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PubMed1990

The role of intestinal barrier failure and bacterial translocation in the development of systemic infection and multiple organ failure.

Traditionally, evaluation of intestinal function has been limited largely to monitoring gastric pH and intestinal motility. This clinical approach has led clinicians to equate normal intestinal motility with normal intestinal function and to assume that if stress-induced gastric bleeding can be prevented, all will be well. However, it is becoming increasingly clear that the gastrointestinal tract is not a passive organ and that intestinal dysfunction is not limited to ileus and upper gastrointestinal bleeding. Instead, the gastrointestinal tract is recognized as having important endocrine, metabolic, immunologic, and barrier functions, as well as its traditional role in nutrient absorption. Over the last 5 years, there has been a resurgence of interest in the role of intestinal barrier failure in the development of systemic infection and multiple organ failure in the critically ill or injured patient.

Bacteria↗

PubMed1994

The postischemic gut serves as a priming bed for circulating neutrophils that provoke multiple organ failure.

Our trauma research center program entitled, "Trauma Primes Cells" is based on the fundamental hypothesis that prior exposure to multiple, sequential, sublethal cellular insults primes constructive or destructive pathways of cellular responses of subsequent injury. A major objective is to design therapy that will reduce the incidence of multiple organ failure. Although a number of inflammatory cascades have been incriminated in the pathogenesis of multiple organ failure (MOF), diffuse PMN-mediated tissue injury remains an attractive unifying concept. We have developed a sequential insult rodent model in which the priming event consisted of superior mesenteric arterial (SMA) clamping for 45 minutes followed by 6 hours of reperfusion. Following this priming event, activation was induced with a low dose of endotoxin (2.5 mg/kg). We believe that these studies support our hypothesis: mesenteric ischemic/reperfusion primes circulating PMNs. When these have been activated they can then be provoked by endotoxin to provoke distant organ injury. Primed PMNs are released from the postischemic mesenteric bed and enter the systemic circulation. They subsequently sequester in the pulmonary vascular bed where they are relatively harmless until they are activated by low dose endotoxin. These activated PMNs then migrate across the endothelium cell and release reactive oxygen metabolites.

Animals↗

PubMed1983

[Multiple organ failure--the most important complication in polytraumatized patients].

In 4 1/2 years 78 out of 433 polytrauma-patients came to death in our hospital ( = 18%), half of them because of their brain-trauma. 15 fatalities occurred in connection with pulmonary failure only, 19 in multiple organ failure. Pulmonary failure is of central importance in MOF. Two types of MOF are described: the rapid pattern directly following severe shock with slightly better prognosis and a delayed pattern caused by concomitant sepsis. The hope of further improving these results is connected with five demands: 1. an elaborate scheme of treatment: taking the priorities into account; 2. sufficient treatment of shock; 3. controlled use of the respirator as early as possible and as long as necessary; 4. avoiding any sepsis; 5. close monitoring of system function.

Adolescent↗

PubMed1991

Does selective decontamination of the gastrointestinal tract prevent multiple organ failure? An experimental study.

Gut bacteria have been incriminated as causing or contributing to generalized sepsis with multiple organ failure in severely ill patients, and selective decontamination of the gastrointestinal tract of Enterobacteriaceae has been claimed to decrease septic complications in these patients. We studied the effects of selective decontamination of the gastrointestinal tract on survival and organ function in an experimental model of sepsis with multiple organ failure. Wistar rats were inoculated intraperitoneally with zymosan and randomized into control or treatment groups (trimethoprim or streptomycin sulfate). Selective decontamination effectively prevented bacterial translocation of Enterobacteriaceae. However, only early mortality was decreased, and only so in the streptomycin-treated rats. Selective decontamination did not result in a significantly better condition of the surviving animals on day 12.

Animals↗

PubMed1992

Incommensurate oxygen consumption in response to maximal oxygen availability predicts postinjury multiple organ failure.

Untreated flow-dependent oxygen consumption (VO2) has recently been implicated as an unrecognized risk factor for multiple organ failure (MOF). We therefore prospectively studied 39 severely injured patients with known risk factors for multiple organ failure who were subjected to an established resuscitation protocol aimed at maximizing oxygen delivery (DO2 greater than 600 mL/min.m2) to attain a VO2 goal of greater than 150 mL/min.m2. Fifteen (38%) of these high risk patients did not meet this VO2 goal by 12 hours. These nonresponding patients had significantly elevated lactate levels, suggesting defective aerobic metabolism. Of note, this blunted VO2 response despite maximal efforts to enhance peripheral oxygen availability predicted MOF. These data serve to re-emphasize the importance of the initial shock insult in causing or priming the host for the development of late MOF.

Adult↗

PubMed1989

[Multiple organ failure syndrome in infection caused by ictero-hemorragic Leptospira. Description of a clinical case].

A 53 years old fisherman was admitted to General Intensive Care Unit in Arezzo with signs and symptoms of Weil disease. An early acute respiratory failure developed. Radiological and haemodynamic findings confirmed a diagnosis of ARDS. The patient developed a severe jaundice, acute renal failure and ARDS (MOF multiple organs failure). To support different failures of the organs, CMV (continuous mandatory ventilation: CPPV with PEEP max 10 cm H2; IRV max 2:1) and AMV (assisted mandatory ventilation: Pressure Support Ventilation), haemofiltration, haemoperfusion and plasmapheresis were simultaneously used, that got better and better renal and respiratory performances. Haemodynamic worsening by PEEP during extracorporeal treatment was overcome by PSV very useful new ventilatory procedure even during weaning period. The patient treated in such manner survived without important disabilities. This care confirms that ARDS (non cardiogenic edema) and MOF can develop during Icterohaemorrhagic Leptospirosis.

Acute Kidney Injury↗

PubMed2002

Septic shock and multiple organ failure after hematopoietic stem cell transplantation: treatment with recombinant human activated protein C.

Severe sepsis with multiple organ failure after hematopoietic stem cell transplantation (HSCT) results in extremely high morbidity and mortality. Recent studies have highlighted the importance of sepsis-induced activation of the coagulation system in the pathophysiology of severe sepsis. Activated protein C is an important modulator of coagulation and inflammatory derangements during severe sepsis. Low levels of protein C occur in severe sepsis and are predictive of poor outcome. Recombinant human activated protein C (drotrecogin alfa (activated)) was recently approved by the Food and Drug Administration (FDA) for severe sepsis. The phase III trial that resulted in the approval of this agent, however, enrolled a general sepsis population and excluded patients undergoing HSCT. We report a case of fulminant septic shock and multiple organ failure after HSCT that was treated with drotrecogin alfa (activated) in addition to standard therapy, and recovered. The high mortality rates of patients who develop severe sepsis after HSCT demand that new avenues of treatment be considered for this very high-risk patient population. This case illustrates the potential application of a novel therapeutic approach. Clinical trials are warranted to further investigate the safety and efficacy of drotrecogin alfa (activated) in patients with severe sepsis after HSCT.

Adult↗

PubMed1991

[Two cases of traumatic bladder rupture with multiple organ failure].

We report two cases of traumatic bladder rupture complicated by multiple organ failure (MOF). The first patient had an extraperitoneal bladder rupture and right femoral bone fracture, which were treated conservatively. However, intrapelvic abscess and adult respiratory distress syndrome (ARDS) which was caused by fat embolism resulted in MOF. The second patient who had been under treatment for malignant lymphoma for three years had an intraperitoneal bladder rupture with ruptures of spleen, intestine and diaphragm. We closed the defects in the bladder, intestine, diaphragm and performed splenectomy. We also provided suprapubic cystostomy and a urethral catheter. However, wound abscess and hepatic failure occurred postoperatively. She died of MOF 20 days after the operation. We stress that in the treatment of bladder rupture, intensive chemotherapy for infection must be done when there are complications of other visceral injuries.

Accidents, Traffic↗

PubMed1998

Multiple organ failure can be predicted as early as 12 hours after injury.

BACKGROUND: The failure of therapies aimed at modulating systemic inflammatory response syndrome and decreasing multiple organ failure (MOF) has been attributed in part to the inability to identify early the population at risk. Our objective, therefore, was to develop predictive models for MOF at admission and at 12, 24 and 48 hours after injury. METHODS: Logistic regression models were derived in a data set with 411 adult trauma patients using indicators of tissue injury, shock, host factors, and the Acute Physiology Score-Acute Physiology and Chronic Health Evaluation III (APS-APACHE III). RESULTS: MOF was diagnosed in 78 patients (19%). Injury Severity Score, platelet count, and age emerged as predictors in all models. Transfused blood, inotropes, and lactate were significant predictors at 12, 24, and 48 hours, but not at admission. The APS-APACHE III emerged only in the 0- to 48-hour model and offered minimal improvement in predictive power. Good predictive power was achieved at 12 hours after injury. CONCLUSION: Postinjury MOF can be predicted as early as 12 hours after injury. The APS-APACHE III added little to the predictive power of tissue injury, shock and host factors.

APACHE↗

PubMed1996

Postinjury multiple organ failure: a bimodal phenomenon.

To better define the epidemiology of postinjury multiple organ failure (MOF), we prospectively evaluated 457 high-risk trauma patients who survived more than 48 hours. Overall, 70 (15%) developed MOF. In 27 (39%) patients, the occurrence was early, while in 43 (61%) patients the presentation was delayed. At presentation, early MOF had more cardiac dysfunction, while late MOF had greater hepatic failure. Indices of shock were more critical risk factors for early MOF, while advanced age was more important for late MOF. While early and late MOF had a similar high incidence of major infections, these appeared to be more important in precipitating late MOF. Finally, while mortality is similar, early MOF patients appear to succumb faster. In conclusion, postinjury MOF remains a significant challenge and appears to present in at least two patterns (i.e., early versus late). Better understanding of the relative roles of the dysfunctional inflammation and infections in early MOF versus late MOF may facilitate the development of new strategies for the prevention and treatment of morbid syndrome.

Adolescent↗

PubMed1995

Multiple organ failure: a common problem in surgical intensive care unit patients.

The management of the surgical patient with multiple system organ failure remains a formidable problem. Despite advances in critical care, the mortality of multiple organ failure remains unchanged since the syndrome was characterized almost two decades ago. At the present time there are no modalities that can actively reverse established organ failure, hence the treatment of these patients consists of metabolic and haemodynamic support until the process reverses itself or death occurs. Therefore, the best management of the surgical patient at risk for multiple organ failure is prevention of the syndrome. Strategies to avoid organ failure include early fixation of long bone fractures, prompt restoration of perfusion and oxygen delivery, the aggressive diagnosis and drainage of abdominal infection prior to organ failure, early institution of enteral nutrition and the use of specific nutritional substrates and formulas. This review will examine the current theories in the pathogenesis of multiple organ failure and detail two clinical decisions, early stabilization of fractures and prompt re-exploration for suspected abdominal sepsis, that have been associated with a reduction in the frequency of the development of organ failure.

Humans↗

PubMed2003

Early multiple organ failure after recurrent endotoxemia in the presence of vasoconstrictor-masked hypovolemia.

OBJECTIVE: Critically ill patients who develop multiple organ failure during systemic inflammatory states are often predisposed to hypovolemia and vasoconstrictor therapy. Although numerous investigations have evaluated the sequelae of systemic inflammation, no data are available on the contribution of chronic vasoconstrictor-masked hypovolemia to organ dysfunction and morphology. DESIGN: Prospective, randomized laboratory investigation. SETTING: University research laboratory. SUBJECTS: Eighteen adult chronically instrumented sheep. INTERVENTIONS: The animals were randomly assigned to one of three groups. In the norfenefrine-masked hypovolemia plus endotoxemia (NMH+ENDO) group, mean arterial pressures of 80 mm Hg were maintained by using the alpha1-adrenergic catecholamine norfenefrine for 52 hrs during hypovolemia. Hypovolemia was induced by hemorrhage (about 23 mL x kg(-1)) until mean arterial pressures reached 40 mm Hg. Endotoxin (0.5 microg x k(-1)) was then injected after 4, 16, 28, and 40 hrs. The NMH group received norfenefrine-masked hypovolemia but no endotoxin. In the ENDO group, recurrent endotoxemia was induced during normovolemia. MEASUREMENTS AND MAIN RESULTS: Despite profound differences in fluid management, cardiovascular filling pressures were not statistically different between groups. Endotoxemia induced norfenefrine-refractory shock (p < .05 vs. the other groups) and contributed to renal dysfunction only during vasoconstrictor-masked hypovolemia. Norfenefrine-masked hypovolemia caused disseminated cardiac cell necrosis independent of endotoxemia (p < .05 vs. ENDO). CONCLUSIONS: Hypovolemia can be masked when volume status is monitored by filling pressures. In this new model of endotoxemia-associated multiple organ failure, chronic vasoconstrictor-masked hypovolemia turned systemic inflammation into a life-threatening condition with renal and cardiovascular failure. Cardiomyocyte necroses were caused by vasoconstrictor-masked hypovolemia but were unrelated to cardiovascular failure.

Adrenergic alpha-Agonists↗

PubMedDate not supplied

Plasma levels of endotoxin and anaphylatoxin in patients with multiple organ failure.

Plasma concentrations of endotoxin and anaphylatoxins were studied inpatients with multiple organ failure (MOF). Thirty one blood samples from nine patients with MOF and twenty samples from preoperative patients as control were determined. The average plasma concentration of endotoxin was 188.7 +/- 37.0 pg-ml-1 (Mean + S.E.) in MOF patients and 12.4 +/- 3.3 pg.ml-1 in control patients (p less than 0.05). Plasma anaphylatoxin (C3a, C5a) levels increased significantly and C4 level decreased in MOF patients as compared with those in control patients. However, no significant correlation was found between plasma endotoxin and anaphylatoxin levels. Endotoxin does not seem to be a major factor in activating of the complement system in patients with MOF.

Adult↗

PubMed1993

Scoring systems and blood lactate concentrations in relation to the development of adult respiratory distress syndrome and multiple organ failure in severely traumatized patients.

In 56 patients with multiple trauma with ISSs > or = 33 we prospectively collected data of seven scoring systems (ISS, TS, TRISS, GCS, PTS, APACHE II, SSS) and sequentially determined blood lactate concentrations. These data were analyzed in relation to the patients later developing adult respiratory distress syndrome (ARDS) and multiple organ failure (MOF). Twenty-two patients developed ARDS, and 18 developed MOF. Of the mentioned scoring systems only ISS, PTS, and SSS were predictive of subsequent ARDS, and only ISS and SSS were predictive of subsequent MOF. Lactate concentrations at days 2, 3, and 4 were significantly different between patients with and without subsequent ARDS, MOF, or both. Surprisingly, APACHE II scores did not correlate with subsequent ARDS or MOF, nor did they show any significant relation with lactate concentrations at any time. By stepwise regression analysis ISS, SSS, and lactate level at day 3 were the most significant variables toward the development of ARDS and MOF. It is concluded that scoring systems directly grading the severity of groups of trauma patients have predictive value for late and remote complications such as ARDS and MOF, whereas scoring systems that grade the physiologic response to trauma--although clearly related to mortality--have no such predictive value.

Adolescent↗

PubMed1998

Death in the burn unit: sterile multiple organ failure.

It has been our impression over the years that the most common cause of death in our burn patients is multiple organ failure, despite the clinical absence of uncontrolled infection at the time of death. A six year review of all deaths in our unit confirmed this impression, revealing that multiorgan failure is indeed the most common cause of death (48 patients, 67 per cent), followed rather distantly by early withdrawal of support (15 patients, 21 per cent), resuscitation failure (4 patients, 6 per cent) and isolated pulmonary failure (4 patients, 6 per cent). Finally, we found that our patients dying of multiorgan failure, although often having had multiple small infections during their course, were indeed clinically uninfected at the time of death. These findings are consistent with the supposition that uncontrolled systemic inflammation, initially triggered by tissue injury and isolated infection, persists despite control of these infections and leads to multiple organ failure and death.

Adolescent↗

PubMed1989

Use of extracorporeal supportive techniques as additional treatment for septic-induced multiple organ failure patients.

We compared retrospectively four similar groups of patients with multiple organ failure (MOF) due to sepsis. All of them were treated initially with conventional therapy, aprotinin as protease inhibitor and vitamin C with allopurinol as possible scavengers of oxygen-free radicals, were also added. After 24 h of no clinical progress, continuous arteriovenous hemofiltration (CAVH), CAVH/dialysis (CAVH/D), and sequential plasmafilter-dialysis with slow continuous hemofiltration (CAVHP/D) were respectively added to groups 2 (n = 14), 3 (n = 6), and 4 (n = 11). Mortality was 87% for group 1, 71% for group 2, 50% for group 3, and 36% for group 4. In the latter we were able to remove possible MOF-inducing mediators from the bloodstream, to give fluids without restriction (even in oliguric patients), and to improve removal of metabolic waste products. It is possible that these extracorporeal supports, associated with conventional therapy, and pharmacologic drugs such as protease inhibitors and possible scavengers of oxygen-free radicals, helped to reduce the mortality rate. We conclude that, although the number of study patients was too small to reach firm conclusions, the good results observed with CAVHP/D suggest clinical trials to assess the efficacy of this technique.

Adult↗

PubMed1994

Timing and predictors of death in pediatric patients with multiple organ system failure.

OBJECTIVES: To describe the timing of onset of organ system failure, multiple organ system failure diagnosis, and the subsequent death in children admitted to a pediatric intensive care unit (ICU). Second, to identify independent risk markers of death in pediatric patients with multiple organ system failure. DESIGN: Review of a database. SETTING: Pediatric ICU within a tertiary care center. PATIENTS: We analyzed the pediatric ICU course of 777 consecutive patients aged < 18 yrs. MEASUREMENTS AND MAIN RESULTS: Eighty-five (10.9%) of 777 children had multiple organ system failure, defined as the simultaneous occurrence of at least two organ system failures. Of 85 children, 37 (43.5%) were postoperative cardiac surgery patients and 48 (56.5%) patients were in the ICU for other reasons. The diagnostic criteria for multiple organ system failure were met on the day of admission by 73 (86%) of 85 patients. The maximum number of organ system failures occurred within 72 hrs in 74 (87%) children. The mortality rate for all patients with multiple organ system failure was 50.6%. Thirty-eight (88.4%) of deaths occurred within 7 days after the diagnosis of multiple organ system failure. Survival analysis was comparable for both postoperative cardiac surgery patients and patients with other diagnoses. Multivariate analysis identified three factors as independent risk markers of death in pediatric patients with multiple organ system failure: maximum number of simultaneous organ system failures during the pediatric ICU stay: odds ratio, 55.9 (95% confidence interval, 7.9 to 396.1); age < or = 12 months: odds ratio, 17.1 (95% confidence interval, 1.8 to 158.7); and the Pediatric Risk of Mortality (PRISM) score on the day of admission: odds ratio, 1.25 (95% confidence interval, 1.1 to 1.5). CONCLUSIONS: The mortality rate associated with multiple organ system failure in pediatric patients is high. The maximum number of simultaneous organ system failures during pediatric ICU stay, age < or = 12 months, and the PRISM score on the day of admission are independent risk markers of death. Diagnosis of multiple organ system failures, development of maximum number of organ system failures, and deaths occur remarkably early after pediatric ICU admission; the rationale for using prophylactic therapy under such circumstances is unclear.

Adolescent↗

PubMed2005

Temporal changes in whole-blood and plasma glutathione in ICU patients with multiple organ failure.

OBJECTIVE: This study investigated the temporal changes in whole-blood and plasma glutathione in ICU patients with multiple organ failure. DESIGN AND SETTING: Prospective and descriptive pilot study performed in an ICU with eight beds at a university hospital. PATIENTS: Critically ill patients (n=11) with multiple organ failure and ICU stay of at least 6 days were consecutively included. Patients with chronic obstructive pulmonary disease (n=21) and healthy volunteers (n=10) were used as reference groups. MEASUREMENTS AND RESULTS: Whole-blood and plasma glutathione were measured every 72 h. Total glutathione and the reduced fraction were determined in whole blood. The oxidized fraction and the redox status were calculated from these values. In plasma only the total concentration was determined. Patients were studied for 6-15 days. Nutrition was supplied according to routines supplying basal needs including glutamine. Both total and reduced glutathione was found to be depleted in whole blood compared to the reference groups. Redox status indicated continuing oxidative stress. Plasma glutathione showed higher values in total concentrations than the reference groups. CONCLUSIONS: This study demonstrates that glutathione remains depleted in whole blood. This contrasts to what has previously been shown in skeletal muscle where a restitution of glutathione concentration is seen.

Adult↗