Steroids and Post-resuscitation Infectious (Septic) Complications
NCT ID: NCT02408939
Last Updated: 2024-01-17
Study Results
Results pending
The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.
Basic Information
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Recruitment Status
COMPLETED
Total Enrollment
191 participants
Study Classification
OBSERVATIONAL
Study Start Date
2015-03-31
Study Completion Date
2015-08-31
Brief Summary
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Postresuscitation disease is characterized by post-insult systemic inflammation, adrenal insufficiency, and circulatory failure. Such severe pathology may be associated with increased susceptibility to infectious complications and increased risk of death due to postresuscitation septic shock. The latter may be attenuated by stress-dose steroids. In this re-analysis of synthesized randomized clinical trial (RCT) data, the investigators will use individual patient data from two prior RCTs of in-hospital cardiac arrest (NCT00411879 \& NCT00729794), in order to determine the effect of stress-dose steroids on the severity of postresuscitation infectious complications, and more specifically, on the risk of septic shock-associated death.
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Detailed Description
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BACKGROUND AND RATIONALE Patients successfully resuscitated after cardiac arrest experience a "sepsis-like" syndrome characterized by cytokine storm, endotoxemia, coagulopathy, and various degrees of adrenal insufficiency. These pathophysiological mechanisms contribute to the development of circulatory failure, i.e. post-resuscitation shock. Post-resuscitation shock patients resuscitated from vasopressor-requiring cardiac arrest are frequently poorly responsive to high-rate vasopressor infusions (e.g. norepinephrine ≥0.5 μg/kg/min) and intravenous fluids.
The postresuscitation systemic inflammatory response syndrome (SIRS) may be partly caused and subsequently amplified by ischemia/reperfusion (I/R)-associated disruption of the intestinal mucosal barrier. Steroids may suppress key events of I/R injury propagation. Furthermore, in shock states, stress-dose steroids improve vascular responsiveness to vasopressors and preserve monocyte and neutrophil phagocytosis, and dendritic cell function. Low-dose steroids may reduce the mortality of severely ill patients with septic shock.
Nosocomial infections constitute an important cause of postresuscitation mortality. We hypothesized that exposure to stress-dose steroids during and/or after CPR may be associated with reduced risk of death due to postresuscitation infectious complications. To test this hypothesis, we combined data from two prior, prospective studies of in-hospital cardiac arrest. These studies compared the combination of vasopressin, steroids, and epinephrine (VSE) to epinephrine alone, with respect to survival to hospital discharge and good functional outcome. Patients with post-resuscitation shock of the VSE groups received stress dose hydrocortisone (300 mg/day for 7 days maximum, followed by gradual taper at a rate of 100 mg / day and discontinuation on day 10). Patients with post-resuscitation shock of the control groups received saline placebo. Follow-up rates were high in both studies and the reported incidence of post-resuscitation infectious complications was similar in the VSE and control groups.
METHODS Study Design Retrospective analysis of prospectively collected data from two randomized, clinical studies. Study participants were hospitalized in intensive or coronary care units (ICUs or CCUs) of three tertiary care centers: Evaggelismos General Hospital and 401 Greek Army Hospital (both in Athens, Greece), and University Hospital of Larissa, Larissa, Greece.
Ethics and Approval The present analysis is not associated with any clinical intervention, and therefore, the investigators have applied for a waiver of informed consent from either the patient or his/her next of kin. Moreover, the investigators have requested the permission to confirm previously recorded microbiological data through the hospitals' electronic databases The institutional review boards (IRBs) of the aforementioned hospitals have granted their approval for the current study. Evaggelismos Hospital approval No. 14/9/1/2015; 401 Greek Army Hospital approval No. 3/2015/5/2/2015; Larissa University Hospital approval No. 58905/2014/14/1/2015. Modifications of statistical terminology \[from individual patient data (IPD) meta-analysis to IPD re-analysis\] and of infections' classification in the definition of the primary outcome were also approved by the Evaggelismos IRB (respective Approval Nos. 30/25/2/2016 and 29/25/2/2016) and communicated to the other 2, aforementioned IRBs. These approvals were ratified by the IRBs of the other 2 participating centers (401 Greek Army Hospital, IRB Decision No.: 4-2016/6/4/2016; Larissa University Hospital, IRB Decision No.: 5/19-5-2016/Θ.18). Additional, significant amendments of the analysis protocol aimed at primarily evaluating the effect of stress-dose steroids on lethal septic shock were approved by the Evaggelismos IRB (Approval No. 9/26/1/2017) and appropriately communicated to the other 2, aforementioned IRBs.
Analysis Endpoints are presented in the dedicated subsection. Patients The reference study population consists of 368 patients (Evaggelismos Hospital, n=288/368=78.2%) with in-hospital cardiac arrest, who required epinephrine during cardiopulmonary resuscitation (CPR) according to the 2005 Guidelines for Resuscitation. During CPR, VSE group patients (n=178) also received vasopressin and methylprednisolone and controls (n=190) the respective saline placebos. At 4 hours after CPR, there were 211 surviving patients (VSE group, n=115), who were evaluated for postresuscitation shock. One hundred three VSE group patients were then assigned to stress-dose hydrocortisone and 88 controls to saline placebo. One hundred two VSE group patients and 15 controls were actually treated with stress-dose hydrocortisone (n=117). One VSE group patient did not receive stress dose hydrocortisone due to pharmacist error; however, the patient did receive 40 mg of methylprednisolone during CPR.
Definitions Essential prerequisites for the applicability of the below-provided definitions of infections to determine their (prior) occurence in the participants of the included studies will include the presence of confirmatory investigator recordings (for the prior diagnoses of these infections) and also the retrieval of confirmatory microbiological data from hospital records.
Ventilator-associated pneumonia (VAP) will be defined as new (or worsening if already present) chest x-ray infiltrate and at least 2 of the following 3 findings: worsening of respiratory secretions (to purulent or muco-purulent), leucocytosis or leucopenia (\>11000/μL or \<4000/μL respectively), and fever or hypothermia (\>38 degrees Celcius or \<36 degrees Celcius respectively). VAP diagnosis will require at least 48 hours of postresuscitation endotracheal intubation and mechanical ventilation. VAP will be confirmed by a positive tracheobronchial aspirate sample with ≥1000000 Colony Forming Units (CFUs)/μL\] and / or a concurrent blood culture positive for the same pathogen.
Ventilator-associated tracheobronchitis (VAT) will be defined as fever (\>38 degrees Celcius) not attributable to another infectious complication and positive tracheobronchial aspirate culture (with ≥1000000 CFUs/μL) yielding a new bacteria (not present at intubation), and no radiographic signs of new pneumonia.
Bacteremia (or Fungemia) will be defined as isolation of a pathogen from at least one blood culture set (in cases of coagulase negative Staphylococcus species, or Corynebacterium species, 2 positive blood culture sets will be required). Septic shock will be defined as bacteremia / fungemia plus circulatory failure with at least 30% increase in norepinephrine infusion requirements after day 3 postarrest.
Urinary tract infection will be defined as fever or hypothermia and presence of at least one pathogen in a urine sample culture at a concentration of ≥100000 CFUs/μL.
Post-resuscitation shock, organ / system failures, acute respiratory distress syndrome, hyperglycemia, and survival to hospital discharge with good functional outcome will be defined as in the 2 included VSE studies. Organ failure free days and ventilator free days will be determined as in the 2 included VSE studies.
Statistical Analysis Plan All analyses will be performed with the Statistical Package for Social Sciences version 22.0 (IBM, Armonk, NY, USA). As this is not a randomized study, patient baseline characteristics will be compared between the Steroids and No Steroids groups. Distribution normality will be tested by Kolmogorov-Smirnov test. Dichotomous and categorical variables will be compared by a two-sided chi-square or Fisher's exact test. Continuous variables will be compared by a two-tailed, independent samples t test or Mann-Whitney exact U test.
We will conduct a cumulative incidence competing risks analysis (CICR) to determine cause-specific hazard ratios (CSHRs) and their 95% confidence intervals (CIs) for death due to a postresuscitation infection, i.e., lethal septic shock, death due to a noninfectious cause, and poor inhospital outcome (as defined in the outcome measures subsection).
Prespecified risk factors for physical death or poor inhospital outcome will be group (Intervention vs. Control); cardiac arrest cause (cardiac vs. non-cardiac); cardiac arrest area (monitored vs. non-monitored), initial cardiac arrest rhythm (shockable vs. non-shockable); cardiac arrest time (i.e. weekday vs. holiday and nighttime vs. morning-to-late evening), advanced life support (ALS)-related bicarbonate dose; time from resuscitation team call to ALS initiation plus ALS duration; and therapeutic hypothermia (yes vs. no).
Additional analyses will include addition of early postresuscitation mean arterial pressure as covariate to the multivariable CICR Cox models
The postresuscitation systemic inflammatory response syndrome (SIRS) may be partly caused and subsequently amplified by ischemia/reperfusion (I/R)-associated disruption of the intestinal mucosal barrier. Steroids may suppress key events of I/R injury propagation. Furthermore, in shock states, stress-dose steroids improve vascular responsiveness to vasopressors and preserve monocyte and neutrophil phagocytosis, and dendritic cell function. Low-dose steroids may reduce the mortality of severely ill patients with septic shock.
Nosocomial infections constitute an important cause of postresuscitation mortality. We hypothesized that exposure to stress-dose steroids during and/or after CPR may be associated with reduced risk of death due to postresuscitation infectious complications. To test this hypothesis, we combined data from two prior, prospective studies of in-hospital cardiac arrest. These studies compared the combination of vasopressin, steroids, and epinephrine (VSE) to epinephrine alone, with respect to survival to hospital discharge and good functional outcome. Patients with post-resuscitation shock of the VSE groups received stress dose hydrocortisone (300 mg/day for 7 days maximum, followed by gradual taper at a rate of 100 mg / day and discontinuation on day 10). Patients with post-resuscitation shock of the control groups received saline placebo. Follow-up rates were high in both studies and the reported incidence of post-resuscitation infectious complications was similar in the VSE and control groups.
METHODS Study Design Retrospective analysis of prospectively collected data from two randomized, clinical studies. Study participants were hospitalized in intensive or coronary care units (ICUs or CCUs) of three tertiary care centers: Evaggelismos General Hospital and 401 Greek Army Hospital (both in Athens, Greece), and University Hospital of Larissa, Larissa, Greece.
Ethics and Approval The present analysis is not associated with any clinical intervention, and therefore, the investigators have applied for a waiver of informed consent from either the patient or his/her next of kin. Moreover, the investigators have requested the permission to confirm previously recorded microbiological data through the hospitals' electronic databases The institutional review boards (IRBs) of the aforementioned hospitals have granted their approval for the current study. Evaggelismos Hospital approval No. 14/9/1/2015; 401 Greek Army Hospital approval No. 3/2015/5/2/2015; Larissa University Hospital approval No. 58905/2014/14/1/2015. Modifications of statistical terminology \[from individual patient data (IPD) meta-analysis to IPD re-analysis\] and of infections' classification in the definition of the primary outcome were also approved by the Evaggelismos IRB (respective Approval Nos. 30/25/2/2016 and 29/25/2/2016) and communicated to the other 2, aforementioned IRBs. These approvals were ratified by the IRBs of the other 2 participating centers (401 Greek Army Hospital, IRB Decision No.: 4-2016/6/4/2016; Larissa University Hospital, IRB Decision No.: 5/19-5-2016/Θ.18). Additional, significant amendments of the analysis protocol aimed at primarily evaluating the effect of stress-dose steroids on lethal septic shock were approved by the Evaggelismos IRB (Approval No. 9/26/1/2017) and appropriately communicated to the other 2, aforementioned IRBs.
Analysis Endpoints are presented in the dedicated subsection. Patients The reference study population consists of 368 patients (Evaggelismos Hospital, n=288/368=78.2%) with in-hospital cardiac arrest, who required epinephrine during cardiopulmonary resuscitation (CPR) according to the 2005 Guidelines for Resuscitation. During CPR, VSE group patients (n=178) also received vasopressin and methylprednisolone and controls (n=190) the respective saline placebos. At 4 hours after CPR, there were 211 surviving patients (VSE group, n=115), who were evaluated for postresuscitation shock. One hundred three VSE group patients were then assigned to stress-dose hydrocortisone and 88 controls to saline placebo. One hundred two VSE group patients and 15 controls were actually treated with stress-dose hydrocortisone (n=117). One VSE group patient did not receive stress dose hydrocortisone due to pharmacist error; however, the patient did receive 40 mg of methylprednisolone during CPR.
Definitions Essential prerequisites for the applicability of the below-provided definitions of infections to determine their (prior) occurence in the participants of the included studies will include the presence of confirmatory investigator recordings (for the prior diagnoses of these infections) and also the retrieval of confirmatory microbiological data from hospital records.
Ventilator-associated pneumonia (VAP) will be defined as new (or worsening if already present) chest x-ray infiltrate and at least 2 of the following 3 findings: worsening of respiratory secretions (to purulent or muco-purulent), leucocytosis or leucopenia (\>11000/μL or \<4000/μL respectively), and fever or hypothermia (\>38 degrees Celcius or \<36 degrees Celcius respectively). VAP diagnosis will require at least 48 hours of postresuscitation endotracheal intubation and mechanical ventilation. VAP will be confirmed by a positive tracheobronchial aspirate sample with ≥1000000 Colony Forming Units (CFUs)/μL\] and / or a concurrent blood culture positive for the same pathogen.
Ventilator-associated tracheobronchitis (VAT) will be defined as fever (\>38 degrees Celcius) not attributable to another infectious complication and positive tracheobronchial aspirate culture (with ≥1000000 CFUs/μL) yielding a new bacteria (not present at intubation), and no radiographic signs of new pneumonia.
Bacteremia (or Fungemia) will be defined as isolation of a pathogen from at least one blood culture set (in cases of coagulase negative Staphylococcus species, or Corynebacterium species, 2 positive blood culture sets will be required). Septic shock will be defined as bacteremia / fungemia plus circulatory failure with at least 30% increase in norepinephrine infusion requirements after day 3 postarrest.
Urinary tract infection will be defined as fever or hypothermia and presence of at least one pathogen in a urine sample culture at a concentration of ≥100000 CFUs/μL.
Post-resuscitation shock, organ / system failures, acute respiratory distress syndrome, hyperglycemia, and survival to hospital discharge with good functional outcome will be defined as in the 2 included VSE studies. Organ failure free days and ventilator free days will be determined as in the 2 included VSE studies.
Statistical Analysis Plan All analyses will be performed with the Statistical Package for Social Sciences version 22.0 (IBM, Armonk, NY, USA). As this is not a randomized study, patient baseline characteristics will be compared between the Steroids and No Steroids groups. Distribution normality will be tested by Kolmogorov-Smirnov test. Dichotomous and categorical variables will be compared by a two-sided chi-square or Fisher's exact test. Continuous variables will be compared by a two-tailed, independent samples t test or Mann-Whitney exact U test.
We will conduct a cumulative incidence competing risks analysis (CICR) to determine cause-specific hazard ratios (CSHRs) and their 95% confidence intervals (CIs) for death due to a postresuscitation infection, i.e., lethal septic shock, death due to a noninfectious cause, and poor inhospital outcome (as defined in the outcome measures subsection).
Prespecified risk factors for physical death or poor inhospital outcome will be group (Intervention vs. Control); cardiac arrest cause (cardiac vs. non-cardiac); cardiac arrest area (monitored vs. non-monitored), initial cardiac arrest rhythm (shockable vs. non-shockable); cardiac arrest time (i.e. weekday vs. holiday and nighttime vs. morning-to-late evening), advanced life support (ALS)-related bicarbonate dose; time from resuscitation team call to ALS initiation plus ALS duration; and therapeutic hypothermia (yes vs. no).
Additional analyses will include addition of early postresuscitation mean arterial pressure as covariate to the multivariable CICR Cox models
Conditions
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Infections
Cardiac Arrest
Study Design
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Observational Model Type
OTHER
Study Time Perspective
RETROSPECTIVE
Study Groups
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Intervention
Patients resuscitated from in-hospital cardiac arrest and treated with stress-dose hydrocortisone for postresuscitation shock
Stress-dose hydrocortisone
Intervention Type
DRUG
Patients with postresuscitation shock received stress-dose (300 mg) of hydrocortisone for 7 days maximum followed by gradual taper and discontinuation over 48 hours after either the resolution of their hemodynamic instability or day 7 of treatment.
Control
Patients resuscitated from in-hospital cardiac arrest and treated according to contemporary standards that did not include stress-dose steroids for postresuscitation shock
No interventions assigned to this group
Interventions
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Stress-dose hydrocortisone
Patients with postresuscitation shock received stress-dose (300 mg) of hydrocortisone for 7 days maximum followed by gradual taper and discontinuation over 48 hours after either the resolution of their hemodynamic instability or day 7 of treatment.
Intervention Type
DRUG
Other Intervention Names
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Solucortef
Eligibility Criteria
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Inclusion Criteria
* Adult patients with refractory inhospital cardiac arrest, defined as epinephrine requirement for ventricular fibrillation/tachycardia or asystole/pulseless electrical activity according to guidelines for resuscitation 2005
Exclusion Criteria
* Age \< 18 years
* Terminal illness or do-not resuscitate status
* Cardiac arrest due to exsanguination
* Cardiac arrest before hospital admission
* Pre-arrest treatment with intravenous corticosteroids
* Previous enrollment in or exclusion from the 2 studies included in the re-analysis
* Terminal illness or do-not resuscitate status
* Cardiac arrest due to exsanguination
* Cardiac arrest before hospital admission
* Pre-arrest treatment with intravenous corticosteroids
* Previous enrollment in or exclusion from the 2 studies included in the re-analysis
Minimum Eligible Age
18 Years
Eligible Sex
ALL
Accepts Healthy Volunteers
No
Sponsors
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University of Thessaly
OTHER
Sponsor Role
collaborator
University of Athens
OTHER
Sponsor Role
lead
Responsible Party
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Spyros D. Mentzelopoulos
Associate Professor in Intensive Care Medicine
Responsibility Role
PRINCIPAL_INVESTIGATOR
Principal Investigators
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Spyros D Mentzelopoulos, MD, PhD
Role: PRINCIPAL_INVESTIGATOR
University of Athens Medical School
Spyros D Mentzelopoulos, MD, PhD
Role: STUDY_DIRECTOR
University of Athens Medical School
Spyros G Zakynthinos, MD, PhD
Role: STUDY_CHAIR
University of Athens Medical School
Locations
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Service d'anesthésie et des réanimations chirurgicales, ôHôpitaux Universitaires Henri Mondor, Assistance Publique des Hôpitaux de Paris, Université Paris Est, Faculté de Médecine
Créteil, , France
Site Status
Department of Intensive Care Medicine, Evaggelismos Hospital
Athens, Attica, Greece
Site Status
401 General Military Hospital of Athens
Athens, Attica, Greece
Site Status
University General Hospital of Larissa
Larissa, Thessaly, Greece
Site Status
President Hellenic Society of Cardiopulmonary Resuscitation
Athens, , Greece
Site Status
Countries
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France
Greece
References
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Adrie C, Adib-Conquy M, Laurent I, Monchi M, Vinsonneau C, Fitting C, Fraisse F, Dinh-Xuan AT, Carli P, Spaulding C, Dhainaut JF, Cavaillon JM. Successful cardiopulmonary resuscitation after cardiac arrest as a "sepsis-like" syndrome. Circulation. 2002 Jul 30;106(5):562-8. doi: 10.1161/01.cir.0000023891.80661.ad.
Reference Type
BACKGROUND
Adrie C, Laurent I, Monchi M, Cariou A, Dhainaou JF, Spaulding C. Postresuscitation disease after cardiac arrest: a sepsis-like syndrome? Curr Opin Crit Care. 2004 Jun;10(3):208-12. doi: 10.1097/01.ccx.0000126090.06275.fe.
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BACKGROUND
Pene F, Hyvernat H, Mallet V, Cariou A, Carli P, Spaulding C, Dugue MA, Mira JP. Prognostic value of relative adrenal insufficiency after out-of-hospital cardiac arrest. Intensive Care Med. 2005 May;31(5):627-33. doi: 10.1007/s00134-005-2603-7. Epub 2005 Apr 19.
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BACKGROUND
Kim JJ, Lim YS, Shin JH, Yang HJ, Kim JK, Hyun SY, Rhoo I, Hwang SY, Lee G. Relative adrenal insufficiency after cardiac arrest: impact on postresuscitation disease outcome. Am J Emerg Med. 2006 Oct;24(6):684-8. doi: 10.1016/j.ajem.2006.02.017.
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BACKGROUND
Hekimian G, Baugnon T, Thuong M, Monchi M, Dabbane H, Jaby D, Rhaoui A, Laurent I, Moret G, Fraisse F, Adrie C. Cortisol levels and adrenal reserve after successful cardiac arrest resuscitation. Shock. 2004 Aug;22(2):116-9. doi: 10.1097/01.shk.0000132489.79498.c7.
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BACKGROUND
Tsai MS, Huang CH, Chang WT, Chen WJ, Hsu CY, Hsieh CC, Yang CW, Chiang WC, Ma MH, Chen SC. The effect of hydrocortisone on the outcome of out-of-hospital cardiac arrest patients: a pilot study. Am J Emerg Med. 2007 Mar;25(3):318-25. doi: 10.1016/j.ajem.2006.12.007.
Reference Type
BACKGROUND
Schultz CH, Rivers EP, Feldkamp CS, Goad EG, Smithline HA, Martin GB, Fath JJ, Wortsman J, Nowak RM. A characterization of hypothalamic-pituitary-adrenal axis function during and after human cardiac arrest. Crit Care Med. 1993 Sep;21(9):1339-47. doi: 10.1097/00003246-199309000-00018.
Reference Type
BACKGROUND
Nolan JP, Deakin CD, Soar J, Bottiger BW, Smith G; European Resuscitation Council. European Resuscitation Council guidelines for resuscitation 2005. Section 4. Adult advanced life support. Resuscitation. 2005 Dec;67 Suppl 1:S39-86. doi: 10.1016/j.resuscitation.2005.10.009. No abstract available.
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BACKGROUND
Keh D, Boehnke T, Weber-Cartens S, Schulz C, Ahlers O, Bercker S, Volk HD, Doecke WD, Falke KJ, Gerlach H. Immunologic and hemodynamic effects of "low-dose" hydrocortisone in septic shock: a double-blind, randomized, placebo-controlled, crossover study. Am J Respir Crit Care Med. 2003 Feb 15;167(4):512-20. doi: 10.1164/rccm.200205-446OC. Epub 2002 Nov 8.
Reference Type
BACKGROUND
American Thoracic Society; Infectious Diseases Society of America. Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia. Am J Respir Crit Care Med. 2005 Feb 15;171(4):388-416. doi: 10.1164/rccm.200405-644ST. No abstract available.
Reference Type
BACKGROUND
Mermel LA, Allon M, Bouza E, Craven DE, Flynn P, O'Grady NP, Raad II, Rijnders BJ, Sherertz RJ, Warren DK. Clinical practice guidelines for the diagnosis and management of intravascular catheter-related infection: 2009 Update by the Infectious Diseases Society of America. Clin Infect Dis. 2009 Jul 1;49(1):1-45. doi: 10.1086/599376.
Reference Type
BACKGROUND
Hooton TM, Bradley SF, Cardenas DD, Colgan R, Geerlings SE, Rice JC, Saint S, Schaeffer AJ, Tambayh PA, Tenke P, Nicolle LE; Infectious Diseases Society of America. Diagnosis, prevention, and treatment of catheter-associated urinary tract infection in adults: 2009 International Clinical Practice Guidelines from the Infectious Diseases Society of America. Clin Infect Dis. 2010 Mar 1;50(5):625-63. doi: 10.1086/650482.
Reference Type
BACKGROUND
Dellinger RP, Levy MM, Rhodes A, Annane D, Gerlach H, Opal SM, Sevransky JE, Sprung CL, Douglas IS, Jaeschke R, Osborn TM, Nunnally ME, Townsend SR, Reinhart K, Kleinpell RM, Angus DC, Deutschman CS, Machado FR, Rubenfeld GD, Webb S, Beale RJ, Vincent JL, Moreno R; Surviving Sepsis Campaign Guidelines Committee including The Pediatric Subgroup. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock, 2012. Intensive Care Med. 2013 Feb;39(2):165-228. doi: 10.1007/s00134-012-2769-8. Epub 2013 Jan 30.
Reference Type
BACKGROUND
ARDS Definition Task Force; Ranieri VM, Rubenfeld GD, Thompson BT, Ferguson ND, Caldwell E, Fan E, Camporota L, Slutsky AS. Acute respiratory distress syndrome: the Berlin Definition. JAMA. 2012 Jun 20;307(23):2526-33. doi: 10.1001/jama.2012.5669.
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BACKGROUND
A randomized clinical trial of calcium entry blocker administration to comatose survivors of cardiac arrest. Design, methods, and patient characteristics. The Brain Resuscitation Clinical Trial II Study Group. Control Clin Trials. 1991 Aug;12(4):525-45. doi: 10.1016/0197-2456(91)90011-a.
Reference Type
BACKGROUND
Vollmar B, Menger MD. Intestinal ischemia/reperfusion: microcirculatory pathology and functional consequences. Langenbecks Arch Surg. 2011 Jan;396(1):13-29. doi: 10.1007/s00423-010-0727-x. Epub 2010 Nov 19.
Reference Type
BACKGROUND
Davies KJ, Walters JH, Kerslake IM, Greenwood R, Thomas MJ. Early antibiotics improve survival following out-of hospital cardiac arrest. Resuscitation. 2013 May;84(5):616-9. doi: 10.1016/j.resuscitation.2012.11.004. Epub 2012 Nov 12.
Reference Type
BACKGROUND
Chalkias A, Scheetz MH, Gulati A, Xanthos T. Periarrest intestinal bacterial translocation and resuscitation outcome. J Crit Care. 2016 Feb;31(1):217-20. doi: 10.1016/j.jcrc.2015.09.015. Epub 2015 Sep 25.
Reference Type
BACKGROUND
Haller B, Schmidt G, Ulm K. Applying competing risks regression models: an overview. Lifetime Data Anal. 2013 Jan;19(1):33-58. doi: 10.1007/s10985-012-9230-8. Epub 2012 Sep 26.
Reference Type
BACKGROUND
Trzeciak S, Jones AE, Kilgannon JH, Milcarek B, Hunter K, Shapiro NI, Hollenberg SM, Dellinger P, Parrillo JE. Significance of arterial hypotension after resuscitation from cardiac arrest. Crit Care Med. 2009 Nov;37(11):2895-903; quiz 2904. doi: 10.1097/ccm.0b013e3181b01d8c.
Reference Type
BACKGROUND
Tsai MS, Chuang PY, Yu PH, Huang CH, Tang CH, Chang WT, Chen WJ. Glucocorticoid use during cardiopulmonary resuscitation may be beneficial for cardiac arrest. Int J Cardiol. 2016 Nov 1;222:629-635. doi: 10.1016/j.ijcard.2016.08.017. Epub 2016 Aug 4.
Reference Type
BACKGROUND
Callaway CW, Soar J, Aibiki M, Bottiger BW, Brooks SC, Deakin CD, Donnino MW, Drajer S, Kloeck W, Morley PT, Morrison LJ, Neumar RW, Nicholson TC, Nolan JP, Okada K, O'Neil BJ, Paiva EF, Parr MJ, Wang TL, Witt J; Advanced Life Support Chapter Collaborators. Part 4: Advanced Life Support: 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Circulation. 2015 Oct 20;132(16 Suppl 1):S84-145. doi: 10.1161/CIR.0000000000000273. No abstract available.
Reference Type
BACKGROUND
Mentzelopoulos SD, Zakynthinos SG, Tzoufi M, Katsios N, Papastylianou A, Gkisioti S, Stathopoulos A, Kollintza A, Stamataki E, Roussos C. Vasopressin, epinephrine, and corticosteroids for in-hospital cardiac arrest. Arch Intern Med. 2009 Jan 12;169(1):15-24. doi: 10.1001/archinternmed.2008.509.
Reference Type
RESULT
Mentzelopoulos SD, Malachias S, Chamos C, Konstantopoulos D, Ntaidou T, Papastylianou A, Kolliantzaki I, Theodoridi M, Ischaki H, Makris D, Zakynthinos E, Zintzaras E, Sourlas S, Aloizos S, Zakynthinos SG. Vasopressin, steroids, and epinephrine and neurologically favorable survival after in-hospital cardiac arrest: a randomized clinical trial. JAMA. 2013 Jul 17;310(3):270-9. doi: 10.1001/jama.2013.7832.
Reference Type
RESULT
Mentzelopoulos SD, Mongardon N, Xanthos T, Zakynthinos SG. Possible significance of hemodynamic and immunomodulatory effects of early stress-dose steroids in cardiac arrest. Crit Care. 2016 Jul 20;20(1):211. doi: 10.1186/s13054-016-1384-4. No abstract available.
Reference Type
DERIVED
Other Identifiers
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14/9/1/2015 IPDRA
Identifier Type: -
Identifier Source: org_study_id
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TERMINATED
PHASE4
Efficacy of Hydrocortisone in Treatment of Severe Sepsis/Septic Shock Patients With Acute Lung Injury/Acute Respiratory Distress Syndrome (ARDS)
NCT01284452
COMPLETED
NA
Early Intravenous Hydrocortisone in Sepsis
NCT06217939
RECRUITING
NA
Stress Doses of Hydrocortisone on Coagulation Dysfunction in Patients With Septic Shock
NCT02266589
COMPLETED
PHASE3
Early Versus Conventional Cessation of Hydrocortisone in Septic Shock
NCT05818826
RECRUITING
PHASE2
Natriuresis as a Predictor of the Haemodynamic Response to Steroid Replacement Therapy in Patients in Septic Shock
NCT03258619
COMPLETED
Activated Protein C and Corticosteroids for Human Septic Shock
NCT00625209
COMPLETED
PHASE3
Effects of Fludrocortisone and Hydrocortisone in Healthy Volunteers With Aldosterone Induced Suppression
NCT00673270
TERMINATED
PHASE1/PHASE2
Hydrocortisone Versus Hydrocortisone Plus Fludrocortisone for the Treatment of Adrenal Insufficiency in Severe Sepsis
NCT00368381
WITHDRAWN
PHASE4
Septic Shock em Steroids
NCT01047670
UNKNOWN
PHASE2/PHASE3
Rapid Recognition of Corticosteroid Resistant or Sensitive Sepsis
NCT04280497
RECRUITING
NA
Initiation of Hydrocortisone for the Treatment of Septic Shock
NCT02580240
COMPLETED
NA
Evaluation of the Role of Hydrocortisone Either Alone or Combined With Fludrocortisone in the Outcome of Septic Shock in Adults
NCT04492280
COMPLETED
PHASE4
Effects of Fludrocortisone on Norepinephrine-mean Arterial Pressure Dose-response in Septic Shock
NCT02069288
WITHDRAWN
PHASE3
Hydrocortisone for COVID-19 and Severe Hypoxia
NCT04348305
COMPLETED
PHASE3
ADjunctive coRticosteroid trEatment iN criticAlly ilL Patients With Septic Shock
NCT01448109
COMPLETED
PHASE4
Metabolic Resuscitation Using Ascorbic Acid, Thiamine, and Glucocorticoids in Sepsis.
NCT03422159
COMPLETED
PHASE2
Effects of Stress Doses of Hydrocortisone on Coagulation Dysfunction in Patients With Septic Shock
NCT02114710
COMPLETED
PHASE3
Diagnostic Study of Adrenal Cortical Function in Children With Septic Shock
NCT00005890
COMPLETED
NA
Effects of Hydrocortison Treatment on Angiotensin II and Angiotensin II Receptors in Patients With Septic Shock
NCT04647552
COMPLETED
Preemptive Resuscitation for Eradication of Septic Shock
NCT01449721
COMPLETED
NA
Corticosteroid Therapy of Septic Shock - Corticus
NCT00147004
COMPLETED
PHASE3
Evaluation of Corticosteroid Therapy in Childhood Severe Sepsis - a Randomised Pilot Study
NCT00732277
COMPLETED
PHASE2