Urgent need for individual mobile phone and institutional reporting of at home, hospitalized, and intensive care unit cases of SARS-CoV-2 (COVID-19) infection.

Approximately 90 days of the SARS-CoV-2 (COVID-19) spreading originally from Wuhan, China, and across the globe has led to a widespread chain of events with imminent threats to the fragile relationship between community health and economic health. Despite near hourly reporting on this crisis, there has been no regular, updated, or accurate reporting of hospitalizations for COVID-19. It is known that many test-positive individuals may not develop symptoms or have a mild self-limited viral syndrome consisting of fever, malaise, dry cough, and constitutional symptoms. However some individuals develop a more fulminant syndrome including viral pneumonia, respiratory failure requiring oxygen, acute respiratory distress syndrome requiring mechanical ventilation, and in substantial fractions leading to death attributable to COVID-19. The pandemic is evolving in a clustered, non-inform fashion resulting in many hospitals with preparedness but few or no cases, and others that are completely overwhelmed. Thus, a considerable risk of spread when personal protection equipment becomes exhausted and a large fraction of mortality in those not offered mechanical ventilation are both attributable to a crisis due to maldistribution of resources. The pandemic is amenable to self-reporting through a mobile phone application that could obtain critical information on suspected cases and report on the results of self testing and actions taken. The only method to understand the clustering and the immediate hospital resource needs is mandatory, uniform, daily reporting of hospital censuses of COVID-19 cases admitted to hospital wards and intensive care units. Current reports of hospitalizations are delayed, uncertain, and wholly inadequate. This paper urges all the relevant stakeholders to take up self-reporting and reporting of hospitalizations of COVID-19 as an urgent task in combating this devastating pandemic.

Acute Kidney Stress and Prevention of Acute Kidney Injury.

Critical care physicians continue to be challenged to recognize an environment that has the potential to result in acute kidney injury, with its associated short- and long-term consequences. The recent development of cell cycle arrest biomarkers that signal the potential development of acute kidney injury is part of an evolution in the molecular diagnosis and understanding of acute kidney injury. A preinjury phase that may lead to acute kidney injury has been described as "acute kidney stress." This concept has the potential to stimulate research and innovation that will lead to early implementation of measures to prevent or reverse acute kidney injury.

Validation of a Real-Time Minute-to-Minute Urine Output Monitor and the Feasibility of Its Clinical Use for Patients Undergoing Cardiac Surgery.

Acute kidney injury after cardiac surgery is associated with increased morbidity and mortality. Methods for measuring urine output in real time may better ensure renal perfusion perioperatively in contrast to the current standard of care where urine output is visually estimated after empiric epochs of time. In this study, we describe an accurate method for monitoring urine output continuously during cardiopulmonary bypass. This may provide a means for setting patient-specific targets for blood pressure and cardiopulmonary bypass flow as a potential strategy to reduce the risk for acute kidney injury.

Acute kidney stress--a useful term based on evolution in the understanding of acute kidney injury.

Critical care physicians have debated an appropriate term for the clinical phase preceding acute kidney injury (AKI). The recent development of cell cycle arrest biomarkers that signal the potential development of AKI is part of an evolution in the molecular diagnosis and understanding of AKI. It is proposed that the pre-injury phase that leads to AKI can be described as "acute kidney stress". This term has the potential to expand horizons in regard to the early detection of situations that will lead to AKI and the early implementation of corrective measures.

Implantable left ventricular assist devices and the kidney.

The use of left ventricular assist devices (LVADs) in treating patients with advanced heart failure restores cardiac output resulting in improved perfusion to multiple organ systems with important clinical benefits. Renal pathophysiology during LVAD support remains an evolving, poorly understood, and potentially dynamic problem. Changes in renal function after LVAD placement have been investigated in multiple studies with contradictory results. Renal dysfunction is common prior to LVAD placement, which complicates postoperative clinical outcomes. The purpose of this review is to assess the latest information regarding the effects of LVADs on renal function with regard to hemodynamics, physiology, pathology and clinical issues prior to and after placement of the devices. The review should then aid in identifying patients best suited to benefit from this technology and to refine the therapy to reduce associated risks.

Cardiac surgery-associated acute kidney injury.

Cardiac surgery-associated acute kidney injury (CSA-AKI) is a common and serious postoperative complication of cardiac surgery requiring cardiopulmonary bypass (CPB), and it is the second most common cause of AKI in the intensive care unit. Although the complication has been associated with the use of CPB, the etiology is likely multifactorial and related to intraoperative and early postoperative management including pharmacologic therapy. To date, very little evidence from randomized trials supporting specific interventions to protect from or prevent AKI in broad cardiac surgery populations has been found. The definition of AKI employed by investigators influences not only the incidence of CSA-AKI, but also the identification of risk variables. The advent of novel biomarkers of kidney injury has the potential to facilitate the subclinical diagnosis of CSA-AKI, the assessment of its severity and prognosis, and the early institution of interventions to prevent or reduce kidney damage. Further studies are needed to determine how to optimize cardiac surgical procedures, CPB parameters, and intraoperative and early postoperative blood pressure and renal blood flow to reduce the risk of CSA-AKI. No pharmacologic strategy has demonstrated clear efficacy in the prevention of CSA-AKI; however, some agents, such as the natriuretic peptide nesiritide and the dopamine agonist fenoldopam, have shown promising results in renoprotection. It remains unclear whether CSA-AKI patients can benefit from the early institution of such pharmacologic agents or the early initiation of renal replacement therapy.

Blood pressure excursions below the cerebral autoregulation threshold during cardiac surgery are associated with acute kidney injury.

OBJECTIVES: To determine whether mean arterial blood pressure excursions below the lower limit of cerebral blood flow autoregulation during cardiopulmonary bypass are associated with acute kidney injury after surgery. SETTING: Tertiary care medical center. PATIENTS: Four hundred ten patients undergoing cardiac surgery with cardiopulmonary bypass. DESIGN: Prospective observational study. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Autoregulation was monitored during cardiopulmonary bypass by calculating a continuous, moving Pearson's correlation coefficient between mean arterial blood pressure and processed near-infrared spectroscopy signals to generate the variable cerebral oximetry index. When mean arterial blood pressure is below the lower limit of autoregulation, cerebral oximetry index approaches 1, because cerebral blood flow is pressure passive. An identifiable lower limit of autoregulation was ascertained in 348 patients. Based on the RIFLE criteria (Risk, Injury, Failure, Loss of kidney function, End-stage renal disease), acute kidney injury developed within 7 days of surgery in 121 (34.8%) of these patients. Although the average mean arterial blood pressure during cardiopulmonary bypass did not differ, the mean arterial blood pressure at the limit of autoregulation and the duration and degree to which mean arterial blood pressure was below the autoregulation threshold (mm Hg × min/hr of cardiopulmonary bypass) were both higher in patients with acute kidney injury than in those without acute kidney injury. Excursions of mean arterial blood pressure below the lower limit of autoregulation (relative risk 1.02; 95% confidence interval 1.01 to 1.03; p < 0.0001) and diabetes (relative risk 1.78; 95% confidence interval 1.27 to 2.50; p = 0.001) were independently associated with for acute kidney injury. CONCLUSIONS: Excursions of mean arterial blood pressure below the limit of autoregulation and not absolute mean arterial blood pressure are independently associated with for acute kidney injury. Monitoring cerebral oximetry index may provide a novel method for precisely guiding mean arterial blood pressure targets during cardiopulmonary bypass.

Effect of percutaneous ventricular assist devices on renal function.

Ventricular assist devices (VADs) are used to improve the systemic circulation and to decrease ventricular loading in patients with hemodynamic instability that is refractory to pharmacologic therapies. During an acute critical event, percutaneous devices are preferred because of their rapid deployment, since implantable devices require more extensive procedures. Implantable devices are used for patients with established end-stage heart failure as a bridge to heart transplantation, recovery or destination therapy. This report reviews mechanical principles and clinical studies regarding percutaneous VAD to address their potential renal effects. Since the focus of this study is set on devices that are dedicated to cardiac support only, extracorporeal membrane oxygenation systems are not included.

State of the art: Proceedings of the American Association for Thoracic Surgery Enhanced Recovery After Cardiac Surgery Summit.

Despite the benefits established for multiple surgical specialties, enhanced recovery after surgery has been underused in cardiac surgery. A cardiac enhanced recovery after surgery summit was convened at the 102nd American Association for Thoracic Surgery annual meeting in May 2022 for experts to convey key enhanced recovery after surgery concepts, best practices, and applicable results for cardiac surgery. Topics included implementation of enhanced recovery after surgery, prehabilitation and nutrition, rigid sternal fixation, goal-directed therapy, and multimodal pain management.

Biomarkers in kidney and heart disease.

There is much symptomatic similarity between acute kidney disease and acute heart disease. Both may present with shortness of breath and chest discomfort, and thus it is not surprising that biomarkers of acute myocardial and renal disease often coexist in many physicians' diagnostic work-up schedules. In this review we explore the similarities and differences between current and future tests of myocardial and renal injury and function, with particular emphasis on the diagnostic utility of currently available biomarkers to assist with the diagnosis of cardiorenal syndromes. Imaging studies have not traditionally been viewed as clinical biomarkers, but as tests of structure and function; they contribute to the diagnostic process, and we believe that they should be considered alongside more traditional biomarkers such as blood and urine measurements of circulating proteins and metabolites. We discuss the place of natriuretic peptides, novel tests of kidney damage as well as kidney function and conclude with a discussion of their place in guiding future research studies whose goals must include better characterization of the degree of dysfunction imposed on one organ system by failure of the other.

Cardio-renal syndromes: report from the consensus conference of the acute dialysis quality initiative.

A consensus conference on cardio-renal syndromes (CRS) was held in Venice Italy, in September 2008 under the auspices of the Acute Dialysis Quality Initiative (ADQI). The following topics were matter of discussion after a systematic literature review and the appraisal of the best available evidence: definition/classification system; epidemiology; diagnostic criteria and biomarkers; prevention/protection strategies; management and therapy. The umbrella term CRS was used to identify a disorder of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. Different syndromes were identified and classified into five subtypes. Acute CRS (type 1): acute worsening of heart function (AHF-ACS) leading to kidney injury and/or dysfunction. Chronic cardio-renal syndrome (type 2): chronic abnormalities in heart function (CHF-CHD) leading to kidney injury and/or dysfunction. Acute reno-cardiac syndrome (type 3): acute worsening of kidney function (AKI) leading to heart injury and/or dysfunction. Chronic reno-cardiac syndrome (type 4): chronic kidney disease leading to heart injury, disease, and/or dysfunction. Secondary CRS (type 5): systemic conditions leading to simultaneous injury and/or dysfunction of heart and kidney. Consensus statements concerning epidemiology, diagnosis, prevention, and management strategies are discussed in the paper for each of the syndromes.

Pathophysiological Basis and Rationale for Early Outpatient Treatment of SARS-CoV-2 (COVID-19) Infection.

Approximately 9 months of the severe acute respiratory syndrome coronavius-2 (SARS-CoV-2 [COVID-19]) spreading across the globe has led to widespread COVID-19 acute hospitalizations and death. The rapidity and highly communicable nature of the SARS-CoV-2 outbreak has hampered the design and execution of definitive randomized, controlled trials of therapy outside of the clinic or hospital. In the absence of clinical trial results, physicians must use what has been learned about the pathophysiology of SARS-CoV-2 infection in determining early outpatient treatment of the illness with the aim of preventing hospitalization or death. This article outlines key pathophysiological principles that relate to the patient with early infection treated at home. Therapeutic approaches based on these principles include 1) reduction of reinoculation, 2) combination antiviral therapy, 3) immunomodulation, 4) antiplatelet/antithrombotic therapy, and 5) administration of oxygen, monitoring, and telemedicine. Future randomized trials testing the principles and agents discussed will undoubtedly refine and clarify their individual roles; however, we emphasize the immediate need for management guidance in the setting of widespread hospital resource consumption, morbidity, and mortality.

Early diagnosis of acute kidney injury: the promise of novel biomarkers.

The incidence of acute kidney injury (AKI) formerly referred to as acute renal failure (ARF) is increasing to epidemic proportions. Development of AKI portends excessive morbidity and mortality. AKI is associated with prolonged hospital stay, increased healthcare costs and high mortality especially in critically ill patients. The mortality rate has remained largely unchanged for many decades. Delay in the diagnosis of AKI using conventional biomarkers like urine output and serum creatinine has been one of the important obstacles in applying effective early interventions. Several new biomarkers are being evaluated in a quest for early diagnosis of AKI, among which neutrophil gelatinase-associated lipocalin (NGAL) appears to be one of the most promising. This review summarizes the recent literature on these biomarkers.

Financial Impact of Acute Kidney Injury After Cardiac Operations in the United States.

BACKGROUND: Acute kidney injury (AKI) after major cardiac operations is a potentially avoidable complication associated with increased morbidity, death, and costly long-term treatment. The financial impact of AKI at the population level has not been well defined. We sought to determine the incremental index hospital cost associated with the development of AKI. METHODS: All patients undergoing coronary artery bypass grafting (CABG) or valve replacement operations, or both (clinical classification software codes 43 and 44), between 2008 and 2011 were identified from the Nationwide Inpatient Sample. AKI was identified using International Classification of Diseases, 9th Revision, Clinical Modification diagnosis codes (584.xx); patients with chronic renal failure were excluded. Mean total index hospitalization costs were compared between patients with and without AKI. RESULTS: At the population level, 1,078,036 individuals underwent major cardiac procedures from 2008 to 2011, with AKI developing in 105,648 (9.8%). Specifically, AKI developed in 8.0% of CABG, 11.4% of valve replacement, and 17.0% of CABG plus valve replacement patients (p < 0.001). Death was more common among patients with AKI vs those without (13.9% vs 1.3%, p < 0.001). Mean total index hospitalization cost was $77,178 for patients with AKI vs $38,820 for those without (p < 0.001). At the national level, the overall incremental annual index hospitalization cost associated with AKI was $1.01 billion. CONCLUSIONS: AKI developed in 1 in every 10 patients nationwide after a cardiac operation. Achieving a 10% reduction in AKI in this population would likely result in an annual savings of approximately $100,000,000 in index-hospital costs alone. Support for research on mechanisms to detect impending damage and prevent AKI may lead to reduced patient morbidity and death and to substantial health care cost savings.

Lactate concentration gradient from right atrium to pulmonary artery.

INTRODUCTION: We compared simultaneous measurements of blood lactate concentration ([Lac]) in the right atrium (RA) and in the pulmonary artery (PA). Our aim was to determine if the mixing of right atrial with coronary venous blood, having substantially lower [Lac], results in detectable decreases in [Lac] from the RA to the PA. METHODS: A prospective, sequential, observational study was conducted in a medical-surgical intensive care unit. We enrolled 45 critically ill adult individuals of either sex requiring pulmonary artery catheters (PACs) to guide fluid therapy. Immediately following the insertion of the PAC, one paired set of blood samples per patient was drawn in random order from the PAC's proximal and distal ports for measurement of hemoglobin concentration, O2 saturation (SO2) and [Lac]. We defined Delta[Lac] as ([Lac]ra - [Lac]pa), DeltaSO2 as (SraO2 - SpaO2) and the change in O2 consumption (DeltaVO2) as the difference in systemic VO2 calculated using Fick's equation with either SraO2 or SpaO2 in place of mixed venous SO2. Data were compared by paired Student's t-test, Spearman's correlation analysis and by the method of Bland and Altman. RESULTS: We found SraO2 > SpaO2 (74.2 +/- 9.1 versus 69.0 +/- 10.4%; p < 0.001) and [Lac]ra > [Lac]pa (3.9 +/- 3.0 versus 3.7 +/- 3.0 mmol x l-1; p < 0.001). Delta[Lac] correlated with DeltaVO2 (r2 = 0.34; p < 0.001). CONCLUSION: We found decreases in [Lac] from the RA to PA in this sample of critically ill individuals. We conclude that parallel decreases in SO2 and [Lac] from the RA to PA support the hypothesis that these gradients are produced by mixing RA with coronary venous blood of lower SO2 and [Lac]. The present study is a preliminary observation of this phenomenon and further work is needed to define the physiological and clinical significance of Delta[Lac].

Extracorporeal Membrane Oxygenation and the Kidney.

BACKGROUND: Extracorporeal membrane oxygenation (ECMO) is an effective therapy for patients with reversible cardiac and/or respiratory failure. Acute kidney injury (AKI) often occurs in patients supported with ECMO; it frequently evolves into chronic kidney damage or end-stage renal disease and is associated with a reported 4-fold increase in mortality rate. Although AKI is generally due to the hemodynamic alterations associated with the baseline disease, ECMO itself may contribute to maintaining kidney dysfunction through several mechanisms. SUMMARY: AKI may be related to conditions derived from or associated with extracorporeal therapy, leading to a reduction in renal oxygen delivery and/or to inflammatory damage. In particular, during pathological conditions requiring ECMO, the biological defense mechanisms maintaining central perfusion by a reduction of perfusion to peripheral organs (such as the kidney) have been identified as pretreatment and patient-related risk factors for AKI. Hormonal pathways are also impaired in patients supported with ECMO, leading to failures in mechanisms of renal homeostasis and worsening fluid overload. Finally, inflammatory damage, due to the primary disease, heart and lung crosstalk with the kidney or associated with extracorporeal therapy itself, may further increase the susceptibility to AKI. Renal replacement therapy can be integrated into the main extracorporeal circuit during ECMO to provide for optimal fluid management and removal of inflammatory mediators. KEY MESSAGES: AKI is frequently observed in patients supported with ECMO. The pathophysiology of the associated AKI is chiefly related to a reduction in renal oxygen delivery and/or to inflammatory damage. Risk factors for AKI are associated with a patient's underlying disease and ECMO-related conditions.

Nadir Oxygen Delivery on Bypass and Hypotension Increase Acute Kidney Injury Risk After Cardiac Operations.

BACKGROUND: Acute kidney injury (AKI) continues to complicate cardiac operations. We sought to determine whether nadir oxygen delivery (DO2) on cardiopulmonary bypass (CPB) was a risk factor for AKI while also accounting for other postoperative factors. METHODS: Using propensity scoring, we matched 85 patients who developed AKI after cardiac operations on CPB with 85 control patients who did not. We analyzed the following variables through midnight on postoperative day 1 (POD1): DO2, antibiotics, blood products and vasopressors (intraoperatively and postoperatively), and hemodynamic variables. RESULTS: Univariable analysis revealed AKI patients had lower nadir DO2 on CPB (208 vs 230 mL O2/min/m(2) body surface area, p = 0.03), lower intensive care unit admission blood pressure gradient across the kidney (mean arterial pressure minus central venous pressure; 60 vs 68 mm Hg; p < 0.001), a greater proportion of patients with mean arterial pressure of less than 60 mm Hg for more than 15 minutes in the postoperative period (70% vs 42%, p < 0.001), a greater chance of having a cardiac index of less than 2.2 (74% vs 49%, p = 0.02), and greater total vasopressor use through the end of POD1 (5.2 vs 2.3 mg, p = 0.002). On multivariable analysis, predictors of AKI were a DO2 on CPB of less than 225 mL O2/min/m(2) (odds ratio, 2.46; 95% confidence interval, 1.21 to 5.03; p = 0.01) and postoperative mean arterial pressure of less than 60 mm Hg for more than 15 minutes (odds ratio, 3.96; 95% confidence interval, 1.92 to 8.20; p < 0.001). An average postoperative pressor dose greater than 0.03 µg/kg/min did not reach significance (odds ratio, 1.98; 95% confidence interval, 0.95 to 4.11; p = 0.07). CONCLUSIONS: Postoperative hypotension on POD0 or POD1 and low DO2 on CPB both independently increase the AKI risk in cardiac surgical patients.