[Acute renal failure in patients with multiple organ failure].
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Acute Kidney Injury↗
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Results for “Multiple Organ Failure”
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[Developmental modalities of septic states. Multiple organ failure syndrome].
Sepsis syndrome occurs when an acute infection results in an host generalized inflammatory response including cytokines production. Death is a frequent and unpredictable sequel of this pathological condition. It may be due either to uncontrolled circulatory failure, or to multiple organ failure. With the advent of nitric oxide in the arena of the most potent vasodilatator agents, we now better understand the mechanisms of low vascular resistance during hyperkinetic septic shock. However a closer understanding of the mechanisms of multiple organ failure is actually required to improve survival rates during severe human sepsis.
Humans↗
[The changes in serum angiotensin-converting enzyme and their relationships to pulmonary failure in experimental model of multiple organ failure].
The correlation of serum angiotensin-converting enzyme (SACE), PaO2 and pulmonary coefficient in rabbit model of multiple system organ failure (MOF). 16 rabbits were fed E coli (0.5-3.0 x 10(11)/kg B.W.) by gastrogavage, were induced hemorrhagic shock (5.33 kPa arterial pressure for an hour) and were rapidly reinfused with shed blood and dextran. According to the criteria of pulmonary failure, that is respiratory rates greater than 100/min, PaO2 less than 8.00 kPa, pulmonary coefficient greater than 6.0, 8 rabbits developed pulmonary failure. They showed a significantly low SACE values, decreased PaO2 values and increased pulmonary coefficients, while in other 8 control animals the values of SACE and PaO2 did not significantly change.
Animals↗
Revision of the multiple organ failure score.
BACKGROUND AND AIM: The multiple organ failure (MOF) score published by Goris et al. in 1985 was one of the first attempts to quantify severity of organ dysfunction and failure based on expert opinion in surgical intensive care unit patients. Fifteen years later a reassessment of this score is mandatory. PATIENTS AND METHODS: Daily MOF scores were documented in patients admitted to the surgical ICUs in Nijmegen (NL) and Cologne (D). Patients with an ICU stay < or = 3 days were excluded. Organ dysfunction (1 point) and organ failure (2 points) were recorded for the following organ systems: lung, heart, kidney, liver, blood, gastrointestinal tract (GI), and central nervous system (CNS). Maximum scores were computed, and logistic regression analysis was used to optimize point weights for each organ system. Predictive power was analyzed using receiver operating characteristic (ROC) curves. RESULTS: In all, 147 patients, mean age 56 years, were included with a total of 2,354 observation days. Hospital mortality was 30.6%. GI failure was present on only 3.3% of days, without impact on mortality. Valid evaluation of CNS was impossible in most cases due to sedation and ventilation. Reweighting of the score items revealed only marginal improvements in prediction. Mortality consistently increased with increase in number of failed organs. This phenomenon was even more pronounced in older patients, e.g., 55% mortality (age > or = 60) versus 0% (age < 60) with two failing organs. CONCLUSION: Due to problems in definition and assessment (reliability) CNS and GI should not be considered in future assessments of the MOF score. The original point weights in the remaining five organ systems provide a valid and reliable risk stratification, at least in surgical ICU patients.
Adult↗
Paediatric sepsis and multiple organ failure.
Mortality from paediatric sepsis and multiple organ failure has fallen over the last half century, but both remain significant causes of death and morbidity among children and infants in the intensive care unit. This article provides a basic guide for front-line clinicians involved in paediatric resuscitation, addressing nomenclature, epidemiology and suggestions for early treatment.
Anti-Bacterial Agents↗
Continuous veno-venous hemofiltration in critically ill patients with multiple organ failure.
18 critically ill patients, with multiple organ failure (MOF) (from shock either septic, n = 15, or cardiogenic, n = 3), oliguria and increase in BUN and creatinine were treated with pump driven, high flux continuous veno-venous hemofiltration (CVVH). Replacement fluids were administered in predilution mode. All patients were under respiratory support and vasoactive drugs, and received early nutritional support (N input: 0.2-0.3 g/kg/day). Mean duration of treatment was 9.2 days and mean ultrafiltrate production was 21.4 l/day; treatment resulted in a significant reduction of both urea nitrogen and creatinine blood levels (-20 and -40% of initial values respectively) in spite of a very severe catabolism. The total amount of urea nitrogen removed through CVVH ranged from 15 to 73 g/day (mean 33.5), the median value of urea nitrogen clearance was 12.8 ml/min with a median ultrafiltration coefficient of 0.8. The mean duration of hemofilters was 69 hours (38-108); the efficacy of filters remained stable throughout the entire lifespan and changes were made in case of sudden decrease of ultrafiltration (< ml/min). No major complication was observed in over than 4000 hours of treatment. Pump driven, high flux CVVH proved effective in the control of water electrolyte balance and metabolic homeostasis in a group of critically ill, hemodynamically unstable, catabolic patients with MOF and acute renal failure. In no case we had to add intermittent hemodialysis or to use hemodiafiltration. The constant extracorporeal blood flow and the stable efficacy of hemofilters allowed an easy control of the overall effectiveness of this technique.
Adult↗
Can body composition in multiple organ failure be favorably influenced by feeding?
Multiple organ failure is the final common path of numerous medical conditions whereby the various organ systems fail and are supported by pharmacologic or mechanical means. The patient appears septic but often no septic focus can be found. Whole body protein dynamics are similar to severe sepsis with an elevation of both synthesis and breakdown. Lean body mass is not maintained even in the presence of an apparently adequate energy intake. The more common methods of assessing body composition are all confounded by fluid retention, which also limits parenteral nutrient intake. There are also difficulties with the tolerance of enteral feeding. In the long term, pharmacologic methods are going to be required if it is deemed that the maintenance of body mass is desirable, but in the interim, a robust noninvasive method is required of monitoring body mass in the presence of severe edema.
Body Composition↗
Multiple-organ failure. Generalized autodestructive inflammation?
As multiple-organ failure (MOF) has been generally associated with sepsis, the importance of bacterial sepsis was evaluated retrospectively in 55 trauma and 37 intra-abdominal-sepsis patients with MOF. The severity of MOF was graded, and an analysis was made of day of onset, incidence, severity, sequence, and mortality of organ failures. No difference was found between groups in sequence, severity, or mortality of organ failures. In contrast, bacterial sepsis was found in 65% of intra-abdominal-sepsis patients but only in 33% of trauma patients. It is concluded that sepsis is probably not the essential cause of MOF. Instead, an alternative hypothesis is presented involving massive activation of inflammatory mediators by severe tissue trauma or intra-abdominal sepsis, resulting in systemic damage to vascular endothelia, permeability edema, and impaired oxygen availability to the mitochondria despite adequate arterial oxygen transport.
Adolescent↗
Elevated pulmonary vascular resistance in patients dying from multiple organ failure.
Twenty-one patients with multiple organ failure were studied with hemodynamic monitoring. The five survivors were compared with the 16 nonsurvivors. Significant differences were found in the cardiac index (CI), the left ventricular stroke work index (LVSWI), and the pulmonary vascular resistance index (PVRI). The CI was higher in survivors (4.38 +/- 1.71) than in nonsurvivors (3.43 +/- 1.49). The LVSWI was also higher (43.0 +/- 16.8, 28.7 +/- 12.8) than in nonsurvivors (47.4 +/- 2.91). The PVRI was lower in survivors (168 +/- 122) than in nonsurvivors (474 +/- 291). It is postulated that the elevated PVRI in MOF is related to the adult respiratory distress syndrome.
Adult↗
Treatment of acute renal failure in patients with multiple organ failure by continuous spontaneous hemofiltration.
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Acute Kidney Injury↗
Multiple organ failure. Pathophysiology and potential future therapy.
Multiple organ failure (MOF) has reached epidemic proportions in most intensive care units and is fast becoming the most common cause of death in the surgical intensive care unit. Furthermore, in spite of the development of successive generations of new and more powerful antibiotics and increasing sophisticated techniques of organ support, our ability to salvage patients once MOF has become established has not appreciably improved over the last two decades. Clearly, new therapeutic strategies aimed at preventing or limiting the development of the physiologic abnormalities that induce organ failure are needed to improve survival in these critically ill patients. Based on our rapidly increasing knowledge of the mechanisms of MOF and the fruits of molecular biology, a number of new therapeutic approaches are in various stages of development. To effectively use these new therapeutic options as they become available, it is necessary to have a clear understanding of the pathophysiology of MOF. Thus, the goals of this review are to integrate the vast amount of new information on the basic biology of MOF and to focus special attention on the potential therapeutic consequences of these recent advances in our understanding of this complex and perplexing syndrome.
Bacterial Infections↗
[Case report: multiple organ failure following trauma].
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Adult↗
Muscle thickness, measured with ultrasound, may be an indicator of lean tissue wasting in multiple organ failure in the presence of edema.
Multiple organ failure (MOF) is accompanied by muscle wasting, but changes in body composition are frequently obscured by fluid retention (edema), mainly in superficial and visceral tissue. There is a need to assess body composition and changes in body composition in these circumstances independently of edema. A relation was sought between fat-free (lean tissue) mass [calculated from body weight and skinfold thicknesses and measured by using dual-energy X-ray absorptiometry (DXA)] and muscle thickness (measured using ultrasound at a variety of sites accessible in an unconscious supine subject) to determine which sites correlated best with lean body mass. The three best sites were midbiceps, midforearm anteriorly, and midthigh anteriorly: R2 for the simple sum of the three sites correlated with fat-free mass from skinfold thicknesses was 71.1%, and with lean tissue mass from DXA was 76.1%. Serial measurements of both muscle thickness and midupper-arm circumference in nine patients with MOF showed a complete dissociation; in all nine there was a significant negative correlation of muscle thickness with time (P < 0.05) but changes in arm circumference were random. Only one patient showed a significant negative correlation with time, seven showed no change, and one other showed a significant increase. The muscle thicknesses that correlate best with lean body mass are measured over the biceps, anterior forearm, and anterior thigh. Monitoring muscle thicknesses at these three sites identifies wasting in edematous patients as it is happening.
Absorptiometry, Photon↗
Inflammatory mediators, infection, sepsis, and multiple organ failure after severe trauma.
The relation of (multiple) organ failure (OF) to the release of inflammatory mediators and the incidence of infection and sepsis was studied prospectively in 100 patients with multiple trauma (injury severity score = 37). Sixteen patients died of OF, 47 patients survived OF, and 37 patients had no OF. Fifteen (24%) of the patients with OF showed no signs of infection. In patients with early onset of OF (n=45), infection followed with a lag of 2 or more days. In 16 (44%) of these patients, infection led to a deterioration in organ function. With late onset of OF (n=18), infection preceded OF in nine patients. Polymorphonuclear leukocyte-elastase, neopterin, C-reactive protein, lactate, antithrombin III, and phospholipase A discriminated significantly among the three outcome groups. Of all factors, only polymorphonuclear leukocyte-elastase showed a difference between patients with and without infection or sepsis, respectively. These data indicate that infection might not play a crucial role in the pathogenesis of posttraumatic OF in a substantial portion of patients with trauma. Early OF, especially, seems to be mainly influenced by the direct sequelae of tissue damage and shock (eg, the release of inflammatory mediators). Since infection and sepsis did not lead to an augmented release of mediators in patients with trauma, the role of both entities remains unclear.
Adult↗
Fatal outcome after polytrauma: multiple organ failure or cerebral damage?
To assess the relative importance of multiple organ failure (MOF) and cerebral damage on the mortality rate following trauma we analyzed retrospectively the records from 99 polytrauma patients admitted to a multidisciplinary European intensive care unit in a 2 year period. In all, 93% of the trauma was non-penetrating and 73% was the result of road accidents. 28 patients died giving an overall mortality of 28.3%. The cause of death was cerebral lesions in 19 patients, hemorrhagic shock in eight and multiple organ failure in one patient who had an injury severity score (ISS) of 13. Most deaths (78%) occurred within 24 h of admission, 15 of these were due to extensive cerebral lesions and seven due to hemorrhagic shock. A total of six deaths occurred after 24 h, four due to extensive cerebral lesions, one due to hemorrhagic shock and one due to multiple organ failure. In our experience, cerebral damage was a more common cause of death than MOF following multiple non-penetrating trauma.
Adolescent↗
Prognostic implications of hyperlactatemia, multiple organ failure, and systemic inflammatory response syndrome in patients with acetaminophen-induced acute liver failure.
OBJECTIVE: Hyperlactatemia has been suggested as a prognostic marker in acetaminophen-induced fulminant hepatic failure, and a modification of the King's College Hospital criteria to incorporate arterial lactate measurements has recently been proposed. The aims of the present study were to further evaluate arterial lactate as a prognostic marker in acetaminophen-induced fulminant hepatic failure and to analyze its relationship to known causes of hyperlactatemia such as multiple organ failure and inflammation. DESIGN: Data were collected early after admission and again at the time of onset of grade 3-4 hepatic encephalopathy from acetaminophen-induced fulminant hepatic failure. Multiple organ failure and inflammatory response were assessed by the sequential organ failure assessment (SOFA) score and manifestation of the severe inflammatory response syndrome (SIRS), respectively. SETTING: A specialized liver intensive care unit at a tertiary liver center. PATIENTS: One hundred and one consecutive patients with acetaminophen-induced fulminant hepatic failure and grade 3-4 hepatic encephalopathy. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Arterial lactate was higher in nonsurvivors than in survivors both early after admission (9.8 +/- 6.5 mmol/L vs. 5.2 +/- 4.2 mmol/L, p = .00004) and at the time of onset of hepatic encephalopathy (6.9 +/- 5.6 mmol/L vs. 3.2 +/- 2.0 mmol/L, p < .00001). At both time points, arterial lactate significantly correlated with SOFA score and the number of SIRS components fulfilled. Applying the lactate modification of the King's College Hospital criteria increased their sensitivity but reduced their specificity to <50%. CONCLUSIONS: The study confirmed arterial lactate as a prognostic marker in acetaminophen-induced fulminant hepatic failure. Arterial lactate correlated with SOFA score and with the number of SIRS components fulfilled. The lactate modification of the King's College Hospital criteria showed no obvious advantages over the existing selection criteria.
Acetaminophen↗
Multiple organ failure: is it disappearing?
The incidence of multiple organ failure (MOF) during the last decade has been reported variously as 2% to 25%, depending on the patient population examined. The mortality rate from this devastating complication ranges from 40% to 80%. Although the incidence has not changed during the last decade, it does not mean that there has been no progress. Tertiary centers are now seeing trauma and nontrauma patients who have more significant underlying disease and injuries. Likewise, a higher percentage of our trauma patients are now referred from outside institutions where there may not be the facilities to administer the complex, rapid resuscitation these patients require. Prevention of MOF remains its best treatment. Rapid, adequate volume resuscitation, adequate nutrition, appropriate antibiotic usage, and aggressive pulmonary management are important for preventing the downward physiologic spiral that leads to MOF and death. Once MOF has occurred, it is not clear that these same measures are as effective in altering outcome.
APACHE↗
Prevention of multiple organ failure.
Physicians are still largely ignorant of the underlying biology of SIRS and multiple organ failure. Nonetheless, strategies to prevent multiple organ failure are possible. These include aggressive resuscitation of hemodynamically unstable patients, careful assessment to avoid missing clinically significant injuries, early operative treatment of all possible injuries with debridement of all nonviable tissue, early nutritional support, and the early diagnosis and prompt treatment of infectious complications. Treatment of patients with established multiple organ failure is still largely supportive and has made little impact on the patient mortality rate over the past 20 years. Future treatment strategies must focus on multimodality combination therapy aimed at specifically suppressing excessive activation of the inflammatory response while preserving immune competence and normal antimicrobial defenses. Only then are physicians likely to begin to see a reduction in the mortality rate of patients with this complex and challenging condition.
Combined Modality Therapy↗