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PubMed1998

Pentoxifylline decreases the incidence of multiple organ failure in patients after major cardio-thoracic surgery.

We assessed the safety and efficacy of intravenous pentoxifylline [3,7-dimethyl-1-(5-oxohexyl)-xanthine] in patients at risk for developing multiple organ failure after major cardio-thoracic surgery in a single-center, randomized, placebo-controlled study. Of 816 consecutive patients who underwent major cardio-thoracic surgery, 40 who had Acute Physiology and Chronic Health Evaluation II score values > or = 19 at the first postoperative day after the surgery were included. Patients were randomized to receive either placebo (control; n = 25) or intravenous pentoxifylline treatment (pentoxifylline; n = 15) at a dosage of 1.5 mg/kg/h as an adjunct to standard supportive therapy. Main outcome measurements were duration of required ventilator support, intensive care unit stay, and incidence of renal failure. Thirty-seven patients were eligible for evaluation. No significant adverse events related to pentoxifylline treatment were observed. The duration of mechanical ventilation was significantly greater for control patients (8.3 +/- 3.1 days) compared with pentoxifylline-treated patients (3.1 +/- .9 days; p < .05). Patients treated with pentoxifylline experienced fewer days on hemofiltration (1.2 +/- .8 vs. 6.8 +/- 3.3; p < .05) and a shorter intensive care unit stay (5.2 +/- 1.1 vs. 11.4 +/- 3.1 days). There were no intergroup differences in mortality. Mortality was 33% in the pentoxifylline group and 36% among control group patients. In conclusion, supplemental pentoxifylline treatment may decrease the incidence of multiple organ failure in patients at risk of systemic inflammatory response syndrome after cardiac surgery. Additional studies are required to determine the validity of the observed effects.

APACHE↗
PubMedDate not supplied

Multiple organ failure in a kidney transplant patient receiving both colchicine and cyclosporine.

Colchicine is a relatively safe and effective medication when given at appropriate doses to patients with normal kidney and liver function. A clinical picture of multiple organ failure has been described in cases of colchicine poisoning and in kidney graft recipients treated with usual doses of colchicine during cyclosporine therapy. We report a case of multiple organ failure in a renal transplant patient who received appropriate doses of colchicine in combination with cyclosporine therapy. Interaction between colchicine and cyclosporine is postulated but boosting of CSA toxicity was excluded because of the low CSA blood through levels before and throughout the episode, in the presence of relatively stable renal function and for the prompt CSA withdrawal. Mechanism of toxicity and modulation of the P-glycoprotein by cyclosporine are reviewed. Although the proscription of the drug in cyclosporine-treated patients is not justified, caution is recommended in prescribing colchicine to patients receiving cyclosporine therapy, particularly in the presence of suboptimal kidney graft function.

Colchicine↗
PubMed1997

[Anesthetic and perioperative management of a neonatal vein of Galen malformation with multiple organ failure].

We treated a neonate in intractable cardiac failure due to a vein of Galen malformation. She manifested severe multiple organ failure. Perioperative problems are cardiac failure, respiratory failure, renal as well as hepatic dysfunction, and coagulopathy. Direct clipping of the feeding arteries improved her symptoms. Anesthetic problems encountered in this patient are massive bleeding and drastic circulatory changes while clipping the feeding arteries, increased intracranial pressure and brain ischemia, and other underlying complications; hepatic and renal dysfunction, respiratory failure and coagulopathy.

Anesthesia, General↗
PubMed2002

Coagulation/fibrinolysis abnormality and vascular endothelial damage in the pathogenesis of thrombocytopenic multiple organ failure.

OBJECTIVE: Until recently, attention has been directed to disseminated intravascular coagulation as a cause of multiple organ failure (MOF). On the other hand, it has now become clear that humoral mediators play important roles in the pathogenesis of MOF. Therefore, we performed the present study in patients with thrombocytopenic MOF to investigate the relationship between various humoral mediators and vascular endothelial damage reported to be triggered by such humoral mediators in the pathogenesis of MOF. DESIGN: A retrospective clinical study. SETTING: Intensive care unit of a university hospital. PATIENTS: The study included 18 thrombocytopenic patients whose conditions progressed to septic MOF (MOF group) and 20 others who did not progress to MOF (non-MOF group). The MOF group and non-MOF group were also presented with infection and with platelet counts of <100,000/mm3. MEASUREMENTS AND MAIN RESULTS: The MOF group had fibrinolysis abnormality, as indicated by increased plasminogen activator inhibitor-1 level. On the other hand, the MOF group had increased polymorphonuclear elastase and polymorphonuclear-mediated fibrinogen degradation product levels with consequent prolonged elevation of thrombomodulin. In addition, both polymorphonuclear elastase and polymorphonuclear-fibrinogen degradation products were significantly positively correlated with thrombomodulin in the MOF group, but no such positive correlation was observed between interleukin-6 or plasminogen activator inhibitor-1 and thrombomodulin. In the non-MOF group, on the other hand, thrombomodulin exhibited no significant positive correlation with polymorphonuclear elastase, polymorphonuclear-fibrinogen degradation products, interleukin-6, or plasminogen activator inhibitor-1. CONCLUSIONS: Our study provided evidence that vascular endothelial damage was the primary cause of organ failures in patients with thrombocytopenic MOF and that humoral mediators played a major role in the development of vascular endothelial damage in such patients. These results suggest that it is important to treat thrombocytopenic MOF as a condition of vascular endothelial damage, with weight placed on countermeasures against disorders of humoral mediators.

Adult↗
PubMed1999

Age of transfused blood is an independent risk factor for postinjury multiple organ failure.

BACKGROUND: Blood transfusion has repeatedly been demonstrated to be an independent risk factor for postinjury multiple organ failure (MOF). Previously believed to represent a surrogate for shock, packed red blood cell (PRBC) transfusion has recently been shown to result in neutrophil priming and pulmonary endothelial cell activation. We have previously observed that the generation of inflammatory mediators is related to the length of PRBC unit storage. The purpose of this study was to determine if age of transfused PRBC is a risk factor for the development of postinjury MOF. METHODS: Using our prospective database of trauma patients at risk for developing MOF, we identified patients who developed MOF (MOF+) and received 6 to 20 units of PRBCs in the first 12 hours following injury. A similar cohort of patients, matched for ISS and transfusion requirement, who did not develop MOF (MOF-) were also identified. The age of each unit of PRBC transfused in the first 6 hours was determined. Multiple logistic regression was performed to determine if age of transfused blood is an independent risk factor. RESULTS: Sixty-three patients were identified, 23 of whom were MOF+. There was no difference in ISS and transfusion requirement between MOF+ and MOF- groups. MOF+ patients, however, were significantly older (46+/-4.7 years versus 33+/-2.3 years). Moreover, mean age of transfused blood was greater in the MOF+ patients (30.5+/-1.6 days versus 24+/-0.5 days). Similarly, the mean number of units older than 14 and 21 days old were greater in the MOF+ patients. Multivariate analysis identified mean age of blood, number of units older than 14 days, and number of units older than 21 days as independent risk factors for MOF. CONCLUSION: The age of transfused PRBCs transfused in the first 6 hours is an independent risk factor for postinjury MOF. This suggests that current blood bank processing and storage technique should be reexamined. Moreover, fresh blood may be more appropriate for the initial resuscitation of trauma patients requiring transfusion.

Adult↗
PubMed2003

Clinical and laboratory effects of recombinant human activated protein C in the treatment of a patient with sepsis-induced multiple organ failure.

OBJECTIVES: To evaluate clinical and laboratory effects of the administration of recombinant human activated protein C (rhAPC) in the treatment of a 25-year-old patient with septic shock and multiple organ failure secondary to perinephritic abscesses. INTERVENTIONS: Intravenous administration of rhAPC-or drotrecogin alfa (activated)-(24 mcg/kg/h) for a total of 80 h as an adjunct to antimicrobial therapy, mechanical ventilation, hemodynamic support, hemodiafiltration and surgical intervention. MEASUREMENTS AND MAIN RESULTS: The administration of rhAPC was associated with a rapid recovery of the patient's clinical condition reflected by decreasing Sepsis-related Organ Failure Assessment (SOFA) scores. Laboratory parameters monitoring inflammation and coagulopathy improved during the treatment. No drug-related adverse events were noted. CONCLUSIONS: RhAPC has been observed to have anticoagulant, anti-inflammatory and profibrinolytic properties in vitro and in vivo. This report describes the effects of rhAPC administration on standard laboratory parameters indicating that no single laboratory parameter exists that is capable of monitoring the effects of rhAPC on the coagulation cascade and the clinical course of sepsis. This description of a patient suffering from sepsis-induced multiple organ failure may illustrate a possible beneficial effect of rhAPC on the course of coagulopathy and systemic inflammatory response and provides evidence for rhAPC complementing standard intensive care therapy in severe sepsis.

Adult↗
PubMed1991

[Rat multiple organ failure model caused by zymosan injections: a pathomorphological study].

We succeeded in developing a Wistar rat multiple organ failure (MOF) model by intraperitoneal injection of Zymosan. 80 rats were divided into the experimental and control groups. On alternative days (1, 2, 4-5 day), rats were killed after their blood specimens were examined. In the experimental group, changes in PaO2, GPT and Cr were apparently significant as compared with those in the control group. Symptoms included lethargy, hyporeaction, and alimentary tract hemorrhage. By combining function with pathology changes at the cellular and subcellular level and histochemical aspects, we listed MOF pathological features for the diagnosis of DIC at its different stages.

Animals↗
PubMed1988

Multiple organ failure without sepsis following surgical treatment of advanced gastric carcinoma.

Two patients, a 58-year-old male and a 41-year-old female, who had poorly differentiated adenocarcinoma with signet ring cells of the stomach, developed progressive multiple organ failure following their surgical treatment, even though they did not have any direct surgical complications. Their abdominal explorations revealed primary gastric tumors with deep infiltration and metastases to the regional lymph nodes. Their clinical courses were characterized by acute renal failure and respiratory distress associated with disseminated intravascular coagulation. Histopathological examination at autopsy revealed diffuse cortical necrosis of the kidneys and marked congestion, edema, and hemorrhage with or without alveolar fibrosis of the lungs. Fibrin thrombi in the lesions of the kidneys and lungs strongly suggested the existence of disseminated intravascular coagulation. It is likely that the widely spreading cancer cells themselves produced the subclinical background for disseminated intravascular coagulation, which appeared to play an important role in the development of the multiple organ failure.

Adenocarcinoma, Mucinous↗
PubMed1991

Energy expenditure and outcome in patients with multiple organ failure following abdominal surgery.

A possible relationship between hypermetabolism (energy expenditure expressed as percentage above the estimated basal metabolic rate) and clinical outcome was investigated in 29 artificially ventilated patients with infection and multiple organ failure following abdominal surgery. The average energy expenditure and hypermetabolism were 126 +/- 19 kJ (30 +/- 5 kcal)/kg/24 h and 36 +/- 12%, respectively. Survivors of the intensive care period (n = 20) had a 15% higher hypermetabolism (41 +/- 11 vs 26 +/- 8%, p less than 0.01) than patients who died in the intensive care unit (n = 9). Six of the patients died after intensive care. On comparing hypermetabolism in survivors (n = 14) and non-survivors (n = 15) of the period of hospitalization, no significant difference was discernible. The results demonstrate that patients with multiple organ failure have a moderate hypermetabolism and suggest that the hypermetabolism is comparatively reduced in patients with a fatal outcome during intensive care.

Aged↗
PubMed1994

Elevated levels of soluble ICAM-1 correlate with the development of multiple organ failure in severely injured trauma patients.

Serum levels of interleukin-6, interleukin-8, the soluble receptor for tumor necrosis factor (sTNFr), and the soluble receptor for intercellular adhesion molecule-1 (sICAM-1) were measured serially in a series of 13 severely injured trauma patients to determine if any of these elements of the inflammatory response are predictive of multiple organ failure (MOF). Six of the 13 patients developed MOF as determined by a MOF scoring system. At the completion of resuscitation (when oxygen delivery and consumption were maximized) sICAM-1 levels were significantly higher in MOF patients before the development of clinical evidence of organ failure (700 +/- 67 ng/mL) compared with non-MOF patients (302 +/- 18 ng/mL). There was a significant correlation between the absolute level of sICAM-1 at the time of resuscitation and the severity of subsequent MOF. This finding suggests that leukocyte-endothelial cell interactions are upregulated immediately after injury and may be implicated in the end-organ injury that leads to MOF.

Adult↗
PubMed1998

Mechanism of gram-positive shock: identification of peptidoglycan and lipoteichoic acid moieties essential in the induction of nitric oxide synthase, shock, and multiple organ failure.

The incidence of septic shock caused by gram-positive bacteria has risen markedly in the last few years. It is largely unclear how gram-positive bacteria (which do not contain endotoxin) cause shock and multiple organ failure. We have discovered recently that two cell wall fragments of the pathogenic gram-positive bacterium Staphylococcus aureus, lipoteichoic acid (LTA) and peptidoglycan (PepG), synergize to cause the induction of nitric oxide (NO) formation, shock, and organ injury in the rat. We report here that a specific fragment of PepG, N-acetylglucosamine-beta-[1--> 4]-N-acetylmuramyl-L-alanine-D-isoglutamine, is the moiety within the PepG polymer responsible for the synergism with LTA (or the cytokine interferon gamma) to induce NO formation in the murine macrophage cell line J774.2. However, this moiety is also present in the PepG of the nonpathogenic bacterium Bacillus subtilis. We have discovered subsequently that S. aureus LTA synergizes with PepG from either bacterium to cause enhanced NO formation, shock, and organ injury in the rat, whereas the LTA from B. subtilis does not synergize with PepG of either bacterium. Thus, we propose that the structure of LTA determines the ability of a particular bacterium to cause shock and multiple organ failure (pathogenicity), while PepG acts to amplify any response induced by LTA.

Animals↗
PubMed1988

[Metabolic abnormalities and nutritional management in postoperative multiple organ failure].

Despite its importance, very little has been known on metabolic abnormalities in the patients with postoperative multiple organ failure (POMOF). The present study was undertaken to investigate the metabolic abnormalities and to establish effective nutritional management on these patients. Systemic energy metabolism and hepatocellular mitochondrial function were studied with indirect calorimetry and arterial ketone body ratio measurements on 30 POMOF patients treated between 1984 and 1985. The POMOF patients were hypermetabolic and their hepatic mitochondrial function was impaired. Their caloric intake was depleted for the limitation in administrable water volume due to renal failure. Some of them could not utilize exogenous glucose given by total parenteral nutrition (TPN). To overcome these problems, on 26 POMOF patients treated between 1986 and 1987 continuous hemofiltration (CHF) was applied to remove excess water and ATP-Mg was administered to improve hepatic mitochondrial function during TPN. The sufficiency rate of energy intake (caloric intake/energy expenditure) was improved from 73.3 +/- 14.7% to 92.0 +/- 8.1% with simultaneous CHF and the hepatic mitochondrial function was also improved with ATP-Mg resulting in better utilization of exogenous glucose. These results indicate that CHF and ATP-Mg administration are effective adjunctive treatments in the nutritional management for POMOF.

Adenosine Triphosphate↗
PubMed2004

Heat shock protein 72 and apoptosis indicate cardiac decompensation during early multiple organ failure in sheep.

OBJECTIVE: Inducible heat shock protein 72 (HSP 72) preserves myocardial function and prevents apoptosis. We investigated the expression and localization of HSP 72 and apoptosis in our previously described new model of multiple organ failure. DESIGN: Eighteen adult-instrumented sheep and three healthy controls were randomly assigned to one of three groups: (a) norfenefrine-masked hypovolemia plus endotoxemia (NMH+ENDO); (b) norfenefrine-masked hypovolemia without endotoxemia (NMH); (c) recurrent endotoxemia during normovolemia (ENDO); and (d) normovolemia without endotoxemia (CONTROLS). MEASUREMENTS AND RESULTS: Hearts were analyzed by light microscopy, Western blots, immunohistochemistry, and TUNEL staining. HSP 72 expression was approximately threefold increased in NMH+ENDO compared with the other groups ( p<0.05) and was localized mainly in left ventricular cardiomyocytes. HSP 72 was elevated in animals with norfenefrine-refractory shock compared to survivors ( p=0.015). TUNEL-positive cells in the left ventricle were significantly elevated in the NMH+ENDO group ( p=0.05) and correlated with HSP 72 expression (r=0.51, p=0.018). HSP 72 correlated positively with heart rate (r=0.76, p<0.0001), the prefinal hourly dose of norfenefrine (r=0.88, p<0.0001), and negatively with left ventricular stroke work index (r=-0.52, p=0.028). Double staining revealed TUNEL-positive cells with and without HSP 72 expression. Micronecroses were only detectable in NMH and NMH+ENDO without intergroup difference or correlations with hemodynamics. CONCLUSION: HSP 72 overexpression and apoptosis, but not necrosis, indicate cardiovascular decompensation and poor outcome during early multiple organ failure.

Animals↗
PubMed1996

Nitrite/nitrate (NOx) and sFas antigen levels in patients with multiple organ failure.

We assessed the plasma levels of nitrite/nitrate (NOx) and soluble Fas antigen (sFas) in patients with multiple organ failure (MOF). The NOx levels showed high levels in MOF patients with sepsis and without infection. A significant difference was not seen between the MOF patients complicated by sepsis and uncomplicated by infection, although the NOx levels in the former group tended to be higher. There was a significant correlation between NOx levels and sFas levels in MOF patients. Both sFas and NOx levels were high during MOF, and rapidly decreased when MOF was relieved. These findings suggest that sFas and NOx contribute to the development of MOF.

Humans↗
PubMed2005

Apoptosis as an early event in the development of multiple organ failure?

We have recently developed a simple method of plasma free DNA detection, which enables us to distinguish between apoptotic and genomic (necrotic) DNA. After applying this method to the critically ill, we revealed apoptotic DNA on the day of admission to be higher than later when multiple-organ failure developed. Moreover, apoptotic DNA contributed to total plasma DNA much more than DNA from necrotic cells and its increase predicted future development of multiple-organ failure and death.

Apoptosis↗
PubMed1997

Comparison of acute physiology and chronic health evaluation III and II for prediction of mortality in multiple organ failure patients treated by plasma exchange.

This study examined the efficacy of a different scoring system for multiple organ failure (MOF) patients treated by plasma exchange (PE). Twenty-five patients with MOF resulting from fulminant hepatitis who had been treated by PE for a total number of 91 PEs in a consecutive period of 22 months were included in our study. Data were collected from each patient to compute acute physiology and chronic health evaluation (APACHE) II and APACHE (AP) III scores. The sensitivity, specificity, and correct prediction of outcomes were measured. The correct prediction of outcomes was 86.5%in AP III and 77.5% in AP II. For the prediction of patient mortality, the AP III system seems to be more reliable than AP II.

APACHE↗
PubMed1991

The cell in shock: the origin of multiple organ failure.

The immediate organ damage seen after multiple trauma and in shock is a typical example of non-bacterial inflammation triggered by activation of various mediators of both the humoral and cellular systems. Anaphylatoxins and the low-flow syndrome during the shock phase account for increased PMN* margination, which in turn causes pulmonary leukostasis and may provoke massive mediator release by PMN (oxygen radicals, proteinases, eicosanoids, PAF etc). This probably leads to severe endothelial cell damage, especially in the lung. Adherence of PMN to the endothelium appears to create the micro-environment where high concentrations of proteolytic enzymes and reactive oxygen radicals exert a deleterious effect on the cell membrane. Endothelial cell membrane injury leads to increased vascular permeability and cell edema. The development of the 'organ in shock' may require a few hours and initially cause minor or no functional impairment at all. Only when shock is severe is there early organ failure, which in this stage may still be an expression of non-bacterial inflammation. Numerous studies have reported the existence of shock-induced cardiodepressant substances in association with various forms of circulatory shock. We have determined a net negative inotropic effect of the low-molecular-weight plasma fraction in severe hypovolemic-traumatic shock and have isolated a cardiodepressant factor (CDF), which by blockade of the calcium inward current has a negative inotropic a chronotropic effect. The intestine as a shock organ appears to range first among the organs involved. The translocation of bacteria from the intestinal tract, the 'intestine in shock' represents the trigger reaction that eventually leads from the 'organ in shock', early organ failure to late (septic) organ failure. Here the most prominent factor is endotoxin (LPS) as a basic mediator of gram-negative bacteria, which also triggers the activation of humoral and cellular systems. The posttraumatic hyperdynamic phase commonly starts on days 3-5 and is mainly caused by bacteremia and/or endotoxemia. Macrophages have a major impact on the late phase of organ failure. At present, the most prominent cellular mediator of the lethal effect of endotoxin is thought to be cachectin, which is identical with the tumor necrotising factor (TNF). TNF is secreted by monocytes/macrophages (MO/MA) in response to LPS. Via macrophage derived cytokines and by LPS there is activation of endothelial cells, with increased adhesiveness for PMN. Both due to this increased adhesiveness and the presence of LPS and cytokines, PMN undergo massive activation, which causes mediator release and tissue damage.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗