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      Efficacy of Left Ventricular Outflow Tract and Carotid Artery Velocity Time Integral as Predictors of Fluid Responsiveness in Patients with Sepsis and Septic Shock

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          A bstract

          Background: Transthoracic echocardiography is a reliable method to measure a dynamic change in left ventricular outflow tract velocity time integral (LVOTVTI) and stroke volume (SV) in response to passive leg raising (PLR) and can predict fluid responsiveness in critically ill patients. Measuring carotid artery velocity time integral (CAVTI) is easier, does not depend on adequate cardiac window, and requires less skill and expertise than LVOTVTI. The aim of this study is to identify the efficacy of ΔCAVTI and ΔLVOTVTI pre- and post-PLR in predicting fluid responsiveness in critically ill patients with sepsis and septic shock.

          Methods: After the institutional ethics committee's clearance and informed written consent, 60 critically ill mechanically ventilated patients aged 18–65 years were recruited in this prospective parallel-group study with 20 patients in each group: sepsis (group S), septic shock (group SS), and control (group C). Demographic parameters and baseline acute physiology, age and chronic health evaluation-II and sequential organ failure assessment scores were noted. LVOTVTI, SV, and CAVTI were measured before and after PLR along with other hemodynamic variables. Patients having a change in SV more than 15% following PLR were defined as “responders.”

          Results: Twenty-three patients (38.33%) were responders. Area under receiver-operating characteristic curve for ΔCAVTI could predict responders in control and sepsis patients only. The correlation coefficients between pre- and post-PLR ΔCAVTI and ΔLVOTVTI were 0.530 ( p = 0.016), 0.440 ( p = 0.052), and 0.044 ( p = 0.853) in control, sepsis, and septic shock patients, respectively.

          Conclusion: Following PLR, ΔCAVTI does not predict fluid responsiveness in septic shock patients and the correlation between ΔCAVTI and ΔLVOTVTI is weak in septic shock patients and only modest in sepsis patients.

          How to cite this article: Chowhan G, Kundu R, Maitra S, Arora MK, Batra RK, Subramaniam R, et al. Efficacy of Left Ventricular Outflow Tract and Carotid Artery Velocity Time Integral as Predictors of Fluid Responsiveness in Patients with Sepsis and Septic Shock. Indian J Crit Care Med 2021;25(3):310–316.

          CTRI/Trial Reg No: www.ctri.nic.in, CTRI/2017/11/010434

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          Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016.

          To provide an update to "Surviving Sepsis Campaign Guidelines for Management of Sepsis and Septic Shock: 2012".
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            Surviving Sepsis Campaign

            To provide an update to the "Surviving Sepsis Campaign Guidelines for Management of Severe Sepsis and Septic Shock," last published in 2008. A consensus committee of 68 international experts representing 30 international organizations was convened. Nominal groups were assembled at key international meetings (for those committee members attending the conference). A formal conflict of interest policy was developed at the onset of the process and enforced throughout. The entire guidelines process was conducted independent of any industry funding. A stand-alone meeting was held for all subgroup heads, co- and vice-chairs, and selected individuals. Teleconferences and electronic-based discussion among subgroups and among the entire committee served as an integral part of the development. The authors were advised to follow the principles of the Grading of Recommendations Assessment, Development and Evaluation (GRADE) system to guide assessment of quality of evidence from high (A) to very low (D) and to determine the strength of recommendations as strong (1) or weak (2). The potential drawbacks of making strong recommendations in the presence of low-quality evidence were emphasized. Some recommendations were ungraded (UG). Recommendations were classified into three groups: 1) those directly targeting severe sepsis; 2) those targeting general care of the critically ill patient and considered high priority in severe sepsis; and 3) pediatric considerations. Key recommendations and suggestions, listed by category, include: early quantitative resuscitation of the septic patient during the first 6 hrs after recognition (1C); blood cultures before antibiotic therapy (1C); imaging studies performed promptly to confirm a potential source of infection (UG); administration of broad-spectrum antimicrobials therapy within 1 hr of recognition of septic shock (1B) and severe sepsis without septic shock (1C) as the goal of therapy; reassessment of antimicrobial therapy daily for de-escalation, when appropriate (1B); infection source control with attention to the balance of risks and benefits of the chosen method within 12 hrs of diagnosis (1C); initial fluid resuscitation with crystalloid (1B) and consideration of the addition of albumin in patients who continue to require substantial amounts of crystalloid to maintain adequate mean arterial pressure (2C) and the avoidance of hetastarch formulations (1C); initial fluid challenge in patients with sepsis-induced tissue hypoperfusion and suspicion of hypovolemia to achieve a minimum of 30 mL/kg of crystalloids (more rapid administration and greater amounts of fluid may be needed in some patients) (1C); fluid challenge technique continued as long as hemodynamic improvement, as based on either dynamic or static variables (UG); norepinephrine as the first-choice vasopressor to maintain mean arterial pressure ≥ 65 mm Hg (1B); epinephrine when an additional agent is needed to maintain adequate blood pressure (2B); vasopressin (0.03 U/min) can be added to norepinephrine to either raise mean arterial pressure to target or to decrease norepinephrine dose but should not be used as the initial vasopressor (UG); dopamine is not recommended except in highly selected circumstances (2C); dobutamine infusion administered or added to vasopressor in the presence of a) myocardial dysfunction as suggested by elevated cardiac filling pressures and low cardiac output, or b) ongoing signs of hypoperfusion despite achieving adequate intravascular volume and adequate mean arterial pressure (1C); avoiding use of intravenous hydrocortisone in adult septic shock patients if adequate fluid resuscitation and vasopressor therapy are able to restore hemodynamic stability (2C); hemoglobin target of 7-9 g/dL in the absence of tissue hypoperfusion, ischemic coronary artery disease, or acute hemorrhage (1B); low tidal volume (1A) and limitation of inspiratory plateau pressure (1B) for acute respiratory distress syndrome (ARDS); application of at least a minimal amount of positive end-expiratory pressure (PEEP) in ARDS (1B); higher rather than lower level of PEEP for patients with sepsis-induced moderate or severe ARDS (2C); recruitment maneuvers in sepsis patients with severe refractory hypoxemia due to ARDS (2C); prone positioning in sepsis-induced ARDS patients with a PaO2/FIO2 ratio of ≤ 100 mm Hg in facilities that have experience with such practices (2C); head-of-bed elevation in mechanically ventilated patients unless contraindicated (1B); a conservative fluid strategy for patients with established ARDS who do not have evidence of tissue hypoperfusion (1C); protocols for weaning and sedation (1A); minimizing use of either intermittent bolus sedation or continuous infusion sedation targeting specific titration endpoints (1B); avoidance of neuromuscular blockers if possible in the septic patient without ARDS (1C); a short course of neuromuscular blocker (no longer than 48 hrs) for patients with early ARDS and a Pao2/Fio2 180 mg/dL, targeting an upper blood glucose ≤ 180 mg/dL (1A); equivalency of continuous veno-venous hemofiltration or intermittent hemodialysis (2B); prophylaxis for deep vein thrombosis (1B); use of stress ulcer prophylaxis to prevent upper gastrointestinal bleeding in patients with bleeding risk factors (1B); oral or enteral (if necessary) feedings, as tolerated, rather than either complete fasting or provision of only intravenous glucose within the first 48 hrs after a diagnosis of severe sepsis/septic shock (2C); and addressing goals of care, including treatment plans and end-of-life planning (as appropriate) (1B), as early as feasible, but within 72 hrs of intensive care unit admission (2C). Recommendations specific to pediatric severe sepsis include: therapy with face mask oxygen, high flow nasal cannula oxygen, or nasopharyngeal continuous PEEP in the presence of respiratory distress and hypoxemia (2C), use of physical examination therapeutic endpoints such as capillary refill (2C); for septic shock associated with hypovolemia, the use of crystalloids or albumin to deliver a bolus of 20 mL/kg of crystalloids (or albumin equivalent) over 5 to 10 mins (2C); more common use of inotropes and vasodilators for low cardiac output septic shock associated with elevated systemic vascular resistance (2C); and use of hydrocortisone only in children with suspected or proven "absolute"' adrenal insufficiency (2C). Strong agreement existed among a large cohort of international experts regarding many level 1 recommendations for the best care of patients with severe sepsis. Although a significant number of aspects of care have relatively weak support, evidence-based recommendations regarding the acute management of sepsis and septic shock are the foundation of improved outcomes for this important group of critically ill patients.
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              Mortality related to severe sepsis and septic shock among critically ill patients in Australia and New Zealand, 2000-2012.

              Severe sepsis and septic shock are major causes of mortality in intensive care unit (ICU) patients. It is unknown whether progress has been made in decreasing their mortality rate. To describe changes in mortality for severe sepsis with and without shock in ICU patients. Retrospective, observational study from 2000 to 2012 including 101,064 patients with severe sepsis from 171 ICUs with various patient case mix in Australia and New Zealand. Hospital outcome (mortality and discharge to home, to other hospital, or to rehabilitation). Absolute mortality in severe sepsis decreased from 35.0% (95% CI, 33.2%-36.8%; 949/2708) to 18.4% (95% CI, 17.8%-19.0%; 2300/12,512; P < .001), representing an overall decrease of 16.7% (95% CI, 14.8%-18.6%), an annual rate of absolute decrease of 1.3%, and a relative risk reduction of 47.5% (95% CI, 44.1%-50.8%). After adjusted analysis, mortality decreased throughout the study period with an odds ratio (OR) of 0.49 (95% CI, 0.46-0.52) in 2012, using the year 2000 as the reference (P < .001). The annual decline in mortality did not differ significantly between patients with severe sepsis and those with all other diagnoses (OR, 0.94 [95% CI, 0.94-0.95] vs 0.94 [95% CI, 0.94-0.94]; P = .37). The annual increase in rates of discharge to home was significantly greater in patients with severe sepsis compared with all other diagnoses (OR, 1.03 [95% CI, 1.02-1.03] vs 1.01 [95% CI, 1.01-1.01]; P < .001). Conversely, the annual increase in the rate of patients discharged to rehabilitation facilities was significantly less in severe sepsis compared with all other diagnoses (OR, 1.08 [95% CI, 1.07-1.09] vs 1.09 [95% CI, 1.09-1.10]; P < .001). In the absence of comorbidities and older age, mortality was less than 5%. In critically ill patients in Australia and New Zealand with severe sepsis with and without shock, there was a decrease in mortality from 2000 to 2012. These findings were accompanied by changes in the patterns of discharge to home, rehabilitation, and other hospitals.
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                Author and article information

                Contributors
                Journal
                Indian J Crit Care Med
                Indian J Crit Care Med
                IJCCM
                Indian Journal of Critical Care Medicine : Peer-reviewed, Official Publication of Indian Society of Critical Care Medicine
                Jaypee Brothers Medical Publishers
                0972-5229
                1998-359X
                March 2021
                : 25
                : 3
                : 310-316
                Affiliations
                [1,3,5–8 ]Department of Anaesthesiology, Pain Medicine and Critical Care, All India Institute of Medical Sciences, New Delhi, India
                [2 ]Department of Critical Care Medicine, Manipal Hospitals, Dwarka, New Delhi, India
                [4 ]Department of Liver Transplant, Anaesthesia and Critical Care, Institute of Liver and Biliary Sciences, New Delhi, India
                Author notes
                Dalim K Baidya, Department of Anaesthesiology, Pain Medicine and Critical Care, All India Institute of Medical Sciences, New Delhi, India, Phone: +91 1126593212, e-mail: dalimkumar.ab8@ 123456gmail.com
                Article
                10.5005/jp-journals-10071-23764
                7991757
                33790513
                91728e03-ac57-42e8-80a5-d32256fdeac0
                Copyright © 2021; Jaypee Brothers Medical Publishers (P) Ltd.

                © Jaypee Brothers Medical Publishers. 2021 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( https://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted use, distribution, and non-commercial reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Categories
                Original Research

                Emergency medicine & Trauma
                fluid responsiveness,passive leg raising,sepsis,transthoracic echocardiography,velocity time integral

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