Clinical experience with intra-aortic balloon counterpulsation over 10 years: a retrospective cohort study of 459 patients

OBJECTIVE: The objective of this study was to identify prognostic predictors for the patients experiencing cardiogenic shock who required the institution of intra-aortic balloon counterpulsation (IABP). DESIGN, SETTING, AND PATIENTS: Patients with cardiogenic shock were retrieved from the clinical information system in National Taiwan University Hospital and classified according to their etiology: acute coronary syndrome (ACS), ST segment elevation myocardial infarction (STEMI), congestive heart failure (CHF), hemodynamic instability after post-coronary bypass graft operation (post-CABG) or after percutaneous intervention (post-PCI), and out-of-hospital cardiac arrest (OHCA) victims. MEASUREMENTS: Kaplan-Meier curves and Cox regression model were applied to evaluate the factors associated with survival. MAIN RESULTS: A total of 459 patients were found to belong to one of six etiology categories between 1995 and 2004. The 30-day mortality was highest in the OHCA group, followed by the STEMI, CHF, ACS, post-PCI, and post-CABG groups in a decreasing frequency (log rank p<0.001). Peak troponin I level was negatively associated with survival, and its effect largely paralleled with underlying etiology. Age and renal impairment were significant prognostic predictors for 30-day mortality (hazard ratio=1.031, p<0.001 and hazard ratio=1.266, p<0.001). Comparing to those manifested as OHCA who had the worst outcome, patients in the other etiology groups had significantly better survival. CONCLUSIONS: This study has illustrated that age, renal function, and etiology-related cardiac injury are predictors for in-hospital course and mortality in those who experienced cardiogenic shock with IABP. The optimal strategy for revascularization in this high-risk group needs further validation.     

Interleukin-6 is the strongest predictor of 30-day mortality in patients with cardiogenic shock due to myocardial infarction

ABSTRACT: INTRODUCTION: Cardiogenic shock (CS) remains the leading cause of death in patients hospitalized for myocardial infarction (MI). Systemic inflammation with inappropriate vasodilatation is observed in many patients with CS and may contribute to an excess mortality rate. The purpose of this study was to determine the predictive role of serial measurements of Nt-proBNP, interleukin-6 (IL-6) and procalcitonin (PCT) for 30-day mortality in patients with CS due to MI. METHODS: The present study is a prospective single-center-study including 87 patients with MI complicated by CS treated with acute revascularization and intra-aortic-balloon-counterpulsation (IABP) support. Predictive values of plasma levels at admission (T0), after 24 hours (T1), and after 72 hours (T2) were examined according to 30-day mortality. RESULTS: Significant differences between survivors (n=59) and non-survivors (n=28) were seen for Nt-proBNP at T0, for IL-6 at T0 and T1, and for PCT at T1 and T2. According to ROC analyses, highest accuracy predicting 30-day mortality was seen at T0 for IL-6, at T1 for PCT, and at T2 for PCT. In univariate analysis significant values were found for Nt-proBNP at T1, for IL-6 and PCT at all points of time. Within the multivariate analysis, age, creatinine and IL-6 were significant determinants of 30-day mortality in which IL-6 showed the highest level of significance. CONCLUSIONS: In patients with MI complicated by CS, IL-6 represented a reliable independent early prognostic marker of 30-day mortality. PCT revealed a significant value at later points of time whereas Nt-proBNP seemed to be of lower relevance.     

Does intra-aortic balloon support for myocardial infarction with cardiogenic shock improve outcome?

Expanded abstract

Citation

Thiele H, Zeymer U, Neumann FJ, Ferenc M, Olbrich HG, Hausleiter J, Richardt G, Hennersdorf M, Empen K, Fuernau G, Desch S, Eitel I, Hambrecht R, Fuhrmann J, Böhm M, Ebelt H, Schneider S, Schuler G, Werdan K; IABP-SHOCK II Trial Investigators: Intraaortic balloon support for myocardial infarction with cardiogenic shock. N Engl J Med 2012, 367:1287-1296.

Background

In the current international guidelines, intra-aortic balloon pump (IABP) counterpulsation is considered a class I treatment for acute myocardial infarction complicated by cardiogenic shock. However, evidence is based mainly on registry data, and there is a paucity of randomized clinical trials.

Methods

Objective

To test the hypothesis that IABP counterpulsation, as compared with the best available medical therapy alone, results in a reduction in mortality among patients with acute myocardial infarction complicated by cardiogenic shock for whom early revascularization is planned.

Design

Randomized, prospective, open-label, multicenter trial.

Setting

Thirty-seven centers in Germany.

Subjects

All adults had acute myocardial infarction complicated by cardiogenic shock and were expected to undergo early revascularization (by means of percutaneous coronary intervention or bypass surgery).

Intervention

After enrollment, 600 patients were randomly assigned to intra-aortic balloon counterpulsation (IABP group, 301 patients) or no IABP counterpulsation (control group, 299 patients).

Outcomes

The primary efficacy endpoint is 30-day all-cause mortality.

Results

At 30 days, 119 patients in the IABP group (39.7%) and 123 patients in the control group (41.3%) had died (relative risk with IABP, 0.96; 95% confidence interval, 0.79 to 1.17; P = 0.69). There were no significant differences in secondary endpoints or in process-of-care measures, including the time to hemodynamic stabilization, the length of stay in the intensive care unit, serum lactate levels, the dose and duration of catecholamine therapy, and renal function.

Conclusions

The use of IABP counterpulsation did not significantly reduce 30-day mortality in patients with acute myocardial infarction complicated by cardiogenic shock for whom an early revascularization strategy was planned.     

Delayed vasopressor initiation is associated with increased mortality in patients with septic shock

PurposeMortality rate for septic shock, despite advancements in knowledge and treatment, remains high. Treatment includes administration of broad-spectrum antibiotics and stabilization of the mean arterial pressure (MAP) with intravenous fluid resuscitation. Fluid-refractory shock warrants vasopressor initiation. There is a paucity of evidence regarding the timing of vasopressor initiation and its effect on patient outcomes.Materials and methodsThis retrospective, single-centered, cohort study included patients with septic shock from January 2017 to July 2017. Time from initial hypotension to vasopressor initiation was measured for each patient. The primary outcome was 30-day mortality.ResultsOf 530 patients screened,119 patients were included. There were no differences in baseline patient characteristics. Thirty-day mortality was higher in patients who received vasopressors after 6 h (51.1% vs 25%, p < .01). Patients who received vasopressors within the first 6 h had more vasopressor-free hours at 72 h (34.5 h vs 13.1, p = .03) and shorter time to MAP of 65 mmHg (1.5 h vs 3.0, p < .01).ConclusionVasopressor initiation after 6 h from shock recognition is associated with a significant increase in 30-day mortality. Vasopressor administration within 6 h was associated with shorter time to achievement of MAP goals and higher vasopressor-free hours within the first 72 h.     

Safety and efficacy of affinity-purified, anti-tumor necrosis factor-alpha, ovine fab for injection (CytoFab) in severe sepsis

OBJECTIVE: Tumor necrosis factor (TNF) is a critical inflammatory mediator in sepsis. This trial was designed to evaluate the safety and effectiveness of polyclonal ovine anti-TNF fragment antigen binding (Fab) fragments (CytoFab) on plasma TNF-alpha, interleukin-6 (IL-6), and interleukin-8 (IL-8) concentrations and the number of shock-free and ventilator-free days in severely septic patients. DESIGN: Phase II, randomized, blinded, placebo-controlled trial conducted from September 1997 to July 1998. SETTING: Nineteen intensive care units in the United States and Canada. PATIENTS: Eighty-one septic patients with either shock or two organ dysfunctions. INTERVENTIONS: Patients were randomized to receive CytoFab, infused as a 250-units/kg loading dose, followed by nine doses of 50 units/kg every 12 hrs, or 5 mg/kg human albumin as placebo. MEASUREMENTS AND MAIN RESULTS: CytoFab promptly reduced plasma TNF-alpha (p = .001) and IL-6 concentrations (p = .002) compared with placebo. CytoFab also significantly decreased TNF-alpha in bronchoalveolar lavage (BAL) fluid (p < .001). The number of shock-free days did not differ between CytoFab and placebo (10.7 vs. 9.4, respectively) (p = .270). CytoFab increased mean ventilator-free days (15.0 vs. 9.8 for placebo; p = .040) and ICU-free days (12.6 vs. 7.6 for placebo; p = .030) at day 28. All-cause, 28-day mortality rates were 37% (14/38) for placebo recipients, compared with 26% (11/43) for CytoFab recipients (p = .274). No differences in incidences of adverse events, laboratory, or vital sign abnormalities were observed between groups. Although 41% of CytoFab-treated patients developed detectable plasma levels of human anti-sheep antibodies, none demonstrated clinical manifestations during the 28-day study. CONCLUSIONS: CytoFab is well tolerated in patients with severe sepsis, effectively reducing serum and BAL TNF-alpha and serum IL-6 concentrations and increasing the number of ventilator-free and ICU-free days at day 28.     

Plasma granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor levels in critical illness including sepsis and septic shock: relation to disease severity, multiple organ dysfunction, and mortality

OBJECTIVE: To define the circulating levels of granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) during critical illness and to determine their relationship to the severity of illness as measured by the Acute Physiology and Chronic Health Evaluation (APACHE) II score, the development of multiple organ dysfunction, or mortality. DESIGN: Prospective cohort study. SETTING: University hospital intensive care unit. PATIENTS: A total of 82 critically ill adult patients in four clinically defined groups, namely septic shock (n = 29), sepsis without shock (n = 17), shock without sepsis (n = 22), and nonseptic, nonshock controls (n = 14). INTERVENTIONS: None. MEASUREMENT AND MAIN RESULTS: During day 1 of septic shock, peak plasma levels of G-CSF, interleukin (IL)-6, and leukemia inhibitory factor (LIF), but not GM-CSF, were greater than in sepsis or shock alone (p < .001), and were correlated among themselves (rs = 0.44-0.77; p < .02) and with the APACHE II score (rs = 0.25-0.40; p = .03 to .18). G-CSF, IL-6, and UF, and sepsis, shock, septic shock, and APACHE II scores were strongly associated with organ dysfunction or 5-day mortality by univariate analysis. However, multiple logistic regression analysis showed that only septic shock remained significantly associated with organ dysfunction and only APACHE II scores and shock with 5-day mortality. Similarly, peak G-CSF, IL-6, and LIF were poorly predictive of 30-day mortality. CONCLUSIONS: Plasma levels of G-CSF, IL-6, and LIF are greatly elevated in critical illness, including septic shock, and are correlated with one another and with the severity of illness. However, they are not independently predictive of mortality, or the development of multiple organ dysfunction. GM-CSF was rarely elevated, suggesting different roles for G-CSF and GM-CSF in human septic shock.     

Impact of neutropenia duration on short-term mortality in neutropenic critically ill cancer patients

OBJECTIVE: To identify predictors of 30-day mortality and to assess the impact of neutropenia recovery (NR) on 30-day mortality in critically ill cancer patients (CICPs). DESIGN AND SETTING: Retrospective review of the medical records of the 102 neutropenic CICPs admitted to a medical intensive care unit (ICU) over a 10-year period. INTERVENTION: None. MEASUREMENTS AND RESULTS: Malignancies consisted of acute leukemia (n=42), lymphoma (n=23), myeloma (n=28), and solid tumors (n=9). Reasons for ICU admission were acute respiratory failure (n=81), shock (n=58), acute renal failure (n=33), and coma (n=13). Seventy patients needed conventional mechanical ventilation (MV) and 21 noninvasive MV, 67 vasopressor agents, and 28 dialysis. Sixty-two patients experienced NR during their ICU stay. In a multivariate logistic regression model, 30-day mortality was higher in patients with acute respiratory or renal failure and lower in patients with NR (OR, 0.09 [0.01-0.86]). This model assumed that patients who experienced NR in the ICU were merely these who did not die early in the ICU. To take into account the effect of time to occurrence of NR on time to death we secondarily used a Cox model including neutropenia duration and NR as time-dependent variables. In this second model, the only significant predictors of 30-day mortality were age, respiratory failure, renal failure, and coma. CONCLUSION: Organ failure but not disease progression or neutropenia duration affect 30-day mortality in neutropenic CICPs. ICU-acquired events might be modeled as time-dependent variables in a Cox model, rather than standard covariates in logistic regression models.     

Update on the management of cardiogenic shock

PURPOSE OF REVIEW: Cardiogenic shock is a life-threatening emergency that occurs frequently with acute coronary syndromes. If rapid myocardial reperfusion following acute myocardial infarction is not obtained, either with thrombolytics or by revascularization, cardiogenic shock frequently develops and the mortality rate is high. This review summarizes recent advances in the pathophysiology, incidence and treatment of cardiogenic shock. Particular attention is given to pharmacologic advances. RECENT FINDINGS: Cardiogenic shock continues to occur in 5-10% of patients who suffer a myocardial infarction and the mortality remains over 50% in most studies. Treatment preference is referral to a cardiac center capable of reperfusion using multiple therapies. While no delay in reperfusion is acceptable, emphasis on implementing supportive treatment such as vasopressors, inotropes, and fluids remains critical. There is a wide variance in treatment standards despite established guidelines. Overall mortality from cardiogenic shock has decreased but the incidence remains unchanged. SUMMARY: Emerging pharmacological interventions designed to counteract the underlying proinflammatory pathophysiologic mechanisms may, in combination with early revascularization, result in improved patient outcomes, but there is no magic bullet on the horizon. Attention to the timeliness of transport and treatment of patients with a focus on revascularization is required for cardiogenic shock patients.     

急性心肌梗死后心源性休克患者早期发生急性肾功能衰竭与预后的关系

目的　了解急性心肌梗死后心源性休克患者中早期发生急性肾功能衰竭与预后的关系。方法回顾性分析解放军总医院 1993— 2 0 0 3年因急性心肌梗死或冠心病心绞痛住院、并出现心源性休克患者的临床资料。以 2 4 h内是否出现急性肾功能衰竭为标准 ,比较其住院期间病死率 ;并采用多元 logistic回归分析 ,评估早期发生急性肾功能衰竭对患者预后的影响。结果　 172例患者中 ,5 1例 ( 30 % )于 2 4 h内出现急性肾功能衰竭。早期是否发生急性肾功能衰竭患者的住院病死率分别为 90 % ( 4 6 / 5 1例 )和 5 6 % ( 6 8/ 12 1例 )。逐步回归分析表明 ,早期发生急性肾功能衰竭是影响急性心肌梗死后心源性休克患者预后的独立因素 ,相对危险度 ( OR) =6 .7,95 %可信区间为 2 .5～ 18.0 ,P<0 .0 0 1。结论　急性心肌梗死后心源性休克患者 ,早期急性肾功能衰竭的发生与患者住院病死率显著相关 ,可作为判断患者预后不良的指标     

Nitric oxide inhibition rapidly increases blood pressure with no change in outcome in cardiogenic shock: the TRIUMPH trial

The TRIUMPH study, recently published in Journal of the American Medical Association, was a prospective randomized placebo-controlled trial testing the hypothesis that tilarginine (a non-specific inhibitor of nitric oxide synthase), when compared with placebo, would reduce 30-day mortality by 25% in patients with myocardial infarction complicated by refractory cardiogenic shock despite successful revascularization of the infarct-related artery. Patients received an intravenous bolus of the drug followed by 5 hours of intravenous infusion of the drug or a matching placebo. Although tilarginine increased systolic blood pressure by 5 mmHg at 2 hours, no effect on mortality was observed at 30 days. There was, however, a 6% absolute increase in 30-day mortality in the tilarginine group (48%, versus 42% in the placebo). This definitive trial gave strong indications for stopping any further trial using non-specific inhibitors of nitric oxide synthase in cardiogenic shock and possibly also in any other cardiovascular area.     

A phase II randomized, controlled trial of continuous hemofiltration in sepsis

OBJECTIVE: To study the effect of early and continuous venovenous hemofiltration (CVVH) on the plasma concentrations of several humoral mediators of inflammation and subsequent organ dysfunction in septic patients. DESIGN: Randomized, controlled trial. SETTING: Intensive care unit of a tertiary hospital. PATIENTS: Twenty-four patients with early septic shock or septic organ dysfunction. INTERVENTIONS: Random allocation to receive 48 hrs of isovolemic CVVH at 2 L/hr of fluid exchange or no hemofiltration. MEASUREMENTS AND MAIN RESULTS: We measured the plasma concentrations of complement fractions C3a and C5a, interleukins 6, 8, and 10, and tumor necrosis factor alpha at baseline and 2, 24, 26, 48, and 72 hrs. A multiple organ dysfunction score (MODS) was calculated daily for each patient until death or discharge from the intensive care unit. The concentrations of most mediators decreased between baseline and 72 hrs. Some significant falls in concentration could be identified between specific time points, but CVVH was not associated with an overall reduction in any plasma cytokine concentrations. There was also no difference between the mean cumulative MODS for control survivors (43.3 +/- 19.7) and CVVH survivors (33.2 +/- 19.0; p = .30), and no difference between the average MODS calculated for all controls (4.1 +/- 1.9) and all CVVH subjects (3.3 +/- 1.7; p = .26). CVVH did not improve oxygenation, lower the platelet count, or reduce the duration of vasopressor support and mechanical ventilation. CONCLUSIONS: Early use of CVVH at 2 L/hr did not reduce the circulating concentrations of several cytokines and anaphylatoxins associated with septic shock, or the organ dysfunction that followed severe sepsis. CVVH using current technology cannot be recommended as an adjunct to the treatment of septic shock unless severe acute renal failure is present.     

Lenercept (p55 tumor necrosis factor receptor fusion protein) in severe sepsis and early septic shock: a randomized, double-blind, placebo-controlled, multicenter phase III trial with 1,342 patients

OBJECTIVE: Phase III study to confirm a trend observed in a previous phase II study showing that a single dose of lenercept, human recombinant p55 tumor necrosis factor receptor-immunoglobulin G1 (TNFR55-IgG1) fusion protein, decreased mortality in patients with severe sepsis or early septic shock. DESIGN: Multicenter, double-blind, phase III, placebo-controlled, randomized study. SETTING: A total of 108 community and university-affiliated hospitals in the United States (60), Canada (6) and Europe (42). PATIENTS: A total of 1,342 patients were recruited who fulfilled the entry criteria within the 12-hr period preceding the study drug administration. INTERVENTION: After randomization, an intravenous dose of 0.125 mg/kg lenercept or placebo was given. The patient was monitored for up to 28 days, during which standard diagnostic, supportive, and therapeutic care was provided. MEASUREMENTS AND MAIN RESULTS: The primary outcome measure was 28-day all-cause mortality. Baseline characteristics were as follows: a total of 1,342 patients were randomized; 662 received lenercept and 680 received placebo. The mean age was 60.5 yrs (range, 17-96 yrs); 39% were female; 65% had medical admissions, 8% had scheduled surgical admissions, and 27% had unscheduled surgical admissions; 73% had severe sepsis without shock, and 27% had severe sepsis with early septic shock. Lenercept and placebo groups were similar at baseline with respect to demographic characteristics, simplified acute physiology score II-predicted mortality, profiles of clinical site of infection and microbiological documentation, number of dysfunctioning organs, and interleukin-6 (IL-6) plasma concentration. Lenercept pharmacokinetics were similar in severe sepsis and early septic shock patients. Tumor necrosis factor was bound in a stable manner to lenercept as reflected by the accumulation of total serum tumor necrosis factor alpha concentrations. There were 369 deaths, 177 on lenercept (27% mortality) and 192 on placebo (28% mortality). A one-sided Cochran-Armitage test, stratified by geographic region and baseline, predicted 28-day all-cause mortality (simplified acute physiology score II), gave a p value of .141 (one-sided). Lenercept treatment had no effect on incidence or resolution of organ dysfunctions. There was no evidence that lenercept was detrimental in the overall population. CONCLUSION: Lenercept had no significant effect on mortality in the study population.     

Rapid decrease in plasma D-lactate as an early potential predictor of diminished 28-day mortality in critically ill septic shock patients.

BACKGROUND: Splanchnic ischemia plays a major role in the development of organ failure during septic shock. Plasma D-lactate has been proposed as a better marker of splanchnic hypoperfusion than L-lactate. We studied the prognostic ability of plasma D- and L-lactate levels. METHODS: A prospective study was performed in an intensive care unit and included patients with septic shock. Two samples for plasma D- and L-lactate determination were collected: the first within 6 h after the patient met the criteria for septic shock (day 1) and the second 24 h later (day 2). RESULTS: In univariate analysis, day 1 plasma D- and L-lactate values were associated with 28-day mortality. For plasma D- and L- lactate, the area under the receiver operating characteristic curve was 0.68+/-0.09 and 0.84+/-0.07 on day 1 (p=0.09), and 0.74+/-0.10 and 0.90+/-0.07 on day 2 (p=0.06), respectively. In survivors, D-lactate levels decreased between day 1 and day 2 (p=0.03), but L-lactate did not (p=0.29). In septic shock patients, plasma D- and L-lactate levels reliably discriminate between survivors and non-survivors. The prognostic ability of plasma L-lactate was better than that of plasma D-lactate. CONCLUSION: A rapid decrease in plasma D-lactate during the course of septic shock could indicate reduced 28-day mortality.     

Serum concentrations of immune parameters during acute cardiogenic pulmonary edema.

OBJECTIVE: To evaluate the effect of acute cardiogenic pulmonary edema on the concentrations of immune parameters in serum. DESIGN: Prospective, controlled study. SETTING: Medical ICU. PATIENTS: Twenty-four consecutive patients with acute pulmonary edema who had significant clinical improvement within 30 mins and did not show any evidence of either tissue damage or infection. For comparison, 25 healthy, age-matched controls and 25 patients with mild chronic heart failure were also studied. INTERVENTIONS: Treatment with oxygen, nitrates, and loop diuretics. MEASUREMENTS: Lymphokines, acute-phase reactants, and cortisol concentrations were measured in serial serum and plasma samples. MAIN RESULTS: Serum concentrations of soluble CD-8 antigen (soluble CD-8) decreased from 928 +/- 124 (SEM) U/mL on admission to 712 +/- 112 and 579 +/- 67 U/mL after 2 and 6 hrs, respectively (p less than .05, p less than .01), and returned to baseline values within 48 hrs (853 +/- 109 U/mL). Concentrations of soluble interleukin-2 receptor increased from 721 +/- 71 to 1078 +/- 112 and 1226 +/- 128 U/mL 12 and 36 hrs, respectively, after admission (p less than .05, p less than .01). Plasma cortisol concentrations were markedly increased on admission (56.9 +/- 4.7 vs. 13.1 +/- 1.3 micrograms/dL after recovery, p less than .001). Increased cortisol concentrations coincided with the nadir of soluble CD-8. Tumor necrosis factor-alpha remained within normal limits in all patients. Neither acute-phase reactants nor angiotensin converting enzyme activity showed significant changes during the observation period. CONCLUSION: The present results indicate significant alterations in the serum concentrations of immune parameters as an effect of an uncomplicated acute cardiogenic pulmonary edema.     

Relative adrenal insufficiency as a predictor of disease severity, mortality, and beneficial effects of corticosteroid treatment in septic shock

OBJECTIVE: To evaluate the concept of relative adrenal insufficiency necessitating corticosteroid therapy in septic shock. DESIGN: Retrospective study. SETTING: Medical-surgical intensive care unit of a university hospital. PATIENTS: We studied 218 consecutive patients with septic shock in a 3-yr period who underwent a short 250-microg adrenocorticotropic hormone test because of >6 hrs of hypotension requiring repeated fluid challenges and/or vasopressor/inotropic treatment. INTERVENTIONS: The test was performed by intravenously injecting 250 mug of synthetic adrenocorticotropic hormone and measuring cortisol immediately before and 30 and 60 mins postinjection. MEASUREMENTS AND MAIN RESULTS: Intensive care unit mortality until day 28 was 22%. Nonsurvivors had greater disease severity, as exemplified by higher Simplified Acute Physiology Score II and Sequential Organ Failure Assessment score, on the day of adrenocorticotropic hormone testing. Cortisol levels directly correlated with albumin levels. Simplified Acute Physiology Score II and Sequential Organ Failure Assessment score increased with higher strata of baseline cortisol/albumin or lower cortisol increases/albumin ratios as measures of free cortisol. Baseline cortisol, cortisol increases, and albumin levels did not independently contribute to mortality prediction by disease severity and absence of corticosteroid (hydrocortisone) treatment in a Cox proportional hazard model, although adrenocorticotropic hormone-induced cortisol increase <100 nmol/L (n = 53) predicted mortality (p = .007). Posttest treatment by corticosteroids (n = 161, 74%) was associated with higher survival in patients with cortisol increase <100 nmol/L (p = .0296). CONCLUSIONS: In intensive care unit patients with septic shock, the cortisol response to adrenocorticotropic hormone inversely relates to disease severity, independent of blood cortisol binding. An adrenocorticotropic hormone-induced cortisol increase <100 nmol/L predicts mortality and beneficial effects of corticosteroid treatment. The data favor relative adrenal insufficiency.     

Before-after study of a standardized hospital order set for the management of septic shock

OBJECTIVE: To evaluate a standardized hospital order set for the management of septic shock in the emergency department. DESIGN: Before-after study design with prospective consecutive data collection. SETTING: Emergency department of a 1,200-bed academic medical center. PATIENTS: A total of 120 patients with septic shock. INTERVENTIONS: Implementation of a standardized hospital order set for the management of septic shock. MEASUREMENTS AND MAIN RESULTS: A total of 120 consecutive patients with septic shock were identified. Sixty patients (50.0%) were managed before the implementation of the standardized order set, constituting the before group, and 60 (50.0%) were evaluated after the implementation of the standardized order set, making up the after group. Demographic variables and severity of illness measured by the Acute Physiology and Chronic Health Evaluation II were similar for both groups. Patients in the after group received statistically more intravenous fluids while in the emergency department (2825 +/- 1624 mL vs. 3789 +/- 1730 mL, p = .002), were more likely to receive intravenous fluids of >20 mL/kg body weight before vasopressor administration (58.3% vs. 88.3%, p < .001), and were more likely to be treated with an appropriate initial antimicrobial regimen (71.7% vs. 86.7%, p = .043) compared with patients in the before group. Patients in the after group were less likely to require vasopressor administration at the time of transfer to the intensive care unit (100.0% vs. 71.7%, p < .001), had a shorter hospital length of stay (12.1 +/- 9.2 days vs. 8.9 +/- 7.2 days, p = .038), and a lower risk for 28-day mortality (48.3% vs. 30.0%, p = .040). CONCLUSIONS: Our study found that the implementation of a standardized order set for the management of septic shock in the emergency department was associated with statistically more rigorous fluid resuscitation of patients, greater administration of appropriate initial antibiotic treatment, and a lower 28-day mortality. These data suggest that the use of standardized order sets for the management of septic shock should be routinely employed.     

主动脉内球囊反搏在急性心肌梗死并发心源性休克中的应用

目的　评价主动脉内球囊反搏 (IABP)对急性心肌梗死合并心源性休克患者在不同血管再通治疗中的疗效和短期生存的影响。方法　回顾性分析了 10 8例接受IABP治疗的急性心肌梗死合并心源性休克患者 ,分别分析了溶栓治疗组、介入治疗组和冠脉搭桥 (CABG)手术治疗组患者的基本特征和血流动力学情况 ,并比较IABP治疗对住院病死率和 30d病死率的影响。结果　患者的基本特征包括年龄、冠心病的危险因子等在各组间差异无显著性意义 (P >0 0 5 ) ,但手术治疗组的男性患者显著少于其它两组 (P <0 0 5 ) ;IABP治疗前血流动力学状态各组间也无显著性意义 ,住院病死率和 30d病死率手术治疗组均显著低于溶栓组和介入组 ,分别为 18 9%、 6 2 8%和 6 0 7% ,16 2 %、 6 0 5 %和 6 0 7% ,P值均 <0 0 0 1。结论　IABP支持下进行CABG治疗可显著减低心肌梗死合并心源性休克患者的近期死亡率 ,且显著优于溶栓治疗和介入治疗     

急性心肌梗死合并心源性休克的血运重建策略

尽管早期血运重建的广泛开展,急性心肌梗死合并心源性休克仍是治疗的重点和难点。另外,急性心肌梗死伴心源性休克患者往往合并多支血管病变,其最佳血运重建策略尚无定论。本文就心源性休克定义及病因,急性心肌梗死合并心源性休克早期血运重建的重要性及血运重建策略选择方面做一综述。     

Combination antibiotic therapy improves survival in patients with community-acquired pneumonia and shock

OBJECTIVE: To assess whether combination antibiotic therapy improves outcome of severe community-acquired pneumonia in the subset of patients with shock. DESIGN: Secondary analysis of a prospective observational, cohort study. SETTING: Thirty-three intensive care units (ICUs) in Spain. PATIENTS: Patients were 529 adults with community-acquired pneumonia requiring ICU admission. INTERVENTIONS: None. MEASUREMENT AND MAIN RESULTS: Two hundred and seventy (51%) patients required vasoactive drugs and were categorized as having shock. The effects of combination antibiotic therapy and monotherapy on survival were compared using univariate analysis and a Cox regression model. The adjusted 28-day in-ICU mortality was similar (p = .99) for combination antibiotic therapy and monotherapy in the absence of shock. However, in patients with shock, combination antibiotic therapy was associated with significantly higher adjusted 28-day in-ICU survival (hazard ratio, 1.69; 95% confidence interval, 1.09-2.60; p = .01) in a Cox hazard regression model. Even when monotherapy was appropriate, it achieved a lower 28-day in-ICU survival than an adequate antibiotic combination (hazard ratio, 1.64; 95% confidence interval, 1.01-2.64). CONCLUSIONS: Combination antibiotic therapy does not seem to increase ICU survival in all patients with severe community-acquired pneumonia. However, in the subset of patients with shock, combination antibiotic therapy improves survival rates.     

Continuous plasmafiltration in sepsis syndrome. Plasmafiltration in Sepsis Study Group.

OBJECTIVE: To assess the effect of plasmafiltration (PF) on biochemical markers of inflammation, cytokines, organ dysfunction, and 14-day mortality in human sepsis. DESIGN: Multicenter, prospective, randomized, controlled clinical trial. SETTING: Seven university-affiliated intensive care units. PATIENTS: Thirty patients (22 adults, eight children) with new (<24 hrs) clinical evidence of infection and sepsis syndrome were enrolled. Fourteen of 30 (nine adults, five children) were randomized to PF. INTERVENTIONS: All patients received protocol-driven supportive intensive care, and those randomized to PF received continuous plasma exchange for 34 hrs using a hollow-fiber plasma filter. MEASUREMENTS AND MAIN RESULTS: Illness severity and risk of death were calculated with the Pediatric Risk of Mortality (children) and the Acute Physiology and Chronic Health Evaluation II (adults) scales. Plasma samples (0, 6, 24, and 48 hrs) were assayed for acute-phase proteins (albumin, globulin, C-reactive protein, alpha1-antitrypsin, haptoglobin), inflammatory mediators (complement fragment C3, thromboxane B2), and cytokines (interleukin-6, granulocyte colony-stimulating factor, leukemia inhibitory factor). Sieving coefficients were estimated from filtrate concentrations at 3 hrs. The two groups were matched for incidence of septic shock (13 of 14 vs. 11 of 16), refractory shock (three of 14 vs. six of 16), bacteremia (six of 14 vs. five of 16), severity of illness, and calculated risk of death (0.68 vs. 0.64). There was no difference in mortality. Eight of 14 PF patients (57%) and eight of 16 controls (50%) survived for 14 days (p = .73, Fisher's exact test). Multiple logistic regression revealed age (odds ratio, 16.4:1; 95% confidence interval, 2.12-infinity) and shock (10.6:1; 1.32-infinity) as significant predictors of death; plasmafiltration was associated with a nonsignificant reduction in the risk of death (odds ratio, 1.78:1; 95% confidence interval, 0.20-18.1). The mean (SD) number of organs failing in the first 7 days in the PF group was 2.57 (0.94) vs. 2.94 (0.85) in controls (p = .37, Mann-Whitney U test). Both groups had similarly elevated plasma concentrations of all inflammatory mediators except complement fragment C3 at study entry. Leukemia inhibitory factor was detectable in four patients only. PF did not influence mean concentrations of interleukin-6, granulocyte colony-stimulating factor, thromboxane B2, total white cell count, neutrophil count, or platelet count, but it was associated with significant reductions of alpha1-antitrypsin, haptoglobin, C-reactive protein, and complement fragment C3 in the first 6 hrs (p < .05). The sieving coefficients for all inflammatory mediators approached unity. CONCLUSIONS: PF caused a significant attenuation of the acute-phase response in sepsis. There was no significant difference in mortality, but there was a trend toward fewer organs failing in the PF group that suggests that this procedure might be beneficial.