Postoperative multiple organ failure

Cellular damage is the pathophysiologic basis for the postoperative multiple organ failure syndrome. This damage may be caused by pre- and intraoperative shock. Postoperative organ failure is manifested when cellular repair does not occur. Three factors may contribute to this progression to multiple organ failure: inadequate resuscitation, malnutrition, and sepsis.     

The syndrome of multiple organ failure

Current technology has prolonged the life support of patients with organ failures. The onset of MOF follows an inciting event and develops a clinical pattern of lung, liver, and kidney failure. Laboratory evidence of the syndrome includes hyperbilirubinemia, hyperglycemia, increased blood lactate, and reduced levels of hepatic proteins. Energy expenditure in MOF is increased and severe sepsis or septic shock can initiate the process of hypermetabolism and MOF. Current therapy is aimed at source control, restoration of oxygen transport, and metabolic support. Critical care nursing provides a technological and humanistic approach in developing a supportive environment for patients and families. Scientific study of the effects of nursing interventions on patient outcomes is needed to evaluate critical care nursing activities.     

Hemodynamic aspects of multiple organ failure

Multiple organ failure (MOF) secondary to sepsis is associated with a high mortality. A large body of evidence suggests that the disturbed relationship between oxygen supply and oxygen uptake plays an important role in the pathogenesis of MOF. The relationship between oxygen-supply dependency and MOF and the practical implications of the relationship are reviewed. It is concluded that, apart from the all-important eradication of the source of the sepsis, optimizing oxygen transport is the best method of preventing the development of MOF. Since the effects of hemodynamic and ventilatory treatments on oxygen uptake are often unpredictable, the impact of the treatments on oxygen uptake should be evaluated directly.     

Hemodynamic aspects of multiple organ failure

Multiple organ failure (MOF) secondary to sepsis is associated with a high mortality. A large body of evidence suggests that the disturbed relationship between oxygen supply and oxygen uptake plays an important role in the pathogenesis of MOF. The relationship between oxygen-supply dependency and MOF and the practical implications of the relationship are reviewed. It is concluded that, apart from the all-important eradication of the source of the sepsis, optimizing oxygen transport is the best method of preventing the development of MOF. Since the effects of hemodynamic and ventilatory treatments on oxygen uptake are often unpredictable, the impact of the treatments on oxygen uptake should be evaluated directly.     

Septic shock and multiple organ failure

OBJECTIVE: To assess the frequency and mortality rates of septic shock in ICU patients and the clinical course of multiple organ failure associated with septic shock. DESIGN: Retrospective case survey. SETTING: Tertiary care center. PATIENTS: During a 2-yr period, 2,469 consecutive intensive care patients were studied regarding the frequency and hospital mortality rates of septic shock. A subset of 1,311 patients was further analyzed for the occurrence of organ system failures within 48 hrs of the onset of septic shock and again 4 to 7 days later. MEASUREMENTS AND MAIN RESULTS: The frequency rate of septic shock was 1.9% (n = 48), with a mortality rate of 72.9% (n = 35) in patients with septic shock. Deaths due to septic shock represented 14.6% of all deaths in the ICU during the study period. Eighteen patients died within 72 hrs of the onset of septic shock. Refractory hypotension was the cause of death in 15 of these 18 patients. Beyond 72 hrs, multiple organ failure accounted for eight of 17 deaths. The mean +/- SD number of organ systems failing at 48 hrs was 3.3 +/- 1.3 in survivors and 4.0 +/- 1.1 in nonsurvivors, and at 4 to 7 days was 2.1 +/- 1.5 in survivors and 4.0 +/- 1.5 in nonsurvivors (p less than .05). None of the specific organ system failures had prognostic value. The number of organ system failures was not related to the duration of hypotension, but had a weak correlation (r2 = .26, p less than .05) with the duration of vasoactive treatment at 4 to 7 days. The prolonged need for norepinephrine therapy was associated with an increased occurrence of renal failure. Thirty (62.5%) patients had positive blood cultures and a mortality rate similar to the mortality rate of patients with negative blood cultures. Patients with negative blood cultures died more often with hypotension (p less than .02). CONCLUSIONS: Septic shock is a major cause of death in intensive care patients. Refractory hypotension is a main cause of early deaths. Later on, multiple organ failure becomes the primary clinical problem and cause of mortality.     

Validation of postinjury multiple organ failure scores

Most multiple organ failure (MOF) scores were developed over a decade ago, but little has been done in terms of validation and to understand the differences between populations identified by each of them. Given the lack of a gold standard, validation must rely on association with objective adverse outcomes. Thus, we propose to (a) validate two widely accepted MOF scores (Denver and Marshall), examining their association with adverse outcomes in a postinjury population; and (b) compare risk factors, characteristics, and outcomes of patients identified by each score. The Denver MOF score grades (from 0-3) four organ dysfunctions (lung, kidney, liver, and heart) and defines MOF as a total score more than 3. The Marshall score grades, in addition, central nervous system and hematologic dysfunction (total of six organs on a 0- to 4-point scale). Using a prospectively collected data set, MOF was scored daily by both scores for 1,389 consecutive trauma patients with Injury Severity Score of more than 15 admitted from 1992 to 2004. Risk factors, clinical outcomes (death, ventilator-free days), and resource utilization outcomes (mechanical ventilation time, length of stay in the intensive care unit) were evaluated. Both scores were associated with areas under the receiver operating characteristic curves of 80 or greater (ideal value = 100), with values for the Denver score being slightly greater (albeit not significantly) regarding prediction of most outcomes. Values of sensitivity and specificity were more than 70% for death and ventilator-free days (with the Denver score showing a consistent trend toward greater specificity), but either sensitivity or specificity was less than 70% for mechanical ventilation time and length of stay in the intensive care unit, suggesting that these scores are appropriately biased toward clinical outcomes as opposed to resource utilization. Both scores performed well, with the Denver MOF score showing greater specificity, which, coupled with its simplicity, makes it an attractive tool for both the research and clinical environments. Basic concepts of each score can probably be combined to produce an improved MOF score.     

Metabolic manifestations of multiple systems organ failure

It is apparent that the metabolic response to injury as manifest in hypermetabolism and organ failure is a markedly different process from standard starvation. As such, it seems to have a different set of support principles that are probably better called metabolic support than nutritional support. The best treatment remains prevention by controlling the presence of dead tissue, injured tissue, and infection, and by appropriately restoring and maintaining oxygen transport. With control of the source and the restoration of oxygen transport, the primary mode of support becomes one of metabolic support. This modality is a support tool that appears to "buy time" and help control malnutrition as a comorbidity or comortality. The principles that have evolved in large part have been those of learning to do no harm. The prevention of substrate limited metabolism and effective support of visceral functions is now available until the late stage of the organ failure process. We still cannot control the catabolic stimulus and the autocannibalism of the skeletal muscle mass with the redistribution of nitrogen into the visceral protein mass and the use of amino acids as prime energy sources. The ability to control this stimulus will probably reside in our ability to understand and manipulate the mediator systems. We are now evolving effective support regimens for preserving organ structure and function and for promoting tissue repair. The route of administration as well as the time of administration of the regimen may have some impact on the disease course itself. When metabolic support has been applied in the setting of intelligent surgery and critical care, a progressive reduction in morbidity and mortality has been realized over the last several years such that the current mortality risk for the organ failure syndrome is in the 35 to 40 per cent range overall.     

Mechanism-oriented therapy for multiple systems organ failure

Damage caused by systemic sepsis is only in part caused by the viable microbe and therefore treatable by antibiotics. Most damage is produced by host defenses. The rationale for anti-inflammatory therapy in severely septic patients is based on these concepts. A variety of anti-inflammatory agents are being studied that might help "tide the patient through" the initial phases of the septic event until antimicrobial therapy has had a chance to work. Antibiotics certainly help minimize the suppurative complications of bacteremia/septicemia. The initial approach to the septic patient should be rapid but thorough, permitting data to be gathered that will permit decisions ultimately to be made as to whether or not sepsis was actually present and what appropriate therapeutic agents are best for longer term treatment. The septic patient will continue to provide a challenge to the clinician. The better one understands the mechanisms involved in the pathophysiology of the development of severe sepsis, septic shock, and the syndrome of MSOF, the better will become the clinical management of such patients. Also, development of additional such insights will certainly permit important new therapeutic modalities to evolve.     

Circulatory disturbances in multiple systems organ failure

Circulatory disturbances in MSOF disturb normal metabolic autoregulation, the ability to continuously couple tissue oxygen delivery with oxygen need. These may occur at three levels of the circulation: the heart; the regional circulations; and the microcirculation. This article will summarize evidence demonstrating that MSOF is associated with reduced tissue oxygen delivery by virtue of changes in all three circulatory components governing the inadequacy of metabolic autoregulation in sepsis.     

骨髓间充质干细胞防治多脏器衰竭

Objective The patients with lethal irradiation after sucessful hematopoietic stem cells transplan-tation had blood recovery, but did not avoid to died of multiple organ failure(MOF). To overcome the block, the article investigated mechanisms of mesenchymal stem cells (MSCs) protecting lethal radiated mice from multiple organ failure after haploid bone marrow cells transplantation. Method BALB/c mice irradiated with 8Gy60COγ-rays were randomly divided into two groups: MSCs group, infused MSCs labeled with cm-DiI and bone marrow monocytes of CB6F1 mice; Control group, only infused bone marrow monocytes; normal group, mice were infused cm-DiI marked MSCs without irradiation. The distribution of MSCs and the serous densities of Il-2, Il-10 and TNF-α in the recipients were observed after transplantation. Results MSCs collected in the bone marrow and the intes-tine in normal group at 15 d,in MSCs group MSCs enriched the different organs at 3,15 and 30 d. MSCs regulated down the secretion of IL-2 and TNF-α,and up the IL-10 density. Conclusions MSCs protected mice from multiple organ failure through above effects and may be open a new treatment strategy on acute radiation syndrome by stem cells.     

骨髓间充质干细胞防治多脏器衰竭

Objective The patients with lethal irradiation after sucessful hematopoietic stem cells transplan-tation had blood recovery, but did not avoid to died of multiple organ failure(MOF). To overcome the block, the article investigated mechanisms of mesenchymal stem cells (MSCs) protecting lethal radiated mice from multiple organ failure after haploid bone marrow cells transplantation. Method BALB/c mice irradiated with 8Gy60COγ-rays were randomly divided into two groups: MSCs group, infused MSCs labeled with cm-DiI and bone marrow monocytes of CB6F1 mice; Control group, only infused bone marrow monocytes; normal group, mice were infused cm-DiI marked MSCs without irradiation. The distribution of MSCs and the serous densities of Il-2, Il-10 and TNF-α in the recipients were observed after transplantation. Results MSCs collected in the bone marrow and the intes-tine in normal group at 15 d,in MSCs group MSCs enriched the different organs at 3,15 and 30 d. MSCs regulated down the secretion of IL-2 and TNF-α,and up the IL-10 density. Conclusions MSCs protected mice from multiple organ failure through above effects and may be open a new treatment strategy on acute radiation syndrome by stem cells.     

骨髓间充质干细胞防治多脏器衰竭

目的 探讨骨髓间充质干细胞(MSCs)防治半相合骨髓移植治疗致死剂量照射小鼠的多脏器衰竭(MOF)的作用及机制.方法 BALB/C小鼠8Gy60Coγ射线照射后,分为MSCs组,尾静脉输注经cm-Dil膜染剂标记的CB6F1小鼠的MSCs和骨髓细胞;对照组,只输注CB6F1骨髓细胞.正常组,不照射,输注标记的MSCs细胞.观察移植后不同时间,供者MSCs在受者体内分布,MSCs组和对照组小鼠外周血中IL-2,TNF-α和IL-10血清浓度变化情况.SAS 9.0软件对数据做成组t检验.结果 移植后15 d,正常组,MSCs主要集中在骨髓和小肠.MSC组,移植后不同时间,标记的细胞分别在胸腺、骨髓、小肠中富集.MSCs上调了IL-10的血清质量浓度,下调了IL-2和TNF-α的质量浓度,两组数据有统计学差异.结论 证实MSCs可以通过下调体内的促炎因子IL-2和TNF-α,及上调抑炎因子IL-10,抑制全身炎症反应综合征的发生,及MSCs体内多组织器官分布,发挥防治MOF的作用.     

骨髓间充质干细胞防治多脏器衰竭

Objective The patients with lethal irradiation after sucessful hematopoietic stem cells transplan-tation had blood recovery, but did not avoid to died of multiple organ failure(MOF). To overcome the block, the article investigated mechanisms of mesenchymal stem cells (MSCs) protecting lethal radiated mice from multiple organ failure after haploid bone marrow cells transplantation. Method BALB/c mice irradiated with 8Gy60COγ-rays were randomly divided into two groups: MSCs group, infused MSCs labeled with cm-DiI and bone marrow monocytes of CB6F1 mice; Control group, only infused bone marrow monocytes; normal group, mice were infused cm-DiI marked MSCs without irradiation. The distribution of MSCs and the serous densities of Il-2, Il-10 and TNF-α in the recipients were observed after transplantation. Results MSCs collected in the bone marrow and the intes-tine in normal group at 15 d,in MSCs group MSCs enriched the different organs at 3,15 and 30 d. MSCs regulated down the secretion of IL-2 and TNF-α,and up the IL-10 density. Conclusions MSCs protected mice from multiple organ failure through above effects and may be open a new treatment strategy on acute radiation syndrome by stem cells.     

骨髓间充质干细胞防治多脏器衰竭

Objective The patients with lethal irradiation after sucessful hematopoietic stem cells transplan-tation had blood recovery, but did not avoid to died of multiple organ failure(MOF). To overcome the block, the article investigated mechanisms of mesenchymal stem cells (MSCs) protecting lethal radiated mice from multiple organ failure after haploid bone marrow cells transplantation. Method BALB/c mice irradiated with 8Gy60COγ-rays were randomly divided into two groups: MSCs group, infused MSCs labeled with cm-DiI and bone marrow monocytes of CB6F1 mice; Control group, only infused bone marrow monocytes; normal group, mice were infused cm-DiI marked MSCs without irradiation. The distribution of MSCs and the serous densities of Il-2, Il-10 and TNF-α in the recipients were observed after transplantation. Results MSCs collected in the bone marrow and the intes-tine in normal group at 15 d,in MSCs group MSCs enriched the different organs at 3,15 and 30 d. MSCs regulated down the secretion of IL-2 and TNF-α,and up the IL-10 density. Conclusions MSCs protected mice from multiple organ failure through above effects and may be open a new treatment strategy on acute radiation syndrome by stem cells.     

骨髓间充质干细胞防治多脏器衰竭

Objective The patients with lethal irradiation after sucessful hematopoietic stem cells transplan-tation had blood recovery, but did not avoid to died of multiple organ failure(MOF). To overcome the block, the article investigated mechanisms of mesenchymal stem cells (MSCs) protecting lethal radiated mice from multiple organ failure after haploid bone marrow cells transplantation. Method BALB/c mice irradiated with 8Gy60COγ-rays were randomly divided into two groups: MSCs group, infused MSCs labeled with cm-DiI and bone marrow monocytes of CB6F1 mice; Control group, only infused bone marrow monocytes; normal group, mice were infused cm-DiI marked MSCs without irradiation. The distribution of MSCs and the serous densities of Il-2, Il-10 and TNF-α in the recipients were observed after transplantation. Results MSCs collected in the bone marrow and the intes-tine in normal group at 15 d,in MSCs group MSCs enriched the different organs at 3,15 and 30 d. MSCs regulated down the secretion of IL-2 and TNF-α,and up the IL-10 density. Conclusions MSCs protected mice from multiple organ failure through above effects and may be open a new treatment strategy on acute radiation syndrome by stem cells.     

骨髓间充质干细胞防治多脏器衰竭

Objective The patients with lethal irradiation after sucessful hematopoietic stem cells transplan-tation had blood recovery, but did not avoid to died of multiple organ failure(MOF). To overcome the block, the article investigated mechanisms of mesenchymal stem cells (MSCs) protecting lethal radiated mice from multiple organ failure after haploid bone marrow cells transplantation. Method BALB/c mice irradiated with 8Gy60COγ-rays were randomly divided into two groups: MSCs group, infused MSCs labeled with cm-DiI and bone marrow monocytes of CB6F1 mice; Control group, only infused bone marrow monocytes; normal group, mice were infused cm-DiI marked MSCs without irradiation. The distribution of MSCs and the serous densities of Il-2, Il-10 and TNF-α in the recipients were observed after transplantation. Results MSCs collected in the bone marrow and the intes-tine in normal group at 15 d,in MSCs group MSCs enriched the different organs at 3,15 and 30 d. MSCs regulated down the secretion of IL-2 and TNF-α,and up the IL-10 density. Conclusions MSCs protected mice from multiple organ failure through above effects and may be open a new treatment strategy on acute radiation syndrome by stem cells.