Serum tumor necrosis factor levels in patients with infectious disease and septic shock

The role of tumor necrosis factor (TNF-alpha) in the pathogenesis of septic shock has been assessed by daily measurements of serum TNF-alpha levels in 60 patients admitted to the medical intensive care unit. All patients in the study had infectious disease and were at risk for the development of sepsis and septic shock. Sepsis was diagnosed in 34 patients, 24 of whom died (six within the first 24 hours). The 26 patients who did not evolve toward sepsis served as a control group. The clinical condition of all patients was monitored by daily APACHE II scoring. Blood was drawn once a day and additional samples were taken in patients whose clinical condition underwent sudden deterioration. TNF-alpha levels were measured with a commercially available immunoradiometric assay. At time of patient admission, TNF-alpha levels were higher in the group with sepsis than in the control group (median 79 iqr 329 vs median 0.5 iqr 5; p less than 0.001). In the group with sepsis, extremely high TNF-alpha levels were found in patients who died within 24 hours. These patients had TNF-alpha levels of 917 iqr 755 pg/ml, whereas the patients who died more than 24 hours after admission had TNF-alpha levels of 58 iqr 59 pg/ml. Survivors had lower TNF-alpha levels (26 iqr 347 pg/ml). APACHE II scores correlated with TNF-alpha levels in the total sepsis group (Spearman rank correlation coefficient 0.477; p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)     

Complement activation in septic shock patients

To evaluate the status of the complement system and to determine the effects of corticosteroids on complement component levels in septic shock, C3, C4, and Factor B were measured in 42 patients with severe late septic shock. Serum levels of C4 and Factor B correlated with C3 levels (r = 0.48 and 0.64, respectively; p less than .01) in patients in shock for more than 4 h, but only Factor B correlated with C3 (r = 0.85; p less than .01) in patients in shock for 4 h or less. C3 and Factor B levels were significantly (p less than .05) lower in patients who died (12,174 +/- 1,524 CH50 U/ml and 14 +/- 1 mg/dl, respectively) than in patients who survived (18,418 +/- 2,833 CH50 U/ml and 21 +/- 2 mg/dl, respectively). Corticosteroids did not alter complement component levels. The alternative pathway appears to be activated early in septic shock, whereas the classical pathway is activated later. C3 and Factor B levels may predict survival of patients in septic shock. In this study, corticosteroids did not change the complement component levels of patients in late severe septic shock.     

Terlipressin in catecholamine-resistant septic shock patients

To determine the effects on hemodynamics, laboratory parameters, and renal function of terlipressin used in septic-shock patients with hypotension not responsive to high-dose norepinephrine (>2.0 microg x kg(-1) x min(-1)) and dopamine (25 microg x kg(-1) x min(-1)), a prospective, open-label study was carried out in 17 patients. Patients received one or two boluses of 1 mg of terlipressin. In all patients terlipressin induced a significant increase in mean arterial pressure (MAP), systemic vascular resistance, pulmonary vascular resistance, and left and right ventricular stroke work. The increase in MAP was accompanied by a significant decrease in heart rate and cardiac index, but stroke volume remained unchanged. Oxygen delivery and consumption were significantly decreased. Blood lactate concentrations significantly decreased over the study period. Bilirubin, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were significantly increased. Thrombocytes were significantly decreased. No change in prothrombin time was observed. Renal function, assessed by urine flow and creatinine clearance, was significantly improved. Pulmonary function assessed by Pao2/Fio2 ratio was not affected. A significant reduction in norepinephrine and dopamine infusion rates was observed in all patients. Eight patients died during their ICU stay from late multiple organ failure. Within the limitations of the present study (open-label design, small group of patients), it can be concluded that in septic shock patients with hypotension nonresponsive to fluid resuscitation and high-dose vasopressors, terlipressin can be effective to restore MAP. Cardiac index should be closely monitored because it was significantly decreased by terlipressin. Renal function was significantly improved. Mesenteric circulation was not evaluated, but hepatic function was altered during the study period. Further studies are required to determine whether terlipressin is safe in terms of outcome in septic shock patients.     

Pre-hospital mechanical ventilation in septic shock patients

BackgroundMechanical ventilation can cause deleterious effects on the lung and thus alter patient's prognosis.The aim of this study was to describe the characteristics of prehospital mechanical ventilation in patients with septic shock requiring mechanical ventilation in the prehospital setting.MethodsPatients with septic shock subjected to pre-hospital intubation and mechanical ventilation by a mobile intensive care unit were consecutively included and retrospectively analysed. Septic shock was defined according to the international sepsis-3 consensus conference. Patient's characteristics, interventions, prehospital ventilatory parameters and outcome were retrieved from medical records. The association between the tidal volume indexed on ideal body weight (VTIBW) and mortality at day 28 was evaluated.ResultsFifty-nine patients were included. Septic shock was mainly associated with pulmonary (64%) infection. Mean pre-hospital VTIBW was 7 ± 1 ml.kg^?1 in the overall population. Mortality reached 42%. The AUC of VTIBW was 0.83 [0.72–0.94].Using logistic regression model including: age, prehospital mean blood pressure, volume infused in the prehospital setting, FiO₂ and length of stay in the intensive care unit, the association with mortality remained significant for VTIBW (OR adjusted [CI95] = 4.11 [1.89–10.98]), VTIBW >8 ml·kg^?1 (OR adjusted [CI95] = 8.29 [2.35–34.98]) and VTIBW <8 ml·kg^?1 (OR adjusted [CI95] = 0.12 [0.03–0.43]).ConclusionIn this retrospective study, we observed an association between mortality at day 28 and prehospital VTIBW in pre-hospital mechanically ventilated patients with septic shock. A VTIBW <8 ml·kg^?1 was associated with a decrease and a VTIBW >8 ml·kg^?1 with an increase in mortality.     

Serum thiamine concentration and oxidative stress as predictors of mortality in patients with septic shock

Purpose

The purpose of the study is to determine the influence of serum thiamine, glutathione peroxidase (GPx) activity, and serum protein carbonyl concentrations in hospital mortality in patients with septic shock.

Materials and Methods

This prospective study included all patients with septic shock on admission or during intensive care unit (ICU) stay, older than 18 years, admitted to 1 of the 3 ICUs of the Botucatu Medical School, from January to August 2012. Demographic information, clinical evaluation, and blood sample were taken within the first 72 hours of the patient's admission or within 72 hours after septic shock diagnosis for serum thiamine, GPx activity, and protein carbonyl determination.

Results

One hundred eight consecutive patients were evaluated. The mean age was 57.5 ± 16.0 years, 63% were male, 54.6% died in the ICU, and 71.3% had thiamine deficiency. Thiamine was not associated with oxidative stress. Neither vitamin B1 levels nor the GPx activity was associated with outcomes in these patients. However, protein carbonyl concentration was associated with increased mortality.

Conclusions

In patients with septic shock, oxidative stress was associated with mortality. On the other hand, thiamine was not associated with oxidative stress or mortality in these patients.     

Plasma cortisol levels in patients with septic shock

To investigate the endogenous adrenocortical response to sepsis, plasma cortisol concentrations were measured in 37 patients (53 +/- 3 yr of age) with septic shock. Patients were studied 11 +/- 2 h after shock commenced. Vasopressor therapy was required in 35 of 37 patients (median dopamine infusion rate of 11 micrograms/kg.min, range 3 to 74). Plasma cortisol concentrations were increased markedly (median 50.7 micrograms/dl, range 15.6 to 400) above normal values (10 to 20 micrograms/dl) in patients with septic shock. Neither patients who reversed their shock nor those who survived to hospital discharge had significantly different plasma cortisol concentrations from those who did not. Patients with Gram-positive infections had increased cortisol levels compared with those who had Gram-negative infections (median 83 micrograms/dl, range 32 to 400 vs. median 44 micrograms/dl, range 16 to 81, respectively; p less than .05). The source of infection, amount of vasopressors infused, and severity of shock were not associated with differences in cortisol concentrations. The length of time in shock before collection of the blood sample for measurements of cortisol and mean arterial pressure at the time of blood collection had significant but weak negative correlations with cortisol concentrations (p less than .05, rs = .37 and p less than .05, rs = -.40, respectively). We conclude that plasma cortisol concentrations are increased in patients with septic shock, but that the degree of increase is variable. This variability may, in part, be related to type of infection, length of time in shock, and BP at the time of blood sampling.(ABSTRACT TRUNCATED AT 250 WORDS)     

Right ventricular dysfunction in patients with septic shock

Using a rapid computerized thermodilution method, we examined the evolution of right ventricular performance in 23 patients with septic shock. Nine survived the episode of septic shock. The other 14 patients died of refractory circulatory shock. Significant right ventricular systolic dysfunction, defined as decreased ejection fraction (-39%) and right ventricular dilation (+38%) was observed in all patients with septic shock. However, in the survivors, increased right ventricular preload may prevent hemodynamic evidence of right ventricular pump failure by utilizing the Frank-Starling mechanism to maintain stroke volume. Conversely, in the nonsurvivors, right ventricular dysfunction was more prononced two days after the onset of septic shock, leading to a fall in stroke. In the last patients, a decrease in contractility appears to be the major factor accounting for decreased right ventricular performance, as evidenced by the marked increase in end-systolic volume (+27%) without significant change in pulmonary artery pressure, during the later stage of septic shock. The observed right ventricular pump failure then appears associated with an alteration in diastolic mechanical properties of this ventricle, as suggested by a leftward displacement of the individual pressure-volume curves.     

Adrenal function testing in patients with septic shock

Introduction  

Adrenal failure (AF) is associated with increased mortality in septic patients. Nonetheless, there is no agreement regarding the best diagnostic criteria for AF. We compared the diagnosis of AF considering different baseline total cortisol cutoff values and Δmax values after low (1 μg) and high (249 μg) doses of corticotropin, we analyzed the impact of serum albumin on AF identification and we correlated laboratorial AF with norepinephrine removal.     

老年肺炎合并感染性休克患者预后相关因素分析

目的 探讨老年肺炎合并感染性休克患者预后相关因素.方法 分析88例老年肺炎合并感染性休克患者的临床资料,用单因素分析比较不同预后组患者预后可能相关因素,再将有统计学差异的因素用多因素回归分析筛选出与死亡相关的独立危险因素.结果 老年肺炎合并感染性休克患者病死率56.8％,单因素分析结果提示死亡组年龄、APACHEⅡ评分、功能不全脏器的数量、干预前及治疗6h后血乳酸水平均显著高于存活组（均P ＜0.05）,且神经、凝血、肾功能不全的发生率均高于存活组（均P＜0.05）,多因素Logistic分析提示入ICU时APACHEⅡ评分≥26.5分、治疗6h后血乳酸水平≥4.0 mmol/L、器官衰竭数量≥3.6个、神经功能不全为不良预后的独立危险因素.结论 老年肺炎患者一旦合并感染性休克病死率就会高,其治疗前病情危重程度、早期干预后血乳酸水平、脏器功能不全的数量（尤其是脑）与预后密切相关,因此如何尽早干预以降低血乳酸水平、避免脏器功能受损对患者预后有极其重要的意义.     

Increased muscle-to-serum lactate gradient predicts progression towards septic shock in septic patients

Purpose  

During septic shock, muscle produces lactate and pyruvate by way of an exaggerated Na⁺, K⁺-ATPase-stimulated aerobic glycolysis associated with epinephrine stimulation. We hypothesized that patients with sepsis without shock and increased epinephrine levels or an increased muscle-to-serum lactate gradient are likely to evolve towards septic shock. Thus, in sepsis patients, we investigated (1) whether muscle produces lactate and pyruvate, and (2) whether muscle lactate production is linked to epinephrine levels and the severity of the patient's condition.     

Immunological parameters in diabetic patients with septic shock

The paper describes early postoperative changes in the parameters of phagocytosis, cellular and humoral immunities in 33 patients with type 2 diabetes mellitus in the phase of decompensation along with diffuse purulent peritonitis and septic shock. Just on admission to an intensive care unit, the patients were found to have secondary immune deficiency and the performed therapy failed to correct the parameters of phagocytosis and cellular and humoral immunities. Impaired immunological responsiveness progressed to the maximum manifestations by the end of 7 days.     

细节护理干预在感染性休克患者中的应用效果

目的探究细节护理干预在感染性休克患者中的应用效果。方法采用便利抽样法,选取2017年1月—2018年6月四川大学华西医院收治的感染性休克患者70例,按随机数字表法将其分为对照组(n=35)和观察组(n=35)。对照组给予常规护理,观察组在对照组的基础上给予细节护理干预。共干预两周。比较两组患者干预前后的临床疗效、血流动力学指标、健康状况及格拉斯格昏迷指数(GCS)评分。结果观察组感染性休克患者治疗有效率为88.57%,高于对照的65.71%,差异有统计学意义(P<0.05)。观察组住院时间、呼吸机使用时间、意识恢复时间、症状体征消失时间均短于对照组,血清C反应蛋白水平低于对照组,差异均有统计学意义(P<0.01)。干预后观察组患者心脏指数、平均动脉压和静脉血氧饱和度均高于对照组,心率低于对照组,差异均有统计学意义(P<0.05)。干预后,观察组患者健康状况评分低于对照组,GCS评分高于对照组,差异有统计学意义(P<0.05)。结论对感染性休克患者实施细节护理干预,可以改善患者生存质量,对血流动力学的影响较小,值得临床推广应用。     

Antibiotic selection for patients with septic shock

Early recognition of the sepsis syndrome, prompt administration of broad-spectrum antibiotics, surgical intervention when indicated, and aggressive supportive care in intensive care units remain the therapeutic strategies for patients with sepsis. Antibiotic selection is based on many factors including the most probable source of infection, the most likely pathogens, and knowledge of antibiotic susceptibility patterns for community- and hospital-acquired infections. Unfortunately, with this approach, mortality remains unacceptably high. Adjuvant therapies such as antiendotoxin antibodies, cytokine antagonists, and anti-inflammatory agents aimed at blunting the host immune response to bacterial infection have provided little clinical benefit to date. As our understanding of the pathophysiology of sepsis progresses, perhaps newer modalities will improve clinical outcome. At this time, preventive strategies, including optimal vaccine use, effective infection control practices, judicious use and care of intravascular lines and indwelling urinary catheters, and appropriate use of anti-infective agents to prevent microbial resistance should be used to decrease the incidence of infection and subsequent sepsis.     

Leukocyte phenotyping to stratify septic shock patients

In a recent study conducted in a cohort of 52 septic patients, Monserrat and coworkers found that profound failure of peripheral T cells to convert from a naïve phenotype to an activated phenotype has positive predictive value in identifying patients who do not recover. These data support the hypothesis that failure of the innate immune system to engage the T-cell compartment contributes to sepsis mortality and provides motivation for the development and clinical evaluation of immunostimulatory therapies for patients with sepsis.