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Djillali Annane - One of the best experts on this subject based on the ideXlab platform.
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the neuropathology of Septic Shock
Brain Pathology, 2004Co-Authors: Tarek Sharshar, Djillali Annane, Geoffroy Lorin De La Gradmaison, Jeanphilippe Brouland, Nicholas S Hopkinson, Françoise GrayAbstract:The neuropathological correlates of encephalopathy and autonomic dysfunction in Septic Shock are unclear. We performed post mortem analysis of 5 brain areas susceptible to ischemia and 5 autonomic nuclei (AN) in 23 patients who had died in our intensive care unit (ICU) from Septic Shock and 8 dying from non-Septic Shock as well as 5 controls who had died suddenly from extracranial injury. Proinflammatory cytokine (IL1-beta and TNF-alpha) and inducible nitric oxide synthase (iNOS) expression was assessed by immunocytochemistry. Abnormalities in Septic Shock were: hemorrhages (26%), hypercoagulability syndrome (9%), micro-abscesses (9%), multifocal necrotizing leukoencephalopathy (9%) and ischemia (100%). The incidence of cerebral hemorrhage or hypercoagulability syndrome was not related to clotting disturbances. The intensity of ischemia within susceptible areas was the same in both ICU groups, but more pronounced in the autonomic centers of Septic patients (P < 0.0001). Neuronal apoptosis assessed using anti-caspase 3 immunocytochemistry and in situ end labeling was more pronounced in the autonomic nuclei of Septic patients. (P < 0.0001). TNF-alpha expression did not differ between groups but vascular iNOS expression assessed by immunocytochemistry was higher in sepsis (P<0.0001) and correlated with autonomic center neuronal apoptosis (P < 0.02). We conclude that Septic Shock is associated with diffuse cerebral damage and specific autonomic neuronal apoptosis which may be due to circulating factors particularly iNOS.
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The neuropathology of Septic Shock
Brain pathology (Zurich Switzerland), 2004Co-Authors: Tarek Sharshar, Djillali Annane, Geoffroy Lorin De La Gradmaison, Jeanphilippe Brouland, Nicholas S Hopkinson, Françoise GrayAbstract:The neuropathological correlates of encephalopathy and autonomic dysfunction in Septic Shock are unclear. We performed post mortem analysis of 5 brain areas susceptible to ischemia and 5 autonomic nuclei (AN) in 23 patients who had died in our intensive care unit (ICU) from Septic Shock and 8 dying from non-Septic Shock as well as 5 controls who had died suddenly from extracranial injury. Proinflammatory cytokine (IL1-beta and TNF-alpha) and inducible nitric oxide synthase (iNOS) expression was assessed by immunocytochemistry. Abnormalities in Septic Shock were: hemorrhages (26%), hypercoagulability syndrome (9%), micro-abscesses (9%), multifocal necrotizing leukoencephalopathy (9%) and ischemia (100%). The incidence of cerebral hemorrhage or hypercoagulability syndrome was not related to clotting disturbances. The intensity of ischemia within susceptible areas was the same in both ICU groups, but more pronounced in the autonomic centers of Septic patients (P < 0.0001). Neuronal apoptosis assessed using anti-caspase 3 immunocytochemistry and in situ end labeling was more pronounced in the autonomic nuclei of Septic patients. (P < 0.0001). TNF-alpha expression did not differ between groups but vascular iNOS expression assessed by immunocytochemistry was higher in sepsis (P
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circulating vasopressin levels in Septic Shock
Critical Care Medicine, 2003Co-Authors: Tarek Sharshar, Anne Blanchard, Michel Paillard, Jean Claude Raphael, Philippe Gajdos, Djillali AnnaneAbstract:ObjectiveTo assess the frequency of vasopressin deficiency in Septic Shock.DesignProspective cohort study.SettingIntensive care unit at Raymond Poincare University Hospital.PatientsA cohort of 44 patients who met the usual criteria for Septic Shock for <7 days. A second cohort of 18 Septic Shock pat
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Neuropathology of Septic Shock
Neuropathology and Applied Neurobiology, 2002Co-Authors: Françoise Gray, Tarek Sharshar, G. Lorin De La Grandmaison, Djillali AnnaneAbstract:Introduction: Septic Shock is the most frequent cause of death in intensive care units. It is often complicated by an encephalopathy and there is increasing evidence that central autonomic nervous system (CANS) dysfunction plays a crucial role in the onset and persistance of the haemodynamic failure. However, only a few neuropathological studies are available; they are always retrospective and often disagree. Material and methods: Twenty consecutive patient who died from Septic Shock were examined and compared with eight patients who died from nonSeptic Shock in the same unit and five ‘normal’ controls collected from the Forensic Medicine Service. Results and conclusion: A variety of lesions, including microabscesses, multifocal necrotizing leukoencephalopathy, haemorrhages and disseminated intravascular coagulation, were found, and were most probably related to the biological disturbances associated with sepsis. These lesions may contribute to the ‘Septic encephalopathy’. Ischaemic changes in ‘susceptible’ areas were comparable in Septic Shock and in nonSeptic Shock. In contrast, ischaemic changes in the nuclei of the CANS were significantly more severe in Septic Shock than in nonSeptic Shock. Neuronal apoptosis in these nuclei was significantly more frequent and more severe in Septic Shock; apoptosis did not correlate exactly with neuronal ischaemia and was associated with only mild microglial activation suggesting that circulating factors may also play a role in its causation.
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Corticosteroids for Septic Shock.
Critical care medicine, 2001Co-Authors: Djillali AnnaneAbstract:Objective: To gather the data to provide a rationale for using replacement therapy with hydrocortisone in Septic Shock patients. Data Sources: The Medline and the Cochrane Library databases. Study Selection: Studies in animals and in humans were considered when significant data were available about the mechanisms of action of corticosteroids or about their use in severe sepsis. Data Summary: Corticosteroids were the first anti-inflammatory drugs tested in Septic patients. Randomized trials clearly showed that a short course of a large dose of anti-inflammatory steroids is ineffective and potentially harmful in patients with severe sepsis. Recent demonstrations of altered hypothalamic-pituitary-adrenal axis response to Septic insult have led to a reappraisal of the use of steroids in Septic Shock. Randomized trials in catecholamine-dependent Septic Shock patients strongly suggest that replacement therapy with hydrocortisone may alleviate the symptoms of systemic inflammatory response, reduce the duration of Shock, and favorably affect survival. Conclusions: Current evidence that the therapeutic interest of replacement therapy with corticosteroids increases suggests that low doses of hydrocortisone should be offered to patients with catecholamine-dependent Septic Shock.
Keith R. Walley - One of the best experts on this subject based on the ideXlab platform.
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the Septic Shock 3 0 definition and trials a vasopressin and Septic Shock trial experience
Critical Care Medicine, 2017Co-Authors: James A. Russell, Terry Lee, Joel Singer, John H Boyd, Keith R. WalleyAbstract:Objectives:The Septic Shock 3.0 definition could alter treatment comparisons in randomized controlled trials in Septic Shock. Our first hypothesis was that the vasopressin versus norepinephrine comparison and 28-day mortality of patients with Septic Shock 3.0 definition (lactate > 2 mmol/L) differ f
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Arginine vasopressin in the treatment of vasodilatory Septic Shock.
Best practice & research. Clinical anaesthesiology, 2008Co-Authors: Cheryl L. Holmes, Keith R. WalleyAbstract:Vasodilatory Septic Shock is characterized by profound vasodilation of the peripheral circulation, relative refractoriness to catecholamines and a relative deficiency of the posterior pituitary hormone, vasopressin. Arginine vasopressin is effective in restoring vascular tone in vasodilatory Septic Shock and may be associated with decreased mortality in less severe Septic Shock as well as improved mortality and decreased renal failure in Septic Shock patients at risk for renal failure.
Joseph E. Parrillo - One of the best experts on this subject based on the ideXlab platform.
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Mycobacterium tuberculosis Septic Shock
Chest, 2013Co-Authors: Shravan Kethireddy, R. Bruce Light, Yazdan Mirzanejad, Dennis G. Maki, Yaseen M. Arabi, Stephen E. Lapinsky, David M. Simon, Aseem Kumar, Joseph E. Parrillo, Anand KumarAbstract:Background Septic Shock due to Mycobacterium tuberculosis (MTB) is an uncommon but well-recognized clinical syndrome. The objective of this study was to describe the unique clinical characteristics, epidemiologic risk factors, and covariates of survival of patients with MTB Septic Shock in comparison with other bacterial Septic Shock. Methods A retrospective nested cohort study was conducted of patients given a diagnosis of MTB Septic Shock derived from a trinational, 8,670-patient database of patients with Septic Shock between 1996 and 2007. Results In the database, 53 patients had been given a diagnosis of MTB Shock compared with 5,419 with Septic Shock associated with isolation of more common bacterial pathogens. Patients with MTB and other bacterial Septic Shock had in-hospital mortality rates of 79.2% and 49.7%, respectively ( P P = .0114). Ten patients (18.9%) did not receive anti-MTB therapy; all died. The median time to appropriate antimicrobial therapy for MTB Septic Shock was 31.0 h (interquartile range, 18.9-71.9 h). Only 11 patients received anti-MTB therapy within 24 h of documentation of hypotension; six of these (54.5%) survived. Only one of 21 patients (4.8%) who started anti-MTB therapy after 24 h survived ( P = .0003 vs Conclusions MTB Septic Shock behaves similarly to bacterial Septic Shock. As with bacterial Septic Shock, early appropriate antimicrobial therapy appears to improve mortality.
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The Pathophysiology of Septic Shock
Critical care clinics, 2009Co-Authors: O. Okorie Nduka, Joseph E. ParrilloAbstract:There is a profound cellular dysfunction in sepsis, that clinically manifests as a continuum from simple, uncomplicated sepsis to severe sepsis, and finally to Septic Shock. Septic Shock remains a significant challenge for clinicians. Recent advances in cellular and molecular biology have significantly improved our understanding of its pathogenetic mechanisms. These improvements will translate to better care and improved outcomes for these patients.
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Pathogenetic Mechanisms of Septic Shock
The New England journal of medicine, 1993Co-Authors: Joseph E. ParrilloAbstract:One of the most frequent and serious problems confronting clinicians is the management of a serious infection and the systemic response to infection, a syndrome termed sepsis. When this syndrome results in hypotension and organ dysfunction, it is called Septic Shock. Septic Shock is the most common cause of death in intensive care units,1 and it is the 13th most common cause of death in the United States2. The incidence of the two disorders continues to rise: 400,000 cases of sepsis and 200,000 episodes of Septic Shock are estimated to occur annually, resulting in more than 100,000 deaths1. . . .
Fabio Guarracino - One of the best experts on this subject based on the ideXlab platform.
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Septic Shock and the Heart
Current Anesthesiology Reports, 2019Co-Authors: Pietro Bertini, Fabio GuarracinoAbstract:Purpose of Review The aim of this review is to analyze the cardiovascular pathophysiology of Septic Shock. Using visual representations of a left ventricular cycle in the pressure/volume plane, we describe hemodynamic derangement occurring in Septic Shock and subsequent changes at each step of treatment allowing a rapid understanding of complex alterations. Recent Findings Acute circulatory failure during sepsis has to be counterbalanced rapidly and appropriately. The most recent guidelines rely on volume expansion, vasoactive, and inotropic support but underlining patients’ pathophysiology is often undetermined. Summary Diagnosis of the hemodynamic substrate needs to be carried out thoroughly, using echocardiography, now commonplace for the intensivist. A pathophysiological approach as we describe might help to understand complicated patterns allowing updates during resuscitation steps. Finally, in our beliefs, clinicians should address Septic Shock resuscitation using a tailored approach and specific protocols, but their applicability needs to be investigated.
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Septic Shock and the Heart
Current Anesthesiology Reports, 2019Co-Authors: Pietro Bertini, Fabio GuarracinoAbstract:The aim of this review is to analyze the cardiovascular pathophysiology of Septic Shock. Using visual representations of a left ventricular cycle in the pressure/volume plane, we describe hemodynamic derangement occurring in Septic Shock and subsequent changes at each step of treatment allowing a rapid understanding of complex alterations. Acute circulatory failure during sepsis has to be counterbalanced rapidly and appropriately. The most recent guidelines rely on volume expansion, vasoactive, and inotropic support but underlining patients’ pathophysiology is often undetermined. Diagnosis of the hemodynamic substrate needs to be carried out thoroughly, using echocardiography, now commonplace for the intensivist. A pathophysiological approach as we describe might help to understand complicated patterns allowing updates during resuscitation steps. Finally, in our beliefs, clinicians should address Septic Shock resuscitation using a tailored approach and specific protocols, but their applicability needs to be investigated.
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Ventriculoarterial decoupling in human Septic Shock
Critical care (London England), 2014Co-Authors: Fabio Guarracino, Baldassare Ferro, Andrea Morelli, Pietro Bertini, Rubia Baldassarri, Michael R. PinskyAbstract:Introduction Septic Shock is the most severe manifestation of sepsis. It is characterized as a hypotensive cardiovascular state associated with multiorgan dysfunction and metabolic disturbances. Management of Septic Shock is targeted at preserving adequate organ perfusion pressure without precipitating pulmonary edema or massive volume overload. Cardiac dysfunction often occurs in Septic Shock patients and can significantly affect outcomes. One physiologic approach to detect the interaction between the heart and the circulation when both are affected is to examine ventriculoarterial coupling, which is defined by the ratio of arterial elastance (Ea) to left ventricular end-systolic elastance (Ees). In this study, we analyzed ventriculoarterial coupling in a cohort of patients admitted to ICUs who presented with vs without Septic Shock.
James A. Russell - One of the best experts on this subject based on the ideXlab platform.
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the Septic Shock 3 0 definition and trials a vasopressin and Septic Shock trial experience
Critical Care Medicine, 2017Co-Authors: James A. Russell, Terry Lee, Joel Singer, John H Boyd, Keith R. WalleyAbstract:Objectives:The Septic Shock 3.0 definition could alter treatment comparisons in randomized controlled trials in Septic Shock. Our first hypothesis was that the vasopressin versus norepinephrine comparison and 28-day mortality of patients with Septic Shock 3.0 definition (lactate > 2 mmol/L) differ f
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Vasopressin in vasodilatory and Septic Shock.
Current Opinion in Critical Care, 2007Co-Authors: James A. RussellAbstract:PURPOSE OF REVIEW The aim of this article is to review mechanisms of action of vasopressin and clinical studies of vasopressin in Septic Shock. RECENT FINDINGS Arginine vasopressin is an important stress hormone that has both vasoactive and antidiuretic properties. The vasoactive properties of vasopressin have been more applicable clinically because of the discovery by Landry and colleagues that there is a deficiency of vasopressin in Septic Shock and that infusion of relatively low doses of vasopressin improves responsiveness to infused catecholamines (such as norepinephrine). There are at least 16 clinical studies of infusion of vasopressin in patients who have Septic Shock. The majority of studies found that vasopressin infusion increased blood pressure and urine output, and decreased the dose requirement of norepinephrine. Several studies showed that vasopressin infusion increased urine output. Both vasopressin and norepinephrine have important adverse effects including decreased cardiac output, decreased heart rate, arrhythmias, myocardial ischemia, mesenteric ischemia, and digital ischemia. SUMMARY It is still unclear whether there is net benefit from low dose vasopressin infusion in patients who have Septic Shock. There may be certain patients who benefit but there are few studies of a prolonged vasopressin infusion to determine which patients benefit.
