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PubMed1996

Reduction of circulating prostaglandin E2 level by antiserum against core lipopolysaccharide in a rabbit model of multiple organ failure.

OBJECTIVE: To determine the potential role of prostaglandin E2 (PGE2) in the development of multiple organ dysfunction or failure (MOF), the possible effects of antiserum directed against Re chemotype lipopolysaccharide (LPS, from Re mutant of Escherichia coli F515) on circulating PGE2 level and survival rate, and whether there is an elevation in the plasma LPS concentration that could account for the induction of arachidonic acid metabolite in a rabbit model of MOF caused by acute hypovolemic insult. DESIGN, MATERIALS, AND METHODS: An animal model of MOF in rabbits, engendered by feeding live Escherichia coli O111:B4 before hemorrhagic shock (35-40 mm Hg for 60 min), was used in the present study. Re-LPS antiserum was given intravenously in the treatment group at the onset of hemorrhage and 4 hours after resuscitation. The animals that received equal volumes of normal rabbit serum and antiserum served as the control group. MEASUREMENTS AND MAIN RESULTS: The circulating PGE2 level was not increased at the end of shock (p > 0.05), but it was found to be significantly elevated 24 hours after hemorrhage and resuscitation in both groups. However, Re-LPS antiserum administration markedly decreased peak PGE2 level (p < 0.05) and attenuated multiple organ damage caused by acute insult. Concomitantly, there were also lower LPS concentrations in the treatment group as compared with the control group (p < 0.05-0.01). The survival rate was significantly increased in antiserum-treated rabbits 96 hours postinjury (treatment vs. control: 58.0% vs. 11.1%, p < 0.01). CONCLUSIONS: The results suggest that an excessive generation and release of PGE2 may be involved in the pathogenesis of immunosuppression and MOF following hemorrhage and resuscitation. Re-LPS antiserum has an inhibitory effect on overproduction of circulating PGE2 and the ability to improve survival with MOF. Gut-derived endotoxemia, bacterial translocation, or both, could account, at least in part, for the PGE2 formation and release in animals response to acute hypovolemic insult.

Animals↗
PubMed2003

Possible role of increased oxidant stress in multiple organ failure after systemic inflammatory response syndrome.

OBJECTIVE: Host response to infection and other forms of tissue injury have been termed systemic inflammatory response syndrome (SIRS). This inflammatory response can frequently be accompanied by oxidative injury in one or more organ systems in the body. The objective of this report was to clarify the possible role of oxidative stress in the development of multiple organ failure (MOF) in patients with SIRS. DESIGN: Prospective clinical study. SETTING: Intensive care unit in a university hospital. PATIENTS: A total of 214 consecutive patients (mean age, 57.1 +/- 17.4 yrs; range, 13 to 84 yrs; 148 men and 66 women). At the time of admission, 139 patients fulfilled the clinical criteria for SIRS. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: We measured plasma concentrations of thiobarbituric acid reactant substances (TBARS), as an index of oxidative stress, every day from the point of admission to the intensive care unit until discharge or death. Furthermore, all variables of the SIRS score and the Sequential Organ Failure Assessment score were collected every day. At the time of admission, plasma TBARS concentrations in SIRS patients with MOF were significantly higher than those in SIRS patients without MOF (2.3 +/- 0.9 vs. 1.9 +/- 0.6 nmol/mL, p <.01), and there was a significant correlation between plasma TBARS concentration and Sequential Organ Failure Assessment score (r2 =.18, p <.001). Furthermore, the duration of SIRS persistence was significantly associated with the percentage increase in plasma TBARS concentration during SIRS persistence in those patients in whom the duration of SIRS was confirmed (r2 =.73, p <.001). The duration of SIRS was significantly higher in patients who developed MOF than in patients who did not develop MOF (6.9 vs. 3.2 days, p <.001). The percentage increase in plasma TBARS concentration during SIRS was also significantly higher in patients who developed MOF than in patients who did not develop MOF (57.1% vs. 15.8%, p <.001). CONCLUSIONS: It can be concluded that processes of oxidative stress in connection with continued SIRS may promote the development of MOF.

Adolescent↗
PubMed2000

Multiple organ failure--the discrepancy between our scientific knowledge and understanding and the management of our patients.

The excitement of molecular biology and of genetic knowledge and their possibilities must be balanced against our limitations in using this information for the care of our patients. There is a great discrepancy between what we know and what we can do. There are many reasons for this. A major one is that science must simplify/reduce the variables in experimentation and then generalize in terms of a specific factor or effect, whereas patients are complex with variables that we do not yet understand completely. This powerful science is now teaching us about the genetic diversity in both susceptibility and outcome of disease, and the diversity in life experiences and antigen exposures. Clinicians have tried to lump together and treat in a similar way many diverse human diseases. This has not worked well. Pancreatitis and perforated diverticulitis both produce inflammation and sepsis, but they are different processes and may both lead to multiple organ failure. This lumping together has contributed to the failure of so-called magic bullets. There are new contributors to organ damage. Gender, lifestyle and prior disease differences also complicate the care of patients. Despite this, we are slowly and gradually improving the care of our surgical patients by careful pre-, intra- and postoperative support and better, simpler and safer operations.

Animals↗
PubMed2005

Heat stroke with multiple organ failure treated with cold hemodialysis and cold continuous hemodiafiltration: a case report.

A 23-year-old comatose man was presented in the emergency room. He had been working inside a building under construction on a hot summer's day. His core body temperature was 42.1 degrees C and he was diagnosed with heat stroke. Urgent cooling procedures, including applying cold vapor to the patient's skin, a gastric lavage with cold water and an intravenous cold saline infusion, were not completely successful and his body temperature remained above 40 degrees C. Because his high temperature was refractory to conventional cooling procedures and we suspected that acute renal failure (ARF) by rhabdomyolysis would develop, we applied hemodialysis (HD) using cold dialysate (initially 30 degrees C and later 35 degrees C), followed by continuous hemodiafiltration (CHDF) with cold dialysate (35 degrees C) at a high flow rate of 18,000 mL per hour. The patient's body temperature fell below 38.0 degrees C within 3 h and was kept below 38.0 degrees C. Continuous hemodiafiltration was continued for one week. During the first week, the patient suffered from multiple organ failure (MOF) involving renal failure, as well as the failure of heart, liver, lung, and central nervous systems. Disseminated intravascular coagulation also developed. However, by virtue of cold CHDF, he almost recovered 3 weeks after the onset, except for remaining mild liver and renal dysfunction. In severe heat stroke, cold HD and high flow, cold CHDF should be a therapeutic choice for cooling and treatment of MOF. Considering mild liver and renal dysfunction still remained, this case suggested these procedures should be initiated at the very beginning of the treatment of severe heat stroke.

Adult↗
PubMed2004

[Sepsis and multiple organ failure after BCG instillation in bladder cancer].

Local Bacillus Calmette-Guerin (BCG) immunotherapy is an effective and widely used treatment for superficial bladder carcino-ma. Local side effects are frequent, where-as systemic side effects are rare, but more serious. Systemic BCG infection as a life-threatening complication of intravesical BCG instillation should be suspected in any patient who presents with persistent fever after BCG instillation for bladder cancer.A 62-year-old patient had been treated with 6 intravesical BCG instillations for recurrent, multifocal bladder carcinoma.4 weeks after the last instillation, he presented with fever, malaise and scleral icterus. Laboratory tests revealed abnormal li-ver function tests, panzytopenia and signs of coagulation disorder. Bone marrow biopsy and liver biopsy showed non-caseating granulomas. Systemic BCG infection was suspected and antituberculous therapy combined with steroids was started. The patient developed severe sepsis and suffered from multiple organ failure. Despite partial improvement, the course was complicated by intracranial sinus thrombosis, and the patient died two month after admission.

Adjuvants, Immunologic↗
PubMed1993

Fish oil increases the release of tumour necrosis factor and interleukin-6, and has no effect on the incidence of multiple organ failure in rats with peritonitis.

OBJECTIVE: To find out if fish oil given intraperitoneally would cause a reduction in the release of tumour necrosis factor and interleukin-6 in abdominal exudate and blood (experiment A), and if it reduces the incidence of organ failure in rats with peritonitis (experiment B). DESIGN: Laboratory experiment. SETTING: University animal laboratory. MATERIAL: Thirty-six selectively decontaminated rats in each experiment. INTERVENTIONS: All rats were pretreated with 2 ml fish oil, lecithin, or saline, intraperitoneally for one or six weeks before intraperitoneal injection of zymosan. Experiment A: Samples of abdominal exudate and plasma were taken regularly for 24 hours after the zymosan had been given. Experiment B: Clinical, biochemical, and histological variables were measured over a 12-day period after the zymosan had been given. MAIN OUTCOME MEASURES: Experiment A: Concentrations of tumour necrosis factor and interleukin-6 in abdominal exudate and plasma. Experiment B: Incidence of multiple organ failure. RESULTS: Experiment A: Concentrations of tumour necrosis factor and interleukin-6 in abdominal exudate and plasma were significantly higher in rats pretreated with fish oil, compared with control rats. This effect was more pronounced after six weeks of pretreatment. Experiment B: There were no significant differences between the groups for any variable. CONCLUSION: Fish oil given intraperitoneally increased rather than reduced local and systemic release of tumour necrosis factor and interleukin-6, and did not reduce the incidence of organ failure in rats with sterile peritonitis.

Animals↗
PubMed1996

[An investigation on the changes of coagulation and fibrinolytic system in intensive infection with multiple organs failure].

An investigation was made for the significance of changes of coagulation and fibronolytic system in intensive infection with multiple system organ failure (MSOF). In 68 cases with various degrees of infection, hematological examinations, including estimation of PT, APTT, Fg, Fn and D-Dimer, activation of coagulation factor II, VII, X, XII (F II, F VII, F X, F XII), AT-III, PLG, alpha(2)-AP, t-PA and count of platelets were carried out. The results were as follows: In intensive infection with MSOF, PT and APTT increased significantly; activity of F II, F VII, F X and F XII decreased significantly platelet count and Fn decreased markedly; concentration of Fg and D-Dimer increased significantly; activity of PAI increased markedly; activity of t-PA and alpha(2)-AP decreased slightly. The incidence of MSOF not combined with DIC was 38.5%, but that combined with DIC was 79.7% (P < 0.01). It is suggested that DIC is the most important factor in the disorder of coagulation and fibrinolytic system. It play an important role in the pathogenesis and development of MSOF.

Adult↗
PubMed2004

[Sepsis and multiple organ failure after BCG-instillation for bladder cancer].

Local Bacillus Calmette-Guérin (BCG) immunotherapy is an effective and widely used treatment for superficial bladder carcinoma. Local side effects are frequent, whereas systemic side effects are rare, but more serious. Systemic BCG infection as a life-threatening complication of intravesical BCG instillation should be suspected in any patient who presents with persistent fever after BCG instillation for bladder cancer. A 62-year-old patient had been treated with 6 intravesical BCG instillations for recurrent, multifocal bladder carcinoma. 4 weeks after the last instillation, he presented with fever, malaise and scleral icterus. Laboratory tests revealed abnormal liver function tests, panzytopenia and signs of coagulation disorder. Bone marrow biopsy and liver biopsy showed noncaseating granulomas. Systemic BCG infection was suspected and antituberculous therapy combined with steroids was started. The patient developed severe sepsis and suffered from multiple organ failure. Despite partial improvement, the course was complicated by intracranial sinus thrombosis, and the patient died two month after admission.

Adjuvants, Immunologic↗
PubMed1995

The cell wall components peptidoglycan and lipoteichoic acid from Staphylococcus aureus act in synergy to cause shock and multiple organ failure.

Although the incidence of Gram-positive sepsis has risen strongly, it is unclear how Gram-positive organisms (without endotoxin) initiate septic shock. We investigated whether two cell wall components from Staphylococcus aureus, peptidoglycan (PepG) and lipoteichoic acid (LTA), can induce the inflammatory response and multiple organ dysfunction syndrome (MODS) associated with septic shock caused by Gram-positive organisms. In cultured macrophages, LTA (10 micrograms/ml), but not PepG (100 micrograms/ml), induces the release of nitric oxide measured as nitrite. PepG, however, caused a 4-fold increase in the production of nitrite elicited by LTA. Furthermore, PepG antibodies inhibited the release of nitrite elicited by killed S. aureus. Administration of both PepG (10 mg/kg; i.v.) and LTA (3 mg/kg; i.v.) in anesthetized rats resulted in the release of tumor necrosis factor alpha and interferon gamma and MODS, as indicated by a decrease in arterial oxygen pressure (lung) and an increase in plasma concentrations of bilirubin and alanine aminotransferase (liver), creatinine and urea (kidney), lipase (pancreas), and creatine kinase (heart or skeletal muscle). There was also the expression of inducible nitric oxide synthase in these organs, circulatory failure, and 50% mortality. These effects were not observed after administration of PepG or LTA alone. Even a high dose of LTA (10 mg/kg) causes only circulatory failure but no MODS. Thus, our results demonstrate that the two bacterial wall components, PepG and LTA, work together to cause systemic inflammation and multiple systems failure associated with Gram-positive organisms.

Animals↗
PubMed1997

Reduced PAF-acetylhydrolase activity is associated with postinjury multiple organ failure.

Our basic laboratory work has identified the postischemic gut as a source of platelet-activating factor (PAF), which primes circulating neutrophils for the production of reactive oxygen metabolites (ROMs) leading to distant organ injury. Circulating PAF-acetylhydrolase (PAF-AH) hydrolyzes PAF to lyso-PAF. Recently, ROMs have been shown to rapidly and irreversibly inactivate human PAF-AH. Consequently, our study hypothesis was that reduced levels of PAF-AH in severely injured patients would be associated with the development of multiple organ failure (MOF). Over a 16 mo period, 26 patients at known risk for MOF (Injury Severity Score (ISS) > or = 25 or an ISS > 15 with > or = 6 U of blood transfused within the first 6 h) had blood sampled on postinjury days 0, 1, 2, 3, and 5. PAF-AH activity was assessed by measuring the percentage of 3H-labeled PAF hydrolyzed. MOF was defined by a standard score. The mean age of the 26 study patients was 34 +/- 2 yr; 19 (73%) were male. The injury mechanism was blunt in 18 (69%), and the mean ISS was 31 +/- 2. Eight patients (31%) developed MOF. In the MOF patients, plasma PAF-AH activity was significantly lower on the day of injury and remained depressed throughout the ensuing 5 days compared with the non-MOF patients. Reduced PAF-AH activity is associated with the development of postinjury MOF. With the recent molecular cloning of human plasma PAF-AH, repleting this circulating, anti-inflammatory enzyme may represent useful therapy for these high risk patients.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1992

Multiple organ failure syndrome.

Tissue injury, whether from infection, blood or volume loss, trauma, or inflammation such as pancreatitis, induces local and systemic responses. The systemic responses include shock, reperfusion, systemic inflammation (hypermetabolism) with primary organ dysfunction, and secondary organ dysfunction that either becomes progressive and leads to death or from which the patient recovers and enters into a period of prolonged rehabilitation. Each of these responses has its pathogenesis and treatments that are appropriate and effective. The research indicates that the responses may contribute to the development of cell and organ injury and to progressive multiple organ failure syndrome and death, particularly in the case of the systemic inflammatory response. Current therapy is designed to rapidly remove the cause of injury, resuscitate the microcirculation, and institute nutrition therapy to prevent single and generalized nutrient deficiencies and promote repair and healing. Newer therapies are designed to modulate the inflammatory response itself to minimize its injury potential and promote tissue repair and recovery of the patient. Genetic regulation of metabolism is also a pathogenetic mechanism. Its role in these responses is just starting to be understood--new therapies will need to await this understanding. Once the patient begins to recover, rehabilitation tends to be long and problematic. Nonetheless, significant survival rates are now occurring, with continued improvements expected in response to the newer therapeutic approaches. Planned rehabilitation thus becomes an important component of effective recovery. Professionals trained in critical care and well versed in cellular and molecular biology provide the milieu within which continued improvements in prevention, therapy, and outcome will continue to occur.

Combined Modality Therapy↗
PubMed1991

Role of granulocyte elastase in tissue injury in patients with septic shock complicated by multiple-organ failure.

To better understand the role of granulocyte elastase (GE) in mediating tissue injury during sepsis, GE levels were measured in plasma and bronchoalveolar lavage fluid (BALF) in patients with septic shock (n = 16) and hemorrhagic shock (n = 30). Granulocyte elastase levels were compared to levels of alpha 1-protease inhibitor (alpha 1-PI). Results show that although plasma GE-alpha 1-PI complex was initially elevated in patients with hemorrhagic and septic shock, elevations in plasma GE-alpha 1-PI complex (831 +/- 241 micrograms/L) persisted in septic shock patients. alpha 1-Protease inhibitor levels in serum were increased, resulting in an inhibition of serum GE activity. Granulocyte elastase activity in BALF, however, was significantly higher in those patients with septic, as compared to hemorrhagic shock (31.4 +/- 25.8 versus 3.7 +/- 4.0 U/L, respectively). In addition GE levels were compared to other parameters, including respiratory index, blood neutrophil count, and plasma levels of endotoxin, fibronectin, and coagulation factor XIII. Significant correlations were observed between GE-alpha 1-PI and increased endotoxin concentration and decreased fibronectin and coagulation factor XIII levels. Significant correlation was found also between GE activity in BALF and respiratory index. These findings suggest that severe tissue damage occurred in patients with septic shock complicated by multiple-organ failure. Although GE activity appeared to be adequately inhibited by alpha 1-PI in blood, increased GE activity in local tissues, such as lung alveoli, may be responsible for significant local tissue injury during septic shock.

Bronchoalveolar Lavage Fluid↗
PubMed1992

Septic shock, multiple organ failure, and disseminated intravascular coagulation. Compared patterns of antithrombin III, protein C, and protein S deficiencies.

STUDY OBJECTIVE: Our aim was to document the following in patients with septic shock and disseminated intravascular coagulation (DIC): (1) the influence of DIC in the mortality rate and the occurrence of organ failure; (2) the comparative prognostic value of initial antithrombin III (ATIII), protein C (PC), and protein S (PS) levels; and (3) the compared pattern of sequential ATIII, PC, and PS levels according to clinical outcome. DESIGN: Demographic data, criteria of severity, mortality in ICU, frequency of organ failure, hemodynamic and oxygenation parameters, and laboratory findings were compared in patients with septic shock according to the occurrence of DIC. Initial and sequential levels of ATIII (activity), PC (antigen and activity), PS (total and free), and C4b binding protein (C4bBP) were compared according to the outcome in patients with DIC. PATIENTS: Sixty patients with septic shock were studied. Forty-four entered the group DIC+; 16 entered the group DIC-. RESULTS: Simplified acute physiologic score (SAPS), frequency of acquired organ failure, blood lactate, and transaminase values were significantly higher in the group DIC+. The mortality rate reached 77 percent in group DIC+ vs 32 percent in DIC- (p less than 0.001). In patients with DIC, a fatal outcome was associated with higher bilirubin and transaminase levels, lower PaO2/FIo2 ratio, Vo2, Do2 and O2 extraction. In the group DIC+, all patients but two had severe deficiencies in ATIII and PC levels. Significant correlations were found between initial ATIII and PC levels, PC and free PS levels, and free PS and C4bBP levels. Initial ATIII levels had the best prognostic value for prediction of subsequent death. Serial measurements were consistent with a prolonged ATIII and PC deficiency with significantly different levels between survivors and nonsurvivors. CONCLUSIONS: DIC is a strong predictor of death and multiple organ failure in patients with septic shock. Sequential ATIII, PC, and PS measurements were consistent with prolonged consumption or inhibition that might account for a sustained procoagulant state and inhibition of fibrinolysis. The initial ATIII level was the best laboratory predictor of death in these patients.

Antithrombin III Deficiency↗
PubMed2006

Decreased progression of postinjury lung dysfunction to the acute respiratory distress syndrome and multiple organ failure.

BACKGROUND: Postinjury organ dysfunction is a result of unbridled systemic hyperinflammation. According to the two-event construct, patients are resuscitated into an early vulnerable window of systemic hyperinflammation (primed) in which a second otherwise innocuous event precipitates uncontrolled hyperinflammation, leading to secondary organ damage and dysfunction (activated). Recent efforts to decrease postinjury morbidity have focused on limiting the potential of second events and systemic inflammation. We hypothesized that the collective effects of recently implemented therapeutic strategies have resulted in decreased activation of the systemic inflammatory response relative to priming in recent years. METHODS: Data were collected prospectively on trauma patients at risk for postinjury multiple organ failure (MOF). Inclusion criteria were age >15 years, trauma intensive care unit admission, Injury Severity Score >15 and survival >48 hours. Isolated head injuries and head injuries with an extracranial abbreviated injury score <2 were excluded. Daily physiologic and laboratory data were collected through surgical intensive care unit day 28, and clinical events were recorded thereafter until death or hospital discharge. Organ failure was characterized with the use of the Denver MOF Scale. Acute respiratory distress syndrome (ARDS) was defined according to the consensus definition. RESULTS: Over a 6.5-year period 897 patients were studied; 271 (31%) developed ARDS, and 226 (25%) developed MOF. Early lung dysfunction, as a measure of systemic priming, did not change over the study period. In contrast, the incidence of ARDS and MOF decreased from 43% to 25% and 33% to 12%, respectively. The incidence of early MOF decreased from 22% to 7% over the study period. CONCLUSIONS: Priming of the postinjury inflammatory response is an early event and is primarily influenced by the injury itself. Recent advances in postinjury care such as judicious blood transfusion, lung protective ventilation, treatment of adrenal insufficiency, and tight glucose control are known to attenuate systemic inflammation. Step-wise adoption of these therapies is coincident with a decrease in the destructive processes resulting in ARDS and MOF. The global effect is a decrease in activation of the systemic inflammatory response over recent years.

Adult↗
PubMed1999

Cardiopulmonary bypass renders patients at risk for multiple organ failure via early neutrophil priming and late neutrophil disability.

BACKGROUND: Cardiopulmonary bypass (CPB) is associated with a systemic inflammatory response syndrome (SIRS) and these patients are recognized to be at increased risk for delayed infectious complications. We have documented that circulating neutrophils (PMNs) from patients manifesting SIRS have evidence of early postinjury priming for cytotoxicity. Consequently, we hypothesized that CPB would result in early postoperative PMN hyperresponsiveness (priming). MATERIALS AND METHODS: Six patients (mean age 50 +/- 2.9 years) who underwent CPB for CABG had sequential blood samples obtained perioperatively. PMNs were isolated and superoxide anion (O(-)(2)) generation (nmol O(-)(2)/3.75 x 10(5) PMNs/min) was measured by reduction of cytochrome c after exposure to fMLP, C5a, or PMA; elastase release (% total PMN elastase content) was measured by cleavage of AAPV-pNA after exposure to fMLP or C5a. RESULTS: PMNs were activated for increased elastase release 6 h after initiation of CPB. Significant PMN priming for O(-)(2) production was discovered at 3, 6, and 12 h following CPB and for elastase release at 3 and 6 h after CPB. At 2 to 3 days after CPB, O(-)(2) generation was significantly less than that of the preoperative control. Neutrophil primability with PAF was detected at 6 h after CPB. A similar defect in PAF-primable O(-)(2) production was seen 2 and 3 days post-CPB. Direct PMN interrogation with the receptor-independent activator PMA revealed loss of integrity of the NADPH oxidase at 2 and 3 days following CPB. CONCLUSIONS: A vulnerable window exists between 3 and 12 h after CPB when PMNs are primed for enhanced cytotoxicity via O(-)(2) production and elastase release. Paradoxically, PMN oxidase integrity becomes deficient 48 h post-CPB, while protease degranulation remains intact. These events render the bypass patient at risk for multiple organ failure via both early PMN-mediated tissue injury and delayed infectious complications.

Adolescent↗