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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.
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.
86 arison and 28-day mortality of patients with Septic Shock 3.0 definition (lactate > 2 mmol/L) differ
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]).
95 s in critically ill patients with sepsis and septic shock, acute respiratory distress syndrome, and m
101 metabolites between sepsis and severe sepsis/septic shock also varied according to the underlying typ
104 with septic shock, plasma from patients with septic shock and acute kidney injury inhibited neutrophi
107 al to 18 years old with severe sepsis and/or septic shock and antimicrobial administration within 24
111 are frequently elevated in severe sepsis or septic shock and have relevant prognostic value, which m
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
117 GITB in transplant patients, complicated by septic shock and multiple organ failure, including acute
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
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
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
133 model for end stage liver disease (MELD) and septic shock are the independent predictors of 50 days i
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
140 s associated with improved outcomes in adult septic shock, but pediatric guidelines do not endorse it
142 sis of sepsis but enables the development of septic shock by maintaining NK cell numbers and integrit
145 s proinflammatory cytokine production during septic shock caused by cecal ligation and puncture or en
149 ne the outcomes of patients meeting Sepsis-3 septic shock criteria versus patients meeting the "old"
151 defined as suspected infection and suspected septic shock decreased significantly after the intervent
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
158 without hydrocortisone, in an ovine model of septic shock did not markedly alter norepinephrine requi
160 study included adult patients with sepsis or septic shock due to bloodstream infections caused by GNB
162 12 of whom 58,045 received a vasopressor for septic shock during the first 2 days of hospitalization.
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
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
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.
186 ate of neutrophil activation associated with septic shock-induced disseminated intravascular coagulat
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
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
208 hrombocytopenia within the first 24 hours of septic shock onset as a prognostic marker of survival at
210 n or equal to two organ failures at day 7 of septic shock or 28-day mortality, had a higher percentag
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
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
221 outcome of 6-hour mean arterial pressure in septic shock patients receiving vasopressin who were on
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
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
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
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
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
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
256 redictive strategies to identify a pediatric septic shock subgroup responsive to corticosteroids.
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
263 apy (2C), presence of RV dysfunction (2C) in septic shock, the reason for cardiac arrest to assist in
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,
268 in plasma cytokine levels in Vasopressin and Septic Shock Trial for lactate less than or equal to 2 v
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
279 rial of mesenchymal stromal cells (MSCs) for septic shock, we applied systematic review methodology t
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
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
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
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