Multiple Organ Failure In Patients Research Articles

Harnessing HLA‐E‐restricted CD8 T lymphocytes for adoptive cell therapy of patients with severe COVID‐19

SARS-CoV-2 is spreading worldwide, and is a pandemic virus that has infected almost 5 million individuals and causing 300.000 deaths, as of mid-May 2020. Because SARS-CoV-2 is a new virus in humans there are currently no vaccines, monoclonal antibodies (mAbs) or even effective drugs available. Human convalescent plasma transfusion is an option for either prophylactic or therapeutic treatment of COVID-19 patients, but its administration to patients who are affected by severe pulmonary disease is associated with increased risk of transfusion-related acute lung injury (TRALI).

Hyperhomocysteinemia Associated with Multiple Organ Failure in Acute Pancreatitis Patients.

Objective This study aimed to evaluate the potential effect of hyperhomocysteinemia on multiple organ failure (MOF) in patients with acute pancreatitis (AP). Method In this cohort study, a total of 1880 AP patients were enrolled and divided into the hyperhomocysteinemia group (study group) and the control group based on serum homocysteine (HCY) levels. Clinical data including demographics, clinical outcomes, and characteristics were collected for analysis. Risk factors of MOF in AP patients were determined by univariate and multivariate logistic regression analyses. Results The hyperhomocysteinemia group showed higher multiple organ failure rates (31.83% vs 20.77%, P < 0.001), compared with the control group. A positive correlation between homocysteine level and APACHE II score was obtained by Pearson correlation analysis (r = 0.420, P < 0.001), compared with the control group. A positive correlation between homocysteine level and APACHE II score was obtained by Pearson correlation analysis (P < 0.001), compared with the control group. A positive correlation between homocysteine level and APACHE II score was obtained by Pearson correlation analysis (Conclusion A high serum homocysteine level may be an independent risk factor of multiple organ failure in patients with acute pancreatitis.

Immunity and Its Effect on the Incidence of Multiple Organ Failure in Patients after the Heart Surgery

The purpose of the study is to identify the components of immunity, which might predict the development of multiple organ failure in patients after heart surgery.Material and methods. The study included 40 patients who were operated in cardiac surgery Department. The inclusion criteria were the presence of indications for cardiac surgery. The exclusion criteria were the presence of infective endocarditis in patients. Before the operation and after 24 hours we studied the blood level of leukocytes and lymphocytes. We analyzed the phenotype of immune cells using monoclonal antibodies, serum levels of procalcitonin and C3 and C4 complement components. All patients were evaluated for multiple organ disfunction (MOD) using the SOFA scale.The results showed that cardiac surgery leads to the development of MOD, statistically significant multidirectional changes in both quantitative and qualitative composition of all cells of the immune system, significant changes in the level of C3 and C4 components of the cascade of complement and plasma level of pro-calcitonin. ROC analysis was revealed that the relative content of monocytes is less than 7.1% of the number of leukocytes as well as the absolute content of monocytes with the CD14 + HLA-DR + phenotype less than 0.32_109/l in the preoperative period, and the C3 level of the complement component less than 0.52 g/l, as well as the maximum SOFA score in the postoperative period, were the best predictors of MOD after the procedures.Conclusion. The components of innate immunity make it possible to predict the complication of the cardiac surgery, earlier than the SOFA scale.

Plasma mitochondrial DNA level as an early marker of systemic inflammatory response syndrome and organ failure in patients undergoing cardiac surgery

Aim. To assess whether plasma mitochondrial DNA (mtDNA) levels in the early postoperative period can predict the development of systemic inflammatory response syndrome (SIRS) and multiple organ failure in patients undergoing cardiac surgery. Methods. This pilot, prospective, observational, cohort study included 85 patients undergoing cardiac surgery. Plasma mtDNA levels were determined immediately after the surgery, and the development of SIRS, acute kidney injury, acute heart failure, and adult respiratory distress syndrome was assessed. Results. The mtDNA levels showed good potential for predicting the development of SIRS within 1-2 days after the surgery (area under the curve = 0.74). Regarding the cut-off point, a mtDNA level of &gt;0.54 ng/mL predicted the development of SIRS in the early postoperative period with a sensitivity of 73.7% and a specificity of 66%. The odds ratio for the development of acute kidney injury with/without SIRS was 3.4 [confidence interval (CI) = 1.27–9.08; p = 0.0149]; acute heart failure, 5.7 (CI = 2.20–14.84; p = 0.0003); and adult respiratory distress syndrome, 3.6 (CI = 1.01–11.10; p = 0.047). Conclusion. The plasma mtDNA levels in the early postoperative period can be used as a predictive marker for the development of SIRS and multiple organ failure in patients undergoing cardiac surgery. Moreover, SIRS is associated with the development of acute kidney injury, acute heart failure, and adult respiratory distress syndrome. Received 25 March 2019. Revised 3 April 2019. Accepted 8 April 2019. Funding: The study did not have sponsorship. Conflict of interest: Authors declare no conflict of interest.

Autophagy and mitochondrial biogenesis impairment contribute to age‐dependent liver injury in experimental sepsis: dysregulation of AMP‐activated protein kinase pathway

Age is an independent risk factor of multiple organ failure in patients with sepsis. However, the age-related mechanisms of injury are not known. AMPK is a crucial regulator of energy homeostasis, which controls mitochondrial biogenesis by activation of peroxisome proliferator-activated receptor-γ coactivator-α (PGC-1α) and disposal of defective organelles by autophagy. We investigated whether AMPK dysregulation might contribute to age-dependent liver injury in young (2-3 mo) and mature male mice (11-13 mo) subjected to sepsis. Liver damage was higher in mature mice than in young mice and was associated with impairment of hepatocyte mitochondrial function, structure, and biogenesis and reduced autophagy. At molecular analysis, there was a time-dependent nuclear translocation of the active phosphorylated catalytic subunits AMPKα1/α2 and PGC-1α in young, but not in mature, mice after sepsis. Treatment with the AMPK activator 5-amino-4-imidazolecarboxamide riboside-1-β-d-ribofuranoside (AICAR) improved liver mitochondrial structure in both age groups compared with vehicle. In loss-of-function studies, young knockout mice with systemic deficiency of AMPKα1 exhibited greater liver injury than did wild-type mice after sepsis. Our study suggests that AMPK is important for liver metabolic recovery during sepsis. Although its function may diminish with age, pharmacological activation of AMPK may be of therapeutic benefit.-Inata, Y., Kikuchi, S., Samraj, R. S., Hake, P. W., O'Connor, M., Ledford, J. R., O'Connor, J., Lahni, P., Wolfe, V., Piraino, G., Zingarelli, B. Autophagy and mitochondrial biogenesis impairment contribute to age-dependent liver injury in experimental sepsis: dysregulation of AMP-activated protein kinase pathway.

Acute-on-Chronic Liver Failure with Complicating Pancreatitis After Autochthonous Hepatitis E Infection

: Hepatitis E virus infection (HEV) is the most common cause of acute viral hepatitis in the world. Genotypes 1 and 2 are responsible for large outbreaks and sporadic cases in the developing countries, whereas genotypes 3 and 4 are zoonotic infections and cause sporadic autochthonous disease with usually mild course in the immunocompetent host without preexisting liver damage. Acute pancreatitis is acknowledged as an extrahepatic complication of acute viral hepatitis, most often related to acute hepatitis A to C. More than 50 cases of HEV-associated acute pancreatitis are reported from South Asia where HEV genotype 1 prevails. The current study reports the case of an 85-year-old male with autochthonous acute HEV infection, which progressed into acute-on-chronic liver failure (ACLF) and was complicated by severe acute pancreatitis. This case underlines autochthonous HEV infection as a cause of multiple organ failure in patients with pre-existing liver disease and suggests an association with acute pancreatitis. Clinicians should be aware of life-threatening complications of autochthonous HEV infection, especially in patients with cirrhosis.

Age-Dependent Changes in AMPK Metabolic Pathways in the Lung in a Mouse Model of Hemorrhagic Shock.

The development of multiple organ failure in patients with hemorrhagic shock is significantly influenced by patient age. Adenosine monophosphate-activated protein kinase (AMPK) is a crucial regulator of energy homeostasis, which coordinates metabolic repair during cellular stress. We investigated whether AMPK-regulated signaling pathways are age-dependent in hemorrhage-induced lung injury and whether AMPK activation by 5-amino-4-imidazole carboxamide riboside (AICAR) affords lung protective effects. Male C57/BL6 young mice (3-5 mo), mature adult mice (9-12 mo), and young AMPKα1 knockout mice (3-5 mo) were subjected to hemorrhagic shock by blood withdrawing, followed by resuscitation with shed blood and lactated Ringer's solution. Plasma proinflammatory cytokines were similarly elevated in C57/BL6 young and mature adult mice after hemorrhagic shock. However, mature adult mice exhibited more severe lung edema and neutrophil infiltration, and higher mitochondrial damage in alveolar epithelial type II cells, than did young mice. No change in autophagy was observed. At molecular analysis, the phosphorylation of the catalytic subunit AMPKα1 was associated with nuclear translocation of peroxisome proliferator-activated receptor γ co-activator-α in young, but not mature, adult mice. Treatment with AICAR ameliorated the disruption of lung architecture in mice of both ages; however, effects in mature adult mice were different than young mice and also involved inhibition of nuclear factor-κB. In young AMPKα1 knockout mice, AICAR failed to improve hypotension and lung neutrophil infiltration. Our data demonstrate that during hemorrhagic shock, AMPK-dependent metabolic repair mechanisms are important for mitigating lung injury. However, these mechanisms are less competent with age.

Endothelial adhesion molecules and multiple organ failure in patients with severe sepsis

ObjectiveTo determine if serum levels of endothelial adhesion molecules were associated with the development of multiple organ failure (MOF) and in-hospital mortality in adult patients with severe sepsis. DesignThis study was a secondary data analysis of a prospective cohort study. SettingPatients were admitted to two tertiary intensive care units in San Antonio, TX, between 2007 and 2012. PatientsPatients with severe sepsis at the time of intensive care unit (ICU) admission were enrolled. Inclusion criteria were consistent with previously published criteria for severe sepsis or septic shock in adults. Exclusion criteria included immunosuppressive medications or conditions. InterventionsNone. MeasurementsBaseline serum levels of the following endothelial cell adhesion molecules were measured within the first 72h of ICU admission: Intracellular Adhesion Molecule 1 (ICAM-1), Vascular Cell Adhesion Molecule-1 (VCAM-1), and Vascular Endothelial Growth Factor (VEGF). The primary and secondary outcomes were development of MOF (⩾2 organ dysfunction) and in-hospital mortality, respectively. Main resultsForty-eight patients were enrolled in this study, of which 29 (60%) developed MOF. Patients that developed MOF had higher levels of VCAM-1 (p=0.01) and ICAM-1 (p=0.01), but not VEGF (p=0.70) compared with patients without MOF (single organ failure only). The area under the curve (AUC) to predict MOF according to VCAM-1, ICAM-1 and VEGF was 0.71, 0.73, and 0.54, respectively. Only increased VCAM-1 levels were associated with in-hospital mortality (p=0.03). These associations were maintained even after adjusting for APACHE and SOFA scores using logistic regression. ConclusionsHigh levels of serum ICAM-1 was associated with the development of MOF. High levels of VCAM-1 was associated with both MOF and in-hospital mortality.

Impact of Serum Triglycerides on Clinical Outcomes in Acute Pancreatitis: Findings from a Regional Integrated Healthcare System

Introduction: Hypertriglyceridemia is an established risk factor for acute pancreatitis. This study seeks to evaluate the effect of serum triglycerides on the development of persistent or multiple organ failure in patients with acute pancreatitis. Methods: A retrospective cohort study was conducted using data from an integrated healthcare system. Patients hospitalized for acute pancreatitis between January 1, 2006 and December 31, 2013 were included in the study. Triglyceride levels measured prior to and within 72 hours of admission were compared. In addition, the impact of serum triglycerides on the development of persistent or multiple organ failure during hospitalization for acute pancreatitis was assessed using Poisson regression models adjusting for age and sex. Results: Among 2,519 patients, 267 patients (10.6%) developed organ failure, of which 75 patients (28.1%) developed multiple system organ failure and 82 patients (30.7%) developed persistent organ failure. Serum triglyceride levels in patients who developed organ failure were initially much higher than in patients who did not develop organ failure, but by 72 hours into the admission, approached levels of the patients who did not develop organ failure. Approximately 7% of patients had very high serum triglyceride levels (>500 mg/dL), which correlated with similarly high triglycerides levels prior to admission. Conclusion: Increased TG levels were associated with the development of multiple or persistent organ failure in this study of patients hospitalized with acute pancreatitis. Patients with high triglyceride levels at the time of admission for acute pancreatitis were likely to have high triglyceride levels prior to admission.

A modified Sequential Organ Failure Assessment score using the Richmond Agitation-Sedation Scale in critically ill patients.

In the January 2016 issue of Critical Care Medicine , Vasilevskis et al . (1) reported the validation study of a modified Sequential Organ Failure Assessment (SOFA) score using the Richmond Agitation-Sedation Scale (RASS) (2) instead of the Glasgow Coma Scale (GCS) for the neurological component. As explained by the authors, the SOFA score, first shown to describe multiple organ failure in patients with sepsis, is now widely used for risk stratification in a wide panel of ICU patients. Unfortunately, the GCS component is subject to implementation difficulties for some patients, such as those who are intubated, and is not highly reliable when assessing neurologic disorders such as delirium and agitation.

Impact of bacterial sepsis on organ failure in patients with liver cirrhosis

Objective The aim of this study was to examine the evidence for impact of bacterial sepsis and multiple organ failure in patients with liver cirrhosis. Data sources A review of contemporary (1995 to present) English medical literature using the terms bacterial infection, hepatic encephalopathy, multiple organ dysfunction, and spontaneous bacterial peritonitis was conducted. Study selection Abstracts were reviewed independently by two authors, and relevant articles were then evaluated. Exclusion criteria included editorials, non-English language, comments, and letters. Data extraction Level of evidence was assigned in accordance with the Oxford Center for Evidence-based Medicine guidance (levels I-V). Results Thirty-seven articles met the inclusion criteria; of which, 11 were of level III, 22 of level IV, and four of level V evidence. Bacterial sepsis and multiple organ failure are common in patients with liver cirrhosis. There was level III evidence that third-generation cephalosporins are the treatment of choice for infections in patients with liver cirrhosis. Conclusion This review indicates that bacterial sepsis and multiple organ failure are common in patients with liver cirrhosis, supported principally by level III/IV evidence.

Abdominal sepsis and oxidative stress

Oxidative stress deserves special attention in the pathogenesis of sepsis. The study included 96 patients with abdominal sepsis caused by advanced suppurative peritonitis and destructive pancreatitis. All patients were divided into 3 groups depending on the severity of sepsis. Level of malondialdehyde (MDA) was determined to evaluate the intensity of lipid peroxidation (LPO). Proteins oxidative modification was assessed according to level of sulfhydryl groups (SH-groups) and carbonyls in proteins. State of anti-oxidant system (AOS) was defined based on activity of catalase, peroxidase, superoxide dismutase and glutathione peroxidase in erythrocytes. There was no relationship between severity of multiple organ failure, MDA concentration, SH-groups and anti-oxidant enzymes levels. At the same time positive correlation between severity of multiple organ failure and carbonyls content in proteins was revealed. In surgical patients sepsis develops on background of oxidative stress. Significant reduction of SH-groups in proteins by the moment of sepsis diagnosis is an unfavorable factor for outcome. The degree of multiple organ failure in patients with abdominal sepsis correlates with oxidative injury of proteinic structures.

Strongyloidosis, Cause of Multiple Organ Failure in Patients with Renal Transplantation

Strongyloidosis, Cause of Multiple Organ Failure in Patients with Renal Transplantation

0733. Impact of endotoxin challenge on disseminated intravascular coagulation in obese minipigs

An early activation of coagulation and fibrinolysis occurs during sepsis and results in a marked increase of thrombin and fibrin formation, leading to the syndrome of disseminated intravascular coagulation (DIC). DIC is a strong predictor of death and multiple organ failure in patients with septic shock [1]. Obesity has been demonstrated to be a hypercoagulable [2] and hypofibrinolytic [3] state but its impact on coagulation and fibrinolysis during sepsis has never been studied.

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Introduction: Hemophagocytic lymphohistiocytosis (HLH) is a syndrome of pathologic immune activation. The clinical phenotype of HLH-induced multiple organ failure (MOF) is very similar to other phenotypes of MOF in critically ill children such as thrombocytopenia-associated MOF (TAMOF) syndrome and immune paralysis/lymphoid depletion syndrome. Methods: We reviewed consecutive autopsy reports of children who died with a diagnosis of HLH between 2005-2012 in a tertiary care university-based pediatric hospital. Two autopsies were limited - one with liver/spleen/bone marrow, and the other with chest/abdomen. Results: Twelve autopsy reports were analyzed. All patients had received treatment with dexamethosone and etoposide. 83.3% (10/12) of patients met criteria for TAMOF at death: platelet count < 100K/mm3 and at least 3 failing organs. 60% (6/10) of patients who met criteria for TAMOF had evidence of microvascular thrombosis on autopsy, 50% (3/6) had evidence of microvascular thrombosis in more than one organ: 2/6 brain, 2/6 heart, 1/6 in lungs, 1/6 in liver, 3/6 in kidneys, 1/6 in pancreas and 2/6 in spleen. Two thirds (4/6) patients also had hypocellular bone marrow. Of the 4 patients who met criteria for TAMOF without microvascular thrombosis on autopsy, 3 had hypocellular bone marrow and one had occlusive aggregates of septated hyphae in blood vessels and no bone marrow was obtained at autopsy. 83% (10/12) of patients had evidence of infection at time of autopsy, categorized as: bacterial (58%), viral (50%), fungal (42%), and 42% of patients had infections in more than one category. 50% (6/12) of patients had lymphocyte depletion in spleen, thymus or bone marrow, and 66% (4/6) of whom were chronically lymphopenic (>7 days absolute lymphocyte count <1000/microliter), and 83% (5/6) with infection on autopsy. Conclusions: Many patients who died with HLH have 1) clinical evidence of TAMOF syndrome and autopsy evidence of disseminated microvascular thrombosis and 2) clinical lymphopenia and autopsy evidence of lymphoid depletion and unresolved infection. These autopsy findings suggest that MOF in patients with HLH is complex with overlapping MOF phenotypes. Further studies are warranted.

Protective Mechanisms Of Inter-Alpha Inhibitor Protein On Extracellular Histone Toxicity

Sepsis is almost invariably associated with hemostatic abnormalities ranging from isolated thrombocytopenia to acute disseminated intravascular coagulation (DIC). Recent evidence indicates that extracellular histones are important mediators and therapeutic targets in sepsis, inflammation and thrombosis. Baboons challenged with E. coli release large amounts of histones into systemic blood circulation. Conversely, infusion of histones into mice and baboons directly induces an inflammatory response, fibrin and platelet deposition in the tissues, leading to organ failure and death. In vitro, histones cytotoxicity is significantly decreased in the presence of plasma or serum. Here, we demonstrate that Inter-alpha Inhibitor Protein (IAIP), an abundant plasma protein, effectively neutralizes the cytotoxic effects of histones and decreases platelet aggregation in vitro and in vivo. IAIP consists of three polypeptides: two heavy chains (HC) and one light chain called bikunin. Bikunin, which has anti-proteolytic activity, carries a chondroitin sulfate (CS) chain to which the heavy chains are covalently linked. The heavy chains can be transferred from IAIP to hyaluronan (HA) and become covalently linked to form HC-HA complex. The mechanism of histone inhibition by IAIP is unclear. Since histones are cationic molecules and can be electrostatically attracted to the negatively charged glycosaminoglycans, we hypothesize that the inhibitory activity of IAIP against histone toxicity could be at least in part mediated by HA and CS. The major aim of this study is to investigate the interaction of IAIP and its components (bikunin, CS, and HA) with histones and to validate the protective effect of IAIP against histone induced thrombocytopenia, prolonged bleeding time, and organ injury.We first determined the effect of the different components of IAIP on histone-induced toxicity, by incubating HL60 cells with histones +/- IAIP, CS, high molecular weight HA (HMW-HA) or bikunin. Cell damage was measured by flow cytometry for propidium iodide (PI) staining. We also tested the effects of IAIP, CS, HMW-HA, and CS on histone-induced platelet aggregation. Interestingly, IAIP, HMW-HA and CS, but not bikunin prevented histone-induced toxicity and platelet aggregation in a concentration dependent manner. Next, we determined if HA or CS are partly responsible for the protective effect of IAIP by pre-incubating IAIP with hyaluronidase or chondoritinase. Hyaluronidase, but not chondoritinase, slightly decreased the protective effects of IAIP on histone-induced platelet aggregation and cytotoxicity, suggesting that HA has a partial role. In addition, using BIACORE 3000, we proved that both IAIP and HMW HA bind to recombinant histone H4 in a dose dependent manner.To validate the protective effect against histone toxicity in vivo, we injected C57BL/6 mice with intravenous calf thymus histones (50 mg/kg) with/without IAIP (50 mg/kg) or HMW HA (90 mg/kg). Platelets were measured before and 30 minutes after histone challenge. As expected, mice injected with only histones developed severe thrombocytopenia (up to ∼ 90%) and prolonged bleeding time (> 10 minutes). Co-injecting mice with histones and IAIP or HMW HA significantly reduced histone-induced thrombocytopenia, with platelet consumption of 82% in the histone-only group versus 37% in the histone + IAIP group and 23% in the histone + HMW-HA group. Both treatments also reduced tail bleeding time from 10 minutes for histone only group to 2.4 minutes in histone + IAIP group and 2.2 minutes for histone + HMW-HA. In addition, mice co-injected with histones and IAIP or HMW HA had significantly reduced proinflammatory cytokine levels (IL-1β, IL-6, TNF-α, KC, MCP-1) and lung injury markers, such as decreased neutrophil infiltration, decreased fibrin deposition and microvascular thrombosis, as noted by immunofluorescence and electron microscopy.In conclusion, our data demonstrate that IAIP and HMW-HA could protect against histone-induced cytotoxicity, platelet activation and microthrombosis, prevent thrombocytopenia and prolonged bleeding time, and protect against systemic inflammation and organ injury. It is likely that IAIP protective effects are at least partially mediated by the HA associated with this protein. Our data suggest that IAIP and HMW-HA could be developed as novel therapies for multiple organ failure in patients with sepsis and trauma. Disclosures:No relevant conflicts of interest to declare.

Efficiency of substitutive renal therapy in the complex intensive care of multiple organ failure in patients with polytrauma

This study was to evaluate the efficiency of the early start of intermittent substitutive renal therapy in patients with polytrauma complicated by multiple organ failure syndrome.

Effects of the Antioxidant-Enriched Concentrated Liquid Diet ANOM on Oxidative Stress and Multiple Organ Injury in Patients with Septic Shock: A Pilot Study

Purpose: In patients with septic shock, excessive production of reactive oxygen species (ROS) by activated neutrophils injures the vascular endothelium. The body responds by recruiting systemic antioxidants, among which vitamin C most rapidly responds. Excessive and prolonged ROS production quickly depletes vitamin C, which is not synthesized by the human body. To improve the prognosis of patients with septic shock, we evaluated the ability of an antioxidant-enriched liquid diet to alleviate oxidative stress and multiple organ failure. Methods: We evaluated 15 patients with septic shock complicated by multiple organ failure who underwent treatment with ANOM® (antioxidant-enriched concentrated liquid diet, Otsuka Pharmaceutical Co, Tokushima, Japan). Vitamin C concentration was determined by measuring serum levels of vitamin C radicals (VCR) with electron spin resonance (ESR) spectroscopy. Results: Serum VCR concentration was significantly increased from the baseline level of 0.155±0.026 after 1 day of ANOM infusion, reaching the normal range at day 3, and 0.642±0.059 at day 7. Serum 8-hydroxydeoxyguanosine (8-OHdG) concentration, a measure of ROS-induced oxidative injury, was 0.495±0.061 ng/mL at day 7, which was significantly lower than the baseline level of 0.896±0.065 ng/mL. The Sepsis-related Organ Failure Assessment (SOFA) score, a measure of multiple organ failure, decreased significantly from 10.9±1.9 at baseline to 6.2±1.7 at day 7. Conclusions: These findings show that ANOM rapidly restores vitamin C levels, suggesting that it protects against excessive oxidative stress and alleviates multiple organ failure in patients with septic shock.

Iron metabolism disturbance as a marker of the severity of pathology in resuscitation patients

Forty-eight patients of resuscitation wards were examined, including 15 patients with purulent peritonitis, 12 patients with acute pancreatitis, 11 patients with thermal skin damages, and 10 patients with severe acetic acid intoxication. An increase in the serum iron, ferritin, and free hemoglobin contents of blood plasma influenced the severity of endotoxicosis. This was expressed in progressive fever, increase in the leukocytic intoxication index and concentrations of low-and middle-molecular-weight substances on erythrocytes and in the blood plasma, intensification of lipid peroxidation, and insufficiency of the antioxidant defense system, which resulted in the development of multiple organ failure in patients with the above-mentioned diseases.

Invasive pulmonary aspergillosis in patients with decompensated cirrhosis: case series

BackgroundOpportunistic invasive fungal infections are increasingly frequent in intensive care patients. Their clinical spectrum goes beyond the patients with malignancies, and for example invasive pulmonary aspergillosis has recently been described in critically ill patients without such condition. Liver failure has been suspected to be a risk factor for aspergillosis.Case presentationWe describe three cases of adult respiratory distress syndrome with sepsis, shock and multiple organ failure in patients with severe liver failure among whom two had positive Aspergillus antigenemia and one had a positive Aspergillus serology. In all cases bronchoalveolar lavage fluid was positive for Aspergillus fumigatus. Outcome was fatal in all cases despite treatment with voriconazole and agressive symptomatic treatment.ConclusionInvasive aspergillosis should be among rapidly raised hypothesis in cirrhotic patients developing acute respiratory symptoms and alveolar opacities.