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1 causes of death were respiratory failure and septic shock.
2           Patients with severe sepsis and/or septic shock.
3 h a liberal strategy in cancer patients with septic shock.
4 e important implications for trial design in septic shock.
5 coid receptors in murine endotoxic and human septic shock.
6 on of antibiotics to patients with sepsis or septic shock.
7 hemodynamic support of newborn and pediatric septic shock.
8 ative bradycardia will benefit patients with septic shock.
9  and nonobese patients with severe sepsis or septic shock.
10 treatment in patients with severe sepsis and septic shock.
11 information regarding the pathophysiology of septic shock.
12 increased odds of mortality were greatest in septic shock.
13 repinephrine, the first-line vasopressor for septic shock.
14  were largely resistant to endotoxin-induced septic shock.
15       Six hundred twenty-eight patients with septic shock.
16 ance to endotoxin- and polymicrobial-induced septic shock.
17 mparisons in randomized controlled trials in septic shock.
18 utralizing IgG M96 failed to protect against septic shock.
19 th and without hydrocortisone, in a model of septic shock.
20 onditions, including immune paralysis during septic shock.
21 th severe sepsis prevents the development of septic shock.
22 negative bacteria can be a potent inducer of septic shock.
23 ion/cardiogenic shock, injury, and infection/septic shock.
24  lactate level, and base deficit to identify septic shock.
25 ry, mortality, and plasma cytokines in human septic shock.
26 uirements, organ dysfunction, and death from septic shock.
27 timate baseline mortality risk for pediatric septic shock.
28 d eighty-four patients (25.0%) progressed to septic shock.
29 of cecal ligation and puncture (CLP)-induced septic shock.
30  and function over time in an ovine model of septic shock.
31 cquired pneumonia in sepsis or severe sepsis/septic shock.
32 ve long-term outcomes of 28-day survivors of septic shock.
33 in the first 24 hours following the onset of septic shock.
34 sma proinflammatory cytokine levels in human septic shock.
35 athogenic neutrophil subset in patients with septic shock.
36 llness myopathy and those with severe sepsis/septic shock.
37 trategies (two protocols vs. usual care) for septic shock.
38 ysfunction plus infection, severe sepsis, or septic shock.
39 esponse syndrome, sepsis, severe sepsis, and septic shock.
40 ent an easy "alert system" among patients in septic shock.
41 splenia and community-acquired severe sepsis/septic shock.
42  mechanism underlying CD300b augmentation of septic shock.
43 on is associated with long-term mortality of septic shock.
44 Health Medical Intensive Care Unit (ICU) for septic shock.
45  patients with severe sepsis who were not in septic shock.
46 y lethal immune collapse syndrome similar to septic shock.
47 ents within 24 hours of meeting criteria for septic shock.
48 ts in inflammatory disease models, including septic shock.
49 l factors are involved in the development of septic shock.
50 psis at various stages, from early sepsis to septic shock.
51 t frequently used initial vasopressor during septic shock.
52 uscitation of patients presenting with early septic shock.
53 ur of shock recognition in severe sepsis and septic shock.
54 n D levels in patients with severe sepsis or septic shock.
55 bacteria may not be the only factor inducing septic shock.
56 mortality in patients with severe sepsis and septic shock.
57 ion that causes widespread tissue damage and septic shock.
58 hway in host resistance to endotoxin-induced septic shock.
59 pisodes of suspected infection and suspected septic shock.
60 T lymphocytes facilitate the pathobiology of septic shock.
61 stablished mortality of IL-15 KO mice during septic shock.
62 ate baseline mortality risk in children with septic shock.
63 that was ongoing at the time of death due to septic shock.
64 lt male C57Black 6 mice, adult patients with septic shock.
65 phrine use of at least 60% for patients with septic shock.
66 ical Modification codes for severe sepsis or septic shock.
67 pathogens is probably critical to outcome in septic shock.
68 surgical ICU patients with severe sepsis and septic shock.
69 d 2015 for fluid-refractory severe sepsis or septic shock.
70 ociated with progression of severe sepsis to septic shock.
71 iated with a 8.0% increase in progression to septic shock.
72 olfactomedin-4+ neutrophils in patients with septic shock.
73 ze neutrophil heterogeneity in children with septic shock.
74  stratification according to the presence of septic shock.
75 ir, and metabolism in the pathophysiology of septic shock.
76 he current study is limited to patients with septic shock.
77 nt survival, particularly in the presence of septic shock.
78 ents who are relatively bradycardic while in septic shock.
79 or hRetn in lipopolysaccharide (LPS)-induced septic shock.
80 mponent of G(-) bacterial cell wall) induced septic shock.
81       Interventional study in a rat model of septic shock (128 adult males) to assess the effects of
82 .01-1.10), P = 0.02), and presence of sepsis/septic shock (2.70 (1.17-6.28), P = 0.02).
83 ol for rapid identification of patients with septic shock, 2) a "resuscitation and stabilization bund
84 linical Modification codes for severe sepsis/septic shock, 2) Martin approach, and 3) Angus approach.
85                      Among 378 patients with septic shock, 207 of 378 (55%; 50-60%) were febrile by h
86 arison and 28-day mortality of patients with Septic Shock 3.0 definition (lactate > 2 mmol/L) differ
87                                          The Septic Shock 3.0 definition and our findings have import
88                                          The Septic Shock 3.0 definition could alter treatment compar
89                                          The Septic Shock 3.0 definition decreased sample size by hal
90                                          The Septic Shock 3.0 definition would have decreased sample
91 .9% received starch, and among patients with septic shock, 68.3% had lactate measured and 64% receive
92 pticemia (038.x), severe sepsis (995.92), or septic shock (785.52), as well as all subsequent hospita
93 day], ventricular fibrillation [120 mg/day], septic shock [80 mg/day], and neutropenia [120 mg/day]).
94  measured by the pSOFA score, and sepsis and septic shock according to the Sepsis-3 definitions.
95 s in critically ill patients with sepsis and septic shock, acute respiratory distress syndrome, and m
96              Consecutive adult patients with septic shock admitted between November 2009 and Septembe
97              The cohort included adults with septic shock admitted to study hospitals between July 1,
98        In emergency department patients with septic shock, afebrile patients received lower rates of
99                             In patients with septic shock, AKI is common and associated with adverse
100 te kidney injury compared with patients with septic shock alone.
101 metabolites between sepsis and severe sepsis/septic shock also varied according to the underlying typ
102                             In patients with septic shock, alterations in inflammation, coagulation,
103  mortality rate of 12.1%, and 347 (4.0%) had septic shock and a mortality rate of 32.3%.
104 with septic shock, plasma from patients with septic shock and acute kidney injury inhibited neutrophi
105 oes not correct this defect in patients with septic shock and acute kidney injury.
106 an important role in acute injury, including septic shock and acute lung injury.
107 al to 18 years old with severe sepsis and/or septic shock and antimicrobial administration within 24
108 role in many inflammatory diseases including septic shock and atherosclerosis.
109                                Patients with septic shock and controls do not differ in their median
110 tcomes in the overall group of patients with septic shock and elevated lactate.
111  are frequently elevated in severe sepsis or septic shock and have relevant prognostic value, which m
112  element in the management of severe sepsis, septic shock and in sports performance evaluation.
113 th increased progression of severe sepsis to septic shock and increased mortality.
114 ical criteria currently reported to identify septic shock and inform the Delphi process; (2) a Delphi
115 ine concentration in plasma decreases during septic shock and may contribute to multiple organ dysfun
116 reatment by the investigator (pneumonia, and septic shock and multiorgan failure).
117  GITB in transplant patients, complicated by septic shock and multiple organ failure, including acute
118  development of secondary conditions such as septic shock and multiple-organ failure.
119 lying immune status impacts on the course of septic shock and on the susceptibility to ICU-acquired c
120 fficacy of plasma exchange for children with septic shock and TAMOF indicated PERSEVERE-II-based stra
121 rched for terms related to severe sepsis and septic shock and terms related to polymyxin B hemoperfus
122         We tested PERSEVERE in children with septic shock and thrombocytopenia-associated multiple or
123 s us to reevaluate the current management of septic shock and to assess whether we are inadvertently
124 his study we selected patients admitted with septic shock and treated for more than 4 days from a pro
125 given intravenous Escherichia coli to induce septic shock, and five acted as controls.
126 rminologies are currently in use for sepsis, septic shock, and organ dysfunction, leading to discrepa
127 lure to rescue included acute renal failure, septic shock, and postoperative pulmonary complications.
128 ubpopulation of neutrophils in patients with septic shock, and those with a high percentage of olfact
129                                   Sepsis and septic shock are common and, at times, fatal in pediatri
130                                   Sepsis and septic shock are commonly present in the ICU and accompa
131                            Severe sepsis and septic shock are life-threatening conditions, with Gram-
132 mmon in septic shock, but many patients with septic shock are relatively bradycardic.
133 model for end stage liver disease (MELD) and septic shock are the independent predictors of 50 days i
134                    Sepsis, severe sepsis and septic shock are the main cause of mortality in non-card
135  bradycardia (heart rate, < 80 beats/min) in septic shock are unknown.
136                                          The septic shock-associated crude mortality was 46.5% (95% C
137     All adults treated with severe sepsis or septic shock between 2005 and 2014, using administrative
138 ce of acute decompensation, 20 patients with septic shock but no cirrhosis or liver disease, and 20 h
139                     Tachycardia is common in septic shock, but many patients with septic shock are re
140 s associated with improved outcomes in adult septic shock, but pediatric guidelines do not endorse it
141        Furthermore, niacin rescued mice from septic shock by diminishing inflammatory symptoms and th
142 sis of sepsis but enables the development of septic shock by maintaining NK cell numbers and integrit
143                                Patients with septic shock can be clinically identified by a vasopress
144                          Adult patients with septic shock can be identified using the clinical criter
145 s proinflammatory cytokine production during septic shock caused by cecal ligation and puncture or en
146          IL-15 SA treatment also exacerbated septic shock caused by cecal ligation and puncture when
147                            It is unclear how septic shock causes acute kidney injury (AKI) and whethe
148  expressed gene in nonsurvivors of pediatric septic shock, compared with survivors.
149 ne the outcomes of patients meeting Sepsis-3 septic shock criteria versus patients meeting the "old"
150                                              Septic shock currently refers to a state of acute circul
151 defined as suspected infection and suspected septic shock decreased significantly after the intervent
152                              As mortality of septic shock decreases, new therapies focus on improving
153 from the emergency department with sepsis or septic shock (defined: infection, >/= 2 systemic inflamm
154 A subset of patients with sepsis progress to septic shock, defined by profound circulatory, cellular,
155 cohort studies to achieve consensus on a new septic shock definition and clinical criteria; and (3) c
156                Evidence for and agreement on septic shock definitions and criteria.
157 e (19 participants) to revise current sepsis/septic shock definitions.
158 without hydrocortisone, in an ovine model of septic shock did not markedly alter norepinephrine requi
159 , 57% of patients meeting old definition for septic shock did not meet Sepsis-3 criteria.
160 study included adult patients with sepsis or septic shock due to bloodstream infections caused by GNB
161        Compared with hospital admission with septic shock during quarters of normal use, hospital adm
162 12 of whom 58,045 received a vasopressor for septic shock during the first 2 days of hospitalization.
163 r hospitalization, 149 (65.0%) had sepsis or septic shock during their course.
164 nrolled 3,663 patients with severe sepsis or septic shock during three 4-month periods between 2011 a
165 ensive care-supported model of gram-negative septic shock, early AKI was not associated with changes
166 and one each of acute myocardial infarction, septic shock, encephalopathy, general deterioration in p
167 rian using the keywords: sepsis, septicemia, septic shock, endotoxemia, persistent pulmonary hyperten
168 ch study subject was allocated to one of two septic shock endotypes, based on a 100-gene signature re
169 improvement initiative for severe sepsis and septic shock focused on the resuscitation bundle on 90-d
170 he most important cause of severe sepsis and septic shock following splenectomy.
171 ve patients presenting with severe sepsis or septic shock from 2011 to 2013.
172         Two hundred sixty-five patients with septic shock from four ICUs were consecutively enrolled.
173 ional normalized ratio, acute kidney injury, septic shock, hepatic encephalopathy and model for end s
174 recommended as the first-line vasopressor in septic shock; however, early vasopressin use has been pr
175 dney injury was 2.212 (95% CI: 1.334-3.667), septic shock (HR = 1.895, 95% CI: 1.081-3.323) and model
176 ions, but can also lead to sepsis and lethal septic shock if overactivated.
177 atients were further categorized as Sepsis-3 septic shock if they demonstrated hypotension, received
178 d consecutive patients with severe sepsis or septic shock in 2 intensive care units in the Netherland
179 rtile range, 57-79 years]; 47.0% women) with septic shock in 26 hospitals that demonstrated at least
180 sopressors, and renal replacement therapy in septic shock in 28-day survivors was associated with 1-,
181 mortality in patients with severe sepsis and septic shock in specific disease severity subgroups.
182                   Adult cancer patients with septic shock in the first 6 hours of ICU admission.
183                          Among patients with septic shock in US hospitals affected by the 2011 norepi
184 orepinephrine, the cornerstone treatment for septic shock, in sepsis-induced immunoparalysis.
185                                           In septic shock, indices of GAG fragmentation correlated wi
186 ate of neutrophil activation associated with septic shock-induced disseminated intravascular coagulat
187                                              Septic shock is a common cause of acute kidney injury (A
188                                              Septic shock is a major cause of death worldwide and a c
189                                              Septic shock is associated with increased long-term morb
190        Relative bradycardia in patients with septic shock is associated with lower mortality, even af
191 tematic review, surveys, and cohort studies, septic shock is defined as a subset of sepsis in which u
192 ng of sepsis, neutrophils from patients with septic shock likewise exhibited a significantly increase
193 alance, this candidate pathway might benefit septic shock management.
194  not affect mouse survival in an LPS-induced septic shock model.
195           Secondary outcomes were time until septic shock, mortality in the intensive care unit or ho
196 ocortisone and placebo groups for time until septic shock; mortality in the intensive care unit or in
197 e blood culture Staphylococcus haemolyticus, septic shock, multiple organ failure including acute res
198 ched an asymptote near 20% for the infection/septic shock, myocardial infarction/cardiogenic shock (n
199 survival was more favorable in the infection/septic shock (n=1076; hazard ratio, 0.61; 95% confidence
200 onia [n=2], interstitial lung disease [n=1], septic shock [n=1], and unknown [n=1]) and two (<1%) of
201 uses in the combination group (sepsis [n=2], septic shock [n=1], congestive cardiac failure [n=1], an
202 residence in a nursing home, recent surgery, septic shock, NF, meningitis, isolated bacteremia, pneum
203                                              Septic shock occurred in 36 of 170 patients (21.2%) in t
204            We identified 1,554 patients with septic shock, of whom 686 (44%) met criteria for relativ
205                Sheep given E. coli developed septic shock, oliguria, increased serum creatinine, and
206  the Surviving Sepsis Campaign in refractory septic shock only.
207 atients meeting the "old" (1991) criteria of septic shock only.
208 hrombocytopenia within the first 24 hours of septic shock onset as a prognostic marker of survival at
209 d risk of death within the 28 days following septic shock onset.
210 n or equal to two organ failures at day 7 of septic shock or 28-day mortality, had a higher percentag
211 ce of two or more organ failures at day 7 of septic shock or 28-day mortality.
212 y and in-hospital mortality in patients with septic shock or ARDS.
213 this molecule as a new class of drug against septic shock or other inflammatory diseases.
214  = 9.17; 95% CI, 8.84-9.50), the presence of septic shock (OR = 2.43; 95% CI, 2.20-2.69) or ventilato
215 matic review identified 44 studies reporting septic shock outcomes (total of 166,479 patients) from a
216  patients aged >/=10 years and patients with septic shock (P-values </=.001).
217  Consecutive sample of all severe sepsis and septic shock patients (defined: infection, >/= 2 systemi
218 talloid resuscitation provided to sepsis and septic shock patients at initial presentation and 2) det
219                             Adult sepsis and septic shock patients captured in a prospective quality
220                 Inadequate stratification of septic shock patients may result in inappropriate treatm
221  outcome of 6-hour mean arterial pressure in septic shock patients receiving vasopressin who were on
222       To compare the hemodynamic response in septic shock patients receiving vasopressin who were on
223                                 Samples from septic shock patients were obtained at day 3 and compare
224 study evaluates whether emergency department septic shock patients without a fever (reported or measu
225 irus reactivations were documented in 68% of septic shock patients without prior immunodeficiency and
226  to one bundle element for severe sepsis and septic shock patients.
227 d b) in cardiomyocytes exposed to serum from septic shock patients.
228                         Within severe sepsis/septic shock, patients with bloodstream infection could
229          Testing PERSEVERE in the context of septic shock phenotypes prompted a revision incorporatin
230 known how PERSEVERE performs within distinct septic shock phenotypes.
231      Compared with plasma from patients with septic shock, plasma from patients with septic shock and
232 placement therapy, plasma from patients with septic shock plus acute kidney injury still showed eleva
233 equirement of mechanical ventilator, sepsis, septic shock, readmission, and reoperation.
234         Among patients with severe sepsis or septic shock receiving antimicrobials in the emergency d
235 ity improvement initiatives to improve early septic shock recognition and first-hour compliance to th
236 ears or older who survived sepsis (including septic shock), recruited from 9 intensive care units (IC
237 d May 2015, enrolling adult patients who had septic shock requiring vasopressors despite fluid resusc
238                          Adult patients with septic shock requiring vasopressors.
239  in patients with sepsis, severe sepsis, and septic shock, respectively.
240  5 mg Fe/kg in the cirrhosis group induced a septic shock response at 24 h with elevated serum levels
241 er might therefore occur in the absence of a septic shock response because of the inhibiting effect o
242                           Prior instances of septic shock resulted in a 6.91-fold (95% CI, 5.34- to 8
243 ary analysis of two clinical trials of early septic shock resuscitation.
244 d the Early Management Bundle, Severe Sepsis/Septic Shock (SEP-1) performance measure to the Hospital
245 ational Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) criteria for objective and consi
246 ational Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) criteria in the emergency depart
247 ational Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) present clinical criteria for th
248 ational Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) uses the Sequential Organ Failur
249                               One infant had septic shock shortly after transplantation, resulting in
250                                              Septic shock should be defined as a subset of sepsis in
251 ynamic Support of Neonates and Children with Septic Shock." Society of Critical Care Medicine members
252 ted to the early management of severe sepsis/septic shock (SS/SS) in Emergency Department (ED) has ye
253 74 patients within 12 hours of severe sepsis/septic shock (SS/SS), and at set intervals out to 28 day
254                  The case-fatality rates for septic shock, STSS, and NF were 45%, 38%, and 29%, respe
255 /critical illness myopathy and severe sepsis/septic shock studies.
256 redictive strategies to identify a pediatric septic shock subgroup responsive to corticosteroids.
257 ital stays in patients with severe sepsis or septic shock subsequently admitted to the ICU.
258 ge, population-based cohort of patients with septic shock that allows for assessment of outcomes in c
259 for >/= 3 days at full dose in patients with septic shock that is not responsive to fluid and moderat
260 e studied data from patients with sepsis and septic shock that were reported to the New York State De
261 irical treatment of patients with sepsis and septic shock, that is, moxifloxacin, meropenem, and pipe
262                            Among adults with septic shock, the early use of vasopressin compared with
263 apy (2C), presence of RV dysfunction (2C) in septic shock, the reason for cardiac arrest to assist in
264                Among survivors of sepsis and septic shock, the use of a primary care-focused team-bas
265  died while on-study from cardiac arrest and septic shock; the latter was deemed possibly related to
266 rected therapy (EGDT) reduced mortality from septic shock, three multicenter trials (ProCESS, ARISE,
267 Retrospective study of patients admitted for septic shock to study ICUs during 2005-2013.
268 in plasma cytokine levels in Vasopressin and Septic Shock Trial for lactate less than or equal to 2 v
269            The Protocol-based Care for Early Septic Shock trial found no differences across alternati
270  28- and 90-day mortality in Vasopressin and Septic Shock Trial in lactate subgroups.
271 2 % higher than the original Vasopressin and Septic Shock Trial mortality.
272 epinephrine and mortality in Vasopressin and Septic Shock Trial.
273  to the ProCESS (Protocolized Care for Early Septic Shock) trial of alternative resuscitation strateg
274 olysaccharide (LPS), resulting in sepsis and septic shock, two major causes of death worldwide, signi
275 ance: Among adults with severe sepsis not in septic shock, use of hydrocortisone compared with placeb
276 in regulating the pathogenesis of sepsis and septic shock via their effects on neutrophil survival an
277 tumumab group (the most common being sepsis, septic shock, viral sepsis, and pneumonia).
278           The incidence of severe sepsis and septic shock was 9.7%.
279 rial of mesenchymal stromal cells (MSCs) for septic shock, we applied systematic review methodology t
280    Patients from 5 days to 18 years old with septic shock were enrolled.
281 dependency observational unit with sepsis or septic shock were evaluated.
282 d three hundred and thirty-one patients with septic shock were included from 2000-2004.
283 arrival with a diagnosis of severe sepsis or septic shock were included.
284                    Definitions of sepsis and septic shock were last revised in 2001.
285 similar sensitivity toward endotoxin-induced septic shock when compared to control mice.
286 iberal transfusion strategy in patients with septic shock when compared with the restrictive strategy
287  its spectrum of diseases (severe sepsis and septic shock), which are leading causes of death in inte
288 abase and found that patients with sepsis or septic shock who had a positive blood culture and were h
289 ers can identify a subgroup of children with septic shock who may be more likely to benefit from cort
290                    Identifying children with septic shock who may benefit from corticosteroids remain
291       Medical and surgical ICU patients with septic shock who received vasopressin infusion added to
292 tients meeting criteria for severe sepsis or septic shock who were admitted to the ICU from the emerg
293 in was significantly higher in patients with septic shock with acute kidney injury compared with pati
294     Fifty-two patients with severe sepsis or septic shock with asplenia and 52 without asplenia were
295                                Patients with septic shock with lactate greater than 2 mmol/L or less
296 nderlying immune conditions on the course of septic shock with respect to both mortality and the deve
297 ects of plasma samples from 13 patients with septic shock (with or without severe acute kidney injury
298 ared with placebo did not reduce the risk of septic shock within 14 days.
299 ures: The primary outcome was development of septic shock within 14 days.
300                       Patients diagnosed for septic shock within the first 48 hours of ICU admission

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