We report the neuropathological findings of a patient who died from complications of COVID-19. The decedent was initially hospitalized for surgical management of underlying coronary artery disease. ...He developed post-operative complications and was evaluated with chest imaging studies. The chest computed tomography (CT) imaging results were indicative of COVID-19 and he was subsequently tested for SARS-CoV-2, which was positive. His condition worsened and he died after more than 2 weeks of hospitalization and aggressive treatment. The autopsy revealed a range of neuropathological lesions, with features resembling both vascular and demyelinating etiologies. Hemorrhagic white matter lesions were present throughout the cerebral hemispheres with surrounding axonal injury and macrophages. The subcortical white matter had scattered clusters of macrophages, a range of associated axonal injury, and a perivascular acute disseminated encephalomyelitis (ADEM)-like appearance. Additional white matter lesions included focal microscopic areas of necrosis with central loss of white matter and marked axonal injury. Rare neocortical organizing microscopic infarcts were also identified. Imaging and clinical reports have demonstrated central nervous system complications in patients’ with COVID-19, but there is a gap in our understanding of the neuropathology. The lesions described in this case provide insight into the potential parainfectious processes affecting COVID-19 patients, which may direct clinical management and ongoing research into the disease. The clinical course of the patient also illustrates that during prolonged hospitalizations neurological complications of COVID may develop, which are particularly difficult to evaluate and appreciate in the critically ill.
Acute kidney injury (AKI) is a common complication of critical illnesses and has a significant impact on outcomes, including mortality and morbidities. Unfortunately, apart from prophylactic ...measures, no effective treatment for this syndrome is known. Therefore, early recognition of AKI not only can provide better opportunities for preventive interventions, but also opens many gates for research and development of effective therapeutic options. Over the last few years, several new AKI biomarkers have been discovered and validated to improve early detection, differential diagnosis, and differentiation of patients into risk groups for progressive renal failure, need for renal replacement therapy (RRT), or death. These novel AKI biomarkers complement serum creatinine (SCr) and urine output, which are the standard diagnostic tools for AKI detection. In this article, we review the available literature on characteristics of promising AKI biomarkers that are currently the focus of preclinical and clinical investigations. These biomarkers include neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule 1 (KIM-1), liver-type fatty acid-binding protein, interleukin 18 (lL-18), insulin-like growth factor-binding protein 7, tissue inhibitor of metalloproteinase 2 (TIMP-2), calprotectin, urine angiotensinogen (AGT), and urine microRNA. We then describe the clinical performance of these biomarkers for diagnosis and prognostication. We also appraise each AKI biomarker's advantages and limitations as a tool for early AKI recognition and prediction of clinical outcomes after AKI. Finally, we review the current and future states of implementation of biomarkers in the clinical practice.
Automated acute kidney injury alerts Kashani, Kianoush B.
Kidney international,
September 2018, 2018-09-00, 20180901, Letnik:
94, Številka:
3
Journal Article
Recenzirano
Odprti dostop
Acute kidney injury (AKI) is one of the most common and probably one of the more consequential complications of critical illnesses. Recent information indicates that it is at least partially ...preventable; however, progress in its prevention, management, and treatment has been hindered by the scarcity of knowledge for effective interventions, inconsistencies in clinical practices, late identification of patients at risk for or with AKI, and limitations of access to best practices for prevention and management of AKI. Growing use of electronic health records has provided a platform for computer science to engage in data mining and processing, not only for early detection of AKI but also for the development of risk-stratification strategies and computer clinical decision–support (CDS) systems. Despite promising perspectives, the literature regarding the impact of AKI electronic alerts and CDS systems has been conflicting. Some studies have reported improvement in care processes and patient outcomes, whereas others have shown no effect on clinical outcomes and yet demonstrated an increase in the use of resources. These discrepancies are thought to be due to multiple factors that may be related to technology, human factors, modes of delivery of information to clinical providers, and level of expectations regarding the impact on patient outcomes. This review appraises the current body of knowledge and provides some outlines regarding research into and clinical aspects of CDS systems for AKI.
Creatinine: From physiology to clinical application Kashani, Kianoush; Rosner, Mitchell H.; Ostermann, Marlies
European journal of internal medicine,
February 2020, 2020-02-00, 20200201, Letnik:
72
Journal Article
Recenzirano
•Estimating kidney function is challenging and critically ill patients.•Creatinine is a widely used functional biomarker and has substantial shortcomings.•Use of novel functional biomarkers with ...creatinine provides additional information.•Creatinine could be used for the estimation of muscle mass or clinical outcomes.•New technologies for direct GFR measurement could overcome creatinine limitations.
Estimating static kidney function accurately and detecting changes in kidney function in a timely fashion are challenging but critically important tasks. Serum creatinine is the most widely used functional biomarker of the kidney. However, its use is associated with substantial shortcomings. Understanding these shortcomings is critical in allowing accurate interpretation of creatinine values and translating them into changes in kidney function. In this review, the pathways involved in creatinine generation and metabolism as well as the techniques involved in measuring creatinine concentrations are discussed. This allows for the discussion of the value and pitfalls in using creatinine as a marker of kidney function. In addition, information regarding alternative functional biomarkers of the kidney is provided.
Although 28% to 49% of severe sepsis hospitalizations have been described as being "culture negative," there are very limited data on the epidemiology and outcomes of those with culture-negative ...severe sepsis (CNSS). The objectives of this study were to investigate the proportion and trends of CNSS and its association with mortality.
Using the Nationwide Inpatient Sample (NIS) database from 2000 to 2010, we identified adults hospitalized with severe sepsis. Those without any specific organism codes were identified as "with CNSS." We examined the proportion of CNSS hospitalizations and rates of mortality associated with it. We also assessed the independent effect of CNSS on mortality.
Of 6,843,279 admissions of patients with severe sepsis, 3,226,406 (47.1%) had culture-negative results. The age-adjusted proportion of CNSS increased from 33.9% in 2000 to 43.5% in 2010 (P < .001). Those with CNSS had more comorbidities, acute organ dysfunction (respiratory, cardiac, hepatic, and renal dysfunction), and in-hospital mortality (34.6% vs 22.7%; P < .001), although acute kidney injury requiring dialysis was less frequent (5.3% vs 6.1%; P < .001). CNSS was an independent predictor of mortality in those with severe sepsis (OR, 1.75; 95% CI, 1.72-1.77).
CNSS among hospitalized patients is common, and its proportion is on the rise. CNSS is associated with greater acute organ dysfunction and mortality. Having CNSS is an independent predictor of death.
Sarcopenia is associated with a poor prognosis in the ICU. The purpose of this study was to describe a simple sarcopenia index using routinely available renal biomarkers and evaluate its association ...with muscle mass and patient outcomes.
A retrospective cohort study.
A tertiary-care medical center.
High-risk adult ICU patients from October 2008 to December 2010.
The gold standard for muscle mass was quantified with the paraspinal muscle surface area at the L4 vertebrae in the subset of individuals with an abdominal CT scan. Using Pearson's correlation coefficient, serum creatinine-to-serum cystatin C ratio was found to be the best performer in the estimation of muscle mass. The relationship between sarcopenia index and hospital and 90-day mortality, and the length of mechanical ventilation was evaluated.
Out of 226 enrolled patients, 123 (54%) were female, and 198 (87%) were white. Median (interquartile range) age, body mass index, and body surface area were 68 (57-77) years, 28 (24-34) kg/m, and 1.9 (1.7-2.2) m, respectively. The mean (± SD) Acute Physiology and Chronic Health Evaluation III was 70 (± 22). ICU, hospital, and 90-day mortality rates were 5%, 12%, and 20%, respectively. The correlation (r) between sarcopenia index and muscle mass was 0.62 and coefficient of determination (r) was 0.27 (p < 0.0001). After adjustment for Acute Physiology and Chronic Health Evaluation III, body surface area, and age, sarcopenia index was independently predictive of both hospital (p = 0.001) and 90-day mortality (p < 0.0001). Among the 131 patients on mechanical ventilator, the duration of mechanical ventilation was significantly lower on those with higher sarcopenia index (-1 d for each 10 unit of sarcopenia index 95% CI, -1.4 to -0.2; p = 0.006).
The sarcopenia index is a fair measure for muscle mass estimation among ICU patients and can modestly predict hospital and 90-day mortality among patients who do not have acute kidney injury at the time of measurement.
Acute kidney injury (AKI) is common in critically ill patients and is associated with high morbidity and mortality. Early identification of high-risk patients provides an opportunity to develop ...strategies for prevention, early diagnosis and treatment of AKI.
We undertook this multicenter prospective cohort study to develop and validate a risk score for predicting AKI in patients admitted to an intensive care unit (ICU). Patients were screened for predictor variables within 48 h of ICU admission. Baseline and acute risk factors were recorded at the time of screening and serum creatinine was measured daily for up to 7 days. A risk score model for AKI was developed with multivariate regression analysis combining baseline and acute risk factors in the development cohort (573 patients) and the model was further evaluated on a test cohort (144 patients). Validation was performed on an independent prospective cohort of 1300 patients. The discriminative ability of the risk model was assessed by the area under the receiver operating characteristic curve (AUROC) and model calibration was evaluated by Hosmer-Lemeshow statistic. AKI was defined by the Kidney Disease: Improving Global Outcomes criteria (absolute change of 0.3 mg/dL or relative change of 50% from baseline serum creatinine in 48 h to 7 days, respectively).
AKI developed in 754 (37.2%) patients. In the multivariate model, chronic kidney disease, chronic liver disease, congestive heart failure, hypertension, atherosclerotic coronary vascular disease, pH ≤ 7.30, nephrotoxin exposure, sepsis, mechanical ventilation and anemia were identified as independent predictors of AKI and the AUROC for the model in the test cohort was 0.79 95% confidence interval (CI) 0.70-0.89. On the external validation cohort, the AUROC value was 0.81 (95% CI 0.78-0.83). The risk model demonstrated good calibration in both cohorts. Positive and negative predictive values for the optimal cutoff value of ≥ 5 points in test and validation cohorts were 22.7 and 96.1% and 31.8 and 95.4%, respectively.
A risk score model integrating chronic comorbidities and acute events at ICU admission can identify patients at high risk to develop AKI. This risk assessment tool could help clinicians to stratify patients for primary prevention, surveillance and early therapeutic intervention to improve care and outcomes of ICU patients.
Management of Refractory Vasodilatory Shock Jentzer, Jacob C.; Vallabhajosyula, Saraschandra; Khanna, Ashish K. ...
Chest,
August 2018, 2018-08-00, 20180801, Letnik:
154, Številka:
2
Journal Article
Recenzirano
Refractory shock is a lethal manifestation of cardiovascular failure defined by an inadequate hemodynamic response to high doses of vasopressor medications. Approximately 7% of critically ill ...patients will develop refractory shock, with short-term mortality exceeding 50%. Refractory vasodilatory shock develops from uncontrolled vasodilation and vascular hyporesponsiveness to endogenous vasoconstrictors, causing failure of physiologic vasoregulatory mechanisms. Standard approaches to the initial management of shock include fluid resuscitation and initiation of norepinephrine. When these measures are inadequate to restore BP, vasopressin or epinephrine can be added. Few randomized studies exist to guide clinical management and hemodynamic stabilization in patients who do not respond to this standard approach. Adjunctive therapies, such as hydrocortisone, thiamine, and ascorbic acid, may increase BP in severe shock and should be considered when combination vasopressor therapy is needed. Novel vasopressor agents, such as synthetic human angiotensin II, can increase BP and reduce the need for high doses of catecholamine vasopressors in severe or refractory vasodilatory shock. Few effective rescue therapies exist for established refractory shock, which emphasizes the importance of aggressive intervention before refractory shock develops, including the earlier initiation of rational combination vasopressor therapy. The present review discusses the diagnosis and management of refractory shock to offer guidance for management of this important clinical problem and to provide a framework for future research.
PDF
