are at greater risk of pneumonia and readmission. Moreover, we discovered lower rates of cardiac surgery in patients who are HIV+, which may reflect limited access to surgery when indicated. Today's risk-adjusted scoring systems in cardiac surgery need to better account for the modern patient who is HIV+.

Community Size and Lung Cancer Resection Outcomes: Studying The Society of Thoracic Surgeons Database.

BACKGROUND: Socioeconomic factors play key roles in surgical outcomes. Socioeconomic data within The Society of Thoracic Surgeons (STS) General Thoracic Surgery Database (GTSD) are limited. Therefore, we utilized community size as a surrogate to understand socioeconomic differences in lung cancer resection outcomes. METHODS: We retrospectively reviewed all lung cancer resections from January 2012 to January 2017 in the STS GTSD. This captured 68,722 patients from 286 centers nationwide. We then linked patient zip codes with 2013 Rural-Urban Continuum Codes to understand the association between community size and postoperative outcomes. Demographic and clinical variables were evaluated for relationships with 30-day mortality, major morbidity, and readmission. RESULTS: Zip codes were included in 47.2% of patients. Zip-coded patients were older, were more comorbid, had less advanced disease, and were more commonly treated with minimally invasive approaches than were those without zip code classification. For geocoded patients, multivariable analyses demonstrated that sex, insurance payor, and hospital region were associated with all 3 major endpoints. Community size, based on Rural-Urban Continuum Codes coding, was not associated with any primary endpoint. Invasive mediastinal staging was related to morbidity, greater pathological stage predicted mortality, and worsened clinical stage was associated with readmission. More invasive surgery and greater extent of lung resection were associated with all primary endpoints. CONCLUSIONS: Incomplete data capture can promote selection bias within the STS GTSD and skew outcomes reporting. Moreover, community size is an insufficient surrogate, compared with sex, insurance payor, hospital region, for understanding socioeconomic differences in lung cancer resection outcomes.

Factors Associated With Survival Following Extracorporeal Cardiopulmonary Resuscitation in Children.

OBJECTIVES: We examined a large single-institution experience in extracorporeal cardiopulmonary resuscitation (ECPR) in children having cardiac arrest refractory to conventional resuscitation measures with focus on factors affecting survival. METHODS: Between 2002 and 2017, 184 children underwent ECPR at our institution. We entered demographic, anatomic, clinical, surgical, and ECPR support details into a multivariable logistic regression models to determine factors associated with mortality. RESULTS: Median age was 54 days (interquartile range [IQR]: 11-272). In all, 157 (85%) patients had primary cardiac disease, including 136 (74%) with congenital heart disease (71 with single ventricle). Extracorporeal cardiopulmonary resuscitation occurred following cardiac surgery in 124 (67%) patients. Median cardiopulmonary resuscitation (CPR) duration was 27 minutes (IQR: 18-40) and median support duration was 3.0 days (IQR: 1.6-5.3). Overall, ECPR was weaned in 115 (63%), with 79 (43%) surviving to hospital discharge. Survival for patients with congenital heart disease, noncongenital cardiac, and noncardiac pathologies was 44%, 71%, and 15%, respectively. On multivariable regression analysis, risk factors associated with mortality were presupport pH <7.1 (odds ratio [OR] = 3.7, 95% confidence interval [CI]: 1.11-12.41, P = .033), mechanical complications (OR = 8.33, 95% CI: 1.91-36.25, P = .005), neurologic complications (OR = 6.27, 95% CI: 1.40-28.10, P = .017), and renal replacement therapy (OR = 3.31, 95% CI: 1.03-10.66, P = .045). CONCLUSIONS: Extracorporeal cardiopulmonary resuscitation plays a valuable role salvaging children with refractory cardiac arrest. Survival varies with underlying pathology and can be expected even with relatively longer CPR durations. Efforts to improve systemic output before and after institution of ECPR might mitigate some of the significant risk factors for mortality.

Aortobronchial Fistula after Thoracic Endovascular Aortic Repair (TEVAR) for Descending Thoracic Aortic Aneurysm.

Continued enlargement of the aneurysm sac after thoracic endovascular aortic repair (TEVAR) is a known risk after endovascular treatment of thoracic aortic aneurysms. For this reason, periodic outpatient follow-up is required to identify situations that require repair. Here, we describe an aortobronchial fistula (ABF) in a patient lost to follow-up, that presented 3 years after an elective TEVAR done for a primary, descending thoracic aortic aneurysm. Our patient arrived in extremis and suffered massive hemoptysis leading to her demise. Computed tomography (CT) angiogram near the time of her death demonstrated a bleeding ABF immediately distal to her previous TEVAR repair. Aortic aneurysmal disease remains life threatening even after repair. Improved endovascular techniques and devices have resulted in decreased need for reintervention. However, this case demonstrates the risk of thoracic aortic disease progression and highlights the importance of establishing consistent, long-term follow-up after TEVAR.

Computed Tomography-guided Pericardiocentesis: An alternative approach for accessing the pericardium.

Pericardial effusions compress the heart, decrease cardiac output, and lead to haemodynamic collapse. Ultrasound (US)-guided pericardiocentesis is the gold standard for treating pericardial effusions. Recently, the incorporation of computed tomography (CT) guidance has increased patient safety while entering the pericardium. Despite the superior performance of CT-guided pericardiocentesis in smaller, complex effusions, this procedure is not routinely performed by cardiologists and surgeons. Unlike those with an intact pericardium, patients with mediastinal trauma, pericardial adhesions, temporary pacing wires, and vascular conduits are high risk for pericardiocentesis. Tamponade physiology also increases patient susceptibility to the hypotensive effects of anaesthesia during surgical drainage. Here we illustrate the technique of CT-guided pericardiocentesis and demonstrate its application in specific clinical scenarios. We conclude that CT-guided pericardiocentesis provides a useful, alternative strategy for treating cardiac tamponade in high risk patients.

Drug and alcohol use complicate traumatic peripheral vascular injury.

BACKGROUND: Drug and alcohol use complicate the presentation and management of traumatic injuries. Impaired hemodynamic recovery and host defense in substance users also predispose these patients to worse outcomes after trauma. We hypothesized that substance abuse, particularly when drugs and alcohol are combined, complicates the presentation, management, and patient outcomes following isolated traumatic peripheral vascular injury. METHODS: This is a retrospective analysis of patients admitted with isolated peripheral vascular injury to our Level 1 trauma center between 2006 and 2012. Demographics, presentation, substance use, resuscitation, operative management, intensive care needs, and length of hospital stay were analyzed. RESULTS: From 257 patients admitted, 158 patients experienced isolated peripheral vascular injury. Patients were subdivided by blood alcohol level (BAL) and urinary toxicology (utox) screens; negative BAL/negative utox (nonintoxicated, n = 90), negative BAL/positive utox (drug users, n = 27), positive BAL/negative utox (alcohol users, n = 22), and positive BAL/positive utox (polysubstance users, n = 19). Compared with nonintoxicated patients, more polysubstance users experienced lower-extremity injury (79% vs. 47%) and presented more often than alcohol users with proximal injury (83% vs. 45%), lower-extremity injury (79% vs. 36%), and as a result of assault (68.4% vs. 31.8%). Polysubstance users required greater resuscitation, more operations, and more frequently experienced complications than any other cohort. Subsequently, these patients had a greater need for intensive care management and longer hospital stay than nonintoxicated and alcohol users. Moreover, using multivariate logistic regression analysis, we found that polysubstance use, alcohol use, and lower-extremity injury are each independent risk factors for infectious complications. CONCLUSION: Our data show that polysubstance users with isolated peripheral vascular injury experience more proximal and lower-extremity injuries, require greater resuscitation, and undergo more operations compared with nonintoxicated patients. Treatment of these patients is more frequently complicated by infection, vascular complications, and increased hospital length of stay.

Alcohol impairs the myeloid proliferative response to bacteremia in mice by inhibiting the stem cell antigen-1/ERK pathway.

Enhancement of stem cell Ag-1 (Sca-1) expression by myeloid precursors promotes the granulopoietic response to bacterial infection. However, the underlying mechanisms remain unclear. ERK pathway activation strongly enhances proliferation of hematopoietic progenitor cells. In this study, we investigated the role of Sca-1 in promoting ERK-dependent myeloid lineage proliferation and the effects of alcohol on this process. Thirty minutes after i.p. injection of alcohol, mice received i.v. challenge with 5 × 10(7) Escherichia coli for 8 or 24 h. A subset of mice received i.v. BrdU injection 20 h after challenge. Bacteremia increased Sca-1 expression, ERK activation, and proliferation of myeloid and granulopoietic precursors. Alcohol administration suppressed this response and impaired granulocyte production. Sca-1 expression positively correlated with ERK activation and cell cycling, but negatively correlated with myeloperoxidase content in granulopoietic precursors. Alcohol intoxication suppressed ERK activation in granulopoietic precursors and proliferation of these cells during bacteremia. Granulopoietic precursors in Sca-1(-/-) mice failed to activate ERK signaling and could not increase granulomacrophagic CFU activity following bacteremia. These data indicate that Sca-1 expression promotes ERK-dependent myeloid cell proliferation during bacteremia. Suppression of this response could represent an underlying mechanism for developing myelosuppression in alcohol-abusing hosts with severe bacterial infection.

Neonatal sepsis and neutrophil insufficiencies.

Sepsis has continuously been a leading cause of neonatal morbidity and mortality despite current advances in chemotherapy and patient intensive care facilities. Neonates are at high risk for developing bacterial infections due to quantitative and qualitative insufficiencies of innate immunity, particularly granulocyte lineage development and response to infection. Although antibiotics remain the mainstay of treatment, adjuvant therapies enhancing immune function have shown promise in treating sepsis in neonates. This article reviews current strategies for the clinical management of neonatal sepsis and analyzes mechanisms underlying insufficiencies of neutrophil defense in neonates with emphasis on new directions for adjuvant therapy development.

Regulation of prenatal human retinal neurosphere growth and cell fate potential by retinal pigment epithelium and Mash1.

During development of the central nervous system, stem and progenitor cell proliferation and differentiation are controlled by complex inter- and intracellular interactions that orchestrate the precise spatiotemporal production of particular cell types. Within the embryonic retina, progenitor cells are located adjacent to the retinal pigment epithelium (RPE), which differentiates prior to the neurosensory retina and has the capacity to secrete a multitude of growth factors. We found that secreted proteinaceous factors in human prenatal RPE conditioned medium (RPE CM) prolonged and enhanced the growth of human prenatal retinal neurospheres. The growth-promoting activity of RPE CM was mitogen-dependent and associated with an acute increase in transcription factor phosphorylation. Expanded populations of RPE CM-treated retinal neurospheres expressed numerous neurodevelopmental and eye specification genes and markers characteristic of neural and retinal progenitor cells, but gradually lost the potential to generate neurons upon differentiation. Misexpression of Mash1 restored the neurogenic potential of long-term cultures, yielding neurons with phenotypic characteristics of multiple inner retinal cell types. Thus, a novel combination of extrinsic and intrinsic factors was required to promote both progenitor cell proliferation and neuronal multipotency in human retinal neurosphere cultures. These results support a pro-proliferative and antiapoptotic role for RPE in human retinal development, reveal potential limitations of human retinal progenitor culture systems, and suggest a means for overcoming cell fate restriction in vitro.